@article{Shadrin:2015,
	Abstract = {Cardiac cell therapies involving bone marrow-derived human mesenchymal stem cells (hMSCs) have shown promising results, although their mechanisms of action are still poorly understood. Here, we investigated direct interactions between hMSCs and cardiomyocytes in vitro. Using a genetic Ca(2+) indicator gCaMP3 to efficiently label hMSCs in co-cultures with neonatal rat ventricular myocytes (NRVMs), we determined that 25-40% of hMSCs (from 4 independent donors) acquired periodic Ca(2+) transients and cardiac markers through spontaneous fusion with NRVMs. Sharp electrode and voltage-clamp recordings in fused cells showed action potential properties and Ca(2+) current amplitudes in between those of non-fused hMSCs and NRVMs. Time-lapse video-microscopy revealed the first direct evidence of active fusion between hMSCs and NRVMs within several hours of co-culture. Application of blebbistatin, nifedipine or verapamil caused complete and reversible inhibition of fusion, suggesting potential roles for actomyosin bridging and Ca(2+) channels in the fusion process. Immunostaining for Cx43, Ki67, and sarcomeric α-actinin showed that fused cells remain strongly coupled to surrounding NRVMs, but downregulate sarcomeric structures over time, acquiring a non-proliferative and non-contractile phenotype. Overall, these results describe the phenotype and mechanisms of hybrid cell formation via fusion of hMSCs and cardiomyocytes with potential implications for cardiac cell therapy. },
	Author = {Shadrin, Ilya Y and Yoon, Woohyun and Li, Liqing and Shepherd, Neal and Bursac, Nenad},
	Date-Added = {2018-07-16 22:01:58 +0000},
	Date-Modified = {2018-07-16 22:01:58 +0000},
	Doi = {10.1038/srep12043},
	Journal = {Sci Rep},
	Journal-Full = {Scientific reports},
	Mesh = {Actinin; Action Potentials; Animals; Caffeine; Calcium; Calcium Channels, L-Type; Cell Fusion; Cell Movement; Cells, Cultured; Coculture Techniques; Connexin 43; Humans; Ions; Mesenchymal Stromal Cells; Microscopy, Video; Myocytes, Cardiac; Myosin Type II; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Time-Lapse Imaging; Troponin T},
	Month = {Jul},
	Pages = {12043},
	Pmc = {PMC4498233},
	pmid = {26159124},
	Pst = {epublish},
	Title = {Rapid fusion between mesenchymal stem cells and cardiomyocytes yields electrically active, non-contractile hybrid cells},
	Volume = {5},
	Year = {2015},
	url = {papers/Shadrin_SciRep2015.pdf}}

@article{De-Biase:2017,
	Abstract = {Microglia play critical roles in tissue homeostasis and can also modulate neuronal function and synaptic connectivity. In contrast to astrocytes and oligodendrocytes, which arise from multiple progenitor pools, microglia arise from yolk sac progenitors and are widely considered to be equivalent throughout the CNS. However, little is known about basic properties of deep brain microglia, such as those within the basal ganglia (BG). Here, we show that microglial anatomical features, lysosome content, membrane properties, and transcriptomes differ significantly across BG nuclei. Region-specific phenotypes of BG microglia emerged during the second postnatal week and were re-established following genetic or pharmacological microglial ablation and repopulation in the adult, indicating that local cues play an ongoing role in shaping microglial diversity. These findings demonstrate that microglia in the healthy brain exhibit a spectrum of distinct functional states and provide a critical foundation for defining microglial contributions to BG circuit function.},
	Author = {De Biase, Lindsay M and Schuebel, Kornel E and Fusfeld, Zachary H and Jair, Kamwing and Hawes, Isobel A and Cimbro, Raffaello and Zhang, Hai-Ying and Liu, Qing-Rong and Shen, Hui and Xi, Zheng-Xiong and Goldman, David and Bonci, Antonello},
	Date-Added = {2018-02-28 22:15:11 +0000},
	Date-Modified = {2018-02-28 22:15:11 +0000},
	Doi = {10.1016/j.neuron.2017.06.020},
	Journal = {Neuron},
	Journal-Full = {Neuron},
	Keywords = {RNA sequencing; density; development; electrophysiology; heterogeneity; microglia; morphology; nucleus accumbens; substantia nigra; ventral tegmental area},
	Mesh = {Animals; Basal Ganglia; Cues; Mice, Transgenic; Microglia; Neurons; Phenotype},
	Month = {Jul},
	Number = {2},
	Pages = {341-356.e6},
	Pmc = {PMC5754189},
	pmid = {28689984},
	Pst = {ppublish},
	Title = {Local Cues Establish and Maintain Region-Specific Phenotypes of Basal Ganglia Microglia},
	Volume = {95},
	Year = {2017},
	url = {papers/DeBiase_Neuron2017.pdf},
	Bdsk-File-2 = {papers/DeBiase_Neuron2017a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2017.06.020}}


@article{Li:2002d,
	Abstract = {We examined whether Gbx2 is required after embryonic day 9 (E9) to repress Otx2 in the cerebellar anlage and position the midbrain/hindbrain organizer. In contrast to Gbx2 null mutants, mice lacking Gbx2 in rhombomere 1 (r1) after E9 (Gbx2-CKO) are viable and develop a cerebellum. A Gbx2-independent pathway can repress Otx2 in r1 after E9. Mid/hindbrain organizer gene expression, however, continues to be dependent on Gbx2. We found that Fgf8 expression normally correlates with the isthmus where cells undergo low proliferation and that in Gbx2-CKO mutants this domain is expanded. We propose that Fgf8 permits lateral cerebellar development through repression of Otx2 and also suppresses medial cerebellar growth in Gbx2-CKO embryos. Our work has uncovered distinct requirements for Gbx2 during cerebellum formation and provided a model for how a transcription factor can play multiple roles during development.},
	Author = {Li, James Y H and Lao, Zhimin and Joyner, Alexandra L},
	Date-Added = {2018-01-24 23:14:27 +0000},
	Date-Modified = {2018-01-24 23:14:27 +0000},
	Journal = {Neuron},
	Journal-Full = {Neuron},
	Mesh = {Animals; Body Patterning; Cell Differentiation; Cerebellum; Female; Fetus; Gene Expression Regulation, Developmental; Homeodomain Proteins; Mesencephalon; Mice; Mice, Knockout; Nerve Tissue Proteins; Otx Transcription Factors; Proto-Oncogene Proteins; Rhombencephalon; Trans-Activators; Wnt Proteins; Zebrafish Proteins},
	Month = {Sep},
	Number = {1},
	Pages = {31-43},
	pmid = {12367504},
	Pst = {ppublish},
	Title = {Changing requirements for Gbx2 in development of the cerebellum and maintenance of the mid/hindbrain organizer},
	Volume = {36},
	Year = {2002},
	url = {papers/Li_Neuron2002.pdf}}


@article{Murabe:1983,
	Abstract = {Immunohistochemical studies with the use of the peroxidase-antiperoxidase (PAP) method revealed that "amoeboid microglial cells", in the brains of neonatal rats and "brain macrophages" in lesioned brains of adult rats react positively to an antiserum raised against macrophages. In brains of neonatal rats, "amoeboid microglial cells" stained by means of the PAP-method were observed in the corpus callosum, internal capsule, dorso-lateral region of the thalamus, subventricular zone of the lateral ventricle, and the subependymal layer of the ventricular system. These cellular elements were not detected in brains of rats aged 21 days or older. Resting microglial cells displaying a typical ramified structure were not specifically stained. Cells reacting positively to the macrophage antiserum appeared (i) in the cerebral cortex of adult rats following placement of a stab wound, or (ii) in the hippocampal formation after kainic acid-induced lesions; in the damaged areas immunoreactive cells exhibited the typical features of "brain macrophages". "Brain macrophages" and "amoeboid microglial cells" are considered to belong to the class of exudate macrophages derived from blood monocytes. Thus, elements of hematogenous origin do exist in the intact brain parenchyma of neonatal rats and in lesioned brains of adult rats. The relationship between brain macrophages and resting microglial cells is discussed.},
	Author = {Murabe, Y and Sano, Y},
	Date-Added = {2018-01-18 00:40:34 +0000},
	Date-Modified = {2018-01-18 00:40:34 +0000},
	Journal = {Cell Tissue Res},
	Journal-Full = {Cell and tissue research},
	Mesh = {Animals; Animals, Newborn; Brain; Immunoenzyme Techniques; Macrophages; Neuroglia; Rats},
	Number = {1},
	Pages = {85-95},
	pmid = {6339067},
	Pst = {ppublish},
	Title = {Morphological studies on neuroglia. VII. Distribution of "brain macrophages" in brains of neonatal and adult rats, as determined by means of immunohistochemistry},
	Volume = {229},
	Year = {1983}}


@article{Reep:1988,
	Abstract = {The cerebral isocortex is usually considered to be a 6-layered structure. Our anatomical findings suggest that layer VII be recognized as a distinct entity in rodent isocortex. This conclusion is based on cytoarchitectural, fiberarchitectural, connectional and developmental data.},
	Author = {Reep, R L and Goodwin, G S},
	Date-Added = {2018-01-18 00:39:05 +0000},
	Date-Modified = {2018-01-18 00:39:05 +0000},
	Journal = {Neurosci Lett},
	Journal-Full = {Neuroscience letters},
	Mesh = {Animals; Cerebral Cortex; Fluorescent Dyes; Leucine; Rats; Somatosensory Cortex; Stilbamidines; Visual Cortex},
	Month = {Jul},
	Number = {1-2},
	Pages = {15-20},
	pmid = {3412636},
	Pst = {ppublish},
	Title = {Layer VII of rodent cerebral cortex},
	Volume = {90},
	Year = {1988},
	url = {papers/Reep_NeurosciLett1988.pdf}}


@article{Minocha:2015,
	Abstract = {Guidepost cells present at and surrounding the midline provide guidance cues that orient the growing axons through commissures. Here we show that the transcription factor Nkx2.1 known to control the specification of GABAergic interneurons also regulates the differentiation of astroglia and polydendrocytes within the mouse anterior commissure (AC). Nkx2.1-positive glia were found to originate from three germinal regions of the ventral telencephalon. Nkx2.1-derived glia were observed in and around the AC region by E14.5. Thereafter, a selective cell ablation strategy showed a synergistic role of Nkx2.1-derived cells, both GABAergic interneurons and astroglia, towards the proper formation of the AC. Finally, our results reveal that the Nkx2.1-regulated cells mediate AC axon guidance through the expression of the repellent cue, Slit2. These results bring forth interesting insights about the spatial and temporal origin of midline telencephalic glia, and highlight the importance of neurons and astroglia towards the formation of midline commissures.},
	Author = {Minocha, Shilpi and Valloton, Delphine and Ypsilanti, Athena R and Fiumelli, Hubert and Allen, Elizabeth A and Yanagawa, Yuchio and Marin, Oscar and Ch{\'e}dotal, Alain and Hornung, Jean-Pierre and Lebrand, C{\'e}cile},
	Date-Added = {2018-01-16 22:49:01 +0000},
	Date-Modified = {2018-01-16 22:49:01 +0000},
	Doi = {10.1038/ncomms7887},
	Journal = {Nat Commun},
	Journal-Full = {Nature communications},
	Mesh = {Animals; Anterior Cerebellar Commissure; Astrocytes; Axons; Cell Movement; Electroporation; Embryo, Mammalian; GABAergic Neurons; Gene Expression Regulation, Developmental; Immunohistochemistry; In Vitro Techniques; Intercellular Signaling Peptides and Proteins; Interneurons; Mice; Nerve Tissue Proteins; Neuroglia; Neurons; Nuclear Proteins; Telencephalon; Thyroid Nuclear Factor 1; Transcription Factors},
	Month = {Apr},
	Pages = {6887},
	Pmc = {PMC4423212},
	pmid = {25904499},
	Pst = {epublish},
	Title = {Nkx2.1-derived astrocytes and neurons together with Slit2 are indispensable for anterior commissure formation},
	Volume = {6},
	Year = {2015},
	url = {papers/Minocha_NatCommun2015.pdf}}


@article{Srivatsa:2014,
	Abstract = {The pyramidal neurons of the mammalian neocortex form two major types of long-range connections-corticocortical and cortico-subcortical. The transcription factors Satb2 and Ctip2 are critical regulators of neuronal cell fate that control interhemispheric versus corticofugal connections respectively. Here, we investigate the axon guidance molecules downstream of Satb2 and Ctip2 that establish these connections. We show that the expression of two Netrin1 receptors- DCC and Unc5C is under direct negative regulation by Satb2 and Ctip2, respectively. Further, we show that the Netrin1-Unc5C/DCC interaction is involved in controlling the interhemispherical projection in a subset of early born, deep layer callosal neurons.},
	Author = {Srivatsa, Swathi and Parthasarathy, Srinivas and Britanova, Olga and Bormuth, Ingo and Donahoo, Amber-Lee and Ackerman, Susan L and Richards, Linda J and Tarabykin, Victor},
	Date-Added = {2018-01-16 22:48:47 +0000},
	Date-Modified = {2018-01-16 22:48:47 +0000},
	Doi = {10.1038/ncomms4708},
	Journal = {Nat Commun},
	Journal-Full = {Nature communications},
	Mesh = {Animals; Chromatin Immunoprecipitation; Corpus Callosum; DCC Receptor; DNA Primers; Electroporation; Gene Expression Regulation, Developmental; In Situ Hybridization; Luciferases; Mice; Morphogenesis; Netrin Receptors; Plasmids; Receptors, Cell Surface; Receptors, Nerve Growth Factor; Tumor Suppressor Proteins},
	Month = {Apr},
	Pages = {3708},
	Pmc = {PMC3997811},
	pmid = {24739528},
	Pst = {epublish},
	Title = {Unc5C and DCC act downstream of Ctip2 and Satb2 and contribute to corpus callosum formation},
	Volume = {5},
	Year = {2014},
	url = {papers/Srivatsa_NatCommun2014.pdf}}


@article{Sulak:2016,
	Abstract = {A major constraint on the evolution of large body sizes in animals is an increased risk of developing cancer. There is no correlation, however, between body size and cancer risk. This lack of correlation is often referred to as 'Peto's Paradox'. Here, we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Proboscidean) lineage. Furthermore, we show that several of the TP53 retrogenes (TP53RTGs) are transcribed and likely translated. While TP53RTGs do not appear to directly function as transcription factors, they do contribute to the enhanced sensitivity of elephant cells to DNA damage and the induction of apoptosis by regulating activity of the TP53 signaling pathway. These results suggest that an increase in the copy number of TP53 may have played a direct role in the evolution of very large body sizes and the resolution of Peto's paradox in Proboscideans.},
	Author = {Sulak, Michael and Fong, Lindsey and Mika, Katelyn and Chigurupati, Sravanthi and Yon, Lisa and Mongan, Nigel P and Emes, Richard D and Lynch, Vincent J},
	Date-Added = {2018-01-16 22:40:23 +0000},
	Date-Modified = {2018-01-16 22:40:23 +0000},
	Doi = {10.7554/eLife.11994},
	Journal = {Elife},
	Journal-Full = {eLife},
	Keywords = {African elephant; Asian elephant; aardvark; armadillo; cell biology; evolutionary biology; genomics; hyrax},
	Mesh = {Animals; Apoptosis; Body Size; DNA Repair; Elephants; Evolution, Molecular; Gene Dosage; Gene Expression Profiling; Genes, p53; Protein Biosynthesis; Signal Transduction; Transcription, Genetic},
	Month = {09},
	Pmc = {PMC5061548},
	pmid = {27642012},
	Pst = {epublish},
	Title = {TP53 copy number expansion is associated with the evolution of increased body size and an enhanced DNA damage response in elephants},
	Volume = {5},
	Year = {2016},
	url = {papers/Sulak_Elife2016.pdf}}


@article{Bogaert:2018,
	Abstract = {We conducted a direct test of an immunological explanation of the finding that gay men have a greater number of older brothers than do heterosexual men. This explanation posits that some mothers develop antibodies against a Y-linked protein important in male brain development, and that this effect becomes increasingly likely with each male gestation, altering brain structures underlying sexual orientation in their later-born sons. Immune assays targeting two Y-linked proteins important in brain development-protocadherin 11 Y-linked (PCDH11Y) and neuroligin 4 Y-linked (NLGN4Y; isoforms 1 and 2)-were developed. Plasma from mothers of sons, about half of whom had a gay son, along with additional controls (women with no sons, men) was analyzed for male protein-specific antibodies. Results indicated women had significantly higher anti-NLGN4Y levels than men. In addition, after statistically controlling for number of pregnancies, mothers of gay sons, particularly those with older brothers, had significantly higher anti-NLGN4Y levels than did the control samples of women, including mothers of heterosexual sons. The results suggest an association between a maternal immune response to NLGN4Y and subsequent sexual orientation in male offspring.},
	Author = {Bogaert, Anthony F and Skorska, Malvina N and Wang, Chao and Gabrie, Jos{\'e} and MacNeil, Adam J and Hoffarth, Mark R and VanderLaan, Doug P and Zucker, Kenneth J and Blanchard, Ray},
	Date-Added = {2018-01-16 22:37:59 +0000},
	Date-Modified = {2018-01-16 22:37:59 +0000},
	Doi = {10.1073/pnas.1705895114},
	Journal = {Proc Natl Acad Sci U S A},
	Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},
	Keywords = {NLGN4Y; fraternal birth order; homosexuality; maternal immune hypothesis; sexual orientation},
	Month = {Jan},
	Number = {2},
	Pages = {302-306},
	pmid = {29229842},
	Pst = {ppublish},
	Title = {Male homosexuality and maternal immune responsivity to the Y-linked protein NLGN4Y},
	Volume = {115},
	Year = {2018},
	url = {papers/Bogaert_ProcNatlAcadSciUSA2018.pdf}}


@article{Clarkson:2016,
	Abstract = {Sex differences in brain neuroanatomy and neurophysiology underpin considerable physiological and behavioural differences between females and males. Sexual differentiation of the brain is regulated by testosterone secreted by the testes predominantly during embryogenesis in humans and the neonatal period in rodents. Despite huge advances in understanding how testosterone, and its metabolite oestradiol, sexually differentiate the brain, little is known about the mechanism that actually generates the male-specific neonatal testosterone surge. This review examines the evidence for the role of the hypothalamus, and particularly the gonadotropin-releasing hormone (GnRH) neurons, in generating the neonatal testosterone surge in rodents and primates. Kisspeptin-GPR54 signalling is well established as a potent and critical regulator of GnRH neuron activity during puberty and adulthood, and we argue here for an equally important role at birth in driving the male-specific neonatal testosterone surge in rodents. The presence of a male-specific population of preoptic area kisspeptin neurons that appear transiently in the perinatal period provide one possible source of kisspeptin drive to neonatal GnRH neurons in the mouse.},
	Author = {Clarkson, Jenny and Herbison, Allan E},
	Date-Added = {2018-01-16 22:30:11 +0000},
	Date-Modified = {2018-01-16 22:30:11 +0000},
	Doi = {10.1098/rstb.2015.0115},
	Journal = {Philos Trans R Soc Lond B Biol Sci},
	Journal-Full = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
	Keywords = {GPR54; GnRH; kisspeptin; sexual differentiation; testosterone},
	Mesh = {Animals; Animals, Newborn; Gene Expression Regulation, Developmental; Gonadotropin-Releasing Hormone; Hypothalamus; Male; Testosterone},
	Month = {Feb},
	Number = {1688},
	Pages = {20150115},
	Pmc = {PMC4785901},
	pmid = {26833836},
	Pst = {ppublish},
	Title = {Hypothalamic control of the male neonatal testosterone surge},
	Volume = {371},
	Year = {2016},
	url = {papers/Clarkson_PhilosTransRSocLondBBiolSci2016.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1098/rstb.2015.0115}}


@article{Furchtgott:2017,
	Abstract = {Computational analysis of gene expression to determine both the sequence of lineage choices made by multipotent cells and to identify the genes influencing these decisions is challenging. Here we discover a pattern in the expression levels of a sparse subset of genes among cell types in B- and T-cell developmental lineages that correlates with developmental topologies. We develop a statistical framework using this pattern to simultaneously infer lineage transitions and the genes that determine these relationships. We use this technique to reconstruct the early hematopoietic and intestinal developmental trees. We extend this framework to analyze single-cell RNA-seq data from early human cortical development, inferring a neocortical-hindbrain split in early progenitor cells and the key genes that could control this lineage decision. Our work allows us to simultaneously infer both the identity and lineage of cell types as well as a small set of key genes whose expression patterns reflect these relationships.},
	Author = {Furchtgott, Leon A and Melton, Samuel and Menon, Vilas and Ramanathan, Sharad},
	Date-Added = {2018-01-16 21:58:50 +0000},
	Date-Modified = {2018-01-16 21:58:50 +0000},
	Doi = {10.7554/eLife.20488},
	Journal = {Elife},
	Journal-Full = {eLife},
	Keywords = {Transcriptomics; computational biology; developmental biology; human; mouse; stem cells; systems biology},
	Month = {Mar},
	Pmc = {PMC5352226},
	pmid = {28296636},
	Pst = {epublish},
	Title = {Discovering sparse transcription factor codes for cell states and state transitions during development},
	Volume = {6},
	Year = {2017},
	url = {papers/Furchtgott_Elife2017.pdf}}


@article{Hammock:2013,
	Abstract = {UNLABELLED: Oxytocin (OXT) has drawn increasing attention as a developmentally relevant neuropeptide given its role in the brain regulation of social behavior. It has been suggested that OXT plays an important role in the infant brain during caregiver attachment in nurturing familial contexts, but there is incomplete experimental evidence. Mouse models of OXT system genes have been particularly informative for the role of the OXT system in social behavior, however, the developing brain areas that could respond to ligand activation of the OXT receptor (OXTR) have yet to be identified in this species. Here we report new data revealing dynamic ligand-binding distribution of OXTR in the developing mouse brain. Using male and female C57BL/6J mice at postnatal days (P) 0, 7, 14, 21, 35, and 60 we quantified OXTR ligand binding in several brain areas which changed across development. Further, we describe OXTR ligand binding in select tissues of the near-term whole embryo at E18.5. Together, these data aid in the interpretation of findings in mouse models of the OXT system and generate new testable hypotheses for developmental roles for OXT in mammalian systems. We discuss our findings in the context of developmental disorders (including autism), attachment biology, and infant physiological regulation.
SUMMARY: Quantitative mapping of selective OXTR ligand binding during postnatal development in the mouse reveals an unexpected, transient expression in layers II/III throughout the mouse neocortex. OXTR are also identified in several tissues in the whole late embryo, including the adrenal glands, brown adipose tissue, and the oronasal cavity.},
	Author = {Hammock, Elizabeth A D and Levitt, Pat},
	Date-Added = {2017-12-09 14:28:14 +0000},
	Date-Modified = {2017-12-09 14:28:14 +0000},
	Doi = {10.3389/fnbeh.2013.00195},
	Journal = {Front Behav Neurosci},
	Journal-Full = {Frontiers in behavioral neuroscience},
	Keywords = {adrenal gland; autism; autoradiography; experience-dependent plasticity; kidney; neocortex; oronasal cavity; oxytocin},
	Pages = {195},
	Pmc = {PMC3858721},
	pmid = {24376405},
	Pst = {epublish},
	Title = {Oxytocin receptor ligand binding in embryonic tissue and postnatal brain development of the C57BL/6J mouse},
	Volume = {7},
	Year = {2013},
	url = {papers/Hammock_FrontBehavNeurosci2013.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.3389/fnbeh.2013.00195}}

@article{Ryden:1969,
	Abstract = {Using tritium-labelled oxytocin with a high specific activity, the halflife in the blood and the urinary excretion of intravenously injected oxytocin were followed in the female. The following groups of patients were studied: normally menstruating women during different phases of the menstrual cycle, women using a combination of gestagenic and oestrogenic hormones for oral contraception, and pregnant women in the first and second trimester. The pregnant women were admitted to the hospital for legal abortion in the 10th--20th week of gestation.

In the proliferative phase, t½ was 272 seconds (n = 14), in the secretory phase 221 seconds (n = 5), and in women using oral contraceptives 199 seconds (n = 10). In pregnant women during the first trimester, t½ was 178 seconds (n = 6). The corresponding value in women examined during the 14th--17th weeks and during the 18th--20th weeks of gestation was 295 seconds (n = 6) and 282 seconds (n = 6), respectively. T½ was also determined within 24 h of abortion in patients in the second trimester, where the abortion was induced by intra-amniotic instillation of 50% glucose. In all cases a decrease in t½ was found. The decrease was most marked in women during the 18th--20th weeks of gestation. Altogether 25--50% of the radioactivity injected was recovered in the urine from pregnant women within 3 h of the injection. Thin-layer chromatography of the urine did not reveal the presence of any intact oxytocin.

The results demonstrate that the disappearance of oxytocin from the blood seems to be influenced by the sex hormones. Thus, an oestrogendominated stage shows a lower disappearance rate, whereas gestagens produce the reverse effect. The pronounced decrease in t½ in pregnant women immediately after abortion might be due to a change to a more progesterone-dominated stage induced by the death of the foetus, or by an alteration in the affinity of oxytocin to the myometrium. },
	Author = {Ryd{\'e}n, G and Sj{\"o}holm, I},
	Date-Added = {2017-12-09 14:26:15 +0000},
	Date-Modified = {2017-12-09 14:27:00 +0000},
	Journal = {Acta Endocrinol (Copenh)},
	Journal-Full = {Acta endocrinologica},
	Mesh = {Abortion, Legal; Chromatography, Thin Layer; Contraceptives, Oral; Female; Gestational Age; Humans; Oxytocin; Pregnancy; Tritium},
	Month = {Jul},
	Number = {3},
	Pages = {425-31},
	pmid = {5820054},
	Pst = {ppublish},
	Title = {Half-life of oxytocin in blood of pregnant and non-pregnant women},
	Volume = {61},
	Year = {1969}}

@article{Greenwood:2017,
	Abstract = {Oxytocin (OXT) is a pleiotropic regulator of physiology and behavior. An emerging body of evidence demonstrates a role for OXT in the transition to postnatal life of the infant. To identify potential sites of OXT action via the OXT receptor (OXTR) in the newborn mouse, we performed receptor autoradiography on 20 μm sagittal sections of whole postnatal day 0 male and female mice on a C57BL/6J background using the 125iodinated ornithine vasotocin analog ([125I]-OVTA) radioligand. A competitive binding assay on both wild-type (WT) and OXTR knockout (OXTR KO) tissue was used to assess the selectivity of [125I]-OVTA for neonatal OXTR. Radioactive ligand (0.05 nM [125I]-OVTA) was competed against concentrations of 0 nM, 10 nM, and 1000 nM excess unlabeled OXT. Autoradiographs demonstrated the high selectivity of the radioligand for infant peripheral OXTR. Specific ligand binding activity for OXTR was observed in the oronasal cavity, the eye, whisker pads, adrenal gland, and anogenital region in the neonatal OXTR WT mouse, but was absent in neonatal OXTR KO. Nonspecific binding was observed in areas with a high lipid content such as the scapular brown adipose tissue and the liver: in these regions, binding was present in both OXTR WT and KO mice, and could not be competed away with OXT in either WT or KO mice. Collectively, these data confirm novel OXT targets in the periphery of the neonate. These peripheral OXTR sites, coupled with the immaturity of the neonate's own OXT system, suggest a role for exogenous OXT in modulating peripheral physiology and development.},
	Author = {Greenwood, Maria A and Hammock, Elizabeth A D},
	Date-Added = {2017-12-09 04:27:42 +0000},
	Date-Modified = {2017-12-09 04:27:42 +0000},
	Doi = {10.1371/journal.pone.0172904},
	Journal = {PLoS One},
	Journal-Full = {PloS one},
	Mesh = {Adipose Tissue, Brown; Adrenal Glands; Animals; Animals, Newborn; Binding Sites; Eye; Female; Liver; Male; Mice, Inbred C57BL; Organ Specificity; Oxytocin; Periodontium; Protein Binding; Receptors, Oxytocin; Tooth; Vibrissae},
	Number = {2},
	Pages = {e0172904},
	Pmc = {PMC5325587},
	pmid = {28235051},
	Pst = {epublish},
	Title = {Oxytocin receptor binding sites in the periphery of the neonatal mouse},
	Volume = {12},
	Year = {2017},
	url = {papers/Greenwood_PLoSOne2017.pdf}}

@article{Ojo:2016,
	Abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field.},
	Author = {Ojo, Joseph O and Mouzon, Benoit C and Crawford, Fiona},
	Date-Added = {2017-11-14 21:43:20 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1016/j.expneurol.2015.06.003},
	Journal = {Exp Neurol},
	Journal-Full = {Experimental neurology},
	Keywords = {Animal models; Astroglial tangles; CTE; Concussion; Neurobehaviour; Neurofibrillary tangles; Neuropathology; Repetitive TBI; Tau; Transgenic mice; concussion},
	Mesh = {Animals; Brain Injury, Chronic; Craniocerebral Trauma; Disease Models, Animal; Humans; Mice; Translational Medical Research; tau Proteins},
	Month = {Jan},
	Pages = {389-404},
	pmid = {26054886},
	Pst = {ppublish},
	Title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
	Volume = {275 Pt 3},
	Year = {2016},
	url = {papers/Ojo_ExpNeurol2016.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2015.06.003}}

@article{McKee:2013,
	Abstract = {Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behaviour. Eighteen age- and gender-matched individuals without a history of repetitive mild traumatic brain injury served as control subjects. In chronic traumatic encephalopathy, the spectrum of hyperphosphorylated tau pathology ranged in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions, including the medial temporal lobe, thereby allowing a progressive staging of pathology from stages I-IV. Multifocal axonal varicosities and axonal loss were found in deep cortex and subcortical white matter at all stages of chronic traumatic encephalopathy. TAR DNA-binding protein 43 immunoreactive inclusions and neurites were also found in 85% of cases, ranging from focal pathology in stages I-III to widespread inclusions and neurites in stage IV. Symptoms in stage I chronic traumatic encephalopathy included headache and loss of attention and concentration. Additional symptoms in stage II included depression, explosivity and short-term memory loss. In stage III, executive dysfunction and cognitive impairment were found, and in stage IV, dementia, word-finding difficulty and aggression were characteristic. Data on athletic exposure were available for 34 American football players; the stage of chronic traumatic encephalopathy correlated with increased duration of football play, survival after football and age at death. Chronic traumatic encephalopathy was the sole diagnosis in 43 cases (63%); eight were also diagnosed with motor neuron disease (12%), seven with Alzheimer's disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lobar degeneration (6%). There is an ordered and predictable progression of hyperphosphorylated tau abnormalities through the nervous system in chronic traumatic encephalopathy that occurs in conjunction with widespread axonal disruption and loss. The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein.},
	Author = {McKee, Ann C and Stern, Robert A and Nowinski, Christopher J and Stein, Thor D and Alvarez, Victor E and Daneshvar, Daniel H and Lee, Hyo-Soon and Wojtowicz, Sydney M and Hall, Garth and Baugh, Christine M and Riley, David O and Kubilus, Caroline A and Cormier, Kerry A and Jacobs, Matthew A and Martin, Brett R and Abraham, Carmela R and Ikezu, Tsuneya and Reichard, Robert Ross and Wolozin, Benjamin L and Budson, Andrew E and Goldstein, Lee E and Kowall, Neil W and Cantu, Robert C},
	Date-Added = {2017-11-14 21:41:39 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1093/brain/aws307},
	Journal = {Brain},
	Journal-Full = {Brain : a journal of neurology},
	Keywords = {concussion},
	Mesh = {Adolescent; Adult; Aged; Aged, 80 and over; Athletes; Brain; Brain Injury, Chronic; Disease Progression; Football; Humans; Male; Middle Aged; Neurofibrillary Tangles; Tauopathies; Veterans; tau Proteins},
	Month = {Jan},
	Number = {Pt 1},
	Pages = {43-64},
	Pmc = {PMC3624697},
	pmid = {23208308},
	Pst = {ppublish},
	Title = {The spectrum of disease in chronic traumatic encephalopathy},
	Volume = {136},
	Year = {2013},
	url = {papers/McKee_Brain2013.pdf}}

@article{Smith:2013a,
	Abstract = {Traumatic brain injury (TBI) has long been recognized to be a risk factor for dementia. This association has, however, only recently gained widespread attention through the increased awareness of 'chronic traumatic encephalopathy' (CTE) in athletes exposed to repetitive head injury. Originally termed 'dementia pugilistica' and linked to a career in boxing, descriptions of the neuropathological features of CTE include brain atrophy, cavum septum pellucidum, and amyloid-β, tau and TDP-43 pathologies, many of which might contribute to clinical syndromes of cognitive impairment. Similar chronic pathologies are also commonly found years after just a single moderate to severe TBI. However, little consensus currently exists on specific features of these post-TBI syndromes that might permit their confident clinical and/or pathological diagnosis. Moreover, the mechanisms contributing to neurodegeneration following TBI largely remain unknown. Here, we review the current literature and controversies in the study of chronic neuropathological changes after TBI.},
	Author = {Smith, Douglas H and Johnson, Victoria E and Stewart, William},
	Date-Added = {2017-11-14 21:40:36 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1038/nrneurol.2013.29},
	Journal = {Nat Rev Neurol},
	Journal-Full = {Nature reviews. Neurology},
	Keywords = {concussion},
	Mesh = {Aged; Athletic Injuries; Brain; Brain Injuries; Chronic Disease; Dementia; Disease Progression; Humans; Male; Neurofibrillary Tangles; Risk Factors; Young Adult},
	Month = {Apr},
	Number = {4},
	Pages = {211-21},
	Pmc = {PMC4513655},
	pmid = {23458973},
	Pst = {ppublish},
	Title = {Chronic neuropathologies of single and repetitive TBI: substrates of dementia?},
	Volume = {9},
	Year = {2013},
	url = {papers/Smith_NatRevNeurol2013.pdf}}

@article{Hay:2016,
	Abstract = {Almost a century ago, the first clinical account of the punch-drunk syndrome emerged, describing chronic neurological and neuropsychiatric sequelae occurring in former boxers. Thereafter, throughout the twentieth century, further reports added to our understanding of the neuropathological consequences of a career in boxing, leading to descriptions of a distinct neurodegenerative pathology, termed dementia pugilistica. During the past decade, growing recognition of this pathology in autopsy studies of nonboxers who were exposed to repetitive, mild traumatic brain injury, or to a single, moderate or severe traumatic brain injury, has led to an awareness that it is exposure to traumatic brain injury that carries with it a risk of this neurodegenerative disease, not the sport or the circumstance in which the injury is sustained. Furthermore, the neuropathology of the neurodegeneration that occurs after traumatic brain injury, now termed chronic traumatic encephalopathy, is acknowledged as being a complex, mixed, but distinctive pathology, the detail of which is reviewed in this article.},
	Author = {Hay, Jennifer and Johnson, Victoria E and Smith, Douglas H and Stewart, William},
	Date-Added = {2017-11-14 21:39:50 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1146/annurev-pathol-012615-044116},
	Journal = {Annu Rev Pathol},
	Journal-Full = {Annual review of pathology},
	Keywords = {CTE; amyloid; axons; neurodegeneration; tau; traumatic brain injury; concussion},
	Mesh = {Animals; Brain Injuries, Traumatic; Chronic Traumatic Encephalopathy; Humans},
	Month = {May},
	Pages = {21-45},
	Pmc = {PMC5367053},
	pmid = {26772317},
	Pst = {ppublish},
	Title = {Chronic Traumatic Encephalopathy: The Neuropathological Legacy of Traumatic Brain Injury},
	Volume = {11},
	Year = {2016},
	url = {papers/Hay_AnnuRevPathol2016.pdf}}

@article{Cherry:2017,
	Abstract = {CCL11, a protein previously associated with age-associated cognitive decline, is observed to be increased in the brain and cerebrospinal fluid (CSF) in chronic traumatic encephalopathy (CTE) compared to Alzheimer's disease (AD). Using a cohort of 23 deceased American football players with neuropathologically verified CTE, 50 subjects with neuropathologically diagnosed AD, and 18 non-athlete controls, CCL11 was measured with ELISA in the dorsolateral frontal cortex (DLFC) and CSF. CCL11 levels were significantly increased in the DLFC in subjects with CTE (fold change = 1.234, p < 0.050) compared to non-athlete controls and AD subjects with out a history of head trauma. This increase was also seen to correlate with years of exposure to American football (β = 0.426, p = 0.048) independent of age (β = -0.046, p = 0.824). Preliminary analyses of a subset of subjects with available post-mortem CSF showed a trend for increased CCL11 among individuals with CTE (p = 0.069) mirroring the increase in the DLFC. Furthermore, an association between CSF CCL11 levels and the number of years exposed to football (β = 0.685, p = 0.040) was observed independent of age (β = -0.103, p = 0.716). Finally, a receiver operating characteristic (ROC) curve analysis demonstrated CSF CCL11 accurately distinguished CTE subjects from non-athlete controls and AD subjects (AUC = 0.839, 95% CI 0.62-1.058, p = 0.028). Overall, the current findings provide preliminary evidence that CCL11 may be a novel target for future CTE biomarker studies.},
	Author = {Cherry, Jonathan D and Stein, Thor D and Tripodis, Yorghos and Alvarez, Victor E and Huber, Bertrand R and Au, Rhoda and Kiernan, Patrick T and Daneshvar, Daniel H and Mez, Jesse and Solomon, Todd M and Alosco, Michael L and McKee, Ann C},
	Date-Added = {2017-11-14 21:44:33 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1371/journal.pone.0185541},
	Journal = {PLoS One},
	Journal-Full = {PloS one},
	Keywords = {concussion},
	Mesh = {Aged; Aged, 80 and over; Alzheimer Disease; Biomarkers; Brain; Chemokine CCL11; Chronic Traumatic Encephalopathy; Female; Football; Humans; Male; Middle Aged},
	Number = {9},
	Pages = {e0185541},
	Pmc = {PMC5614644},
	pmid = {28950005},
	Pst = {epublish},
	Title = {CCL11 is increased in the CNS in chronic traumatic encephalopathy but not in Alzheimer's disease},
	Volume = {12},
	Year = {2017},
	url = {papers/Cherry_PLoSOne2017.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pone.0185541}}

@article{Montenigro:2015,
	Abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is most often identified in postmortem autopsies of individuals exposed to repetitive head impacts, such as boxers and football players. The neuropathology of CTE is characterized by the accumulation of hyperphosphorylated tau protein in a pattern that is unique from that of other neurodegenerative diseases, including Alzheimer's disease. The clinical features of CTE are often progressive, leading to dramatic changes in mood, behavior, and cognition, frequently resulting in debilitating dementia. In some cases, motor features, including parkinsonism, can also be present. In this review, the historical origins of CTE are revealed and an overview of the current state of knowledge of CTE is provided, including the neuropathology, clinical features, proposed clinical and pathological diagnostic criteria, potential in vivo biomarkers, known risk factors, and treatment options.},
	Author = {Montenigro, Philip H and Corp, Daniel T and Stein, Thor D and Cantu, Robert C and Stern, Robert A},
	Date-Added = {2017-11-14 21:39:33 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1146/annurev-clinpsy-032814-112814},
	Journal = {Annu Rev Clin Psychol},
	Journal-Full = {Annual review of clinical psychology},
	Keywords = {chronic traumatic encephalopathy; concussion; football; history; neurodegenerative disorders; traumatic brain injury; concussion},
	Mesh = {Biomarkers; Boxing; Brain; Brain Injury, Chronic; Football; History, 20th Century; History, 21st Century; Humans; Neuroimaging; Risk Factors},
	Pages = {309-30},
	pmid = {25581233},
	Pst = {ppublish},
	Title = {Chronic traumatic encephalopathy: historical origins and current perspective},
	Volume = {11},
	Year = {2015},
	url = {papers/Montenigro_AnnuRevClinPsychol2015.pdf}}

@article{McKee:2016,
	Abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. Like many other neurodegenerative conditions, at present, CTE can only be definitively diagnosed by post-mortem examination of brain tissue. As the first part of a series of consensus panels funded by the NINDS/NIBIB to define the neuropathological criteria for CTE, preliminary neuropathological criteria were used by 7 neuropathologists to blindly evaluate 25 cases of various tauopathies, including CTE, Alzheimer's disease, progressive supranuclear palsy, argyrophilic grain disease, corticobasal degeneration, primary age-related tauopathy, and parkinsonism dementia complex of Guam. The results demonstrated that there was good agreement among the neuropathologists who reviewed the cases (Cohen's kappa, 0.67) and even better agreement between reviewers and the diagnosis of CTE (Cohen's kappa, 0.78). Based on these results, the panel defined the pathognomonic lesion of CTE as an accumulation of abnormal hyperphosphorylated tau (p-tau) in neurons and astroglia distributed around small blood vessels at the depths of cortical sulci and in an irregular pattern. The group also defined supportive but non-specific p-tau-immunoreactive features of CTE as: pretangles and NFTs affecting superficial layers (layers II-III) of cerebral cortex; pretangles, NFTs or extracellular tangles in CA2 and pretangles and proximal dendritic swellings in CA4 of the hippocampus; neuronal and astrocytic aggregates in subcortical nuclei; thorn-shaped astrocytes at the glial limitans of the subpial and periventricular regions; and large grain-like and dot-like structures. Supportive non-p-tau pathologies include TDP-43 immunoreactive neuronal cytoplasmic inclusions and dot-like structures in the hippocampus, anteromedial temporal cortex and amygdala. The panel also recommended a minimum blocking and staining scheme for pathological evaluation and made recommendations for future study. This study provides the first step towards the development of validated neuropathological criteria for CTE and will pave the way towards future clinical and mechanistic studies.},
	Author = {McKee, Ann C and Cairns, Nigel J and Dickson, Dennis W and Folkerth, Rebecca D and Keene, C Dirk and Litvan, Irene and Perl, Daniel P and Stein, Thor D and Vonsattel, Jean-Paul and Stewart, William and Tripodis, Yorghos and Crary, John F and Bieniek, Kevin F and Dams-O'Connor, Kristen and Alvarez, Victor E and Gordon, Wayne A and {TBI/CTE group}},
	Date-Added = {2017-11-14 21:38:47 +0000},
	Date-Modified = {2017-11-14 21:46:24 +0000},
	Doi = {10.1007/s00401-015-1515-z},
	Journal = {Acta Neuropathol},
	Journal-Full = {Acta neuropathologica},
	Keywords = {Brain trauma; Chronic traumatic encephalopathy; Neurodegenerative disorders; Tauopathy; Traumatic brain injury; concussion},
	Mesh = {Alzheimer Disease; Autopsy; Brain Injury, Chronic; Humans; National Institute of Biomedical Imaging and Bioengineering (U.S.); National Institute of Neurological Disorders and Stroke; Neurofibrillary Tangles; Neurons; Tauopathies; United States; tau Proteins},
	Month = {Jan},
	Number = {1},
	Pages = {75-86},
	Pmc = {PMC4698281},
	pmid = {26667418},
	Pst = {ppublish},
	Title = {The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy},
	Volume = {131},
	Year = {2016},
	url = {papers/McKee_ActaNeuropathol2016.pdf}}

@article{Yagita:2005,
	Abstract = {We have generated 362 bp and 547 bp partial sequences for Rana pipiens ephrin-A2 and ephrin-A5 mRNA, respectively. Translation homologies for the comparable segments of cDNA of chicken, mouse and human are 90.8, 86.9 and 84.4% for the ephrin-A2 sequence and 85.7, 85.0 and 85.0% for the ephrin-A5 sequence. Digoxigenin-labeled riboprobes were prepared and applied by means of in situ hybridization to whole-mounts of the brains of mature adults and expression patterns in tadpoles were also explored. The RNA probes revealed similar posterior (high) to anterior (low) expression gradients in the adult tectum, demonstrating that both ephrin-As are expressed in the adult Ranid frog tectum. Only the ephrin-A2 probe was tested on tadpole brain, yielding an appropriately graded expression pattern similar to the adult.},
	Author = {Yagita, Yoshiki and Barjis, Isaac and Hecht, Michael and Bach, Helene and Feldheim, David A and Scalia, Frank},
	Date-Added = {2017-11-01 21:08:33 +0000},
	Date-Modified = {2017-11-01 21:08:33 +0000},
	Doi = {10.1016/j.devbrainres.2005.06.016},
	Journal = {Brain Res Dev Brain Res},
	Journal-Full = {Brain research. Developmental brain research},
	Mesh = {Animals; Chickens; Conserved Sequence; DNA, Complementary; Ephrin-A2; Ephrin-A5; Evolution, Molecular; Gene Expression Regulation, Developmental; Humans; Larva; Mice; Molecular Sequence Data; Nucleotides; RNA, Messenger; Rana pipiens; Sequence Homology, Amino Acid; Sequence Homology, Nucleic Acid; Superior Colliculi},
	Month = {Sep},
	Number = {1},
	Pages = {72-7},
	pmid = {16083970},
	Pst = {ppublish},
	Title = {Partial nucleotide sequences and expression patterns of frog (Rana pipiens) ephrin-A2 and ephrin-A5 mRNA},
	Volume = {159},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.devbrainres.2005.06.016}}

@article{Kramer:2004,
	Abstract = {This paper describes a simple method for the preparation and characterization of protein density gradients on solid supports. The method employs colloidal metal nanoparticles as protein carriers and optical tags and is capable of forming linear, exponential, 1D, 2D, and multiprotein gradients of varying slope without expensive or sophisticated surface patterning techniques. Surfaces patterned with proteins using the procedures described within are shown to support cell growth and are thus suitable for studies of protein-cell interactions.},
	Author = {Kr{\"a}mer, Stephan and Xie, Huan and Gaff, John and Williamson, John R and Tkachenko, Alexander G and Nouri, Navid and Feldheim, David A and Feldheim, Daniel L},
	Date-Added = {2017-11-01 21:08:22 +0000},
	Date-Modified = {2017-11-01 21:08:22 +0000},
	Doi = {10.1021/ja031674n},
	Journal = {J Am Chem Soc},
	Journal-Full = {Journal of the American Chemical Society},
	Mesh = {Animals; Axons; Cattle; Cell Division; Cells, Cultured; Chromatography, High Pressure Liquid; Gold Colloid; Hippocampus; Metals; Microscopy, Fluorescence; Nanotechnology; Neurons; Polylysine; Rats; Serum Albumin, Bovine; Spectrophotometry},
	Month = {May},
	Number = {17},
	Pages = {5388-95},
	pmid = {15113210},
	Pst = {ppublish},
	Title = {Preparation of protein gradients through the controlled deposition of protein-nanoparticle conjugates onto functionalized surfaces},
	Volume = {126},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1021/ja031674n}}

@article{Jiao:2008,
	Abstract = {In the central nervous system (CNS) of adult mammals, neurogenesis occurs in only two restricted areas, the subgranular zone (SGZ) of the hippocampus and the subventricular zone (SVZ). Isolation of multipotent progenitor cells from other CNS regions suggests that their neurogenic potential is dictated by local environmental cues. Here, we report that astrocytes in areas outside of the SGZ and SVZ of adult mice express high levels of ephrin-A2 and -A3, which present an inhibitory niche, negatively regulating neural progenitor cell growth. Adult mice lacking both ephrin-A2 and -A3 display active ongoing neurogenesis throughout the CNS. These findings suggest that neural cell replacement therapies for neurodegeneration or injury in the adult CNS may be achieved by manipulating ephrin signaling pathways.},
	Author = {Jiao, Jian-Wei and Feldheim, David A and Chen, Dong Feng},
	Date-Added = {2017-11-01 21:08:18 +0000},
	Date-Modified = {2017-11-01 21:08:18 +0000},
	Doi = {10.1073/pnas.0708861105},
	Journal = {Proc Natl Acad Sci U S A},
	Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},
	Mesh = {Animals; Astrocytes; Cell Differentiation; Central Nervous System; Ephrin-A2; Ephrin-A3; Ephrins; Mice; Mice, Transgenic; Neurons; Receptor, EphA7; Signal Transduction},
	Month = {Jun},
	Number = {25},
	Pages = {8778-83},
	Pmc = {PMC2438395},
	pmid = {18562299},
	Pst = {ppublish},
	Title = {Ephrins as negative regulators of adult neurogenesis in diverse regions of the central nervous system},
	Volume = {105},
	Year = {2008},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0708861105}}

@article{Triplett:2014,
	Abstract = {BACKGROUND: There are numerous functional types of retinal ganglion cells (RGCs), each participating in circuits that encode a specific aspect of the visual scene. This functional specificity is derived from distinct RGC morphologies and selective synapse formation with other retinal cell types; yet, how these properties are established during development remains unclear. Islet2 (Isl2) is a LIM-homeodomain transcription factor expressed in the developing retina, including approximately 40% of all RGCs, and has previously been implicated in the subtype specification of spinal motor neurons. Based on this, we hypothesized that Isl2+ RGCs represent a related subset that share a common function.
RESULTS: We morphologically and molecularly characterized Isl2+ RGCs using a transgenic mouse line that expresses GFP in the cell bodies, dendrites and axons of Isl2+ cells (Isl2-GFP). Isl2-GFP RGCs have distinct morphologies and dendritic stratification patterns within the inner plexiform layer and project to selective visual nuclei. Targeted filling of individual cells reveals that the majority of Isl2-GFP RGCs have dendrites that are monostratified in layer S3 of the IPL, suggesting they are not ON-OFF direction-selective ganglion cells. Molecular analysis shows that most alpha-RGCs, indicated by expression of SMI-32, are also Isl2-GFP RGCs. Isl2-GFP RGCs project to most retino-recipient nuclei during early development, but specifically innervate the dorsal lateral geniculate nucleus and superior colliculus (SC) at eye opening. Finally, we show that the segregation of Isl2+ and Isl2- RGC axons in the SC leads to the segregation of functional RGC types.
CONCLUSIONS: Taken together, these data suggest that Isl2+ RGCs comprise a distinct class and support a role for Isl2 as an important component of a transcription factor code specifying functional visual circuits. Furthermore, this study describes a novel genetically-labeled mouse line that will be a valuable resource in future investigations of the molecular mechanisms of visual circuit formation.},
	Author = {Triplett, Jason W and Wei, Wei and Gonzalez, Cristina and Sweeney, Neal T and Huberman, Andrew D and Feller, Marla B and Feldheim, David A},
	Date-Added = {2017-11-01 21:08:07 +0000},
	Date-Modified = {2017-11-01 21:08:07 +0000},
	Doi = {10.1186/1749-8104-9-2},
	Journal = {Neural Dev},
	Journal-Full = {Neural development},
	Mesh = {Animals; Axons; Dendrites; Geniculate Bodies; LIM-Homeodomain Proteins; Mice; Mice, Transgenic; Neural Pathways; Retinal Ganglion Cells; Superior Colliculi; Transcription Factors},
	Month = {Feb},
	Pages = {2},
	Pmc = {PMC3937143},
	pmid = {24495295},
	Pst = {epublish},
	Title = {Dendritic and axonal targeting patterns of a genetically-specified class of retinal ganglion cells that participate in image-forming circuits},
	Volume = {9},
	Year = {2014},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1749-8104-9-2}}

@article{Sweeney:2014,
	Abstract = {There are ∼20 types of retinal ganglion cells (RGCs) in mice, each of which has distinct molecular, morphological, and physiological characteristics. Each RGC type sends axon projections to specific brain areas that execute light-dependent behaviors. Here, we show that the T-box transcription factor Tbr2 is required for the development of several RGC types that participate in non-image-forming circuits. These types are molecularly distinct, project to non-image-forming targets, and include intrinsically photosensitive RGCs. Tbr2 mutant mice have reduced retinal projections to non-image-forming nuclei and an attenuated pupillary light reflex. These data demonstrate that Tbr2 acts to execute RGC type choice and/or survival in a set of RGCs that mediates light-induced subconscious behaviors.},
	Author = {Sweeney, Neal T and Tierney, Hannah and Feldheim, David A},
	Date-Added = {2017-11-01 21:08:01 +0000},
	Date-Modified = {2017-11-01 21:08:01 +0000},
	Doi = {10.1523/JNEUROSCI.0035-14.2014},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Keywords = {TBR2; axon projections; retina; visual circuit},
	Mesh = {Age Factors; Animals; Animals, Newborn; Axons; Cadherins; Calbindin 2; Female; Gene Expression Regulation; Green Fluorescent Proteins; Male; Mice; Mice, Transgenic; Mutation; Pupil; Receptors, Dopamine D4; Reflex; Retinal Ganglion Cells; T-Box Domain Proteins; Visual Pathways},
	Month = {Apr},
	Number = {16},
	Pages = {5447-53},
	Pmc = {PMC3988404},
	pmid = {24741035},
	Pst = {ppublish},
	Title = {Tbr2 is required to generate a neural circuit mediating the pupillary light reflex},
	Volume = {34},
	Year = {2014},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0035-14.2014}}

@article{Scalia:2009,
	Abstract = {Eph/ephrin-receptor/ligand A and B families play a variety of roles during CNS development, including patterning the retinotectal projection. However, the alignment of their expression gradients with developing retinotectal maps and gradients of cellular development is not well understood in species whose midbrain tecta undergo a protracted anterior to posterior development. By using anatomical tracing methods and (3)H-thymidine neuronography, we have mapped the retinotectal projection and the spatiotemporal progression of tectal cellular development onto Eph/ephrin expression patterns in the tectum of larval Rana pipiens, as studied by means of in situ affinity analysis with fusion proteins. EphA expression is maximal in anterior tectum (and temporal retina); ephrin-A expression is maximal at the posterior pole (and nasal retina). EphB expression is graded in the early larva, where it is maximal in the posterior tectum just anterior to the posterior pole (and in the ventral retina). Tectal EphB expression becomes uniform at later stages and remains so in the adult, although its retinal expression remains maximal ventrally. In the early larva, EphA, EphB, and ephrin-A protein gradients are parallel to each other and align with the temporonasal axis of the retinal projection. The early EphB expression maximum overlaps the boundary between the mantle layer of newly postmitotic cells and the posterior, epithelial region of cell proliferation, suggesting that the expression maximum is associated with the initial migrations of the postmitotic cells. Ephrin-B expression was detected in the olfactory bulb and dorsal retina at all ages, but not in the tectum.},
	Author = {Scalia, Frank and Currie, Julia R and Feldheim, David A},
	Date-Added = {2017-11-01 21:07:01 +0000},
	Date-Modified = {2017-11-01 21:07:01 +0000},
	Doi = {10.1002/cne.21968},
	Journal = {J Comp Neurol},
	Journal-Full = {The Journal of comparative neurology},
	Mesh = {Animals; Ephrins; Larva; Prosencephalon; Rana pipiens; Receptors, Eph Family; Retina; Tectum Mesencephali; Visual Pathways},
	Month = {May},
	Number = {1},
	Pages = {30-48},
	pmid = {19260054},
	Pst = {ppublish},
	Title = {Eph/ephrin gradients in the retinotectal system of Rana pipiens: developmental and adult expression patterns},
	Volume = {514},
	Year = {2009},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.21968}}

@article{Himanen:2004,
	Abstract = {The interactions between Eph receptor tyrosine kinases and their ephrin ligands regulate cell migration and axon pathfinding. The EphA receptors are generally thought to become activated by ephrin-A ligands, whereas the EphB receptors interact with ephrin-B ligands. Here we show that two of the most widely studied of these molecules, EphB2 and ephrin-A5, which have never been described to interact with each other, do in fact bind one another with high affinity. Exposure of EphB2-expressing cells to ephrin-A5 leads to receptor clustering, autophosphorylation and initiation of downstream signaling. Ephrin-A5 induces EphB2-mediated growth cone collapse and neurite retraction in a model system. We further show, using X-ray crystallography, that the ephrin-A5-EphB2 complex is a heterodimer and is architecturally distinct from the tetrameric EphB2-ephrin-B2 structure. The structural data reveal the molecular basis for EphB2-ephrin-A5 signaling and provide a framework for understanding the complexities of functional interactions and crosstalk between A- and B-subclass Eph receptors and ephrins.},
	Author = {Himanen, Juha-Pekka and Chumley, Michael J and Lackmann, Martin and Li, Chen and Barton, William A and Jeffrey, Phillip D and Vearing, Christopher and Geleick, Detlef and Feldheim, David A and Boyd, Andrew W and Henkemeyer, Mark and Nikolov, Dimitar B},
	Date-Added = {2017-11-01 21:04:20 +0000},
	Date-Modified = {2017-11-01 21:04:20 +0000},
	Doi = {10.1038/nn1237},
	Journal = {Nat Neurosci},
	Journal-Full = {Nature neuroscience},
	Mesh = {Alkaline Phosphatase; Animals; Animals, Newborn; Cell Line; Chromatography, Gel; Chromatography, Ion Exchange; Cricetinae; Cricetulus; Crystallography; Electrophoresis; Ephrin-A5; Ephrin-B2; Fluorescent Antibody Technique; Green Fluorescent Proteins; Humans; Infection; Luminescent Proteins; Mice; Neurites; Neuroblastoma; Phosphorylation; Protein Binding; Receptor, EphA3; Receptor, EphB2; Signal Transduction; Sindbis Virus; Spectrometry, Fluorescence; Surface Plasmon Resonance; Time Factors; Transfection; Video Recording},
	Month = {May},
	Number = {5},
	Pages = {501-9},
	pmid = {15107857},
	Pst = {ppublish},
	Title = {Repelling class discrimination: ephrin-A5 binds to and activates EphB2 receptor signaling},
	Volume = {7},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1237}}

@article{Zhang:2012,
	Abstract = {Self-avoidance is a mechanism by which dendrites from the same neuron repel one another in order to establish uniform coverage of the dendritic field. The importance of self-avoidance for the development of complex arborization patterns has been highlighted by studies of Drosophila sensory and mouse retinal neurons. However, it is unclear whether branch patterning in the mammalian central nervous system is also governed by this strategy. We reduced Satb2 expression in a population of layer II/III pyramidal neurons in vivo by RNA interference and found that the somas of Satb2-deficient neurons clumped together, and their dendrites failed to expand laterally but instead formed fascicles. Furthermore, experiments showed that reducing Satb2 caused the adhesion of not only neighboring Satb2-deficient neurons but also neighboring wild-type neurons. Our results indicate a cell autonomous and non-cell autonomous role for Satb2 in regulating the adhesive and/or repulsive properties of cerebral pyramidal neurons.},
	Author = {Zhang, Lei and Song, Ning-Ning and Chen, Jia-Yin and Huang, Ying and Li, He and Ding, Yu-Qiang},
	Date-Added = {2017-07-05 17:41:29 +0000},
	Date-Modified = {2017-07-05 17:41:29 +0000},
	Doi = {10.1093/cercor/bhr215},
	Journal = {Cereb Cortex},
	Journal-Full = {Cerebral cortex (New York, N.Y. : 1991)},
	Mesh = {Animals; Animals, Newborn; Cell Adhesion; Cell Communication; Cell Enlargement; Cells, Cultured; Dendrites; Matrix Attachment Region Binding Proteins; Mice; Pyramidal Cells; Transcription Factors},
	Month = {Jul},
	Number = {7},
	Pages = {1510-9},
	pmid = {21885532},
	Pst = {ppublish},
	Title = {Satb2 is required for dendritic arborization and soma spacing in mouse cerebral cortex},
	Volume = {22},
	Year = {2012},
	url = {papers/Zhang_CerebCortex2012.pdf}}

@article{Lu2021,
  title = {An analog of psychedelics restores functional neural circuits disrupted by unpredictable stress.},
  author = {Lu, Ju and Tjia, Michelle and Mullen, Brian and Cao, Bing and Lukasiewicz, Kacper and Shah-Morales, Sajita and Weiser, Sydney and Cameron, Lindsay P and Olson, David E and Chen, Lu and Zuo, Yi},
  journal = {Mol Psychiatry},
  volume = {26},
  number = {11},
  year = {2021},
  month = {11},
  pages = {6237-6252},
  abstract = {Psychological stress affects a wide spectrum of brain functions and poses risks for many mental disorders. However, effective therapeutics to alleviate or revert its deleterious effects are lacking. A recently synthesized psychedelic analog tabernanthalog (TBG) has demonstrated anti-addictive and antidepressant potential. Whether TBG can rescue stress-induced affective, sensory, and cognitive deficits, and how it may achieve such effects by modulating neural circuits, remain unknown. Here we show that in mice exposed to unpredictable mild stress (UMS), administration of a single dose of TBG decreases their anxiety level and rescues deficits in sensory processing as well as in cognitive flexibility. Post-stress TBG treatment promotes the regrowth of excitatory neuron dendritic spines lost during UMS, decreases the baseline neuronal activity, and enhances whisking-modulation of neuronal activity in the somatosensory cortex. Moreover, calcium imaging in head-fixed mice performing a whisker-dependent texture discrimination task shows that novel textures elicit responses from a greater proportion of neurons in the somatosensory cortex than do familiar textures. Such differential response is diminished by UMS and is restored by TBG. Together, our study reveals the effects of UMS on cortical neuronal circuit activity patterns and demonstrate that TBG combats the detrimental effects of stress by modulating basal and stimulus-dependent neural activity in cortical networks.},
  keywords = {Animals; Hallucinogens; Mice; Neurons; Somatosensory Cortex; Vibrissae; },
  pmid = {34035476},
  doi = {10.1038/s41380-021-01159-1},
  pii = {10.1038/s41380-021-01159-1},
  pmc = {PMC8613316},
  mid = {NIHMS1701193},
  url = {papers/Lu_MolPsychiatry2022-34035476.pdf},
  nlmuniqueid = {9607835}
}

@article{Yokoyama:2001,
	Abstract = {To investigate Eph-ephrin bidirectional signaling, a series of mutations were generated in the ephrin-B3 locus. The absence of both forward and reverse signaling resulted in mice with mirror movements as typified by a hopping locomotion. The corticospinal tract was defective as axons failed to respect the midline boundary of the spinal cord and bilaterally innervated both contralateral and ipsilateral motor neuron populations. A second mutation that expresses a truncated ephrin-B3 protein lacking its cytoplasmic domain did not lead to hopping, indicating that reverse signaling is not required for corticospinal innervation. Ephrin-B3 is concentrated at the spinal cord midline, while one of its receptors, EphA4, is expressed in postnatal corticospinal neurons as their fibers pathfind down the contralateral spinal cord. Our data indicate ephrin-B3 functions as a midline-anchored repellent to stimulate forward signaling in EphA4-expressing axons.},
	Author = {Yokoyama, N and Romero, M I and Cowan, C A and Galvan, P and Helmbacher, F and Charnay, P and Parada, L F and Henkemeyer, M},
	Date-Added = {2017-05-24 23:48:35 +0000},
	Date-Modified = {2017-05-24 23:48:35 +0000},
	Journal = {Neuron},
	Journal-Full = {Neuron},
	Mesh = {Alleles; Animals; Axons; Electric Stimulation; Ephrin-B3; Female; Fetal Proteins; Gait Disorders, Neurologic; Homozygote; Male; Membrane Proteins; Mice; Mice, Neurologic Mutants; Motor Cortex; Mutagenesis, Site-Directed; Pyramidal Tracts; Receptor Protein-Tyrosine Kinases; Receptor, EphA4; Signal Transduction; Spinal Cord},
	Month = {Jan},
	Number = {1},
	Pages = {85-97},
	pmid = {11182083},
	Pst = {ppublish},
	Title = {Forward signaling mediated by ephrin-B3 prevents contralateral corticospinal axons from recrossing the spinal cord midline},
	Volume = {29},
	Year = {2001},
	url = {papers/Yokoyama_Neuron2001.pdf}}

@article{Dottori:1998,
	Abstract = {Members of the Eph family of tyrosine kinase receptors have been implicated in the regulation of developmental processes and, in particular, axon guidance in the developing nervous system. The function of the EphA4 (Sek1) receptor was explored through creation of a null mutant mouse. Mice with a null mutation in the EphA4 gene are viable and fertile but have a gross motor dysfunction, which is evidenced by a loss of coordination of limb movement and a resultant hopping, kangaroo-like gait. Consistent with the observed phenotype, anatomical studies and anterograde tracing experiments reveal major disruptions of the corticospinal tract within the medulla and spinal cord in the null mutant animals. These results demonstrate a critical role for EphA4 in establishing the corticospinal projection.},
	Author = {Dottori, M and Hartley, L and Galea, M and Paxinos, G and Polizzotto, M and Kilpatrick, T and Bartlett, P F and Murphy, M and K{\"o}ntgen, F and Boyd, A W},
	Date-Added = {2017-05-24 23:42:32 +0000},
	Date-Modified = {2017-05-24 23:42:32 +0000},
	Journal = {Proc Natl Acad Sci U S A},
	Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},
	Mesh = {Animals; Base Sequence; Fetal Proteins; Gait; Gene Expression Regulation, Developmental; Genotype; Homozygote; Medulla Oblongata; Mice; Mice, Knockout; Molecular Sequence Data; Movement Disorders; Nerve Fibers; Nerve Tissue Proteins; Neural Pathways; Polymerase Chain Reaction; Receptor Protein-Tyrosine Kinases; Receptor, EphA4; Recombination, Genetic; Restriction Mapping; Spinal Cord; Stem Cells},
	Month = {Oct},
	Number = {22},
	Pages = {13248-53},
	Pmc = {PMC23772},
	pmid = {9789074},
	Pst = {ppublish},
	Title = {EphA4 (Sek1) receptor tyrosine kinase is required for the development of the corticospinal tract},
	Volume = {95},
	Year = {1998},
	url = {papers/Dottori_ProcNatlAcadSciUSA1998.pdf}}

@article{Kullander:2001,
	Abstract = {The EphA4 receptor tyrosine kinase regulates the formation of the corticospinal tract (CST), a pathway controlling voluntary movements, and of the anterior commissure (AC), connecting the neocortical temporal lobes. To study EphA4 kinase signaling in these processes, we generated mice expressing mutant EphA4 receptors either lacking kinase activity or with severely downregulated kinase activity. We demonstrate that EphA4 is required for CST formation as a receptor for which it requires an active kinase domain. In contrast, the formation of the AC is rescued by kinase-dead EphA4, suggesting that in this structure EphA4 acts as a ligand for which its kinase activity is not required. Unexpectedly, the cytoplasmic sterile-alpha motif (SAM) domain is not required for EphA4 functions. Our findings establish both kinase-dependent and kinase-independent functions of EphA4 in the formation of major axon tracts.},
	Author = {Kullander, K and Mather, N K and Diella, F and Dottori, M and Boyd, A W and Klein, R},
	Date-Added = {2017-05-24 23:39:19 +0000},
	Date-Modified = {2017-05-24 23:39:19 +0000},
	Journal = {Neuron},
	Journal-Full = {Neuron},
	Mesh = {Animals; Axons; Brain Stem; Ephrin-A4; Ephrin-B2; Fetal Proteins; In Situ Hybridization; Membrane Proteins; Mice; Mice, Knockout; Mice, Mutant Strains; Molecular Sequence Data; Motor Cortex; Organ Specificity; Prosencephalon; Protein Structure, Tertiary; Pyramidal Tracts; RNA, Messenger; Receptor Protein-Tyrosine Kinases; Receptor, EphA4; Signal Transduction; Temporal Lobe},
	Month = {Jan},
	Number = {1},
	Pages = {73-84},
	pmid = {11182082},
	Pst = {ppublish},
	Title = {Kinase-dependent and kinase-independent functions of EphA4 receptors in major axon tract formation in vivo},
	Volume = {29},
	Year = {2001},
	url = {papers/Kullander_Neuron2001.pdf}}

@article{Leighton:2001,
	Abstract = {The search to understand the mechanisms regulating brain wiring has relied on biochemical purification approaches in vertebrates and genetic approaches in invertebrates to identify molecular cues and receptors for axon guidance. Here we describe a phenotype-based gene-trap screen in mice designed for the large-scale identification of genes controlling the formation of the trillions of connections in the mammalian brain. The method incorporates an axonal marker, which helps to identify cell-autonomous mechanisms in axon guidance, and has generated a resource of mouse lines with striking patterns of axonal labelling, which facilitates analysis of the normal wiring diagram of the brain. Studies of two of these mouse lines have identified an in vivo guidance function for a vertebrate transmembrane semaphorin, Sema6A, and have helped re-evaluate that of the Eph receptor EphA4.},
	Author = {Leighton, P A and Mitchell, K J and Goodrich, L V and Lu, X and Pinson, K and Scherz, P and Skarnes, W C and Tessier-Lavigne, M},
	Date-Added = {2017-05-24 22:51:25 +0000},
	Date-Modified = {2017-05-24 22:51:25 +0000},
	Doi = {10.1038/35065539},
	Journal = {Nature},
	Journal-Full = {Nature},
	Mesh = {Alkaline Phosphatase; Animals; Axons; Brain; Cell Adhesion Molecules, Neuronal; Cell Movement; Cells, Cultured; Female; Fetal Proteins; GPI-Linked Proteins; Genetic Techniques; Genetic Vectors; Humans; Isoenzymes; Male; Mice; Mice, Inbred C57BL; Mutation; Nerve Tissue Proteins; Neural Pathways; Neurons; Phenotype; Receptor Protein-Tyrosine Kinases; Receptor, EphA4; Ribosomes; Semaphorins; Sensory Receptor Cells; Thalamus},
	Month = {Mar},
	Number = {6825},
	Pages = {174-9},
	pmid = {11242070},
	Pst = {ppublish},
	Title = {Defining brain wiring patterns and mechanisms through gene trapping in mice},
	Volume = {410},
	Year = {2001},
	url = {papers/Leighton_Nature2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35065539}}

@article{Gallarda:2008,
	Abstract = {Execution of motor behaviors relies on circuitries effectively integrating immediate sensory feedback to efferent pathways controlling muscle activity. It remains unclear how, during neuromuscular circuit assembly, sensory and motor projections become incorporated into tightly coordinated, yet functionally separate pathways. We report that, within axial nerves, establishment of discrete afferent and efferent pathways depends on coordinate signaling between coextending sensory and motor projections. These heterotypic axon-axon interactions require motor axonal EphA3/EphA4 receptor tyrosine kinases activated by cognate sensory axonal ephrin-A ligands. Genetic elimination of trans-axonal ephrin-A --> EphA signaling in mice triggers drastic motor-sensory miswiring, culminating in functional efferents within proximal afferent pathways. Effective assembly of a key circuit underlying motor behaviors thus critically depends on trans-axonal signaling interactions resolving motor and sensory projections into discrete pathways.},
	Author = {Gallarda, Benjamin W and Bonanomi, Dario and M{\"u}ller, Daniel and Brown, Arthur and Alaynick, William A and Andrews, Shane E and Lemke, Greg and Pfaff, Samuel L and Marquardt, Till},
	Date-Added = {2017-05-24 22:50:00 +0000},
	Date-Modified = {2017-05-24 22:50:00 +0000},
	Doi = {10.1126/science.1153758},
	Journal = {Science},
	Journal-Full = {Science (New York, N.Y.)},
	Mesh = {Afferent Pathways; Animals; Axons; Cells, Cultured; Coculture Techniques; Efferent Pathways; Electrophysiology; Ephrins; Ganglia, Spinal; Growth Cones; Ligands; Mice; Mice, Transgenic; Motor Activity; Motor Neurons; Muscle, Skeletal; Mutation; Neurons, Afferent; Peripheral Nerves; Receptor, EphA3; Receptor, EphA4; Signal Transduction},
	Month = {Apr},
	Number = {5873},
	Pages = {233-6},
	Pmc = {PMC3158657},
	pmid = {18403711},
	Pst = {ppublish},
	Title = {Segregation of axial motor and sensory pathways via heterotypic trans-axonal signaling},
	Volume = {320},
	Year = {2008},
	url = {papers/Gallarda_Science2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1153758}}

@article{Armentano:2007,
	Abstract = {We used cortex-specific deletion of the transcription factor gene COUP-TFI (also known as Nr2f1) in mice to demonstrate previously unknown fundamental roles for it in patterning mammalian neocortex into areas. The highest COUP-TFI expression is observed in the cortical progenitors and progeny in parietal and occipital cortex that form sensory areas, and the lowest expression was observed in frontal cortex that includes motor areas. Cortical deletion of COUP-TFI resulted in massive expansion of frontal areas, including motor, to occupy most of neocortex, paralleled by marked compression of sensory areas to caudal occipital cortex. These area patterning changes are preceded and paralleled by corresponding changes in molecular markers of area identity and altered axonal projections to maintain patterned area-specific input and output connections. We conclude that COUP-TFI is required for balancing patterning of neocortex into frontal/motor and sensory areas by acting in its expression domain to repress frontal/motor area identities and to specify sensory area identities.},
	Author = {Armentano, Maria and Chou, Shen-Ju and Tomassy, Giulio Srubek and Leing{\"a}rtner, Axel and O'Leary, Dennis D M and Studer, Mich{\`e}le},
	Date-Added = {2017-05-25 00:09:44 +0000},
	Date-Modified = {2017-05-25 00:09:44 +0000},
	Doi = {10.1038/nn1958},
	Journal = {Nat Neurosci},
	Journal-Full = {Nature neuroscience},
	Mesh = {Animals; Body Patterning; COUP Transcription Factor I; Embryo, Mammalian; Fibroblast Growth Factor 8; Gene Expression Regulation, Developmental; Homeodomain Proteins; Mice; Mice, Inbred C57BL; Mice, Transgenic; Motor Cortex; Neural Pathways; PAX2 Transcription Factor; Serotonin; Somatosensory Cortex; Transcription Factors},
	Month = {Oct},
	Number = {10},
	Pages = {1277-86},
	pmid = {17828260},
	Pst = {ppublish},
	Title = {COUP-TFI regulates the balance of cortical patterning between frontal/motor and sensory areas},
	Volume = {10},
	Year = {2007},
	url = {papers/Armentano_NatNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1958}}

@article{Bedogni:2010,
	Abstract = {Areas and layers of the cerebral cortex are specified by genetic programs that are initiated in progenitor cells and then, implemented in postmitotic neurons. Here, we report that Tbr1, a transcription factor expressed in postmitotic projection neurons, exerts positive and negative control over both regional (areal) and laminar identity. Tbr1 null mice exhibited profound defects of frontal cortex and layer 6 differentiation, as indicated by down-regulation of gene-expression markers such as Bcl6 and Cdh9. Conversely, genes that implement caudal cortex and layer 5 identity, such as Bhlhb5 and Fezf2, were up-regulated in Tbr1 mutants. Tbr1 implements frontal identity in part by direct promoter binding and activation of Auts2, a frontal cortex gene implicated in autism. Tbr1 regulates laminar identity in part by downstream activation or maintenance of Sox5, an important transcription factor controlling neuronal migration and corticofugal axon projections. Similar to Sox5 mutants, Tbr1 mutants exhibit ectopic axon projections to the hypothalamus and cerebral peduncle. Together, our findings show that Tbr1 coordinately regulates regional and laminar identity of postmitotic cortical neurons.},
	Author = {Bedogni, Francesco and Hodge, Rebecca D and Elsen, Gina E and Nelson, Branden R and Daza, Ray A M and Beyer, Richard P and Bammler, Theo K and Rubenstein, John L R and Hevner, Robert F},
	Date-Added = {2017-05-24 20:46:48 +0000},
	Date-Modified = {2017-05-24 20:46:48 +0000},
	Doi = {10.1073/pnas.1002285107},
	Journal = {Proc Natl Acad Sci U S A},
	Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},
	Mesh = {Animals; Biomarkers; DNA-Binding Proteins; Down-Regulation; Gene Expression Regulation, Developmental; Mice; Mitosis; Mutation; Neocortex; Neurons; Nuclear Proteins; Oligonucleotide Array Sequence Analysis; Organ Specificity; Protein Binding; Transcriptional Activation; Up-Regulation},
	Month = {Jul},
	Number = {29},
	Pages = {13129-34},
	Pmc = {PMC2919950},
	pmid = {20615956},
	Pst = {ppublish},
	Title = {Tbr1 regulates regional and laminar identity of postmitotic neurons in developing neocortex},
	Volume = {107},
	Year = {2010},
	url = {papers/Bedogni_ProcNatlAcadSciUSA2010.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.1002285107}}

@article{Kalil:2011,
	Abstract = {Precise wiring of cortical circuits during development depends upon axon extension, guidance, and branching to appropriate targets. Motile growth cones at axon tips navigate through the nervous system by responding to molecular cues, which modulate signaling pathways within axonal growth cones. Intracellular calcium signaling has emerged as a major transducer of guidance cues but exactly how calcium signaling pathways modify the actin and microtubule cytoskeleton to evoke growth cone behaviors and axon branching is still mysterious. Axons must often pause their extension in tracts while their branches extend into targets. Some evidence suggests a competition between growth of axons and branches but the mechanisms are poorly understood. Since it is difficult to study growing axons deep within the mammalian brain, much of what we know about signaling pathways and cytoskeletal dynamics of growth cones comes from tissue culture studies, in many cases, of non-mammalian species. Consequently it is not well understood how guidance cues relevant to mammalian neural development in vivo signal to the growth cone cytoskeleton during axon outgrowth and guidance. In this review we describe our recent work in dissociated cultures of developing rodent sensorimotor cortex in the context of the current literature on molecular guidance cues, calcium signaling pathways, and cytoskeletal dynamics that regulate growth cone behaviors. A major challenge is to relate findings in tissue culture to mechanisms of cortical development in vivo. Toward this goal, we describe our recent work in cortical slices, which preserve the complex cellular and molecular environment of the mammalian brain but allow direct visualization of growth cone behaviors and calcium signaling. Findings from this work suggest that mechanisms regulating axon growth and guidance in dissociated culture neurons also underlie development of cortical connectivity in vivo.},
	Author = {Kalil, Katherine and Li, Li and Hutchins, B Ian},
	Date-Added = {2017-05-23 05:43:57 +0000},
	Date-Modified = {2017-05-23 05:43:57 +0000},
	Doi = {10.3389/fnana.2011.00062},
	Journal = {Front Neuroanat},
	Journal-Full = {Frontiers in neuroanatomy},
	Keywords = {CaMKII; Wnt5a; axon branching; axon guidance; axon outgrowth; calcium signaling; corpus callosum; microtubules},
	Pages = {62},
	Pmc = {PMC3202218},
	pmid = {22046148},
	Pst = {epublish},
	Title = {Signaling mechanisms in cortical axon growth, guidance, and branching},
	Volume = {5},
	Year = {2011},
	url = {papers/Kalil_FrontNeuroanat2011.pdf}}

@article{Huang:2012,
	Abstract = {BACKGROUND: Adolescent alcohol abuse remains a serious public health concern, with nearly a third of high school seniors reporting heavy drinking in the previous month.
METHODS: Using the high ethanol-consuming C57BL/6J mouse strain, we examined the effects of ethanol (3.75 g/kg, IP, daily for 45 days) on body weight and brain region mass (cerebral cortex, cerebellum, corpus callosum) during peri-adolescence (postnatal day [P]25 to 70) or adulthood (P180 to 225) of both males and females.
RESULTS: In control peri-adolescent animals, body weight gain was greater in males compared with females. In the peri-adolescent exposure group, ethanol significantly reduced body weight gain to a similar extent in both male and female mice (82 and 84% of controls, respectively). In adult animals, body weight gain was much less than that of the peri-adolescent mice, with ethanol having a small but significant effect in males but not females. Between the control peri-adolescent and adult cohorts (measurements taken at P70 and 225, respectively), there were no significant differences in the mass of the cerebral cortex or the cerebellum from either male or female mice, although the rostro-caudal length of the corpus callosum increased slightly but significantly (6.1%) between these time points.
CONCLUSIONS: Ethanol treatment significantly reduced the mass of the cerebral cortex in peri-adolescent (-3.1%), but not adult, treated mice. By contrast, ethanol significantly reduced the length of the corpus callosum in adult (-5.4%), but not peri-adolescent, treated mice. Future studies at the histological level may yield additional details concerning ethanol and the peri-adolescent brain.},
	Author = {Huang, Chiming and Titus, Jennifer A and Bell, Richard L and Kapros, Tamas and Chen, Jie and Huang, Rosa},
	Date-Added = {2017-05-19 17:17:59 +0000},
	Date-Modified = {2017-05-19 17:17:59 +0000},
	Doi = {10.1111/j.1530-0277.2012.01759.x},
	Journal = {Alcohol Clin Exp Res},
	Journal-Full = {Alcoholism, clinical and experimental research},
	Mesh = {Age Factors; Alcoholism; Animals; Body Weight; Brain; Corpus Callosum; Disease Models, Animal; Ethanol; Female; Male; Mice; Mice, Inbred C57BL; Organ Size},
	Month = {Oct},
	Number = {10},
	Pages = {1728-37},
	pmid = {22433022},
	Pst = {ppublish},
	Title = {A mouse model for adolescent alcohol abuse: stunted growth and effects in brain},
	Volume = {36},
	Year = {2012},
	url = {papers/Huang_AlcoholClinExpRes2012.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1530-0277.2012.01759.x}}

@article{Pollard:2006,
	Abstract = {The developmental and evolutionary mechanisms behind the emergence of human-specific brain features remain largely unknown. However, the recent ability to compare our genome to that of our closest relative, the chimpanzee, provides new avenues to link genetic and phenotypic changes in the evolution of the human brain. We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that the most dramatic of these 'human accelerated regions', HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal-Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal-Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology.},
	Author = {Pollard, Katherine S and Salama, Sofie R and Lambert, Nelle and Lambot, Marie-Alexandra and Coppens, Sandra and Pedersen, Jakob S and Katzman, Sol and King, Bryan and Onodera, Courtney and Siepel, Adam and Kern, Andrew D and Dehay, Colette and Igel, Haller and Ares, Jr, Manuel and Vanderhaeghen, Pierre and Haussler, David},
	Date-Added = {2017-05-05 21:57:52 +0000},
	Date-Modified = {2017-05-05 21:59:46 +0000},
	Doi = {10.1038/nature05113},
	Journal = {Nature},
	Journal-Full = {Nature},
	Keywords = {Neocortex; isocortex; Evolution},
	Mesh = {Aging; Animals; Base Sequence; Cell Adhesion Molecules, Neuronal; Cerebral Cortex; Evolution, Molecular; Extracellular Matrix Proteins; Gene Expression Profiling; Gene Expression Regulation, Developmental; Humans; Macaca; Molecular Sequence Data; Mutation; Neocortex; Nerve Tissue Proteins; Nucleic Acid Conformation; Organ Specificity; RNA Stability; RNA, Untranslated; Serine Endopeptidases; Time Factors},
	Month = {Sep},
	Number = {7108},
	Pages = {167-72},
	pmid = {16915236},
	Pst = {ppublish},
	Title = {An RNA gene expressed during cortical development evolved rapidly in humans},
	Volume = {443},
	Year = {2006},
	url = {papers/Pollard_Nature2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature05113}}

@article{Uziel:2002,
	Abstract = {Axon guidance cues of the ephrin ligand family have been hypothesized to regulate the formation of thalamocortical connections, but in vivo evidence for such a role has not been examined directly. To test whether ephrin-mediated repulsive cues participate in sorting the projections originating from distinct thalamic nuclei, we analyzed the organization of somatosensory and anterior cingulate afferents postnatally in mice lacking ephrin-A5 gene expression. Projections from ventrobasal and laterodorsal nuclei to their respective sensory and limbic cortical areas developed normally. However, a portion of limbic thalamic neurons from the laterodorsal nucleus also formed additional projections to somatosensory cortical territories, thus maintaining inappropriate dual projections to multiple cortical regions. These results suggest that ephrin-A5 is not required for the formation of normal cortical projections from the appropriate thalamic nuclei, but rather acts as a guidance cue that restricts limbic thalamic axons from inappropriate neocortical regions.},
	Author = {Uziel, Daniela and M{\"u}hlfriedel, Sven and Zarbalis, Kostas and Wurst, Wolfgang and Levitt, Pat and Bolz, J{\"u}rgen},
	Date-Added = {2017-05-05 19:04:13 +0000},
	Date-Modified = {2017-05-05 19:04:13 +0000},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Mesh = {Animals; Cell Count; Cerebral Cortex; Ephrin-A5; Fluorescent Dyes; Gyrus Cinguli; Homozygote; Limbic System; Mice; Mice, Knockout; Nervous System Malformations; Neurons; Thalamic Nuclei; Thalamus},
	Month = {Nov},
	Number = {21},
	Pages = {9352-7},
	pmid = {12417660},
	Pst = {ppublish},
	Title = {Miswiring of limbic thalamocortical projections in the absence of ephrin-A5},
	Volume = {22},
	Year = {2002},
	url = {papers/Uziel_JNeurosci2002.pdf}}

@article{Sigalas:2015,
	Abstract = {UNLABELLED: Nicotinic acetylcholine receptors (nAChRs) play an important role in the modulation of many cognitive functions but their role in integrated network activity remains unclear. This is at least partly because of the complexity of the cholinergic circuitry and the difficulty in comparing results from in vivo studies obtained under diverse experimental conditions and types of anesthetics. Hence the role of nAChRs in the synchronization of cortical activity during slow-wave sleep is still controversial, with some studies showing they are involved in ACh-dependent EEG desynchronization, and others suggesting that this effect is mediated exclusively by muscarinic receptors. Here we use an in vitro model of endogenous network activity, in the form of recurring self-maintained depolarized states (Up states), which allows us to examine the role of high-affinity nAChRs on network dynamics in a simpler form of the cortical microcircuit. We find that mice lacking nAChRs containing the β2-subunit (β2-nAChRs) have longer and more frequent Up states, and that this difference is eliminated when β2-nAChRs in wild-type mice are blocked. We further show that endogenously released ACh can modulate Up/Down states through the activation of both β2- and α7-containing nAChRs, but through distinct mechanisms: α7-nAChRs affect only the termination of spontaneous Up states, while β2-nAChRs also regulate their generation. Finally we provide evidence that the effects of β2-subunit-containing, but not α7-subunit-containing nAChRs, are mediated through GABAB receptors. To our knowledge this is the first study documenting direct nicotinic modulation of Up/Down state activity.
SIGNIFICANCE STATEMENT: Through our experiments we were able to uncover a clear and previously disputed effect of nicotinic signaling in synchronized activity of neuronal networks of the cortex. We show that both high-affinity receptors (containing the β2-subunit, β2-nAChRs) and low-affinity receptors (containing the α7-subunit, α7-nAChRs) can regulate cortical network function exhibited in the form of Up/Down states. We further show that the effects of β2-nAChRs, but not α7-nAChRs, are mediated through the activation of GABAB receptors. These results suggest a possible synthesis of seemingly contradictory results in the literature and could be valuable for informing computational models of cortical function and for guiding the search for therapeutic interventions.},
	Author = {Sigalas, Charalambos and Rigas, Pavlos and Tsakanikas, Panagiotis and Skaliora, Irini},
	Date-Added = {2017-05-05 18:50:13 +0000},
	Date-Modified = {2017-05-05 18:50:13 +0000},
	Doi = {10.1523/JNEUROSCI.5222-14.2015},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Keywords = {barrel cortex; cholinergic; network activity; oscillations; persistent activity; β2-nAChR},
	Mesh = {Animals; Cells, Cultured; Cerebral Cortex; Excitatory Postsynaptic Potentials; In Vitro Techniques; Mice; Mice, Knockout; Neurons; Nicotine; Patch-Clamp Techniques; Receptors, Nicotinic; alpha7 Nicotinic Acetylcholine Receptor},
	Month = {Aug},
	Number = {32},
	Pages = {11196-208},
	pmid = {26269630},
	Pst = {ppublish},
	Title = {High-Affinity Nicotinic Receptors Modulate Spontaneous Cortical Up States In Vitro},
	Volume = {35},
	Year = {2015},
	url = {papers/Sigalas_JNeurosci2015.pdf}}

@article{Alcamo:2008,
	Abstract = {Satb2 is a DNA-binding protein that regulates chromatin organization and gene expression. In the developing brain, Satb2 is expressed in cortical neurons that extend axons across the corpus callosum. To assess the role of Satb2 in neurons, we analyzed mice in which the Satb2 locus was disrupted by insertion of a LacZ gene. In mutant mice, beta-galactosidase-labeled axons are absent from the corpus callosum and instead descend along the corticospinal tract. Satb2 mutant neurons acquire expression of Ctip2, a transcription factor that is necessary and sufficient for the extension of subcortical projections by cortical neurons. Conversely, ectopic expression of Satb2 in neural stem cells markedly decreases Ctip2 expression. Finally, we find that Satb2 binds directly to regulatory regions of Ctip2 and induces changes in chromatin structure. These data suggest that Satb2 functions as a repressor of Ctip2 and regulatory determinant of corticocortical connections in the developing cerebral cortex.},
	Author = {Alcamo, Elizabeth A and Chirivella, Laura and Dautzenberg, Marcel and Dobreva, Gergana and Fari{\~n}as, Isabel and Grosschedl, Rudolf and McConnell, Susan K},
	Date-Added = {2017-05-05 18:44:08 +0000},
	Date-Modified = {2017-05-05 18:45:16 +0000},
	Doi = {10.1016/j.neuron.2007.12.012},
	Journal = {Neuron},
	Journal-Full = {Neuron},
	Mesh = {Animals; Animals, Newborn; Bromodeoxyuridine; Cells, Cultured; Cerebral Cortex; Chromatin Immunoprecipitation; Electrophoretic Mobility Shift Assay; Embryo, Mammalian; Gene Expression Regulation, Developmental; Matrix Attachment Region Binding Proteins; Mice; Mice, Transgenic; Mutation; Nerve Tissue Proteins; Neural Pathways; Neurons; Stem Cells; Transcription Factors},
	Month = {Feb},
	Number = {3},
	Pages = {364-77},
	pmid = {18255030},
	Pst = {ppublish},
	Title = {Satb2 regulates callosal projection neuron identity in the developing cerebral cortex},
	Volume = {57},
	Year = {2008},
	url = {papers/Alcamo_Neuron2008.pdf},
	Bdsk-File-2 = {papers/Alcamo_Neuron2008a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.12.012}}

@article{Lieberoth:2009,
	Abstract = {Although carbohydrates have been implicated in cell interactions in the nervous system, the molecular bases of their functions have remained largely obscure. Here, we show that promotion or inhibition of neurite outgrowth of cerebellar or dorsal root ganglion neurons, respectively, induced by the mucin-type adhesion molecule CD24 depends on alpha2,3-linked sialic acid and Lewis(x) present on glia-specific CD24 glycoforms. Alpha2,3-sialyl residues of CD24 bind to a structural motif in the first fibronectin type III domain of the adhesion molecule L1. Following the observation that the adhesion molecules TAG-1 and Contactin show sequence homologies with fucose-specific lectins, we obtained evidence that TAG-1 and Contactin mediate Lewis(x)-dependent CD24-induced effects on neurite outgrowth. Thus, L1, TAG-1, and Contactin function as lectin-like neuronal receptors. Their cis interactions with neighboring adhesion molecules, e.g., Caspr1 and Caspr2, and with their triggered signal transduction pathways elicit cell type-specific promotion or inhibition of neurite outgrowth induced by glial CD24 in a glycan-dependent trans interaction.},
	Author = {Lieberoth, Annika and Splittstoesser, Frauke and Katagihallimath, Nainesh and Jakovcevski, Igor and Loers, Gabriele and Ranscht, Barbara and Karagogeos, Domna and Schachner, Melitta and Kleene, Ralf},
	Date-Added = {2017-05-04 23:34:33 +0000},
	Date-Modified = {2017-05-04 23:34:33 +0000},
	Doi = {10.1523/JNEUROSCI.4361-08.2009},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Mesh = {Animals; Animals, Newborn; Antigens, CD15; Antigens, CD24; Binding Sites; Cell Adhesion Molecules, Neuronal; Cells, Cultured; Cerebellum; Contactin 2; Contactins; Cricetinae; Cricetulus; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Ganglia, Spinal; Glycosylation; Immunoprecipitation; Leukocyte L1 Antigen Complex; Locomotion; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurites; Neurons; Peptides; Protein Binding; Recovery of Function; Sialic Acids; Spinal Cord Injuries; Transfection},
	Month = {May},
	Number = {20},
	Pages = {6677-90},
	pmid = {19458237},
	Pst = {ppublish},
	Title = {Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth},
	Volume = {29},
	Year = {2009},
	url = {papers/Lieberoth_JNeurosci2009.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4361-08.2009}}

@article{Vernes:2008,
	Abstract = {BACKGROUND: Rare mutations affecting the FOXP2 transcription factor cause a monogenic speech and language disorder. We hypothesized that neural pathways downstream of FOXP2 influence more common phenotypes, such as specific language impairment.
METHODS: We performed genomic screening for regions bound by FOXP2 using chromatin immunoprecipitation, which led us to focus on one particular gene that was a strong candidate for involvement in language impairments. We then tested for associations between single-nucleotide polymorphisms (SNPs) in this gene and language deficits in a well-characterized set of 184 families affected with specific language impairment.
RESULTS: We found that FOXP2 binds to and dramatically down-regulates CNTNAP2, a gene that encodes a neurexin and is expressed in the developing human cortex. On analyzing CNTNAP2 polymorphisms in children with typical specific language impairment, we detected significant quantitative associations with nonsense-word repetition, a heritable behavioral marker of this disorder (peak association, P=5.0x10(-5) at SNP rs17236239). Intriguingly, this region coincides with one associated with language delays in children with autism.
CONCLUSIONS: The FOXP2-CNTNAP2 pathway provides a mechanistic link between clinically distinct syndromes involving disrupted language.},
	Author = {Vernes, Sonja C and Newbury, Dianne F and Abrahams, Brett S and Winchester, Laura and Nicod, J{\'e}r{\^o}me and Groszer, Matthias and Alarc{\'o}n, Maricela and Oliver, Peter L and Davies, Kay E and Geschwind, Daniel H and Monaco, Anthony P and Fisher, Simon E},
	Date-Added = {2017-05-04 23:31:28 +0000},
	Date-Modified = {2017-05-04 23:31:28 +0000},
	Doi = {10.1056/NEJMoa0802828},
	Journal = {N Engl J Med},
	Journal-Full = {The New England journal of medicine},
	Mesh = {Child; Chromatin Immunoprecipitation; Down-Regulation; Female; Forkhead Transcription Factors; Gene Expression Regulation; Genetic Markers; Genome-Wide Association Study; Haplotypes; Humans; Language Development Disorders; Male; Membrane Proteins; Nerve Tissue Proteins; Phenotype; Polymerase Chain Reaction; Polymorphism, Single Nucleotide},
	Month = {Nov},
	Number = {22},
	Pages = {2337-45},
	Pmc = {PMC2756409},
	pmid = {18987363},
	Pst = {ppublish},
	Title = {A functional genetic link between distinct developmental language disorders},
	Volume = {359},
	Year = {2008},
	url = {papers/Vernes_NEnglJMed2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa0802828}}

@article{Strauss:2006,
	Abstract = {Contactin-associated protein-like 2 (CASPR2) is encoded by CNTNAP2 and clusters voltage-gated potassium channels (K(v)1.1) at the nodes of Ranvier. We report a homozygous mutation of CNTNAP2 in Old Order Amish children with cortical dysplasia, focal epilepsy, relative macrocephaly, and diminished deep-tendon reflexes. Intractable focal seizures began in early childhood, after which language regression, hyperactivity, impulsive and aggressive behavior, and mental retardation developed in all children. Resective surgery did not prevent the recurrence of seizures. Temporal-lobe specimens showed evidence of abnormalities of neuronal migration and structure, widespread astrogliosis, and reduced expression of CASPR2.},
	Author = {Strauss, Kevin A and Puffenberger, Erik G and Huentelman, Matthew J and Gottlieb, Steven and Dobrin, Seth E and Parod, Jennifer M and Stephan, Dietrich A and Morton, D Holmes},
	Date-Added = {2017-05-04 23:20:58 +0000},
	Date-Modified = {2017-05-04 23:20:58 +0000},
	Doi = {10.1056/NEJMoa052773},
	Journal = {N Engl J Med},
	Journal-Full = {The New England journal of medicine},
	Mesh = {Child; Child, Preschool; Electroencephalography; Epilepsies, Partial; Gene Expression; Homozygote; Humans; Magnetic Resonance Angiography; Membrane Proteins; Mutation; Nerve Tissue Proteins; Phenotype; Reflex, Stretch; Secondary Prevention; Seizures; Temporal Lobe},
	Month = {Mar},
	Number = {13},
	Pages = {1370-7},
	pmid = {16571880},
	Pst = {ppublish},
	Title = {Recessive symptomatic focal epilepsy and mutant contactin-associated protein-like 2},
	Volume = {354},
	Year = {2006},
	url = {papers/Strauss_NEnglJMed2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1056/NEJMoa052773}}

@article{Lepe-Zuniga:1987,
	Author = {Lepe-Zuniga, J L and Zigler, Jr, J S and Gery, I},
	Date-Added = {2017-05-04 21:46:52 +0000},
	Date-Modified = {2017-05-04 21:46:52 +0000},
	Journal = {J Immunol Methods},
	Journal-Full = {Journal of immunological methods},
	Mesh = {Culture Media; HEPES; Hydrogen Peroxide; Piperazines},
	Month = {Oct},
	Number = {1},
	Pages = {145},
	pmid = {3655381},
	Pst = {ppublish},
	Title = {Toxicity of light-exposed Hepes media},
	Volume = {103},
	Year = {1987}}

@article{Swartz:2017,
	Abstract = {Identifying biological mechanisms through which the experience of adversity emerges as individual risk for mental illness is an important step toward developing strategies for personalized treatment and, ultimately, prevention. Preclinical studies have identified epigenetic modification of gene expression as one such mechanism. Recent clinical studies have suggested that epigenetic modification, particularly methylation of gene regulatory regions, also acts to shape human brain function associated with risk for mental illness. However, it is not yet clear whether differential gene methylation as a function of adversity contributes to the emergence of individual risk for mental illness. Using prospective longitudinal epigenetic, neuroimaging and behavioral data from 132 adolescents, we demonstrate that changes in gene methylation associated with lower socioeconomic status (SES) predict changes in risk-related brain function. Specifically, we find that lower SES during adolescence is associated with an increase in methylation of the proximal promoter of the serotonin transporter gene, which predicts greater increases in threat-related amygdala reactivity. We subsequently demonstrate that greater increases in amygdala reactivity moderate the association between a positive family history for depression and the later manifestation of depressive symptoms. These initial results suggest a specific biological mechanism through which adversity contributes to altered brain function, which in turn moderates the emergence of general liability as individual risk for mental illness. If replicated, this prospective pathway may represent a novel target biomarker for intervention and prevention among high-risk individuals.},
	Author = {Swartz, J R and Hariri, A R and Williamson, D E},
	Date-Added = {2017-04-25 00:10:58 +0000},
	Date-Modified = {2017-04-25 00:10:58 +0000},
	Doi = {10.1038/mp.2016.82},
	Journal = {Mol Psychiatry},
	Journal-Full = {Molecular psychiatry},
	Month = {Feb},
	Number = {2},
	Pages = {209-214},
	Pmc = {PMC5122474},
	pmid = {27217150},
	Pst = {ppublish},
	Title = {An epigenetic mechanism links socioeconomic status to changes in depression-related brain function in high-risk adolescents},
	Volume = {22},
	Year = {2017},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/mp.2016.82}}

@article{McGowan:2009,
	Abstract = {Maternal care influences hypothalamic-pituitary-adrenal (HPA) function in the rat through epigenetic programming of glucocorticoid receptor expression. In humans, childhood abuse alters HPA stress responses and increases the risk of suicide. We examined epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history of childhood abuse and those from either suicide victims with no childhood abuse or controls. We found decreased levels of glucocorticoid receptor mRNA, as well as mRNA transcripts bearing the glucocorticoid receptor 1F splice variant and increased cytosine methylation of an NR3C1 promoter. Patch-methylated NR3C1 promoter constructs that mimicked the methylation state in samples from abused suicide victims showed decreased NGFI-A transcription factor binding and NGFI-A-inducible gene transcription. These findings translate previous results from rat to humans and suggest a common effect of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression.},
	Author = {McGowan, Patrick O and Sasaki, Aya and D'Alessio, Ana C and Dymov, Sergiy and Labont{\'e}, Benoit and Szyf, Moshe and Turecki, Gustavo and Meaney, Michael J},
	Date-Added = {2017-04-25 00:01:42 +0000},
	Date-Modified = {2017-04-25 00:01:42 +0000},
	Doi = {10.1038/nn.2270},
	Journal = {Nat Neurosci},
	Journal-Full = {Nature neuroscience},
	Mesh = {Adult; Adult Survivors of Child Abuse; Base Sequence; Cell Line; DNA Methylation; Epigenesis, Genetic; Female; Hippocampus; Humans; Male; Middle Aged; Molecular Sequence Data; Promoter Regions, Genetic; Receptors, Glucocorticoid; Suicide; Young Adult},
	Month = {Mar},
	Number = {3},
	Pages = {342-8},
	Pmc = {PMC2944040},
	pmid = {19234457},
	Pst = {ppublish},
	Title = {Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse},
	Volume = {12},
	Year = {2009},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn.2270}}

@article{Guemez-Gamboa:2014,
	Abstract = {Activity-dependent neurotransmitter switching engages genetic programs regulating transmitter synthesis, but the mechanism by which activity is transduced is unknown. We suppressed activity in single neurons in the embryonic spinal cord to determine whether glutamate-gamma-aminobutyric acid (GABA) switching is cell autonomous. Transmitter respecification did not occur, suggesting that it is homeostatically regulated by the level of activity in surrounding neurons. Graded increase in the number of silenced neurons in cultures led to graded decrease in the number of neurons expressing GABA, supporting non-cell-autonomous transmitter switching. We found that brain-derived neurotrophic factor (BDNF) is expressed in the spinal cord during the period of transmitter respecification and that spike activity causes release of BDNF. Activation of TrkB receptors triggers a signaling cascade involving JNK-mediated activation of cJun that regulates tlx3, a glutamate/GABA selector gene, accounting for calcium-spike BDNF-dependent transmitter switching. Our findings identify a molecular mechanism for activity-dependent respecification of neurotransmitter phenotype in developing spinal neurons.},
	Author = {Guemez-Gamboa, Alicia and Xu, Lin and Meng, Da and Spitzer, Nicholas C},
	Date-Added = {2017-04-19 19:20:49 +0000},
	Date-Modified = {2017-04-19 19:20:49 +0000},
	Doi = {10.1016/j.neuron.2014.04.029},
	Journal = {Neuron},
	Journal-Full = {Neuron},
	Mesh = {Animals; Brain-Derived Neurotrophic Factor; Calcium; Cells, Cultured; Female; Glutamic Acid; JNK Mitogen-Activated Protein Kinases; Neurons; Phosphorylation; Proto-Oncogene Proteins c-jun; Signal Transduction; Spinal Cord; Xenopus laevis; gamma-Aminobutyric Acid},
	Month = {Jun},
	Number = {5},
	Pages = {1004-16},
	Pmc = {PMC4072120},
	pmid = {24908484},
	Pst = {ppublish},
	Title = {Non-cell-autonomous mechanism of activity-dependent neurotransmitter switching},
	Volume = {82},
	Year = {2014},
	url = {papers/Guemez-Gamboa_Neuron2014.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2014.04.029}}

@article{Ballesteros-Yanez:2010,
	Abstract = {The neuronal nicotinic acetylcholine receptors (nAChRs) are allosteric membrane proteins involved in multiple cognitive processes, including attention, learning, and memory. The most abundant form of heterooligomeric nAChRs in the brain contains the beta2- and alpha4- subunits and binds nicotinic agonists with high affinity. In the present study, we investigated in the mouse the consequences of the deletion of one of the nAChR components: the beta2-subunit (beta2(-/-)) on the microanatomy of cortical pyramidal cells. Using an intracellular injection method, complete basal dendritic arbors of 650 layer III pyramidal neurons were sampled from seven cortical fields, including primary sensory, motor, and associational areas, in both beta2(-/-) and WT animals. We observed that the pyramidal cell phenotype shows significant quantitative differences among different cortical areas in mutant and WT mice. In WT mice, the density of dendritic spines was rather similar in all cortical fields, except in the prelimbic/infralimbic cortex, where it was significantly higher. In the absence of the beta2-subunit, the most significant reduction in the density of spines took place in this high-order associational field. Our data suggest that the beta2-subunit is involved in the dendritic morphogenesis of pyramidal neurons and, in particular, in the circuits that contribute to the high-order functional connectivity of the cerebral cortex.},
	Author = {Ballesteros-Y{\'a}{\~n}ez, Inmaculada and Benavides-Piccione, Ruth and Bourgeois, Jean-Pierre and Changeux, Jean-Pierre and DeFelipe, Javier},
	Date-Added = {2017-04-18 20:27:46 +0000},
	Date-Modified = {2017-04-18 20:27:46 +0000},
	Doi = {10.1073/pnas.1006269107},
	Journal = {Proc Natl Acad Sci U S A},
	Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},
	Mesh = {Animals; Cerebral Cortex; Dendrites; Dendritic Cells; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Biological; Mutation; Neurons; Phenotype; Pyramidal Cells; Receptors, Nicotinic},
	Month = {Jun},
	Number = {25},
	Pages = {11567-72},
	Pmc = {PMC2895077},
	pmid = {20534523},
	Pst = {ppublish},
	Title = {Alterations of cortical pyramidal neurons in mice lacking high-affinity nicotinic receptors},
	Volume = {107},
	Year = {2010},
	url = {papers/Ballesteros-Yáñez_ProcNatlAcadSciUSA2010.pdf}}

@article{Aden:2003,
	Abstract = {BACKGROUND AND PURPOSE: Cerebral hypoxic ischemia (HI) is an important cause of brain injury in the newborn infant. Adenosine is believed to protect against HI brain damage. However, the roles of the different adenosine receptors are unclear, particularly in young animals. We examined the role of adenosine A2A receptors (A2AR) using 7-day-old A2A knockout (A2AR(-/-)) mice in a model of HI.
METHODS: HI was induced in 7-day-old CD1 mice by exposure to 8% oxygen for 30 minutes after occlusion of the left common carotid artery. The resulting unilateral focal lesion was evaluated with the use of histopathological scoring and measurements of residual brain areas at 5 days, 3 weeks, and 3 months after HI. Behavioral evaluation of brain injury by locomotor activity, rotarod, and beam-walking test was made 3 weeks and 3 months after HI. Cortical cerebral blood flow, assessed by laser-Doppler flowmetry, and rectal temperature were measured during HI.
RESULTS: Reduction in cortical cerebral blood flow during HI and rectal temperature did not differ between wild-type (A2AR(+/+)) and knockout mice. In the A2AR(-/-) animals, brain injury was aggravated compared with wild-type mice. The A2AR(-/-) mice subjected to HI displayed increased forward locomotion and impaired rotarod performance in adulthood compared with A2AR(+/+) mice subjected to HI, whereas beam-walking performance was similarly defective in both groups.
CONCLUSIONS: These results suggest that, in contrast to the situation in adult animals, A2AR play an important protective role in neonatal HI brain injury.},
	Author = {Ad{\'e}n, Ulrika and Halldner, Linda and Lagercrantz, Hugo and Dalmau, Ishar and Ledent, Catherine and Fredholm, Bertil B},
	Date-Added = {2017-01-19 20:33:07 +0000},
	Date-Modified = {2017-01-19 20:33:07 +0000},
	Doi = {10.1161/01.STR.0000060204.67672.8B},
	Journal = {Stroke},
	Journal-Full = {Stroke},
	Mesh = {Animals; Animals, Newborn; Atmosphere Exposure Chambers; Behavior, Animal; Blood Flow Velocity; Body Temperature; Brain; Carotid Arteries; Cerebrovascular Circulation; Disease Models, Animal; Disease Progression; Hypoxia, Brain; Hypoxia-Ischemia, Brain; Laser-Doppler Flowmetry; Ligation; Mice; Mice, Knockout; Receptor, Adenosine A2A; Receptors, Purinergic P1; Survival Rate},
	Month = {Mar},
	Number = {3},
	Pages = {739-44},
	pmid = {12624301},
	Pst = {ppublish},
	Title = {Aggravated brain damage after hypoxic ischemia in immature adenosine A2A knockout mice},
	Volume = {34},
	Year = {2003},
	url = {papers/Adén_Stroke2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.STR.0000060204.67672.8B}}

@article{Guadiana:2013,
	Abstract = {The formation of primary cilia is a highly choreographed process that can be disrupted in developing neurons by overexpressing neuromodulatory G-protein-coupled receptors GPCRs or by blocking intraflagellar transport. Here, we examined the effects of overexpressing the ciliary GPCRs, 5HT6 and SSTR3, on cilia structure and the differentiation of neocortical neurons. Neuronal overexpression of 5HT6 and SSTR3 was achieved by electroporating mouse embryo cortex in utero with vectors encoding these receptors. We found that overexpression of ciliary GPCRs in cortical neurons, especially 5HT6, induced the formation of long (>30 μm) and often forked cilia. These changes were associated with increased levels of intraflagellar transport proteins and accelerated ciliogenesis in neonatal neocortex, the induction of which required Kif3a, an anterograde motor critical for cilia protein trafficking and growth. GPCR overexpression also altered the complement of signaling molecules within the cilia. We found that SSTR3 and type III adenylyl cyclase (ACIII), proteins normally enriched in neuronal cilia, were rarely detected in 5HT6-elongated cilia. Intriguingly, the changes in cilia structure were accompanied by changes in neuronal morphology. Specifically, disruption of normal ciliogenesis in developing neocortical neurons, either by overexpressing cilia GPCRs or a dominant-negative form of Kif3a, significantly impaired dendrite outgrowth. Remarkably, coexpression of ACIII with 5HT6 restored ACIII to cilia, normalized cilia structure, and restored dendrite outgrowth, effects that were not observed in neurons coexpressing ACIII and dominant-negative form of Kif3a. Collectively, our data suggest the formation of neuronal dendrites in developing neocortex requires structurally normal cilia enriched with ACIII.},
	Author = {Guadiana, Sarah M and Semple-Rowland, Susan and Daroszewski, Daniel and Madorsky, Irina and Breunig, Joshua J and Mykytyn, Kirk and Sarkisian, Matthew R},
	Date-Added = {2016-03-18 17:31:34 +0000},
	Date-Modified = {2016-03-18 17:31:34 +0000},
	Doi = {10.1523/JNEUROSCI.2906-12.2013},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Mesh = {Adenylyl Cyclases; Animals; Cells, Cultured; Cilia; Dendrites; Female; Kinesin; Male; Mice; NIH 3T3 Cells; Neocortex; Neurogenesis; Neurons; Pregnancy; Receptors, Serotonin},
	Month = {Feb},
	Number = {6},
	Pages = {2626-38},
	pmid = {23392690},
	Pst = {ppublish},
	Title = {Arborization of dendrites by developing neocortical neurons is dependent on primary cilia and type 3 adenylyl cyclase},
	Volume = {33},
	Year = {2013},
	url = {papers/Guadiana_JNeurosci2013.pdf}}

@article{Breunig:2015,
	Abstract = {As the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma.},
	Author = {Breunig, Joshua J and Levy, Rachelle and Antonuk, C Danielle and Molina, Jessica and Dutra-Clarke, Marina and Park, Hannah and Akhtar, Aslam Abbasi and Kim, Gi Bum and Hu, Xin and Bannykh, Serguei I and Verhaak, Roel G W and Danielpour, Moise},
	Date-Added = {2016-03-18 17:31:15 +0000},
	Date-Modified = {2016-03-18 17:31:15 +0000},
	Doi = {10.1016/j.celrep.2015.06.012},
	Journal = {Cell Rep},
	Journal-Full = {Cell reports},
	Month = {Jul},
	Number = {2},
	Pages = {258-71},
	pmid = {26146073},
	Pst = {ppublish},
	Title = {Ets Factors Regulate Neural Stem Cell Depletion and Gliogenesis in Ras Pathway Glioma},
	Volume = {12},
	Year = {2015},
	url = {papers/Breunig_CellRep2015.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.celrep.2015.06.012}}

@article{Zeisel:2015,
	Abstract = {The mammalian cerebral cortex supports cognitive functions such as sensorimotor integration, memory, and social behaviors. Normal brain function relies on a diverse set of differentiated cell types, including neurons, glia, and vasculature. Here, we have used large-scale single-cell RNA sequencing (RNA-seq) to classify cells in the mouse somatosensory cortex and hippocampal CA1 region. We found 47 molecularly distinct subclasses, comprising all known major cell types in the cortex. We identified numerous marker genes, which allowed alignment with known cell types, morphology, and location. We found a layer I interneuron expressing Pax6 and a distinct postmitotic oligodendrocyte subclass marked by Itpr2. Across the diversity of cortical cell types, transcription factors formed a complex, layered regulatory code, suggesting a mechanism for the maintenance of adult cell type identity.},
	Author = {Zeisel, Amit and Mu{\~n}oz-Manchado, Ana B and Codeluppi, Simone and L{\"o}nnerberg, Peter and La Manno, Gioele and Jur{\'e}us, Anna and Marques, Sueli and Munguba, Hermany and He, Liqun and Betsholtz, Christer and Rolny, Charlotte and Castelo-Branco, Gon{\c c}alo and Hjerling-Leffler, Jens and Linnarsson, Sten},
	Date-Added = {2016-03-17 21:14:22 +0000},
	Date-Modified = {2016-03-17 21:15:48 +0000},
	Doi = {10.1126/science.aaa1934},
	Journal = {Science},
	Journal-Full = {Science (New York, N.Y.)},
	Keywords = {mouse; mice; technique; Methods; RNAseq},
	Mesh = {Animals; CA1 Region, Hippocampal; Eye Proteins; Gene Expression; Genetic Markers; Homeodomain Proteins; Inositol 1,4,5-Trisphosphate Receptors; Interneurons; Mice; Oligodendroglia; Paired Box Transcription Factors; Phylogeny; Repressor Proteins; Sequence Analysis, RNA; Single-Cell Analysis; Somatosensory Cortex; Transcription Factors; Transcriptome},
	Month = {Mar},
	Number = {6226},
	Pages = {1138-42},
	pmid = {25700174},
	Pst = {ppublish},
	Title = {Cell types in the mouse cortex and hippocampus revealed by single-cell RNA-seq},
	Volume = {347},
	Year = {2015},
	url = {papers/Zeisel_Science2015.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.aaa1934}}

@article{Perez-Cadahia:2011,
	Abstract = {Immediate-early genes have important roles in processes such as brain development, learning, and responses to drug abuse. Further, immediate-early genes play an essential role in cellular responses that contribute to long-term neuronal plasticity. Neuronal plasticity is a characteristic of the nervous system that is not limited to the first stages of brain development but persists in adulthood and seems to be an inherent feature of everyday brain function. The plasticity refers to the neuron's capability of showing short- or long-lasting phenotypic changes in response to different stimuli and cellular scenarios. In this review, we focus on the immediate-early genes encoding transcription factors (AP-1 and Egr) that are relevant for neuronal responses. Our current understanding of the mechanisms involved in the induction of the immediate-early genes is presented.},
	Author = {P{\'e}rez-Cadah{\'\i}a, Beatriz and Drobic, Bojan and Davie, James R},
	Date-Added = {2016-03-17 21:12:26 +0000},
	Date-Modified = {2016-03-17 21:13:09 +0000},
	Doi = {10.1139/O10-138},
	Journal = {Biochem Cell Biol},
	Journal-Full = {Biochemistry and cell biology = Biochimie et biologie cellulaire},
	Keywords = {Immediate-Early; gene; IEG; Transcription Factors; activity-development; activity manipulation},
	Mesh = {Animals; Brain; Early Growth Response Protein 1; Genes, Immediate-Early; Humans; Nervous System Physiological Phenomena; Neuronal Plasticity; Neurons; Signal Transduction; Transcription Factor AP-1; Transcription Factors; Transcriptional Activation},
	Month = {Feb},
	Number = {1},
	Pages = {61-73},
	pmid = {21326363},
	Pst = {ppublish},
	Title = {Activation and function of immediate-early genes in the nervous system},
	Volume = {89},
	Year = {2011},
	url = {papers/Pérez-Cadahía_BiochemCellBiol2011.pdf}}

@article{Meyza:2015,
	Abstract = {Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized, in part, by an inability to adequately respond to social cues. Patients diagnosed with ASD are often devoid of empathy and impaired in understanding other people's emotional perspective. The neuronal correlates of this impairment are not fully understood. Replicating such a behavioral phenotype in a mouse model of autism would allow us insight into the neuronal background of the problem. Here we tested BTBR T(+)Itpr3(tf)/J (BTBR) and c57BL/6J (B6) mice in two behavioral paradigms: the Transfer of Emotional Information test and the Social Proximity test. In both tests BTBR mice displayed asocial behavior. We analyzed c-Fos protein expression in several brain regions after each of these tests, and found that, unlike B6 mice, BTBR mice react to a stressed cagemate exposure in the Transfer of Emotional Information test with no increase of c-Fos expression in either the prefrontal cortex or the amygdala. However, after Social Proximity exposure we observed a strong increase in c-Fos expression in the CA3 field of the hippocampus and two hypothalamic regions of BTBR brains. This response was accompanied by a strong activation of periaqueductal regions related to defensiveness, which suggests that BTBR mice find unavoidable social interaction highly aversive.},
	Author = {Meyza, Ksenia and Nikolaev, Tomasz and Kondrakiewicz, Kacper and Blanchard, D Caroline and Blanchard, Robert J and Knapska, Ewelina},
	Date-Added = {2016-03-17 21:12:03 +0000},
	Date-Modified = {2016-03-17 21:12:03 +0000},
	Doi = {10.3389/fnbeh.2015.00199},
	Journal = {Front Behav Neurosci},
	Journal-Full = {Frontiers in behavioral neuroscience},
	Keywords = {BTBR; autism; c-Fos; empathy; mouse model},
	Pages = {199},
	Pmc = {PMC4526814},
	pmid = {26300749},
	Pst = {epublish},
	Title = {Neuronal correlates of asocial behavior in a BTBR T (+) Itpr3(tf)/J mouse model of autism},
	Volume = {9},
	Year = {2015},
	url = {papers/Meyza_FrontBehavNeurosci2015.pdf}}

@article{Darmanis:2015,
	Abstract = {The human brain is a tissue of vast complexity in terms of the cell types it comprises. Conventional approaches to classifying cell types in the human brain at single cell resolution have been limited to exploring relatively few markers and therefore have provided a limited molecular characterization of any given cell type. We used single cell RNA sequencing on 466 cells to capture the cellular complexity of the adult and fetal human brain at a whole transcriptome level. Healthy adult temporal lobe tissue was obtained during surgical procedures where otherwise normal tissue was removed to gain access to deeper hippocampal pathology in patients with medical refractory seizures. We were able to classify individual cells into all of the major neuronal, glial, and vascular cell types in the brain. We were able to divide neurons into individual communities and show that these communities preserve the categorization of interneuron subtypes that is typically observed with the use of classic interneuron markers. We then used single cell RNA sequencing on fetal human cortical neurons to identify genes that are differentially expressed between fetal and adult neurons and those genes that display an expression gradient that reflects the transition between replicating and quiescent fetal neuronal populations. Finally, we observed the expression of major histocompatibility complex type I genes in a subset of adult neurons, but not fetal neurons. The work presented here demonstrates the applicability of single cell RNA sequencing on the study of the adult human brain and constitutes a first step toward a comprehensive cellular atlas of the human brain.},
	Author = {Darmanis, Spyros and Sloan, Steven A and Zhang, Ye and Enge, Martin and Caneda, Christine and Shuer, Lawrence M and Hayden Gephart, Melanie G and Barres, Ben A and Quake, Stephen R},
	Date-Added = {2016-03-17 21:11:49 +0000},
	Date-Modified = {2016-03-17 21:11:49 +0000},
	Doi = {10.1073/pnas.1507125112},
	Journal = {Proc Natl Acad Sci U S A},
	Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},
	Keywords = {RNAseq; human brain; interneurons; neurons; single cells},
	Mesh = {Adult; Brain; HLA Antigens; Humans; Neurons; Sequence Analysis, RNA; Single-Cell Analysis; Transcriptome},
	Month = {Jun},
	Number = {23},
	Pages = {7285-90},
	Pmc = {PMC4466750},
	pmid = {26060301},
	Pst = {ppublish},
	Title = {A survey of human brain transcriptome diversity at the single cell level},
	Volume = {112},
	Year = {2015},
	url = {papers/Darmanis_ProcNatlAcadSciUSA2015.pdf}}

@article{Zhang:2014a,
	Abstract = {The major cell classes of the brain differ in their developmental processes, metabolism, signaling, and function. To better understand the functions and interactions of the cell types that comprise these classes, we acutely purified representative populations of neurons, astrocytes, oligodendrocyte precursor cells, newly formed oligodendrocytes, myelinating oligodendrocytes, microglia, endothelial cells, and pericytes from mouse cerebral cortex. We generated a transcriptome database for these eight cell types by RNA sequencing and used a sensitive algorithm to detect alternative splicing events in each cell type. Bioinformatic analyses identified thousands of new cell type-enriched genes and splicing isoforms that will provide novel markers for cell identification, tools for genetic manipulation, and insights into the biology of the brain. For example, our data provide clues as to how neurons and astrocytes differ in their ability to dynamically regulate glycolytic flux and lactate generation attributable to unique splicing of PKM2, the gene encoding the glycolytic enzyme pyruvate kinase. This dataset will provide a powerful new resource for understanding the development and function of the brain. To ensure the widespread distribution of these datasets, we have created a user-friendly website (http://web.stanford.edu/group/barres_lab/brain_rnaseq.html) that provides a platform for analyzing and comparing transciption and alternative splicing profiles for various cell classes in the brain.},
	Author = {Zhang, Ye and Chen, Kenian and Sloan, Steven A and Bennett, Mariko L and Scholze, Anja R and O'Keeffe, Sean and Phatnani, Hemali P and Guarnieri, Paolo and Caneda, Christine and Ruderisch, Nadine and Deng, Shuyun and Liddelow, Shane A and Zhang, Chaolin and Daneman, Richard and Maniatis, Tom and Barres, Ben A and Wu, Jian Qian},
	Date-Added = {2016-03-17 21:06:04 +0000},
	Date-Modified = {2016-03-17 21:06:54 +0000},
	Doi = {10.1523/JNEUROSCI.1860-14.2014},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Keywords = {alternative splicing; astrocytes; microglia; oligodendrocytes; transcriptome; vascular cells; Methods; RNAseq; technique},
	Mesh = {Alternative Splicing; Animals; Cerebral Cortex; Databases, Nucleic Acid; Endothelium, Vascular; Mice; Neuroglia; Neurons; Sequence Analysis, RNA; Transcriptome},
	Month = {Sep},
	Number = {36},
	Pages = {11929-47},
	Pmc = {PMC4152602},
	pmid = {25186741},
	Pst = {ppublish},
	Title = {An RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex},
	Volume = {34},
	Year = {2014},
	url = {papers/Zhang_JNeurosci2014.pdf}}

@article{Sekar:2016,
	Abstract = {Schizophrenia is a heritable brain illness with unknown pathogenic mechanisms. Schizophrenia's strongest genetic association at a population level involves variation in the major histocompatibility complex (MHC) locus, but the genes and molecular mechanisms accounting for this have been challenging to identify. Here we show that this association arises in part from many structurally diverse alleles of the complement component 4 (C4) genes. We found that these alleles generated widely varying levels of C4A and C4B expression in the brain, with each common C4 allele associating with schizophrenia in proportion to its tendency to generate greater expression of C4A. Human C4 protein localized to neuronal synapses, dendrites, axons, and cell bodies. In mice, C4 mediated synapse elimination during postnatal development. These results implicate excessive complement activity in the development of schizophrenia and may help explain the reduced numbers of synapses in the brains of individuals with schizophrenia.},
	Author = {Sekar, Aswin and Bialas, Allison R and de Rivera, Heather and Davis, Avery and Hammond, Timothy R and Kamitaki, Nolan and Tooley, Katherine and Presumey, Jessy and Baum, Matthew and Van Doren, Vanessa and Genovese, Giulio and Rose, Samuel A and Handsaker, Robert E and {Schizophrenia Working Group of the Psychiatric Genomics Consortium} and Daly, Mark J and Carroll, Michael C and Stevens, Beth and McCarroll, Steven A},
	Date-Added = {2016-01-29 22:14:49 +0000},
	Date-Modified = {2016-01-29 22:14:49 +0000},
	Doi = {10.1038/nature16549},
	Journal = {Nature},
	Journal-Full = {Nature},
	Month = {Jan},
	pmid = {26814963},
	Pst = {aheadofprint},
	Title = {Schizophrenia risk from complex variation of complement component 4},
	Year = {2016},
	url = {papers/Sekar_Nature2016.pdf}}

@article{Rash:2011,
	Abstract = {The processes regulating cortical surface area expansion during development and evolution are unknown. We show that loss of function of all fibroblast growth factor receptors (FgfRs) expressed at the earliest stages of cortical development causes severe deficits in surface area growth by embryonic day 12.5 (E12.5) in the mouse. In FgfR mutants, accelerated production of neurons led to severe loss of radial progenitors and premature termination of neurogenesis. Nevertheless, these mutants showed remarkably little change in cortical layer structure. Birth-dating experiments indicated that a greater proportion of layer fates was generated during early neurogenic stages, revealing that FgfR activity normally slows the temporal progression of cortical layer fates. Electroporation of a dominant-negative FgfR at E11.5 increased cortical neurogenesis in normal mice--an effect that was blocked by simultaneous activation of the Notch pathway. Together with changes in the expression of Notch pathway genes in FgfR mutant embryos, these findings indicate that Notch lies downstream of FgfR signaling in the same pathway regulating cortical neurogenesis and begin to establish a mechanism for regulating cortical surface expansion.},
	Author = {Rash, Brian G and Lim, H David and Breunig, Joshua J and Vaccarino, Flora M},
	Date-Added = {2014-02-28 19:42:16 +0000},
	Date-Modified = {2014-02-28 19:44:58 +0000},
	Doi = {10.1523/JNEUROSCI.4439-11.2011},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Keywords = {development; Cerebral Cortex; Neocortex; radial glia; neurogenesis; Mouse},
	Mesh = {Age Factors; Analysis of Variance; Animals; Brain; Bromodeoxyuridine; Caspase 3; Cell Count; Cell Differentiation; Cells, Cultured; Cerebral Cortex; DNA-Binding Proteins; Electroporation; Embryo, Mammalian; Eye Proteins; Fatty Acid-Binding Proteins; Fibroblast Growth Factors; Gene Expression Regulation, Developmental; Green Fluorescent Proteins; Homeodomain Proteins; Ki-67 Antigen; Mice; Mice, Transgenic; Mutation; Nerve Tissue Proteins; Neurogenesis; Neurons; Paired Box Transcription Factors; Receptors, Fibroblast Growth Factor; Receptors, Notch; Repressor Proteins; Signal Transduction; Stem Cells; T-Box Domain Proteins; Transcription Factors},
	Month = {Oct},
	Number = {43},
	Pages = {15604-17},
	Pmc = {PMC3235689},
	pmid = {22031906},
	Pst = {ppublish},
	Title = {FGF signaling expands embryonic cortical surface area by regulating Notch-dependent neurogenesis},
	Volume = {31},
	Year = {2011},
	url = {papers/Rash_JNeurosci2011.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4439-11.2011}}

@article{Shitamukai:2011,
	Abstract = {Radial glia cells function as neural stem cells in the developing brain and generate self-renewing and differentiating daughter cells by asymmetric cell divisions. During these divisions, the apical process or basal process of the elongated epithelial structure is asymmetrically partitioned into daughter cells, depending on developmental contexts. However, in mammalian neurogenesis, the relationship between these subcellular structures and self-renewability is largely unknown. We induced oblique cleavages of radial glia cells to split the apical and basal processes into two daughters, and investigated the fate and morphology of the daughters in slice cultures. We observed that the more basal daughter cell that inherits the basal process self-renews outside of the ventricular zone (VZ), while the more apical daughter cell differentiates. These self-renewing progenitors, termed "outer VZ progenitors," retain the basal but not the apical process, as recently reported for the outer subventricular zone (OSVZ) progenitors in primates (Fietz et al., 2010; Hansen et al., 2010); to self-renew, they require clonal Notch signaling between sibling cells. We also found a small endogenous population of outer VZ progenitors in the mouse embryonic neocortex, consistent with a low frequency of oblique radial glia divisions. Our results describe the general role of the basal process in the self-renewal of neural progenitors and implicate the loss of the apical junctions during oblique divisions as a possible mechanism for generating OSVZ progenitors. We propose that mouse outer VZ progenitors, induced by oblique cleavages, provide a model to study both progenitor self-renewal and OSVZ progenitors.},
	Author = {Shitamukai, Atsunori and Konno, Daijiro and Matsuzaki, Fumio},
	Date-Added = {2014-02-28 19:30:03 +0000},
	Date-Modified = {2014-02-28 19:31:20 +0000},
	Doi = {10.1523/JNEUROSCI.4773-10.2011},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Keywords = {development; radial glia; cortical columns; Cerebral Cortex; Neocortex},
	Mesh = {Analysis of Variance; Animals; Cell Differentiation; Cell Lineage; Cells, Cultured; Immunohistochemistry; Mice; Mice, Inbred ICR; Neocortex; Neuroglia; Neurons; Stem Cells},
	Month = {Mar},
	Number = {10},
	Pages = {3683-95},
	pmid = {21389223},
	Pst = {ppublish},
	Title = {Oblique radial glial divisions in the developing mouse neocortex induce self-renewing progenitors outside the germinal zone that resemble primate outer subventricular zone progenitors},
	Volume = {31},
	Year = {2011},
	url = {papers/Shitamukai_JNeurosci2011.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4773-10.2011}}

@article{Rash:2013,
	Abstract = {Gyrification allows an expanded cortex with greater functionality to fit into a smaller cranium. However, the mechanisms of gyrus formation have been elusive. We show that ventricular injection of FGF2 protein at embryonic day 11.5-before neurogenesis and before the formation of intrahemispheric axonal connections-altered the overall size and shape of the cortex and induced the formation of prominent, bilateral gyri and sulci in the rostrolateral neocortex. We show increased tangential growth of the rostral ventricular zone (VZ) but decreased Wnt3a and Lef1 expression in the cortical hem and adjacent hippocampal promordium and consequent impaired growth of the caudal cortical primordium, including the hippocampus. At the same time, we observed ectopic Er81 expression, increased proliferation of Tbr2-expressing (Tbr2(+)) intermediate neuronal progenitors (INPs), and elevated Tbr1(+) neurogenesis in the regions that undergo gyrification, indicating region-specific actions of FGF2 on the VZ and subventricular zone (SVZ). However, the relative number of basal radial glia-recently proposed to be important in gyrification-appeared to be unchanged. These findings are consistent with the hypothesis that increased radial unit production together with rapid SVZ growth and heightened localized neurogenesis can cause cortical gyrification in lissencephalic species. These data also suggest that the position of cortical gyri can be molecularly specified in mice. In contrast, a different ligand, FGF8b, elicited surface area expansion throughout the cortical primordium but no gyrification. Our findings demonstrate that individual members of the diverse Fgf gene family differentially regulate global as well as regional cortical growth rates while maintaining cortical layer structure.},
	Author = {Rash, Brian G and Tomasi, Simone and Lim, H David and Suh, Carol Y and Vaccarino, Flora M},
	Date-Added = {2014-02-28 19:33:06 +0000},
	Date-Modified = {2014-02-28 19:34:43 +0000},
	Doi = {10.1523/JNEUROSCI.3621-12.2013},
	Journal = {J Neurosci},
	Journal-Full = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	Keywords = {development; Cerebral Cortex; Neocortex; Mouse; radial glia; neurogenesis},
	Mesh = {Animals; Antimetabolites; Axons; Brain Chemistry; Bromodeoxyuridine; Cell Count; Cerebral Cortex; Cerebral Ventricles; DNA, Complementary; Densitometry; Dependovirus; Female; Fibroblast Growth Factor 2; Green Fluorescent Proteins; Immunohistochemistry; In Situ Hybridization; Lymphoid Enhancer-Binding Factor 1; Mice; Neocortex; Pregnancy; RNA; Real-Time Polymerase Chain Reaction; Wnt3A Protein},
	Month = {Jun},
	Number = {26},
	Pages = {10802-14},
	Pmc = {PMC3693057},
	pmid = {23804101},
	Pst = {ppublish},
	Title = {Cortical gyrification induced by fibroblast growth factor 2 in the mouse brain},
	Volume = {33},
	Year = {2013},
	url = {papers/Rash_JNeurosci2013.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3621-12.2013}}

@article{Inamura:2011,
	Abstract = {Neuronal differentiation is a crucial event during neural development. Recent studies have characterized the development of the diencephalon; however, the origins of the primarily GABAergic prethalamic nuclei, including the zona incerta (ZI), ventral lateral geniculate nucleus (vLG) and reticular thalamic nucleus (RT), remain unclear. Here we characterize Olig2 lineage cells in the developing prethalamus using mice in which tamoxifen-induced recombination permanently labels Olig2-expressing cells. We show that GABAergic neurons in the prethalamic nuclei, including the RT, ZI and vLG, originate from prethalamic Olig2 lineage cells. Based on these data and on those derived from short-term lineage-tracing data using Olig3-lacZ mice and previous reports, we suggest that vLG cells originate from the ventricular zone of the thalamus, zona limitans intrathalamica and prethalamus.},
	Author = {Inamura, Naoko and Ono, Katsuhiko and Takebayashi, Hirohide and Zalc, Bernard and Ikenaka, Kazuhiro},
	Date-Added = {2013-08-07 13:38:36 +0000},
	Date-Modified = {2013-08-07 13:39:45 +0000},
	Doi = {10.1159/000328974},
	Journal = {Dev Neurosci},
	Journal-Full = {Developmental neuroscience},
	Keywords = {development; visual system; thalamus; migration; Gene Expression; GABA; Interneurons},
	Mesh = {Animals; Basic Helix-Loop-Helix Transcription Factors; Cell Differentiation; Cell Lineage; Cell Movement; Female; GABAergic Neurons; Gene Expression Regulation, Developmental; Geniculate Bodies; Immunohistochemistry; In Situ Hybridization; Mice; Mice, Transgenic; Models, Animal; Nerve Tissue Proteins; Stem Cells; Subthalamus; Tamoxifen; Ventral Thalamic Nuclei},
	Number = {2},
	Pages = {118-29},
	pmid = {21865661},
	Pst = {ppublish},
	Title = {Olig2 lineage cells generate GABAergic neurons in the prethalamic nuclei, including the zona incerta, ventral lateral geniculate nucleus and reticular thalamic nucleus},
	Volume = {33},
	Year = {2011},
	url = {papers/Inamura_DevNeurosci2011.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000328974}}

@article{Dimos:2008,
	Abstract = {The generation of pluripotent stem cells from an individual patient would enable the large-scale production of the cell types affected by that patient's disease. These cells could in turn be used for disease modeling, drug discovery, and eventually autologous cell replacement therapies. Although recent studies have demonstrated the reprogramming of human fibroblasts to a pluripotent state, it remains unclear whether these induced pluripotent stem (iPS) cells can be produced directly from elderly patients with chronic disease. We have generated iPS cells from an 82-year-old woman diagnosed with a familial form of amyotrophic lateral sclerosis (ALS). These patient-specific iPS cells possess properties of embryonic stem cells and were successfully directed to differentiate into motor neurons, the cell type destroyed in ALS.},
	Author = {Dimos, John T and Rodolfa, Kit T and Niakan, Kathy K and Weisenthal, Laurin M and Mitsumoto, Hiroshi and Chung, Wendy and Croft, Gist F and Saphier, Genevieve and Leibel, Rudy and Goland, Robin and Wichterle, Hynek and Henderson, Christopher E and Eggan, Kevin},
	Date-Added = {2013-07-05 20:54:00 +0000},
	Date-Modified = {2013-07-05 21:11:18 +0000},
	Doi = {10.1126/science.1158799},
	Journal = {Science},
	Journal-Full = {Science (New York, N.Y.)},
	Keywords = {Stem Cells; Pluripotent Stem Cells; development; gene; Regeneration},
	Mesh = {Aged, 80 and over; Amyotrophic Lateral Sclerosis; Cell Differentiation; Cell Line; Embryonic Stem Cells; Female; Fibroblasts; Gene Expression; Humans; Motor Neurons; Neuroglia; Nuclear Reprogramming; Pluripotent Stem Cells; Retroviridae; Spinal Cord; Superoxide Dismutase; Transcription Factors; Transduction, Genetic},
	Month = {Aug},
	Number = {5893},
	Pages = {1218-21},
	pmid = {18669821},
	Pst = {ppublish},
	Title = {Induced pluripotent stem cells generated from patients with ALS can be differentiated into motor neurons},
	Volume = {321},
	Year = {2008},
	url = {papers/Dimos_Science2008.pdf}}

@article{Warren:2008,
	Abstract = {We present a draft genome sequence of the platypus, Ornithorhynchus anatinus. This monotreme exhibits a fascinating combination of reptilian and mammalian characters. For example, platypuses have a coat of fur adapted to an aquatic lifestyle; platypus females lactate, yet lay eggs; and males are equipped with venom similar to that of reptiles. Analysis of the first monotreme genome aligned these features with genetic innovations. We find that reptile and platypus venom proteins have been co-opted independently from the same gene families; milk protein genes are conserved despite platypuses laying eggs; and immune gene family expansions are directly related to platypus biology. Expansions of protein, non-protein-coding RNA and microRNA families, as well as repeat elements, are identified. Sequencing of this genome now provides a valuable resource for deep mammalian comparative analyses, as well as for monotreme biology and conservation.},
	Author = {Warren, Wesley C and Hillier, LaDeana W and Marshall Graves, Jennifer A and Birney, Ewan and Ponting, Chris P and Gr{\"u}tzner, Frank and Belov, Katherine and Miller, Webb and Clarke, Laura and Chinwalla, Asif T and Yang, Shiaw-Pyng and Heger, Andreas and Locke, Devin P and Miethke, Pat and Waters, Paul D and Veyrunes, Fr{\'e}d{\'e}ric and Fulton, Lucinda and Fulton, Bob and Graves, Tina and Wallis, John and Puente, Xose S and L{\'o}pez-Ot{\'\i}n, Carlos and Ord{\'o}{\~n}ez, Gonzalo R and Eichler, Evan E and Chen, Lin and Cheng, Ze and Deakin, Janine E and Alsop, Amber and Thompson, Katherine and Kirby, Patrick and Papenfuss, Anthony T and Wakefield, Matthew J and Olender, Tsviya and Lancet, Doron and Huttley, Gavin A and Smit, Arian F A and Pask, Andrew and Temple-Smith, Peter and Batzer, Mark A and Walker, Jerilyn A and Konkel, Miriam K and Harris, Robert S and Whittington, Camilla M and Wong, Emily S W and Gemmell, Neil J and Buschiazzo, Emmanuel and Vargas Jentzsch, Iris M and Merkel, Angelika and Schmitz, Juergen and Zemann, Anja and Churakov, Gennady and Kriegs, Jan Ole and Brosius, Juergen and Murchison, Elizabeth P and Sachidanandam, Ravi and Smith, Carly and Hannon, Gregory J and Tsend-Ayush, Enkhjargal and McMillan, Daniel and Attenborough, Rosalind and Rens, Willem and Ferguson-Smith, Malcolm and Lef{\`e}vre, Christophe M and Sharp, Julie A and Nicholas, Kevin R and Ray, David A and Kube, Michael and Reinhardt, Richard and Pringle, Thomas H and Taylor, James and Jones, Russell C and Nixon, Brett and Dacheux, Jean-Louis and Niwa, Hitoshi and Sekita, Yoko and Huang, Xiaoqiu and Stark, Alexander and Kheradpour, Pouya and Kellis, Manolis and Flicek, Paul and Chen, Yuan and Webber, Caleb and Hardison, Ross and Nelson, Joanne and Hallsworth-Pepin, Kym and Delehaunty, Kim and Markovic, Chris and Minx, Pat and Feng, Yucheng and Kremitzki, Colin and Mitreva, Makedonka and Glasscock, Jarret and Wylie, Todd and Wohldmann, Patricia and Thiru, Prathapan and Nhan, Michael N and Pohl, Craig S and Smith, Scott M and Hou, Shunfeng and Nefedov, Mikhail and de Jong, Pieter J and Renfree, Marilyn B and Mardis, Elaine R and Wilson, Richard K},
	Date-Added = {2013-06-13 15:43:25 +0000},
	Date-Modified = {2013-06-13 15:43:25 +0000},
	Doi = {10.1038/nature06936},
	Journal = {Nature},
	Journal-Full = {Nature},
	Mesh = {Animals; Base Composition; Dentition; Evolution, Molecular; Female; Genome; Genomic Imprinting; Humans; Immunity; Male; Mammals; MicroRNAs; Milk Proteins; Phylogeny; Platypus; Receptors, Odorant; Repetitive Sequences, Nucleic Acid; Reptiles; Sequence Analysis, DNA; Spermatozoa; Venoms; Zona Pellucida},
	Month = {May},
	Number = {7192},
	Pages = {175-83},
	Pmc = {PMC2803040},
	pmid = {18464734},
	Pst = {ppublish},
	Title = {Genome analysis of the platypus reveals unique signatures of evolution},
	Volume = {453},
	Year = {2008},
	url = {papers/Warren_Nature2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06936}}

@article{Derecki:2012a,
	Abstract = {Rett syndrome is an X-linked autism spectrum disorder. The disease is characterized in most cases by mutation of the MECP2 gene, which encodes a methyl-CpG-binding protein. Although MECP2 is expressed in many tissues, the disease is generally attributed to a primary neuronal dysfunction. However, as shown recently, glia, specifically astrocytes, also contribute to Rett pathophysiology. Here we examine the role of another form of glia, microglia, in a murine model of Rett syndrome. Transplantation of wild-type bone marrow into irradiation-conditioned Mecp2-null hosts resulted in engraftment of brain parenchyma by bone-marrow-derived myeloid cells of microglial phenotype, and arrest of disease development. However, when cranial irradiation was blocked by lead shield, and microglial engraftment was prevented, disease was not arrested. Similarly, targeted expression of MECP2 in myeloid cells, driven by Lysm(cre) on an Mecp2-null background, markedly attenuated disease symptoms. Thus, through multiple approaches, wild-type Mecp2-expressing microglia within the context of an Mecp2-null male mouse arrested numerous facets of disease pathology: lifespan was increased, breathing patterns were normalized, apnoeas were reduced, body weight was increased to near that of wild type, and locomotor activity was improved. Mecp2(+/-) females also showed significant improvements as a result of wild-type microglial engraftment. These benefits mediated by wild-type microglia, however, were diminished when phagocytic activity was inhibited pharmacologically by using annexin V to block phosphatydilserine residues on apoptotic targets, thus preventing recognition and engulfment by tissue-resident phagocytes. These results suggest the importance of microglial phagocytic activity in Rett syndrome. Our data implicate microglia as major players in the pathophysiology of this devastating disorder, and suggest that bone marrow transplantation might offer a feasible therapeutic approach for it.},
	Author = {Derecki, No{\"e}l C and Cronk, James C and Lu, Zhenjie and Xu, Eric and Abbott, Stephen B G and Guyenet, Patrice G and Kipnis, Jonathan},
	Date-Added = {2013-04-01 16:18:07 +0000},
	Date-Modified = {2013-04-01 16:18:44 +0000},
	Doi = {10.1038/nature10907},
	Journal = {Nature},
	Journal-Full = {Nature},
	Keywords = {downloads},
	Mesh = {Animals; Annexin A5; Apoptosis; Body Weight; Bone Marrow Transplantation; Brain; Disease Models, Animal; Disease Progression; Female; Insulin-Like Growth Factor I; Locomotion; Male; Methyl-CpG-Binding Protein 2; Mice; Mice, Inbred C57BL; Microglia; Phagocytosis; Phosphatidylserines; Respiration; Rett Syndrome; Rotarod Performance Test},
	Month = {Apr},
	Number = {7392},
	Pages = {105-9},
	Pmc = {PMC3321067},
	pmid = {22425995},
	Pst = {epublish},
	Title = {Wild-type microglia arrest pathology in a mouse model of Rett syndrome},
	Volume = {484},
	Year = {2012},
	url = {papers/Derecki_Nature2012a.pdf}}

@article{Johansson:2008,
	Abstract = {Transplanted bone marrow-derived cells (BMDCs) have been reported to fuse with cells of diverse tissues, but the extremely low frequency of fusion has led to the view that such events are biologically insignificant. Nonetheless, in mice with a lethal recessive liver disease (tyrosinaemia), transplantation of wild-type BMDCs restored liver function by cell fusion and prevented death, indicating that cell fusion can have beneficial effects. Here we report that chronic inflammation resulting from severe dermatitis or autoimmune encephalitis leads to robust fusion of BMDCs with Purkinje neurons and formation of hundreds of binucleate heterokaryons per cerebellum, a 10-100-fold higher frequency than previously reported. Single haematopoietic stem-cell transplants showed that the fusogenic cell is from the haematopoietic lineage and parabiosis experiments revealed that fusion can occur without irradiation. Transplantation of rat bone marrow into mice led to activation of dormant rat Purkinje neuron-specific genes in BMDC nuclei after fusion with mouse Purkinje neurons, consistent with nuclear reprogramming. The precise neurological role of these heterokaryons awaits elucidation, but their frequency in brain after inflammation is clearly much higher than previously appreciated.},
	Author = {Johansson, Clas B and Youssef, Sawsan and Koleckar, Kassie and Holbrook, Colin and Doyonnas, Regis and Corbel, Stephane Y and Steinman, Lawrence and Rossi, Fabio M V and Blau, Helen M},
	Date-Added = {2012-11-05 17:39:47 +0000},
	Date-Modified = {2012-11-05 17:40:43 +0000},
	Doi = {10.1038/ncb1720},
	Journal = {Nat Cell Biol},
	Journal-Full = {Nature cell biology},
	Keywords = {Stem Cells; Cell Fusion; macrophage; microglia; neuron; Immune System;},
	Mesh = {Animals; Bone Marrow Cells; Cell Fusion; Dermatitis; Encephalomyelitis, Autoimmune, Experimental; Female; Green Fluorescent Proteins; Hematopoietic Stem Cells; Inflammation; Lipopolysaccharides; Mesenchymal Stem Cell Transplantation; Mice; Mice, Inbred C57BL; Purkinje Cells; Rats; Rats, Sprague-Dawley; Transplantation Chimera},
	Month = {May},
	Number = {5},
	Pages = {575-83},
	pmid = {18425116},
	Pst = {ppublish},
	Title = {Extensive fusion of haematopoietic cells with Purkinje neurons in response to chronic inflammation},
	Volume = {10},
	Year = {2008},
	url = {papers/Johansson_NatCellBiol2008.pdf}}

@article{Lam:2012,
	Abstract = {A variety of genetically encoded reporters use changes in fluorescence (or F{\"o}rster) resonance energy transfer (FRET) to report on biochemical processes in living cells. The standard genetically encoded FRET pair consists of CFPs and YFPs, but many CFP-YFP reporters suffer from low FRET dynamic range, phototoxicity from the CFP excitation light and complex photokinetic events such as reversible photobleaching and photoconversion. We engineered two fluorescent proteins, Clover and mRuby2, which are the brightest green and red fluorescent proteins to date and have the highest F{\"o}rster radius of any ratiometric FRET pair yet described. Replacement of CFP and YFP with these two proteins in reporters of kinase activity, small GTPase activity and transmembrane voltage significantly improves photostability, FRET dynamic range and emission ratio changes. These improvements enhance detection of transient biochemical events such as neuronal action-potential firing and RhoA activation in growth cones.},
	Author = {Lam, Amy J and St-Pierre, Fran{\c c}ois and Gong, Yiyang and Marshall, Jesse D and Cranfill, Paula J and Baird, Michelle A and McKeown, Michael R and Wiedenmann, J{\"o}rg and Davidson, Michael W and Schnitzer, Mark J and Tsien, Roger Y and Lin, Michael Z},
	Date-Added = {2012-11-05 17:30:58 +0000},
	Date-Modified = {2012-11-05 17:33:08 +0000},
	Doi = {10.1038/nmeth.2171},
	Journal = {Nat Methods},
	Journal-Full = {Nature methods},
	Keywords = {Technique; optical imaging; microscopy; FRET; Transgenes; Reporter/genetics; optical physiology; Neurophysiology;},
	Month = {Oct},
	Number = {10},
	Pages = {1005-12},
	Pmc = {PMC3461113},
	pmid = {22961245},
	Pst = {ppublish},
	Title = {Improving FRET dynamic range with bright green and red fluorescent proteins},
	Volume = {9},
	Year = {2012},
	url = {papers/Lam_NatMethods2012.pdf}}

@article{Murchison:2010,
	Abstract = {The Tasmanian devil, a marsupial carnivore, is endangered because of the emergence of a transmissible cancer known as devil facial tumor disease (DFTD). This fatal cancer is clonally derived and is an allograft transmitted between devils by biting. We performed a large-scale genetic analysis of DFTD with microsatellite genotyping, a mitochondrial genome analysis, and deep sequencing of the DFTD transcriptome and microRNAs. These studies confirm that DFTD is a monophyletic clonally transmissible tumor and suggest that the disease is of Schwann cell origin. On the basis of these results, we have generated a diagnostic marker for DFTD and identify a suite of genes relevant to DFTD pathology and transmission. We provide a genomic data set for the Tasmanian devil that is applicable to cancer diagnosis, disease evolution, and conservation biology.},
	Author = {Murchison, Elizabeth P and Tovar, Cesar and Hsu, Arthur and Bender, Hannah S and Kheradpour, Pouya and Rebbeck, Clare A and Obendorf, David and Conlan, Carly and Bahlo, Melanie and Blizzard, Catherine A and Pyecroft, Stephen and Kreiss, Alexandre and Kellis, Manolis and Stark, Alexander and Harkins, Timothy T and Marshall Graves, Jennifer A and Woods, Gregory M and Hannon, Gregory J and Papenfuss, Anthony T},
	Date-Added = {2010-09-15 13:28:32 -0400},
	Date-Modified = {2011-09-13 09:45:17 -0400},
	Journal = {Science},
	Journal-Full = {Science (New York, N.Y.)},
	Keywords = {Grants; ideas;; microRNAs; development},
	Mesh = {Animals; Bites and Stings; Cell Differentiation; Facial Neoplasms; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Genes, Neoplasm; Genome, Mitochondrial; Genotype; Marsupialia; Membrane Proteins; MicroRNAs; Microsatellite Repeats; Myelin Basic Proteins; Nerve Sheath Neoplasms; Schwann Cells; Sequence Analysis, DNA; Tumor Markers, Biological},
	Month = {Jan},
	Number = {5961},
	Pages = {84-7},
	pmid = {20044575},
	Pst = {ppublish},
	Title = {The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer},
	Volume = {327},
	Year = {2010},
	url = {papers/Murchison_Science2010.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1180616}}

@article{Alonso:2003,
	Abstract = {Tissue stem cells form the cellular base for organ homeostasis and repair. Stem cells have the unusual ability to renew themselves over the lifetime of the organ while producing daughter cells that differentiate into one or multiple lineages. Difficult to identify and characterize in any tissue, these cells are nonetheless hotly pursued because they hold the potential promise of therapeutic reprogramming to grow human tissue in vitro, for the treatment of human disease. The mammalian skin epithelium exhibits remarkable turnover, punctuated by periods of even more rapid production after injury due to burn or wounding. The stem cells responsible for supplying this tissue with cellular substrate are not yet easily distinguishable from neighboring cells. However, in recent years a significant body of work has begun to characterize the skin epithelial stem cells, both in tissue culture and in mouse and human skin. Some epithelial cells cultured from skin exhibit prodigious proliferative potential; in fact, for >20 years now, cultured human skin has been used as a source of new skin to engraft onto damaged areas of burn patients, representing one of the first therapeutic uses of stem cells. Cell fate choices, including both self-renewal and differentiation, are crucial biological features of stem cells that are still poorly understood. Skin epithelial stem cells represent a ripe target for research into the fundamental mechanisms underlying these important processes.},
	Address = {Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, NY 10021, USA.},
	Author = {Alonso, Laura and Fuchs, Elaine},
	Crdt = {2003/08/13 05:00},
	Da = {20031001},
	Date = {2003 Sep 30},
	Date-Added = {2009-03-25 23:03:31 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Dcom = {20031104},
	Dep = {20030811},
	Edat = {2003/08/13 05:00},
	Gr = {R01-AR31737/AR/NIAMS NIH HHS/United States},
	Issn = {0027-8424 (Print)},
	Jid = {7505876},
	Journal = {Proc Natl Acad Sci U S A},
	Jt = {Proceedings of the National Academy of Sciences of the United States of America},
	Language = {eng},
	Lr = {20081120},
	Mh = {Animals; Cell Differentiation; Cells, Cultured; Epithelial Cells/cytology; Hair Follicle/cytology; Humans; Keratinocytes/cytology/transplantation; Skin/*cytology; Stem Cells/*cytology/physiology},
	Mhda = {2003/11/05 05:00},
	Month = {Sep},
	Oid = {NLM: PMC304094},
	Own = {NLM},
	Pages = {11830--11835},
	Phst = {2003/08/11 {$[$}aheadofprint{$]$}},
	Pii = {1734203100},
	Pl = {United States},
	Pmc = {PMC304094},
	pmid = {12913119},
	Pst = {ppublish},
	Pt = {Journal Article; Research Support, U.S. Gov't, P.H.S.; Review},
	Rf = {64},
	Sb = {IM},
	Status = {MEDLINE},
	Title = {Stem cells of the skin epithelium},
	Volume = {100 Suppl 1},
	Year = {2003},
	url = {papers/Alonso_ProcNatlAcadSciUSA2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.1734203100}}

@article{Tumbar:2004,
	Abstract = {Many adult regenerative cells divide infrequently but have high proliferative capacity. We developed a strategy to fluorescently label slow-cycling cells in a cell type-specific fashion. We used this method to purify the label-retaining cells (LRCs) that mark the skin stem cell (SC) niche. We found that these cells rarely divide within their niche but change properties abruptly when stimulated to exit. We determined their transcriptional profile, which, when compared to progeny and other SCs, defines the niche. Many of the >100 messenger RNAs preferentially expressed in the niche encode surface receptors and secreted proteins, enabling LRCs to signal and respond to their environment.},
	Address = {Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, Rockefeller University, New York, NY 10021, USA.},
	Author = {Tumbar, Tudorita and Guasch, Geraldine and Greco, Valentina and Blanpain, Cedric and Lowry, William E and Rendl, Michael and Fuchs, Elaine},
	Crdt = {2003/12/13 05:00},
	Da = {20040116},
	Date = {2004 Jan 16},
	Date-Added = {2009-03-25 23:08:42 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Dcom = {20040209},
	Dep = {20031211},
	Edat = {2003/12/13 05:00},
	Gr = {R01 AR050452-04/AR/NIAMS NIH HHS/United States},
	Issn = {1095-9203 (Electronic)},
	Jid = {0404511},
	Journal = {Science},
	Jt = {Science (New York, N.Y.)},
	Language = {eng},
	Lr = {20081120},
	Mh = {Animals; Cell Cycle; Cell Division; Cell Separation; Epidermis/*cytology/physiology; Epithelial Cells/*cytology/physiology; Gene Expression Profiling; Gene Expression Regulation; Green Fluorescent Proteins; Hair Follicle/*cytology/physiology; Histones/genetics/metabolism; Keratinocytes/cytology; Luminescent Proteins/genetics/metabolism; Mice; Mice, Transgenic; Microscopy, Fluorescence; Multipotent Stem Cells/cytology/*physiology; Oligonucleotide Array Sequence Analysis; RNA, Messenger/genetics/metabolism; Reverse Transcriptase Polymerase Chain Reaction; Transcription, Genetic},
	Mhda = {2004/02/11 05:00},
	Mid = {NIHMS44867},
	Month = {Jan},
	Number = {5656},
	Oid = {NLM: NIHMS44867; NLM: PMC2405920},
	Own = {NLM},
	Pages = {359--363},
	Phst = {2003/12/11 {$[$}aheadofprint{$]$}},
	Pii = {1092436},
	Pl = {United States},
	Pmc = {PMC2405920},
	pmid = {14671312},
	Pst = {ppublish},
	Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},
	Rn = {0 (Histones); 0 (Luminescent Proteins); 0 (RNA, Messenger); 147336-22-9 (Green Fluorescent Proteins)},
	Sb = {IM},
	Status = {MEDLINE},
	Title = {Defining the epithelial stem cell niche in skin},
	Volume = {303},
	Year = {2004},
	url = {papers/Tumbar_Science2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1092436}}

@article{Aaronson:1971,
	Author = {Aaronson, S. A. and Todaro, G. J. and Scolnick, E. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {15 ERVs retroelements;Embryo;Clone Cells;RNA Viruses;Enzyme Induction;24 Pubmed search results 2008;Cell Line;15 Retrovirus mechanism;Mice;Bromodeoxyuridine;DNA Nucleotidyltransferases;Cells, Cultured;Animals},
	Medline = {72042139},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5},
	Pages = {157-9},
	Pubmed = {5119627},
	Title = {Induction of murine C-type viruses from clonal lines of virus-free BALB-3T3 cells},
	Uuid = {6E4A3F07-22B3-41A2-9CF0-E6CE79B42132},
	Volume = {174},
	Year = {1971}}

@article{Abbott:2004,
	Author = {Abbott, Alison},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Cerebrovascular Accident;21 Neurodegenerative;21 Neurophysiology;Nerve Regeneration;Human;Stem Cells;Cell Division;Tissue Therapy;Male;Brain;Neurons;news},
	Month = {5},
	Nlm_Id = {0410462},
	Number = {6990},
	Pages = {338-9},
	Pii = {429338a},
	Pubmed = {15164032},
	Title = {Striking back},
	Uuid = {7236B95F-747D-43F4-B5E1-8479D47AE6FE},
	Volume = {429},
	Year = {2004},
	url = {papers/Abbott_Nature2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/429338a}}

@article{Abdel-Aziz:2000,
	Abstract = {PURPOSE: An intact and fully functional multiprotein DNA replication complex (DNA synthesome) from human as well as from murine mammary carcinoma cells was first isolated and characterized in our laboratory. The human cell synthesome supports the in vitro origin-specific simian virus 40 (SV40) DNA replication reaction in the presence of the viral large T-antigen using a semiconservative mechanism and has been shown to contain all the proteins and enzymes required to support DNA synthesis. We are currently using the DNA synthesome as a unique model for analyzing the mechanism of action of anticancer drugs affecting DNA replication. The purpose of this study was to further investigate the mechanism of action of ara-C using the DNA synthesome isolated from the human breast cancer cell line MDA MB-468. METHODS: Synthesome-mediated SV40 DNA replication was performed in the presence of various concentrations of ara-CTP (the active metabolite of ara-C) and the types of daughter DNA molecules produced were analyzed lusing neutral and alkaline gel electrophoresis. We also examined the effect of ara-C on intact MDA MB-468 cell DNA synthesis and on cell proliferation. In addition, we studied the effect of ara-CTP on the activity of some of the synthesome target proteins (the DNA polymerases alpha and delta). RESULTS: Full-length daughter DNA molecules were obtained in the presence of low concentrations of ara-CTP while at higher concentrations, there was an inhibition of full-length daughter DNA synthesis. The findings suggest that specifically the initiation phase of DNA synthesis was inhibited by ara-CTP since the production of the short Okazaki fragments was suppressed at all concentrations of the drug above 10 microM. In addition, it was found that the IC50 of ara-CTP for inhibition of synthesome-mediated in vitro DNA replication was comparable to that required to inhibit intact cell DNA synthesis. Further experimentation has shown that ara-CTP preferentially inhibits the activity of the synthesome-associated DNA polymerase alpha enzyme while the DNA polymerase delta seems to be resistant to the inhibitory effect of that drug. CONCLUSIONS: Our results indicate that ara-C's action on DNA replication is mediated primarily through DNA polymerase alpha and suggest that this enzyme plays a key role in DNA synthetic initiation events. The results also provide definitive support for the use of the DNA synthesome as a unique and powerful model for analyzing the mechanism of action of anticancer drugs which directly affect DNA replication. 0344-5704 Journal Article},
	Author = {Abdel-Aziz, W. and Jiang, H. Y. and Hickey, R. J. and Malkas, L. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Journal = {Cancer Chemother Pharmacol},
	Keywords = {EE pdf;Tumor Cells, Cultured;Cell Division/drug effects;DNA Replication/*drug effects;Antimetabolites, Antineoplastic/*pharmacology;DNA Polymerase III/biosynthesis;DNA, Neoplasm/*biosynthesis;Human;08 Aberrant cell cycle;Breast Neoplasms/metabolism;Cytarabine/*pharmacology;Antigens, Polyomavirus Transforming/metabolism;Replicon/drug effects;Support, U.S. Gov't, P.H.S.;DNA Polymerase I/biosynthesis;Arabinofuranosylcytosine Triphosphate/pharmacology},
	Number = {4},
	Organization = {University of Maryland School of Medicine, Department of Pharmacology and Experimental Therapeutics, Baltimore, MD 21201, USA.},
	Pages = {312-9},
	Title = {Ara-C affects formation of cancer cell DNA synthesome replication intermediates},
	Uuid = {5ABDDBB5-1C18-4F45-AF57-A7FF63707641},
	Volume = {45},
	Year = {2000},
	url = {papers/Abdel-Aziz_CancerChemotherPharmacol2000.pdf}}

@article{Abe:2003,
	Abstract = {BACKGROUND: BM cells have been shown to give rise to progeny of various cell lineages, including cells in lung and liver. This investigation evaluated whether purified BM mononuclear cells and side population (SP) cells that have hematopoietic stem-cell activity also had this property; whether a TBI preparative regimen was necessary for engraftment; and where BM-derived cells were engrafted. METHODS: Either 1-3 million BM mononuclear cells or 2000 BM SP cells from transgenic enhanced green fluorescent protein-expressing (EGFP) mice were transplanted i.v. to unirradiated or 7-9.5 Gy irradiated recipients. RESULTS: Flow cytometric analysis showed that lung cells (mean 45\%, range 4-70\%) and liver cells (mean 4\%, range 0.4-8.3\%) from irradiated, but not unirradiated recipients, were EGFP donor-derived. Similar results were obtained transplanting BM mononuclear cells or SP cells. Morphologically, donor-derived cells in the lung were primarily monocytes and macrophages. Additionally, lung fibroblasts and Type I, but not Type II, alveolar cells and rare cells in the bronchial epithelium were donor BM derived. In the liver, Kupffer cells, inflammatory cells and small clusters of hepatocytes, but not bile duct cells, were donor-derived. DISCUSSION: BM mononuclear and SP cells generated progeny in some compartments of the lung and liver, but only in TBI recipients. Stem cells in BM can contribute to repair of tissue injury in some compartments, but not to the same extent in the lung and liver.},
	Author = {Abe, S. and Lauby, G. and Boyer, C. and Rennard, S. I. and Sharp, J. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1465-3249},
	Journal = {Cytotherapy},
	Keywords = {Research Support, Non-U.S. Gov't;Gamma Rays;Animals;Blood Cells;Whole-Body Irradiation;Bone Marrow Transplantation;Serum Albumin;Female;Cell Count;Mice, Transgenic;Liver;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Keratin;Immune Tolerance;Bone Marrow Cells;Survival Rate;Flow Cytometry;Mice;Immunohistochemistry;Graft Survival;Luminescent Proteins;Spleen;Lung},
	Nlm_Id = {100895309},
	Number = {6},
	Organization = {Department of Internal Medicine Pulmonary Section, University of Nebraska Medical Center, Omaha, NE 986395, USA.},
	Pages = {523-33},
	Pii = {0RJXN5LLRQL82P13},
	Pubmed = {14660048},
	Title = {Transplanted BM and BM side population cells contribute progeny to the lung and liver in irradiated mice},
	Uuid = {54F89858-5CAB-4886-91C0-D937E0BA898E},
	Volume = {5},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1080/14653240310003576}}

@article{Abe:1998,
	Abstract = {In the absence of envelope gene expression, retrovirus packaging cell lines expressing Moloney murine leukemia virus (MLV) gag and pol genes produce large amounts of noninfectious virus-like particles that contain reverse transcriptase, processed Gag protein, and viral RNA (gag-pol RNA particles). We demonstrate that these particles can be made infectious in an in vitro, cell-free system by the addition of a surrogate envelope protein, the G spike glycoprotein of vesicular stomatitis virus (VSV-G). The appearance of infectivity is accompanied by physical association of the G protein with the immature, noninfectious virus particles. Similarly, exposure in vitro of wild-type VSV-G to a fusion-defective pseudotyped virus containing a mutant VSV-G markedly increases the infectivity of the virus to titers similar to those of conventional VSV-G pseudotyped viruses. Furthermore, similar treatment of an amphotropic murine leukemia virus significantly allows infection of BHK cells not otherwise susceptible to infection with native amphotropic virus. The partially cell-free virus maturation system reported here should be useful for studies aimed at the preparation of tissue-targeted retrovirus vectors and will also aid in studies of nucleocapsid-envelope interactions during budding and of virus assembly and virus-receptor interactions during virus uptake into infected cells. It may also represent a potentially useful step toward the eventual development of a completely cell-free retrovirus assembly system.},
	Author = {Abe, A. and Chen, S. T. and Miyanohara, A. and Friedmann, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {RNA, Viral;Animals;Humans;Vesicular stomatitis-Indiana virus;Cell Line, Transformed;15 Retrovirus mechanism;Virion;Hela Cells;Viral Envelope Proteins;Cell Line;Research Support, U.S. Gov't, P.H.S.;Moloney murine leukemia virus;Membrane Glycoproteins;Fusion Proteins, gag-pol;Cell-Free System;Cricetinae;24 Pubmed search results 2008;Culture Media;15 PS VSVG receptor;Research Support, Non-U.S. Gov't},
	Medline = {98325147},
	Month = {8},
	Nlm_Id = {0113724},
	Number = {8},
	Organization = {Department of Pediatrics, Center for Molecular Genetics, University of California, San Diego, La Jolla, California 92093-0634, USA.},
	Pages = {6356-61},
	Pubmed = {9658075},
	Title = {In vitro cell-free conversion of noninfectious Moloney retrovirus particles to an infectious form by the addition of the vesicular stomatitis virus surrogate envelope G protein},
	Uuid = {6BA86AC4-4324-11DB-A5D2-000D9346EC2A},
	Volume = {72},
	Year = {1998},
	url = {papers/Abe_JVirol1998.pdf}}

@article{Abedi:2004,
	Abstract = {OBJECTIVE: Murine marrow cells are capable of repopulating skeletal muscle fibers. A point of concern has been the "robustness" of such conversions. We have investigated the impact of type of cell delivery, muscle injury, nature of delivered cell, and stem cell mobilizations on marrow-to-muscle conversion. METHODS: We transplanted green fluorescence protein (GFP)-transgenic marrow into irradiated C57BL/6 mice and then injured anterior tibialis muscle by cardiotoxin. One month after injury, sections were analyzed by standard and deconvolutional microscopy for expression of muscle and hematopoietic markers. RESULTS: Irradiation was essential to conversion, although whether by injury or induction of chimerism is not clear. Cardiotoxin- and, to a lesser extent, PBS-injected muscles showed significant number of GFP(+) muscle fibers, while uninjected muscles showed only rare GFP(+) cells. Marrow conversion to muscle was increased by two cycles of G-CSF mobilization and to a lesser extent by G-CSF and steel or GM-CSF. Transplantation of female GFP to male C57BL/6 and GFP to ROSA26 mice showed fusion of donor cells to recipient muscle. High numbers of donor-derived muscle colonies and up to 12\%GFP(+) muscle cells were seen after mobilization or direct injection. These levels of donor muscle chimerism approach levels that could be clinically significant in developing strategies for the treatment of muscular dystrophies. CONCLUSION: In summary, the conversion of marrow to skeletal muscle cells is based on cell fusion and is critically dependent on injury. This conversion is also numerically significant and increases with mobilization.},
	Author = {Abedi, Mehrdad and Greer, Deborah A. and Colvin, Gerald A. and Demers, Delia A. and Dooner, Mark S. and Harpel, Jasha A. and Weier, Heinz-Ulrich U. and Lambert, Jean-Francois F. and Quesenberry, P. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0301-472X},
	Journal = {Exp Hematol},
	Keywords = {Hematopoietic Stem Cell Mobilization;Animals;Bone Marrow Transplantation;Muscle Cells;Female;Cell Fusion;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Male;Transplantation Chimera;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Muscle, Skeletal;Mice;Muscle Fibers;Luminescent Proteins;Colony-Stimulating Factors;Regeneration},
	Month = {5},
	Nlm_Id = {0402313},
	Number = {5},
	Organization = {Roger Williams Medical Center, Department of Research, Providence, RI 02864, USA. mabedi\@rwmc.org},
	Pages = {426-34},
	Pii = {S0301472X04000645},
	Pubmed = {15145210},
	Title = {Robust conversion of marrow cells to skeletal muscle with formation of marrow-derived muscle cell colonies: a multifactorial process},
	Uuid = {07AF3ACE-D12E-4AAD-90CE-357A8D1F16E7},
	Volume = {32},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.exphem.2004.02.007}}

@article{Aberg:2000,
	Abstract = {In several species, including humans, the dentate granule cell layer (GCL) of the hippocampus exhibits neurogenesis throughout adult life. The ability to regulate adult neurogenesis pharmacologically may be of therapeutic value as a mechanism for replacing lost neurons. Insulin- like growth factor-I (IGF-I) is a growth-promoting peptide hormone that has been shown to have neurotrophic properties. The relationship between IGF-I and adult hippocampal neurogenesis is to date unknown. The aim of this study was to investigate the effect of the peripheral administration of IGF-I on cellular proliferation in the dentate subgranular proliferative zone, which contains neuronal progenitor cells, and on the subsequent migration and differentiation of progenitor cells within the GCL. Using bromodeoxyuridine (BrdU) labeling, we found a significant increase of BrdU-immunoreactive progenitors in the GCL after 6 d of peripheral IGF-I administration. To determine the cell fate in progenitor progeny, we characterized the colocalization of BrdU-immunolabeled cells with cell-specific markers. In animals treated with IGF-I for 20 d, BrdU-positive cells increased significantly. Furthermore, the fraction of newly generated neurons in the GCL increased, as evaluated by the neuronal markers Calbindin D(28K), microtubule-associated protein-2, and NeuN. There was no difference in the fraction of newly generated astrocytes. Thus, our results show that peripheral infusion of IGF-I increases progenitor cell proliferation and selectively induces neurogenesis in the progeny of adult neural progenitor cells. This corresponds to a 78 +/- 17\%(p <0.001) increase in the number of new neurons in IGF-I-treated animals compared with controls.},
	Author = {Aberg, M. A. and Aberg, N. D. and Hedbacker, H. and Oscarsson, J. and Eriksson, P. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurosci},
	Keywords = {Hippocampus/cytology/*drug effects/metabolism;Rats;Female;Bromodeoxyuridine/metabolism;Dentate Gyrus/cytology/drug effects;Animal;Stem Cells/*drug effects/metabolism;Insulin-Like Growth Factor I/*pharmacology;04 Adult neurogenesis factors;Hypophysectomy;Support, Non-U.S. Gov't;Male;C-13},
	Number = {8},
	Organization = {Institute of Clinical Neuroscience, Sahlgrenska University Hospital, Goteborg University, Goteborg, Sweden.},
	Pages = {2896-903.},
	Title = {Peripheral infusion of IGF-I selectively induces neurogenesis in the adult rat hippocampus},
	Uuid = {52A63FBA-C95F-4154-B7BB-38DA461BA72A},
	Volume = {20},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10751442%20http://www.jneurosci.org/cgi/content/full/20/8/2896%20http://www.jneurosci.org/cgi/content/abstract/20/8/2896}}

@article{Aboody:2000,
	Abstract = {One of the impediments to the treatment of brain tumors (e.g., gliomas) has been the degree to which they expand, infiltrate surrounding tissue, and migrate widely into normal brain, usually rendering them "elusive"to effective resection, irradiation, chemotherapy, or gene therapy. We demonstrate that neural stem cells (NSCs), when implanted into experimental intracranial gliomas in vivo in adult rodents, distribute themselves quickly and extensively throughout the tumor bed and migrate uniquely in juxtaposition to widely expanding and aggressively advancing tumor cells, while continuing to stably express a foreign gene. The NSCs "surround"the invading tumor border while "chasing down"infiltrating tumor cells. When implanted intracranially at distant sites from the tumor (e.g., into normal tissue, into the contralateral hemisphere, or into the cerebral ventricles), the donor cells migrate through normal tissue targeting the tumor cells (including human glioblastomas). When implanted outside the CNS intravascularly, NSCs will target an intracranial tumor. NSCs can deliver a therapeutically relevant molecule-cytosine deaminase-such that quantifiable reduction in tumor burden results. These data suggest the adjunctive use of inherently migratory NSCs as a delivery vehicle for targeting therapeutic genes and vectors to refractory, migratory, invasive brain tumors. More broadly, they suggest that NSC migration can be extensive, even in the adult brain and along nonstereotypical routes, if pathology (as modeled here by tumor) is present. 0027-8424 Journal Article},
	Author = {Aboody, K. S. and Brown, A. and Rainov, N. G. and Bower, K. A. and Liu, S. and Yang, W. and Small, J. E. and Herrlinger, U. and Ourednik, V. and Black, P. M. and Breakefield, X. O. and Snyder, E. Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {G;Human;Animals;Stem Cells/cytology/*physiology;Nucleoside Deaminases/*genetics;Rats;Brain/*pathology;Neurons/cytology/*physiology;Gene Therapy/methods;Female;11 Glia;Disease Models, Animal;Glioblastoma/*pathology/therapy;Hematopoietic Stem Cell Transplantation;Mice, Nude;Tropism;Rats, Inbred F344;Support, Non-U.S. Gov't;Brain Neoplasms/*pathology/therapy;Cytosine Deaminase;Support, U.S. Gov't, P.H.S.;Cell Movement/physiology;Mice},
	Number = {23},
	Organization = {Departments of Neurology, Pediatrics, and Neurosurgery, Children's Hospital, Boston, MA, USA.},
	Pages = {12846-51},
	Pubmed = {11070094},
	Title = {Neural stem cells display extensive tropism for pathology in adult brain: evidence from intracranial gliomas},
	Uuid = {62D215A2-5535-4A50-92C3-B7564C9732F0},
	Volume = {97},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11070094}}

@article{Abraham:2004,
	Abstract = {In the fetal human hippocampus, Cajal-Retzius (CR) cells coexpress p73, a p53-family member involved in cell survival and apoptosis, and the glycoprotein reelin, crucial for radial migration. We distinguish two populations of putative CR cells. (1). p73/reelin expressing cells appear around 10 gestational weeks (GW) at the cortico-choroid border in the temporal horn of the lateral ventricle (the ventral cortical hem) and occupy the marginal zone (MZ) overlying the ammonic and dentate primordia. (2). Additional p73-positive cells appear from 14 GW onward in the neuroepithelium near the dentate-fimbrial boundary and spread toward the pial surface, flanking the migrating secondary dentate matrix. From 13 to 17 GW, large parts of the dentate gyrus are almost devoid of CR cells. p73/Reelin-positive CR cells appear in the MZ of the suprapyramidal blade at 16 GW and around 21 GW in the infrapyramidal blade. The p73-positive cells of the dentate-fimbrial boundary express reelin when they are close to the pial surface, suggesting that they differentiate into CR cells of the infrapyramidal blade. Reelin-positive, p73-negative interneurons are prominent in the prospective strata lacunosum-moleculare and radiatum of cornu ammonis as early as 14 GW; in the dentate molecular layer and hilus they appear around midgestation. We propose that CR cells of the human hippocampal formation belong to two distinct cell populations: an early one derived from the ventral cortical hem and mainly related to migration of the ammonic and dentate plates and a later appearing one derived from the dentate-fimbrial neuroepithelium, which may be related to the protracted neurogenesis and migration of dentate granule cells, particularly of the infrapyramidal blade.},
	Author = {Abraham, Hajnalka and P{\'e}rez-Garc{\'\i}a, Carlos Gustavo and Meyer, Gundela},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {10 Development;10 Hippocampus;Tissue Distribution;DNA-Binding Proteins;Humans;Cells, Cultured;Neocortex;Hippocampus;Serine Endopeptidases;Cell Adhesion Molecules, Neuronal;Cerebellar Nuclei;Genes, Tumor Suppressor;Extracellular Matrix Proteins;Neurons;Nuclear Proteins;Cell Division;Gestational Age;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Month = {5},
	Nlm_Id = {9110718},
	Number = {5},
	Organization = {Department of Anatomy, Faculty of Medicine, University La Laguna, Tenerife, Spain.},
	Pages = {484-95},
	Pii = {bhh010},
	Pubmed = {15054064},
	Title = {p73 and Reelin in Cajal-Retzius cells of the developing human hippocampal formation},
	Uuid = {CFFD61AC-FCC4-4363-8966-4C2FE1B31F51},
	Volume = {14},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhh010}}

@article{Agiostratidou:2001,
	Abstract = {Human somatic cells cultured in vitro exhibit a limited number of divisions. In contrast immortal cells have lost their growth regulatory mechanisms and, thus, continue to divide indefinitely. Cyclin-dependent kinase inhibitors (CDKIs) represent one of the most important regulatory factors in both mortality and immortality, as they are over-expressed in senescent cells and are down-regulated in a number of human cancers. In the present study we determined the effect of CDKIs on the proliferation ability of human osteosarcoma cell lines. Transient expression of various CDKIs (p15INK4b, p16INK4a and p21CIP1/WAF1) in KHOS cells resulted in growth arrest and the cells failed to enter the S-phase of the cell cycle as shown by a DNA synthesis inhibition assay. In addition, stable transfection of p21CIP1/WAF1 and p16INK4a genes in two osteosarcoma cell lines (KHOS and U2-OS cells) showed that p21CIP1/WAF1 was able to repress the immortal phenotype in both cell lines, whereas temporary over-expression of p16INK4a reversibly inhibited the cell growth. Therefore this study indicates that CDKIs mediate growth arrest in human osteosarcoma cell lines and provides further evidence of the existence of molecular links between cellular mortality and immortality. 0258-851x Journal Article},
	Author = {Agiostratidou, G. and Derventzi, A. and Gonos, E. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {In Vivo},
	Keywords = {Human;DNA, Neoplasm/biosynthesis;Cell Aging/genetics;Transfection;Comparative Study;Genes, p16;Cell Transformation, Neoplastic/genetics;DNA Replication;08 Aberrant cell cycle;Osteosarcoma/*pathology;Cell Cycle Proteins/genetics/*physiology;Neoplasm Proteins/antagonists &inhibitors/physiology;Support, Non-U.S. Gov't;Recombinant Fusion Proteins/physiology;Cell Division/genetics;Cell Cycle/genetics;Bone Neoplasms/*pathology;Tumor Cells, Cultured/cytology/metabolism;Cyclins/genetics/*physiology;Cyclin-Dependent Kinases/antagonists &inhibitors/physiology;EE, G abstr;Protein p16/genetics/*physiology},
	Number = {5},
	Organization = {National Hellenic Research Foundation, Institute of Biological Research and Biotechnology, 48 Vas. Constantinou Ave., Athens 11635, Greece.},
	Pages = {443-6},
	Pubmed = {11695244},
	Title = {Over-expression of CDKIs p15INK4b, p16INK4a and p21CIP1/WAF1 genes mediate growth arrest in human osteosarcoma cell lines},
	Uuid = {AE1DDA71-C0B3-4E49-891A-6541E79B61A5},
	Volume = {15},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11695244%20Polaris:Users:ackman:Desktop:query.fcgi}}

@article{Agrawal:1996,
	Abstract = {As hematopoietic stem and progenitor cells have a low mitotic index, we have quantitated the impact of cytokine combinations on cell cycling of CD34+ cells and, using VSV-G pseudotyped retroviral vectors, correlated our findings with ex vivo gene transfer. We tested nine different combinations of cytokines for induction of human peripheral blood CD34+ cells into cell cycle over 72 hours. Using the 5-bromodeoxyuridine-Hoechst 33258 (BrdU-Hoechst) assay, we measured the cell-cycle kinetics. The combinations of cytokines tested that were most efficient in inducing the CD34+ cells into cycle were stem cell factor (SCF) plus one of the following: interleukin-1 (IL-1), IL-3, granulocyte colony-stimulating factor (G-CSF). The maximum numbers of cells in S+G2M phase were observed after 48 hours of culture. At least 35 +/- 5\%of the CD34+ cells remained quiescent in the first G0/G1 phase, however, no matter which cytokine combination was used. Cell-cycle analysis of the CD34+CD38- subset by 7-amino actinomycin D staining did not detect cycling cells during 72 hours of culture with any of the cytokines tested. To investigate whether the cells could be infected by the VSV-G pseudotyped virus containing the neomycin phospho-transferase gene (neo), we exposed CD34+ cells to the virus for 7-8 hours after 0, 36, and 48 hours of cytokine stimulation. Total CD34+ cells and the CD34+CD38- subset were analyzed by polymerase chain reaction (PCR) for reverse-transcribed viral DNA of the neomycin resistance gene (RT-neoDNA). Immediately after exposure to the virus, RT-neoDNA was detectable in CD34+ cells that have been cultured with or without cytokines for 36 to 48 hours. Forty-eight hours postinfection, however, RT-neoDNA could be detected only with cytokine combinations that induced mitosis of the CD34+ cells, consistent with the requirement for mitotic activity for retroviral integration. Similar experiments performed with the 34+CD38- subset showed that RT-reoDNA could not be detected at any time point. Thus, postinfection RT-neoDNA could be immediately detected in noncycling CD34+ cells but not in CD34+CD38- cells. These results suggest during short-term liquid culture, there may be blocks for reverse transcription of retroviral RNA in CD34+CD38-cells in addition to the lack of mitotic activity.},
	Author = {Agrawal, Y. P. and Agrawal, R. S. and Sinclair, A. M. and Young, D. and Maruyama, M. and Levine, F. and Ho, A. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0301-472X},
	Journal = {Exp Hematol},
	Keywords = {N-Glycosyl Hydrolases;Transduction, Genetic;ADP-ribosyl Cyclase;Cells, Cultured;Base Sequence;Humans;Blood Cells;Cell Cycle;Vesicular stomatitis-Indiana virus;Antigens, Differentiation;Apoptosis;Antigens, CD;15 Retrovirus mechanism;RNA-Directed DNA Polymerase;Antigens, CD34;Retroviridae;Immunophenotyping;Proviruses;Genetic Vectors;Research Support, U.S. Gov't, P.H.S.;DNA Primers;Gene Transfer Techniques;Membrane Glycoproteins;Hematopoietic Stem Cells;24 Pubmed search results 2008;Molecular Sequence Data;Antigens, CD38;Research Support, Non-U.S. Gov't},
	Medline = {96221566},
	Month = {5},
	Nlm_Id = {0402313},
	Number = {6},
	Organization = {Department of Medicine, University of California, San Diego School of Medicine, USA.},
	Pages = {738-47},
	Pubmed = {8635530},
	Title = {Cell-cycle kinetics and VSV-G pseudotyped retrovirus-mediated gene transfer in blood-derived CD34+ cells},
	Uuid = {C11022E1-692D-403F-92C8-FE9038664D61},
	Volume = {24},
	Year = {1996}}

@article{Aguirre:2002,
	Abstract = {Acquired resistance to the CNS pathogen Cryptococcus neoformans is mediated by CD4(+) T lymphocytes primed by exposure to antigen in the context of major histocompatibility class II (MHC II) molecules. In mouse brain, parenchymal and perivascular microglial cells may express interferon-gamma (IFN-gamma)-inducible MHC class II marker and thus interact with CD4(+) T cells. Primed effector T cells are retained in the infected CNS if antigen is encountered in proper MHC context and may deliver signals that potentiate microglia to enhanced fungistasis. Vaccinated C57BL6/J mice resist an ordinarily lethal C. neoformans rechallenge, but identically treated congenic Abeta(o/o) mice (MHC class II-deficient; CD4(+) T-cell-deficient) do not. Nor can Abeta(o/o) mice be adoptively immunized by infusion of lymphocytes from vaccinated C57BL6/J donors, as are severe combined immunodeficient (SCID) mice (MHC class II-intact, lymphocyte-deficient). Chimeric (C57BL/6J:Abeta(o/o)) mice with class II expression likely on perivascular microglia only were, like SCID mice, capable of adoptive immunization against C. neoformans brain infection. To the contrary, chimeric mice with class II expression likely only on parenchymal microglia were not capable of effective adoptive immunization against C. neoformans brain infection. Therefore, in order to mediate resistance to infection, primed CD4(+) T cells must interact with the replenishable perivascular microglial subset that lies in close proximity to cerebral vasculature. Although T cells may supply help in the form of inflammatory cytokines to parenchymal microglia, expression of class II on these cells appears unnecessary for antifungal activity.},
	Author = {Aguirre, Karen and Miller, Shannon},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Research Support, Non-U.S. Gov't;Cryptococcus neoformans;Animals;Meningitis, Cryptococcal;Bone Marrow Transplantation;Brain;Microglia;Cell Communication;Mice, Inbred C57BL;11 Glia;Transplantation Chimera;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Mice, Knockout;Immunization;Antigen Presentation;Mice;CD4-Positive T-Lymphocytes;Immunity, Natural;Histocompatibility Antigens Class II;Blood Vessels},
	Medline = {22106034},
	Month = {8},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Biology Department, Clarkson University, Potsdam, New York 13699, USA. kmaguirr\@clarkson.edu},
	Pages = {184-8},
	Pubmed = {12112369},
	Title = {MHC class II-positive perivascular microglial cells mediate resistance to Cryptococcus neoformans brain infection},
	Uuid = {AF0B08A6-3BA7-45E1-9206-1123AD503BD8},
	Volume = {39},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10093}}

@article{Aguirre:2004a,
	Abstract = {The subventricular zone (SVZ) is a source of neural progenitors throughout brain development. The identification and purification of these progenitors and the analysis of their lineage potential are fundamental issues for future brain repair therapies. We demonstrate that early postnatal NG2-expressing (NG2+) progenitor cells located in the SVZ self-renew in vitro and display phenotypic features of transit-amplifier type C-like multipotent cells. NG2+ cells in the SVZ are highly proliferative and express the epidermal growth factor receptor, the transcription factors Dlx, Mash1, and Olig2, and the Lewis X (LeX) antigen. We show that grafted early postnatal NG2+ cells generate hippocampal GABAergic interneurons that propagate action potentials and receive functional glutamatergic synaptic inputs. Our work identifies Dlx+/Mash1+/LeX+/NG2+/GFAP-negative cells of the SVZ as a new class of postnatal multipotent progenitor cells that may represent a specific cellular reservoir for renewal of postnatal and adult inhibitory interneurons in the hippocampus.},
	Author = {Aguirre, Adan A. and Chittajallu, Ramesh and Belachew, Shibeshih and Gallo, Vittorio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {gamma-Aminobutyric Acid;Cell Differentiation;Animals;Receptor, Epidermal Growth Factor;DNA-Binding Proteins;Antigens, CD15;Cells, Cultured;Stem Cell Transplantation;Transcription Factors;Synaptic Transmission;Proteoglycans;Homeodomain Proteins;Cell Movement;Mice, Transgenic;Hippocampus;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;Animals, Newborn;Antigens;Action Potentials;Support, U.S. Gov't, P.H.S.;Mice;Interneurons;Cell Division;Stem Cells;Nerve Tissue Proteins;Neural Inhibition;Lateral Ventricles},
	Month = {5},
	Nlm_Id = {0375356},
	Number = {4},
	Organization = {Center for Neuroscience Research, Children's Research Institute, Rm. 5345, Children's National Medical Center, 111 Michigan Ave., N.W., Washington, DC 20010, USA.},
	Pages = {575-89},
	Pii = {jcb.200311141},
	Pubmed = {15159421},
	Title = {NG2-expressing cells in the subventricular zone are type C-like cells and contribute to interneuron generation in the postnatal hippocampus},
	Uuid = {243E49F9-1744-4893-8C3A-2BA0A320F178},
	Volume = {165},
	Year = {2004},
	url = {papers/Aguirre_JCellBiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200311141}}

@article{Aguirre:2004,
	Abstract = {We used a 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP)-enhanced green fluorescent protein (EGFP) transgenic mouse to study postnatal subventricular zone (SVZ) progenitor fate, with a focus on the olfactory bulb (OB). The postnatal OB of the CNP-EGFP mouse contained EGFP+ interneurons and oligodendrocytes. In the anterior SVZ, the majority of EGFP+ progenitors were NG2+. These NG2+/EGFP+ progenitors expressed the OB interneuron marker Er81, the neuroblast markers doublecortin (DC) and Distalless-related homeobox (DLX), or the oligodendrocyte progenitor marker Nkx2.2. In the rostral migratory stream (RMS), EGFP+ cells displayed a migrating phenotype. A fraction of these cells were either NG2-/Er81+/DC+/DLX+ or NG2+/Nkx2.2+. DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate) injection into the lateral ventricle (LV) of early postnatal mice demonstrated that NG2+/EGFP+ progenitors migrate from the SVZ through the RMS into the OB. Moreover, fluorescence-activated cell-sorting-purified NG2+/CNP-EGFP+ or NG2+/beta-actin-enhanced yellow fluorescent protein-positive (EYFP+) progenitors transplanted into the early postnatal LV displayed extensive rostral and caudal migration. EYFP+ or EGFP+ graft-derived cells within the RMS were DLX+/Er81+ or Nkx2.2+, migrated to the OB, and differentiated to interneurons and oligodendrocytes. In the subcortical white matter (SCWM), grafted cells differentiated to either oligodendrocytes or astrocytes. Transplantation of NG2+/EYFP+ progenitors selectively purified from the SVZ showed that these cells were migratory and generated glia and neurons in the OB, hippocampus, and striatum. In contrast, cortical, OB, or cerebellar NG2+ cells had a very limited migratory potential and gave rise to glia in the SCWM and striatum. Our findings indicate region-specific differences between NG2+ progenitor cells and show that NG2+ cells can migrate throughout the RMS and contribute to both gliogenesis and neurogenesis in the postnatal OB.},
	Author = {Aguirre, Adan and Gallo, Vittorio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {03 Adult neurogenesis progenitor source},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {46},
	Organization = {Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC 20010, USA.},
	Pages = {10530-41},
	Pii = {24/46/10530},
	Pubmed = {15548668},
	Title = {Postnatal neurogenesis and gliogenesis in the olfactory bulb from NG2-expressing progenitors of the subventricular zone},
	Uuid = {605802AA-0DA0-42A7-9BCD-A25F5E8B514A},
	Volume = {24},
	Year = {2004},
	url = {papers/Aguirre_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3572-04.2004}}

@article{Aguzzi:2003,
	Abstract = {The incidence of Alzheimer's disease (AD) and that of prion disorders (PrD) could not be more different. One-third of octogenarians succumb to AD, whereas Creutzfeldt-Jakob disease typically affects one individual in a million each year. However, these diseases have many common features impinging on the metabolism of neuronal membrane proteins: the amyloid precursor protein APP in the case of AD, and the cellular prion protein PrPC in PrD. APP begets the Abeta peptide, whereas PrPC begets the malignant prion protein PrPSc. Both Abeta and PrPSc are associated with disease, but we do not know what triggers their accumulation and neurotoxicity. A great deal has been learned, however, about protein folding, misfolding, and aggregation; an entirely new class of intramembrane proteases has been identified; and unsuspected roles for the immune system have been uncovered. There is reason to expect that prion research will profit from advances in the understanding of AD, and vice versa.},
	Author = {Aguzzi, Adriano and Haass, Christian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:40 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Creutzfeldt-Jakob Syndrome;Human;Animals;Prion Diseases;Amyloid beta-Protein;review, tutorial;Endopeptidases;Protein Folding;Brain;review;Mutation;21 Neurodegenerative;PrPSc Proteins;Terminology;Amyloid beta-Protein Precursor;Alzheimer Disease;21 Neurophysiology;PrPC Proteins;Membrane Proteins},
	Medline = {22954843},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5646},
	Organization = {Institute of Neuropathology, University Hospital of Zurich, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland. adriano\@pathol.unizh.ch},
	Pages = {814-8},
	Pii = {302/5646/814},
	Pubmed = {14593165},
	Title = {Games played by rogue proteins in prion disorders and Alzheimer's disease},
	Uuid = {FAEE579A-15C4-422B-BC56-9F1D346349F6},
	Volume = {302},
	Year = {2003},
	url = {papers/Aguzzi_Science2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1087348}}

@article{Aharoni:2005,
	Abstract = {Brain insults such as the autoimmune inflammatory process in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) induce a measure of neurogenesis, but its regenerative therapeutic consequence is limited, because it fails to regenerate functional neurons and compensate the damage. Here, we investigated whether peripheral immunomodulatory treatment for MS/EAE, glatiramer acetate (GA), can enhance neurogenesis and generate neuroprotection in the CNS of EAE-inflicted mice. EAE was induced by myelin oligodendrocyte glycoprotein peptide, either in yellow fluorescent protein (YFP) 2.2 transgenic mice, which selectively express YFP on their neuronal population, or in C57BL/6 mice. The in situ effect of GA was studied in various brain regions; neuroprotection and neurogeneration were evaluated and quantified by measuring the expression of different neuronal antigens and in vivo proliferation markers. The results demonstrated that in EAE-inflicted mice, neuroproliferation was initially elevated after disease appearance but subsequently declined below that of naive mice. In contrast, GA treatment in various stages of the disease led to sustained reduction in the neuronal/axonal damage typical to the neurodegenerative disease course. Moreover, three processes characteristic of neurogenesis, namely cell proliferation, migration, and differentiation, were augmented and extended by GA treatment in EAE mice compared with EAE-untreated mice and naive controls. The newborn neuroprogenitors manifested massive migration through exciting and dormant migration pathways, into injury sites in brain regions, which do not normally undergo neurogenesis, and differentiated to mature neuronal phenotype. This suggests a direct linkage between immunomodulation, neurogenesis, and an in situ therapeutic consequence in the CNS.},
	Author = {Aharoni, Rina and Arnon, Ruth and Eilam, Raya},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {36},
	Organization = {Department of Immunology, The Weizmann Institute of Science, Rehovot, 76100, Israel.},
	Pages = {8217-28},
	Pii = {25/36/8217},
	Pubmed = {16148229},
	Title = {Neurogenesis and neuroprotection induced by peripheral immunomodulatory treatment of experimental autoimmune encephalomyelitis},
	Uuid = {C07570D7-9994-49AE-8549-0CF3B9E9CB96},
	Volume = {25},
	Year = {2005},
	url = {papers/Aharoni_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1859-05.2005}}

@article{Ahmed:2001,
	Abstract = {Lewis rats, on recovery from monophasic clinical experimental allergic encephalomyelitis (EAE), can be induced to develop repeated paralytic relapses with a graded reduction in clinical severity following intraperitoneal administration of IL-12. By the time of the third relapse, the number and size of inflammatory cuffs in the spinal cord were reduced with the makeup of the cellular infiltrate shifting to a significantly increased number of B cells. Serum levels of myelin basic protein (MBP)-specific IgG1 and IgG2b were found to rise over time while MBP and MBP peptide-positive macrophages and microglia became evident in perivascular cuffs and in spinal cord parenchyma, indicative of myelin phagocytosis. Axonal death was observed in semithin and EM sections of spinal cord in third relapse animals in association with iNOS and tPA immunostaining throughout gray and white matter. These neurotoxic or excitotoxic agents may contribute to axonal damage directly or indirectly by activated microglia and macrophages, leading to limited damage of the axonal-myelin unit.},
	Author = {Ahmed, Z. and Gveric, D. and Pryce, G. and Baker, D. and Leonard, J. P. and Cuzner, M. L. and Diemel, L. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Interleukin-12;Rats, Inbred Lew;Animals;Myelin Sheath;Encephalomyelitis, Experimental Autoimmune;Acute Disease;Rats;Interleukins;Immunoglobulin G;Myelin Basic Proteins;Transforming Growth Factor beta;Paralysis;Female;Axons;Macrophage Activation;Autoantibodies;Not relevant;11 Glia;Spinal Cord;Leukocyte Count;Support, Non-U.S. Gov't;Tissue Plasminogen Activator;Recurrence},
	Medline = {21288683},
	Month = {6},
	Nlm_Id = {0370502},
	Number = {6},
	Organization = {Neuroinflammation Group, Department of Neurochemistry, Institute of Neurology, University College London, London, United Kingdom. z.ahmed\@ion.ucl.ac.uk},
	Pages = {2127-38},
	Pubmed = {11395390},
	Title = {Myelin/axonal pathology in interleukin-12 induced serial relapses of experimental allergic encephalomyelitis in the Lewis rat},
	Uuid = {2209A3A0-BF0E-4165-ACDC-F2189A791E9A},
	Volume = {158},
	Year = {2001}}

@article{Ahmed:1995,
	Abstract = {We have previously reported the isolation of an EGF-responsive precursor from the embryonic and adult mouse striatum. This precursor exhibits self renewal and the ability to produce a sphere of undifferentiated cells which can be induced to differentiate into neurons and glia. RT-PCR analysis of these spheres of undifferentiated cells revealed the expression of mRNA for the trkB neurotrophin receptor, both with and without the catalytic domain, and little or no expression of trkA or trkC. We examined the actions of BDNF on the fate of EGF-generated neural precursors. Ten days after a one-time exposure to BDNF, single EGF-generated spheres showed a twofold increase in neuron number and a marked enhancement in neurite outgrowth. Examination of neuronal nuclei with immunochemical probes for c-fos and bromodeoxyuridine revealed that the actions of BDNF were directly upon neuronal cells and did not involve division of neuronal precursors. The twofold increase in neuronal number due to BDNF, observed after 10 d in vitro, was significantly reduced after 21 d in vitro and was not apparent at 27 d in vitro. Quantitative analyses revealed that while repeated application of BDNF did not prevent the loss of neuron number over time, it did result in a significant increase in neurite numbers. Moreover, delayed addition of BDNF mimicked the increase in neuronal numbers seen when BDNF was present throughout. These BDNF actions did not appear to involve the enhancement of a novel neuronal phenotype, with all effects being due to increase in the numbers and neurite outgrowth of neurons that colocalize GABA and substance P. These findings suggest that BDNF markedly enhances the antigenic and morphologic differentiation of EGF-generated neuronal precursors. BDNF alone does not appear to act as a survival factor for neuronal precursors nor is it sufficient for preventing their death over time. 0270-6474 Journal Article},
	Author = {Ahmed, S. and Reynolds, B. A. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation/drug effects;Animals;Cell Survival/drug effects;Cells, Cultured;Neurons/*cytology/physiology;Nerve Growth Factors/pharmacology;Phenotype;Brain-Derived Neurotrophic Factor;Central Nervous System/*cytology;C abstr;Cell Count/drug effects;Stem Cells/*cytology;Time Factors;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Nerve Tissue Proteins/administration &dosage/*pharmacology;Neurites/ultrastructure;04 Adult neurogenesis factors;Mice},
	Number = {8},
	Organization = {Department of Anatomy, University of Calgary Faculty of Medicine, Alberta, Canada.},
	Pages = {5765-78},
	Pubmed = {7643217},
	Title = {BDNF enhances the differentiation but not the survival of CNS stem cell-derived neuronal precursors},
	Uuid = {390254C7-325F-4704-AF59-312F7DF3770D},
	Volume = {15},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7643217}}

@article{Ahn:2005,
	Abstract = {Sonic hedgehog (Shh) has been implicated in the ongoing neurogenesis in postnatal rodent brains. Here we adopted an in vivo genetic fate-mapping strategy, using Gli1 (GLI-Kruppel family member) as a sensitive readout of Shh activity, to systematically mark and follow the fate of Shh-responding cells in the adult mouse forebrain. We show that initially, only a small population of cells (including both quiescent neural stem cells and transit-amplifying cells) responds to Shh in regions undergoing neurogenesis. This population subsequently expands markedly to continuously provide new neurons in the forebrain. Our study of the behaviour of quiescent neural stem cells provides in vivo evidence that they can self-renew for over a year and generate multiple cell types. Furthermore, we show that the neural stem cell niches in the subventricular zone and dentate gyrus are established sequentially and not until late embryonic stages.},
	Author = {Ahn, Sohyun and Joyner, Alexandra L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Tamoxifen;Research Support, Non-U.S. Gov't;Trans-Activators;Immunohistochemistry;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Signal Transduction;Time Factors;Research Support, N.I.H., Extramural;Cell Division;Mice;Animals;Brain;Neurons;Cell Lineage},
	Month = {10},
	Nlm_Id = {0410462},
	Number = {7060},
	Organization = {Howard Hughes Medical Institute, Developmental Genetics Program, Skirball Institute of Biomolecular Medicine and Department of Cell Biology, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.},
	Pages = {894-7},
	Pii = {nature03994},
	Pubmed = {16208373},
	Title = {In vivo analysis of quiescent adult neural stem cells responding to Sonic hedgehog},
	Uuid = {AD8B3337-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {437},
	Year = {2005},
	url = {papers/Ahn_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03994}}

@article{Ailles:2002,
	Abstract = {A major challenge in gene therapy is to achieve efficient transduction of hematopoietic stem cells (HSC). It has previously been shown that lentiviral vectors (LV) transduce efficiently human cord blood-derived NOD/SCID mouse repopulating cells (SRC). Here we studied the effect of cytokines during the short ex vivo incubation with vector. Although SRC transduction was efficient without stimulation, the presence of cytokines significantly improved it. The treatment did not affect the engraftment level or the SRC frequency, but seemed to enhance SRC susceptibility to LV. SRC transduced in both conditions repopulated primary and secondary recipients, maintaining stable multi-lineage transgene expression. Using linear amplification-mediated PCR, we then analyzed vector integration in the bone marrow and CFC of the engrafted mice to monitor the clonal activity of the transduced SRC in vivo. We showed polyclonal engraftment, multi-lineage differentiation, and propagation to secondary recipients of individual SRC. We observed multiple integrations in most clones. These results provide the first formal demonstration that primitive human HSC with self-renewal and multi-lineage repopulation capacities were transduced by LV. Our findings are relevant for the design of clinical protocols that exploit this system to reach significant engraftment by genetically modified HSC in the absence of in vivo selection or strong conditioning regimens.},
	Author = {Ailles, Laurie and Schmidt, Manfred and Santoni de Sio, Francesca Romana and Glimm, Hanno and Cavalieri, Simona and Bruno, Stefania and Piacibello, Wanda and Von Kalle, Christof and Naldini, Luigi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {1525-0016},
	Journal = {Mol Ther},
	Keywords = {Cytokines;Transgenes;Cell Differentiation;Animals;Cell Separation;Humans;Bone Marrow Transplantation;Cell Cycle;Lentivirus;Mice, SCID;Antigens, CD34;11 Glia;Green Fluorescent Proteins;Hela Cells;Genetic Vectors;Cell Line;Cell Lineage;Gene Transfer Techniques;Flow Cytometry;Polymerase Chain Reaction;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22297657},
	Month = {11},
	Nlm_Id = {100890581},
	Number = {5},
	Organization = {Laboratory for Gene Transfer and Therapy, University of Torino Medical School, Candiolo, Italy.},
	Pages = {615-26},
	Pii = {S1525001602907203},
	Pubmed = {12409260},
	Title = {Molecular evidence of lentiviral vector-mediated gene transfer into human self-renewing, multi-potent, long-term NOD/SCID repopulating hematopoietic cells},
	Uuid = {DC5CEB18-8F71-4AD7-86C2-F071293D1A60},
	Volume = {6},
	Year = {2002}}

@article{Airaksinen:1997,
	Abstract = {Intracellular calcium-binding proteins are abundantly expressed in many neuronal populations. Previous evidence suggests that calcium-binding proteins can modulate various neuronal properties, presumably by their action as calcium buffers. The importance of calcium-binding proteins for nervous system function in an intact integrated system is, however, less clear. To investigate the physiological role of a major endogenous calcium-binding protein, calbindin D28k (calbindin) in vivo, we have generated calbindin null mutant mice by gene targeting. Surprisingly, calbindin deficiency does not affect general parameters of development and behavior or the structure of the nervous system at the light microscopic level. Null mutants are, however, severely impaired in tests of motor coordination, suggesting functional deficits in cerebellar pathways. Purkinje neurons, the only efferent of the cerebellar cortex, and inferior olive neurons, the source of the climbing fiber afferent, have previously been shown to express calbindin. Correlated with this unusual type of ataxia, confocal calcium imaging of Purkinje cells in cerebellar slices revealed marked changes of synaptically evoked postsynaptic calcium transients. Their fast, but not their slow, decay component had larger amplitudes in null mutant than in wild-type mice. We conclude that endogenous calbindin is of crucial importance for integrated nervous system function.},
	Author = {Airaksinen, M. S. and Eilers, J. and Garaschuk, O. and Thoenen, H. and Konnerth, A. and Meyer, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Ataxia;Signal Transduction;Purkinje Cells;Animals;Synapses;Evoked Potentials;Mice, Mutant Strains;Up-Regulation;Mice, Inbred C57BL;Calcium;Calcium-Binding Protein, Vitamin D-Dependent;Behavior, Animal;Embryonic and Fetal Development;Dendrites;research support, non-u.s. gov't ;21 Calcium imaging;21 Neurophysiology;Calcium-Binding Proteins;Cerebellum;Mice;Psychomotor Performance;24 Pubmed search results 2008;Nerve Tissue Proteins},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {4},
	Organization = {Department of Neurochemistry, Max Planck Institute for Psychiatry, Martinsried, Germany.},
	Pages = {1488-93},
	Pubmed = {9037080},
	Title = {Ataxia and altered dendritic calcium signaling in mice carrying a targeted null mutation of the calbindin D28k gene},
	Uuid = {9EDDBBAF-1CD7-4624-B0E4-4A8BBB83094F},
	Volume = {94},
	Year = {1997},
	url = {papers/Airaksinen_ProcNatlAcadSciUSA1997.pdf}}

@article{Akaaboune:2002,
	Abstract = {We show that fluorescently tagged ligands with high affinity for their targets can be reversibly unbound by focused laser excitation. By sequential unbinding and relabeling with different colors of alpha-bungarotoxin, we selectively labeled adjacent pools of acetylcholine receptors (AChRs) at neuromuscular junctions of adult mice. Timelapse imaging in vivo revealed that synaptic AChRs completely intermingle over approximately 4 days and many extrasynaptic AChRs are incorporated into the synapse each day. In mice that lacked alpha-dystrobrevin, a component of the dystrophin-glycoprotein complex, rates of AChR turnover, and intermingling were increased approximately 4- to 5-fold. These results demonstrate remarkable molecular dynamism underlying macroscopic stability of the postsynaptic membrane, and establish alpha-dystrobrevin as a key control point for regulation of mobility and turnover.},
	Author = {Akaaboune, Mohammed and Grady, R. Mark and Turney, Steve and Sanes, Joshua R. and Lichtman, Jeff W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Cytoskeletal Proteins;Fluorescent Dyes;Animals;research support, u.s. gov't, p.h.s. ;Female;Microscopy, Fluorescence;research support, non-u.s. gov't ;Receptors, Cholinergic;Dystrophin-Associated Proteins;Neuromuscular Junction;21 Neurophysiology;Light;Receptors, Neurotransmitter;Mice;24 Pubmed search results 2008;Membrane Proteins;Ligands;Binding, Competitive},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.},
	Pages = {865-76},
	Pii = {S0896627302007390},
	Pubmed = {12086635},
	Title = {Neurotransmitter receptor dynamics studied in vivo by reversible photo-unbinding of fluorescent ligands},
	Uuid = {511762F9-B9E1-48D9-B2B4-D02CD36A4745},
	Volume = {34},
	Year = {2002},
	url = {papers/Akaaboune_Neuron2002.pdf}}

@article{Akiyama:2000,
	Abstract = {Dendritic cells (DC) that have been genetically modified to express cytokine genes may be novel tools for inducing antitumor immune responses. In the present study, the pMX retroviral vector was modified to express the mouse IL-2 (mIL-2pMX) and mouse IL-12 (mIL-12pMX) genes. Supernatants from 293 cells transfected with pMX retroviral vectors were harvested and used to transduce mouse lin- bone marrow (BM) progenitor cells. After 48 h co-culture with pseudotype retrovirus, BM cells were cultured for 12 days in the presence of mGM-CSF, mSCF and mTNF-alpha to obtain a DC-enriched fraction. Flow cytometric analysis showed that GFP protein expression in these cultures was 20-40\%and that 40-50\%of the cultured BM cells were positive for the DC marker, DEC205. About 60\%of cells sorted for DEC205 also expressed GFP. The supernatants of DC-mIL-2 and DC-mIL-12 cultured for 48 h contained 5.2 +/- 0.15 and 33.9 +/- 2.6 ng cytokine protein per milliliter, respectively. Intratumoral injection of DC-mIL-2 or DC-mIL-12 on days 8 and 15 after the intradermal injection of 1 x 105 B16F10 cells, resulted in a significant reduction in tumor size by day 21, as compared with mice treated with unmodified DC or DC-GFP. Longer term analysis as assessed at day 42 revealed that B16 tumor-bearing mice treated with cytokine gene-modified DC survived significantly longer than mice from other groups. Spleen cells obtained from DC-treated mice were specifically sensitized for the generation of CTL by subsequent restimulation with gene-modified DC. These results suggested that DC genetically modified to express IL-2 or IL-12 can induce potent antitumor responses against well-established, poorly immunogenic B16F10 tumors. Gene Therapy (2000) 7, 2113-2121.},
	Author = {Akiyama, Y. and Watanabe, M. and Maruyama, K. and Ruscetti, F. W. and Wiltrout, R. H. and Yamaguchi, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Interleukin-12;Transduction, Genetic;Animals;Injections, Intralesional;Mice, Inbred C57BL;Retroviridae;Dendritic Cells;11 Glia;Green Fluorescent Proteins;Interleukin-2;Genetic Vectors;Gene Therapy;Melanoma, Experimental;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Gene Expression;Immunotherapy, Adoptive;Research Support, Non-U.S. Gov't},
	Medline = {21127469},
	Month = {12},
	Nlm_Id = {9421525},
	Number = {24},
	Organization = {Growth Factor Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104, Japan.},
	Pages = {2113-21},
	Pubmed = {11223993},
	Title = {Enhancement of antitumor immunity against B16 melanoma tumor using genetically modified dendritic cells to produce cytokines},
	Uuid = {B899B656-FD22-43F2-B391-C5F8112797BE},
	Volume = {7},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3301353}}

@article{Albertson:2003,
	Abstract = {Asymmetric cell division is important in generating cell diversity from bacteria to mammals. Drosophila melanogaster neuroblasts are a useful model system for investigating asymmetric cell division because they establish distinct apical-basal cortical domains, have an asymmetric mitotic spindle aligned along the apical-basal axis, and divide unequally to produce a large apical neuroblast and a small basal daughter cell (GMC). Here we show that Discs large (Dlg), Scribble (Scrib) and Lethal giant larvae (Lgl) tumour suppressor proteins regulate multiple aspects of neuroblast asymmetric cell division. Dlg/Scrib/Lgl proteins show apical cortical enrichment at prophase/metaphase, and then have a uniform cortical distribution. Mutants have defects in basal protein targeting, a reduced apical cortical domain and reduced apical spindle size. Defects in apical cell and spindle pole size result in symmetric or inverted neuroblast cell divisions. Inverted divisions correlate with the appearance of abnormally small neuroblasts and large GMCs, showing that neuroblast/GMC identity is more tightly linked to cortical determinants than cell size. We conclude that Dlg/Scrib/Lgl are important in regulating cortical polarity, cell size asymmetry and mitotic spindle asymmetry in Drosophila neuroblasts. 1465-7392 Journal Article},
	Author = {Albertson, R. and Doe, C. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Nat Cell Biol},
	Keywords = {Support, U.S. Gov't, P.H.S.;Insect Proteins/genetics/*metabolism;Cell Division/physiology;10 Development;Cell Cycle Proteins/genetics/metabolism;Drosophila melanogaster/physiology;*Cell Size;Neurons/cytology/*physiology;Drosophila Proteins/genetics/*metabolism;F;Microscopy, Fluorescence;Membrane Proteins/genetics/*metabolism;Animals;Tumor Suppressor Proteins/genetics/*metabolism;Support, Non-U.S. Gov't;Cell Polarity;Mitotic Spindle Apparatus/*metabolism},
	Number = {2},
	Organization = {Institute of Molecular Biology, Institute of Neuroscience, Howard Hughes Medical Institute, University of Oregon 1254, Eugene, OR 97403, USA.},
	Pages = {166-70},
	Pubmed = {12545176},
	Title = {Dlg, Scrib and Lgl regulate neuroblast cell size and mitotic spindle asymmetry},
	Uuid = {8DB3F1B1-88A0-41F0-9639-E9B2D25A5BB3},
	Volume = {5},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12545176}}

@article{Albrecht:2002,
	Abstract = {At focal CNS injury sites, several cytokines accumulate, including ciliary neurotrophic factor (CNTF) and interleukin-1beta (IL-1beta). Additionally, the CNTF alpha receptor is induced on astrocytes, establishing an autocrine/paracrine loop. How astrocyte function is altered as a result of CNTF stimulation remains incompletely characterized. Here, we demonstrate that direct injection of CNTF into the spinal cord increases GFAP expression and astroglial size and that primary cultures of spinal cord astrocytes treated with CNTF, IL-1beta, or leukemia inhibitory factor exhibit nuclear hypertrophy comparable to that observed in vivo. Using a coculture bioassay, we further demonstrate that CNTF treatment of astrocytes increases their ability to support ChAT(+) ventral spinal cord neurons (presumably motor neurons) more than twofold compared with untreated astrocytes. Also, the complexity of neurites was significantly increased in neurons cultured with CNTF-treated astrocytes compared with untreated astrocytes. RT-PCR analysis demonstrated that CNTF increased levels of FGF-2 and nerve growth factor (NGF) mRNA and that IL-1beta increased NGF and hepatocyte growth factor mRNA levels. Furthermore, both CNTF and IL-1beta stimulated the release of FGF-2 from cultured spinal cord astrocytes. These findings demonstrate that cytokine-activated astrocytes better support CNS neuron survival via the production of neurotrophic molecules. We also show that CNTF synergizes with FGF-2, but not epidermal growth factor, to promote DNA synthesis in spinal cord astrocyte cultures. The significance of these findings is discussed by presenting a new model depicting the sequential activation of astrocytes by cytokines and growth factors in the context of CNS injury and repair. 21634366 0014-4886 Journal Article},
	Author = {Albrecht, P. J. and Dahl, J. P. and Stoltzfus, O. K. and Levenson, R. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Exp Neurol},
	Keywords = {RNA, Messenger/biosynthesis;Drug Synergism;Motor Neurons/cytology/*drug effects;Cells, Cultured;Cell Survival/drug effects;Rats;Ciliary Neurotrophic Factor/*pharmacology;Fibroblast Growth Factor 2/*biosynthesis/genetics;Spinal Cord/cytology/*drug effects/metabolism;Neurites/drug effects;Animal;Rats, Sprague-Dawley;Nerve Growth Factors/genetics/metabolism;11 Glia;G abstr;Male;Astrocytes/cytology/*drug effects/metabolism;Reverse Transcriptase Polymerase Chain Reaction;DNA/biosynthesis;Support, Non-U.S. Gov't;Coculture;Growth Inhibitors/pharmacology;Lymphokines/pharmacology;Cell Nucleus/drug effects;Cell Division/drug effects;Interleukin-1/pharmacology},
	Number = {1},
	Organization = {Department of Neuroscience and Anatomy, Milton S. Hershey College of Medicine, Pennsylvania State University, Hershey, Pennsylvania 17033, USA.},
	Pages = {46-62},
	Pubmed = {11771938},
	Title = {Ciliary neurotrophic factor activates spinal cord astrocytes, stimulating their production and release of fibroblast growth factor-2, to increase motor neuron survival},
	Uuid = {7F176A66-569A-4287-AD32-E9FCBC410931},
	Volume = {173},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11771938}}

@article{Albrieux:2004,
	Abstract = {In mouse, the first neurons are generated at embryonic day (E) 12 and form the preplate (PP), which contains a mix of future marginal zone cells, including Cajal-Retzius cells, and subplate cells. To detect developmental changes in channel populations in these earliest-generated neurons of the cerebral cortex, we studied the electrophysiological properties of proliferative cells of the ventricular zone and postmitotic neurons of the PP at E12 and E13, using whole-cell patch-clamp recordings. We found an inward sodium current in 55\%of PP cells. To determine whether sodium currents occur in a specific cell type, we stained recorded cells with an antibody for calretinin, a calcium-binding protein found specifically in Cajal-Retzius cells. All calretinin-positive cells had sodium currents, although so did some calretinin-negative cells. To correlate the Na current expression to Na channel gene expression with the Cajal-Retzius cell phenotype, we performed single-cell reverse transcription-PCR on patch-clamp recorded cells to detect expression of the Cajal-Retzius cell marker reelin and the Na channel isoforms SCN 1, 2, and 3. These results showed that virtually all Cajal-Retzius cells (97\%), as judged by reelin expression, express the SCN transcript identified as the SCN3 isoform. Of these, 41\%presented a functional Na current. There is, however, a substantial SCN-positive population in the PP (27\%of SCN-positive cells) that does not express reelin. These results raise the possibility that populations of pioneer neurons of the PP, including Cajal-Retzius cells, gain neuronal physiological properties early in development via expression of the Na(v)1.3 (SCN3) Na channel isoform.},
	Author = {Albrieux, Mireille and Platel, Jean-Claude C. and Dupuis, Alain and Villaz, Michel and Moody, William J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Sodium Channels;research support, u.s. gov't, p.h.s. ;Neocortex;Patch-Clamp Techniques;in vitro ;Mice, Inbred C57BL;RNA, Messenger;Calcium-Binding Protein, Vitamin D-Dependent;Reverse Transcriptase Polymerase Chain Reaction;research support, non-u.s. gov't ;Potassium;21 Neurophysiology;21 Circuit structure-function;Sodium;Neurons;Protein Isoforms;Mice;24 Pubmed search results 2008;Gestational Age},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {7},
	Organization = {Department of Biology, University of Washington, Seattle, Washington 98195, USA.},
	Pages = {1719-25},
	Pii = {24/7/1719},
	Pubmed = {14973256},
	Title = {Early expression of sodium channel transcripts and sodium current by cajal-retzius cells in the preplate of the embryonic mouse neocortex},
	Uuid = {96377479-CAFD-4B91-9430-0DE9938BF02F},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3548-02.2004}}

@article{Albright:1998,
	Abstract = {Human herpesvirus-6 (HHV-6) is a betaherpesvirus that has been frequently associated with pediatric encephalitis. In 1995 Challoner et al reported that HHV-6 variant B (HHV-6B) was linked to multiple sclerosis (MS) due to the presence of viral DNA and antigen in the oligodendrocytes surrounding MS plaques. These findings led us to examine HHV-6B's in vitro tropism for primary neural cells. HIV-6B mediated cell-to-cell fusion in cultured adult oligodendroglia. Infection of oligodendrocytes was further confirmed by transmission electron microscopy (EM), which showed the presence of intracellular HHV-6 particles, and by PCR for HHV-6 DNA. However, the release of infectious virus was low or undetectable in multiple experiments. Microglia were also susceptible to infection by HHV-6B, as demonstrated by an antigen capture assay. We did not detect infection of a differentiated neuronal cell line (NT2D). Our findings suggest that HHV-6B infection of oligodendrocytes and/or microglia could potentially play a role in neuropathogenesis.},
	Author = {Albright, A. V. and Lavi, E. and Black, J. B. and Goldberg, S. and O'Connor, M. J. and Gonz{\'a}lez-Scarano, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {1355-0284},
	Journal = {J Neurovirol},
	Keywords = {Human;Multiple Sclerosis;Cytopathogenic Effect, Viral;Cells, Cultured;Microglia;Oligodendroglia;Cell Fusion;Not relevant;11 Glia;Alpha;Cell Line;Support, Non-U.S. Gov't;Herpesvirus 6, Human;Cell Size;Neurons;Adult;Support, U.S. Gov't, P.H.S.;Polymerase Chain Reaction;Temporal Lobe;Enzyme-Linked Immunosorbent Assay;Microscopy, Electron;Virus Replication;Cell Death},
	Medline = {99053381},
	Month = {10},
	Nlm_Id = {9508123},
	Number = {5},
	Organization = {Department of Neurology, University of Pennsylvania Medical Center, Philadelphia 19104-6146, USA.},
	Pages = {486-94},
	Pubmed = {9839646},
	Title = {The effect of human herpesvirus-6 (HHV-6) on cultured human neural cells: oligodendrocytes and microglia},
	Uuid = {3C8B9860-B294-43F3-A9F0-4BA3FD379556},
	Volume = {4},
	Year = {1998}}

@article{Alcantara:2005,
	Abstract = {The present study utilizes nestin-BDNF transgenic mice, which offer a model for early increased brain-derived neurotrophic factor (BDNF) signalling, to examine the role of BDNF in the development of cortical architecture. Our results demonstrate that the premature and homogeneous expression of BDNF, while preserving tangential migration from the ganglionic eminence to the cortex, impairs the final radial migration of GABAergic neurons, as well as their integration in the appropriate cortical layers. Moreover, Cajal-Retzius (CR) cells and GABAergic neurons segregate in the cortical marginal zone (MZ) in response to BDNF signalling, leading to an alternating pattern and a columnar cortical organization, within which the migration of different neuronal populations is specifically affected. These results suggest that both CR and GABAergic neurons play a role in directing the radial migration of late-generated cortical neurons, and that the spatial distribution of these cells in the MZ is critical for the development of correct cortical organization. In addition, reelin secreted by CR cells in the MZ is not sufficient to direct the migration of late-born neurons to the upper cortical layers, which most likely requires the presence of reelin-secreting interneurons in layers V-VI. We propose that in addition to modulating reelin expression, BDNF regulates the patched distribution of CR and GABAergic neurons in the MZ, and that this spatial distribution is involved in the formation of anatomical and/or functional columns and convoluted structures.},
	Author = {Alc{\'a}ntara, and Pozas, and Iba\~{n}ez, and Soriano,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {9110718},
	Organization = {Department of Cell Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain; Present address: Department of Experimental Pathology and Therapeutics, School of Medicine, University of Barcelona, Spain.},
	Pii = {bhi128},
	Pubmed = {16000651},
	Title = {BDNF-modulated Spatial Organization of Cajal-Retzius and GABAergic Neurons in the Marginal Zone Plays a Role in the Development of Cortical Organization},
	Uuid = {8F5EBE02-C07B-43A7-A936-729BF38E2139},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhi128}}

@article{Aldskogius:1999,
	Abstract = {We review three principally different forms of injury-induced synaptic alterations. (1) Displacement of presynaptic terminals from perikarya and dendrites of axotomized neurons, (2) central changes in primary afferent terminals of peripherally axotomized sensory ganglion cells, and (3) anterograde Wallerian-type degeneration following interruption of central axonal pathways. All these instances rapidly activate astrocytes and microglia in the vicinity of the affected synaptic terminals. The evidence suggests that activated astrocytes play important and direct roles in synapse elimination and in the processes mediating collateral reinnervation. The roles of microglia are enigmatic. They undergo activation close to axotomized motoneuron perikarya, where synapse displacement occurs, but not adjacent to axotomized intrinsic central nervous system neurons, where synapse displacement also occurs. Microglia are also rapidly activated around central primary sensory terminals of peripherally axotomized sensory ganglion cells. Occasional phagocytosis of degenerating axon terminals by microglia occur in the latter situation. However, the role of microglia may be more oriented toward the general tissue conditions rather than specifically toward synaptic terminals.},
	Author = {Aldskogius, H. and Liu, L. and Svensson, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Nervous System Diseases;Synapses;Neuroglia;Motor Neurons;Human;Neuronal Plasticity;Not relevant;11 Glia;Microglia;review, tutorial;Spinal Cord;Neurons, Afferent;Animals;Brain;Support, Non-U.S. Gov't;Neurons;review},
	Medline = {99423707},
	Month = {10},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuroscience, Biomedical Center, Uppsala, Sweden. hakan.aldskogius\@anatomi.uu.se},
	Pages = {33-41},
	Pii = {10.1002/(SICI)1097-4547(19991001)58:1<33::AID-JNR5>3.0.CO;2-M},
	Pubmed = {10491570},
	Title = {Glial responses to synaptic damage and plasticity},
	Uuid = {8CED6A53-EE26-11DA-8605-000D9346EC2A},
	Volume = {58},
	Year = {1999}}

@article{Aldskogius:2001,
	Abstract = {Microglia has the potential to produce and release a range of factors that directly and/or indirectly promote regeneration in the injured nervous system. The overwhelming evidence indicates, however, that this potential is generally not expressed in vivo. Activated microglia may enhance neuronal degeneration following axotomy, thereby counteracting functional recovery. Microglia does not seem to contribute significantly to axonal outgrowth after peripheral nerve injury, since this process proceeds uneventful even if perineuronal microglia is eliminated. The phagocytic phenotype of microglia is highly suppressed during Wallerian degeneration in the central nervous system. Therefore, microglia is incapable of rapid and efficient removal of myelin debris and its putative growth inhibitory components. In this way, microglia may contribute to regeneration failure in the central nervous system. Structural and temporal correlations are compatible with participation by perineuronal microglia in axotomy-induced shedding of presynaptic terminals, but direct evidence for such participation is lacking. Currently, the most promising case for a promoting effect on neural repair by activated microglia appears to be as a mediator of collateral sprouting, at least in certain brain areas. However, final proof for a critical role of microglia in these instances is still lacking. Results from in vitro studies demonstrate that microglia can develop a regeneration supportive phenotype. Altering the microglial involvement following neural injury from a typically passive or even counterproductive state and into a condition where these cells are actively supporting regeneration and plasticity is, therefore, an exciting challenge and probably a realistic goal.},
	Author = {Aldskogius, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {1059-910X},
	Journal = {Microsc Res Tech},
	Keywords = {Central Nervous System;Nerve Degeneration;Nerve Regeneration;Human;Neuronal Plasticity;Not relevant;11 Glia;Microglia;review, tutorial;Support, Non-U.S. Gov't;Phagocytosis;review},
	Medline = {21417960},
	Month = {7},
	Nlm_Id = {9203012},
	Number = {1},
	Organization = {Department of Neuroscience, Biomedical Center, Uppsala, Sweden. Hakan.Aldskogius\@neuro.uu.se},
	Pages = {40-6},
	Pii = {10.1002/jemt.1119},
	Pubmed = {11526956},
	Title = {Microglia in neuroregeneration},
	Uuid = {98BE2D07-FB09-4697-8D1E-FB07B84B5EEE},
	Volume = {54},
	Year = {2001}}

@article{Aldskogius:1998,
	Abstract = {Axon injury rapidly activates microglial and astroglial cells close to the axotomized neurons. Following motor axon injury, astrocytes upregulate within hour(s) the gap junction protein connexin-43, and within one day glial fibrillary acidic protein (GFAP). Concomitantly, microglial cells proliferate and migrate towards the axotomized neuron perikarya. Analogous responses occur in central termination territories of peripherally injured sensory ganglion cells. The activated microglia express a number of inflammatory and immune mediators. When neuron degeneration occurs, microglia act as phagocytes. This is uncommon after peripheral nerve injury in the adult mammal, however, and the functional implications of the glial cell responses in this situation are unclear. When central axons are injured, the glial cell responses around the affected neuron perikarya appears to be minimal or absent, unless neuron degeneration occurs. Microglia proliferate, and astrocytes upregulate GFAP along central axons undergoing anterograde, Wallerian, degeneration. Although microglia develop into phagocytes, they eliminate the disintegrating myelin very slowly, presumably because they fail to release molecules which facilitate phagocytosis. During later stages of Wallerian degeneration, oligodendrocytes express clusterin, a glycoprotein implicated in several conditions of cell degeneration. A hypothetical scheme for glial cell activation following axon injury is discussed, implying the injured neurons initially interact with adjacent astrocytes. Subsequently, neighbouring resting microglia are activated. These glial reactions are amplified by paracrine and autocrine mechanisms, in which cytokines appear to be important mediators. The specific functional properties of the activated glial cells will determine their influence on neuronal survival, axon regeneration, and synaptic plasticity. The control of the induction and progression of these responses are therefore likely to be critical for the outcome of, for example, neurotrauma, brain ischemia and chronic neurodegenerative diseases.},
	Author = {Aldskogius, H. and Kozlova, E. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0301-0082},
	Journal = {Prog Neurobiol},
	Keywords = {Neurons;Neuroglia;Central Nervous System;Cell Communication;Human;11 Glia;review, tutorial;Axotomy;Support, Non-U.S. Gov't;Animals;review;Axons},
	Medline = {98265208},
	Month = {5},
	Nlm_Id = {0370121},
	Number = {1},
	Organization = {Department of Neuroscience, Biomedical Center, Uppsala, Sweden. Hakan.Aldskogius\@anatomi.uu.se},
	Pages = {1-26},
	Pii = {S0301008297000932},
	Pubmed = {9602498},
	Title = {Central neuron-glial and glial-glial interactions following axon injury},
	Uuid = {70E11CE7-63ED-4BFC-BBF9-404F5CEC9791},
	Volume = {55},
	Year = {1998}}

@article{Alonso:1999,
	Abstract = {In the adult rodent brain, it is now well established that neurons are continuously generated from proliferating neuronal progenitor cells located in the subventricular zone of the lateral ventricle (SVZ) and the dentate gyrus of the hippocampus. Recently, it has been shown that neurons can also be generated in vitro from various regions of the adult brain and spinal cord ventricular neuroaxis. As the highly polysialylated neural cell adhesion molecule (PSA-NCAM) has been shown to be specifically expressed by neuronal progenitor cells of the SVZ and the hippocampus, the present study was designed to determine whether cells expressing this molecule could be detected in the vicinity of the ventricular system of the adult rat brain and spinal cord. After double or triple immunostaining for different neuronal and glial markers, confocal microscopy was used to examine the surface of the ventricular neuroaxis in either 40- to 50-microm-thick transverse vibratome sections cut through different brain regions, or in 200- to 300-microm-thick tissue slices including the intact surface of the brain ventricles or of the spinal cord central canal. In untreated rats, PSA-NCAM, microtubule associated protein 2 (MAP2) and class III- beta-tubulin were found to be associated with a number of neuron-like cells located on the surface of the third and fourth ventricles and of the spinal cord central canal. The proliferation of the PSA-NCAM- immunoreactive (IR) neuron-like cells detected on the surface of the third and fourth ventricles was not affected by injection of epidermal growth factor (EGF) or basic fibroblast growth factor (bFGF) into these ventricles, but was stimulated by the combined injection of EGF + bFGF. These data indicate that cells exhibiting features of neuronal progenitors are present on the ependymal surface of the adult rat brain and spinal cord ventricular axis.},
	Author = {Alonso, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Fibroblast Growth Factor, Basic/pharmacology;Rats;Stem Cells/chemistry/*cytology;Neurons/chemistry/*cytology;Fourth Ventricle/chemistry/cytology;Spinal Canal/chemistry/cytology;02 Adult neurogenesis migration;Cell Division/drug effects/physiology;Central Nervous System/*cytology/physiology;Animal;Antimetabolites;Injections, Intraventricular;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Sialic Acids/*analysis/metabolism;B;Neural Cell Adhesion Molecules/*analysis/metabolism;Age Factors;Rats, Sprague-Dawley/*physiology;Lateral Ventricles/chemistry/cytology;Third Ventricle/chemistry/cytology;Biological Markers;Bromodeoxyuridine},
	Number = {2},
	Organization = {INSERM U336, University of Montpellier II, 34095 Montpellier, France. galonso\@crit.univ-montp2.fr},
	Pages = {149-66.},
	Title = {Neuronal progenitor-like cells expressing polysialylated neural cell adhesion molecule are present on the ventricular surface of the adult rat brain and spinal cord},
	Uuid = {92774D6C-F7E5-4CB5-A572-7948BE041489},
	Volume = {414},
	Year = {1999},
	url = {papers/Alonso_JCompNeurol1999.pdf}}

@article{Alonso:1999a,
	Abstract = {In the brain of adult rodents, young neurons arising from the subventricular zone (SVZ) of the lateral ventricle migrate tangentially along the rostral migratory stream (RMS) toward the olfactory bulb. The aim of this study was to determine whether surgical lesions placed through the RMS could affect the rostral migration of these newly formed neurons. Confocal and electron microscopy were used to characterize their anatomical organization within the intact and lesioned forebrains. As soon as 7 days and up to 45 days after placing a surgical lesion through the proximal portions of the RMS, numerous cells immunostained for polysialylated neural cell adhesion molecule (PSA-NCAM) were detected both (1) throughout the lesional cavity extending from the cortex to the anterior commissura, and (2) within the tissue located caudal to the lesion. In both regions, these PSA- NCAM-immunostained cells were labeled for neuronal markers but were negative for glial fibrillary acidic protein (GFAP). After administration of the proliferation marker bromodeoxyuridine (BrdU), nuclear labeling was associated with cells immunostained for PSA-NCAM but GFAP-negative, that accumulated within the lesional cavity and in the tissue caudal to the lesion. For the longest postlesional delays, a number of the PSA-NCAM-immunostained neurons located in various portions of the lesional cavity exhibited intense immunostaining for gamma-aminobutyric acid, whereas only a few of them exhibited faint immunostaining for tyrosine hydroxylase. These data indicate that surgical lesions placed through the RMS of adult rats impede the migration toward the olfactory bulb of the neuroblasts arising from the SVZ, inducing their accumulation and their partial differentiation in forebrain regions caudal to the lesion.},
	Author = {Alonso, G. and Prieto, M. and Chauvet, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Cerebral Ventricles;B-13;24 Pubmed search results 2008;Immunohistochemistry;Sialic Acids;Male;Brain Diseases;Neural Cell Adhesion Molecule L1;Animals;Cell Movement;Brain Diseases/pathology/*physiopathology;Neural Cell Adhesion Molecules/metabolism;Neural Pathways;Microscopy, Electron;Sialic Acids/metabolism;Prosencephalon/pathology/*physiopathology;Animal;Neural Pathways/physiopathology;Rats, Sprague-Dawley;02 Adult neurogenesis migration;Prosencephalon;Rats;Cell Movement/physiology;Neurons/*physiology;Neural Cell Adhesion Molecules;Microscopy, Confocal;Support, Non-U.S. Gov't;Research Support, Non-U.S. Gov't;Neurons},
	Medline = {99196578},
	Month = {3},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {INSERM U 336, Developpement, Plasticite et Vieillissement du Systeme Nerveux, Universite Montpellier II, Montpellier, France. galonso\@crit.univ-mont2.fr},
	Pages = {508-28.},
	Pii = {10.1002/(SICI)1096-9861(19990322)405:4<508::AID-CNE5>3.0.CO;2-5},
	Pubmed = {10098942},
	Title = {Tangential migration of young neurons arising from the subventricular zone of adult rats is impaired by surgical lesions passing through their natural migratory pathway},
	Uuid = {796753F8-381C-476C-AAD7-8ACCC3B39794},
	Volume = {405},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10098942%20Polaris:Users:ackman:Desktop:citmgr_endnote}}

@article{Alonso:2006,
	Abstract = {In the olfactory bulb (OB), new neurons are added throughout life, forming an integral part of the functioning circuit. Yet only some of them survive more than a month. To determine whether this turnover depends on olfactory learning, we examined the survival of adult newborn cells labeled with the cell division marker BrdU, administered before learning in an olfactory discrimination task. We report that discrimination learning increases the number of newborn neurons in the adult OB by prolonging their survival. Simple exposure to the pair of olfactory cues did not alter neurogenesis, indicating that the mere activation of sensory inputs during the learning task was insufficient to alter neurogenesis. The increase in cell survival after learning was not uniformly distributed throughout angular sectors of coronal sections of the OB. Monitoring odor activation maps using patterns of Zif268 immediate early gene expression revealed that survival was greater in regions more activated by the non-reinforced odorant. We conclude that sensory activation in a learning context not only controls the total number of newborn neurons in the adult OB, but also refines their precise location. Shaping the distribution of newborn neurons by influencing their survival could optimize the olfactory information processing required for odor discrimination.},
	Author = {Alonso, Mariana and Viollet, C{\'e}cile and Gabellec, Marie-Madeleine M. and Meas-Yedid, Vannary and Olivo-Marin, Jean-Christophe C. and Lledo, Pierre-Marie M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:16 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Neurons;Odors;24 Pubmed search results 2008;Smell;Discrimination Learning;Female;research support, non-u.s. gov't ;Olfactory Receptor Neurons;Cell Survival;Animals, Newborn;Olfactory Bulb;Age Factors;comparative study ;Animals;Male;Mice},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {41},
	Organization = {Perception and Memory Laboratory, Centre National de la Recherche Scientifique, Unit{\'e} de Recherche Associ{\'e}e 2182, Pasteur Institute, 75724 Paris Cedex 15, France.},
	Pages = {10508-13},
	Pii = {26/41/10508},
	Pubmed = {17035535},
	Title = {Olfactory discrimination learning increases the survival of adult-born neurons in the olfactory bulb},
	Uuid = {315A7389-5006-429B-986D-CAAF64EA28A3},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2633-06.2006}}

@article{Alvarez:2006,
	Abstract = {RNA interference (RNAi), which allows selective gene silencing, has been proposed for functional genomic analysis and for the treatment of human disease. However, induction of RNAi in mammalian cells by expression of double-stranded RNA can activate innate antiviral response pathways that perturb off-target gene expression. The activation and functional consequences of these effects in neurons are unknown. We find that expression of subsets of short hairpin RNAs (shRNAs) in rat hippocampal pyramidal neurons can have off-target effects that reduce the complexity of dendritic arbors and trigger the loss of dendritic spines. Morphological changes are accompanied by electrophysiological perturbations in passive membrane properties and a decrease in the number and strength of excitatory and inhibitory synapses. These perturbations depend on the shRNA sequence and are independent of the identity of the targeted protein. Our results indicate that off-target effects of RNAi severely perturb neuronal structure and function and may lead to the functional withdrawal of affected cells from the brain circuitry.},
	Author = {Alvarez, Veronica A. and Ridenour, Dennis A. and Sabatini, Bernardo L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Synapses;Dendrites;Rats, Sprague-Dawley;21 Neurophysiology;Hippocampus;Rats;Nerve Tissue Proteins;23 RNAi;Research Support, N.I.H., Extramural;RNA Interference;Adaptation, Physiological;Cells, Cultured;Animals;24 Pubmed search results 2008;23 Technique;21 Epilepsy},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {30},
	Organization = {Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {7820-5},
	Pii = {26/30/7820},
	Pubmed = {16870727},
	Title = {Retraction of synapses and dendritic spines induced by off-target effects of RNA interference},
	Uuid = {FEC9AC84-48A4-11DB-A317-000D9346EC2A},
	Volume = {26},
	Year = {2006},
	url = {papers/Alvarez_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1957-06.2006}}

@article{Alvarez-Buylla:1992,
	Abstract = {Neurogenesis, typically a developmental phenomenon, continues into adult life in song birds. Cells born in the walls of the lateral ventricle migrate and differentiate throughout the adult telencephalon. I will argue here that birds take advantage of these new neurons as a form of plasticity. Most of the neurons connecting the different song control nuclei are born early in development. One important exception is the central efferent motor pathway for learned vocalization. This pathway is formed by projection neurons born during juvenile and adult life. Recruitment of new projection neurons at different times of the year and in different species correlates with vocal learning. Adult neurogenesis as a form of plasticity may serve learning and it may also teach us how to repair the damaged brain.},
	Author = {Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Exp Neurol},
	Keywords = {01 Adult neurogenesis general;Neurons/*physiology;Canaries/physiology;Brain/*physiology;*Neuronal Plasticity;A abstr;Animal;Support, U.S. Gov't, P.H.S.;Vocalization, Animal/physiology;Birds/*physiology;*Nerve Regeneration},
	Number = {1},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {110-4.},
	Pubmed = {1728556},
	Title = {Neurogenesis and plasticity in the CNS of adult birds},
	Uuid = {311B716B-7FC9-44B4-8489-E234E57C2632},
	Volume = {115},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=1728556&dopt=Citation}}

@article{Alvarez-Buylla:1990,
	Abstract = {Adult neurogenesis in birds offers unique opportunities to study basic questions addressing the birth, migration and differentiation of neurons. Neurons in adult canaries originate from discrete proliferative regions on the walls of the lateral ventricles. They migrate away from their site of birth, initially at high rates, along the processes of radical cells. The rates of dispersal diminish as the young neurons invade regions devoid of radial fibers, probably under the guidance of other cues. The discrete sites of birth in the ventricular zone generate neurons that end up differentiating throughout the telencephalon. New neurons may become interneurons or projection neurons; the latter connect two song control nuclei between neostriatum and archistriatum. Radial cells, that in mammals disappear as neurogenesis comes to an end, persist in the adult avian brain. The presence of radial cells may be key to adult neurogenesis. Not only do they serve as guides for initial dispersal, they also divide and may be the progenitors of new neurons.},
	Author = {Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Experientia},
	Keywords = {01 Adult neurogenesis general;Cell Differentiation;Cerebral Ventricles/cytology/growth &development;Telencephalon/cytology/embryology/growth &development;Birds/*growth &development;A abstr;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Cell Movement;Brain/cytology/*growth &development},
	Number = {9},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {948-55.},
	Pubmed = {2209804},
	Title = {Mechanism of neurogenesis in adult avian brain},
	Uuid = {93D98BA6-6D29-4C52-BFE2-2E6D52EC69EB},
	Volume = {46},
	Year = {1990},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=2209804&dopt=Citation}}

@article{Alvarez-Buylla:1990a,
	Author = {Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Experientia},
	Keywords = {*Cell Movement;02 Adult neurogenesis migration;Cell Differentiation;Brain/cytology/embryology/*growth &development;Animal;Neurons/*cytology;B abstr},
	Number = {9},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {879-82.},
	Pubmed = {2209795},
	Title = {Commitment and migration of young neurons in the vertebrate brain},
	Uuid = {D464D0CC-883F-488B-A1C4-BF461DCA6842},
	Volume = {46},
	Year = {1990},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=2209795&dopt=Citation}}

@article{Alvarez-Buylla:1994,
	Abstract = {Neurogenesis occurs in adult song birds, which suggests that neurons born after hatching may contribute to histogenesis and plasticity of the avian brain. However, little is known about the overall contribution to the mature brain of neurons born in juveniles and adults, and how this process affects different regions of the avian brain. In fact, studies of the histogenesis of the avian forebrain have made the classical assumption that neuronal birth ends before hatching. Here we determined the contribution of neurons born before and after hatching to different regions throughout the adult canary brain. Male canaries were injected with [3H]-thymidine at different times during embryonic, juvenile, and adult life. The position of labeled neurons was mapped in parasagittal brain sections. Because all birds were killed as adults, results indicate the time of birth of neurons that survived to adulthood in different structures of the avian brain. Injection at embryonic day (E) 5 or E9 resulted in labeled neurons in all regions of the neuroaxis. The vast majority of neurons outside of the telencephalon were born before E9. One exception was a discrete region in the dorsal thalamus, a part of the song-control circuit, where neurons continued to be born after E9. Most regions of the telencephalon had a high proportion of its neurons labeled by the embryonic injections. In particular, archistriatum, anterior neostriatum, and the hippocampus had most of their neurons labeled before hatching. This indicates that many of the telencephalic neurons born in the embryo are long lived and are not replaced by other neurons that continue to be added to the telencephalon after hatching. Neurons labeled by [3H]-thymidine injections after hatching were restricted to the telencephalon and contributed importantly to many regions. In particular, the avian striatum (lobus parolfactorius, LPO) received a large number of its neurons during the first 20 days of life, but continued to incorporate new neurons throughout juvenile and adult life. Neurons continued to be added to the telencephalon of adults (even in 4-year-old birds). The distribution of labeled neurons after [3H]-thymidine injections in adults was similar to that observed in latter stages of juvenile development. The contribution of neurons born at different ages from embryonic development to adulthood varied among different anatomical subdivisions of the canary brain. this could, in part, explain differences in the cytoarchitecture and plasticity between brain regions. Neurogenesis after hatching may allow the modification of selected brain circuits as the bird matures and ages.},
	Author = {Alvarez-Buylla, A. and Ling, C. Y. and Yu, W. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Telencephalon/physiology;Neuronal Plasticity/physiology;Neurons/cytology/*physiology;Corpus Striatum/physiology;Animal;Cell Survival/physiology;Time Factors;Canaries/embryology/growth &development/*physiology;01 Adult neurogenesis general;Male;*Brain Mapping;Support, Non-U.S. Gov't;Embryo, Nonmammalian/cytology;Hippocampus/physiology;Support, U.S. Gov't, P.H.S.;Vocalization, Animal/*physiology;A abstr;Thalamic Nuclei/physiology},
	Number = {2},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {233-48.},
	Title = {Contribution of neurons born during embryonic, juvenile, and adult life to the brain of adult canaries: regional specificity and delayed birth of neurons in the song-control nuclei},
	Uuid = {D8129FB6-6035-4968-BD94-8DDFAC283A9A},
	Volume = {347},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7814666}}

@article{Alvarez-Buylla:1992a,
	Abstract = {It is generally thought that most circuits of the adult central nervous system (CNS) are sculpted, in part at least, by selective elimination of some of the neurons present in an initial overabundant set. In this scenario, the birth of neurons precedes the period when brain functions, such as learning, first occur. In contrast to this form of brain assembly, we describe here the delayed development of the high vocal center (HVC) and one of its efferent pathways in canaries. The retrograde tracer Fluoro-Gold (FG) was injected into one of HVC's two efferent targets, the nucleus robustus archistriatalis (RA), to define the boundaries of HVC. The HVC grows markedly between 1 and 4 months, invading neighboring territories of the caudal telencephalon. During this same period, 0.43\%-0.64\%of the HVC neurons present at 1 year of age are labeled per day of [3H]-thymidine injection. [3H]-Thymidine labeling is a marker of cell birth, and during the first 4 months HVC neuron number increases, probably accounting for part of the HVC growth observed. Thereafter, the number of HVC neurons remains constant, but neuronal birth persists. We infer from this that neuronal replacement starts as early as 4 months after hatching and perhaps before then. About half of the neurons born after posthatching day 10 grow an axon to RA to form the main efferent pathway exiting from HVC. HVC growth, neurogenesis, axogenesis, and the observed replacement of neurons happen during the period of juvenile vocal learning. However, the recruitment of neurons that are still present at 1 year shows no particular inflections corresponding to the various stages in song learning, and continues at essentially the same rate after the more stereotyped adult song has been acquired. We suggest that a combination of neurogenesis and neuronal replacement provides unique advantages for learning.},
	Author = {Alvarez-Buylla, A. and Ling, C. Y. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurobiol},
	Keywords = {01 Adult neurogenesis general;Neuronal Plasticity/drug effects/physiology;Thymidine/pharmacology;Neurons/drug effects/*physiology;A abstr;Fluorescent Dyes;Animal;Support, U.S. Gov't, P.H.S.;Histocytochemistry;Birds/*physiology;Male;Efferent Pathways/cytology/drug effects/*growth &development;Vocalization, Animal/drug effects/*physiology},
	Number = {4},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {396-406.},
	Title = {High vocal center growth and its relation to neurogenesis, neuronal replacement and song acquisition in juvenile canaries},
	Uuid = {C8FDE220-2941-4285-BA49-18308C5080D1},
	Volume = {23},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed?term=1634887}}

@article{Alvarez-Buylla:1997,
	Abstract = {Neurogenesis continues in the brain of adult birds. These cells are born in the ventricular zone of the lateral ventricles. Young neurons then migrate long distances guided, in part, by radial cell processes and become incorporated throughout most of the telencephalon. In songbirds, the high vocal center (HVC), which is important for the production of learned song, receives many of its neurons after hatching. HVC neurons which project to the robust nucleus of the archistriatum to form part of the efferent pathway for song production, and HVC interneurons continue to be added throughout life. In contrast, Area X-projecting HVC cells, thought to be part of a circuit necessary for song learning but not essential for adult song production, are only born in the embryo. New neurons in HVC of juvenile and adult birds replace older cells that die. There is a correlation between seasonal cell turnover rates (addition and loss) and testosterone levels in adult male canaries. Available evidence suggests that steroid hormones control the recruitment and/or survival of new HVC neurons, but not their production. The functions of neuronal replacement in adult birds remain unclear. However, rates of HVC neuron turnover are highest at times of year when canaries modify their songs. Replaceable HVC neurons may participate in the modification of perceptual memories or motor programs for song production. In contrast, permanent HVC neurons could hold long-lasting song-related information. The unexpected large-scale production of neurons in the adult brain holds important clues about brain function and, in particular, about the neural control of a learned behavior--birdsong.},
	Author = {Alvarez-Buylla, A. and Kirn, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurobiol},
	Keywords = {A;01 Adult neurogenesis general;Neurons/*physiology;Female;Cell Death/physiology;Animal;Brain/*cytology/*growth &development;Support, U.S. Gov't, P.H.S.;Birds/*physiology;Cell Movement/*physiology;Support, Non-U.S. Gov't;Vocalization, Animal/*physiology;Male},
	Number = {5},
	Organization = {Rockefeller University, New York, New York 10021, USA.},
	Pages = {585-601.},
	Title = {Birth, migration, incorporation, and death of vocal control neurons in adult songbirds},
	Uuid = {934E17E6-72D5-4BAA-B293-E45AC691C1FE},
	Volume = {33},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9369461}}

@article{Alvarez-Buylla:1998,
	Author = {Alvarez-Buylla, A. and Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {J Neurobiol},
	Keywords = {Neurons/*physiology;02 Adult neurogenesis migration;B both;Embryo/physiology;Aging/physiology;Nervous System/cytology/*embryology/*growth &development;Animal;Support, U.S. Gov't, P.H.S.;Stem Cells/*physiology},
	Number = {2},
	Organization = {Rockefeller University, New York, New York 10021, USA.},
	Pages = {105-10.},
	Title = {Stem cells in the developing and adult nervous system},
	Uuid = {4D7512D1-D06A-11DA-8A8C-000D9346EC2A},
	Volume = {36},
	Year = {1998},
	url = {papers/Alvarez-Buylla_JNeurobiol1998.pdf}}

@article{Alvarez-Buylla:1988,
	Abstract = {Frontal and coronal sections of adult male and female canary brain were stained with a monoclonal antibody to vimentin using an immunoperoxidase technique; some sections were counterstained with cresyl violet. The position of radial glia cells was mapped using a computer-linked microscope. The telencephalon was found to have a rich set of radial glia. The long processes of these radial glia showed a mediolateral orientation, and were much more abundant in some parts of the telencephalon (e.g., hyperstriatum, caudal neostriatum, and lobus parolfactorius) than in others (e.g., anterior neostriatum, archistriatum, and septum), which had few or no radial glia fibers. A small, elongated cell type not previously described in adult avian brain was frequently seen to be associated with the long processes of the radial glia, oriented in the same direction and often in close apposition. The position of these cells was also systematically mapped, and they were found to be virtually absent outside of the telencephalon. The relation between radial glia fibers and the small, elongated cells was most commonly seen close to the lateral ventricle of the forebrain, where the radial glia cells have their cell bodies. The above observations suggest that there may be a functional relation between radial glia and the small, elongated cells. We hypothesize that the latter cells are young migrating neurons. This hypothesis is tested in a separate publication (A. Alvarez-Buylla and F. Nottebohm, unpublished observations).},
	Author = {Alvarez-Buylla, A. and Theelen, M. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurosci},
	Keywords = {02 Adult neurogenesis migration;Neurons/*classification/cytology;Antibodies, Monoclonal/diagnostic use;03 Adult neurogenesis progenitor source;Female;Neuroglia/*cytology;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Birds/*anatomy &histology;Male;Brain/*cytology;BB abstr},
	Number = {8},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {2707-12.},
	Title = {Mapping of radial glia and of a new cell type in adult canary brain},
	Uuid = {EE9962C0-1103-40F8-8E35-3B7D139ABA6C},
	Volume = {8},
	Year = {1988},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=3411349}}

@article{Alvarez-Buylla:1998a,
	Abstract = {New neurons continue to be born in the ventricular zone (VZ) of the lateral ventricles in the brain of adult birds. On the basis of serial section reconstruction and electron microscopy, we determined that the VZ of the adult canary brain is composed of three main cell types (A, B, and E). Type A cells were never found in contact with the ventricle and had microtubule-rich processes typical of young migrating neurons. Type B cells were organized as a pseudostratified epithelium, all contacted the ventricle, and most had a characteristic single cilium. Type E cells, also in contact with ventricle, were ultrastructurally similar to the mammalian multiciliated ependymal cells. After six injections of [3H]-thymidine (1 every 12 hr), Types A and B cells were found labeled. Type E cells were never [3H]-thymidine labeled. One to two hours after a single injection of [3H]-thymidine, all labeled cells corresponded to Type B cells. At survivals of 5, 24, and 74 hr after [3H]-thymidine injection, the proportion of labeled Type B cells decreased and that of Type A cells increased, indicating that Type B cells were the primary precursors. Most [3H]-labeled nuclei at 1-2 hr after [3H]-thymidine injection were separated from the ventricular cavity, but most of the mitotic cells were adjacent to the ventricle. This observation and measurements of the distance between labeled nuclei and the ventricular surface at 1, 5, 7, and 11 hr after [3H]- thymidine injection indicate that Type B cell nuclei move toward the ventricle to divide. This work reveals the architecture of the VZ in an adult vertebrate brain, identifies the primary precursor of new neurons, and describes nuclear translocation of these precursors during the cell cycle.},
	Author = {Alvarez-Buylla, A. and Garcia-Verdugo, J. M. and Mateo, A. S. and Merchant-Larios, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {J Neurosci},
	Keywords = {Cerebral Ventricles/*cytology;Cell Movement/*physiology;Neurons/*cytology/ultrastructure;Mitosis/physiology;Thymidine/pharmacokinetics;Female;Cell Count;02 Adult neurogenesis migration;Animal;Ependyma/*cytology;Cell Survival/physiology;03 Adult neurogenesis progenitor source;BB pdf;Canaries;Cell Division/physiology;Stem Cells/*cytology/ultrastructure;Cell Nucleus/physiology;Tritium/diagnostic use;Support, U.S. Gov't, P.H.S.;Age Factors;Microscopy, Electron;Cilia/ultrastructure},
	Number = {3},
	Organization = {The Rockefeller University Field Research Center, Tyrrel Road, Millbrook, New York 12545, USA.},
	Pages = {1020-37.},
	Title = {Primary neural precursors and intermitotic nuclear migration in the ventricular zone of adult canaries},
	Uuid = {D08CA836-2B73-4C9B-B317-3D347D82CEE6},
	Volume = {18},
	Year = {1998},
	url = {papers/Alvarez-Buylla_JNeurosci1998.pdf}}

@article{Alvarez-Buylla:2002,
	Author = {Alvarez-Buylla, A. and Garcia-Verdugo, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;Astrocytes/cytology/physiology;Human;Neurons/*cytology/physiology;Regeneration/physiology;A both;Cell Differentiation/physiology;Animal;Lateral Ventricles/*cytology/growth &development;Support, U.S. Gov't, P.H.S.;Stem Cells/cytology/physiology;Support, Non-U.S. Gov't;Cell Movement/physiology},
	Number = {3},
	Organization = {Department of Neurological Surgery, Brain Tumor Research Center, San Francisco, California 94143-0520, USA. abuylla\@itsa.ucsf.edu},
	Pages = {629-34.},
	Title = {Neurogenesis in adult subventricular zone},
	Uuid = {33573890-BF2C-45BC-A8AB-4969A6B33E00},
	Volume = {22},
	Year = {2002},
	url = {papers/Alvarez-Buylla_JNeurosci2002.pdf}}

@article{Alvarez-Buylla:2001,
	Abstract = {For many years, it was assumed that neurons and glia in the central nervous system were produced from two distinct precursor pools that diverged early during embryonic development. This theory was partially based on the idea that neurogenesis and gliogenesis occurred during different periods of development, and that neurogenesis ceased perinatally. However, there is now abundant evidence that neural stem cells persist in the adult brain and support ongoing neurogenesis in restricted regions of the central nervous system. Surprisingly, these stem cells have the characteristics of fully differentiated glia. Neuroepithelial stem cells in the embryonic neural tube do not show glial characteristics, raising questions about the putative lineage from embryonic to adult stem cells. In the developing brain, radial glia have long been known to produce cortical astrocytes, but recent data indicate that radial glia might also divide asymmetrically to produce cortical neurons. Here we review these new developments and propose that the stem cells in the central nervous system are contained within the neuroepithelial -->radial glia -->astrocyte lineage.},
	Author = {Alvarez-Buylla, A. and Garcia-Verdugo, J. M. and Tramontin, A. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {Models, Biological;Astrocytes/cytology;B both;Aging;Embryo/cytology;Neuroglia/*cytology;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Epithelial Cells/cytology;Support, Non-U.S. Gov't;*Cell Lineage;Stem Cells/*cytology},
	Number = {4},
	Pages = {287-93.},
	Title = {A unified hypothesis on the lineage of neural stem cells},
	Uuid = {AD8AE0A4-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {2},
	Year = {2001},
	url = {papers/Alvarez-Buylla_NatRevNeurosci2001.pdf}}

@article{Alvarez-Buylla:2001a,
	Abstract = {For many years, it was assumed that neurons and glia in the central nervous system were produced from two distinct precursor pools that diverged early during embryonic development. This theory was partially based on the idea that neurogenesis and gliogenesis occurred during different periods of development, and that neurogenesis ceased perinatally. However, there is now abundant evidence that neural stem cells persist in the adult brain and support ongoing neurogenesis in restricted regions of the central nervous system. Surprisingly, these stem cells have the characteristics of fully differentiated glia. Neuroepithelial stem cells in the embryonic neural tube do not show glial characteristics, raising questions about the putative lineage from embryonic to adult stem cells. In the developing brain, radial glia have long been known to produce cortical astrocytes, but recent data indicate that radial glia might also divide asymmetrically to produce cortical neurons. Here we review these new developments and propose that the stem cells in the central nervous system are contained within the neuroepithelial -->radial glia -->astrocyte lineage.},
	Author = {Alvarez-Buylla, A. and Garcia-Verdugo, J. M. and Tramontin, A. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {Models, Biological;Astrocytes/cytology;02 Adult neurogenesis migration;Aging;Embryo/cytology;B both;03 Adult neurogenesis progenitor source;BB pdf;Neuroglia/*cytology;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Epithelial Cells/cytology;Support, Non-U.S. Gov't;*Cell Lineage;Stem Cells/*cytology},
	Number = {4},
	Organization = {Arturo Alvarez-Buylla and Anthony D. Tramontin are at the University of California, San Francisco, Department of Neurosurgery Research, Box 0520, Koret Vision Research Laboratories, K-130, 10 Kirkham Street, San Francisco, California 94143, USA.Jose Manuel Garcia-Verdugo is at the University of Valencia, Burjassot-46100, Valencia, Spain. abuylla\@itsa.ucsf.edu},
	Pages = {287-293.},
	Title = {OPINIONA unified hypothesis on the lineage of neural stem cells},
	Uuid = {FE329AE0-0E35-4AE6-BE6B-CEA9E0E09AFF},
	Volume = {2},
	Year = {2001},
	url = {papers/Alvarez-Buylla_NatRevNeurosci2001a.pdf}}

@article{Alvarez-Buylla:1988a,
	Abstract = {Neurons are born in the ventricular walls of the vertebrate central nervous system. From there, the young neurons migrate to their final destinations, where differentiation occurs. Neuronal migration has been described during the ontogeny of the avian and mammalian brain. Whereas in mammals most neurogenesis occurs during early development, in the adult avian forebrain wide-spread neurogenesis continues to occur. How do neurons born in adulthood reach their final destination? We report here that small elongated cells, born in the ventricular zone adjacent to the lateral ventricle, differentiate into mature neurons 20-40 days later, after migrating over distances of up to 5 mm. Migration rates are highest (28 micron h-1) when young neurons migrate through regions which are rich in radial glia. The adult vertebrate brain offers unique opportunities for studying factors that regulate neuronal migration, pathfinding and differentiation.},
	Author = {Alvarez-Buylla, A. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Nature},
	Keywords = {02 Adult neurogenesis migration;Cell Differentiation;B;Brain/*growth &development;Neurons/*growth &development;Birds/*growth &development;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Cell Movement;Cerebral Ventricles/physiology},
	Number = {6188},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {353-4.},
	Title = {Migration of young neurons in adult avian brain},
	Uuid = {798D18E0-0BB4-4E93-BBB4-8BEF61AD6F75},
	Volume = {335},
	Year = {1988},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=3419503}}

@article{Alvarez-Buylla:1990b,
	Abstract = {Neurogenesis in the adult avian brain is restricted to the telencephalon. New neurons originate in the ventricular zone (VZ) from cells that have not been identified. We mapped the position of [3H]thymidine-labeled cells in the walls of the ventricles of the adult canary brain. Labeled VZ cells were restricted to the telencephalon (lateral ventricles) and concentrated in "hot spots". The coincidence of these hot spots with regions rich in radial cells suggested that radial cells may be the cells undergoing mitosis. We used smears prepared from fragments of the VZ containing the hot spots to show directly that radial cells accumulate [3H]thymidine. In addition, grain counts at different survival times demonstrated that these cells divide. Hot spots of VZ cell division also coincided with sites of neuronal origin. We suggest that radial cell division may give rise to new neurons.},
	Author = {Alvarez-Buylla, A. and Theelen, M. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Neuron},
	Keywords = {02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;Female;Neurons/cytology/ultrastructure;Cell Division;Animal;Cerebral Ventricles/*cytology;Support, U.S. Gov't, P.H.S.;Thymidine/blood/diagnostic use;BB;Support, Non-U.S. Gov't;Birds/*anatomy &histology;Male},
	Number = {1},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {101-9.},
	Title = {Proliferation "hot spots"in adult avian ventricular zone reveal radial cell division},
	Uuid = {AB1BFCF8-C194-4F64-8505-3DF168513375},
	Volume = {5},
	Year = {1990},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=2369518}}

@article{Alvarez-Buylla:2004,
	Abstract = {The adult mammalian brain retains neural stem cells that continually generate new neurons within two restricted regions: the subventricular zone (SVZ) of the lateral ventricle and the dentate gyrus subgranular zone (SGZ) of the hippocampus. Though these cellular populations are spatially isolated and subserve different brain systems, common themes begin to define adult neurogenic niches: (1) astrocytes serve as both stem cell and niche cell, (2) a basal lamina and concomitant vasculogenesis may be essential components of the niche, and (3) "embryonic"molecular morphogens and signals persist in these niches and play critical roles for adult neurogenesis. The adult neurogenic niches can be viewed as "displaced"neuroepithelium, pockets of cells and local signals that preserve enough embryonic character to maintain neurogenesis for life. 0896-6273 Journal Article},
	Author = {Alvarez-Buylla, A. and Lim, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Neuron},
	Keywords = {02 Adult neurogenesis migration;10 Development;BB pdf;03 Adult neurogenesis progenitor source;10 Hippocampus},
	Number = {5},
	Organization = {Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA 94143 USA. abuylla\@itsa.ucsf.edu},
	Pages = {683-6},
	Title = {For the long run: maintaining germinal niches in the adult brain},
	Uuid = {F34EB901-698C-11DA-A4B6-000D9346EC2A},
	Volume = {41},
	Year = {2004},
	url = {papers/Alvarez-Buylla_Neuron2004.pdf}}

@article{Alvarez-Buylla:1988b,
	Abstract = {The higher vocal center (HVc) of the canary brain projects to two forebrain nuclei: robustus archistriatalis (RA) and area X of lobus parolfactorius. The time of birth of HVc neurons projecting to these two regions was determined by combining [3H]thymidine autoradiography and retrograde fluorogold uptake. Birds were sacrificed at 13 months of age, 4 days after fluorogold injections into area X or RA. A single injection of [3H]thymidine in ovo (embryonic day 9) labeled 76\%of area X-projecting cells and 0.8\%of cells projecting to RA. The great majority of RA-projecting cells were produced during posthatching development (posthatching day 10-240; P10-P240), with a peak at P60 and a hiatus at P120. HVc reaches full adult size by P240, yet at that age the production of new RA-projecting cells continued at a rate comparable to that recorded during posthatching development. Late production of neurons interconnecting two distant regions of the brain may regulate source to target cell population size. Male canaries start to sing at P40. During subsequent months, they imitate external models and their song becomes more structured and stereotyped. At sexual maturity (P240), song is stable. Three interpretations are offered: (i) neurogenesis of RA-projecting cells is related to learning, and learning continues even after achievement of pattern stability; (ii) neurogenesis of RA-projecting cells is not related to learning; (iii) the production of RA-projecting cells serves different purposes during development and after sexual maturity.},
	Author = {Alvarez-Buylla, A. and Theelen, M. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Aging;01 Adult neurogenesis general;A;*Learning;Brain/embryology/growth &development/*physiology;Female;Neurons/cytology/*physiology;Animal;Support, U.S. Gov't, P.H.S.;DNA Replication;Canaries/*physiology;Support, Non-U.S. Gov't;Male;Vocalization, Animal},
	Number = {22},
	Organization = {Rockefeller University, Field Research Center, Millbrook, NY 12545.},
	Pages = {8722-6.},
	Title = {Birth of projection neurons in the higher vocal center of the canary forebrain before, during, and after song learning},
	Uuid = {76FBD1F9-0919-4A63-8B35-A96C382CCDD1},
	Volume = {85},
	Year = {1988},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=3186755}}

@article{Alvarez-Buylla:2000,
	Abstract = {The subventricular zone (SVZ) is a major germinal zone which persists in the adult brain. The SVZ contains cells that self renew and continuously produce new neurons and glia. In this chapter we discuss the development, architecture and function of the adult SVZ, as well as the fate of SVZ cells after transplantation. We focus on identification of neural stem cells, factors which regulate neurogenesis and mechanisms for neuronal migration through the adult brain. Detailed understanding of these processes is necessary to utilize the SVZ as a source of neuronal and glial precursors for genetic manipulation, transplantation or brain self repair. Using Smart Source Parsing},
	Author = {Alvarez-Buylla, A. and Herrera, D. G. and Wichterle, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Prog Brain Res},
	Keywords = {Prosencephalon/cytology/*embryology/physiology;02 Adult neurogenesis migration;Cell Division/physiology;03 Adult neurogenesis progenitor source;Human;Stem Cells/cytology/physiology/*transplantation;Animal;Brain Injuries/*therapy;Neurons/cytology/physiology/*transplantation;Cell Differentiation/physiology;BB;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Age Factors;Cell Movement/physiology},
	Organization = {Rockefeller University, 1230 York Avenue 210, New York, NY 10021, USA. alvarez\@rockvax.rockefeller.edu},
	Pages = {1-11},
	Title = {The subventricular zone: source of neuronal precursors for brain repair},
	Uuid = {01E1CCC6-4B92-490D-82B9-FA7D4DD570B6},
	Volume = {127},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11142024}}

@article{Alvarez-Buylla:1990c,
	Abstract = {Projection neurons that form part of the motor pathway for song control continue to be produced and to replace older projection neurons in adult canaries and zebra finches. This is shown by combining [3H]thymidine, a cell birth marker, and fluorogold, a retrogradely transported tracer of neuronal connectivity. Species and seasonal comparisons suggest that this process is related to the acquisition of perceptual or motor memories. The ability of an adult brain to produce and replace projection neurons should influence our thinking on brain repair.},
	Author = {Alvarez-Buylla, A. and Kirn, J. R. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Science},
	Keywords = {A;01 Adult neurogenesis general;Neurons/*physiology;*Learning;Brain/*physiology;Axonal Transport;Autoradiography;Thymidine/metabolism;Animal;Canaries/*physiology;Tritium;Motor Activity;Support, U.S. Gov't, P.H.S.;Seasons;Vocalization, Animal},
	Number = {4975},
	Organization = {Rockefeller University Field Research Center, Millbrook, NY 12545.},
	Pages = {1444-6.},
	Title = {Birth of projection neurons in adult avian brain may be related to perceptual or motor learning},
	Uuid = {EFD1758D-EEF4-4CF9-BE99-4B303A9D5A9F},
	Volume = {249},
	Year = {1990},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1698312}}

@article{Alvarez-Buylla:1995,
	Abstract = {It is generally assumed that neurogenesis in the central nervous system ceases before or soon after birth. In the last three decades, however, several studies have reported that new neurons continue to be added into the brain of adult fish, frogs, reptiles, birds and mammals. The precursor cells that give rise to the neurons generated in adulthood are generally located in the walls of the brain ventricles. From these proliferative regions, neuronal precursors migrate toward their final targets where they differentiate; they often traverse long distances through complex brain parenchyma. The identity of the neuronal precursors in the brains of adult animals is still unknown. Experiments in adult birds suggest that proliferating radial cells may be the neuronal precursors. In adult mice, cells present in the subventricular zone can generated neurons in vivo and in vitro. These neuronal precursors can be induced to proliferate in vitro when exposed to growth factors and retain their potential to differentiate into neurons and glia. Whether these putative neural stem cells can differentiate into multiple neuronal types remains to be determined. The neuronal precursors of the adult brain could be used as a source of cells for neuronal transplantation. In addition, these cells could be manipulated in vivo or in vitro to introduce genes into the brain. Adult neurogenesis offers new experimental opportunities to study neuronal birth, migration and differentiation and for the treatment of neurological diseases.},
	Author = {Alvarez-Buylla, A. and Lois, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Stem Cells},
	Keywords = {Neurons/*physiology;02 Adult neurogenesis migration;Vertebrates/growth &development;B-4;*Stem Cells;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Brain/*cytology},
	Number = {3},
	Organization = {Rockefeller University, New York, New York 10021, USA.},
	Pages = {263-72.},
	Title = {Neuronal stem cells in the brain of adult vertebrates},
	Uuid = {E4A85775-6132-444D-AB18-2AC9B6B51079},
	Volume = {13},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7613493}}

@article{Alvarez-Dolado:2003,
	Abstract = {Recent studies have suggested that bone marrow cells possess a broad differentiation potential, being able to form new liver cells, cardiomyocytes and neurons. Several groups have attributed this apparent plasticity to 'transdifferentiation'. Others, however, have suggested that cell fusion could explain these results. Using a simple method based on Cre/lox recombination to detect cell fusion events, we demonstrate that bone-marrow-derived cells (BMDCs) fuse spontaneously with neural progenitors in vitro. Furthermore, bone marrow transplantation demonstrates that BMDCs fuse in vivo with hepatocytes in liver, Purkinje neurons in the brain and cardiac muscle in the heart, resulting in the formation of multinucleated cells. No evidence of transdifferentiation without fusion was observed in these tissues. These observations provide the first in vivo evidence for cell fusion of BMDCs with neurons and cardiomyocytes, raising the possibility that cell fusion may contribute to the development or maintenance of these key cell types. 1476-4687 Journal Article},
	Author = {Alvarez-Dolado, M. and Pardal, R. and Garcia-Verdugo, J. M. and Fike, J. R. and Lee, H. O. and Pfeffer, K. and Lois, C. and Morrison, S. J. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Nature},
	Keywords = {Models, Biological;Purkinje Cells/*cytology;Cell Differentiation;EE pdf;Cell Fusion;Giant Cells/*cytology;Hepatocytes/*cytology;Myocytes, Cardiac/*cytology;Mice, Inbred C57BL;Bone Marrow Transplantation;Support, U.S. Gov't, P.H.S.;Animals;Support, Non-U.S. Gov't;Stem Cells/cytology;Mice;Bone Marrow Cells/*cytology},
	Number = {6961},
	Organization = {Department of Neurological Surgery, University of California at San Francisco, San Francisco, California 94143-0520, USA.},
	Pages = {968-73},
	Title = {Fusion of bone-marrow-derived cells with Purkinje neurons, cardiomyocytes and hepatocytes},
	Uuid = {0236AF83-CEDC-11D9-B244-000D9346EC2A},
	Volume = {425},
	Year = {2003},
	url = {papers/Alvarez-Dolado_Nature2003.pdf}}

@article{Alves:2002,
	Abstract = {In the early postnatal subventricular zone (SVZ), two seemingly unrelated events occur simultaneously: a massive tangential migration of neuroblasts towards the olfactory bulb, known as the rostral migratory stream (RMS), and the outward movement of radial glia (RG) undergoing astrocytic transformation. Because of the orthogonal arrangement between these two sets of cells, little, if any, relevance has been ascribed for their possible interactions. By depositing DiI at the pial surface we have studied RG transformation within the SVZ/RMS, from birth up to the end of the first postnatal week. While still within the SVZ/RMS, RG morphology changed from simple bipolar to highly complex branched profiles, attaining their highest degree of complexity at the interface of the SVZ with the overlying white matter. At this interface cell bodies of radial glia accumulate and their processes run tangentially, surrounding the SVZ/RMS. Processes of RG surrounding the SVZ/RMS could also be observed by immunostaining for vimentin, GFAP, and nestin. In contrast, in the white matter all DiI-labeled RG presented a simple bipolar profile. These results indicate that the outward radial migration of the transforming RG does not occur uniformly. Instead, the different morphologies and cell densities that RG assume when they cross the SVZ/RMS and overlying white matter imply different migratory behaviors. Finally, our data suggest that RG provide a cellular scaffold to the early postnatal SVZ/RMS, much in the same way as astrocytes in the adult RMS.},
	Author = {Alves, Jos{\'e} A. J. and Barone, Patrick and Engelender, Simone and Fr{\'o}es, Maira M. and Menezes, Jo\~{a}o R. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Cytoskeletal Proteins;Glial Fibrillary Acidic Protein;Cell Differentiation;Animals;Astrocytes;Rats;Cell Count;Cell Movement;Vimentin;Rats, Wistar;11 Glia;Olfactory Bulb;03 Adult neurogenesis progenitor source;Pia Mater;Animals, Newborn;Intermediate Filament Proteins;Carbocyanines;Stem Cells;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22198992},
	Month = {9},
	Nlm_Id = {0213640},
	Number = {3},
	Organization = {Lab. de Neuroanatomia Celular, Departamento de Anatomia, Instituto de Ci\^{e}ncias Biom{\'e}dicas, Universidade Federal do Rio de Janeiro, Brazil 21941-590.},
	Pages = {251-65},
	Pubmed = {12210108},
	Title = {Initial stages of radial glia astrocytic transformation in the early postnatal anterior subventricular zone},
	Uuid = {FF999F5D-CAFD-4CAD-A1C9-054C2DD4B39F},
	Volume = {52},
	Year = {2002},
	url = {papers/Alves_JNeurobiol2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.10087}}

@article{Amadio:2006,
	Abstract = {Despite an ever-expanding database of sequenced mammalian genomes to be mined for clues, the emergence of the unique human brain remains an evolutionary enigma. In their new study, trawl the human genome and those of other mammals in search of short conserved DNA elements that show extremely rapid evolution only in humans. As they report in a recent issue of Nature, their scan yielded a gene for a novel noncoding RNA that adopts a human-specific structure and may regulate neurodevelopment.},
	Author = {Amadio, and Walsh,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008;19 Neocortical evolution},
	Month = {9},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {Division of Genetics, Children's Hospital Boston, Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, and Broad Institute of MIT and Harvard, Boston, MA 02115, USA; Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Boston, MA 02115, USA.},
	Pages = {1033-1035},
	Pii = {S0092-8674(06)01154-8},
	Pubmed = {16990130},
	Title = {Brain Evolution and Uniqueness in the Human Genome},
	Uuid = {376BC2C3-E835-4ABF-98E5-1337538DF0BE},
	Volume = {126},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.09.007}}

@article{Amendola:2005,
	Abstract = {Transferring multiple genes into the same cell allows for the combination of genetic correction, marking, selection and conditional elimination of transduced cells or the reconstitution of multisubunit components and synergistic pathways. However, this cannot be reliably accomplished by current gene transfer technologies. Based on the finding that some cellular promoters intrinsically promote divergent transcription, we have developed synthetic bidirectional promoters that mediate coordinate transcription of two mRNAs in a ubiquitous or a tissue-specific manner. Lentiviral vectors incorporating the new promoters enabled efficient dual gene transfer in several tissues in vivo after direct delivery or transgenesis, and in a human gene therapy model. Because divergent gene pairs, likely transcribed from shared promoters, are common in the genome, the synthetic promoters that we developed may mimic a well-represented feature of transcription. Vectors incorporating these promoters should increase the power of gene function studies and expand the reach and safety of gene therapy.},
	Author = {Amendola, Mario and Venneri, Mary Anna and Biffi, Alessandra and Vigna, Elisa and Naldini, Luigi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {23 Technique},
	Month = {1},
	Nlm_Id = {9604648},
	Number = {1},
	Organization = {[1] San Raffaele Telethon Institute for Gene Therapy (HSR-TIGET), San Raffaele Scientific Institute, via Olgettina 58, 20132 Milano, Italy. [2] Vita Salute San Raffaele University, San Raffaele Scientific Institute, via Olgettina 58, 20132 Milano, Italy.},
	Pages = {108-16},
	Pii = {nbt1049},
	Pubmed = {15619618},
	Title = {Coordinate dual-gene transgenesis by lentiviral vectors carrying synthetic bidirectional promoters},
	Uuid = {6A32CF1F-7CF6-45A9-9D29-3A0837FEDC48},
	Volume = {23},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt1049}}

@article{Amrein:2004,
	Abstract = {Abstract Adult neurogenesis in the dentate gyrus occurs at species-specific levels. Wood mice (Apodemus flavicollis) show higher proliferation rates than laboratory mice and voles (Clethrionomys glareolus, Microtus subterraneus). We compare rates of cell death and proliferation and investigate if cell proliferation leads to the long-term recruitment of granule cells. Granule and pyknotic cell numbers were estimated in wild-living rodents in different age classes and compared with laboratory mice of mixed genetic background. All species differ significantly in their number of granule cells, except for the comparison of laboratory mice with European pine voles. Granule cell number is significantly higher in old bank voles and wood mice as compared to adults (23 and 37\%, respectively). The number of pyknotic cells is highest in wood mice and lowest in laboratory mice. Across all species, the numbers of proliferating and pyknotic cells correlate. Despite differences in cell proliferation and cell death, the ratio of proliferating to pyknotic cells does not differ between adults of the wild-living species, but in laboratory mice a significantly lower proportion of cells die compared with the other species. In addition, the ratio of proliferating to pyknotic cells was significantly higher in old wood mice than in adults. We conclude (i) that cell proliferation can lead to an increase in granule cell number in wild-living rodents and (ii) that species- and age-specific changes of the ratio between proliferating and pyknotic cells occur as deviations from a close correlation of these two numbers across all species and age groups.},
	Author = {Amrein, Irmgard and Slomianka, Lutz and Lipp, Hans-Peter P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {01 Adult neurogenesis general},
	Month = {12},
	Nlm_Id = {8918110},
	Number = {12},
	Organization = {Institute of Anatomy, University of Z{\"u}rich-Irchel, Winterthurerstr. 190, 8057 Z{\"u}rich, Switzerland.},
	Pages = {3342-50},
	Pii = {EJN3795},
	Pubmed = {15610166},
	Title = {Granule cell number, cell death and cell proliferation in the dentate gyrus of wild-living rodents},
	Uuid = {678323BC-F18D-4E65-B48C-6B20A49DBDA9},
	Volume = {20},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2004.03795.x}}

@article{Andersen:1981,
	Abstract = {BALB/c mouse sarcoma virus (BALB-MSV) is a spontaneously occurring transforming retrovirus of mouse origin. The integrated form of the viral genome was cloned from the DNA of a BALB-MSV-transformed nonproducer NRK cell line in the Charon 9 strain of bacteriophage lambda. In transfection assays, the 19-kilobase-pair (kbp) recombinant DNA clone transformed NIH/3T3 mouse cells with an efficiency of 3 X 10(4) focus-forming units per pmol. Such transformants possessed typical BALB-MSV morphology and released BALB-MSV after helper virus superinfection. A 6.8-kbp DNA segment within the 19-kbp DNA possessed restriction enzyme sites identical to those of the linear BALB-MSV genome. Long terminal repeats of approximately 0.6 kbp were localized at either end of the viral genome by the presence of a repeated constellation of restriction sites and by hybridization of segments containing these sites with nick-translated Moloney murine leukemia virus long terminal repeat DNA. A continuous segment of at least 0.6 and no more than 0.9 kbp of helper virus-unrelated sequences was localized toward the 3' end of the viral genome in relation to viral RNA. A probe composed of these sequences detected six EcoRI-generated DNA bands in normal mouse cell DNA as well as a smaller number of bands in rat and human DNAs. These studies demonstrate that BALB-MSV, like previously characterized avian and mammalian transforming retroviruses, arose by recombination of a type C helper virus with a well-conserved cellular gene.},
	Author = {Andersen, P. R. and Tronick, S. R. and Aaronson, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Mice, Inbred BALB C;Animals;Cloning, Molecular;Base Sequence;Transfection;15 Retrovirus mechanism;Sarcoma Viruses, Murine;Genes, Viral;Cell Line;DNA, Recombinant;Cell Transformation, Viral;Recombination, Genetic;Mice;DNA Restriction Enzymes;24 Pubmed search results 2008;Helper Viruses;Cell Transformation, Neoplastic;Nucleic Acid Hybridization},
	Medline = {82101074},
	Month = {11},
	Nlm_Id = {0113724},
	Number = {2},
	Pages = {431-9},
	Pubmed = {6275097},
	Title = {Structural organization and biological activity of molecular clones of the integrated genome of a BALB/c mouse sarcoma virus},
	Uuid = {20ACBDE9-5349-4945-BE83-D0E8656BFC20},
	Volume = {40},
	Year = {1981}}

@article{Anderson:2000,
	Abstract = {Recent studies directed toward developing a better understanding of the molecular and cellular biology basis of monocyte-derived multinucleated giant cell formation, function, and biologic activity are presented. In addition, HIV-1-infected T-lymphocyte syncytia and the significance of adhesion molecule/ligand interactions in the formation of these syncytia are described. Interleukin-4 or interleukin-13 induction of monocyte-macrophage fusion provides a model for foreign body giant cell formation. On the other hand, interferon-gamma induction of monocyte-macrophage fusion provides a model for Langhans' giant cell formation. Variations in monocyte-macrophage adhesion and fusion to form foreign body giant cells are provided by substrates with different surface chemistries. Recent advances in osteoclast biology have identified the role of tumor necrosis factor-alpha in regulating osteoclast bone resorption and receptor-ligand interactions and signal pathways for osteoclast activation. Although foreign body giant cells, Langhans' giant cells, and osteoclasts are derived from monocytes or monocyte progenitor cells, the ways in which they are formed, whether induced by cytokines, receptors, or biologic activity, are markedly different.},
	Author = {Anderson, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1065-6251},
	Journal = {Curr Opin Hematol},
	Keywords = {Foreign Bodies;Giant Cells;HIV-1;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;CD4-Positive T-Lymphocytes;Humans;Animals;24 Pubmed search results 2008;Cell Lineage;review},
	Medline = {20074202},
	Month = {1},
	Nlm_Id = {9430802},
	Number = {1},
	Organization = {Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.},
	Pages = {40-7},
	Pubmed = {10608503},
	Title = {Multinucleated giant cells},
	Uuid = {BAD54022-E9E4-11DA-920C-000D9346EC2A},
	Volume = {7},
	Year = {2000},
	url = {papers/Anderson_CurrOpinHematol2000.pdf}}

@article{Anderson:1995,
	Abstract = {In C58 and AKR mice, endogenous N-tropic, ecotropic murine leukemia virus (MuLV) proviruses become activated in rare cells during embryogenesis. Resultant replication-competent progeny viruses then actively infect a large number of cells throughout the fetus, including cells in the developing central nervous system. By in situ hybridization analyses, we have assessed the presence of ecotropic MuLV RNA in the brains of C58 mice as a function of age. Only a few ecotropic MuLV-positive cells were observed in weanling mice, but the number of positive cells in the brain increased progressively with increasing age of the mice. Throughout the lives of the mice, the ecotropic MuLV RNA-positive cells were primarily located in well-defined white-matter tracts of the brain (commissura anterior, corpus callosum, fimbria hippocampi, optical tract, and striatum) and of the spinal cord. Cells of the subventricular zone also expressed ecotropic MuLV RNA, and in older mice a small number of positive cells were present in the grey matter. Infection of endogenous ecotropic MuLV provirus-less CE/J mice in utero with ecotropic MuLV clone AKR-623 resulted in the extensive infection of brain cells. The regional distribution of ecotropic MuLV RNA-containing cells was the same as observed in the brains of C58 mice, in which cells became infected by endogenously activated virus, but the number of positive cells was higher.},
	Author = {Anderson, G. W. and Plagemann, P. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {RNA, Viral;Fetus;Pregnancy;Animals;Aging;Brain;Female;15 Retrovirus mechanism;Species Specificity;Virus Activation;Embryonic and Fetal Development;Leukemia Virus, Murine;Proviruses;Mice, Inbred Strains;Research Support, U.S. Gov't, P.H.S.;Mice;24 Pubmed search results 2008;15 ERVs retroelements;Mice, Inbred AKR;Research Support, Non-U.S. Gov't},
	Medline = {96079065},
	Month = {12},
	Nlm_Id = {0113724},
	Number = {12},
	Organization = {Department of Microbiology, University of Minnesota, Minneapolis 55455, USA.},
	Pages = {8089-95},
	Pubmed = {7494328},
	Title = {Expression of ecotropic murine leukemia virus in the brains of C58/M, DBA2/J, and in utero-infected CE/J mice},
	Uuid = {833A10BF-4326-11DB-A5D2-000D9346EC2A},
	Volume = {69},
	Year = {1995},
	url = {papers/Anderson_JVirol1995.pdf}}

@article{Anderson:2001,
	Abstract = {0896-6273 Journal Article Review Review, Academic},
	Author = {Anderson, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Neuron},
	Keywords = {Body Patterning/*physiology;Neurons/cytology/metabolism;10 Development;Cell Differentiation/*physiology;Human;Gene Expression Regulation, Developmental/physiology;F;Stem Cells/cytology/*metabolism;Support, Non-U.S. Gov't;Animals;Nervous System/cytology/*embryology/growth &development;Stem Cell Transplantation},
	Number = {1},
	Organization = {Division of Biology 216-76, Howard Hughes Medical Institute, California Institute of Technology, Pasadena, CA 91125, USA. mancusog\@caltech.edu},
	Pages = {19-35},
	Pubmed = {11343642},
	Title = {Stem cells and pattern formation in the nervous system: the possible versus the actual},
	Uuid = {5AECD7C5-3713-4512-9D05-0B502E86ED91},
	Volume = {30},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11343642}}

@article{Anderson:1997,
	Abstract = {Although previous analyses indicate that neocortical neurons originate from the cortical proliferative zone, evidence suggests that a subpopulation of neocortical interneurons originates within the subcortical telencephalon. For example, gamma-aminobutyric acid (GABA)- expressing cells migrate in vitro from the subcortical telencephalon into the neocortex. The number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon. Finally, mice lacking the homeodomain proteins DLX-1 and DLX-2 show no detectable cell migration from the subcortical telencephalon to the neocortex and also have few GABA-expressing cells in the neocortex.},
	Author = {Anderson, S. A. and Eisenstat, D. D. and Shi, L. and Rubenstein, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Science},
	Keywords = {DNA-Binding Proteins/*genetics/physiology;Neocortex/*cytology/embryology/metabolism;H;Tissue Culture;Corpus Striatum/*cytology/embryology/metabolism;Animal;Cell Movement;Mutation;Glutamate Decarboxylase/metabolism;Calcium-Binding Protein, Vitamin D-Dependent/analysis;Support, Non-U.S. Gov't;Interneurons/chemistry/*physiology;GABA/analysis;Telencephalon/*cytology/embryology/metabolism;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Homeodomain Proteins/*genetics/physiology;Mice;*Genes, Homeobox;12 Interneuron development},
	Number = {5337},
	Organization = {Nina Ireland Laboratory of Developmental Neurobiology, Center for Neurobiology and Psychiatry, Department of Psychiatry, University of California at San Francisco, CA 94143-0984, USA.},
	Pages = {474-6.},
	Title = {Interneuron migration from basal forebrain to neocortex: dependence on Dlx genes},
	Uuid = {15C1BDC3-6A4F-4628-A7F6-26DD68F2D423},
	Volume = {278},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9334308}}

@article{Andersson:2003,
	Abstract = {Immunologic reactions against gene therapy products may prove to be a frequent problem in clinical gene therapy protocols. Enhanced green fluorescence protein (EGFP) is commonly used as a marker in gene transfer protocols, and immune responses against EGFP-expressing cells have been documented. The present study was designed to investigate the effect of a pharmacologic, nonmyeloablative, conditioning regimen on the development of EGFP+ donor/recipient mixed bone marrow chimerism and ensuing tolerance to EGFP-expressing transplants. To this end, C57BL/6J (B6) mice were treated with soluble formulations of either busulfan (Busulfex) or the closely related compound treosulfan, followed by transplantation of bone marrow cells from EGFP-transgenic (B6-EGFP.Tg) donor mice. Such conditioning regimens resulted in long-term persistence of donor EGFP+ cells among various hematopoietic lineages from blood, bone marrow, and thymus. Stable hematopoietic chimeras transplanted at 10 to 17 weeks after bone marrow transplantation (BMT) with B6-EGFP.Tg skin grafts all accepted their transplants, whereas non-EGFP chimeric B6 control animals were able to mount rejection of the EGFP+ B6 skin grafts. Control third-party grafts from major histocompatibility complex (MHC)-mismatched mice were rejected within 20 days, indicating that acceptance of EGFP-expressing skin grafts was the result of specific immune tolerance induction by the transplantation of EGFP-transgenic bone marrow. Long-term tolerance to EGFP in chimeric recipients was confirmed by the absence of anti-EGFP-reactive T cells and antibodies. These results broaden the therapeutic potential for using hematopoietic molecular chimerism in nonmyeloablated recipients as a means of preventing rejection of genetically modified cells.},
	Author = {Andersson, Goran and Illigens, Ben M. W. and Johnson, Kevin W. and Calderhead, David and LeGuern, Christian and Benichou, Gilles and White-Scharf, Mary E. and Down, Julian D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Transduction, Genetic;Animals;Bone Marrow Transplantation;Busulfan;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Immune Tolerance;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Skin Transplantation;Graft Rejection;Mice;Transplantation Conditioning;Luminescent Proteins;Graft Survival;Transgenes},
	Medline = {22640656},
	Month = {6},
	Nlm_Id = {7603509},
	Number = {11},
	Organization = {BioTransplant Incorporated, Boston, MA 02129, USA.},
	Pages = {4305-12},
	Pii = {2002-06-1649},
	Pubmed = {12576326},
	Title = {Nonmyeloablative conditioning is sufficient to allow engraftment of EGFP-expressing bone marrow and subsequent acceptance of EGFP-transgenic skin grafts in mice},
	Uuid = {5A39B7FD-2B5A-4633-884B-341E1BEBA5CA},
	Volume = {101},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2002-06-1649}}

@article{Andreadis:1997,
	Abstract = {Replication-incompetent recombinant retroviruses are currently used for gene delivery. The limited efficiency of gene transfer using these vectors hampers implementation of gene therapy. Successful integration of Moloney murine leukemia virus (MMuLV)-derived retroviral vectors into the host cell DNA requires cell division. The time difference between virus entry and cell division is variable and prolonged in slowly dividing cells. Therefore, the rate of intracellular decay of internalized vectors between the time of entry into the target cell and cell division may limit the probability of successful integration following viral entry. We present two methods that measure the intracellular stability of MMuLV-derived retroviral vectors in NIH 3T3 cells. The first is based on a temporary interruption of cell cycle progression by using cell detachment. This method provides an estimate, but not a direct measurement, of the half-life. The results show that the MMuLV intracellular half-life is on the order of but shorter than the total cell cycle time. The second method allows the direct measurement of the intracellular half-life by using two cell cycle-specific labels: 5-bromodeoxyuridine, a thymidine analog that labels cells in S-phase; and the viral vector that labels cells in mitosis. By varying the time between the administration of the two labels, the intracellular half-life is measured to be in the range of 5.5 to 7.5 h. Such a short intracellular half-life may restrict the efficiency of gene transfer by retroviral vectors, particularly in slowly dividing target cells.},
	Author = {Andreadis, S. T. and Brott, D. and Fuller, A. O. and Palsson, B. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {beta-Galactosidase;Animals;Cell Cycle;15 Retrovirus mechanism;Kinetics;Trypsin;Genetic Vectors;Cell Adhesion;Half-Life;Gene Transfer Techniques;Moloney murine leukemia virus;3T3 Cells;Flow Cytometry;Mice;Virus Integration;Genes, Reporter;G1 Phase;S Phase},
	Medline = {97456520},
	Month = {10},
	Nlm_Id = {0113724},
	Number = {10},
	Organization = {Department of Chemical Engineering, University of Michigan, Ann Arbor 48109, USA.},
	Pages = {7541-8},
	Pubmed = {9311834},
	Title = {Moloney murine leukemia virus-derived retroviral vectors decay intracellularly with a half-life in the range of 5.5 to 7.5 hours},
	Uuid = {2A31EBB9-5F7C-4795-9254-EB2B7779A40F},
	Volume = {71},
	Year = {1997},
	url = {papers/Andreadis_JVirol1997.pdf}}

@article{Andreassen:2001,
	Abstract = {A "spindle assembly"checkpoint has been described that arrests cells in G1 following inappropriate exit from mitosis in the presence of microtubule inhibitors. We have here addressed the question of whether the resulting tetraploid state itself, rather than failure of spindle function or induction of spindle damage, acts as a checkpoint to arrest cells in G1. Dihydrocytochalasin B induces cleavage failure in cells where spindle function and chromatid segregation are both normal. Notably, we show here that nontransformed REF-52 cells arrest indefinitely in tetraploid G1 following cleavage failure. The spindle assembly checkpoint and the tetraploidization checkpoint that we describe here are likely to be equivalent. Both involve arrest in G1 with inactive cdk2 kinase, hypophosphorylated retinoblastoma protein, and elevated levels of p21(WAF1) and cyclin E. Furthermore, both require p53. We show that failure to arrest in G1 following tetraploidization rapidly results in aneuploidy. Similar tetraploid G1 arrest results have been obtained with mouse NIH3T3 and human IMR-90 cells. Thus, we propose that a general checkpoint control acts in G1 to recognize tetraploid cells and induce their arrest and thereby prevents the propagation of errors of late mitosis and the generation of aneuploidy. As such, the tetraploidy checkpoint may be a critical activity of p53 in its role of ensuring genomic integrity. 1059-1524 Journal Article},
	Author = {Andreassen, P. R. and Lohez, O. D. and Lacroix, F. B. and Margolis, R. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Mol Biol Cell},
	Keywords = {Tubulin/metabolism;Human;Cyclin-Dependent Kinases/metabolism;Animals;Cytochalasin B/analogs &derivatives/*pharmacology;Cell Separation;Rats;*Polyploidy;Chromosomes/metabolism;Protein-Serine-Threonine Kinases/metabolism;*G1 Phase;08 Aberrant cell cycle;Immunoblotting;Actins/antagonists &inhibitors/metabolism;Cell Line;Support, Non-U.S. Gov't;*CDC2-CDC28 Kinases;Cyclins/metabolism;Mitotic Spindle Apparatus/*metabolism;*Cell Division/drug effects;Flow Cytometry;EE, T pdf;Mice;Enzyme Inhibitors/metabolism;Protein p53/*metabolism},
	Number = {5},
	Organization = {Institut de Biologie Structurale Jean-Pierre Ebel (Commissariat a l'Energie Atomique-Centre National de la Recherche Scientifique), 38027 Grenoble Cedex 1, France.},
	Pages = {1315-28},
	Title = {Tetraploid state induces p53-dependent arrest of nontransformed mammalian cells in G1},
	Uuid = {88B57EDF-E9D9-41BE-AB71-A65993031201},
	Volume = {12},
	Year = {2001},
	url = {papers/Andreassen_MolBiolCell2001.pdf}}

@article{Ang:2003,
	Abstract = {We have used time-lapse multiphoton microscopy to map the migration and settling pattern of GABAergic interneurons that originate in the ganglionic eminence of the ventral forebrain and incorporate into the neocortex of the cerebral hemispheres. Imaging of the surface of the cerebral hemispheres in both explant cultures and brains of living mouse embryos revealed that GABAergic interneurons migrating within the marginal zone originate from three different sources and migrate via distinct and independent streams. After reaching their areal destination, interneurons descend into the underlying cortex to assume positions with isochronically generated, radially derived neurons. The dynamics and pattern of cell migration in the marginal zone (see movies, available at www.jneurosci.org) suggest that the three populations of interneurons respond selectively to distinct local cues for directing their migration to the appropriate areas and layers of the neocortex. This approach opens a new avenue for study of normal and abnormal neuronal migration in their native environment and indicate that interneurons have specific programs for their areal and laminar deployment. 1529-2401 Journal Article},
	Author = {Ang, E. S. and Haydar, T. F. and Gluncic, V. and Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurosci},
	Keywords = {Calcium-Binding Protein, Vitamin D-Dependent/biosynthesis;10 Development;Microscopy, Video/methods;Interneurons/*cytology/metabolism;gamma-Aminobutyric Acid/*metabolism;Immunohistochemistry;Bromodeoxyuridine/pharmacokinetics;Time Factors;In Vitro;Support, U.S. Gov't, P.H.S.;Cerebral Cortex/*cytology/*embryology;Animals;Support, Non-U.S. Gov't;Mice;F pdf;Cell Movement/physiology},
	Number = {13},
	Organization = {Department of Neurobiology, Yale Medical School, New Haven, Connecticut 06510, USA.},
	Pages = {5805-15},
	Pubmed = {12843285},
	Title = {Four-dimensional migratory coordinates of GABAergic interneurons in the developing mouse cortex},
	Uuid = {D46856EA-F2AC-4B79-AB02-167160A1A6BC},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12843285}}

@article{Ang:2006a,
	Abstract = {Neurons of the cerebral neocortex in mammals, including humans, are generated during fetal life in the proliferative zones and then migrate to their final destinations by following an inside-to-outside sequence. The present study examined the effect of ultrasound waves (USW) on neuronal position within the embryonic cerebral cortex in mice. We used a single BrdU injection to label neurons generated at embryonic day 16 and destined for the superficial cortical layers. Our analysis of over 335 animals reveals that, when exposed to USW for a total of 30 min or longer during the period of their migration, a small but statistically significant number of neurons fail to acquire their proper position and remain scattered within inappropriate cortical layers and/or in the subjacent white matter. The magnitude of dispersion of labeled neurons was variable but systematically increased with duration of exposure to USW. These results call for a further investigation in larger and slower-developing brains of non-human primates and continued scrutiny of unnecessarily long prenatal ultrasound exposure.},
	Author = {Ang, Eugenius S. B. C. and Gluncic, Vicko and Duque, Alvaro and Schafer, Mark E. and Rakic, Pasko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Embryo;24 Pubmed search results 2008;research support, n.i.h., extramural ;Ultrasonography;Female;Pregnancy;Animals;Cell Movement;Cerebral Cortex;Neurons;Mice},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {34},
	Organization = {*Department of Neurobiology and Kavli Institute for Neuroscience, Yale Medical School, Sterling Hall of Medicine, Room C-318, 333 Cedar Street, New Haven, CT 06510.},
	Pages = {12903-10},
	Pii = {0605294103},
	Pubmed = {16901978},
	Title = {From the Cover: Prenatal exposure to ultrasound waves impacts neuronal migration in mice},
	Uuid = {47E0A42B-2EF0-42A5-AFB1-8A2323EABF8A},
	Volume = {103},
	Year = {2006},
	url = {papers/Ang_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0605294103}}

@article{Angata:2007,
	Abstract = {Polysialic acid, which is synthesized by two polysialyltransferases, ST8SiaII and ST8SiaIV, plays an essential role in brain development by modifying the neural cell adhesion molecule (NCAM). It is currently unclear how polysialic acid functions in different processes of neural development. Here we generated mice doubly mutant in both ST8SiaII and ST8SiaIV to determine the effects of loss of polysialic acid on brain development. In contrast to NCAM-deficient, ST8SiaII-deficient, or ST8SiaIV-deficient single mutant mice, ST8SiaII and ST8SiaIV double mutants displayed severe defects in anatomical organization of the forebrain associated with apoptotic cell death. Loss of polysialic acid affected both tangential and radial migration of neural precursors during cortical development, resulting in aberrant positioning of neuronal and glial cells. Glial cell differentiation was aberrantly increased in vivo and in vitro in the absence of polysialic acid. Consistent with these findings, polysialic acid-deficient mice exhibited increased expression of the glial cell marker glial fibrillary acidic protein and a decrease in expression of Pax6, a transcription factor regulating neural cell migration. These results indicate that polysialic acid regulates cell migration and differentiation of neural precursors crucial for brain development.},
	Author = {Angata, Kiyohiko and Huckaby, Valerie and Ranscht, Barbara and Terskikh, Alexey and Marth, Jamey D. and Fukuda, Minoru},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0270-7306},
	Journal = {Mol Cell Biol},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8109087},
	Number = {19},
	Organization = {Glycobiology Program, Cancer Research Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA.},
	Pages = {6659-68},
	Pii = {MCB.00205-07},
	Pubmed = {17682066},
	Title = {Polysialic acid-directed migration and differentiation of neural precursors are essential for mouse brain development},
	Uuid = {ECB7B6ED-9301-43D1-AB15-9FC964CF5367},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/MCB.00205-07}}

@article{Angelov:1998,

@article{Anthony:2004,
	Abstract = {Radial glial cells function during CNS development as neural progenitors, although their precise contribution to neurogenesis remains controversial. Recent work has argued that regional differences may exist regarding the neurogenic potential of radial glia. Here, we show that the vast majority of neurons in all brain regions derive from radial glia. Cre/loxP fate mapping and clonal analysis demonstrate that radial glia throughout the CNS serve as neuronal progenitors and that radial glia within different regions of the CNS pass through their neurogenic stage of development at distinct time points. Thus, radial glial populations within different CNS regions are not heterogeneous with regard to their potential to generate neurons versus glia. 0896-6273 Journal Article},
	Author = {Anthony, T. E. and Klein, C. and Fishell, G. and Heintz, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Neuron},
	Keywords = {F, G pdf},
	Number = {6},
	Organization = {Laboratory of Molecular Biology, Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021 USA.},
	Pages = {881-90},
	Title = {Radial glia serve as neuronal progenitors in all regions of the central nervous system},
	Uuid = {BCAB79E0-71C2-11DA-A383-000D9346EC2A},
	Volume = {41},
	Year = {2004},
	url = {papers/Anthony_Neuron2004.pdf}}

@article{Anton:2004,
	Abstract = {Neural progenitor proliferation, differentiation and migration are continually active in the rostral migratory stream of the adult brain. Here, we show that the receptor tyrosine kinase ErbB4 is expressed prominently by the neuroblasts present in the subventricular zone and the rostral migratory stream. The neuregulins (NRG1-NRG3), which have been identified as ErbB4 ligands, are detected either in the stream or in adjacent regions. Mice deficient in ErbB4 expressed under the control of either the nestin or the hGFAP promoter have altered neuroblast chain organization and migration and deficits in the placement and differentiation of olfactory interneurons. These findings suggest that ErbB4 activation helps to regulate the organization of neural chains that form the rostral migratory stream and influences the differentiation of olfactory interneuronal precursors.},
	Author = {Anton, and Ghashghaei, and Weber, and McCann, and Fischer, and Cheung, and Gassmann, and Messing, and Klein, and Schwab, and Lloyd, and Lai,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {02 Adult neurogenesis migration},
	Nlm_Id = {9809671},
	Organization = {[1] UNC Neuroscience Center and the Department of Cell and Molecular Physiology, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA. [2] These authors contributed equally to this work.},
	Pii = {nn1345},
	Pubmed = {15543145},
	Title = {Receptor tyrosine kinase ErbB4 modulates neuroblast migration and placement in the adult forebrain},
	Uuid = {8D2509BA-DC5E-4AA8-A5B4-7AB29E45E01E},
	Year = {2004},
	url = {papers/Anton_NatNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1345}}

@article{Anton:1999,
	Abstract = {Changes in specific cell-cell recognition and adhesion interactions between neurons and radial glial cells regulate neuronal migration as well as the establishment of distinct layers in the developing cerebral cortex. Here, we show that alpha3beta1 integrin is necessary for neuron-glial recognition during neuronal migration and that alpha(v) integrins provide optimal levels of the basic neuron-glial adhesion needed to maintain neuronal migration on radial glial fibers. A gliophilic-to-neurophilic switch in the adhesive preference of developing cortical neurons occurs following the loss of alpha3beta1 integrin function. Furthermore, the targeted mutation of the alpha3 integrin gene results in abnormal layering of the cerebral cortex. These results suggest that alpha3beta1 and alpha(v) integrins regulate distinct aspects of neuronal migration and neuron-glial interactions during corticogenesis.},
	Author = {Anton, E. S. and Kreidberg, J. A. and Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Integrin alpha3beta1;Animals;Integrins;Research Support, U.S. Gov't, Non-P.H.S.;Integrin alphaV;Mutation;Antigens, CD;Cell Movement;Embryonic and Fetal Development;Embryo;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Neuroglia;Cell Aggregation;Neurons;Integrin alpha3;Mice;Research Support, Non-U.S. Gov't},
	Medline = {99166864},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510-8001, USA. esa5\@psu.edu},
	Pages = {277-89},
	Pii = {S0896-6273(00)81089-2},
	Pubmed = {10069334},
	Title = {Distinct functions of alpha3 and alpha(v) integrin receptors in neuronal migration and laminar organization of the cerebral cortex},
	Uuid = {AC9B3ADF-E3D7-4E4D-BFCA-3EAAD7518A98},
	Volume = {22},
	Year = {1999},
	url = {papers/Anton_Neuron1999.pdf}}

@article{Antony:2004,
	Abstract = {Human endogenous retroviruses (HERVs) constitute 8\%of the human genome and have been implicated in both health and disease. Increased HERV gene activity occurs in immunologically activated glia, although the consequences of HERV expression in the nervous system remain uncertain. Here, we report that the HERV-W encoded glycoprotein syncytin is upregulated in glial cells within acute demyelinating lesions of multiple sclerosis patients. Syncytin expression in astrocytes induced the release of redox reactants, which were cytotoxic to oligodendrocytes. Syncytin-mediated neuroinflammation and death of oligodendrocytes, with the ensuing neurobehavioral deficits, were prevented by the antioxidant ferulic acid in a mouse model of multiple sclerosis. Thus, syncytin's proinflammatory properties in the nervous system demonstrate a novel role for an endogenous retrovirus protein, which may be a target for therapeutic intervention.},
	Author = {Antony, Joseph M. and van Marle, Guido and Opii, Wycliffe and Butterfield, D. Allan and Mallet, Fran\c{c}ois and Yong, Voon Wee and Wallace, John L. and Deacon, Robert M. and Warren, Kenneth and Power, Christopher},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Gene Products, env;Multiple Sclerosis;Myelin Sheath;Astrocytes;Encephalitis;Rats;Antioxidants;Middle Aged;Humans;Animals;Coumaric Acids;Oligodendroglia;15 Retrovirus mechanism;Endogenous Retroviruses;Recombinant Fusion Proteins;RNA, Messenger;Disease Models, Animal;Oxidation-Reduction;Aged;Cell Line;Adult;Reactive Oxygen Species;Pregnancy Proteins;Mice;24 Pubmed search results 2008;Cell Death;15 ERVs retroelements;Research Support, Non-U.S. Gov't},
	Month = {10},
	Nlm_Id = {9809671},
	Number = {10},
	Organization = {Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta T2N 4N1, Canada.},
	Pages = {1088-95},
	Pii = {nn1319},
	Pubmed = {15452578},
	Title = {Human endogenous retrovirus glycoprotein-mediated induction of redox reactants causes oligodendrocyte death and demyelination},
	Uuid = {3A64ADE8-EE5A-11DA-8605-000D9346EC2A},
	Volume = {7},
	Year = {2004},
	url = {papers/Antony_NatNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1319}}

@article{Araujo:1992,
	Abstract = {The present study characterizes whether basic fibroblast growth factor (bFGF) is present and released from astroglia, microglia, and hippocampal neurons in vitro. For cell content, bFGF-like immunoreactivity (IR) of cell extracts was measured, whereas release was determined by assessing the levels of bFGF-like IR in media. In addition, the effects of lymphokines and trophic factors that are known to be released from these cells on bFGF release were examined. For all three cell types, bFGF-like IR in extracts of cell lysates was detectable. In addition, media content was highest in astroglial cultures and lowest in neuronal cultures. Although bFGF-like IR of neuronal and microglial media appeared to increase with time in culture, this was likely due to significant astroglial proliferation. Thus, notable levels of bFGF are released by astroglia in vitro. In astroglia, bFGF release was enhanced by interleukin-1 (IL-1), IL-6, and epidermal growth factor (EGF), but not by other lymphokines or NGF. In contrast, bFGF in microglial media was reduced by IL-3, EGF, and NGF, but slightly augmented by gamma-interferon (IFN); other lymphokines were ineffective. In addition, no effects were seen in the neuronal cultures. It is likely that the bFGF found in glial media interacts with bFGF receptors since in both glial and neuronal cell types, a single class of low-capacity (Bmax), high-affinity (Kd) bFGF binding sites was evident. The possibility that endogenous bFGF acts as an autocrine factor for astroglia was further supported by experiments that tested the mitogenic effects of exogenous bFGF on glial cells. bFGF significantly enhanced 3H-thymidine uptake into astroglial, but not microglial, cells in vitro. Thus, the present study demonstrates that a complex regulation of glial bFGF release by astroglia and microglia occurs in vitro. Moreover, the results are consistent with an autocrine role for bFGF in astroglial cultures.},
	Author = {Araujo, D. M. and Cotman, C. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Lymphokines;Research Support, Non-U.S. Gov't;Neuroglia;Binding Sites;Alpha;Immunohistochemistry;Nerve Tissue Proteins;Astrocytes;Time Factors;Cell Division;Research Support, U.S. Gov't, P.H.S.;11 Glia;Cells, Cultured;Animals;Fibroblast Growth Factor 2;Nerve Growth Factors;Neurons},
	Medline = {92251446},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {5},
	Organization = {Department of Psychobiology, University of California, Irvine 92717.},
	Pages = {1668-78},
	Pubmed = {1578261},
	Title = {Basic FGF in astroglial, microglial, and neuronal cultures: characterization of binding sites and modulation of release by lymphokines and trophic factors},
	Uuid = {4CA90F3F-3947-447F-BA95-C388B7B97014},
	Volume = {12},
	Year = {1992}}

@article{Arlotta:2003,
	Abstract = {Over most of the past century, it was thought that the adult brain was completely incapable of generating new neurons. However, in the last decade, the development of new techniques has resulted in an explosion of new research showing that (i) neurogenesis, the birth of new neurons, is not restricted to embryonic development, but normally also occurs in two limited regions of the adult mammalian brain (the olfactory bulb and the dentate gyrus of the hippocampus); (ii) that there are significant numbers of multipotent neural precursors in many parts of the adult mammalian brain; and (iii) that it is possible to induce neurogenesis even in regions of the adult mammalian brain, like the neocortex, where it does not normally occur, via manipulation of endogenous multipotent precursors in situ. In the neocortex, recruitment of small numbers of new neurons can be induced in a region-specific, layer-specific, and neuronal type-specific manner, and newly recruited neurons can form long-distance connections to appropriate targets. This suggests that elucidation of the relevant molecular controls over adult neurogenesis from endogenous neural precursors/stem cells may allow the development of neuronal replacement therapies for neurodegenerative disease and other central nervous system injuries that may not require transplantation of exogenous cells. 0077-8923 Journal Article Review Review, Tutorial},
	Author = {Arlotta, P. and Magavi, S. S. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {01 Adult neurogenesis general;Neurons/*physiology;Nerve Regeneration/*physiology;Environment;Support, U.S. Gov't, Non-P.H.S.;Neocortex/cytology/physiology;Support, U.S. Gov't, P.H.S.;Animals;Support, Non-U.S. Gov't;Cells, Cultured;A, D, L pdf;Stem Cells/*physiology},
	Organization = {MGH-HMS Center for Nervous System Repair, Massachusetts General Hospital, Department of Neurosurgery, Harvard Medical School, Boston, Massachusetts 02114, USA.},
	Pages = {229-36},
	Title = {Induction of adult neurogenesis: molecular manipulation of neural precursors in situ},
	Uuid = {8BA4EEF6-7BF5-41F2-8470-0F20DFB1EF6D},
	Volume = {991},
	Year = {2003},
	url = {papers/Arlotta_AnnNYAcadSci2003.pdf}}

@article{Arlotta:2003a,
	Abstract = {Over the past three decades, research exploring potential neuronal replacement therapies have focused on replacing lost neurons by transplanting cells or grafting tissue into diseased regions of the brain. Over most of the past century of modern neuroscience, it was thought that the adult brain was completely incapable of generating new neurons. However, in the last decade, the development of new techniques has resulted in an explosion of new research showing that neurogenesis, the birth of new neurons, normally occurs in two limited and specific regions of the adult mammalian brain, and that there are significant numbers of multipotent neural precursors in many parts of the adult mammalian brain. Recent findings from our lab demonstrate that it is possible to induce neurogenesis de novo in the adult mammalian brain, particularly in the neocortex where it does not normally occur, and that it may become possible to manipulate endogenous multipotent precursors in situ to replace lost or damaged neurons. Recruitment of new neurons can be induced in a region-specific, layer-specific, and neuronal type-specific manner, and newly recruited neurons can form long-distance connections to appropriate targets. Elucidation of the relevant molecular controls may both allow control over transplanted precursor cells and potentially allow the development of neuronal replacement therapies for neurodegenerative disease and other CNS injuries that do not require transplantation of exogenous cells. 0531-5565 Journal Article Review Review, Academic},
	Author = {Arlotta, P. and Magavi, S. S. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Exp Gerontol},
	Keywords = {Neurons/*physiology;Olfactory Bulb/physiology;Human;A, D, L pdf;Animals;Neocortex/physiology;*Stem Cell Transplantation;17 Transplant Regeneration;01 Adult neurogenesis general;Mammals/*physiology;Support, Non-U.S. Gov't;06 Adult neurogenesis injury induced;Hippocampus/physiology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Neurodegenerative Diseases/therapy;*Nerve Regeneration;Mice},
	Number = {1-2},
	Organization = {Division of Neuroscience, Department of Neurology and Program in Neuroscience, Children's Hospital, Harvard Medical School, 320 Longwood Ave., Enders 354, Boston, MA 02115, USA.},
	Pages = {173-82},
	Title = {Molecular manipulation of neural precursors in situ: induction of adult cortical neurogenesis},
	Uuid = {178943B5-72A5-4B5F-86E6-84AF071A0E26},
	Volume = {38},
	Year = {2003},
	url = {papers/Arlotta_ExpGerontol2003}}

@article{Armentano:2006,
	Abstract = {The transcription factor COUP-TFI (NR2F1), an orphan member of the nuclear receptor superfamily, is an important regulator of neurogenesis, cellular differentiation and cell migration. In the forebrain, COUP-TFI controls the connectivity between thalamus and cortex and neuronal tangential migration in the basal telencephalon. Here, we show that COUP-TFI is required for proper axonal growth and guidance of all major forebrain commissures. Fibres of the corpus callosum, the hippocampal commissure and the anterior commissure project aberrantly and fail to cross the midline in COUP-TFI null mutants. Moreover, hippocampal neurons lacking COUP-TFI have a defect in neurite outgrowth and show an abnormal axonal morphology. To search for downstream effectors, we used microarray analysis and showed that, in the absence of COUP-TFI, expression of various cytoskeleton molecules involved in neuronal morphogenesis is affected. Diminished protein levels of the microtubule-associated protein MAP1B and increased levels of the GTP-binding protein RND2 were confirmed in the developing cortex in vivo and in primary hippocampal neurons in vitro. Therefore, based on morphological studies, gene expression profiling and primary cultured neurons, the present data uncover a previously unappreciated intrinsic role for COUP-TFI in axonal growth in vivo and supply one of the premises for COUP-TFI coordination of neuronal morphogenesis in the developing forebrain.},
	Author = {Armentano, Maria and Filosa, Alessandro and Andolfi, Gennaro and Studer, Mich\`{e}le},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {8701744},
	Number = {21},
	Organization = {TIGEM (Telethon Institute of Genetics and Medicine Disorders Program, Via P. Castellino 111, 80131 Napoli, Italy.},
	Pages = {4151-62},
	Pii = {dev.02600},
	Pubmed = {17021036},
	Title = {COUP-TFI is required for the formation of commissural projections in the forebrain by regulating axonal growth},
	Uuid = {73485913-8D33-4F60-8113-1D702EAEA8F4},
	Volume = {133},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.02600}}

@article{Arnhold:2000,
	Abstract = {OBJECT: The aim of this investigation was to assess new information concerning the capacity of transplanted embryonic stem cell (ESC)-derived neuronal cells to migrate into host brain and to evaluate these cells as a possible source for cell replacement therapy in neurodegenerative disorders such as Parkinson's disease (PD). METHODS: The authors investigated the ability of ESC-derived neural precursor cells to migrate and differentiate in a host striatum by using a D3-derived ESC clone that was transfected stably with a chicken beta-actin cytomegalovirus enhancer-driven green fluorescent protein (GFP)-labeled construct. This procedure allowed easy monitoring of all transplanted cells because of the green fluorescent labeling of donor cells. This approach also afforded easy estimation of cell integration and simultaneous observation of the entire transplanted cell population in relation to immunocytochemically identified neuronal and glial differentiation. After selection of nestin-positive neural precursor cells in a synthetic medium, they were implanted into the striatum of male adult Wistar rats. Their integration was analyzed on morphological studies performed 3 days to 4 weeks posttransplantation. CONCLUSIONS: The investigators found that after transplantation, a subpopulation of GFP-labeled cells differentiated into various neural morphological types that were positive for the mouse-specific Thy-1 antigen, which is known be expressed on neurons, as well as being positive for the astroglial marker glial fibrillary acidic protein. Moreover, GFP-expressing cells that were negative for either of these markers remained close to the injection site, presumably representing other derivatives of the neural lineage. Together, these findings contribute to basic research regarding future transplantation strategies in neurodegenerative diseases such as PD.},
	Author = {Arnhold, S. and Lenartz, D. and Kruttwig, K. and Klinz, F. J. and Kolossov, E. and Hescheler, J. and Sturm, V. and Andressen, C. and Addicks, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0022-3085},
	Journal = {J Neurosurg},
	Keywords = {Cell Differentiation;Animals;Stem Cell Transplantation;Corpus Striatum;Humans;Rats;Cell Movement;Parkinson Disease;Antigens, Thy-1;11 Glia;Rats, Wistar;Male;Green Fluorescent Proteins;Fetal Tissue Transplantation;Neurons;Neuroglia;Luminescent Proteins;Stem Cells;Chickens},
	Medline = {21003934},
	Month = {12},
	Nlm_Id = {0253357},
	Number = {6},
	Organization = {Institute of Anatomy I, Department of Stereotactic and Functional Neurosurgery, University of Cologne, Germany. stefan.arnhold\@uni-koeln.de},
	Pages = {1026-32},
	Pubmed = {11117845},
	Title = {Differentiation of green fluorescent protein-labeled embryonic stem cell-derived neural precursor cells into Thy-1-positive neurons and glia after transplantation into adult rat striatum},
	Uuid = {04EC7C34-C5F7-4323-8718-B0D85E8763C7},
	Volume = {93},
	Year = {2000}}

@article{Aronica:2005,
	Abstract = {Cells of the microglia/macrophage lineage represent an important component of different brain tumours. However, there is little information about the microglia/macrophage cell system in glioneuronal tumours and its possible contribution to the high epileptogenecity of these lesions. In the present study, the distribution of cells of the microglia/macrophage lineage was studied by immunocytochemistry for CD68 and human leucocyte antigen (HLA)-DR in a group of glioneuronal tumours, including gangliogliomas (GG, n = 30), and dysembryoplastic neuroepithelial tumours (DNT, n = 17), from patients with chronic intractable epilepsy. A significant number of microglia/macrophage cells were observed in the large majority of glioneuronal tumours, both within the tumour and in the peritumoral region. Activated microglial cells positive for HLA-DR were localized around blood vessels and clustered around tumour neuronal cells. The density of activated microglial cells correlated with the duration of epilepsy, as well as with the frequency of seizures prior to surgical resection. These observations indicate that the presence of cells of the microglial/macrophage cell system is a feature of glioneuronal tumours and is functionally related to epilepsy, either directly in epileptogenesis or through activation following seizure activity.},
	Author = {Aronica, E. and Gorter, J. A. and Redeker, S. and Ramkema, M. and Spliet, W. G. M. and van Rijen, P. C. and Leenstra, S. and Troost, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Epilepsy;Adult;Adolescent;Female;Immunohistochemistry;HLA-DR Antigens;Middle Aged;Microglia;Child, Preschool;Child;11 Glia;Humans;Neoplasms, Neuroepithelial;Brain;Male},
	Month = {6},
	Nlm_Id = {7609829},
	Number = {3},
	Organization = {Department of (Neuro)Pathology, Academic Medical Centre, University of Amsterdam, 1105 AZ Amsterdam, the Netherlands. e.aronica\@amc.uva.nl},
	Pages = {280-91},
	Pii = {NAN636},
	Pubmed = {15885065},
	Title = {Distribution, characterization and clinical significance of microglia in glioneuronal tumours from patients with chronic intractable epilepsy},
	Uuid = {5FCDA117-D840-47C5-96A1-59872617A7E1},
	Volume = {31},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1365-2990.2004.00636.x}}

@article{Arsenijevic:1998,
	Abstract = {Insulin-like growth factor-I (IGF-I) has been reported previously to promote the proliferation, survival, and maturation of sympathetic neuroblasts, the genesis of retinal neurons, and the survival of CNS projection and motor neurons. Here we asked whether IGF-I could promote the in vitro differentiation of postmitotic mammalian CNS neuronal precursors derived from multipotent epidermal growth factor (EGF)-responsive stem cells. In the absence of IGF-I, virtually no neurons were present in cultured stem cell progeny, whereas IGF-I increased neuron number by eight- to 40-fold. Brief exposures (2 hr) to IGF-I were sufficient to allow for neuronal differentiation without affecting proliferation or survival. IGF-I actions could be mimicked by insulin and IGF-II at concentrations that correspond to the pharmacology of the IGF-I receptor, the latter for which the mRNA was detected in undifferentiated stem cell progeny. Although ineffectual alone at low concentrations (10 nM) that would activate its own receptor, insulin was able to potentiate the actions of IGF-I by acting on mitotically active neural precursors. When neuronal precursor differentiation by IGF-I was examined in relation to brain-derived neurotrophic factor (BDNF), two important observations were made: (1) BDNF could potentiate the differentiating actions of IGF-I plus insulin, and (2) BDNF could act on a separate population of precursors that did not require IGF-I plus insulin for differentiation. Taken together, these results suggest that IGF-I and BDNF may act together or sequentially to promote neuronal precursor differentiation. 0270-6474 Journal Article Review Review, Tutorial},
	Author = {Arsenijevic, Y. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurosci},
	Keywords = {C abstr;Stem Cells/*cytology/drug effects/*physiology;Brain/cytology/*physiology;Insulin-Like Growth Factor I/metabolism/pharmacology/*physiology;Mitosis/*physiology;Brain-Derived Neurotrophic Factor/pharmacology/physiology;Neurons/cytology/*physiology;Drug Synergism;Mice/embryology;Cell Differentiation/physiology;04 Adult neurogenesis factors;Insulin/pharmacology;Support, Non-U.S. Gov't;Animals;Cell Count/drug effects;Receptors, Somatomedin/physiology},
	Number = {6},
	Organization = {Department of Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada T2N4N1.},
	Pages = {2118-28},
	Pubmed = {9482798},
	Title = {Insulin-like growth factor-I is a differentiation factor for postmitotic CNS stem cell-derived neuronal precursors: distinct actions from those of brain-derived neurotrophic factor},
	Uuid = {F1D595A9-86B1-4D8E-A311-73B9AF5D807A},
	Volume = {18},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9482798}}

@article{Arvidsson:2001,
	Abstract = {Neurogenesis in the adult rat dentate gyrus was studied following focal ischemic insults produced by middle cerebral artery occlusion (MCAO). Animals were subjected to either 30 min of MCAO, which causes damage confined to the striatum, or 2 h of MCAO, which leads to both striatal and cortical infarction. When compared to sham-operated rats, MCAO-rats showed a marked increase of the number of cells double-labelled for 5- bromo-2'-deoxyuridine-5'-monophosphate (BrdU; injected during 4-6 days postischemia) and neuronal-specific antigen (NeuN; a marker of postmitotic neurons) in the ipsilateral dentate granule cell layer and subgranular zone at 5 weeks following the 2 h insult. Only a modest and variable increase of BrdU-labelled cells was found after 30 min of MCAO. The enhanced neurogenesis was not dependent on cell death in the hippocampus, and its magnitude was not correlated to the degree of cortical damage. Systemic administration of the N-methyl-D-aspartate (NMDA) receptor blocker dizocilpine maleate (MK-801) completely suppressed the elevated neurogenesis following 2 h of MCAO. Our findings indicate that stroke leads to increased neurogenesis in the adult rat dentate gyrus through glutamatergic mechanisms acting on NMDA receptors. This modulatory effect may be mediated through changes in the levels of several growth factors, which occur after stroke, and could influence various regulatory steps of neurogenesis.},
	Author = {Arvidsson, A. and Kokaia, Z. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:39:25 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Recovery of Function/drug effects/physiology;Rats;Excitatory Amino Acid Antagonists/pharmacology;Receptors, N-Methyl-D-Aspartate/antagonists &inhibitors/*metabolism;D both;Infarction, Middle Cerebral Artery/*metabolism/pathology/physiopathology;Animal;Dentate Gyrus/cytology/*growth &development/metabolism;Cell Differentiation/drug effects/*physiology;Rats, Wistar;Male;Support, Non-U.S. Gov't;Neuronal Plasticity/drug effects/*physiology;Cell Division/drug effects/*physiology;Neurons/cytology/drug effects/*metabolism;06 Adult neurogenesis injury induced;Brain Ischemia/metabolism/pathology/physiopathology;Immunohistochemistry;Bromodeoxyuridine/pharmacokinetics;Biological Markers/analysis;Antimetabolites/pharmacokinetics},
	Number = {1},
	Organization = {Section of Restorative Neurology, Wallenberg Neuroscience Center, BMC A11, University Hospital, SE-221 84, Lund, Sweden. andrea.arvidsson\@neurol.lu.se},
	Pages = {10-8.},
	Title = {N-methyl-D-aspartate receptor-mediated increase of neurogenesis in adult rat dentate gyrus following stroke},
	Uuid = {9730EB66-EC81-11DA-8605-000D9346EC2A},
	Volume = {14},
	Year = {2001},
	url = {papers/Arvidsson_EurJNeurosci2001.pdf}}

@article{Arvidsson:2002,
	Abstract = {In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we show that the adult brain has the capacity for self-repair after insults causing extensive neuronal death. If the new neurons are functional and their formation can be stimulated, a novel therapeutic strategy might be developed for stroke in humans. 1078-8956 Journal Article},
	Author = {Arvidsson, A. and Collin, T. and Kirik, D. and Kokaia, Z. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:27:23 -0400},
	Journal = {Nat Med},
	Keywords = {Animals;Cerebrovascular Accident/metabolism/*pathology;Rats;Brain/*pathology;Neurons/metabolism/*pathology;D pdf;Cell Movement;Stem Cells/cytology;Rats, Wistar;Male;DNA-Binding Proteins/metabolism;Homeodomain Proteins/metabolism;Support, Non-U.S. Gov't;Neuropeptides/metabolism;Lateral Ventricles/pathology;Cell Division;Proto-Oncogene Proteins/metabolism;Biological Markers/analysis},
	Number = {9},
	Organization = {Section of Restorative Neurology, Wallenberg Neuroscience Center, Lund University Hospital, Lund, Sweden. andreas.arvidsson\@neurol.lu.se},
	Pages = {963-70},
	Title = {Neuronal replacement from endogenous precursors in the adult brain after stroke},
	Uuid = {BAA16CF7-C26D-11DA-969D-000D9346EC2A},
	Volume = {8},
	Year = {2002},
	url = {../Data/Papers/text/dissertation/dissertation.pdf}}

@article{Arvidsson:2001a,
	Abstract = {Gene expression for glial cell line-derived neurotrophic factor (GDNF) family ligands and receptors was analyzed with in situ hybridization after two focal ischemic insults of different severities. Focal ischemia was induced in rats by either 30 min or 2 h of middle cerebral artery occlusion (MCAO), causing damage to the striatum only, or involving also the parietal cortex, respectively. We found modest, transient elevation of GDNF mRNA in the dentate granule cell layer. In addition, the number of GDNF mRNA-expressing cells increased in the cortex and striatum after 2 h or 30 min of MCAO, respectively. No changes of neurturin or persephin mRNA expression were detected. Both c- Ret and GFRalpha1 mRNA levels were markedly increased in the ipsilateral cortex outside the ischemic lesion at 6-24 h after the 2-h insult, whereas GFRalpha2 expression was decreased in cortical areas both within and outside the lesion. Similar increases of c-Ret and GFRalpha1 mRNA levels were detected in the striatum, and to a lesser extent, in the cortex following 30 min of MCAO. The 2-h insult also gave rise to transient increases of c-Ret and GFRalpha1 mRNA in hippocampal subregions. Thirty minutes and 2 h of MCAO lead to elevated c-Ret, and GFRalpha1 or GFRalpha2 mRNA expression, respectively, in the ipsilateral ventroposterolateral thalamic nucleus. Both insults induced increased levels of GFRalpha1 mRNA in the subventricular zone of the lateral ventricle.Our data indicate major changes of GDNF family signaling in the forebrain, regulated mainly through altered receptor levels, in the post-ischemic phase. These changes could enhance neuroprotective and neuroregenerative responses both to endogenous and exogenous GDNF ligands. Using Smart Source Parsing},
	Author = {Arvidsson, A. and Kokaia, Z. and Airaksinen, M. S. and Saarma, M. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Neuroscience},
	Keywords = {D abstr;06 Adult neurogenesis injury induced},
	Number = {1},
	Pages = {27-41},
	Title = {Stroke induces widespread changes of gene expression for glial cell line-derived neurotrophic factor family receptors in the adult rat brain},
	Uuid = {7BA2B945-00E6-4C0B-829F-33DFF84AFE9F},
	Volume = {106},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11564414}}

@article{Asano:2001,
	Abstract = {G proteins play important roles in transmembrane signal transduction, and various isoforms of each subunit, alpha, beta and gamma, are highly expressed in the brain. The Ggamma5 subunit is a minor isoform in the adult brain, but we have previously shown it to be highly expressed in the proliferative region of the ventricular zone in the rat embryonic brain. We show here that Ggamma5 is also selectively localized in a proliferative region in the adult rat brain, including the subventricular zone of the lateral ventricle and rostral migratory stream. The Galphai2 subunit colocalized with Ggamma5 in these regions, the two subunits being present in neuronal precursors and ependymal cells but not in proliferating astrocytes. In addition, intense staining of Ggamma5 was seen in axons of the olfactory neurons, which are known to regenerate. These results suggest specific roles for Ggamma5 in precursor cells during neurogenesis so that this isoform might be a useful biological marker.},
	Author = {Asano, T. and Shinohara, H. and Morishita, R. and Ueda, H. and Kawamura, N. and Katoh-Semba, R. and Kishikawa, M. and Kato, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Neurochem},
	Keywords = {Lateral Ventricles/*chemistry/cytology/embryology/growth &development;Axons/chemistry;Cell Differentiation;Protein Subunits;Olfactory Bulb/*chemistry/cytology/embryology/growth &development;Rats;Immunoenzyme Techniques;Heterotrimeric GTP-Binding Proteins/*analysis;Cell Movement;Animal;C abstr;Rats, Wistar;Male;Protein Isoforms/*analysis;Support, Non-U.S. Gov't;Interneurons/*chemistry/cytology;Cell Lineage;Stem Cells/*chemistry/cytology;04 Adult neurogenesis factors;Ependyma/*chemistry/cytology;Bromodeoxyuridine/diagnostic use;Gestational Age;Nerve Tissue Proteins/*analysis},
	Number = {6},
	Organization = {Institute for Developmental Research, Aichi Human Service Center, Kasugai, Aichi, Japan. tosano\@inst-hsc.pref.aichi.jp},
	Pages = {1129-35.},
	Title = {Selective localization of G protein gamma5 subunit in the subventricular zone of the lateral ventricle and rostral migratory stream of the adult rat brain},
	Uuid = {607EA09B-2541-41A7-B561-DD05B228E753},
	Volume = {79},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11752054%20http://www.jneurochem.org/cgi/content/full/79/6/1129%20http://www.jneurochem.org/cgi/content/abstract/79/6/1129}}

@article{Aschner:1999,
	Abstract = {Neuroglial cells of the central nervous system include the astrocytes, oligodendrocytes, and microglia. Their counterparts in the peripheral nervous system are the Schwann cells. The term neuroglia comes from an erroneous concept originally coined by Virchow (1850), in which he envisioned the neurons to be embedded in a layer of connective tissue. The term, or its shortened form--glia, has persisted as the preferred generic term for these cells. A reciprocal relationship exists between neurons and glia, and this association is vital for mutual differentiation, development, and functioning of these cell types. Therefore, perturbations in glial cell function, as well as glial metabolism of chemicals to active intermediates, can lead to neuronal dysfunction. The purpose of this review is to explore neuroglial sites of neurotoxicant actions, discuss potential mechanisms of glial-induced or glial-mediated central nervous system and peripheral nervous system damage, and review the role of glial cells in neurotoxicity development.},
	Author = {Aschner, M. and Allen, J. W. and Kimelberg, H. K. and LoPachin, R. M. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0362-1642},
	Journal = {Annu Rev Pharmacol Toxicol},
	Keywords = {Neuroglia;review, academic;Schwann Cells;Human;Not relevant;11 Glia;Support, U.S. Gov't, P.H.S.;Animals;Nervous System Diseases;review},
	Medline = {99261465},
	Nlm_Id = {7607088},
	Organization = {Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA. maschner\@bgsm.edu},
	Pages = {151-73},
	Pubmed = {10331080},
	Title = {Glial cells in neurotoxicity development},
	Uuid = {E718C1D3-9FA7-4271-BD98-E5F97055D5B8},
	Volume = {39},
	Year = {1999},
	Bdsk-Url-1 = {http://dx.doi.org/10.1146/annurev.pharmtox.39.1.151}}

@article{Asensio:2001,
	Abstract = {The CXC chemokine gamma interferon (IFN-gamma)-inducible protein CXCL10/IP-10 is markedly elevated in cerebrospinal fluid and brain of individuals infected with human immunodeficiency virus type 1 (HIV-1) and is implicated in the pathogenesis of HIV-associated dementia (HAD). To explore the possible role of CXCL10/IP-10 in HAD, we examined the expression of this and other chemokines in the central nervous system (CNS) of transgenic mice with astrocyte-targeted expression of HIV gp120 under the control of the glial fibrillary acidic protein (GFAP) promoter, a murine model for HIV-1 encephalopathy. Compared with wild-type controls, CNS expression of the CC chemokine gene CCL2/MCP-1 and the CXC chemokine genes CXCL10/IP-10 and CXCL9/Mig was induced in the GFAP-HIV gp120 mice. CXCL10/IP-10 RNA expression was increased most and overlapped the expression of the transgene-encoded HIV gp120 gene. Astrocytes and to a lesser extent microglia were identified as the major cellular sites for CXCL10/IP-10 gene expression. There was no detectable expression of any class of IFN or their responsive genes. In astrocyte cultures, soluble recombinant HIV gp120 protein was capable of directly inducing CXCL10/IP-10 gene expression a process that was independent of STAT1. These findings highlight a novel IFN- and STAT1-independent mechanism for the regulation of CXCL10/IP-10 expression and directly link expression of HIV gp120 to the induction of CXCL10/IP-10 that is found in HIV infection of the CNS. Finally, one function of IP-10 expression may be the recruitment of leukocytes to the CNS, since the brain of GFAP-HIV gp120 mice had increased numbers of CD3(+) T cells that were found in close proximity to sites of CXCL10/IP-10 RNA expression.},
	Author = {Asensio, V. C. and Maier, J. and Milner, R. and Boztug, K. and Kincaid, C. and Moulard, M. and Phillipson, C. and Lindsley, K. and Krucker, T. and Fox, H. S. and Campbell, I. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {T-Lymphocytes;Animals;HIV-1;DNA-Binding Proteins;Trans-Activators;Astrocytes;Humans;Solubility;Cells, Cultured;Brain;Interferon Type II;Mice, Transgenic;Mice, Inbred C57BL;Recombinant Fusion Proteins;11 Glia;Research Support, U.S. Gov't, P.H.S.;Receptors, Chemokine;Chemokines, CXC;Interferon-alpha;Mice;Gene Expression;HIV Envelope Protein gp120;Glial Fibrillary Acidic Protein},
	Medline = {21329489},
	Month = {8},
	Nlm_Id = {0113724},
	Number = {15},
	Organization = {Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.},
	Pages = {7067-77},
	Pubmed = {11435587},
	Title = {Interferon-independent, human immunodeficiency virus type 1 gp120-mediated induction of CXCL10/IP-10 gene expression by astrocytes in vivo and in vitro},
	Uuid = {2BDE957A-8584-4926-AF47-97B9A1B28190},
	Volume = {75},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.75.15.7067-7077.2001}}

@article{Asheuer:2004,
	Abstract = {In rodents, bone marrow-derived cells enter the brain during adult life. Allogeneic bone marrow transplantation is used to treat genetic CNS diseases, but the fate of human bone marrow and CD34(+) cells within the brain remains to be elucidated. The present study demonstrates that cells derived from human CD34(+) cells, isolated from either cord blood or peripheral blood, migrate into the brain after infusion into nonobese diabetic/severe combined immunodeficient mice. Both types of CD34(+)-derived cells differentiate into perivascular and ramified microglia. The lentiviral transfer of genes into CD34(+) cells before infusion does not modify the differentiation of human CD34(+) cells into microglia, allowing new transgenic proteins to be expressed in these cells. The transplantation of CD34(+) cells could thus be used for the treatment of CNS diseases.},
	Author = {Asheuer, Muriel and Pflumio, Fran\c{c}oise and Benhamida, Sonia and Dubart-Kupperschmitt, Anne and Fouquet, Fran\c{c}oise and Imai, Yoshinori and Aubourg, Patrick and Cartier, Nathalie},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Differentiation;Mice, Inbred NOD;Animals;Humans;Central Nervous System Diseases;Transplantation, Heterologous;Recombinant Proteins;Microglia;Brain;Mice, SCID;Antigens, CD34;11 Glia;Green Fluorescent Proteins;Hematopoietic Stem Cell Transplantation;Fatty Acids;Peripheral Blood Stem Cell Transplantation;Hematopoietic Stem Cells;Infant, Newborn;Mice;Fetal Blood;Luminescent Proteins;Gene Expression;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {7505876},
	Number = {10},
	Organization = {Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale U561, H\^{o}pital Saint-Vincent de Paul, 75014 Paris, France.},
	Pages = {3557-62},
	Pii = {0306431101},
	Pubmed = {14990803},
	Title = {Human CD34+ cells differentiate into microglia and express recombinant therapeutic protein},
	Uuid = {0F3ED2E5-544E-4AEB-97B1-16B50A443B3E},
	Volume = {101},
	Year = {2004},
	url = {papers/Asheuer_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0306431101}}

@article{Ashwell:1990,
	Abstract = {The appearance and distribution of microglia in the developing cerebellum has been examined with the aid of a peroxidase-conjugated lectin derived from Griffonia simplicifolia. This distribution has in turn been correlated with that of pyknotic figures in the same Nissl-counterstained sections, in order to gain an understanding of the role of microglial in the developing cerebellum. Round and ameboid microglia may be recognised in the fetal cerebellum as early as E11. Numbers of microglia increase steadily from that time, with initial concentrations in the region of the dorsal and ventricular surfaces. By P1, concentrations of both pyknotic figures and ameboid microglia begin to appear in the region of the future cerebellar medulla. Ameboid microglia are recognisable in the cerebellar medulla until P10, with particular concentrations where folia branch and in the rostral cerebellar peduncles. After this time only resting microglia are found in the cerebellum. Concentrations of microglia largely match the positions of pyknotic figures throughout development, except at P10 and P14, when cell death is found in the external granular layer without an accompanying concentration of microglia. Electron microscopic examination of the phagosomes of ameboid microglia at P5 and P6 indicates that these cells are mainly concerned with the phagocytosis of entire cells rather than axons. Cell death in the cerebellar medulla may serve to clear pathways for developing cortical afferents and efferents, or to increase the mechanical plasticity of the medulla during cortical folding.},
	Author = {Ashwell, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0165-3806},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Connective Tissue Cells;Lectins;Microscopy, Electron;Not relevant;Cell Survival;Cerebellum;11 Glia;Mice;Animals;Phagocytosis},
	Medline = {91070714},
	Month = {9},
	Nlm_Id = {8908639},
	Number = {2},
	Organization = {School of Anatomy, University of NSW, Kensington, Australia.},
	Pages = {219-30},
	Pubmed = {2253324},
	Title = {Microglia and cell death in the developing mouse cerebellum},
	Uuid = {4A35B912-869C-4437-A987-D6D129D28A2A},
	Volume = {55},
	Year = {1990}}

@article{Ashwell:1989,
	Abstract = {In this study the development of ameboid microglia and resting microglia in the retina of the albino rabbit has been examined by means of a lectin derived from Griffonia simplicifolia. Ameboid microglia are present in the retina as early as E12, when the optic fissure is in the process of closure, and appear to be concentrated initially at the vitreal surface. At E14 many ameboid microglia can be seen to extend processes to the ventricular surface of the cytoblast layer, but in subsequent ages these cells are rare and ameboid microglia are largely confined to the ganglion cell layer, inner plexiform layer, and occasionally the developing inner nuclear layer. By adult life, mature (or resting) microglia are confined to the inner plexiform and ganglion cell layers. Numbers of microglia increase steadily throughout fetal life from a mean of 400 at E14, the earliest age quantified, to a peak of 28,600 at E30. There is a small postnatal drop in numbers to 17,150 at P9. Microglia could only be labelled faintly in animals older than P11, but analysis of two adult (P130) retinas with adequate labelling suggested that numbers rise to a value of about 23,800 at this age. Ameboid microglia thus appear in the retina 11 days prior to the onset of axon loss in the optic nerve (about E23) and 14 days prior to the beginning of the period of reduction of retinal ganglion cell numbers (about E26). The present findings indicate that while some microglial precursors may enter the retina in response to debris generated during the natural retinal ganglion cell death period, most enter the retina well before this period. Also, microglia present a uniform density distribution with apparently regular spacing as early as E16, so the uniform regular distribution cannot simply be the consequence of regularly distributed pyknotic figures as previously suggested.},
	Author = {Ashwell, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Retina;Neuroglia;Female;Not relevant;Cell Division;Cell Survival;Retinal Vessels;11 Glia;Immunoenzyme Techniques;Retinal Ganglion Cells;Animals;Horseradish Peroxidase;Phagocytosis;Rabbits;Male},
	Medline = {89380914},
	Month = {9},
	Nlm_Id = {0406041},
	Number = {3},
	Organization = {Department of Anatomy, University of Sydney, NSW, Australia.},
	Pages = {286-301},
	Pubmed = {2674209},
	Title = {Development of microglia in the albino rabbit retina},
	Uuid = {F90A0688-8CFB-4008-BC71-6875EE003036},
	Volume = {287},
	Year = {1989}}

@article{Ashwell:1989a,
	Abstract = {We have examined the development of microglia in the rat retina, using a peroxidase-conjugated lectin derived from Griffonia simplicifolia. Retinas were studied from animals aged from E(embryonic day)12, just after the invagination of the optic cup and prior to the closure of the optic fissure, to adulthood. The lectin also proved a sensitive label for the endothelial cells of the developing retina. Our results provide some support for the view that microglia are derived from the monocyte-macrophage series of blood cells. At E12, most labeled cells were found at the vitreal surface, suggesting that they had come from the hyaloid circulation, while some had entered the retina and appeared to be migrating towards its ventricular surface. From E14 to early postnatal ages, most labeled cells had processes and resembled the amoeboid microglial cells described in silver carbonate staining studies (Ling, 1982). The number of labeled cells rose from about 700 to E14 to a peak of about 27,000 at P(postnatal day)7, and fell to about 19,600 by P12. As early as E16, a regularity was apparent in the distribution of microglial cells over the surface of the retina, the cells tending to avoid each other. Microglial cells are found throughout the thickness of the very young retina, but as the layers of the retina differentiate, they are increasingly restricted to the inner half of the retina. Our findings indicate that microglia enter the retina well before the period of neuronal death, making it unlikely that they invade the retina solely in response to cell death. Our results confirm however that, once in the retina, microglia become associated with, and appear to phagocytose, the pyknotic debris which appears during the period of neuronal death. They also become closely associated with the retinal vasculature. In the adult, the intensity of the labeling of microglia was much reduced. Those cells which were labeled appeared more differentiated, resembling the "resting microglia" described in earlier studies.},
	Author = {Ashwell, K. W. and Holl{\"a}nder, H. and Streit, W. and Stone, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0952-5238},
	Journal = {Vis Neurosci},
	Keywords = {Embryo;Retina;Rats;Not relevant;Cell Count;Retinal Vessels;11 Glia;Animals, Newborn;Animals;Support, Non-U.S. Gov't;Phagocytosis},
	Medline = {91120244},
	Nlm_Id = {8809466},
	Number = {5},
	Organization = {Department of Anatomy, University of Sydney, NSW, Australia.},
	Pages = {437-48},
	Pubmed = {2487081},
	Title = {The appearance and distribution of microglia in the developing retina of the rat},
	Uuid = {5A1DCF21-9860-43D5-A09B-3869D4B22AF1},
	Volume = {2},
	Year = {1989}}

@article{Ashwood-Smith:1985,
	Abstract = {Cryopreservation of chinese hamster ovary cells in tissue culture with either glycerol or dimethyl sulfoxide did not result in chromosome damage as measured by the sister chromatid exchange technique. These results are consistent with earlier negative reports in which the freezing and thawing of mammalian cells did not increase the frequency of micronuclei. No increases in the spontaneous mutation rates of several bacterial strains at different genetic loci were observed during the course of a number of years of storage at -196 degrees C. It is concluded that standard cryopreservation procedures are without genetic hazards. However, the well-documented effects of dimethyl sulfoxide on cell fusion and gene differentiation suggest caution in its use as a cryopreservative for animal and human embryos. 0011-2240 Journal Article},
	Author = {Ashwood-Smith, M. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Cryobiology},
	Keywords = {Cricetulus;Ovary;Sister Chromatid Exchange/*drug effects;Salmonella typhimurium/cytology/drug effects/*genetics;Glycerol/*pharmacology;EE, DMSO, abstr;Tissue Preservation/*methods;Female;Cell Line;08 Aberrant cell cycle;Escherichia coli/cytology/drug effects/*genetics;Dimethyl Sulfoxide/*pharmacology;Animals;Support, Non-U.S. Gov't;Hamsters;Freezing;*Mutation},
	Number = {5},
	Pages = {427-33},
	Pubmed = {3902368},
	Title = {Genetic damage is not produced by normal cryopreservation procedures involving either glycerol or dimethyl sulfoxide: a cautionary note, however, on possible effects of dimethyl sulfoxide},
	Uuid = {8B040C13-8DE2-4442-A82F-5ECE2DCDAF4D},
	Volume = {22},
	Year = {1985},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3902368}}

@article{Askovic:2001,
	Abstract = {The chimeric murine oncornavirus FrCas(E) causes a rapidly progressive paralytic disease associated with spongiform neurodegeneration throughout the neuroaxis. Neurovirulence is determined by the sequence of the viral envelope gene and by the capacity of the virus to infect microglia. The neurocytopathic effect of this virus appears to be indirect, since the cells which degenerate are not infected. In the present study we have examined the possible role of inflammatory responses in this disease and have used as a control the virus F43. F43 is an highly neuroinvasive but avirulent virus which differs from FrCas(E) only in 3' pol and env sequences. Like FrCas(E), F43 infects large numbers of microglial cells, but it does not induce spongiform neurodegeneration. RNAase protection assays were used to detect differential expression of genes encoding a variety of cytokines, chemokines, and inflammatory cell-specific markers. Tumor necrosis factor alpha (TNF-alpha) and TNF-beta mRNAs were upregulated in advanced stages of disease but not early, even in regions with prominent spongiosis. Surprisingly there was no evidence for upregulation of the cytokines interleukin-1 alpha (IL-1 alpha), IL-1 beta, and IL-6 or of the microglial marker F4/80 at any stage of this disease. In contrast, increased levels of the beta-chemokines MIP-1 alpha and -beta were seen early in the disease and were concentrated in regions of the brain rich in spongiosis, and the magnitude of responses was similar to that observed in the brains of mice injected with the glutamatergic neurotoxin ibotenic acid. MIP-1alpha and MIP-1beta mRNAs were also upregulated in F43-inoculated mice, but the responses were three- to fivefold lower and occurred later in the course of infection than was observed in FrCas(E)-inoculated mice. These results suggest that the robust increase in expression of MIP-1 alpha and MIP-1 beta in the brain represents a correlate of neurovirulence in this disease, whereas the TNF responses are likely secondary events.},
	Author = {Askovic, S. and Favara, C. and McAtee, F. J. and Portis, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Retroviridae Infections;Chemokines, CC;Virulence;Macrophage Inflammatory Protein-1;Ibotenic Acid;Neurodegenerative Diseases;Immunohistochemistry;Inflammation;Retroviridae;Not relevant;11 Glia;Cell Death;RNA, Messenger;Brain;Animals;Mice;Neurons},
	Medline = {21126391},
	Month = {3},
	Nlm_Id = {0113724},
	Number = {6},
	Organization = {Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840, USA.},
	Pages = {2665-74},
	Pubmed = {11222690},
	Title = {Increased expression of MIP-1 alpha and MIP-1 beta mRNAs in the brain correlates spatially and temporally with the spongiform neurodegeneration induced by a murine oncornavirus},
	Uuid = {D3976495-DAC1-4C98-84D8-3F35CEEE9655},
	Volume = {75},
	Year = {2001},
	url = {papers/Askovic_JVirol2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.75.6.2665-2674.2001}}

@article{Athanassakis:2002,
	Abstract = {The development, growth and regeneration of nerve cells remain an unresolved issue. The up-to-date reported brain repair mechanisms are numerous and evidence suggests that, apart from the required trophism, tropism, microenvironment and specificity of the brain, a plethora of chemical, physiological and immunological compounds can contribute to such events. Among these compounds, we concentrated our interest on L- carnitine (L-Cn), which regulates the beta-oxidation of long chain fatty acids necessary for brain development, myelinization and growth. In contrast to fetal brain cells that grow easily in culture, adult brain cells show limited neurogenesis. Here, using adult brain cells from experimental mice, we show that although L-Cn does not improve their proliferative activity in short-term cultures, it accelerates the growth and differentiation of neurons, astrocytes, oligodendrocytes and ependymal cells from neurospheres in long-term cultures. Thus, the formation of a confluent neural network requires a 2-month period in culture. These observations provide new insights for in vivo use of L- Cn to support brain cell development in cases of injury or brain degenerative diseases.},
	Author = {Athanassakis, I. and Zarifi, I. and Evangeliou, A. and Vassiliadis, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Brain Res},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {1-2},
	Organization = {Department of Biology, University of Crete, P.O. Box 2208, 714-09, Crete, Heraklion, Greece},
	Pages = {70-8.},
	Title = {L-Carnitine accelerates the in vitro regeneration of neural network from adult murine brain cells},
	Uuid = {9513C52D-4A71-4829-89F2-EAFEB96F0758},
	Volume = {932},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11911863}}

@article{Awasaki:2004,
	Abstract = {BACKGROUND: Axon pruning is involved in establishment and maintenance of functional neural circuits. During metamorphosis of Drosophila, selective pruning of larval axons is developmentally regulated by ecdysone and caused by local axon degeneration. Previous studies have revealed intrinsic molecular and cellular mechanisms that trigger this pruning process, but how pruning is accomplished remains essentially unknown. RESULTS: Detailed analysis of morphological changes in the axon branches of Drosophila mushroom body (MB) neurons revealed that during early pupal stages, clusters of neighboring varicosities, each of which belongs to different axons, disappear simultaneously shortly before the onset of local axon degeneration. At this stage, bundles of axon branches are infiltrated by the processes of surrounding glia. These processes engulf clusters of varicosities and accumulate intracellular degradative compartments. Selective inhibition of cellular functions, including endocytosis, in glial cells via the temperature-sensitive allele of shibire both suppresses glial infiltration and varicosity elimination and induces a severe delay in axon pruning. Selective inhibition of ecdysone receptors in the MB neurons severely suppressed not only axon pruning but also the infiltration and engulfing action of the surrounding glia. CONCLUSIONS: These findings strongly suggest that glial cells are extrinsically activated by ecdysone-stimulated MB neurons. These glial cells infiltrate the mass of axon branches to eliminate varicosities and break down axon branches actively rather than just scavenging already-degraded debris. We therefore propose that neuron-glia interaction is essential for the precisely coordinated axon-pruning process during Drosophila metamorphosis.},
	Author = {Awasaki, Takeshi and Ito, Kei},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {Ecdysone;Nerve Degeneration;Motor Neurons, Gamma;Pupa;Animals;Mushroom Bodies;Comparative Study;Dynamins;Axons;Alleles;Endocytosis;Neuroglia;Receptors, Steroid;Metamorphosis, Biological;Drosophila;Immunohistochemistry;24 Pubmed search results 2008;Gene Expression;Drosophila Proteins;Research Support, Non-U.S. Gov't},
	Month = {4},
	Nlm_Id = {9107782},
	Number = {8},
	Organization = {Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan. awasaki\@iam.u-tokyo.ac.jp},
	Pages = {668-77},
	Pii = {S0960982204002544},
	Pubmed = {15084281},
	Title = {Engulfing action of glial cells is required for programmed axon pruning during Drosophila metamorphosis},
	Uuid = {534123D7-00AB-11DB-9E68-000D9346EC2A},
	Volume = {14},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2004.04.001}}

@article{Awasaki:2006,
	Abstract = {Axon pruning is a common phenomenon in neural circuit development. Previous studies demonstrate that the engulfing action of glial cells is essential in this process. The underlying molecular mechanisms, however, remain unknown. We show that draper (drpr) and ced-6, which are essential for the clearance of apoptotic cells in C. elegans, function in the glial engulfment of larval axons during Drosophila metamorphosis. The drpr mutation and glia-specific knockdown of drpr and ced-6 by RNA interference suppress glial engulfment, resulting in the inhibition of axon pruning. drpr and ced-6 interact genetically in the glial action. Disruption of the microtubule cytoskeleton in the axons to be pruned occurs via ecdysone signaling, independent of glial engulfment. These findings suggest that glial cells engulf degenerating axons through drpr and ced-6. We propose that apoptotic cells and degenerating axons of living neurons are removed by a similar molecular mechanism.},
	Author = {Awasaki, Takeshi and Tatsumi, Ryoko and Takahashi, Kuniaki and Arai, Kunizo and Nakanishi, Yoshinobu and Ueda, Ryu and Ito, Kei},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Animals;Gene Expression Regulation, Developmental;Rats;10 Structural plasticity;Phosphoproteins;Apoptosis;Axons;Animals, Genetically Modified;comparative study ;research support, non-u.s. gov't ;Nerve Net;Drosophila;Metamorphosis, Biological;Caenorhabditis elegans Proteins;24 Pubmed search results 2008;Membrane Proteins;Drosophila Proteins},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan. takeshi.awasaki\@umassmed.edu},
	Pages = {855-67},
	Pii = {S0896-6273(06)00318-7},
	Pubmed = {16772168},
	Title = {Essential role of the apoptotic cell engulfment genes draper and ced-6 in programmed axon pruning during Drosophila metamorphosis},
	Uuid = {F0D360F1-DAA9-4631-97E7-82FE383861DF},
	Volume = {50},
	Year = {2006},
	url = {papers/Awasaki_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.04.027}}

@article{Axelrod:2006,
	Abstract = {The evolution of cooperation has a well established theoretical framework based on game theory. This approach has made valuable contributions to a wide variety of disciplines, including political science, economics, and evolutionary biology. Existing cancer theory suggests that individual clones of cancer cells evolve independently from one another, acquiring all of the genetic traits or hallmarks necessary to form a malignant tumor. It is also now recognized that tumors are heterotypic, with cancer cells interacting with normal stromal cells within the tissue microenvironment, including endothelial, stromal, and nerve cells. This tumor cell-stromal cell interaction in itself is a form of commensalism, because it has been demonstrated that these nonmalignant cells support and even enable tumor growth. Here, we add to this theory by regarding tumor cells as game players whose interactions help to determine their Darwinian fitness. We marshal evidence that tumor cells overcome certain host defenses by means of diffusible products. Our original contribution is to raise the possibility that two nearby cells can protect each other from a set of host defenses that neither could survive alone. Cooperation can evolve as by-product mutualism among genetically diverse tumor cells. Our hypothesis supplements, but does not supplant, the traditional view of carcinogenesis in which one clonal population of cells develops all of the necessary genetic traits independently to form a tumor. Cooperation through the sharing of diffusible products raises new questions about tumorigenesis and has implications for understanding observed phenomena, designing new experiments, and developing new therapeutic approaches.},
	Author = {Axelrod, Robert and Axelrod, David E. and Pienta, Kenneth J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Models, Biological;Cell Transformation, Neoplastic;research support, n.i.h., extramural ;research support, non-u.s. gov't ;09 Evolutionary dynamics;22 Stem cells;research support, u.s. gov't, non-p.h.s. ;Evolution;Game Theory;Humans;Neoplasms;22 Cancer;review;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {7505876},
	Number = {36},
	Organization = {Gerald R. Ford School of Public Policy and Department of Political Science, University of Michigan, Ann Arbor, MI 48109, USA.},
	Pages = {13474-9},
	Pii = {0606053103},
	Pubmed = {16938860},
	Title = {Evolution of cooperation among tumor cells},
	Uuid = {7D593FF4-0149-4CD5-822A-B54591F4A19A},
	Volume = {103},
	Year = {2006},
	url = {papers/Axelrod_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0606053103}}

@article{Ayala:2007,
	Abstract = {The correct positioning of neurons during development--achieved through directed migration--is the basis for proper brain function. Several decades of research have yielded a comprehensive map illustrating the temporal and spatial events underlying neurogenesis and neuronal migration during development. The discovery of distinct migration modes and pathways has been accompanied by the identification of a large interwoven molecular network that transmits extracellular signals into the cell. Moreover, recent work has shed new light on how the cytoskeleton is regulated and coordinated at the molecular and cellular level to execute neuronal migration.},
	Author = {Ayala, Rams{\'e}s and Shu, Tianzhi and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Neurons;24 Pubmed search results 2008;10 Development;Cytoskeleton;Signal Transduction;Protein Kinases;Animals;Brain;Cell Movement;review;Humans},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Department of Brain and Cognitive Sciences, Picower Institute for Learning and Memory, RIKEN-MIT Neuroscience Research Center, Cambridge, MA 02139, USA.},
	Pages = {29-43},
	Pii = {S0092-8674(06)01648-5},
	Pubmed = {17218253},
	Title = {Trekking across the brain: the journey of neuronal migration},
	Uuid = {751C197D-0524-46E5-898B-CEF60525B832},
	Volume = {128},
	Year = {2007},
	url = {papers/Ayala_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.12.021}}

@article{Ayoub:2003,
	Abstract = {Microglia are the immune cells of the CNS. In the normal adult mammalian brain, the majority of these cells is quiescent and exhibits a ramified morphology. Microglia are perhaps best known for their swift transformation to an activated ameboid morphology in response to pathological insults. Here we have observed the responsiveness of these cells to events surrounding the normal activation of neurosecretory neurons in the hypothalamic supraoptic nucleus (SON), a well studied model of structural plasticity in the CNS. Neurons in the SON were activated by substituting 2\%saline for drinking water. Brain sections were collected from four experimental groups [controls (C), 2 d-dehydrated (2D), 7 d-dehydrated (D7), and 7 d-dehydrated/21 d-rehydrated animals (R21)] and stained with Isolectin-B4-HRP to visualize microglial cells. Based on morphological criteria, we quantified ramified, hypertrophied, and ameboid microglia using unbiased stereological techniques. Statistical analyses showed significant increases in the number of hypertrophied microglia in the D2 and D7 groups. Moreover, there was a significant increase in the number of ameboid microglia in the D7 group. No changes were seen across conditions in the number of ramified cells, nor did we observe any significant phenotypic changes in a control area of the cingulate gyrus. Hence, increased morphological diversity of microglia was found specifically in the SON and was reversible with the cessation of stimulation. These results indicate that phenotypic plasticity of microglia may be a feature of the normal structural remodeling that accompanies neuronal activation in addition to the activation that accompanies brain pathology.},
	Author = {Ayoub, Albert E. and Salm, A. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Gyrus Cinguli;Cell Size;Rats, Sprague-Dawley;Rats;Supraoptic Nucleus;Phenotype;Not relevant;11 Glia;Support, U.S. Gov't, Non-P.H.S.;Microglia;Male;Animals},
	Medline = {22825257},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {21},
	Organization = {Department of Neurobiology and Anatomy, West Virginia University School of Medicine, Morgantown, West Virginia 26506-9128, USA.},
	Pages = {7759-66},
	Pii = {23/21/7759},
	Pubmed = {12944504},
	Title = {Increased morphological diversity of microglia in the activated hypothalamic supraoptic nucleus},
	Uuid = {48B73CDB-CF44-4776-8417-86AC5EF30EBC},
	Volume = {23},
	Year = {2003},
	url = {papers/Ayoub_JNeurosci2003.pdf}}

@article{Azzam:2004,
	Abstract = {Budding yeast protein phosphatase Cdc14 is sequestered in the nucleolus in an inactive state during interphase by the anchor protein Net1. Upon entry into anaphase, the Cdc14 early anaphase release (FEAR) network initiates dispersal of active Cdc14 throughout the cell. We report that the FEARnetwork promotes phosphorylation of Net1 by cyclin-dependent kinase (Cdk) complexed with cyclin B1 or cyclin B2. These phosphorylations appear to be required for FEAR and sustain the proper timing of late mitotic events. Thus, a regulatory circuit exists to ensure that the arbiter of the mitotic state, Cdk, sets in motion events that culminate in exit from mitosis.},
	Author = {Azzam, Ramzi and Chen, Susan L. and Shou, Wenying and Mah, Angie S. and Alexandru, Gabriela and Nasmyth, Kim and Annan, Roland S. and Carr, Steven A. and Deshaies, Raymond J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:41 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {10 Development;Cell Cycle Proteins;Phosphorylation;DNA, Ribosomal;Recombinant Proteins;Metaphase;Mitosis;Mutation;Protein Kinases;Meiosis;Cyclin B;Support, Non-U.S. Gov't;Saccharomyces cerevisiae Proteins;Saccharomyces cerevisiae;Cell Nucleolus;Support, U.S. Gov't, P.H.S.;Protein-Tyrosine-Phosphatase;Cyclin-Dependent Kinases;Anaphase;Nuclear Proteins},
	Month = {7},
	Nlm_Id = {0404511},
	Number = {5683},
	Organization = {Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.},
	Pages = {516-9},
	Pii = {305/5683/516},
	Pubmed = {15273393},
	Title = {Phosphorylation by cyclin B-Cdk underlies release of mitotic exit activator Cdc14 from the nucleolus},
	Uuid = {9BA0C2A1-58AF-4A7F-88CE-5838C67360F5},
	Volume = {305},
	Year = {2004},
	url = {papers/Azzam_Science2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1099402}}

@article{Baba:1997,
	Abstract = {In the main olfactory bulb, neurons are arranged strategically in distinct layers among which translaminar synaptic transmission can be made from the superficial, sensory to the deep, output layers that account for the processing of olfactory information. To search for stimulus-transcription coupling thought to be operated differentially in several cell types, c-Jun expression was examined immunohistochemically in rat olfactory bulb following 30-min odor stimulation with acetic acid and 1-butanol. c-Jun was rapidly induced in neuronal cell nuclei belonging to periglomerular, tufted, mitral and granule cells. The disappearance of c-Jun, however, differed between each cell type. In the glomerular layer, the glomeruli composed of c- Jun-expressing periglomerular cells were seen. Different odors led to labeling of different sets of glomeruli. The labeled periglomerular cells disappeared within 2 h. In all the deeper layers, however, a rather homogeneous label was noted for the tufted, mitral and granule cells present throughout the olfactory bulb, regardless of the difference in odor. In tufted and mitral cells, the c-Jun expression persisted for 4 days after odor stimulation. In the granule cell layer, numerous granule cells increased c-Jun immunoreactivity which lasted for 1 day following odor application. In control rats which were given clean air, the basal amount of c-Jun expression was seen confined to scattered granule cells. The results suggest that c-Jun is expressed in a variety of odorant-stimulated bulb neurons with a time course being dependent on cell type.},
	Author = {Baba, K. and Ikeda, M. and Houtani, T. and Nakagawa, H. and Ueyama, T. and Sato, K. and Sakuma, S. and Yamashita, T. and Tsukahara, Y. and Sugimoto, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {Brain Res},
	Keywords = {Tissue Distribution;Rats, Sprague-Dawley;Neurons, Afferent/drug effects/*metabolism;Olfactory Bulb/cytology/drug effects/*metabolism;Proto-Oncogene Proteins c-jun/*metabolism;Rats;1-Butanol/pharmacology;*Odors;Stimulation, Chemical;Acetic Acid/pharmacology;Animal;I abstr;Support, Non-U.S. Gov't;Male;13 Olfactory bulb anatomy},
	Number = {1-2},
	Organization = {Department of Anatomy, Kansai Medical University, Moriguchi, Osaka, Japan.},
	Pages = {142-8.},
	Title = {Odor exposure reveals non-uniform expression profiles of c-Jun protein in rat olfactory bulb neurons},
	Uuid = {1B19770D-1234-4C85-9BCC-22DAF371525D},
	Volume = {774},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9452202}}

@article{Baba:2004,
	Abstract = {BACKGROUND/AIMS: Recently, several cells found within the liver have been reported to derive from bone marrow (BM). This study sought to examine the commitment of BM cells to hepatic stellate cell (HSC) lineage in mouse liver. METHODS: We transplanted BM cells from green fluorescent protein (GFP) transgenic mice into age-matched C57BL/J mice. Hepatic nonparenchymal cells were isolated from the livers of BM-transplanted mice using density gradient centrifugation with Nycodenz. The expression of lineage markers by the isolated cells was evaluated by RT-PCR and immunostaining. We then examined the histology of liver tissues obtained from BM-transplanted mice with and without carbon tetrachloride-induced injury. RESULTS: GFP-expressing cells with intracytoplasmic lipid droplets comprised 33.4 +/- 2.3\%of the cells isolated by density gradient centrifugation. These cells expressed the HSC lineage markers, such as desmin and glial fibrillary acidic protein (GFAP), by both RT-PCR and immunostaining. During a 7-day culture, GFP-positive cells began to express alpha-smooth muscle actin, a marker of activated HSC. In the liver of BM-transplanted mice, GFP-positive nonparenchymal cells expressed GFAP and extended their process around hepatocytes. Upon liver injury, these cells also co-expressed desmin and alpha-smooth muscle actin. CONCLUSIONS: Nonparenchymal cells, derived from transplanted BM, acquired HSC characteristics in both quiescent and activated states.},
	Author = {Baba, Shinji and Fujii, Hideaki and Hirose, Tetsuro and Yasuchika, Kentaro and Azuma, Hisaya and Hoppo, Toshitaka and Naito, Masato and Machimoto, Takafumi and Ikai, Iwao},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:26 -0400},
	Issn = {0168-8278},
	Journal = {J Hepatol},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Cells, Cultured;Bone Marrow Transplantation;Mice, Transgenic;Liver;Mice, Inbred C57BL;11 Glia;Liver Diseases;Reverse Transcriptase Polymerase Chain Reaction;Green Fluorescent Proteins;Bone Marrow Cells;Cell Lineage;Liver Regeneration;Mice;Genes, Reporter;Luminescent Proteins;Immunohistochemistry;Carbon Tetrachloride},
	Month = {2},
	Nlm_Id = {8503886},
	Number = {2},
	Organization = {Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto City 606-8507, Japan. barbee\@kuhp.kyoto-u.ac.jp},
	Pages = {255-60},
	Pii = {S0168827803005312},
	Pubmed = {14739096},
	Title = {Commitment of bone marrow cells to hepatic stellate cells in mouse},
	Uuid = {12C9C747-8495-4A26-9349-E02B75641BE6},
	Volume = {40},
	Year = {2004}}

@article{Bae:2005,
	Abstract = {After transplantation, adult bone marrow-derived mesenchymal stem cells (BM-MSCs) may undergo transdifferentiation and/or cell fusion in response to new environments. However, the mechanism(s) that govern these cell fate switches remain unknown. Here we demonstrate that the pathology associated with murine Niemann- Pick disease type C (NP-C) cerebellum augments the ability of BM-MSCs to fuse with Purkinje neurons. The results suggest that the degenerative microenvironment of Purkinje neurons in the NP-C cerebellum modulates the cell fate switch of BM-MSCs via cell fusion.},
	Author = {Bae, and Furuya, and Shinoda, and Endo, and Schuchman, and Hirabayashi, and Jin,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1043-0342},
	Journal = {Hum Gene Ther},
	Keywords = {11 Glia},
	Month = {6},
	Nlm_Id = {9008950},
	Notes = {cell fusion, degeneration, dendrites neurons},
	Organization = {College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, South Korea.},
	Pubmed = {16029138},
	Title = {Neurodegeneration Augments the Ability of Bone Marrow-Derived Mesenchymal Stem Cells to Fuse with Purkinje Neurons in Niemann-Pick Type C Mice},
	Uuid = {6B4B22DB-B49D-4217-953F-25612CD7A527},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/hum.2005.16.ft-97}}

@article{Bagri:2002,
	Abstract = {The dentate gyrus is the primary afferent pathway into the hippocampus, but there is little information concerning the molecular influences that govern its formation. In particular, the control of migration and cell positioning of dentate granule cells is not clear. We have characterized more fully the timing and route of granule cell migration during embryogenesis using in utero retroviral injections. Using this information, we developed an in vitro assay that faithfully recapitulates important events in dentate gyrus morphogenesis. In searching for candidate ligands that may regulate dentate granule cell migration, we found that SDF1, a chemokine that regulates cerebellar and leukocyte migration, and its receptor CXCR4 are expressed in patterns that suggest a role in dentate granule cell migration. Furthermore, CXCR4 mutant mice have a defect in granule cell position. Ectopic expression of SDF1 in our explant assay showed that it directly regulates dentate granule cell migration. Our study shows that a chemokine is necessary for the normal development of the dentate gyrus, a forebrain structure crucial for learning and memory.},
	Author = {Bagri, Anil and Gurney, Theresa and He, Xiaoping and Zou, Yong-Rui R. and Littman, Dan R. and Tessier-Lavigne, Marc and Pleasure, Samuel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Organ Culture Techniques;Gestational Age;Stromal Cells;Mice, Knockout;Research Support, Non-U.S. Gov't;Embryonic and Fetal Development;Chemokines, CXC;Female;Dentate Gyrus;Research Support, U.S. Gov't, P.H.S.;Pregnancy;Morphogenesis;Mice;Cell Movement;Animals;Neurons;Receptors, CXCR4},
	Medline = {22170647},
	Month = {9},
	Nlm_Id = {8701744},
	Number = {18},
	Organization = {Neurodevelopmental Disorders Laboratory, Department of Neurology, Program in Neuroscience, University of California, San Francisco, CA 94143-0435, USA.},
	Pages = {4249-60},
	Pubmed = {12183377},
	Title = {The chemokine SDF1 regulates migration of dentate granule cells},
	Uuid = {2415FE0C-7114-11DA-9A4D-000D9346EC2A},
	Volume = {129},
	Year = {2002},
	url = {papers/Bagri_Development2002.pdf}}

@article{Bai:1996,
	Abstract = {The colchicine analog 3-chloroacetyl-3-demthylthio-colchicine (3CTC) is a competitive inhibitor of colchicine binding to tubulin, binds to tubulin at 37 degrees C, but not at 0 degree C, and covalently reacts with beta-tubulin at 37 degree C, but not at 0 degree C, in a reaction inhibited by colchicine site drugs. The approximate intramolecular distance between the oxygen at position C-3 in 3CTC and the chlorine atom of the 3-chloroacetyl group is 3 A. using decylagarose chromatography, we purified beta-tubulin that had reacted with 3-(chloromethyl-[14C] Carbonyl)-3- demethylthiocolchicine ([14C]3CTC). This beta-tubulin that had reacted with 3-(chloromethyl-[14C]carbonyl)- 3-demethythiocolchicine ([14C]3CTC). This beta-tubulin was digested with formic acid, cyanogen bromide, endoproteinase Glu-C, or endoproteinase Lys-C, and the radio-labeled peptide(s) were isolated. The sequences of these peptides indicated that as much as 90\%of the covalent reaction between the [14C]3CTC and beta-tubulin occurred at cysteine 354. This finding indicates that the C-3 oxygen atom of colchicinoids is within 3 A of the sulfur atom of the Cys-354 residue, suggests that the colchicine A ring lies between Cys-354 and Cys-239, based on the known 9 A distance between these residues, and may indicate that the tropolone C ring lies between the peptide region containing Cys-239 and the amino-terminal beta-tubulin sequence, based on the labeling pattern observed following direct photoactivation of tubulin-bound colchicine. 0021-9258 Journal Article},
	Author = {Bai, R. and Pei, X. F. and Boye, O. and Getahun, Z. and Grover, S. and Bekisz, J. and Nguyen, N. Y. and Brossi, A. and Hamel, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:50 -0400},
	Journal = {J Biol Chem},
	Keywords = {Protein Binding;Colchicine/analogs &derivatives/antagonists &;Tubulin/chemistry/*metabolism;EE, T abstr;inhibitors/*metabolism/pharmacology;Cyanogen Bromide;Molecular Sequence Data;08 Aberrant cell cycle;Cysteine/*metabolism;Amino Acid Sequence;Cattle;Chromatography, High Pressure Liquid;Animals},
	Number = {21},
	Organization = {Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.},
	Pages = {12639-45},
	Pubmed = {8647876},
	Title = {Identification of cysteine 354 of beta-tubulin as part of the binding site for the A ring of colchicine},
	Uuid = {DA9F68E4-B3C8-4299-B2D2-0B9261BB6084},
	Volume = {271},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8647876}}

@article{Baker:2006,
	Abstract = {The MRL mouse is unique in its capacity for regenerative healing of wounds. This regenerative ability includes complete closure, with little scarring, of wounds to the ear pinna and repair of cardiac muscle, without fibrosis, following cryoinjury. Here, we examine whether neurogenic zones within the MRL brain show enhanced regenerative capacity. The largest neurogenic zone in the adult brain, the subventricular zone (SVZ), lies adjacent to the lateral wall of the lateral ventricle and is responsible for replacement of interneuron populations within the olfactory bulb. Initial gross observation of the anterior forebrain in MRL mice revealed enlarged lateral ventricles; however, little neurodegeneration was detected within the SVZ or surrounding tissues. Instead, increased proliferation within the SVZ was observed, based on incorporation of the thymidine analogue bromodeoxyuridine. Closer examination using electron microscopy revealed that a significant number of SVZ astrocytes interpolated within the ependyma and established contact with the ventricle. In addition, subependymal, protuberant nests of cells, consisting primarily of neuroblasts, were found along the anterior SVZ of MRL mice. Whole mounts of the lateral wall of the lateral ventricle stained for the neuroblast marker doublecortin revealed normal formation of chains of migratory neuroblasts along the entire wall and introduction of enhanced green fluorescent protein-tagged retrovirus into the lateral ventricles confirmed that newly generated neuroblasts were able to track into the olfactory bulb.},
	Author = {Baker, Kasey L. and Daniels, Stephen B. and Lennington, Jessica B. and Lardaro, Thomas and Czap, Alexandra and Notti, Ryan Q. and Cooper, Oliver and Isacson, Ole and Frasca, Salvatore and Conover, Joanne C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Microscopy, Electron, Transmission;Neurons;02 Adult neurogenesis migration;24 Pubmed search results 2008;Wound Healing;Cell Proliferation;research support, non-u.s. gov't ;Astrocytes;Immunohistochemistry;Stem Cells;Cell Death;Animals;Brain;Cell Movement;Male;Mice},
	Month = {10},
	Nlm_Id = {0406041},
	Number = {6},
	Organization = {Center for Regenerative Biology, University of Connecticut, Storrs, 06269, USA.},
	Pages = {747-61},
	Pubmed = {16927265},
	Title = {Neuroblast protuberances in the subventricular zone of the regenerative MRL/MpJ mouse},
	Uuid = {128FCCB8-33DA-4709-949A-0B985039DF87},
	Volume = {498},
	Year = {2006},
	url = {papers/Baker_JCompNeurol2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.21090}}

@article{Baker:2001,
	Abstract = {A possible source for transplantable neurons in Parkinson's disease are adult olfactory bulb (OB) dopamine (DA) progenitors that originate in the anterior subventricular zone and reach the OB through the rostral migratory stream. We used adult transgenic mice expressing a lacZ reporter directed by an 8.9 kb tyrosine hydroxylase (TH) promoter to investigate the course of DAergic differentiation. Parallel transgene and intrinsic TH mRNA expression occurred during migration of DA interneurons through the mitral and superficial granule cell layers before these cells reached their final periglomerular position. Differential transgene and calcium-calmodulin-dependent protein kinase IV expression distinguished two nonoverlapping populations of interneurons. Transgenic mice carrying a TH8.9kb/lacZ construct with a mutant AP-1 site demonstrated that this element confers OB DA-specific TH gene regulation. These results indicate that DA phenotypic determination is specific to a subset of mobile OB progenitors.},
	Author = {Baker, H. and Liu, N. and Chun, H. S. and Saino, S. and Berlin, R. and Volpe, B. and Son, J. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {J Neurosci},
	Keywords = {13 Olfactory bulb anatomy;I both},
	Number = {21},
	Organization = {Burke Medical Research Institute, Weill Medical College, Cornell University, White Plains, New York 10605.},
	Pages = {8505-13.},
	Title = {Phenotypic differentiation during migration of dopaminergic progenitor cells to the olfactory bulb},
	Uuid = {5F27B1F2-E14D-4C82-9606-52832F65528C},
	Volume = {21},
	Year = {2001},
	url = {papers/Baker_JNeurosci2001.pdf}}

@article{Balci:2007,
	Abstract = {Periventricular nodular heterotopia (PNH) is a rare neuronal migration disorder in which immature neurons fail to undergo a directed migration from the ventricular and subventricular zones to the cerebral cortex. Classic PNH occurs predominantly in females and is associated with periods of epilepsy and near-normal intelligence. One gene associated with PNH was mapped to chromosome Xq28. PNH with learning disability is reported in 15 male patients with several syndromes and various congenital abnormalities such as craniosynostosis, frontonasal malformation, and agenesis of the corpus callosum. We present a 26-year-old male patient who was followed up with the diagnosis of epilepsy from the age of 1 year. Additionally the patient had severe learning disability, obesity, and hypogonadism. Imaging of his brain demonstrated PNH. Klinefelter syndrome was clinically suspected, and analysis of his chromosomes revealed a karyotype 46,XY,der(19)t(X;19) (q11.1-11.2;p13.3). Molecular techniques, such as subtelomere-specific fluorescent in-situ hybridization and multicolour banding, were also used. The same translocation was demonstrated in his mother and his maternal grandmother. This family might help to explain the gene localization of X-linked recessive PNH. In our patient, PNH is associated with familial (X;19) translocation. To our knowledge, this unique combination has not been reported in the medical literature.},
	Author = {Balci, Sevim and Unal, Aysun and Engiz, Ozlem and Aktas, Dilek and Liehr, Thomas and Gross, Madelaine and Mrasek, Kristin and Saygi, Serap},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0012-1622},
	Journal = {Dev Med Child Neurol},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008;21 Epilepsy},
	Month = {3},
	Nlm_Id = {0006761},
	Number = {3},
	Organization = {Department of Clinical Genetics, Faculty of Medicine, Hacettepe University, Ankara, Turkey.},
	Pages = {219-24},
	Pii = {DMCN219},
	Pubmed = {17355480},
	Title = {Bilateral periventricular nodular heterotopia, severe learning disability, and epilepsy in a male patient with 46,XY,der(19)t(X;19) (q11.1-11.2;p13.3)},
	Uuid = {FFFFF166-7DBB-4990-874D-9603CFD4E3A1},
	Volume = {49},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1469-8749.2007.00219.x}}

@article{Ballas:2005,
	Abstract = {Regulation of neuronal gene expression is critical to central nervous system development. Here, we show that REST regulates the transitions from pluripotent to neural stem/progenitor cell and from progenitor to mature neuron. In the transition to progenitor cell, REST is degraded to levels just sufficient to maintain neuronal gene chromatin in an inactive state that is nonetheless poised for expression. As progenitors differentiate into neurons, REST and its co-repressors dissociate from the RE1 site, triggering activation of neuronal genes. In some genes, the level of expression is adjusted further in neurons by CoREST/MeCP2 repressor complexes that remain bound to a site of methylated DNA distinct from the RE1 site. Expression profiling based on this mechanism indicates that REST defines a gene set subject to plasticity in mature neurons. Thus, a multistage repressor mechanism controls the orderly expression of genes during development while still permitting fine tuning in response to specific stimuli.},
	Author = {Ballas, Nurit and Grunseich, Christopher and Lu, Diane D. and Speh, Joan C. and Mandel, Gail},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Research Support, Non-U.S. Gov't;Cell Differentiation;Animals;Genes, Regulator;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Chromatin;Neuronal Plasticity;Cells, Cultured;Nervous System;Transcription Factors;Research Support, U.S. Gov't, P.H.S.;Neurons;Pluripotent Stem Cells;Mice;24 Pubmed search results 2008;Nerve Tissue Proteins;Repressor Proteins;DNA Methylation},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {4},
	Organization = {Howard Hughes Medical Institute, Dept. of Neurology and Behavior, The State University of New York at Stony Brook, Stony Brook, NY 11794, USA. nballas\@notes.cc.sunysb.edu},
	Pages = {645-57},
	Pii = {S0092-8674(05)00285-0},
	Pubmed = {15907476},
	Title = {REST and its corepressors mediate plasticity of neuronal gene chromatin throughout neurogenesis},
	Uuid = {147958CE-0275-455F-ABF0-61E66EF02520},
	Volume = {121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.03.013}}

@article{Baltimore:1971,
	Author = {Baltimore, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0028-4793},
	Journal = {N Engl J Med},
	Keywords = {15 Retrovirus mechanism;RNA, Neoplasm;24 Pubmed search results 2008;Virus Replication;Leukemia;Oncogenic Viruses;Histocytochemistry;Cell-Free System;Humans;RNA, Viral;RNA Viruses;DNA Nucleotidyltransferases;Animals},
	Medline = {71079019},
	Month = {2},
	Nlm_Id = {0255562},
	Number = {5},
	Pages = {273-5},
	Pubmed = {5539352},
	Title = {Reversal of information flow in the growth of RNA tumor viruses},
	Uuid = {FC43FEF6-4D24-4C15-A6B2-7E166BDB1D99},
	Volume = {284},
	Year = {1971}}

@article{Banati:1994,
	Abstract = {The study of microglial cell biology has become the key to understanding the brain's fundamental tissue reactions as well as the cellular mechanisms underlying CNS disease. This article focuses on glial-neuronal interactions with special reference to human pathology. Three important areas of brain pathology are critically reviewed: multiple sclerosis and CNS inflammation, the brain in AIDS and opportunistic infections, and neurodegenerative disorders. Although microglial cytotoxicity may cause bystander damage, e.g. in ischemia, there is little evidence to support the view that microglial activation per se is pathogenic. Results suggesting that one important normal function of microglia is to protect the integrity of the central nervous system are discussed. The concept is proposed that microglia function as a highly developed guardian to the CNS.},
	Author = {Banati, R. B. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Central Nervous System;Inflammation;Cell Survival;11 Glia;Microglia;Animals;Humans;review},
	Medline = {95220173},
	Nlm_Id = {7809375},
	Number = {3-4},
	Organization = {Department of Neuromorphology, Max-Planck-Institute of Psychiatry, Martinsried, Germany.},
	Pages = {114-27},
	Pubmed = {7705219},
	Title = {Surveillance, intervention and cytotoxicity: is there a protective role of microglia?},
	Uuid = {5989FFDF-D935-4DD5-8B7A-9AF082EC85B9},
	Volume = {16},
	Year = {1994}}

@article{Banfield:2003,
	Abstract = {The transsynaptic retrograde transport of the pseudorabies virus Bartha (PRV-Bartha) strain has become an important neuroanatomical tract-tracing technique. Recently, dual viral transneuronal labeling has been introduced by employing recombinant strains of PRV-Bartha engineered to express different reporter proteins. Dual viral transsynaptic tracing has the potential of becoming an extremely powerful method for defining connections of single neurons to multiple neural circuits in the brain. However, the present use of recombinant strains of PRV expressing different reporters that are driven by different promoters, inserted in different regions of the viral genome, and detected by different methods limits the potential of these recombinant virus strains as useful reagents. We previously constructed and characterized PRV152, a PRV-Bartha derivative that expresses the enhanced green fluorescent protein. The development of a strain isogenic to PRV152 and differing only in the fluorescent reporter would have great utility for dual transsynaptic tracing. In this report, we describe the construction, characterization, and application of strain PRV614, a PRV-Bartha derivative expressing a novel monomeric red fluorescent protein, mRFP1. In contrast to viruses expressing DsRed and DsRed2, PRV614 displayed robust fluorescence both in cell culture and in vivo following transsynaptic transport through autonomic circuits afferent to the eye. Transneuronal retrograde dual PRV labeling has the potential to be a powerful addition to the neuroanatomical tools for investigation of neuronal circuits; the use of strain PRV614 in combination with strain PRV152 will eliminate many of the pitfalls associated with the presently used pairs of PRV recombinants. 0022-538x Journal Article},
	Author = {Banfield, B. W. and Kaufman, J. D. and Randall, J. A. and Pickard, G. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {J Virol},
	Keywords = {Suprachiasmatic Nucleus/virology;Rats;Cell Line;Ganglia, Spinal/virology;Herpesvirus 1, Suid/*physiology;Support, U.S. Gov't, P.H.S.;15 Retrovirus mechanism;J, T pdf;Luminescent Proteins/*metabolism;Animals;Support, Non-U.S. Gov't;Synapses/*virology},
	Number = {18},
	Organization = {Department of Microbiology, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Campus Box B175, Denver, CO 80262, USA. bruce.banfield\@uchsc.edu},
	Pages = {10106-12},
	Title = {Development of pseudorabies virus strains expressing red fluorescent proteins: new tools for multisynaptic labeling applications},
	Uuid = {04A30716-3DBD-41E6-B020-A9C693F8303D},
	Volume = {77},
	Year = {2003},
	url = {papers/Banfield_JVirol2003.pdf}}

@article{Bannert:2004,
	Abstract = {Retroelements constitute a large portion of our genomes. One class of these elements, the human endogenous retroviruses (HERVs), is comprised of remnants of ancient exogenous retroviruses that have gained access to the germ line. After integration, most proviruses have been the subject of numerous amplifications and have suffered extensive deletions and mutations. Nevertheless, HERV-derived transcripts and proteins have been detected in healthy and diseased human tissues, and HERV-K, the youngest, most conserved family, is able to form virus-like particles. Although it is generally accepted that the integration of retroelements can cause significant harm by disrupting or disregulating essential genes, the role of HERV expression in the etiology of malignancies and autoimmune and neurologic diseases remains controversial. In recent years, striking evidence has accumulated indicating that some proviral sequences and HERV proteins might even serve the needs of the host and are therefore under positive selection. The remarkable progress in the analysis of host genomes has brought to light the significant impact of HERVs and other retroelements on genetic variation, genome evolution, and gene regulation.},
	Author = {Bannert, Norbert and Kurth, Reinhard},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {15 ERVs retroelements;Endogenous Retroviruses;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Retroviridae Proteins;Microscopy, Electron;Evolution, Molecular;Genome, Human;Gene Expression;15 Retrovirus mechanism;Humans;Antibodies, Viral;Retroelements;Proviruses;review},
	Month = {10},
	Nlm_Id = {7505876},
	Organization = {Robert Koch-Institut, Nordufer 20, 13353 Berlin, Germany. bannertn\@rki.de},
	Pages = {14572-9},
	Pii = {0404838101},
	Pubmed = {15310846},
	Title = {Retroelements and the human genome: new perspectives on an old relation},
	Uuid = {C65C30C1-EE4E-11DA-8605-000D9346EC2A},
	Volume = {101 Suppl 2},
	Year = {2004},
	url = {papers/Bannert_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0404838101}}

@article{Barinaga:2003,
	Abstract = {1095-9203 Comment News},
	Author = {Barinaga, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Science},
	Keywords = {Cell Survival;Neurons/*physiology;Cell Differentiation;Human;Pregnancy;Olfactory Bulb/cytology/physiology;Animals;Rats;Memory;Stem Cells/physiology;Prolactin/*physiology;Female;Receptors, Prolactin/genetics/physiology;Brain/cytology/*physiology;Seasons;Male;Vocalization, Animal;Odors;01 Adult neurogenesis general;A;Dentate Gyrus/cytology/*physiology;Smell;*Learning;Songbirds/physiology;Mice;Cell Division},
	Number = {5603},
	Pages = {32-4},
	Pubmed = {12511626},
	Title = {Developmental biology. Newborn neurons search for meaning},
	Uuid = {F5C8F045-5D06-40A9-A504-B17FFECDBA5A},
	Volume = {299},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12511626}}

@article{Barker:1996,
	Abstract = {Grafts of embryonic ventral mesencephalic tissue placed in the striatum of 6-hydroxydopamine-lesioned rats survive, and make and receive connections to and from the host brain. The dopaminergic neurons of the graft can grow processes into the host brain, and thereby alleviate many of the behavioral deficits of this form of experimental Parkinson's disease. However, when examined some weeks after implantation, grafted substantia nigra only contains about 5\%of the expected complement of dopaminergic neurons. We have examined the time course of loss of grafted neurons. We find that the majority die during the first 7 days after transplantation. However, we have shown previously that three-dimensional cultures with the same dimensions as a graft, made of identical cell suspensions, have much better dopaminergic neuronal survival. There must, therefore, be features in the environment surrounding a graft that are toxic to dopaminergic neurons. A limiting factor in the efficacy of dopaminergic grafts is the small distance over which the neurons are able to grow neurites and form connections in the host brain. We find that the growth of neurites from dopaminergic neurons into the host striatum occurs in two phases. Neurites reach their maximum length within 7 days of transplantation, and this is followed by a much slower process of branch and terminal formation. Since axon growth in the adult brain may be inhibited by a number of factors associated with reactive gliosis, we have immunostained various ages of graft for vimentin, tenascin, chondroitin sulfate proteoglycan (CS-PG) using the CS56 antibody, the DSD-1 proteoglycan, and microglia using the OX-42 antibody. We have compared this staining with that surrounding a simple stab wound. Vimentin staining was initially seen in the graft and in astrocytes immediately surrounding it. By 7 weeks staining was restricted to a ring of astrocytes surrounding the graft. Tenascin, DSD-1, and CS-PG were initially seen in and around the grafts. By 7 weeks they had disappeared from grafts, but CS-PG and tenascin persisted in small amounts around stab wounds. In general, immunostaining of these molecules persisted longer around a stab lesion than around a graft. There was also an intense local microglial reaction surrounding both grafts and stab wounds which had largely resolved by 7 weeks.},
	Author = {Barker, R. A. and Dunnett, S. B. and Faissner, A. and Fawcett, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Dopamine;Animals;Corpus Striatum;Rats;review, tutorial;review;Female;Vimentin;Rats, Sprague-Dawley;Substantia Nigra;11 Glia;Fetal Tissue Transplantation;Time Factors;Support, Non-U.S. Gov't;Neurons;Tyrosine 3-Monooxygenase;Gliosis;Immunohistochemistry;Biological Markers;Cell Death},
	Medline = {96390697},
	Month = {9},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {MRC Cambridge Centre for Brain Repair, University of Cambridge, United Kingdom.},
	Pages = {79-93},
	Pii = {S0014488696901417},
	Pubmed = {8797670},
	Title = {The time course of loss of dopaminergic neurons and the gliotic reaction surrounding grafts of embryonic mesencephalon to the striatum},
	Uuid = {8570C54A-5A0B-4C76-873E-8A3395966092},
	Volume = {141},
	Year = {1996}}

@article{Barker:2005,
	Abstract = {Postnatal hippocampal neurogenesis in wild mammals may play an essential role in spatial memory. We compared two species that differ in their reliance on memory to locate stored food. Yellow-pine chipmunks use a single cache to store winter food; eastern gray squirrels use multiple storage sites. Gray squirrels had three times the density of proliferating cells in the dentate gyrus (determined by Ki-67 immunostaining) than that found in chipmunks, but similar density of young neurons (determined by doublecortin immunostaining). Three explanations may account for these results. First, the larger population of young cells in squirrels may increase the flexibility of the spatial memory system by providing a larger pool of cells from which new neurons can be recruited. Second, squirrels may have a more rapid cell turnover rate. Third, many young cells in the squirrels may mature into glia rather than neurons. The densities of young neurons were higher in juveniles than in adults of both species. The relationship between adult age and cell density was more complex than that has been found in captive populations. In adult squirrels, the density of proliferating cells decreased exponentially with age, whereas in adult chipmunks the density of young neurons decreased exponentially with age.},
	Author = {Barker, J. M. and Wojtowicz, J. M. and Boonstra, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1601-1848},
	Journal = {Genes Brain Behav},
	Keywords = {01 Adult neurogenesis general;06 Adult neurogenesis injury induced;delete_this;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {101129617},
	Number = {2},
	Organization = {Centre for the Neurobiology of Stress, Department of Physiology, and Centre for the Neurobiology of Stress, University of Toronto, Scarborough, Ontario, Canada.},
	Pages = {89-98},
	Pii = {GBB097},
	Pubmed = {15720405},
	Title = {Where's my dinner? Adult neurogenesis in free-living food-storing rodents},
	Uuid = {4D8F4EAC-6ED3-4478-AB1D-3192600984FE},
	Volume = {4},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1601-183X.2004.00097.x}}

@article{Barral-Moran:2003,
	Abstract = {Injury to the nervous system results in reactive astrogliosis that is a critical determinant of neuronal regeneration. To analyze glial responses to mechanical injury and the role of the polysialic neural cell adhesion molecule (PSA-NCAM) in this process, we established primary glia cultures from newborn rat cerebral cortex. Scratching a confluent monolayer of primary glial cells resulted in two major events: rapid migration of oligodendrocyte progenitor-like (O-2A) cells into the wounded area and development of polarized morphology of type 1 astrocytes at the wound edge. Migrating O-2A progenitors had a bipolar morphology and exhibited A2B5 and O4 immunolabeling. Once these cells were established inside the wounded area, they lost A2B5 immunoreactivity and differentiated into glial fibrillary acidic protein-positive astrocytes. Migrating O-2A cells expressed PSA-NCAM, but type 1 astrocytes at the wound edge did not. Treatment of wounded cultures with Endo-N, which specifically removes PSA from the surface of cells, resulted in a significant decrease in O-2A cell migration into the wounded area and completely blocked the wound closure. Video time-lapse analysis showed that, in the presence of Endo-N, O-2A cells remained motile and migrated short distances but did not move away from the monolayer. These results demonstrate that O-2A progenitors contribute to reactive astrogliosis in culture and that PSA-NCAM is involved in this process by regulating cell migration.},
	Author = {Barral-Moran, M-J J. and Calaora, V. and Vutskits, L. and Wang, C. and Zhang, H. and Durbec, P. and Rougon, G. and Kiss, J. Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Oligodendroglia;24 Pubmed search results 2008;Rats, Sprague-Dawley;Neuroglia;Research Support, Non-U.S. Gov't;Rats;Neural Cell Adhesion Molecule L1;Gliosis;Stem Cells;Cells, Cultured;Cell Movement;Cerebral Cortex;Animals;Sialic Acids},
	Medline = {22658406},
	Month = {6},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {Departamento de Ciencias Morfologicas, Facultad de Medicina, Universidad de Zaragoza, Zaragoza, Spain.},
	Pages = {679-90},
	Pubmed = {12774308},
	Title = {Oligodendrocyte progenitor migration in response to injury of glial monolayers requires the polysialic neural cell-adhesion molecule},
	Uuid = {C3CF6E92-7EC6-47A3-B8A5-13D6E448624E},
	Volume = {72},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10627}}

@article{Barres:1999,
	Author = {Barres, B. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Cell},
	Keywords = {02 Adult neurogenesis migration;Cell Differentiation;03 Adult neurogenesis progenitor source;Human;Neuroglia/*cytology;Animal;Neurons/*cytology;Brain/*cytology;BB abstr;Stem Cells/*cytology},
	Number = {6},
	Organization = {Stanford University School of Medicine, Department of Neurobiology, California 94305-5125, USA.},
	Pages = {667-70.},
	Title = {A new role for glia: generation of neurons!},
	Uuid = {8250E315-FE6F-45FD-985C-1F6372B3312A},
	Volume = {97},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10380916}}

@article{Barrett:1999,
	Author = {Barrett, L. B. and Logan, A. and Berry, M. and Ying, W. and Gonzalez, A. M. and Baird, A. and Seymour, L. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0300-5127},
	Journal = {Biochem Soc Trans},
	Keywords = {Hamsters;Cholera Toxin;Animals;Gene Targeting;Polylysine;Rats;Transfection;Nervous System Diseases;11 Glia;PC12 Cells;Green Fluorescent Proteins;Genetic Vectors;Cell Line;Gene Therapy;DNA, Recombinant;Neurons;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {20288925},
	Month = {12},
	Nlm_Id = {7506897},
	Number = {6},
	Organization = {CRC Institute for Cancer Studies, University of Birmingham, Edgbaston, U.K.},
	Pages = {851-7},
	Pubmed = {10830116},
	Title = {Targeted transfection of neuronal cells using a poly(D-lysine)-cholera-toxin b chain conjugate},
	Uuid = {2C7109A5-7244-4207-9C67-21DE14D57DA6},
	Volume = {27},
	Year = {1999}}

@article{Barrette:2000,
	Abstract = {The low levels of transduction of human hematopoietic stem cells (HSCs) with Moloney murine leukemia virus (MLV) vectors have been an obstacle to gene therapy for hematopoietic diseases. It has been demonstrated that lentivirus vectors are more efficient than MLV vectors at transducing nondividing cell lines as well as human CD34(+) cells and severe combined immunodeficiency disease repopulating cells. We compared transduction of cell lines and Lin(-) bone marrow cells, using a vesicular stomatitis virus G (VSV-G)-pseudotyped lentivirus or MLV vectors carrying a green fluorescent protein marker gene. As predicted, the lentivirus vector was more efficient at transducing mouse and human growth-inhibited cell lines. The transduction of mouse HSC by lentivirus vectors was compared directly to MLV vectors in a co-transduction assay. In this assay, transduction by ecotropic MLV is a positive internal control for downstream steps in retrovirus transduction, including cell division. Both the VSV-G lentivirus and MLV vectors transduced mouse HSCs maintained in cytokine-free medium at very low frequency, as did the ecotropic control. The lentivirus vector and the MLV vector were equally efficient at transducing bone marrow HSCs cultured in interleukin 3 (IL-3), IL-6, and stem cell factor for 96 hours. In conclusion, although lentivirus vectors are able to transduce growth-inhibited cell lines, the cell cycle status of HSCs render them resistant to lentivirus-mediated transduction, and it is hypothesized that entry into cycle, not necessarily division, may be a requirement for efficient lentivirus-mediated transduction. 0006-4971 Journal Article},
	Author = {Barrette, S. and Douglas, J. L. and Seidel, N. E. and Bodine, D. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Journal = {Blood},
	Keywords = {Human;Tissue Distribution;Lentivirus/*genetics;Animals;Mice, Mutant Strains;Comparative Study;Female;Moloney murine leukemia virus/*genetics;Mice, Inbred C57BL;DNA/metabolism;08 Aberrant cell cycle;Hematopoietic Stem Cells/*metabolism;Hela Cells;Hematopoietic Stem Cell Transplantation;Blotting, Southern;Transduction, Genetic/*standards;Cell Lineage;3T3 Cells;Titrimetry;Hemoglobins/genetics;Retroviridae;Cytokines/pharmacology;Polymerase Chain Reaction;Mice;Genetic Vectors/genetics/standards;Vesicular stomatitis-Indiana virus/genetics;EE, J pdf},
	Number = {10},
	Organization = {Hematopoiesis Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.},
	Pages = {3385-91},
	Title = {Lentivirus-based vectors transduce mouse hematopoietic stem cells with similar efficiency to moloney murine leukemia virus-based vectors},
	Uuid = {AA1EE43C-211B-43D9-93AE-FED4E4A881E7},
	Volume = {96},
	Year = {2000},
	url = {papers/Barrette_Blood2000.pdf}}

@article{Barron:1979,
	Abstract = {Adult cats survived left lateral funiculotomy 1 to 153 days. The pericruciate cortex was studied electron microscopically in these as well as sham-operated and unoperated animals. Ten days after surgery Betz cells of the right pericruciate cortex displayed disaggregation of cytoplasmic ribosomes; random dispersal and degranulation of the normally compact arrays of cisterns of rough ER; in some cells perinuclear and peripheral disposition of remaining Nissl bodies; retispersion of the Golgi apparatus; and, uncommonly, neurofilamentous hyperplasia. Fourteen days postoperatively cytoplasmic ribosomes were largely regrouped in rosette arrangements and Golgi membranes were evenly distributed in the cytoplasm. Further reversion of the ER toward a normal appearance occurred 28 days postoperatively but substantial perikaryal atrophy had supervened in many neurons by 49-153 days after surgery. Evidence of nerve cell death was not found. Concentric membranous arrays derived from ER and associated with autophagic bodies and mitochondria were identified in dendrites of normals and cats that had been operated upon, perhaps more frequently contralateral to the spinal operation. Electron-dense and electron-lucent degenerative changes in dendrites also occurred, especially early after operation. Degenerating myelin sheaths were detected in the pericruciate cortex of animals that had been operated upon and sometimes were captured in the process of phagocytosis by oligodendrocytes as well as astrocytes and microglia. The long-term persistence of axotomized Betz cells, albeit in an atrophic state, and the reversibility of some of the cytologic responses to axon injury suggest that these neurons may retain a capacity for axon regeneration that could be mobilized, as by pharmacologic means.},
	Author = {Barron, K. D. and Dentinger, M. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Dendrites;Golgi Apparatus;Cats;Myelin Sheath;Not relevant;Endoplasmic Reticulum;11 Glia;Support, U.S. Gov't, P.H.S.;Spinal Cord;Support, Non-U.S. Gov't;Animals;Cerebral Cortex;Cytoplasmic Granules;Axons},
	Medline = {81217517},
	Month = {3},
	Nlm_Id = {2985192R},
	Number = {2},
	Pages = {128-51},
	Pubmed = {261986},
	Title = {Cytologic observations on axotomized feline Betz cells. 1. Qualitative electron microscopic findings},
	Uuid = {C881D963-239E-465C-AB9C-22E0FC0A187F},
	Volume = {38},
	Year = {1979}}

@article{Basu:2002,
	Abstract = {Interleukin-1 (IL-1) is induced immediately after insults to the brain, and elevated levels of IL-1 have been strongly implicated in the neurodegeneration that accompanies stroke, Alzheimer's disease, and multiple sclerosis. In animal models, antagonizing IL-1 has been shown to reduce cell death; however, the basis for this protection has not been elucidated. Here we analyzed the response to penetrating brain injury in mice lacking the type 1 IL-1 receptor (IL-1R1) to determine which cellular and molecular mediators of tissue damage require IL-1 signaling. At the cellular level, fewer amoeboid microglia/macrophages appeared adjacent to the injured brain tissue in IL-1R1 null mice, and those microglia present at early postinjury intervals retained their resting morphology. Astrogliosis also was mildly abrogated. At the molecular level, cyclooxygenase-2 (Cox-2) and IL-6 expression were depressed and delayed. Interestingly, basal levels of Cox-2, IL-1, and IL-6 were significantly lower in the IL-1R1 null mice. In addition, stimulation of vascular cell adhesion molecule-1 mRNA was depressed in the IL-1R1 null mice, and correspondingly, there was reduced diapedesis of peripheral macrophages in the IL-1R1 null brain after injury. This observation correlated with a reduced number of Cox-2+ amoeboid phagocytes adjacent to the injury. In contrast, several molecular aspects of the injury response were normal, including expression of tumor necrosis factor-alpha and the production of nerve growth factor. Because antagonizing IL-1 protects neural cells in experimental models of stroke and multiple sclerosis, our data suggest that cell preservation is achieved by abrogating microglial/macrophage activation and the subsequent self-propagating cycle of inflammation. 22117912 1529-2401 Journal Article},
	Author = {Basu, A. and Krady, J. K. and O'Malley, M. and Styren, S. D. and DeKosky, S. T. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Cytokines/genetics/metabolism;Prostaglandin-Endoperoxide Synthase/genetics/metabolism;Signal Transduction;Macrophages/metabolism/pathology;Prostaglandins/metabolism;Cyclophilins/genetics/metabolism;Isoenzymes/genetics/metabolism;Animal;Cell Count;Interleukin-1/metabolism;Inflammation Mediators/*metabolism;11 Glia;G abstr;Disease Models, Animal;Male;Macrophage Activation;Neurons/metabolism/pathology;Support, Non-U.S. Gov't;Microglia/*metabolism/pathology;Mice, Inbred C57BL;Head Injuries, Penetrating/*physiopathology;Receptors, Interleukin-1/deficiency/genetics/*metabolism;Gliosis/pathology/prevention &control;Interleukin-6/genetics/metabolism;Mice, Knockout;Vascular Cell Adhesion Molecule-1/genetics/metabolism;Mice;RNA, Messenger/metabolism},
	Number = {14},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.},
	Pages = {6071-82},
	Pubmed = {12122068},
	Title = {The type 1 interleukin-1 receptor is essential for the efficient activation of microglia and the induction of multiple proinflammatory mediators in response to brain injury},
	Uuid = {1E802FDB-B489-432F-A9F0-7CCCF5443C0D},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12122068}}

@article{Baszler:1991,
	Abstract = {To determine the biologic basis of ts1 MoMuLV neurovirulence in vivo, newborn CFW/D mice were inoculated with neurovirulent ts1 MoMuLV and nonneurovirulent wt MoMuLV and the temporal response to virus infection in the central nervous system (CNS), spleen, and thymus was studied comparatively. Experimental procedures included single and double labeling in situ immunohistochemistry with selective morphometric analyses, and steady state immunoblotting of viral proteins. Cellular targets for virus infection were identical for both ts1 and wt MoMuLV and consisted sequentially of 1) splenic megakaryocytes, 2) splenic and thymic lymphocytes, 3) CNS capillary endothelial cells, and 4) CNS pericytes and microglia. Resident microglial cells served as the major reservor and amplifier of virus infection in the CNS of ts1 MoMuLV-infected mice; a similar but much less significant role was played by microglia in wt MoMuLV-infected mice. The genesis and progression of severe spongiform lesions in ts1 MoMuLV-infected mice were both temporally and spatially correlated with amplified virus infection of microglia, and hyperplasia and hypertrophy of both virus-infected and nonvirus-infected microglial cells. Direct virus infection of neurons was never observed. The development of clinical neurologic disease and spongiform lesions in ts1 MoMuLV-infected mice correlated with the accumulation of both viral gag and env gene products in the CNS; there was no selective accumulation of env precursor polyprotein Pr80env. When compared to wt MoMuLV-infected mice, the neurovirulence of ts1 MoMuLV-infected mice occurred by an enhanced ability to replicate in the CNS and to infect and activate more microglia, rather than by a fundamental change in cellular tropism or topography of virus infection.},
	Author = {Baszler, T. V. and Zachary, J. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Antibodies, Viral;Mice, Inbred Strains;Virulence;Central Nervous System;Immunoblotting;Moloney murine leukemia virus;Virus Replication;Immunohistochemistry;Not relevant;Thymus Gland;Viral Proteins;11 Glia;Mice;Support, Non-U.S. Gov't;Spleen;Animals;Central Nervous System Diseases},
	Medline = {91157972},
	Month = {3},
	Nlm_Id = {0370502},
	Number = {3},
	Organization = {Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana.},
	Pages = {655-71},
	Pubmed = {2000941},
	Title = {Murine retroviral neurovirulence correlates with an enhanced ability ofvirus to infect selectively, replicate in, and activate resident microglial cells},
	Uuid = {94AC3012-95EB-48DC-9B7D-256DF7B18769},
	Volume = {138},
	Year = {1991}}

@article{Baszler:1990,
	Abstract = {Ts1 Moloney murine leukemia virus (MoMuLV) is a neurovirulent retrovirus that causes a progressive, noninflammatory, spongiform, neurodegenerative disease in mice. The temporal localization of cellular targets for virus replication and the genesis of ultrastructural spongiform changes in the central nervous system (CNS) of CFW/D mice inoculated at birth with neurovirulent ts1 MoMuLV and nonneurovirulent wild type (wt) MoMuLV were studied comparatively by transmission electron microscopy. Cellular targets for both ts1 and wt MoMuLV infection were sequentially (a) splenic megakaryocytes, (b) CNS intravascular platelets and capillary endothelia, and (c) resident CNS pericytes and microglia. When compared with wt MoMuLV-infected mice, ts1 MoMuLV-infected mice had amplified localization of virus to microglia with disease progression that paralleled the development of spongiform changes both temporally and spatially. Virus infection of neurons was never observed. Spongiform lesions originated from the dilated cytocavitary system of proximal neuronal processes (predominantly dendrites) and from vacuolated myelin sheaths of distal axons. As the disease progressed, the severity of the spongiform lesions in ts1 MoMuLV-infected mice increased rapidly and was associated with increased number of virions and virus-infected cells. Lesions in wt MoMuLV-infected mice were not severe and regressed terminally with apparent clearance of virus from the CNS. These studies indicated that murine retroviral-induced spongiform lesions originated from both neuronal and oligodendroglial degeneration; splenic megakaryocytes, platelets, and cell-free viremia contributed to systemic dissemination of virus to the CNS; microglia were the major cell target and reservoir for virus infection in the CNS; and the neurovirulence of ts1 MoMuLV occurred by enhanced replication rather than by a fundamental change in cellular tropism. The identification of microglia as the major CNS cell target for virus infection and the absence of productive virus infection of neurons suggested an indirect mechanism for murine retroviral-induced neuronal dysfunction.},
	Author = {Baszler, T. V. and Zachary, J. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0023-6837},
	Journal = {Lab Invest},
	Keywords = {Mice, Inbred Strains;Mutation;Animals;Neuroglia;Nerve Degeneration;Virus Replication;Not relevant;11 Glia;Support, Non-U.S. Gov't;Spleen;Leukemia Virus, Murine;Central Nervous System Diseases;Mice},
	Medline = {91040713},
	Month = {11},
	Nlm_Id = {0376617},
	Number = {5},
	Organization = {Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana.},
	Pages = {612-23},
	Pubmed = {2172651},
	Title = {Murine retroviral-induced spongiform neuronal degeneration parallels resident microglial cell infection: ultrastructural findings},
	Uuid = {B06DE214-F8F5-48BB-9BFB-5E145F52BDA3},
	Volume = {63},
	Year = {1990}}

@article{Batista:2006,
	Abstract = {Neural stem and progenitor cells are located in the subependyma of the adult forebrain. An increase in adult subependymal cell proliferation is reported after various kinds of brain injury. We demonstrate an expansion of neural precursor cells in the postnatal subependyma in a murine genetic disease model of Huntington's disease (HD), the R6/2 mouse. We used the in vitro neurosphere assay as an index of the number of neural stem cells in vivo and to assess proliferation kinetics in vitro and in vivo bromodeoxyuridine labeling to assess the progenitor cell population and their fates. Disease progression in this model leads to an increase in the numbers of neural stem cells in the adult striatal subependyma. This increase is produced cell non-autonomously by events in the R6/2 brains as the mice become increasingly symptomatic. Once the neural stem cell increase is induced in vivo, it is maintained during in vitro passaging of neural stem cells, but the neural stem cell increase is not reproduced during in vitro passaging of neural stem cells from presymptomatic R6/2 mice. In addition, we show that some of the R6/2 neural progenitor cells show a change from their normal migration destiny toward the olfactory bulb. Instead, some of these cells migrate into the striatum, one of the main affected areas in HD. Our findings demonstrate that HD damage recruits precursor cells in two ways: expansion of neural stem cells and altered migration of progenitor cells.},
	Author = {Batista, Claudia M. C. and Kippin, Tod E. and Willaime-Morawek, Sandrine and Shimabukuro, Mar{\'\i}lia Kimie and Akamatsu, Wado and van der Kooy, Derek},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Mice, Neurologic Mutants;Neurons;24 Pubmed search results 2008;Huntington Disease;Cell Proliferation;research support, non-u.s. gov't ;Stem Cells;Corpus Striatum;Animals;comparative study ;Cell Movement;Humans;Mice},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {41},
	Organization = {Neurobiology Research Group, Department of Medical Genetics and Microbiology, University of Toronto, Toronto, Ontario, Canada M5S 3E1.},
	Pages = {10452-60},
	Pii = {26/41/10452},
	Pubmed = {17035529},
	Title = {A progressive and cell non-autonomous increase in striatal neural stem cells in the Huntington's disease R6/2 mouse},
	Uuid = {39A451D7-1C7B-4290-B384-0D757833C657},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2850-06.2006}}

@article{Battista:2006,
	Abstract = {Adult neural stem cells (NSC) proliferate and differentiate depending on the composition of the cellular and molecular niche in which they are immersed. Until recently, microglial cells have been ignored as part of the neurogenic niche. We studied the dynamics of NSC proliferation and differentiation in the dentate gyrus of the hippocampus (DG) and characterized the changes of the neurogenic niche in adrenalectomized animals (ADX). At the cellular level, we found increased NSC proliferation and neurogenesis in the ADX animals. In addition, a morphologically distinct subpopulation of NSC (Nestin+/GFAP-) with increased proliferating profile was detected. Interestingly, the number of microglial cells at stages 2 and 3 of activation correlated with increased neurogenesis (r(2) = 0.999) and the number of Nestin-positive cells (r(2) = 0.96). At the molecular level, transforming growth factor beta (TGF-beta) mRNA levels were increased 10-fold in ADX animals. Interestingly, TGF-beta levels correlated with the amount of neurogenesis detected (r(2) = 0.99) and the number of stage 2 and 3 microglial cells (r(2) = 0.94). Furthermore, blockade of TGF-beta biological activity by administration of an anti-TGF-beta type II receptor antibody diminished the percentage of 5-bromo-2'-deoxyuridine (BrdU)/PSA-NCAM-positive cells in vivo. Moreover, TGF-beta was able to promote neurogenesis in NSC primary cultures. This work supports the idea that activated microglial cells are not pro- or anti-neurogenic per se, but the balance between pro- and anti-inflammatory secreted molecules influences the final effect of this activation. Importantly, we identified an anti-inflammatory cytokine, TGF-beta, with neurogenic potential in the adult brain.},
	Author = {Battista, Daniela and Ferrari, Carina C. and Gage, Fred H. and Pitossi, Fernando J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {8918110},
	Number = {1},
	Organization = {Laboratory of Neuromodulation, Leloir Institute, CONICET-UBA, University of Buenos Aires, 435 Av Patricias Argentinas, Buenos Aires 1405, Argentina.},
	Pages = {83-93},
	Pii = {EJN4539},
	Pubmed = {16420418},
	Title = {Neurogenic niche modulation by activated microglia: transforming growth factor beta increases neurogenesis in the adult dentate gyrus},
	Uuid = {3721E8EF-BFD2-49D2-90B6-BA3AE6E87EFB},
	Volume = {23},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2005.04539.x}}

@article{Bauer:1995,
	Abstract = {Clinical signs of experimental autoimmune encephalomyelitis (EAE) in rats can be suppressed by treatment with liposomes containing dichloromethylene diphosphonate (Cl2MDP liposomes). Here we investigated whether besides the blood-borne macrophages also ED2+ perivascular cells and microglia are affected by this treatment. For this purpose we examined the central nervous system of bone marrow chimeras in which EAE was induced with encephalitogenic T cells. Quantification of cell numbers of various cell types in inflammatory lesions in the spinal cord showed that after treatment with Cl2MDP liposomes more than 95\%of the bone marrow derived (I1-69+) macrophages were eliminated. In addition the number of ED2+ perivascular cells were seen to be decreased by 68\%as compared to ED2+ cells in control liposome treated animals. However the number of these perivascular cells in Cl2MDP liposome treated animals did not differ from the number of perivascular cells in naive animals, indicating that only newly recruited, inflammation associated, ED2+ macrophages were eliminated. Moreover, detection of degenerating nuclei by in situ nick translation (ISNT) in combination with staining for ED1 or ED2 showed that in the perivascular space no degenerating cells were present. Cl2MDP liposome treatment furthermore decreased the numbers of T cells infiltrating the parenchyma by more than 50\%. Instead T cells were found in large numbers in the perivascular space. Microglia did not seem to be eliminated by Cl2MDP liposome treatment as shown by the absence of ED1+/ISNT+ cells in the CNS parenchyma. However the number of ED1+ (I1-69-) microglial cells decreased by more than 80\%, indicating that the activation of this cell type was impaired. It is concluded that bone marrow derived macrophages play an important role in the pathogenesis of EAE via interactions with lymphocytes and the activation of resident microglia.},
	Author = {Bauer, J. and Huitinga, I. and Zhao, W. and Lassmann, H. and Hickey, W. F. and Dijkstra, C. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Research Support, Non-U.S. Gov't;Central Nervous System;Rats, Inbred Lew;Rats;Research Support, U.S. Gov't, P.H.S.;Encephalomyelitis, Autoimmune, Experimental;T-Lymphocytes;11 Glia;Microglia;Macrophages;Rats, Inbred BN;Spinal Cord;Animals;Spleen},
	Medline = {96275083},
	Month = {12},
	Nlm_Id = {8806785},
	Number = {4},
	Organization = {Department of Cell Biology and Immunology, Vrije Universiteit, Amsterdam, Netherlands.},
	Pages = {437-46},
	Pubmed = {8926037},
	Title = {The role of macrophages, perivascular cells, and microglial cells in the pathogenesis of experimental autoimmune encephalomyelitis},
	Uuid = {369161B7-8ECC-486B-BA35-CD62E11BFCC2},
	Volume = {15},
	Year = {1995}}

@article{Bauer:2005,
	Abstract = {Adult neurogenesis is studied in vivo using thymidine analogues such as bromodeoxyuridine (BrdU) to label DNA synthesis during the S phase of the cell cycle. However, BrdU may also label DNA synthesis events not directly related to cell proliferation, such as DNA repair and/or abortive reentry into the cell cycle, which can occur as part of an apoptotic process in postmitotic neurons. In this study, we used three well-characterized models of injury-induced neuronal apoptosis and the combined visualization of cell birth (BrdU labeling) and death (Tdt-mediated dUTP-biotin nick end labeling) to investigate the specificity of BrdU incorporation in the adult mouse brain in vivo. We present evidence that BrdU is not significantly incorporated during DNA repair and that labeling is not detected in vulnerable or dying postmitotic neurons, even when a high dose of BrdU is directly infused into the brain. These findings have important implications for a controversy surrounding adult neurogenesis: the connection between cell cycle reactivation and apoptosis of terminally differentiated neurons.},
	Author = {Bauer, Sylvian and Patterson, Paul H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {01 Adult neurogenesis general;08 Aberrant cell cycle;06 Adult neurogenesis injury induced},
	Month = {11},
	Nlm_Id = {0375356},
	Number = {4},
	Organization = {Biology Division, California Institute of Technology, Pasadena, CA 91125.},
	Pages = {641-50},
	Pii = {jcb.200505072},
	Pubmed = {16291699},
	Title = {The cell cycle-apoptosis connection revisited in the adult brain},
	Uuid = {B65BD976-AD3C-11DA-B832-000D9346EC2A},
	Volume = {171},
	Year = {2005},
	url = {papers/Bauer_JCellBiol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200505072}}

@article{Bauer:2006,
	Abstract = {Although neural stem cells (NSCs) persist in various areas of the adult brain, their contribution to brain repair after injury is very limited. Treatment with exogenous growth factors can mitigate this limitation, suggesting that the brain environment is normally deficient in permissive cues and that it may be possible to stimulate the latent regenerative potential of endogenous progenitors with appropriate signals. We analyzed the effects of overexpressing the cytokine leukemia inhibitory factor (LIF) on adult neurogenesis in the normal brain. We found that LIF reduces neurogenesis in the olfactory bulb and subventricular zone by acting directly on NSCs. LIF appears to promote NSC self-renewal, preventing the emergence of more differentiated cell types. This ultimately leads to an expansion of the NSC pool. Our results have implications for the development of therapeutic strategies for brain repair and suggest that LIF may be useful, in combination with other factors, in promoting regeneration in the adult brain.},
	Author = {Bauer, Sylvian and Patterson, Paul H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Spheroids, Cellular;Cell Differentiation;Animals;Cells, Cultured;Transfection;Neuronal Plasticity;Telencephalon;Mice, Inbred C57BL;Nerve Growth Factors;research support, non-u.s. gov't;Antimitotic Agents;Cell Proliferation;Nerve Regeneration;Injections, Intraventricular;Male;Genetic Vectors;Leukemia Inhibitory Factor;Neuroglia;Neurons;Adenoviridae;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Bromodeoxyuridine;Stem Cells},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {46},
	Organization = {Biology Division, California Institute of Technology, Pasadena, California 91125, USA.},
	Pages = {12089-99},
	Pii = {26/46/12089},
	Pubmed = {17108182},
	Title = {Leukemia inhibitory factor promotes neural stem cell self-renewal in the adult brain},
	Uuid = {3A19E9E8-DCF7-48A2-A087-61BD11901E4B},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3047-06.2006}}

@article{Baus:2003,
	Abstract = {Although the Cdk inhibitor p21(Waf1/Cip1), one of the transcriptional targets of p53, has been implicated in the maintenance of G(2) arrest after DNA damage, its function at this stage of the cell cycle is not really understood. Here, we show that the exposure of normal human fibroblasts (NHFs) to genotoxic agents provokes permanent cell cycle exit in G(2) phase, whereas mouse embryo fibroblasts and transformed human cells progress through mitosis and arrest in G(1) without intervening cytokinesis. p21(Waf1/Cip1) exerts a key role in driving this G(2) exit both by inhibiting cyclin B1-Cdk1 and cyclin A-Cdk1/2 complexes, which control G(2)/M progression, and by blocking the phosphorylation of pRb family proteins. NHFs with compromised pRb proteins could still efficiently arrest in G(2) but were unable to exit the cell cycle, resulting in cell death. Our experiments show that, when under continuous genotoxic stress, normal cells can reverse their commitment to mitotic progression due to passage through the restriction point and that mechanisms involving p21(Waf1/Cip1) and pocket proteins can induce exit in G(2) and G(1). 0261-4189 Journal Article},
	Author = {Baus, F. and Gire, V. and Fisher, D. and Piette, J. and Dulic, V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:41 -0400},
	Journal = {Embo J},
	Keywords = {EE pdf;*DNA Damage;Human;08 Aberrant cell cycle;Fibroblasts/cytology/metabolism;Piperazines/pharmacology;Bleomycin/pharmacology;Cyclin-Dependent Kinases/metabolism;Cyclins/metabolism;Mitosis;Support, Non-U.S. Gov't;Cells, Cultured;*G2 Phase},
	Number = {15},
	Organization = {CRBM-CNRS FRE 2593, 1919, Route de Mende, 34293 Montpellier, IGMM-CNRS UMR 5535, Montpellier and IGH-CNRS UPR 1142, Montpellier, France.},
	Pages = {3992-4002},
	Title = {Permanent cell cycle exit in G2 phase after DNA damage in normal human fibroblasts},
	Uuid = {EBE2D712-3E34-47DE-BC25-2D0007DA36D7},
	Volume = {22},
	Year = {2003},
	url = {papers/Baus_EmboJ2003.pdf}}

@article{Bayer:1982,
	Abstract = {The total number of granule cells in the dentate gyrus was estimated in 17 male rats, four each aged 30, 120, and 200 days, and five aged 365 days. There is a substantial 35-43\%linear increase between 1 month and 1 year. Two parameters of the granular layer are involved in the numerical change. First, total granular layer volume grows linearly with age. Second, average volume of a single granule cell nucleus in the ventral dentate gyrus decreases with age. Older rats tend to have a larger granular layer filled with more and smaller cells. In another group of 21 male rats, 3H-thymidine injections were given on four consecutive days during juvenile (30-33, n = 6) and adult life (60-63, n = 5; 120-123, n = 6; 180-183, n = 4). All animals survived to 200 days of age. The proportion of labeled mature granule cells and labeled presumptive granule cell precursors were determined in anatomically- matched slices. With older ages at injection, there is a decline in labeled mature granule cells and a concurrent increase in labeled precursors. These data are compatible with the constant level of granule cell increase determined volumetrically. Most of the late granule cells originate nearly simultaneously along the base of the main bulk of the granular layer; very few are found in the dorsal tip (septal extreme) and ventral tip (temporal extreme). This study is the first demonstration of a net numerical gain in a neuronal population during adulthood in the mammalian brain. Since the granule adulthood in the mammalian brain. Since the granule cells play a pivotal role in hippocampal function, these data suggest that their influence grows with age. Using Smart Source Parsing},
	Author = {Bayer, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Exp Brain Res},
	Keywords = {02 Adult neurogenesis migration;Cell Differentiation;10 Development;B;Rats;10 Hippocampus;Autoradiography;Thymidine/metabolism;Cell Division;Cell Count;Hippocampus/*cytology/metabolism;Support, U.S. Gov't, Non-P.H.S.;Animal;Male;Rats, Inbred Strains},
	Number = {3},
	Pages = {315-23},
	Title = {Changes in the total number of dentate granule cells in juvenile and adult rats: a correlated volumetric and 3H-thymidine autoradiographic study},
	Uuid = {FE6D5715-C36A-4362-A5D3-85538781C60F},
	Volume = {46},
	Year = {1982},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7095040}}

@article{Bayer:1983,
	Abstract = {Neurogenesis in the rat olfactory bulb was examined with 3H-thymidine- radiography. For the animals in the prenatal groups, the initial 3H- thymidine exposures were separated by 24 h; they were the offspring of pregnant females given two injections on consecutive embryonic (E) days (E12-E13, E13-E14, . . . E21-E22). For the animals in the postnatal (P) groups, the initial 3H-thymidine injections were separated by 48 h, each group receiving either four (PO-P3, P2-P4, . . . P6-P9) or two (P8- P9, P10-P11, . . . P20-P21) consecutive daily injections. On P60, the percentage of labeled cells and the proportion of cells added during either 24 h or 48 h periods were quantified at several anatomical levels for each neuronal population in the main olfactory bulb (mitral cells, tufted cells, granule cells, interneurons in the external plexiform layer, periglomerular granule cells) and accessory olfactory bulb (output neurons, granule cells, periglomerular granule cells). The total time span of neurogenesis extends from E12 to beyond P20. Output neurons are prenatally generated over 5-9 day periods (with most neurogenesis occurring over 2-4 days) in a strict sequential order beginning with the accessory bulb output neurons (E13-E14) and ending with the interstitial tufted cells lying between the glomeruli in the main bulb (E20-E22). These data are correlated with the main and accessory bulb projection fields in the amygdala and with the chronology of amygdala neurogenesis. With the exception of the granule cells in the accessory bulb (88\%generated between E15-E22), the rest of the interneuronal populations are generated postnatally and nearly simultaneously. While most neurons (75-80\%) originate during the first three weeks of life, all interneuronal populations, including accessory bulb granule cells, show some neurogenesis beyond P20. Injections of 3H- thymidine in juvenile and adult rats indicates neurogenesis up to P60 in the accessory bulb and up to P180 in the main bulb, especially in the main bulb granule cell population. There is circumstantial evidence for turnover of main bulb granule cells during adult life. Using Smart Source Parsing},
	Author = {Bayer, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Exp Brain Res},
	Keywords = {A;01 Adult neurogenesis general;Cell Differentiation;10 Development;Interneurons/cytology;Rats;10 Hippocampus;Cell Division;Animal;Support, U.S. Gov't, Non-P.H.S.;Olfactory Bulb/embryology/*growth &development/metabolism;Thymidine/*metabolism;Rats, Inbred Strains},
	Number = {2-3},
	Pages = {329-40},
	Title = {3H-thymidine-radiographic studies of neurogenesis in the rat olfactory bulb},
	Uuid = {BFFA96EF-4732-48E0-82CB-9D854FE6888E},
	Volume = {50},
	Year = {1983},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=6641865}}

@article{Bayer:1980,
	Author = {Bayer, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Thymidine;Thalamic Nuclei;Cell Differentiation;Septal Nuclei;Hippocampus;Autoradiography;Comparative Study;Neural Pathways;Rats;Limbic System;Female;Pregnancy;Brain Mapping;Morphogenesis;Animals;Neurons},
	Medline = {80204888},
	Month = {3},
	Nlm_Id = {0406041},
	Number = {1},
	Pages = {87-114},
	Pubmed = {7381056},
	Title = {Development of the hippocampal region in the rat. I. Neurogenesis examined with 3H-thymidine autoradiography},
	Uuid = {579E6264-686D-11DA-A4B6-000D9346EC2A},
	Volume = {190},
	Year = {1980},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.901900107}}

@article{Bayer:1980a,
	Author = {Bayer, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Radiation Tolerance;X-Rays;Cell Differentiation;Limbic System;Female;Rats;Epithelium;Hippocampus;Pregnancy;Brain Mapping;Morphogenesis;Animals},
	Medline = {80204878},
	Month = {3},
	Nlm_Id = {0406041},
	Number = {1},
	Pages = {115-34},
	Pubmed = {7381049},
	Title = {Development of the hippocampal region in the rat. II. Morphogenesis during embryonic and early postnatal life},
	Uuid = {AD8AE9E6-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {190},
	Year = {1980},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.901900108}}

@article{Bayer:1982a,
	Abstract = {Volumetric estimates of the total number of granule cells in rats 30, 120, 200, and 365 days old increase linearly by approximately 35 to 43 percent between 1 month and 1 year. Total volume of the granular layer also grows linearly during that time. These results demonstrate a numerical increase in a neuronal population during adulthood in the mammalian brain.},
	Author = {Bayer, S. A. and Yackel, J. W. and Puri, P. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Science},
	Keywords = {B;Rats;Animal;Support, U.S. Gov't, Non-P.H.S.;Hippocampus/cytology/*growth &development;Age Factors;Male},
	Number = {4548},
	Pages = {890-2.},
	Title = {Neurons in the rat dentate gyrus granular layer substantially increase during juvenile and adult life},
	Uuid = {9FB6DC5C-67A7-11DA-A4B6-000D9346EC2A},
	Volume = {216},
	Year = {1982},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7079742}}

@article{Bechmann:2001,
	Abstract = {Virchow-Robin's perivascular spaces lie between the basement membrane around pericytes and the basement membrane at the surface of the glia limitans of the brain vessels. They are directly connected to the subpial space and harbour a population of cells distinct from pericytes, perivascular microglia and other cells within perivascular spaces (e.g. T cells and mast cells) in their ability to quickly phagocytose particles from the cerebrospinal fluid (CSF). Morphology, function, and cell surface proteins of these perivascular cells suggest an origin from the monocyte/macrophage lineage. It is currently unclear to what extent these brain perivascular cells represent a resident population of histiocytes or undergo continuous supplementation from blood monocytes. Using transplants of green-fluorescent-protein (GFP)-transfected bone marrow cells, we therefore investigated the replacement of perivascular cells by blood-borne macrophages in adult mice. GFP-positive cells in the perivascular spaces were found as early as 2 weeks post transplantation. The substitution of host perivascular cells by donor-derived macrophages was then evaluated using immunocytochemistry and intraventricular injection of hydrophilic rhodamine-fluorescent tracers. Such tracers diffuse along perivascular spaces and are subsequently phagocytosed by perivascular cells leading to stable phagocytosis-dependent labelling. Thus, the population of newly immigrated macrophages could be related to the total number of perivascular macrophages. This approach revealed a continuous increase of donor-derived perivascular cells. At 14 weeks post transplantation, all perivascular cells were donor-derived. These data show that brain perivascular cells are a population of migratory macrophages and not resident histiocytes.},
	Author = {Bechmann, I. and Priller, J. and Kovac, A. and B{\"o}ntert, M. and Wehner, T. and Klett, F. F. and Bohsung, J. and Stuschke, M. and Dirnagl, U. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Blood Vessels;Fluorescent Dyes;Rhodamines;Cell Differentiation;Animals;Macrophages;Pericytes;Dextrans;Bone Marrow Transplantation;Brain;Indicators and Reagents;Cell Count;Cell Movement;Mice, Inbred C57BL;11 Glia;Chemotaxis, Leukocyte;Green Fluorescent Proteins;Pia Mater;Immune System;Bone Marrow Cells;Cell Lineage;Mice;Immunohistochemistry;Luminescent Proteins;Biotin;Research Support, Non-U.S. Gov't},
	Medline = {21850280},
	Month = {11},
	Nlm_Id = {8918110},
	Number = {10},
	Organization = {Department of Cell and Neurobiology, Institute of Anatomy, Humboldt-University Hospital Charit{\'e}, Schumannstrasse 20/21, D-10098 Berlin, Germany. ingo.bechmann\@charite.de},
	Pages = {1651-8},
	Pii = {1793},
	Pubmed = {11860459},
	Title = {Immune surveillance of mouse brain perivascular spaces by blood-borne macrophages},
	Uuid = {B96B461E-B550-4DF8-819C-10F012B25DF9},
	Volume = {14},
	Year = {2001},
	url = {papers/Bechmann_EurJNeurosci2001.pdf}}

@article{Bechmann:2001a,
	Abstract = {Brain perivascular spaces harbor a population of cells which exhibit high phagocytic capacity. Therefore, these cells can be labeled by intraventricular injection of tracers. Such perivascular cells at the interface between blood and brain are believed to belong to the monocyte/macrophage lineage and to be involved in antigen presentation. Currently, it is unclear whether these cells undergo a continuous turnover by entering and leaving the bloodstream. Using bone-marrow-chimeric animals, migration of donor macrophages into brain perivascular spaces has been reported. On the other hand, following intracerebral injection of india ink into nontransplanted animals, ink-labeled perivascular cells were still found 2 years after injection, suggesting a high stability of this cell pool. Thus, the turnover of perivascular cells observed in chimeras might be a result of bone marrow transplantation rather than a physiological occurrence. To address this issue, we monitored de novo invasion of macrophages into perivascular spaces of apparently healthy adult rats by applying techniques other than bone marrow transplantation, (i) consecutive injections of different tracers and (ii) ex vivo isolation of macrophages from the blood, cell labeling, and reinjection into the same animal to avoid MHC mismatch. Both approaches revealed vivid de novo invasion of macrophages into perivascular spaces, but not into brain parenchyma, rendering untenable the concept of perivascular cells forming a stable population of macrophages in the brain. Thus, brain perivascular spaces are under permanent immune surveillance of blood borne macrophages in normal adult rats.},
	Author = {Bechmann, I. and Kwidzinski, E. and Kovac, A. D. and Simb{\"u}rger, E. and Horvath, T. and Gimsa, U. and Dirnagl, U. and Priller, J. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Research Support, Non-U.S. Gov't;Basement Membrane;Rats;Rats, Wistar;Fluorescent Dyes;11 Glia;Macrophages;Animals;Oligodendroglia;Brain;Cell Movement},
	Medline = {21159780},
	Month = {4},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Institute of Anatomy, Humboldt-University Hospital Charit{\'e}, Berlin, Germany. ingo.bechmann\@charite.de},
	Pages = {242-9},
	Pii = {S0014488600976180},
	Pubmed = {11259112},
	Title = {Turnover of rat brain perivascular cells},
	Uuid = {8481D47F-D3B7-11D9-A0E9-000D9346EC2A},
	Volume = {168},
	Year = {2001},
	url = {papers/Bechmann_ExpNeurol2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.2000.7618}}

@article{Bechmann:2005,
	Abstract = {In this study, we demonstrate the infiltration of blood-derived monocytic cells and their morphologic transformation into microglia in zones of acute, anterograde (Wallerian) axonal degeneration induced by entorhinal cortex lesion (ECL). ECL was performed in mice which had received green fluorescent protein (GFP)-transduced bone marrow grafts allowing identification of blood-derived elements within the brain. While in the unlesioned hemisphere GFP(+) cells were restricted to perivascular and leptomeningeal sites, many round fluorescent cells appeared in hippocampal zones of axonal degeneration at 24 h post lesion (hpl). Within 72 hpl, these GFP(+) cells acquired ramified, microglia-like morphologies, which persisted for at least 7 days post ECL. Differentiation of GFP(+) cells into glial fibrillary acidic protein (GFAP)(+) astrocytes was never observed. To exclude that this recruitment is an artifact of irradiation or bone marrow transplantation, the fluorescent cell tracker 6-carboxylfluorescein diacetate (CFDA) was injected into spleens of normal mice 1 day before ECL. Again, fluorescent cells appeared at the lesion site and along the layers of axonal degeneration at 48 hpl and CFDA+/MAC-1(+), cells exhibited amoeboid and ramified morphologies. Thus, blood-derived cells infiltrate not only the site of mechanical lesion, but also the layers of anterograde axonal degeneration, where they readily transform into microglia-like elements. A role for infiltrating leukocytes in facilitating or modulating postlesional plasticity, e.g., by phagocytosis of growth-inhibiting myelin should now be considered. Moreover, monocytic cells may serve as vehicles to transport therapeutic substances such as neurotrophic factors or caspase inhibitors to zones of axonal degeneration.},
	Author = {Bechmann, and Goldmann, and Kovac, and Kwidzinski, and Simb{\"u}rger, and Naftolin, and Dirnagl, and Nitsch, and Priller,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:17 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {8804484},
	Number = {6},
	Pages = {647-9},
	Pii = {04-2599fje},
	Pubmed = {15671154},
	Title = {Circulating monocytic cells infiltrate layers of anterograde axonal degeneration where they transform into microglia},
	Uuid = {2598CBB2-F3D0-40DD-BB0C-9C32AE3CC447},
	Volume = {19},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.04-2599fje}}

@article{Bechmann:1997,
	Abstract = {Entorhinal lesion leads to anterograde degeneration of perforant path fibers in their main termination zone in the outer molecular layers of the dentate gyrus. Concomitantly, astrocytes become hypertrophic, and microglial cells alter their phenotype, suggesting participation in anterograde degeneration. This study analyzes the involvement of these lesion-induced activated glial cells in the process of phagocytosis of degenerated axonal debris. We established a phagocytosis-dependent labeling technique that allows for direct and simultaneous visualization of both labeled incorporated axonal debris and incorporating glial cells. Stereotaxic application of small crystals of the biotin- and rhodamine-conjugated dextran amine Mini Ruby (MR) into the entorhinal cortex led to strong and stable axonal staining of perforant path axons. Following entorhinal lesion, labeled terminals and fibers condensed and formed small granules. Incorporation of these rhodamine-fluorescent granules resulted in a phagocytosis-dependent cell labeling. During the first 3 days, we were able to identify these cells as microglia by using double-fluorescence and confocal microscopy. The first unequivocally double-labeled astrocytes were found 6 days post lesion (dpl). Whereas in all stages a subpopulation of microglial cells remained devoid of MR-labeled granules, all astrocytes in the middle molecular layer were double-labeled after long survival times (20 dpl). On the ultrastructural level, labeled granules appeared to be perforant path axons containing the tracer. Both terminals and myelinated fibers could be seen inside the cytoplasm of microglial cells and astrocytes. Thus, anterograde degeneration is a sufficient stimulus to induce axon incorporation by both astrocytes and a subpopulation of microglial cells.},
	Author = {Bechmann, I. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Fluorescent Dyes;Rhodamines;Nerve Degeneration;Astrocytes;Animals;Phagocytosis;Rats;Dextrans;Microglia;Female;Entorhinal Cortex;Axons;Hippocampus;Rats, Wistar;Not relevant;Microscopy, Fluorescence;11 Glia;Male;Axonal Transport;Support, Non-U.S. Gov't;Nerve Fibers;Biotin;Research Support, Non-U.S. Gov't},
	Medline = {97323109},
	Month = {6},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Cell and Neurobiology, Humboldt University Hospital Charit{\'e}, Berlin, Germany.},
	Pages = {145-54},
	Pii = {10.1002/(SICI)1098-1136(199706)20:2<145::AID-GLIA6>3.0.CO;2-8},
	Pubmed = {9179599},
	Title = {Astrocytes and microglial cells incorporate degenerating fibers following entorhinal lesion: a light, confocal, and electron microscopical study using a phagocytosis-dependent labeling technique},
	Uuid = {03618D06-1D73-4A59-B36E-946EB165A511},
	Volume = {20},
	Year = {1997}}

@article{Bechmann:1997a,
	Abstract = {Retrograde and anterograde degeneration have been reported to be sufficient stimuli to activate glial cells, which, in turn, are involved in phagocytosis of degenerating material. Here we describe a double-fluorescence technique which allows for direct and simultaneous visualization of both labeled incorporated axonal debris and incorporating glial cells in the course of anterograde degeneration. Stereotaxic application of small crystals of biotinylated and tetramethylrhodamine (TRITC)-conjugated dextran amine Mini Ruby into the medial entorhinal cortex resulted in a stable rhodamine fluorescence confined to fibers and terminals in the middle molecular layer of the dentate gyrus, the stratum lacunosum-moleculare, and the crossed temporo-hippocampal pathway. Subsequent stereotaxic lesion of the entorhinal cortex induced transformation of rhodamine-fluorescent fibers and terminals into small granules. Incorporation of these granules by microglial cells [labeled by fluorescein isothiocyanate (FITC)-coupled Bandeiraea simplicifolia isolectin B4] or astrocytes (labeled by FITC-coupled glial fibrillary acidic protein antibodies) resulted in phagocytosis-dependent labeling of these non-neuronal cells, which could be identified by double-fluorescence microscopy. Electron microscopical analysis revealed that, following lesion, the tracer remained confined to entorhinal axons which were found to be incorporated by glial cells. Our data show that TRITC- and biotin-conjugated dextran amines are versatile tracers leading to Phaseolus vulgaris leucoagglutinin-like axonal staining. Lesion-induced phagocytosis of anterogradely degenerating axons by immunocytochemically identified glial cells can be directly observed by this technique on the light and electron microscopical levels.},
	Author = {Bechmann, I. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0948-6143},
	Journal = {Histochem Cell Biol},
	Keywords = {Rhodamines;Research Support, Non-U.S. Gov't;Neuroglia;Nerve Degeneration;Female;Rats;Phagocytes;Immunohistochemistry;Rats, Wistar;Fluorescent Dyes;11 Glia;Microscopy, Fluorescence;Biotin;Microscopy, Immunoelectron;Male;Animals;Axons},
	Medline = {97352048},
	Month = {5},
	Nlm_Id = {9506663},
	Number = {5},
	Organization = {Humboldt University Clinic Charit{\'e}, Department of Cell and Neurobiology, Berlin, Germany.},
	Pages = {391-7},
	Pubmed = {9208330},
	Title = {Identification of phagocytic glial cells after lesion-induced anterograde degeneration using double-fluorescence labeling: combination of axonal tracing and lectin or immunostaining},
	Uuid = {1457F59F-FC5F-4C9A-865A-250CE842A6FF},
	Volume = {107},
	Year = {1997}}

@article{Bechmann:2001b,
	Abstract = {In contrast to other organs where the tissue is capable of replacing lost cells and thus regaining tissue function, immune cell recruitment and activation is suppressed in the CNS in order to minimize secondary damage after lesion. This state of immune privilege has its cost because the injured tissue cannot fully benefit from growth-promoting effects accompanying inflammatory responses. These responses include phagocytosis of growth-inhibiting myelin debris by cells of the innate immune system and the recently described protection of surviving fibers by myelin-specifie T cells of the adaptive immune system. While the signals suppressing macrophage functions in the CNS are yet to be defined, it seems that help from T cells is diminished by apoptosis-induction via death-inducing ligands. Indeed, the death ligand CD95L (FasL, APO 1 L) is constitutively found on neurons, microglia and astrocytes. Its upregulation on astrocytes during axonal degeneration in the hippocampus after entorhinal lesion is accompanied by the appearance of apoptotic leukocytes. T cells also express CD95L and TNF-related apoptosis- inducing ligand (TRAIL), and the presence of CD95 (Fas, APOI) and TRAIL-receptors renders brain cells putative targets of T cell-induced apoptosis. Thus, blockade of death ligands could be helpful by simultaneously enhancing T cell survival and blocking T cell-mediated brain cell death. This is only one example of how boosting helpful immune cell functions and abrogating their destructive effects might help to overcome the brain's failure to regenerate after axonal lesions.},
	Author = {Bechmann, I. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0922-6028},
	Journal = {Restor Neurol Neurosci},
	Keywords = {review literature;Central Nervous System;Research Support, Non-U.S. Gov't;Human;Neuronal Plasticity;Neuroimmunomodulation;Not relevant;11 Glia;Animals;Humans;Central Nervous System Diseases;review;Support, Non-U.S. Gov't},
	Medline = {22077803},
	Nlm_Id = {9005499},
	Number = {3-4},
	Organization = {Institute of Anatomy, Department Cell and Neurobiology, Humboldt-University Hospital Charit{\'e}, 10098 Berlin, Germany.},
	Pages = {189-98},
	Pubmed = {12082221},
	Title = {Plasticity following lesion: help and harm from the immune system},
	Uuid = {F86530C0-3FA3-44BD-9A4E-9F302134CC37},
	Volume = {19},
	Year = {2001}}

@article{Beck:2003,
	Abstract = {Bone marrow-derived cells participate in remodeling processes of many ischemia-associated diseases, which has raised hopes for the use of bone marrow as a source for cell-based therapeutic approaches. To study the participation of bone marrow-derived cells in a stroke model, bone marrow from C57BL/6-TgN(ACTbEGFP)1Osb mice that express green fluorescent protein (GFP) in all cells was transplanted into C57BL/6J mice. The recipient mice underwent permanent occlusion of the middle cerebral artery, and bone marrow-derived cells were tracked by fluorescence. The authors investigated the involvement of bone marrow-derived cells in repair processes 6 weeks and 6 months after infarction. Six weeks after occlusion of the artery, more than 90\%of the GFP-positive cells in the infarct border zone were microglial cells. Very few GFP-positive cells expressed endothelial markers in the infarct/infarct border zone, and no bone marrow-derived cells transdifferentiated into astrocytes, neurons, or oligodendroglial cells at all time points investigated. The results indicate the need for additional experimental studies to determine whether therapeutic application of nonselected bone marrow will replenish brain cells beyond an increase in microglial engraftment.},
	Author = {Beck, Heike and Voswinckel, Robert and Wagner, Shawn and Ziegelhoeffer, Tibor and Heil, Matthias and Helisch, Armin and Schaper, Wolfgang and Acker, Till and Hatzopoulos, Antonis K. and Plate, Karl H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0271-678X},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {Research Support, Non-U.S. Gov't;Cell Differentiation;Animals;Infarction, Middle Cerebral Artery;Bone Marrow Transplantation;Microglia;2',3'-Cyclic-Nucleotide Phosphodiesterases;Indicators and Reagents;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Male;Bone Marrow Cells;Choroid Plexus;Age Factors;Mice;Luminescent Proteins;Biological Markers;Lectins;von Willebrand Factor;Glial Fibrillary Acidic Protein},
	Medline = {22681133},
	Month = {6},
	Nlm_Id = {8112566},
	Number = {6},
	Organization = {GSF-Research Center for Environment &Health, Institute for Clinical Molecular Biology and Tumor Genetics, Munich, Germany. Heike.Beck\@gsf.de},
	Pages = {709-17},
	Pubmed = {12796719},
	Title = {Participation of bone marrow-derived cells in long-term repair processes after experimental stroke},
	Uuid = {D455721A-9CEF-4BCA-9994-4B8B9EA8BC59},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1097/01.WCB.0000065940.18332.8D}}

@article{Beck:1995,
	Abstract = {Homozygous Igf1-/- mice at 2 months of age had reduced brain weights, with reductions evenly affecting all major brain areas. The gross morphology of the CNS was normal, but the size of white matter structures in brain and spinal cord was strongly reduced, owing to decreased numbers of axons and oligodendrocytes. Myelinated axons were more strongly reduced in number than unmyelinated axons. The volume of the dentate gyrus granule cell layer was reduced in excess of the decrease in brain weight. Among populations of calcium-binding protein-containing neurons, there was a selective reduction in the number of striatal parvalbumin-containing cells. Numbers of mesencephalic dopaminergic neurons, striatal and basal forebrain cholinergic neurons, and spinal cord motoneurons were unaffected. Cerebellar morphology was unaltered. Our findings suggest cell type- and region-specific functions for IGF-I and emphasize prominent roles in axon growth and maturation in CNS myelination.},
	Author = {Beck, K. D. and Powell-Braxton, L. and Widmer, H. R. and Valverde, J. and Hefti, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Glial Fibrillary Acidic Protein;10 Development;10 Hippocampus;Animals;Myelin Sheath;Astrocytes;Corpus Striatum;Research Support, U.S. Gov't, Non-P.H.S.;Brain;Mutation;Cell Count;Hippocampus;Mice, Inbred C57BL;Axons;Calcium-Binding Protein, Vitamin D-Dependent;Spinal Cord;Research Support, U.S. Gov't, P.H.S.;Parvalbumins;Neurons;Organ Size;Mice;Insulin-Like Growth Factor I;Research Support, Non-U.S. Gov't},
	Medline = {95234311},
	Month = {4},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Department of Neuroscience, Genentech, Incorporated, South San Francisco, California 94080, USA.},
	Pages = {717-30},
	Pubmed = {7718235},
	Title = {Igf1 gene disruption results in reduced brain size, CNS hypomyelination, and loss of hippocampal granule and striatal parvalbumin-containing neurons},
	Uuid = {46334EB3-F160-49A1-A5F2-DF23B1A727B1},
	Volume = {14},
	Year = {1995}}

@article{Becker:2001,
	Abstract = {We analyzed pathway choices of regenerating, mostly supraspinal, descending axons in the spinal cord of adult zebrafish and the cellular changes in the spinal cord caudal to a lesion site after complete spinal transection. Anterograde tracing (by application of the tracer rostral to the spinal lesion site) showed that significantly more descending axons (74\%) regenerated in the spinal gray matter of the caudal spinal cord than would be expected from random growth. Retrograde tracing (by application of the tracer caudal to the spinal lesion site) showed that, rostral to the lesion, most of these axons (80\%) extended into the major white matter tracts. Thus, ventral descending tracts often were devoid of labeled axons caudal to a spinal lesion but contained many axons rostral to the lesion in the same animals, indicating a pathway switch of descending axons from the white matter to the gray matter. Ascending axons of spinal neurons were not observed regrowing to the rostral tracer application site; therefore, they most likely did not contribute to the axonal populations analyzed. A macrophage/microglia response within 2 days of spinal cord transection, along with phagocytosis of myelin, was observed caudal to the transection by immunohistochemistry and electron microscopy. Nevertheless, caudal to the lesion, descending tracts in the white matter were filled with myelin debris during the time of axonal regrowth, at least up to 6 weeks postlesion. We suggest that the spontaneous regeneration of axons of supraspinal origin after spinal cord transection in adult zebrafish may be due in part to the axons' ability to negotiate novel pathways in the spinal cord gray matter.},
	Author = {Becker, T. and Becker, C. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Zebrafish;Neurons, Efferent;Spinal Cord Injuries;Nerve Regeneration;Not relevant;11 Glia;Microglia;Macrophages;Spinal Cord;Neurons, Afferent;Age Factors;Support, Non-U.S. Gov't;Animals;Axons},
	Medline = {21179351},
	Month = {4},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Zentrum f{\"u}r Molekulare Neurobiologie Hamburg, Universit{\"a}t Hamburg, Martinistr. 52, D-20246 Hamburg, Germany. tcbecker\@zmnh.uni-hamburg.de},
	Pages = {131-47},
	Pubmed = {11283955},
	Title = {Regenerating descending axons preferentially reroute to the gray matter in the presence of a general macrophage/microglial reaction caudal to a spinal transection in adult zebrafish},
	Uuid = {3BCC4454-72E3-405A-9F82-C37AFF578B56},
	Volume = {433},
	Year = {2001}}

@article{Becq:2005,
	Abstract = {In the present article we investigated the properties of CA1 and dentate gyrus cell precursors in adult rodents both in vivo and in vitro. Cell proliferation in situ was investigated by rating the number of cells incorporating BrdU after kainate-induced seizures. CA1 precursors displayed a greater proliferation capacity than dentate gyrus precursors. The majority of BrdU-labeled cells in CA1 expressed Nestin and Mash-1, two markers of neural precursors. BrdU-positive cells in the dentate gyrus expressed Nestin, but only a few expressed Mash-1. In animals pretreated with the antimitotic azacytidine, the capacity of kainate to enhance the proliferation was higher in CA1 than in the dentate gyrus. Differences in intrinsic progenitor cell activity could underlie these different expansion capacities. Thus, we compared the renewal- expansion and multipotency of dentate gyrus and CA1 precursors isolated in vitro. We found that the dissected CA1 region, including the periventricular zone, is enriched in neurosphere-forming cells (presumed stem cells), which respond to either EGF or FGF-2. Dentate gyrus contains fewer neurosphere-forming cells and none that respond to FGF-2 alone. Neurospheres generated from CA1 were multipotent and produced neurons, astrocytes, and oligodendrocytes, while dentate gyrus neurospheres mostly produced glial cells. The analysis of the effects of EGF on organotypic cultures of hippocampal slices depicted similar features: BrdU and Nestin immunoreactivities increased after EGF treatment in CA1 but not in the dentate gyrus. These results suggest that CA1 precursors are more stem-cell-like than granule cell precursors, which may represent a more restricted precursor cell.},
	Author = {Becq, H. and Jorquera, I. and Ben-Ari, Y. and Weiss, S. and Represa, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Cell Differentiation;Phosphopyruvate Hydratase;24 Pubmed search results 2008;Immunohistochemistry;Kainic Acid;Animals;Cells, Cultured;Epidermal Growth Factor;Hippocampus;In Vitro;Cell Count;Transcription Factors;Fibroblast Growth Factor 2;Basic Helix-Loop-Helix Transcription Factors;Azacitidine;Statistics, Nonparametric;Analysis of Variance;Intermediate Filament Proteins;Drug Interactions;Excitatory Amino Acid Agonists;Bromodeoxyuridine;21 Epilepsy;DNA-Binding Proteins;Comparative Study;Enzyme Inhibitors;Time Factors;Dose-Response Relationship, Drug;Stem Cells;21 Neurophysiology;Cell Proliferation;Mice;Research Support, Non-U.S. Gov't;Neurons;Nerve Tissue Proteins;Dentate Gyrus},
	Month = {2},
	Nlm_Id = {0213640},
	Number = {2},
	Organization = {INMED/INSERM U29, Marseille, France.},
	Pages = {243-61},
	Pubmed = {15459894},
	Title = {Differential properties of dentate gyrus and CA1 neural precursors},
	Uuid = {2CE64E7C-17EB-4B3E-B606-83B4ED6AB637},
	Volume = {62},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.20089}}

@article{Bedard:2004,
	Abstract = {The subventricular zone (SVZ) is known to be the major source of neural stem cells in the adult brain. In rodents and nonhuman primates, many neuroblasts generated in the SVZ migrate in chains along the rostral migratory stream (RMS) to populate the olfactory bulb (OB) with new granular and periglomerular interneurons. In order to know if such a phenomenon exists in the adult human brain, we applied single and double immunostaining procedures to olfactory bulbs obtained following brain necropsy in normal adult human subjects. Double immunofluorescence labelling with a confocal microscope served to visualize cells that express markers of proliferation and immature neuronal state as well as markers that are specific to olfactory interneurons. Newborn cells that express cell cycle proteins [Ki-67, proliferating cell nuclear antigen (PCNA)] were detected in the granular and glomerular layers (GLs) of the human olfactory bulb; these cells coexpressed markers of immature neuronal state, such as Doublecortin (DCX), NeuroD and Nestin. Numerous differentiating cells expressed molecular markers of early committed neurons [beta-tubulin class III (TuJ1)] and were also immunoreactive for glutamic acid decarboxylase (GAD), a marker of GABAergic neurons, or tyrosine hydroxylase (TH), a marker of dopaminergic neurons. Other early committed neurons expressed the calcium-binding proteins calretinin (CR) or parvalbumin (PV). These results provide strong evidence for the existence of adult neurogenesis in the human olfactory system. Despite its relatively small size compared to that in rodents and nonhuman primates, the olfactory bulb in humans appears to be populated, throughout life, by new granular and periglomerular neurons that express a wide variety of chemical phenotypes. 0165-3806 Journal Article},
	Author = {Bedard, A. and Parent, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {A, B pdf;01 Adult neurogenesis general},
	Number = {1-2},
	Organization = {Centre de recherche Universite Laval Robert-Giffard, 2601, de la Canardiere, Local F-6500, Beauport, Quebec, Canada G1J 2G3.},
	Pages = {159-68},
	Title = {Evidence of newly generated neurons in the human olfactory bulb},
	Uuid = {35520F15-A307-4859-A8BA-960EBF838577},
	Volume = {151},
	Year = {2004},
	url = {papers/Bedard_BrainResDevBrainRes2004.pdf}}

@article{Beech:2004,
	Abstract = {The subventricular zone (SVZ) is a major neurogenic region in the adult brain. Cells from the SVZ give rise to two populations of olfactory bulb interneurons: the granule cells and periglomerular (PG) cells. Currently, little is known about the signaling pathways that direct these newly generated neurons to become either granule or PG neurons. In the present study, we used the nestin promoter and enhancer to direct expression of the tetracycline transactivator (tTA). We generated two independent strains of nestin-tTA transgenic animals and crossed founder mice from both lines to mice containing a tetracycline-regulated transgene (mCREB) whose expression served as a marker for the activity of the nestin-tTA transgene. mCREB expression occurred in a subset of proliferating cells in the SVZ and rostral migratory stream in both lines. Surprisingly, in both lines of nestin-tTA mice transgene expression in the olfactory bulb was limited to PG neurons and was absent from granule cells, suggesting that this nestin promoter construct differentiates between the two interneuronal populations. Transgene expression occurred in several subtypes of PG neurons, including those expressing calretinin, calbindin, GAD67, and tyrosine hydroxylase. These results suggest that a unique subset of SVZ precursor cells gives rise to PG, and not granule cells. The ability to express different transgenes within this subpopulation of neuronal precursors provides a powerful system to define the signals regulating the differentiation and survival of adult-generated neurons in the olfactory bulb.},
	Author = {Beech, Robert D. and Cleary, Muriel A. and Treloar, Helen B. and Eisch, Amelia J. and Harrist, Alexia V. and Zhong, Weimin and Greer, Charles A. and Duman, Ronald S. and Picciotto, Marina R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Transgenes;13 Olfactory bulb anatomy;DNA-Binding Protein, Cyclic AMP-Responsive;03 Adult neurogenesis progenitor source;Comparative Study;Nerve Tissue Proteins;Gene Expression Regulation;Stem Cells;Promoter Regions (Genetics);Mice, Transgenic;Support, U.S. Gov't, P.H.S.;Olfactory Bulb;Animals;Mice;Support, Non-U.S. Gov't;Neurons;Intermediate Filament Proteins},
	Month = {7},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Psychiatry, Yale University School of Medicine, 34 Park Street, 3rd Floor, New Haven, CT 06508, USA. robert.beech\@yale.edu},
	Pages = {128-41},
	Pubmed = {15176089},
	Title = {Nestin promoter/enhancer directs transgene expression to precursors of adult generated periglomerular neurons},
	Uuid = {631DD709-3120-4135-B2C0-5ACA90D3F00E},
	Volume = {475},
	Year = {2004},
	url = {papers/Beech_JCompNeurol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20179}}

@article{Beggs:2003,
	Abstract = {Targeted deletion of focal adhesion kinase (fak) in the developing dorsal forebrain resulted in local disruptions of the cortical basement membrane located between the neuroepithelium and pia-meninges. At disruption sites, clusters of neurons invaded the marginal zone. Retraction of radial glial endfeet, midline fusion of brain hemispheres, and gliosis also occurred, similar to type II cobblestone lissencephaly as seen in congenital muscular dystrophy. Interestingly, targeted deletion of fak in neurons alone did not result in cortical ectopias, indicating that fak deletion from glia is required for neuronal mislocalization. Unexpectedly, fak deletion specifically from meningeal fibroblasts elicited similar cortical ectopias in vivo and altered laminin organization in vitro. These observations provide compelling evidence that FAK plays a key signaling role in cortical basement membrane assembly and/or remodeling. In addition, FAK is required within neurons during development because neuron-specific fak deletion alters dendritic morphology in the absence of lamination defects.},
	Author = {Beggs, Hilary E. and Schahin-Reed, Dorreyah and Zang, Keling and Goebbels, Sandra and Nave, Klaus Armin and Gorski, Jessica and Jones, Kevin R. and Sretavan, David and Reichardt, Louis F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Mice;Focal Adhesion Protein-Tyrosine Kinases;Dystroglycans;Precipitin Tests;Cells, Cultured;Carrier Proteins;Staining and Labeling;Microtubule-Associated Proteins;DNA-Binding Proteins;Mice, Knockout;Protein-Tyrosine Kinase;Transcription Factors;Cerebral Cortex;Fibroblasts;Calcium-Binding Protein, Vitamin D-Dependent;Disease Models, Animal;Basement Membrane;Research Support, U.S. Gov't, P.H.S.;src-Family Kinases;Embryo;Mutation;Neurons;Serine Endopeptidases;Phosphotyrosine;Bacterial Proteins;Immunohistochemistry;Heterozygote;Extracellular Matrix Proteins;Microscopy, Electron;Phosphopyruvate Hydratase;Cytoskeletal Proteins;Comparative Study;Glial Fibrillary Acidic Protein;Astrocytes;Otx Transcription Factors;Lamins;10 Development;Research Support, Non-U.S. Gov't;Animals;Blotting, Western;Infection;Dura Mater;Focal Adhesion Kinase 1;Homeodomain Proteins;Membrane Glycoproteins;Silver Staining;Muscular Dystrophies;Cell Adhesion Molecules, Neuronal;10 Hippocampus;Nerve Tissue Proteins},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, CA 94143, USA. hbeggs\@itsa.ucsf.edu},
	Pages = {501-14},
	Pii = {S0896627303006664},
	Pubmed = {14642275},
	Title = {FAK deficiency in cells contributing to the basal lamina results in cortical abnormalities resembling congenital muscular dystrophies},
	Uuid = {82C60539-F56B-4FCE-A2BF-1921897C9641},
	Volume = {40},
	Year = {2003}}

@article{Belachew:2003,
	Abstract = {Neurogenesis is known to persist in the adult mammalian central nervous system (CNS). The identity of the cells that generate new neurons in the postnatal CNS has become a crucial but elusive issue. Using a transgenic mouse, we show that NG2 proteoglycan-positive progenitor cells that express the 2',3'-cyclic nucleotide 3'-phosphodiesterase gene display a multipotent phenotype in vitro and generate electrically excitable neurons, as well as astrocytes and oligodendrocytes. The fast kinetics and the high rate of multipotent fate of these NG2+ progenitors in vitro reflect an intrinsic property, rather than reprogramming. We demonstrate in the hippocampus in vivo that a sizeable fraction of postnatal NG2+ progenitor cells are proliferative precursors whose progeny appears to differentiate into GABAergic neurons capable of propagating action potentials and displaying functional synaptic inputs. These data show that at least a subpopulation of postnatal NG2-expressing cells are CNS multipotent precursors that may underlie adult hippocampal neurogenesis. 0021-9525 Journal Article},
	Author = {Belachew, S. and Chittajallu, R. and Aguirre, A. A. and Yuan, X. and Kirby, M. and Anderson, S. and Gallo, V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {Spheroids, Cellular;gamma-Aminobutyric Acid/metabolism;Animals, Newborn;Mice;Mice, Transgenic;Support, U.S. Gov't, P.H.S.;Cells, Cultured;03 Adult neurogenesis progenitor source;Recombinant Fusion Proteins/diagnostic use;Promoter Regions (Genetics);2',3'-Cyclic-Nucleotide Phosphodiesterases/genetics/metabolism;Models, Animal;Action Potentials;Antigens/genetics/*metabolism;Cell Differentiation/*genetics;Action Potentials/genetics;Intermediate Filament Proteins;Proteoglycans;Multipotent Stem Cells/cytology/*metabolism;Antigens;Research Support, U.S. Gov't, P.H.S.;Recombinant Fusion Proteins;Phenotype;Hippocampus/cytology/*growth &development/*metabolism;gamma-Aminobutyric Acid;Multipotent Stem Cells;Neural Pathways/cytology/growth &development/metabolism;Neurons;Proteoglycans/genetics/*metabolism;Neural Pathways;Astrocytes/cytology/metabolism;02 Adult neurogenesis migration;Hippocampus;Astrocytes;Promoter Regions (Genetics)/genetics;Neurons/cytology/*metabolism;Dentate Gyrus;BB abstr;Animals;Research Support, Non-U.S. Gov't;Oligodendroglia;Cell Differentiation;Spheroids, Cellular/cytology/metabolism;Intermediate Filament Proteins/metabolism;2',3'-Cyclic-Nucleotide Phosphodiesterases;Dentate Gyrus/cytology/growth &development/metabolism;Oligodendroglia/cytology/metabolism;Support, Non-U.S. Gov't;Nerve Tissue Proteins},
	Medline = {22581681},
	Month = {4},
	Nlm_Id = {0375356},
	Number = {1},
	Organization = {Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC 20010-2970, USA.},
	Pages = {169-86},
	Pii = {jcb.200210110},
	Pubmed = {12682089},
	Title = {Postnatal NG2 proteoglycan-expressing progenitor cells are intrinsically multipotent and generate functional neurons},
	Uuid = {E0CA380F-2C49-4328-BB6D-97EA1D852DCC},
	Volume = {161},
	Year = {2003},
	url = {papers/Belachew_JCellBiol2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200210110}}

@article{Bellander:2004,
	Abstract = {The complement cascade has been suggested to be involved in development of secondary brain damage following traumatic brain injury (TBI). Previous studies have shown that reactive microglia are involved in activation of the complement cascade following various injuries to the nervous system. Macrophages seem to have a significant role in this process, but it is still unclear whether these cells, as well as the complement components, are derived from reactive microglia or if these biological events only can occur as a result from the influx of plasma and monocytes via a disrupted blood-brain barrier (BBB). The aim of this study was to investigate the response of microglial cells and the complement system in the absence of plasma/blood components following a standardized crush injury in an entorhinal-hippocampal slice culture. There was a clear increase in complement component C1q and C5b-9-IR (Membrane Attack Complex, MAC) in the area near the crush injury. MAC-IR appeared as numerous dots in clusters which co-localized with anti-NeuN labelled neurons in the injury border zone. Complement C1q-IR co-localized with reactive microglia, co-labelled with OX42 antisera. These findings show activation of the complement cascade near the injury zone and in particular, formation of MAC at the surface of neurons in this area. There was a distinct activation of microglial cells (OX42-IR) near the site of injury, as well as an increase in ED-1 expressing macrophages. In the absence of blood and plasma components it is likely that ED-1-labelled cells represent reactive microglia transformed into macrophages. In addition, Neurons (Neun-IR) near the injury were found to co-localize with clusterin-IR indicating upregulation of a defense system to the endogenous complement attack. The present study provides evidence that microglia and complement is activated in the injury border zone of the tissue slice in a similar fashion as in vivo following TBI, despite the absence of plasma/blood products and cells. These findings support the hypothesis that reactive microglia have a key role in complement activation following TBI by local synthesis of complement with a potential impact on development of secondary neuronal insults.},
	Author = {Bellander, Bo-Michael M. and Bendel, Olof and Von Euler, Gabriel and Ohlsson, Marcus and Svensson, Mikael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0897-7151},
	Journal = {J Neurotrauma},
	Keywords = {Complement Activation;Male;Rats, Sprague-Dawley;Hippocampus;Immunohistochemistry;Female;Rats;11 Glia;Microglia;Organ Culture;Support, Non-U.S. Gov't;Entorhinal Cortex;Animals;Neurons;Brain Injuries},
	Month = {5},
	Nlm_Id = {8811626},
	Number = {5},
	Organization = {Department of Clinical Neuroscience, Section for Neurosurgery, Karolinska Hospital, Stockholm, Sweden. bob\@ks.se},
	Pages = {605-15},
	Pubmed = {15165368},
	Title = {Activation of microglial cells and complement following traumatic injury in rat entorhinal-hippocampal slice cultures},
	Uuid = {1336ED50-0F9E-4333-B78E-3A7BFA8CF66A},
	Volume = {21},
	Year = {2004},
	url = {papers/Bellander_JNeurotrauma2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/089771504774129937}}

@article{Belmonte:2004,
	Author = {Belmonte, Matthew K. and Allen, Greg and Beckel-Mitchener, Andrea and Boulanger, Lisa M. and Carper, Ruth A. and Webb, Sara J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Fragile X Syndrome;Synapses;10 Development;research support, non-u.s. gov't;Neuronal Plasticity;Neural Pathways;Cerebellum;Autistic Disorder;10 genetics malformation;Child;Humans;Brain;24 Pubmed search results 2008;review},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {42},
	Organization = {Autism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge CB2 2AH, United Kingdom.},
	Pages = {9228-31},
	Pii = {24/42/9228},
	Pubmed = {15496656},
	Title = {Autism and abnormal development of brain connectivity},
	Uuid = {57D644E1-78AC-415A-BD5F-61931A5389DF},
	Volume = {24},
	Year = {2004},
	url = {papers/Belmonte_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3340-04.2004}}

@article{Belvindrah:2002,
	Abstract = {mCD24, a glycosylphosphatidylinositol-anchored highly glycosylated molecule, is expressed on differentiating neurons during development. In the adult CNS, its expression is restricted to immature neurons located in two regions showing ongoing neurogenesis: the subventricular zone (SVZ) of the lateral ventricle pathway and the dentate gyrus (DG) of the hippocampal formation. Here, combining bromodeoxyuridine (BrdU) and proliferating cell nuclear antigen labelings we confirmed that mCD24 is expressed on proliferating cells. To determine whether the inactivation of the molecule may affect adult neurogenesis, we analyzed the phenotype of mCD24-deficient mice (mCD24-/-). We labeled cells in S-phase with a pulse, a long, or a cumulative administration of BrdU and analyzed cells in different zones according to their dividing rate (rapid and slow) both in the control and mCD24-/-. We found a significant increase in the number of rapid (in the SVZ and the DG) and slow (in the SVZ) proliferating cells. Cumulative assays revealed a global reduction of the total cell cycle duration of rapidly proliferating precursors of SVZ. We investigated the fate of supernumerary cells and observed an increased number of apoptotic cells (terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling) in the mutant SVZ. Furthermore, we found no difference in the size of the olfactory bulb between wild-type (WT) and mutant mice. In support, mCD24 deletion did not appear to affect migration in the migratory stream. A comparison of the organization of migrating precursors between WT and mCD24 -/-, both in vivo at the optic and electron microscopic levels and in SVZ cultured explants, did not show any changes in the arrangement of neuroblasts in chain-like structures. Altogether, our data suggest that mCD24 regulates negatively cell proliferation in zones of secondary neurogenesis.},
	Author = {Belvindrah, Richard and Rougon, Genevi\`{e}ve and Chazal, Genevi\`{e}ve},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Phenotype;Cell Cycle;Apoptosis;Proliferating Cell Nuclear Antigen;Antigens, CD;Cell Count;Cell Movement;Mice, Inbred C57BL;Antigens, CD24;Olfactory Bulb;Membrane Glycoproteins;Mice, Knockout;Neurons;Dentate Gyrus;In Situ Nick-End Labeling;Mice;Cell Division;24 Pubmed search results 2008;Stem Cells;Bromodeoxyuridine;Lateral Ventricles;Research Support, Non-U.S. Gov't},
	Medline = {21975474},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {9},
	Organization = {Neurogen\`{e}se et Morphogen\`{e}se dans le d{\'e}veloppement et chez l'adulte/Institut de Biologie du D{\'e}veloppement de Marseille, Centre National de la Recherche Scientifique, Universit{\'e} de la M{\'e}diterran{\'e}e, Campus de Luminy, 13288 Marseille, France.},
	Pages = {3594-607},
	Pii = {22/9/3594},
	Pubmed = {11978835},
	Title = {Increased neurogenesis in adult mCD24-deficient mice},
	Uuid = {433DCD4D-F50A-40BE-AE1F-7ECB915A7BE8},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/20026367}}

@article{Belvindrah:2007,
	Abstract = {The subventricular zone (SVZ) of the lateral ventricle is the major site of neurogenesis in the adult brain. Neuroblasts that are born in the SVZ migrate as chains along the rostral migratory stream (RMS) to the olfactory bulb. Little is known about the mechanisms that control interactions between neuroblasts during their migration. Here we show that migrating neuroblasts express beta1 integrins and that the integrin ligand laminin is localized to cell chains. Using genetically modified mice and time-lapse video recordings of SVZ explants, we demonstrate that beta1 integrins and laminin promote the formation of cell chains. Laminin also induces the aggregation of purified neuroblasts. We conclude that the formation of cell chains in the RMS is controlled in part by beta1 integrins via binding to laminin. In addition, we provide evidence that beta1 class integrins are required for the maintenance of the glial tubes and that defects in the glial tubes lead to the ectopic migration of neuroblasts into the surrounding tissue.},
	Author = {Belvindrah, Richard and Hankel, Sabine and Walker, John and Patton, Bruce L. and M{\"u}ller, Ulrich},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {02 Adult neurogenesis migration;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {10},
	Organization = {The Scripps Research Institute, Department of Cell Biology, Institute for Childhood and Neglected Disease, La Jolla, California 92037, USA.},
	Pages = {2704-17},
	Pii = {27/10/2704},
	Pubmed = {17344408},
	Title = {Beta1 integrins control the formation of cell chains in the adult rostral migratory stream},
	Uuid = {53C5C213-983D-43BF-92E5-A877D8B00F84},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2991-06.2007}}

@article{Ben-Hur:1998,
	Abstract = {Oligodendrocyte-type 2 astrocyte (O-2A) lineage cells are derived from multipotential stem cells of the developing CNS. Precursors of O-2A progenitors express the polysialylated (PSA) form of the neural cell adhesion molecule (NCAM) and are detected in neonatal rat brain glial cultures. It is unclear how such PSA-NCAM+ "pre-progenitors" are related to neural stem cells and whether they still have the potential to differentiate along several neural lineages. Here we isolated PSA-NCAM+ pre-progenitor cells from glial cultures by immunopanning and found that most of these cells expressed nestin and PDGF-receptor-alpha but not O-2A antigens. PSA-NCAM+ cells synthesized transcripts for fibroblast growth factor (FGF) receptors 1, 2, and 3 and responded to FGF2 by survival and proliferation, growing into large clusters resembling neural spheres. FGF2-induced proliferation of PSA-NCAM+ pre-progenitors was significantly enhanced by thyroid hormone (T3), which on its own did not increase cell survival or mitosis. After adhesion and withdrawal of the mitogen, spheres generated mostly oligodendrocytes and astrocytes but very rarely neurons. PSA-NCAM immunopanned cells grown in epidermal growth factor (EGF) also adopted a mostly glial fate after differentiation. In contrast, PSA-NCAM-negative cells and striatal neonatal stem cells, grown in EGF or FGF2, generated the three CNS cell types. Like neural stem cells, PSA-negative cells generated more oligodendrocytes and fewer neurons when expanded in FGF2 and T3. Thus emergence of PSA-NCAM at the surface of neonatal brain precursors coincides with their restriction to a glial fate. T3 modulates these events by enhancing PSA-NCAM+ pre-progenitor growth in FGF2 and favoring an oligodendrocyte fate.},
	Author = {Ben-Hur, T. and Rogister, B. and Murray, K. and Rougon, G. and Dubois-Dalcq, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Astrocytes;Rats;Protein Precursors;Oligodendroglia;Rats, Sprague-Dawley;Fibroblast Growth Factor 2;03 Adult neurogenesis progenitor source;Receptors, Thyroid Hormone;Antigens;Animals, Newborn;Sialic Acids;Cell Lineage;Neural Cell Adhesion Molecule L1;Cell Division;Stem Cells;Nerve Tissue Proteins;Triiodothyronine;Neural Cell Adhesion Molecules},
	Medline = {98337877},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {15},
	Organization = {Unite de Neurovirologie et R{\'e}g{\'e}n{\'e}ration du Syst\`{e}me Nerveux, Institut Pasteur, 75724 Paris, France.},
	Pages = {5777-88},
	Pubmed = {9671666},
	Title = {Growth and fate of PSA-NCAM+ precursors of the postnatal brain},
	Uuid = {0759F17A-CC26-4A91-B288-41DBEE00EE38},
	Volume = {18},
	Year = {1998},
	url = {papers/Ben-Hur_JNeurosci1998.pdf}}

@article{Bengzon:1997,
	Abstract = {Neuronal apoptosis was observed in the rat dentate gyrus in two experimental models of human limbic epilepsy. Five hours after one hippocampal kindling stimulation, a marked increase of in situ terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) of fragmented DNA was observed in nuclei located within and on the hilar border of the granule cell layer and in the polymorphic region. Forty kindling stimulations with 5-min interval produced higher numbers of labeled nuclei compared with one stimulation. The increase of TUNEL-positive nuclei was prevented by the protein synthesis inhibitor cycloheximide but not affected by the N-methyl-D-aspartate receptor antagonist MK-801. Kainic acid-induced seizures lead to a pattern of labeling in the hippocampal formation identical to that evoked by kindling. A large proportion of cells displaying TUNEL-positive nuclei was double-labeled by the neuron-specific antigen NeuN, demonstrating the neuronal identity of apoptotic cells. Either 1 or 40 kindling stimulations also gave rise to a marked increase of the number of cells double-labeled with the mitotic marker bromodeoxyuridine and NeuN in the subgranular zone and on the hilar border of the dentate granule cell layer. The present data show that single and intermittent, brief seizures induce both apoptotic death and proliferation of dentate gyrus neurons. We hypothesize that these processes, occurring early during epileptogenesis, are primary events in the development of hippocampal pathology in animals and possibly also in patients suffering from temporal lobe epilepsy. 0027-8424 Journal Article},
	Author = {Bengzon, J. and Kokaia, Z. and Elmer, E. and Nanobashvili, A. and Kokaia, M. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Rats, Sprague-Dawley;D abstr;Rats;Apoptosis;Cell Division;Limbic System/*pathology/physiopathology;06 Adult neurogenesis injury induced;Dentate Gyrus/*pathology/physiopathology;Support, Non-U.S. Gov't;Animals;Neurons/*pathology;Male;Epilepsy/*pathology/physiopathology},
	Number = {19},
	Organization = {Section of Restorative Neurology, Wallenberg Neuroscience Center, University Hospital, S-221 85 Lund, Sweden. johan.begzon\@neurol.lu.se},
	Pages = {10432-7},
	Pubmed = {9294228},
	Title = {Apoptosis and proliferation of dentate gyrus neurons after single and intermittent limbic seizures},
	Uuid = {67C412E5-EC82-11DA-8605-000D9346EC2A},
	Volume = {94},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9294228}}

@article{Bennett:2003,
	Abstract = {Neurofibromatosis type 1 (NF1) patients are predisposed to learning disabilities, macrocephaly, and brain tumors as well as abnormalities on magnetic resonance imaging that are postulated to result from abnormal myelination. Here we show that Nf1+/- spinal cords in adult mice have more than twofold-increased numbers of NG2+ progenitor cells. Nf1-/- embryonic spinal cords have increased numbers of Olig2+ progenitors. Also, cultures from Nf1 mutant embryos with hemizygous and biallelic Nf1 mutations have dramatically increased numbers of CNS oligodendrocyte progenitor cells. In medium that allows growth of neuroepithelial cells and glial progenitors, mutant cells hyper-respond to FGF2, have increased basal and FGF-stimulated Ras-GTP, and fail to accumulate when treated with a farnesyltransferase inhibitor. Cell accumulation results in part from increased proliferation and decreased cell death. In contrast to wild-type cells, Nf1-/- progenitors express the glial differentiation marker O4 while retaining expression of the progenitor marker nestin. Nf1 mutant progenitors also abnormally coexpress the glial differentiation markers O4 and GFAP. Importantly, Nf1-/- spinal cord-derived oligodendrocyte progenitors, which are amplified 12-fold, retain the ability to form oligodendrocytes after in vivo transplantation. The data reveal a key role for neurofibromin and Ras signaling in the maintenance of CNS progenitor cell pools and also suggest a potential role for progenitor cell defects in the CNS abnormalities of NF1 patients. 1529-2401 Journal Article},
	Author = {Bennett, M. R. and Rizvi, T. A. and Karyala, S. and McKinnon, R. D. and Ratner, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Heterozygote;Spinal Cord/*pathology;Animals;Cells, Cultured;Stem Cell Transplantation;Neurons/pathology;ras Proteins/metabolism;Neurofibromin 1/*genetics;Female;Cell Count;Neurofibromatosis 1/genetics/*pathology;Mutation;Enzyme Inhibitors/pharmacology;11 Glia;Oligodendroglia/*pathology;Male;Mice, Neurologic Mutants;Mice, Inbred C57BL;Support, Non-U.S. Gov't;Cell Division/genetics;Mice, Knockout;Homozygote;Fibroblast Growth Factor 2/pharmacology;Stem Cells/drug effects/metabolism/*pathology;Support, U.S. Gov't, P.H.S.;Support, U.S. Gov't, Non-P.H.S.;Antigens, Differentiation/biosynthesis;Mice;G pdf},
	Number = {18},
	Organization = {Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0521, USA.},
	Pages = {7207-17},
	Pubmed = {12904481},
	Title = {Aberrant growth and differentiation of oligodendrocyte progenitors in neurofibromatosis type 1 mutants},
	Uuid = {243C5C92-2D88-4B09-A7FD-DA2BCA87DD7D},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12904481}}

@article{Benraiss:2001,
	Abstract = {Neural progenitor cells persist throughout the adult forebrain subependyma, and neurons generated from them respond to brain-derived neurotrophic factor (BDNF) with enhanced maturation and survival. To induce neurogenesis from endogenous progenitors, we overexpressed BDNF in the adult ventricular zone by transducing the forebrain ependyma to constitutively express BDNF. We constructed a bicistronic adenovirus bearing BDNF under cytomegalovirus (CMV) control, and humanized green fluorescent protein (hGFP) under internal ribosomal entry site (IRES) control. This AdCMV:BDNF:IRES:hGFP (AdBDNF) was injected into the lateral ventricles of adult rats, who were treated for 18 d thereafter with the mitotic marker bromodeoxyuridine (BrdU). Three weeks after injection, BDNF averaged 1 &mgr;g/gm in the CSF of AdBDNF-injected animals but was undetectable in control CSF. In situ hybridization demonstrated BDNF and GFP mRNA expression restricted to the ventricular wall. In AdBDNF-injected rats, the olfactory bulb exhibited a >2.4-fold increase in the number of BrdU(+)-betaIII-tubulin(+) neurons, confirmed by confocal imaging, relative to AdNull (AdCMV:hGFP) controls. Importantly, AdBDNF-associated neuronal recruitment to the neostriatum was also noted, with the treatment-induced addition of BrdU(+)-NeuN(+)- betaIII-tubulin(+) neurons to the caudate putamen. Many of these cells also expressed glutamic acid decarboxylase, cabindin-D28, and DARPP-32 (dopamine and cAMP-regulated phosphoprotein of 32 kDa), markers of medium spiny neurons of the neostriatum. These newly generated neurons survived at least 5-8 weeks after viral induction. Thus, a single injection of adenoviral BDNF substantially augmented the recruitment of new neurons into both neurogenic and non-neurogenic sites in the adult rat brain. The intraventricular delivery of, and ependymal infection by, viral vectors encoding neurotrophic agents may be a feasible strategy for inducing neurogenesis from resident progenitor cells in the adult brain.},
	Author = {Benraiss, A. and Chmielnicki, E. and Lerner, K. and Roh, D. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {J Neurosci},
	Keywords = {C both;04 Adult neurogenesis factors},
	Number = {17},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021.},
	Pages = {6718-31.},
	Title = {Adenoviral brain-derived neurotrophic factor induces both neostriatal and olfactory neuronal recruitment from endogenous progenitor cells in the adult forebrain},
	Uuid = {ED3188D6-8364-49A6-B474-5BE1935AF1A1},
	Volume = {21},
	Year = {2001},
	url = {papers/Benraiss_JNeurosci2001.pdf}}

@article{Berman:1997,
	Abstract = {Radial glia are present at the earliest stage of cerebral cortical development, and later they transform into astrocytes. Other glial cells including astrocytes and oligodendrocytes are thought to appear only after neuron generation is complete and the cortical layers are formed. Little is known of when and where microglia enter the central nervous system and proliferate. We addressed the question of the origin of these three glial cell types in the developing ferret cerebral cortex. We assessed the temporal pattern of glial cell division by administering [3H]thymidine to label cells in S phase, and by using survival periods of 1-2 h to label dividing cells in situ. Labeled cells were identified in the developing intermediate zone of the ferret cerebral wall. These cells were present at E28, and reached a maximum number at P1. Double labeling experiments identified these cells as astrocytes, oligodendrocytes or microglia. None of the dividing cells expressed neuronal markers. These data show that all three types of glia are generated in the developing subcortical white matter, and that glial progenitors are present in the intermediate zone as soon as it becomes a recognizable structure. These data also show that the period of glial generation overlaps extensively with the period of neuron generation, since neuron generation is not complete until the end of the second postnatal week in the ferret.},
	Author = {Berman, N. E. and Johnson, J. K. and Klein, R. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Neuroglia/metabolism/*physiology;Pregnancy;G;Cerebral Cortex/*cytology/*growth &development/metabolism;Bromodeoxyuridine/pharmacology;Thymidine/metabolism;Microglia/physiology;Phenotype;Female;Cell Count;Animal;11 Glia;Antimetabolites/pharmacology;Support, U.S. Gov't, P.H.S.;Animals, Newborn/physiology;Immunohistochemistry;Biological Markers;Ferrets/*physiology},
	Number = {1-2},
	Organization = {Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City 66160-7400, USA. Nberman\@knmc.edu},
	Pages = {149-64.},
	Title = {Early generation of glia in the intermediate zone of the developing cerebral cortex},
	Uuid = {15C29F53-C9A7-4940-894B-463DD275E459},
	Volume = {101},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9263589}}

@article{Bernad:1994,
	Abstract = {An efficient procedure for the insertion of genetic markers into a large proportion of the mouse haemopoietic system was developed, based on the in vitro expansion of retrovirally infected bone marrow and selection of the transduced cells. Bone marrow cells harvested 4 d after 5-FU treatment were incubated under IL-3/SCF stimulation and their growth dynamic, susceptibility to retroviral infection and reconstitution capacity evaluated throughout the incubation period. On the third day of culture a maximum expansion in the CFU-GM and CFU-S12 progenitor pools was observed (130- and 15-fold, respectively), with no apparent impairment in long-term repopulating precursors. This expansion was, however, accompanied by a net decrease in the CFU-GM susceptibility to the infection by supernatants containing a Moloney-derived ecotropic retroviral vector carrying the neor gene. The designed protocol thus involved the infection of freshly harvested 5-FU-treated bone marrow, followed by expansion under IL-3/SCF stimulation and selection for resistance to G418. This procedure allowed us to harvest up to 780 CFU-GM and 50 CFU-S12 per 10(5) bone marrow cells, free from non-genetically marked progenitors. Most of the animals reconstituted with the transduced marrow bore, for at least 5 months, a very high proportion of bone marrow, spleen and thymus cells tagged with the reporter gene. These results, together with the high percentage of haemopoietic precursors bearing the neor gene and expressing resistance to G418 5 months after the transplantation indicates that long-term lympho-haemopoietic repopulating cells were efficiently transduced and selected in vitro under conditions that preserve their self-renewal and differentiation properties. This gene-transfer methodology may improve the development of gene therapy protocols where the purging of non-transduced precursors would guarantee a lasting and uniform expression of exogenous genes.},
	Author = {Bernad, A. and Varas, F. and Gallego, J. M. and Almendral, J. M. and Bueren, J. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0007-1048},
	Journal = {Br J Haematol},
	Keywords = {Mice, Inbred BALB C;Animals;Hematopoietic Cell Growth Factors;Cells, Cultured;Bone Marrow Transplantation;Recombinant Proteins;Female;Interleukin-3;Mice, Inbred C57BL;Disease Susceptibility;11 Glia;Retroviridae;Genetic Vectors;Blotting, Southern;Male;Bone Marrow Cells;Retroviridae Infections;Gene Transfer Techniques;Mice;Hematopoietic Stem Cells;Stem Cell Factor;Research Support, Non-U.S. Gov't},
	Medline = {95034235},
	Month = {5},
	Nlm_Id = {0372544},
	Number = {1},
	Organization = {Unidad de Biolog{\'\i}a Molecular y Celular, CIEMAT, Madrid, Spain.},
	Pages = {6-17},
	Pubmed = {7524619},
	Title = {Ex vivo expansion and selection of retrovirally transduced bone marrow: an efficient methodology for gene-transfer to murine lympho-haemopoietic stem cells},
	Uuid = {28C4E4E0-8EC7-486F-9950-1845A717E5B1},
	Volume = {87},
	Year = {1994}}

@article{Bernier:2002,
	Abstract = {The subventricular zone remains mitotically active throughout life in rodents. Studies with tritiated thymidine, which is incorporated into the DNA of mitotic cells, have revealed that the rodent subventricular zone produces neuroblasts that migrate toward the olfactory bulb along the rostral migratory stream. A similar migratory stream has been documented in monkeys by using the thymidine analogue BrdUrd. The same approach showed that neurogenesis occurred in the dentate gyrus of adult primates, including humans. In the present study, experiments combining injections of BrdUrd and the dye 1,1'-dioctadecyl-3,3,3',3'-tetramethylindo-carbocyanine, with the immunostaining for molecular markers of neurogenesis (polysialylated neural cell adhesion molecule, beta-tubulin-III, collapsin response mediator protein-4, neuronal nuclear protein) in New World (Saimiri sciureus) and Old World (Macaca fascicularis) monkeys have revealed that new neurons are produced in the amygdala, piriform cortex, and adjoining inferior temporal cortex in adult primates. These newborn neurons expressed the antiapoptotic protein Bcl-2 and formed a more-or-less continuous pathway that extended from the tip of the temporal ventricular horn to the deep portion of the temporal lobe. The production of newborn neurons in the amygdala, piriform cortex, and inferior temporal cortex seems to parallel the continuing addition of neurons in the olfactory bulb. These two concomitant phenomena may ensure structural stability and functional plasticity to the primate olfactory system and temporal lobe. 22177226 0027-8424 Journal Article},
	Author = {Bernier, P. J. and Bedard, A. and Vinet, J. and Levesque, M. and Parent, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {01 Adult neurogenesis general;A both},
	Number = {17},
	Organization = {Centre de Recherche Universite Laval-Robert-Giffard, 2601, Chemin de la Canardiere, Local F-6500, Beauport, QC, Canada G1J 2G3.},
	Pages = {11464-9},
	Title = {Newly generated neurons in the amygdala and adjoining cortex of adult primates},
	Uuid = {F334D8FC-CDEF-11D9-B244-000D9346EC2A},
	Volume = {99},
	Year = {2002},
	url = {papers/Bernier_ProcNatlAcadSciUSA2002.pdf}}

@article{Berns:2004,
	Abstract = {RNA interference (RNAi) is a powerful new tool with which to perform loss-of-function genetic screens in lower organisms and can greatly facilitate the identification of components of cellular signalling pathways. In mammalian cells, such screens have been hampered by a lack of suitable tools that can be used on a large scale. We and others have recently developed expression vectors to direct the synthesis of short hairpin RNAs (shRNAs) that act as short interfering RNA (siRNA)-like molecules to stably suppress gene expression. Here we report the construction of a set of retroviral vectors encoding 23,742 distinct shRNAs, which target 7,914 different human genes for suppression. We use this RNAi library in human cells to identify one known and five new modulators of p53-dependent proliferation arrest. Suppression of these genes confers resistance to both p53-dependent and p19ARF-dependent proliferation arrest, and abolishes a DNA-damage-induced G1 cell-cycle arrest. Furthermore, we describe siRNA bar-code screens to rapidly identify individual siRNA vectors associated with a specific phenotype. These new tools will greatly facilitate large-scale loss-of-function genetic screens in mammalian cells.},
	Author = {Berns, Katrien and Hijmans, E. Marielle and Mullenders, Jasper and Brummelkamp, Thijn R. and Velds, Arno and Heimerikx, Mike and Kerkhoven, Ron M. and Madiredjo, Mandy and Nijkamp, Wouter and Weigelt, Britta and Agami, Reuven and Ge, Wei and Cavet, Guy and Linsley, Peter S. and Beijersbergen, Roderick L. and Bernards, Ren{\'e}},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {RNA, Small Interfering;Genetic Vectors;Down-Regulation;Gene Library;p14ARF Protein;Human;Cell Line, Tumor;Retroviridae;Cell Division;Cyclins;RNA Interference;23 RNAi;Reproducibility of Results;Protein p53;Cloning, Molecular;23 Technique;Fibroblasts},
	Month = {3},
	Nlm_Id = {0410462},
	Number = {6981},
	Organization = {Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.},
	Pages = {431-7},
	Pii = {nature02371},
	Pubmed = {15042092},
	Title = {A large-scale RNAi screen in human cells identifies new components of the p53 pathway},
	Uuid = {B4BD274A-63B0-4649-B973-4BD3490A264D},
	Volume = {428},
	Year = {2004},
	url = {papers/Berns_Nature2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature02371}}

@article{Berry:2002,
	Abstract = {We present evidence that NG2+ glia are an integral part of an oligodendrocyte/synantocyte (OS) lineage stream the progenitors of which begin to produce both glial phenotypes at about birth. The NG2 CSPG is differentially distributed within the OS lineage, being expressed in progenitors and synantocytes but not in oligodendrocytes. All cells in the OS lineage, except the primordial stem cells, express O4. The oligodendrocyte line reacts with CD9, but synantocytes are CD9-. Nonetheless, synantocytes are morphologically complex and specialised glia which contact axolemma in myelinated fibres at nodes of Ranvier and synaptic terminals, and form >99\%of all NG2+ glia in the adult CNS. Thus, the other NG2+ phenotype, the adult oligodendrocyte progenitor cell (AOPC), constitutes a small population of <1\%of all NG2+ glia in the mature CNS. AOPC are a heterogeneous set of cells probably originating from multiple sources which, by definition, produce oligodendrocytes in the adult to replace loss after trauma, demyelination and normal 'wear and tear'. The definitive functions of synantocytes remain undefined. 0300-4864 Journal Article},
	Author = {Berry, M. and Hubbard, P. and Butt, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurocytol},
	Keywords = {11 Glia;G pdf},
	Number = {6-7},
	Organization = {Neural Damage and Repair, Centre for Neuroscience Research, Hodgkin Building, GKT School of Biomedical Sciences, Guy's Campus, London Bridge, London SE1 1UL, UK. martin.berry\@kcl.ac.uk},
	Pages = {457-67},
	Pubmed = {14501216},
	Title = {Cytology and lineage of NG2-positive glia},
	Uuid = {21E0C200-2C7E-4B96-B2C6-40F21160868E},
	Volume = {31},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14501216}}

@article{Bertolotto:1993,
	Abstract = {We used six monoclonal antibodies (MAb) recognizing epitopes within keratan sulfate (KS) chains for an immunocytochemical study of adult rat brain. One of the MAb selectively stained microglia and their ramified processes. KS-positive cells were found throughout the CNS in both paraffin-embedded and cryostat sections; the greatest number were present in hippocampus and brainstem. In the cortex the positive processes of some cells surrounded neuronal somata. In the white matter the processes were both parallel and perpendicular to the axon bundles. Double staining showed that KS-positive cells did not express astrocytic or oligodendroglial markers. By immunoelectron microscopy, the positivity was localized around the perikarya and cell processes of small cells with peripheral chromatin clumps and dark cytoplasm, which often contained secondary lysosomes. The KS-positive cells did not contribute to myelin sheaths and were not surrounded by a basal membrane. In addition to the cellular staining, three other MAb stained the white matter diffusely. Anti-KS MAb are therefore proposed as immunohistochemical markers for ramified microglia in both paraffin and cryostat sections of adult rat brain.},
	Author = {Bertolotto, A. and Caterson, B. and Canavese, G. and Migheli, A. and Schiffer, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0022-1554},
	Journal = {J Histochem Cytochem},
	Keywords = {Support, Non-U.S. Gov't;Paraffin Embedding;Brain Chemistry;Keratan Sulfate;Neuroglia;Rats;Antibodies, Monoclonal;Not relevant;11 Glia;Frozen Sections;Fluorescent Antibody Technique;Peptide Hydrolases;Microscopy, Immunoelectron;Brain;Immunoenzyme Techniques;Animals},
	Medline = {93195291},
	Month = {4},
	Nlm_Id = {9815334},
	Number = {4},
	Organization = {Clinica Neurologica II, Universit\`{a}di Torino, Italy.},
	Pages = {481-7},
	Pubmed = {8450191},
	Title = {Monoclonal antibodies to keratan sulfate immunolocalize ramified microglia in paraffin and cryostat sections of rat brain},
	Uuid = {BF823A1A-292A-4512-A7DE-1ECD161530DF},
	Volume = {41},
	Year = {1993},
	url = {papers/Bertolotto_JHistochemCytochem1993.pdf}}

@article{Besancon:1981,
	Abstract = {0006-291x Journal Article},
	Author = {Besancon, F. and Bourgeade, M. F. and Justesen, J. and Ferbus, D. and Thang, M. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Biochem Biophys Res Commun},
	Keywords = {Cell Transformation, Viral/*drug effects;2',5'-Oligoadenylate Synthetase;Mice, Inbred BALB C;Nucleotidyltransferases/*metabolism;Interferons/pharmacology;Kinetics;EE, DMSO, abstr;Cell Line;08 Aberrant cell cycle;Moloney murine leukemia virus/*genetics;Dimethyl Sulfoxide/*pharmacology;Cell Differentiation/drug effects;Support, Non-U.S. Gov't;Animals;Mice;Butyrates/*pharmacology},
	Number = {1},
	Pages = {16-24},
	Pubmed = {6172125},
	Title = {Two inducers of cell differentiation enhance the 2'5'oligoadenylate synthetase activity in MSV transformed cells},
	Uuid = {AA6A7ABE-4D9C-43F6-9C7F-65E4DB0679B7},
	Volume = {103},
	Year = {1981},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6172125}}

@article{Beschorner:2002,
	Abstract = {The immune response in the central nervous system (CNS) is under tight control of regulatory mechanisms, resulting in the establishment of immune privilege. CNS injury induces an acute inflammatory reaction, composed mainly of invading leukocytes and activated microglial cells/macrophages. The generation of this robust immune response requires binding of receptors such as CD14, a pattern recognition receptor of the immune system. CD14, a surface molecule of monocytic cells, is up-regulated after monocyte stimulation and is involved in cellular activation. To examine CD14 expression in human brain lesions we investigated sections of brains obtained at autopsy from 25 cases following closed traumatic brain injury (TBI) and 5 control brains by immunohistochemistry. Detection of CD14 in controls demonstrated constitutive expression by perivascular cells, but not in parenchymal microglial cells, equivalent to known expression pattern of ED2 in rats. Following TBI, numbers of CD14(+) cells in perivascular spaces and in the brain parenchyma increased in parallel within 1-2 days, both at the lesion and in adjacent perilesional areas. The number of CD14(+) cells in perivascular spaces and in the brain parenchyma reached maximum levels within 4-8 days and remained elevated until weeks after trauma. In contrast to activated parenchymal microglia/macrophages, resting parenchymal microglial cells lacked CD14. Thus, early CD14 expression constitutes an essential part of the acute inflammatory CNS response following trauma.},
	Author = {Beschorner, Rudi and Nguyen, Thai D. and G{\"o}zalan, Fatma and Pedal, Ingo and Mattern, Rainer and Schluesener, Hermann J. and Meyermann, Richard and Schwab, Jan M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Research Support, Non-U.S. Gov't;Adolescent;Monocytes;Antigens, Differentiation, Myelomonocytic;Middle Aged;Macrophages;Humans;Brain;Antigens, Differentiation;Female;Cell Membrane;Extracellular Space;Antigens, CD;Microglia;11 Glia;Chemotaxis, Leukocyte;Antigens, CD14;Male;Calgranulin A;Brain Injuries;Aged;Aged, 80 and over;Calcium-Binding Proteins;Adult;Immunohistochemistry;Histocompatibility Antigens Class II;Blood Vessels},
	Medline = {22005489},
	Month = {6},
	Nlm_Id = {0412041},
	Number = {6},
	Organization = {Institute of Brain Research, University of T{\"u}bingen, Medical School, Calwerstr. 3, 72076, Germany. rudi.beschorner\@med.uni-tuebingen.de},
	Pages = {541-9},
	Pubmed = {12012085},
	Title = {CD14 expression by activated parenchymal microglia/macrophages and infiltrating monocytes following human traumatic brain injury},
	Uuid = {A20AECDF-C0BD-4D7F-BF5F-CD5F3186706F},
	Volume = {103},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00401-001-0503-7}}

@article{Bessis:2007,
	Abstract = {Microglia have long been characterized by their immune function in the nervous system and are still mainly considered in a beneficial versus detrimental dialectic. However a review of literature enables to shed novel lights on microglial function under physiological conditions. It is now relevant to position these cells as full time partners of neuronal function and more specifically of synaptogenesis and developmental apoptosis. Indeed, microglia can actively control neuronal death. It has actually been shown in retina that microglial nerve growth factor (NGF) is necessary for the developmental apoptosis to occur. Similarly, in cerebellum, microglia induces developmental Purkinje cells death through respiratory burst. Furthermore, in spinal cord, microglial TNFalpha commits motoneurons to a neurotrophic dependent developmental apoptosis. Microglia can also control synaptogenesis. This is suggested by the fact that a mutation in KARAP/DAP12, a key protein of microglial activation impacts synaptic functions in hippocampus, and synapses protein content. In addition it has been now demonstrated that microglial brain-derived neurotrophin factor (BDNF) directly regulates synaptic properties in spinal cord. In conclusion, microglia can control neuronal function under physiological conditions and it is known that neuronal activity reciprocally controls microglial activation. We will discuss the importance of this cross-talk which allows microglia to orchestrate the balance between synaptogenesis and neuronal death occurring during development or injuries. (c) 2006 Wiley-Liss, Inc.},
	Author = {Bessis, Alain and B{\'e}chade, Catherine and Bernard, Delphine and Roumier, Anne},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Biologie Cellulaire de la Synapse, Inserm U789, Ecole Normale Sup{\'e}rieure, 46 rue d'Ulm 75005 Paris, France.},
	Pages = {233-8},
	Pubmed = {17106878},
	Title = {Microglial control of neuronal death and synaptic properties},
	Uuid = {45C5A73E-0932-4090-ABF9-C60B4DFD984A},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20459}}

@article{Bessis:2005,
	Abstract = {Tumor necrosis factor-alpha (TNFalpha) is a prototypic inflammatory cytokine up-regulated in most if not all neurodegenerative diseases. Many studies have reported variable roles in the adult or pathological brain. In contrast, the implication of TNFalpha in developmental neuronal cell death has been well documented in few studies. In sympathetic and trigeminal neurons, TNFalpha acts in an autocrine manner to induce immediate cell death on neurotrophic factor deprivation. In the spinal cord, TNFalpha is transiently produced by macrophages and commits motoneurons to become competent to die 2 days later. TNFalpha is also likely to induce immediate and delayed prodeath effects in adult and pathological tissues. Data obtained in embryonic systems will thus help to develop new therapeutic approaches to pathological neuronal death in adults.},
	Author = {Bessis, Alain and Bernard, Delphine and Triller, Antoine},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1073-8584},
	Journal = {Neuroscientist},
	Keywords = {10 Development;11 Glia},
	Month = {8},
	Nlm_Id = {9504819},
	Number = {4},
	Organization = {Laboratoire de Biologie Cellulaire de la Synapse Normale et Pathologique. alain.bessis\@ens.fr.},
	Pages = {277-81},
	Pii = {11/4/277},
	Pubmed = {16061514},
	Title = {Tumor Necrosis Factor-\{alpha\}and Neuronal Development},
	Uuid = {48CC8928-A33C-495B-AEB1-6C3EE4A5949F},
	Volume = {11},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1177/1073858404270905}}

@article{Betarbet:1996,
	Abstract = {Our previous studies have shown that the progeny of the neuronal progenitor cells localized in a discrete region of the anterior part of the neonatal subventricular zone, referred to as the SVZa, migrate tangentially along a stereotypical and extended pathway to the olfactory bulb, and then turn radially into one of the overlying cellular layers. In this study we have examined whether the SVZa cells retain their ability to migrate and disperse when heterotopically transplanted into the striatum. SVZa cells from P0-P2 rat pups were microdissected, dissociated, labeled with the lipophilic, fluorescent dye PKH26 or the cell proliferation marker BrdU, and then transplanted into the neonatal (P0-P2) striatum. Examination of the striatum a few days after transplantation revealed aggregates of heavily labeled BrdU- positive, SVZa cells in the striatum, often situated near blood vessels. Two to four weeks after transplantation, however, the labeled SVZa cells had disseminated from their site of implantation and showed three patterns of distribution. In none of the cases was the implantation site detectable in the striatum, signifying that the cells had become incorporated in the host brain. Of the 12 brains analyzed for cell distribution, transplanted SVZa cells were confined to the striatum in 4 cases. The cells were present as individual cells or in small groups of usually two to four cells. When PKH26 was used, we found that many of the transplanted cells extended processes into the striatum. In 3 out of the 12 animals, the labeled SVZa cells were distributed along the dorsal and lateral aspects of the striatal boundary. In the remaining five animals, labeled SVZa cells appeared in both locations: within the striatum as well as along the striatal boundary. The dispersion of the transplanted cells within the striatum and the presence of the transplanted SVZa cells all along the striatal boundary, a region corresponding to the lateral cortical stream of migration of the developing forebrain, demonstrates that the isochronically transplanted SVZa cells retained their capacity to migrate.},
	Author = {Betarbet, R. and Zigova, T. and Bakay, R. A. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Cell Transplant},
	Keywords = {Fluorescent Dyes;Microinjections;Rats;Cell Movement/*physiology;Female;Animal;Rats, Sprague-Dawley;Stem Cells/*cytology/*transplantation;Retroviridae;*Transplantation, Heterotopic;17 Transplant Regeneration;Cell Survival/physiology;Male;Animals, Newborn;Support, Non-U.S. Gov't;L abstr;Neostriatum;Support, U.S. Gov't, P.H.S.;Cerebral Cortex/cytology;Immunohistochemistry;Bromodeoxyuridine},
	Number = {2},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, GA 30322, USA.},
	Pages = {165-78.},
	Title = {Migration patterns of neonatal subventricular zone progenitor cells transplanted into the neonatal striatum},
	Uuid = {16AE466F-4B4A-48A3-9BA4-F2E7E13A948D},
	Volume = {5},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8689029}}

@article{Betarbet:1996a,
	Abstract = {Earlier studies in our laboratory have demonstrated that a discrete region of the anterior part of the neonatal subventricular zone (SVZa) contains exclusively neuronal progenitor cells. The descendants of the SVZa progenitor cells are destined for the granule cell and glomerular layers of the olfactory bulb, where they differentiate into granule and periglomerular cells, the interneurons of the olfactory bulb, respectively. In the present set of experiments we examined the neurotransmitter phenotype of the SVZa-derived cells. In order to label SVZa-derived cells, the cell proliferation marker bromodeoxyuridine (BrdU) was injected into the SVZa of postnatal day 2 (P2) rats. After 3 weeks, by which time most of the SVZa-derived cells have migrated to their final destination in the bulb, the animals were perfused and their brains processed for immunohistochemistry. To identify the neurotransmitter phenotype of the SVZa-derived cells, sagittal sections of the forebrain, including the olfactory bulb, were double-labeled with an antibody to BrdU in conjunction with an antibody to gamma-amino- butyric acid (GABA) or tyrosine hydroxylase (TH), the rate limiting enzyme in the synthesis of dopamine. Using simultaneous indirect immunofluorescence to detect the presence of single- and double-labeled cells, we found that 59\%and 51\%of the BrdU-positive cells were immunoreactive for GABA in the granule cell and glomerular layers, respectively. In addition, 10\%of the BrdU-positive periglomerular cells were immunoreactive for TH. The presence of double-labeled (BrdU- positive/GABA-positive and BrdU-positive/TH-positive) cells in the olfactory bulb, demonstrates that the SVZa is a source of the GABAergic and dopaminergic interneurons of the olfactory bulb during postnatal development.},
	Author = {Betarbet, R. and Zigova, T. and Bakay, R. A. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:16:09 -0400},
	Journal = {Int J Dev Neurosci},
	Keywords = {I both;Brain/cytology/embryology;Tyrosine 3-Monooxygenase/analysis;Rats, Sprague-Dawley;13 Olfactory bulb anatomy;Female;Rats;Cerebral Ventricles/embryology;Animal;Animals, Newborn;Support, U.S. Gov't, P.H.S.;gamma-Aminobutyric Acid/*analysis;Support, Non-U.S. Gov't;Dopamine/*analysis;Interneurons/chemistry/*cytology;Male;Cell Lineage},
	Number = {7-8},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta GA 30322, USA.},
	Pages = {921-30.},
	Title = {Dopaminergic and GABAergic interneurons of the olfactory bulb are derived from the neonatal subventricular zone},
	Uuid = {16EC1042-E17A-4285-8B41-6C3A41A74A90},
	Volume = {14},
	Year = {1996},
	url = {papers/Betarbet_IntJDevNeurosci1996.pdf}}

@article{Betschinger:2003,
	Abstract = {To generate different cell types, some cells can segregate protein determinants into one of their two daughter cells during mitosis. In Drosophila neuroblasts, the Par protein complex localizes apically and directs localization of the cell fate determinants Prospero and Numb and the adaptor proteins Miranda and Pon to the basal cell cortex, to ensure their segregation into the basal daughter cell. The Par protein complex has a conserved function in establishing cell polarity but how it directs proteins to the opposite side is unknown. We show here that a principal function of this complex is to phosphorylate the cytoskeletal protein Lethal (2) giant larvae (Lgl; also known as L(2)gl). Phosphorylation by Drosophila atypical protein kinase C (aPKC), a member of the Par protein complex, releases Lgl from its association with membranes and the actin cytoskeleton. Genetic and biochemical experiments show that Lgl phosphorylation prevents the localization of cell fate determinants to the apical cell cortex. Lgl promotes cortical localization of Miranda, and we propose that phosphorylation of Lgl by aPKC at the apical neuroblast cortex restricts Lgl activity and Miranda localization to the opposite, basal side of the cell. 0028-0836 Journal Article},
	Author = {Betschinger, J. and Mechtler, K. and Knoblich, J. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Nature},
	Keywords = {Cell Cycle Proteins/metabolism;10 Development;Proteins/*metabolism;Animals;Phosphorylation;Cytoskeleton/*metabolism;Protein Transport;Cell Line;Support, Non-U.S. Gov't;Carrier Proteins/metabolism;Macromolecular Systems;Drosophila Proteins/*metabolism;Protein Kinase C/*metabolism;Drosophila melanogaster/*cytology/*metabolism;Molecular Sequence Data;Cell Division;Amino Acid Sequence;*Cell Polarity;F},
	Number = {6929},
	Organization = {Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria.},
	Pages = {326-30},
	Pubmed = {12629552},
	Title = {The Par complex directs asymmetric cell division by phosphorylating the cytoskeletal protein Lgl},
	Uuid = {819657AE-CF7F-4E49-ADE9-B1F30F5A6CA6},
	Volume = {422},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12629552}}

@article{Betzig:2006,
	Abstract = {We introduce a method for optically imaging intracellular proteins at nanometer spatial resolution. Numerous sparse subsets of photoactivatable fluorescent protein molecules were activated, localized (to approximately 2 to 25 nanometers), and then bleached. The aggregate position information from all subsets was then assembled into a superresolution image. We used this method--termed photoactivated localization microscopy--to image specific target proteins in thin sections of lysosomes and mitochondria; in fixed whole cells, we imaged vinculin at focal adhesions, actin within a lamellipodium, and the distribution of the retroviral protein Gag at the plasma membrane.},
	Author = {Betzig, Eric and Patterson, George H. and Sougrat, Rachid and Lindwasser, O. Wolf and Olenych, Scott and Bonifacino, Juan S. and Davidson, Michael W. and Lippincott-Schwartz, Jennifer and Hess, Harald F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Fluorescence;Lysosomes;research support, n.i.h., extramural ;Organelles;HIV-1;Animals;Photobleaching;Algorithms;Proteins;Mitochondria;Cercopithecus aethiops;Cell Membrane;Focal Adhesions;COS Cells;23 Technique;Recombinant Fusion Proteins;Gene Products, gag;Cell Line;Nanotechnology;Light;Vinculin;Microscopy;24 Pubmed search results 2008;Actins;Luminescent Proteins;Pseudopodia},
	Month = {9},
	Nlm_Id = {0404511},
	Number = {5793},
	Organization = {Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, VA 20147, USA. betzige\@janelia.hhmi.org},
	Pages = {1642-5},
	Pii = {1127344},
	Pubmed = {16902090},
	Title = {Imaging intracellular fluorescent proteins at nanometer resolution},
	Uuid = {ACD71C04-1337-4A14-9EEF-FAA299BE64FA},
	Volume = {313},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1127344}}

@article{Bhardwaj:2006,
	Abstract = {Stem cells generate neurons in discrete regions in the postnatal mammalian brain. However, the extent of neurogenesis in the adult human brain has been difficult to establish. We have taken advantage of the integration of (14)C, generated by nuclear bomb tests during the Cold War, in DNA to establish the age of neurons in the major areas of the human cerebral neocortex. Together with the analysis of the neocortex from patients who received BrdU, which integrates in the DNA of dividing cells, our results demonstrate that, whereas nonneuronal cells turn over, neurons in the human cerebral neocortex are not generated in adulthood at detectable levels but are generated perinatally.},
	Author = {Bhardwaj, Ratan D. and Curtis, Maurice A. and Spalding, Kirsty L. and Buchholz, Bruce A. and Fink, David and Bj{\"o}rk-Eriksson, Thomas and Nordborg, Claes and Gage, Fred H. and Druid, Henrik and Eriksson, Peter S. and Fris{\'e}n, Jonas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Atmosphere;research support, n.i.h., extramural ;Animals;Humans;Aging;Middle Aged;Neocortex;research support, u.s. gov't, non-p.h.s. ;Time Factors;Antimetabolites;Nuclear Warfare;01 Adult neurogenesis general;Aged;research support, non-u.s. gov't ;Autopsy;Carbon Radioisotopes;Aged, 80 and over;24 Pubmed search results 2008;Stem Cells;Bromodeoxyuridine},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {33},
	Organization = {Department of Cell and Molecular Biology, Medical Nobel Institute, and Department of Forensic Medicine, Karolinska Institute, SE-171 77 Stockholm, Sweden.},
	Pages = {12564-8},
	Pii = {0605177103},
	Pubmed = {16901981},
	Title = {Neocortical neurogenesis in humans is restricted to development},
	Uuid = {B51E2E31-1D41-4E60-8507-3B68643AB616},
	Volume = {103},
	Year = {2006},
	url = {papers/Bhardwaj_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0605177103}}

@article{Bi:1995,
	Abstract = {Vesicular stomatitis virus (VSV) causes acute infection of the central nervous system (CNS) when intranasally applied. We have examined cellular inflammatory changes in the CNS following VSV infection. As early as 1 day postinfection (p.i.), astrocytes were activated in the olfactory bulb (OB). This was followed by activation of microglia, first observed in the OB at day 3 p.i. Expression of inducible nitric oxide synthase was observed in activated microglia in the OB at day 3 p.i., and increased inducible nitric oxide synthase expression coincided with decreased virus titers in tissue homogenates. Expression of major histocompatibility complex (MHC) class I molecules on astrocytes and microglial, endothelial, and ependymal cells was also rapidly induced and followed by induced expression of MHC class II molecules on astrocytes and microglial and endothelial cells. Consistent with the pattern of viral dissemination, MHC molecules were expressed temporally from the rostral-to-caudal direction. Infiltration of CD8+ cells was observed as early as 1 day p.i. in the OB. CD4+ cells were detected in the OB at day 4 p.i. Increasing T-cell infiltration coincided with decreased virus titers. In contrast, B-cell infiltration of the CNS was not detected until day 14 p.i., after the virus was cleared and mice were showing behavioral signs of recovery. Breakdown of the blood-brain barrier was detected beginning at day 6 p.i., was most severe at day 8 p.i., and was followed by full recovery. Collectively, these data show that both innate immunity (production of nitric oxide) and acquired immunity (expression of MHC molecules and T-cell infiltration) are activated following VSV infection in the CNS.},
	Author = {Bi, Z. and Barna, M. and Komatsu, T. and Reiss, C. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Histocompatibility Antigens Class I;T-Lymphocytes;Mice, Inbred BALB C;Animals;Astrocytes;Central Nervous System Diseases;Major Histocompatibility Complex;Nitric Oxide Synthase;Vesicular stomatitis-Indiana virus;Microglia;15 Retrovirus mechanism;Rhabdoviridae Infections;11 Glia;Time Factors;Blood-Brain Barrier;Male;Research Support, U.S. Gov't, P.H.S.;Mice;CD4-Positive T-Lymphocytes;24 Pubmed search results 2008;Immunity, Natural;Inflammation;Immunity;Amino Acid Oxidoreductases;Histocompatibility Antigens Class II},
	Medline = {95395984},
	Month = {10},
	Nlm_Id = {0113724},
	Number = {10},
	Organization = {Department of Biology, New York University, New York 10003-6688, USA.},
	Pages = {6466-72},
	Pubmed = {7545248},
	Title = {Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity},
	Uuid = {F1DFFA9D-9A53-4360-90B0-870B109AB77B},
	Volume = {69},
	Year = {1995}}

@article{Bianco:2001,
	Abstract = {The concept of producing 'spare parts'of the body for replacement of damaged or lost organs lies at the core of the varied biotechnological practices referred to generally as tissue engineering. Use of postnatal stem cells has the potential to significantly alter the perspective of tissue engineering. Successful long-term restoration of continuously self-renewing tissues such as skin, for example, depends on the use of extensively self-renewing stem cells. The identification and isolation of stem cells from a number of tissues provides appropriate targets for prospective gene therapies. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Bianco, P. and Robey, P. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Nature},
	Keywords = {F abstr;Bone and Bones/cytology;10 Development;Human;Regeneration;*Stem Cells;*Tissue Engineering/trends;Animals;Support, Non-U.S. Gov't;Skin/cytology;Bone Regeneration},
	Number = {6859},
	Organization = {Dipartimento di Medicina Sperimentale e Patologia, Universita 'La Sapienza', Viale Regina Elena 324, Roma 00161, Italy. p.bianco\@flashnet.it},
	Pages = {118-21},
	Pubmed = {11689957},
	Title = {Stem cells in tissue engineering},
	Uuid = {0486320D-DE95-4C70-8449-6DA7BCB3841D},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689957}}

@article{Biebl:2000,
	Abstract = {The adult central nervous system was thought to be very limited in its regenerative potential; however, the discovery that stem cell populations produce neurons in the adult brain highlights the dynamics of a previously assumed 'static'organ. The continuous generation of new neurons in the adult brain, nevertheless, leads to the question of whether neurogenesis is counterbalanced by an accompanying cell death in the same regions. The objective of this study was to stereologically analyze neurogenesis and programmed cell death in adult brain regions with known neurogenic activity. Using bromodeoxyuridine (BrdU) to identify newborn cells we find that within a few days of BrdU-labeling the adult dentate gyrus and olfactory bulb generate high numbers of newborn neurons. More importantly, dUTP-nick end labeling (TUNEL) reveals that areas of adult neurogenesis also contain high numbers of apoptotic cells. We conclude that programmed cell death may have an important regulatory function by eliminating supernumerous cells from neurogenic regions and may thus contribute to a self-renewal mechanism in the adult mammalian brain.},
	Author = {Biebl, M. and Cooper, C. M. and Winkler, J. and Kuhn, H. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neurosci Lett},
	Keywords = {Neurons/*cytology/metabolism;Rats;Apoptosis/*physiology;Olfactory Bulb/cytology/metabolism;Female;Cell Count;02 Adult neurogenesis migration;Animal;Rats, Wistar;Brain/*cytology/*physiology;Nerve Regeneration;Support, Non-U.S. Gov't;B;In Situ Nick-End Labeling;Dentate Gyrus/cytology/metabolism;Cell Differentiation/physiology;Bromodeoxyuridine;DNA Fragmentation},
	Number = {1},
	Organization = {Department of Neurology, University of Regensburg, Universitatsstrasse 84, D-93053, Regensburg, Germany.},
	Pages = {17-20.},
	Title = {Analysis of neurogenesis and programmed cell death reveals a self- renewing capacity in the adult rat brain},
	Uuid = {29F4B02E-62A0-4228-B6A6-75247B32D5A7},
	Volume = {291},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10962143}}

@article{Bielas:2007,
	Abstract = {The axonal shafts of neurons contain bundled microtubules, whereas extending growth cones contain unbundled microtubule filaments, suggesting that localized activation of microtubule-associated proteins (MAP) at the transition zone may bundle these filaments during axonal growth. Dephosphorylation is thought to lead to MAP activation, but specific molecular pathways have remained elusive. We find that Spinophilin, a Protein-phosphatase 1 (PP1) targeting protein, is responsible for the dephosphorylation of the MAP Doublecortin (Dcx) Ser 297 selectively at the "wrist" of growing axons, leading to activation. Loss of activity at the "wrist" is evident as an impaired microtubule cytoskeleton along the shaft. These findings suggest that spatially restricted adaptor-specific MAP reactivation through dephosphorylation is important in organization of the neuronal cytoskeleton.},
	Author = {Bielas, Stephanie L. and Serneo, Finley F. and Chechlacz, Magdalena and Deerinck, Thomas J. and Perkins, Guy A. and Allen, Patrick B. and Ellisman, Mark H. and Gleeson, Joseph G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Microtubule-Associated Proteins;Magnetic Resonance Imaging;Animals;Cells, Cultured;Humans;Serine;Microfilament Proteins;Phosphoprotein Phosphatases;Phosphorylation;Axons;Neurites;Hippocampus;research support, non-u.s. gov't;Male;Neuropeptides;Microtubules;Mice, Inbred Strains;Mice, Knockout;Neurons;research support, n.i.h., extramural;Mice;Cyclin-Dependent Kinase 5;24 Pubmed search results 2008;Actins;Corpus Callosum;Nerve Tissue Proteins},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {3},
	Organization = {Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.},
	Pages = {579-91},
	Pii = {S0092-8674(07)00389-3},
	Pubmed = {17482550},
	Title = {Spinophilin facilitates dephosphorylation of doublecortin by PP1 to mediate microtubule bundling at the axonal wrist},
	Uuid = {E5ECF94A-43EE-4C7F-B2AA-042156B9CBF9},
	Volume = {129},
	Year = {2007},
	url = {papers/Bielas_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2007.03.023}}

@article{Bielle:2005,
	Abstract = {Cajal-Retzius cells are critical in cortical lamination, but very little is known about their origin and development. The homeodomain transcription factor Dbx1 is expressed in restricted progenitor domains of the developing pallium: the ventral pallium (VP) and the septum. Using genetic tracing and ablation experiments in mice, we show that two subpopulations of Reelin(+) Cajal-Retzius cells are generated from Dbx1-expressing progenitors. VP- and septum-derived Reelin(+) neurons differ in their onset of appearance, migration routes, destination and expression of molecular markers. Together with reported data supporting the generation of Reelin(+) cells in the cortical hem, our results show that Cajal-Retzius cells are generated at least at three focal sites at the borders of the developing pallium and are redistributed by tangential migration. Our data also strongly suggest that distinct Cajal-Retzius subtypes exist and that their presence in different territories of the developing cortex might contribute to region-specific properties.},
	Author = {Bielle, Franck and Griveau, Am{\'e}lie and Narboux-N\^{e}me, Nicolas and Vigneau, S{\'e}bastien and Sigrist, Markus and Arber, Silvia and Wassef, Marion and Pierani, Alessandra},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {10 Development;Tissue Distribution;Animals;Aging;Homeodomain Proteins;Cell Movement;Telencephalon;Cell Adhesion Molecules, Neuronal;Serine Endopeptidases;Recombinant Fusion Proteins;Calcium-Binding Protein, Vitamin D-Dependent;Mice, Neurologic Mutants;Embryo;research support, non-u.s. gov't ;Extracellular Matrix Proteins;Animals, Newborn;tau Proteins;Cerebral Cortex;Neurons;Mice;Cell Division;24 Pubmed search results 2008;Nerve Tissue Proteins;Genetic Techniques;12 Interneuron development},
	Month = {8},
	Nlm_Id = {9809671},
	Number = {8},
	Organization = {Centre National de la Recherche Scientifique-Unit{\'e} Mixte de Recherche 8542, Ecole Normale Sup{\'e}rieure, 46 rue d'Ulm, 75005 Paris, France.},
	Pages = {1002-12},
	Pii = {nn1511},
	Pubmed = {16041369},
	Title = {Multiple origins of Cajal-Retzius cells at the borders of the developing pallium},
	Uuid = {64967ECB-EFDA-4749-95F6-E0C57769C71A},
	Volume = {8},
	Year = {2005},
	url = {papers/Bielle_NatNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1511}}

@article{Bierhuizen:1997,
	Abstract = {The further improvement of gene transfer into hematopoietic stem cells and their direct progeny will be greatly facilitated by markers that allow rapid detection and efficient selection of successfully transduced cells. For this purpose, a retroviral vector was designed and tested encoding a recombinant version of the Aequorea victoria green fluorescent protein that is enhanced for high-level expression in mammalian cells (EGFP). Murine cell lines (NIH 3T3, Rat2) and bone marrow cells transduced with this retroviral vector demonstrated a stable green fluorescence signal readily detectable by flow cytometry. Functional analysis of the retrovirally transduced bone marrow cells showed EGFP expression in in vitro clonogenic progenitors (GM-CFU), day 13 colony-forming unit-spleen (CFU-S), and in peripheral blood cells and marrow repopulating cells of transplanted mice. In conjunction with fluorescence-activated cell sorting (FACS) techniques EGFP expression could be used as a marker to select for greater than 95\%pure populations of transduced cells and to phenotypically define the transduced cells using antibodies directed against specific cell-surface antigens. Detrimental effects of EGFP expression were not observed: fluorescence intensity appeared to be stable and hematopoietic cell growth was not impaired. The data show the feasibility of using EGFP as a convenient and rapid reporter to monitor retroviral-mediated gene transfer and expression in hematopoietic cells, to select for the genetically modified cells, and to track these cells and their progeny both in vitro and in vivo.},
	Author = {Bierhuizen, M. F. and Westerman, Y. and Visser, T. P. and Dimjati, W. and Wognum, A. W. and Wagemaker, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Gene Transfer Techniques;Flow Cytometry;Luminescent Proteins;Research Support, Non-U.S. Gov't;Hematopoietic Stem Cells;Female;Bone Marrow Cells;Retroviridae;Biological Markers;11 Glia;Green Fluorescent Proteins;Humans;Animals;Mice;Cells, Cultured;Genetic Vectors},
	Medline = {98008093},
	Month = {11},
	Nlm_Id = {7603509},
	Number = {9},
	Organization = {Institute of Hematology, Erasmus University Rotterdam, Rotterdam, The Netherlands.},
	Pages = {3304-15},
	Pubmed = {9345012},
	Title = {Enhanced green fluorescent protein as selectable marker of retroviral-mediated gene transfer in immature hematopoietic bone marrow cells},
	Uuid = {CA937BC1-4D60-4482-80EB-4608E094687F},
	Volume = {90},
	Year = {1997}}

@article{Bierhuizen:1999,
	Abstract = {The feasibility of using the enhanced green fluorescent protein (EGFP) as a selectable reporter molecule of retroviral-mediated gene transfer in immature rhesus monkey and human CD34+ hematopoietic cells was examined. Retroviral transduction with the MFG-EGFP retroviral vector resulted in readily detectable EGFP expression in 27\%of human and 11-35\%of rhesus monkey bone marrow cells, and in 17-38\%of rhesus monkey peripheral blood cells mobilized with FLT3 ligand (FL) and granulocyte colony-stimulating factor (G-CSF). In addition, we used the human CD34+ KG1A cell line as a model to study viability and growth of successfully transduced cells. Cultures of mock- and EGFP-transduced KG1A cells generated equal viable cell numbers for at least 1 month, indicating the absence of a cytotoxic effect of EGFP expression in these cells. FACS selection on the basis of EGFP and CD34 expression resulted in enriched subsets (>or = 87\%) of CD34+ EGFP-negative and CD34+ EGFP-positive KG1A, rhesus monkey and human bone marrow cells, demonstrating the potential of obtaining almost pure populations of transduced immature hematopoietic cells. EGFP expression was also readily demonstrated in erythroid and granulocyte/macrophage colonies derived from the CD34+ EGFP-positive rhesus monkey and human bone marrow cells by either inverted fluorescence microscopy or flow cytometry. Using four-color flow cytometry, EGFP expression could also be demonstrated in viable and phenotypically defined immature subpopulations of the CD34+ cells, ie those expressing little or no HLA-DR (rhesus monkey) or CD38 (human) antigens at the cell surface. These results demonstrate that EGFP is a very useful marker to monitor gene transfer efficiency in phenotypically defined immature rhesus monkey and human hematopoietic cell types and to select for these cells by multicolor flow cytometry prior to transplantation.},
	Author = {Bierhuizen, M. F. and Westerman, Y. and Hartong, S. C. and Visser, T. P. and Wognum, A. W. and Wagemaker, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0887-6924},
	Journal = {Leukemia},
	Keywords = {Hematopoietic Stem Cell Mobilization;Colony-Forming Units Assay;Humans;Animals;Cell Separation;Transfection;Feasibility Studies;Antigens, CD34;Retroviridae;Immunophenotyping;11 Glia;Genetic Vectors;Green Fluorescent Proteins;Cell Line;Macaca mulatta;Cell Lineage;Male;Bone Marrow Cells;Recombinant Fusion Proteins;Flow Cytometry;Hematopoietic Stem Cells;Luminescent Proteins;Genes, Reporter;Biological Markers;Gene Expression;Membrane Proteins;Research Support, Non-U.S. Gov't},
	Medline = {99229682},
	Month = {4},
	Nlm_Id = {8704895},
	Number = {4},
	Organization = {Institute of Hematology, Erasmus University Rotterdam, The Netherlands.},
	Pages = {605-13},
	Pubmed = {10214869},
	Title = {Efficient detection and selection of immature rhesus monkey and human CD34+ hematopoietic cells expressing the enhanced green fluorescent protein (EGFP)},
	Uuid = {1A2DDCF9-39D7-48DB-93BB-39E0AF99AAD4},
	Volume = {13},
	Year = {1999}}

@article{Biffi:2004,
	Abstract = {Gene-based delivery can establish a sustained supply of therapeutic proteins within the nervous system. For diseases characterized by extensive CNS and peripheral nervous system (PNS) involvement, widespread distribution of the exogenous gene may be required, a challenge to in vivo gene transfer strategies. Here, using lentiviral vectors (LVs), we efficiently transduced hematopoietic stem cells (HSCs) ex vivo and evaluated the potential of their progeny to target therapeutic genes to the CNS and PNS of transplanted mice and correct a neurodegenerative disorder, metachromatic leukodystrophy (MLD). We proved extensive repopulation of CNS microglia and PNS endoneurial macrophages by transgene-expressing cells. Intriguingly, recruitment of these HSC-derived cells was faster and more robust in MLD mice. By transplanting HSCs transduced with the arylsulfatase A gene, we fully reconstituted enzyme activity in the hematopoietic system of MLD mice and prevented the development of motor conduction impairment, learning and coordination deficits, and neuropathological abnormalities typical of the disease. Remarkably, ex vivo gene therapy had a significantly higher therapeutic impact than WT HSC transplantation, indicating a critical role for enzyme overexpression in the HSC progeny. These results indicate that transplantation of LV-transduced autologous HSCs represents a potentially efficacious therapeutic strategy for MLD and possibly other neurodegenerative disorders.},
	Author = {Biffi, Alessandra and De Palma, Michele and Quattrini, Angelo and Del Carro, Ubaldo and Amadio, Stefano and Visigalli, Ilaria and Sessa, Maria and Fasano, Stefania and Brambilla, Riccardo and Marchesini, Sergio and Bordignon, Claudio and Naldini, Luigi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0021-9738},
	Journal = {J Clin Invest},
	Keywords = {Mice;Cell Differentiation;Research Support, Non-U.S. Gov't;Lentivirus;Mice, Inbred C57BL;11 Glia;Motor Activity;Gene Therapy;Hematopoietic Stem Cell Transplantation;Animals;Nervous System;Cell Movement;Leukodystrophy, Metachromatic;Disease Models, Animal},
	Month = {4},
	Nlm_Id = {7802877},
	Number = {8},
	Organization = {San Raffaele Telethon Institute for Gene Therapy, San Raffaele Scienctific Institute, Milan, Italy.},
	Pages = {1118-29},
	Pubmed = {15085191},
	Title = {Correction of metachromatic leukodystrophy in the mouse model by transplantation of genetically modified hematopoietic stem cells},
	Uuid = {366E2A0F-8DB0-4F47-972C-6DCE833EF2F1},
	Volume = {113},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1172/JCI200419205}}

@article{Binder:1999,
	Abstract = {Recent work suggests that limiting the activation of the trkB subtype of neurotrophin receptor inhibits epileptogenesis, but whether or where neurotrophin receptor activation occurs during epileptogenesis is unclear. Because the activation of trk receptors involves the phosphorylation of specific tyrosine residues, the availability of antibodies that selectively recognize the phosphorylated form of trk receptors permits a histochemical assessment of trk receptor activation. In this study the anatomy and time course of trk receptor activation during epileptogenesis were assessed with immunohistochemistry, using a phospho-specific trk antibody. In contrast to the low level of phosphotrk immunoreactivity constitutively expressed in the hippocampus of adult rats, a striking induction of phosphotrk immunoreactivity was evident in the distribution of the mossy fibers after partial kindling or kainate-induced seizures. The anatomic distribution, time course, and threshold for seizure-induced phosphotrk immunoreactivity correspond to the demonstrated pattern of regulation of BDNF expression by seizure activity. These results provide immunohistochemical evidence that trk receptors undergo activation during epileptogenesis and suggest that the mossy fiber pathway is particularly important in the pro-epileptogenic effects of the neurotrophins.},
	Author = {Binder, D. K. and Routbort, M. J. and McNamara, J. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Electric Stimulation;Receptor Protein-Tyrosine Kinases/*metabolism;Rats, Sprague-Dawley;07 Excitotoxicity Apoptosis;Neural Pathways/metabolism;Kainic Acid/toxicity;Rats;Immunohistochemistry;E-8;Kindling (Neurology);Animal;Support, U.S. Gov't, P.H.S.;Status Epilepticus/chemically induced/metabolism;Mossy Fibers, Hippocampal/*metabolism;Cells, Cultured;Male;Seizures/*metabolism},
	Number = {11},
	Organization = {Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.},
	Pages = {4616-26.},
	Title = {Immunohistochemical evidence of seizure-induced activation of trk receptors in the mossy fiber pathway of adult rat hippocampus},
	Uuid = {CD93E490-14EE-4A5E-856C-18D1B8CCB404},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10341259%20http://www.jneurosci.org/cgi/content/full/19/11/4616}}

@article{Birmingham:2006,
	Abstract = {Off-target gene silencing can present a notable challenge in the interpretation of data from large-scale RNA interference (RNAi) screens. We performed a detailed analysis of off-targeted genes identified by expression profiling of human cells transfected with small interfering RNA (siRNA). Contrary to common assumption, analysis of the subsequent off-target gene database showed that overall identity makes little or no contribution to determining whether the expression of a particular gene will be affected by a given siRNA, except for near-perfect matches. Instead, off-targeting is associated with the presence of one or more perfect 3' untranslated region (UTR) matches with the hexamer or heptamer seed region (positions 2-7 or 2-8) of the antisense strand of the siRNA. These findings have strong implications for future siRNA design and the application of RNAi in high-throughput screening and therapeutic development.},
	Author = {Birmingham, Amanda and Anderson, Emily M. and Reynolds, Angela and Ilsley-Tyree, Diane and Leake, Devin and Fedorov, Yuriy and Baskerville, Scott and Maksimova, Elena and Robinson, Kathryn and Karpilow, Jon and Marshall, William S. and Khvorova, Anastasia},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1548-7091},
	Journal = {Nat Methods},
	Keywords = {Cell Survival;Base Pairing;Humans;Transfection;Oligonucleotide Array Sequence Analysis;Databases, Factual;Base Pair Mismatch;Sensitivity and Specificity;Sequence Alignment;23 Technique;Computational Biology;Silicon;Gene Expression Profiling;Hela Cells;RNA, Small Interfering;RNA, Messenger;Cell Line;Numerical Analysis, Computer-Assisted;21 Neurophysiology;Gene Silencing;23 RNAi;24 Pubmed search results 2008;3' Untranslated Regions},
	Month = {3},
	Nlm_Id = {101215604},
	Number = {3},
	Organization = {Dharmacon Research, 2650 Crescent Drive, \#100, Lafayette, Colorado 80026, USA.},
	Pages = {199-204},
	Pii = {nmeth854},
	Pubmed = {16489337},
	Title = {3' UTR seed matches, but not overall identity, are associated with RNAi off-targets},
	Uuid = {FEC9A130-48A4-11DB-A317-000D9346EC2A},
	Volume = {3},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nmeth854}}

@article{Bittman:1999,
	Abstract = {Proliferating cells of the developing murine neocortex couple together into clusters during neurogenesis. Previously, we have shown that these clusters contain neural precursors in all phases of the cell cycle except M phase, and that they extend a nestin-expressing process from the cluster to the pial surface. In addition, coupling within neocortical cell clusters is a dynamic process related to the cell cycle, with maximal coupling in S/G2 phase, uncoupling in M phase and then recoupling during G1 and S phases of the cell cycle. In the present study, we use immunohistochemistry to demonstrate that cycling neocortical cells as well as radial glial cells express the gap junction proteins connexin 26 and connexin 43. Furthermore, we demonstrate that biocytin labeled clusters extend processes to the pial surface that express the glial cell antigen RC2. Lastly, by combining bromodeoxyuridine and connexin immunohistochemistry on acutely dissociated neocortical cells, we show that the percentage of cycling cells immunoreactive to connexin 26 and connexin 43 changes through the cell cycle. These results indicate that radial glial cells as well as neural precursors couple into clusters, and suggest that through differential regulation of connexins, neocortical precursors may compartmentalize as they progress through the cell cycle.},
	Author = {Bittman, K. S. and LoTurco, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Cereb Cortex},
	Keywords = {Nerve Tissue Proteins/*physiology;10 Development;Fetal Development/physiology;Neocortex/cytology/*embryology;Comparative Study;Cell Cycle/physiology;Stem Cells/physiology;Animal;Connexin 43/*physiology;Mice, Inbred Strains;Antibody Specificity;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Mice;Cell Differentiation/physiology;F;Nerve Fibers/physiology;Connexins/*physiology},
	Number = {2},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, Storrs 06268-4156, USA.},
	Pages = {188-95.},
	Title = {Differential regulation of connexin 26 and 43 in murine neocortical precursors},
	Uuid = {A7512708-70B1-479A-9858-8FDBEC96F031},
	Volume = {9},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10220231}}

@article{Bittman:2002,
	Abstract = {Intercellular communication through gap junction channels is a prominent feature of the developing cerebral cortex. In the first 2 weeks after birth, a time critical in the development of the rat neocortex, extensive cell coupling has been documented that diminishes as the cortex matures. Among the family of gap junction proteins, connexins 26, 36, and 43 are differentially expressed during cortical development. We used intracellular dye injections and connexin immunohistochemistry to investigate the coupling patterns and connexin expression between the different neuronal and glial cell types of the developing cortex of the rat. We found that neurons and glia couple homotypically and heterotypically at postnatal days 7 and 14. Although the prevalence of coupling was homotypic, there was considerable heterotypic coupling that involved pyramidal and nonpyramidal neurons, the principal neuronal cell types of the cortex, or neurons and astrocytes. Coupling between different cell types appeared to be mediated by differential expression of connexins 26, 36, and 43. It may be that coupling between cells in the developing neocortex is a function of the spatial and temporal expression of these and other connexin proteins.},
	Author = {Bittman, Kevin and Becker, David L. and Cicirata, Federico and Parnavelas, John G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Fluorescent Dyes;Connexin 43;Animals;Astrocytes;Gene Expression Regulation, Developmental;Rats;Microscopy, Confocal;Cell Communication;Rats, Sprague-Dawley;Axons;Fluorescein-5-isothiocyanate;Pyramidal Cells;Gap Junctions;Connexins;Dendrites;research support, non-u.s. gov't ;Cerebral Cortex;21 Neurophysiology;Cell Size;Neuroglia;Neurons;Interneurons;24 Pubmed search results 2008;Immunohistochemistry;Biotin},
	Month = {2},
	Nlm_Id = {0406041},
	Number = {3},
	Organization = {Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom.},
	Pages = {201-12},
	Pii = {10.1002/cne.2121},
	Pubmed = {11807831},
	Title = {Connexin expression in homotypic and heterotypic cell coupling in the developing cerebral cortex},
	Uuid = {8CD735F3-2C00-4449-BC3D-F40F4B43C949},
	Volume = {443},
	Year = {2002},
	url = {papers/Bittman_JCompNeurol2002.pdf}}

@article{Bittman:1997,
	Abstract = {Cells within the ventricular zone (VZ) of developing neocortex are coupled together into clusters by gap junction channels. The specific role of clustering in cortical neurogenesis is unknown; however, clustering provides a means for spatially restricted local interactions between subsets of precursors and other cells within the VZ. In the present study, we have used a combination of 5-bromo-2'-deoxyuridine (BrDU) pulse labeling, intracellular biocytin labeling, and immunocytochemistry to determine when in the cell cycle VZ cells couple and uncouple from clusters and to determine what cell types within the VZ are coupled to clusters. Our results indicate that clusters contain radial glia and neural precursors but do not contain differentiating or migrating neurons. In early neurogenesis, all precursors in S and G2 phases of the cell cycle are coupled, and approximately half of the cells in G1 are coupled. In late neurogenesis, however, over half of the cells in both G1 and S phases are not coupled to VZ clusters, whereas all cells in G2 are coupled to clusters. Increased uncoupling in S phase during late neurogenesis may contribute to the greater percentage of VZ cells exiting the cell cycle at this time. Consistent with this hypothesis, we found that pharmacologically uncoupling VZ cells with octanol decreases the percentage of VZ cells that enter S phase. These results demonstrate that cell clustering in the VZ is restricted to neural precursors and radial glia, is dynamic through the cell cycle, and may play a role in regulating neurogenesis.},
	Author = {Bittman, K. and Owens, D. F. and Kriegstein, A. R. and LoTurco, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Pregnancy;Animals;Lysine;Epithelial Cells;Tubulin;Cell Cycle;Female;Cell Communication;Gap Junctions;G2 Phase;Cerebral Ventricles;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;21 Neurophysiology;Mice;G1 Phase;Bromodeoxyuridine;24 Pubmed search results 2008;S Phase;Research Support, Non-U.S. Gov't},
	Medline = {97426553},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {18},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut 06269-4156, USA.},
	Pages = {7037-44},
	Pubmed = {9278539},
	Title = {Cell coupling and uncoupling in the ventricular zone of developing neocortex},
	Uuid = {2F0119C9-3FFA-4514-96A1-838632FCFA8B},
	Volume = {17},
	Year = {1997}}

@article{Bjarnason:2001,
	Abstract = {We studied the relative RNA expression of clock genes throughout one 24-hour period in biopsies obtained from the oral mucosa and skin from eight healthy diurnally active male study participants. We found that the human clock genes hClock, hTim, hPer1, hCry1, and hBmal1 are expressed in oral mucosa and skin, with a circadian profile consistent with that found in the suprachiasmatic nuclei and the peripheral tissues of rodents. hPer1, hCry1, and hBmal1 have a rhythmic expression, peaking early in the morning, in late afternoon, and at night, respectively, whereas hClock and hTim are not rhythmic. This is the first human study to show a circadian profile of expression for all five clock genes as documented in rodents, suggesting their functional importance in man. In concurrent oral mucosa biopsies, thymidylate synthase enzyme activity, a marker for DNA synthesis, had a circadian variation with peak activity in early afternoon, coinciding with the timing of S phase in our previous study on cell-cycle timing in human oral mucosa. The major peak in hPer1 expression occurs at the same time of day as the peak in G(1) phase in oral mucosa, suggesting a possible link between the circadian clock and the mammalian cell cycle. 0002-9440 Clinical Trial Journal Article},
	Author = {Bjarnason, G. A. and Jordan, R. C. and Wood, P. A. and Li, Q. and Lincoln, D. W. and Sothern, R. B. and Hrushesky, W. J. and Ben-David, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Am J Pathol},
	Keywords = {F abstr;10 Development;Cell Cycle/physiology;Trans-Activators/*genetics;Mouth Mucosa/enzymology/*metabolism;Gene Expression Regulation;Circadian Rhythm/genetics/*physiology;Thymidylate Synthase/genetics/metabolism;Support, U.S. Gov't, Non-P.H.S.;Transcription Factors/genetics;Nuclear Proteins/genetics;RNA, Messenger/genetics/metabolism;Support, Non-U.S. Gov't;Flavoproteins/genetics;Skin/*metabolism;Support, U.S. Gov't, P.H.S.},
	Number = {5},
	Organization = {Toronto-Sunnybrook Regional Cancer Centre, Toronto, Ontario, Canada. bjarnason\@srcl.sunnybrook.utoronto.ca},
	Pages = {1793-801},
	Pubmed = {11337377},
	Title = {Circadian expression of clock genes in human oral mucosa and skin: association with specific cell-cycle phases},
	Uuid = {C480EC4E-ED6A-4977-96D7-5D882780048B},
	Volume = {158},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11337377}}

@article{Bjorklund:1992,
	Abstract = {The ability of intrastriatal grafts of fetal mesencephalic dopamine neurons to ameliorate the symptoms of experimental and clinical parkinsonism has raised the question of the mechanisms underlying the transplant-induced functional effects. Recent studies have taken advantage of quantitative cytochemical and in situ hybridization techniques to study functional graft-host interactions at the cellular level in the rat Parkinson model. The results provide evidence that behaviorally functional grafts restore dopaminergic neurotransmission and normalize dopamine receptor function in the denervated striatum, and that these effects are likely to depend on both synaptic and extrasynaptic mechanisms. 0959-4388 Journal Article Review Review, Tutorial},
	Author = {Bjorklund, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Curr Opin Neurobiol},
	Keywords = {Parkinson Disease/*therapy;17 Transplant Regeneration;Human;L abstr;Dopamine/*physiology;*Brain Tissue Transplantation;Animals},
	Number = {5},
	Organization = {Department of Medical Research, University of Lund, Sweden.},
	Pages = {683-9},
	Pubmed = {1422126},
	Title = {Dopaminergic transplants in experimental parkinsonism: cellular mechanisms of graft-induced functional recovery},
	Uuid = {64CEAD3A-EC80-11DA-8605-000D9346EC2A},
	Volume = {2},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1422126}}

@article{Bjorklund:2000,
	Abstract = {In animal models, immature neural precursors can replace lost neurons, restore function and promote brain self-repair. Clinical trials in Parkinson's disease suggest that similar approaches may also work in the diseased human brain. But how realistic is it that cell replacement can be developed into effective clinical therapy? 1097-6256 Journal Article Review Review, Tutorial},
	Author = {Bjorklund, A. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Human;Animals;Huntington Disease/therapy;Rats;Recovery of Function;Parkinson Disease/therapy;*Stem Cell Transplantation;Swine;Central Nervous System Diseases/*therapy;Cerebrovascular Accident/therapy;Epilepsy/therapy;Clinical Trials;Seizures/prevention &control;06 Adult neurogenesis injury induced;Neurons/*transplantation;Cell Transplantation/methods/*trends;Brain/*cytology/embryology;D, L pdf},
	Number = {6},
	Organization = {The authors are at the Wallenberg Neuroscience Center, Lund University, Solvegatan 17, S-223 62 Lund, Sweden. anders.bjorklund\@mphy.lu.se},
	Pages = {537-44},
	Title = {Cell replacement therapies for central nervous system disorders},
	Uuid = {4E694C67-EC7F-11DA-8605-000D9346EC2A},
	Volume = {3},
	Year = {2000},
	url = {papers/Bjorklund_NatNeurosci2000.pdf}}

@article{Black:2001,
	Author = {Black, I. B. and Woodbury, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1079-9796},
	Journal = {Blood Cells Mol Dis},
	Keywords = {Neurons;Cell Differentiation;Research Support, Non-U.S. Gov't;Immunophenotyping;Rats;Bone Marrow Cells;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;review, tutorial;Humans;Animals;Stromal Cells;review},
	Medline = {21375886},
	Nlm_Id = {9509932},
	Number = {3},
	Organization = {Department of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, 675 Hoes Lane, CABM 342, Piscataway, NJ 08854, USA. black\@cabm.rutgers.edu},
	Pages = {632-6},
	Pii = {S1079979601904231},
	Pubmed = {11482877},
	Title = {Adult rat and human bone marrow stromal stem cells differentiate into neurons},
	Uuid = {B3076514-E828-4E6F-949F-99B37396980A},
	Volume = {27},
	Year = {2001},
	url = {papers/Black_BloodCellsMolDis2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/bcmd.2001.0423}}

@article{Blackshaw:2002,
	Abstract = {1097-6256 Comment News},
	Author = {Blackshaw, S. and Cepko, C. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Nat Neurosci},
	Keywords = {17 Transplant Regeneration;Cell Culture/*methods;Human;Brain/cytology/growth &development;Graft Survival/physiology;Nerve Growth Factors/therapeutic use;Cell Differentiation/physiology;Stem Cell Transplantation/*methods;Brain Tissue Transplantation/*methods;L pdf;Animals;Stem Cells/*cytology/metabolism;Neurodegenerative Diseases/*therapy},
	Number = {12},
	Pages = {1251-2},
	Title = {Stem cells that know their place},
	Uuid = {BEE1CD4E-8B22-4E77-A2F2-9468F5F4236E},
	Volume = {5},
	Year = {2002},
	url = {papers/Blackshaw_NatNeurosci2002}}

@article{Blesch:2001,
	Abstract = {Vector systems for the regulated and reversible expression of therapeutic genes are likely to improve the safety and efficacy of gene therapy for medical disease. In the present study, we investigated whether the expression of genes transferred into the central nervous system by ex vivo gene therapy can be regulated in vivo leading to controlled neuronal survival and axonal growth. Primary rat fibroblasts were transfected with a retrovirus containing a tetracycline responsive promoter for the expression of the neurotrophin nerve growth factor (NGF) or green fluorescent protein as a control (GFP). After lesions of basal forebrain cholinergic neurons, NGF-mediated neuronal rescue and axonal growth could be completely controlled over a 2-week period by the addition or removal of the tetracycline modulator doxycycline in the animals' drinking water. Further, continued expression of the reporter gene GFP could be reliably and repeatedly turned on and off in the injured CNS for at least 3 months post-grafting, the longest time point investigated. These data constitute the first report of regulated neuronal rescue and axonal growth by controlled neurotrophin gene delivery and long-term, regulated expression using ex vivo CNS gene therapy.},
	Author = {Blesch, A. and Conner, J. M. and Tuszynski, M. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Animals;Central Nervous System Diseases;Rats;Research Support, U.S. Gov't, Non-P.H.S.;Fibroblasts;Female;Axons;Polysaccharides;Retroviridae;11 Glia;Time Factors;Genetic Vectors;Spinal Cord;Analysis of Variance;Rats, Inbred F344;Research Support, U.S. Gov't, P.H.S.;Green Fluorescent Proteins;Gene Therapy;Neurons;Promoter Regions (Genetics);Anti-Bacterial Agents;Luminescent Proteins;Doxycycline;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {21318992},
	Month = {6},
	Nlm_Id = {9421525},
	Number = {12},
	Organization = {Department of Neurosciences-0626, University of California, San Diego, La Jolla, CA 92093-0626, USA.},
	Pages = {954-60},
	Pubmed = {11426336},
	Title = {Modulation of neuronal survival and axonal growth in vivo by tetracycline-regulated neurotrophin expression},
	Uuid = {8022F549-D6A8-4823-9465-A7760D1F93DA},
	Volume = {8},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301480}}

@article{Blitz:2005,
	Abstract = {Local interneurons provide feed-forward inhibition from retinal ganglion cells (RGCs) to thalamocortical (TC) neurons, but questions remain regarding the timing, magnitude, and functions of this inhibition. Here, we identify two types of inhibition that are suited to play distinctive roles. We recorded excitatory and inhibitory postsynaptic currents (EPSCs/IPSCs) in TC neurons in mouse brain slices and activated individual RGC inputs. In 34\%of TC neurons, we identified EPSCs and IPSCs with identical thresholds that were tightly correlated, indicating activation by the same RGC. Such "locked" IPSCs occurred 1 ms after EPSC onset. The remaining neurons had only "nonlocked" inhibition, in which EPSCs and IPSCs had different thresholds, indicating activation by different RGCs. Nonlocked inhibition may refine receptive fields within the LGN by providing surround inhibition. In contrast, dynamic-clamp recordings suggest that locked inhibition improves the precision of synaptically evoked responses in individual TC neurons by eliminating secondary spikes.},
	Author = {Blitz, Dawn M. and Regehr, Wade G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Excitatory Postsynaptic Potentials;Animals;Synapses;Neuronal Plasticity;research support, u.s. gov't, p.h.s. ;Synaptic Transmission;Patch-Clamp Techniques;Visual Pathways;Organ Culture Techniques;Visual Fields;Time Factors;Vision;Action Potentials;21 Neurophysiology;Mice;Interneurons;24 Pubmed search results 2008;Neural Inhibition;Geniculate Bodies;Retinal Ganglion Cells},
	Month = {3},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Neurobiology Department, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {917-28},
	Pii = {S0896-6273(05)00071-1},
	Pubmed = {15797552},
	Title = {Timing and specificity of feed-forward inhibition within the LGN},
	Uuid = {00047A07-83D4-4D83-868C-5C75CEF9433C},
	Volume = {45},
	Year = {2005},
	url = {papers/Blitz_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.01.033}}

@article{Blumcke:2001,
	Abstract = {A considerable potential for neurogenesis has been identified in the epileptic rat hippocampus. Here, we explore this feature in human patients suffering from chronic mesial temporal lobe epilepsy. Immunohistochemical detection of the neurodevelopmental antigen nestin was used to detect neural precursor cells, and cell-type specific markers were employed to study their histogenetic origin and potential for neuronal or glial differentiation. The ontogenetic regulation of nestin-positive precursors was established in human control brains (week 19 of gestation-15 years of age). A striking increase of nestin- immunoreactive cells within the hilus and dentate gyrus could be observed in a group of young patients with temporal lobe epilepsy (TLE) and surgical treatment before age 2 years compared to adult TLE patients and controls. The cellular morphology and regional distribution closely resembled nestin-immunoreactive granule-cell progenitors transiently expressed during prenatal human hippocampus development. An increased Ki-67 proliferation index and clusters of supragranular nestin-immunoreactive cells within the molecular layer of the dentate gyrus were also noted in the group of young TLE patients. Confocal studies revealed colocalization of nestin and the betaIII isoform of tubulin, indicating a neuronal fate for some of these cells. Vimentin was consistently expressed in nestin-immunoreactive cells, whereas cell lineage-specific markers, i.e., glial fibrillary acidic protein, MAP2, neurofilament protein, NeuN, or calbindin D-28k failed to colocalize. These findings provide evidence for increased neurogenesis in pediatric patients with early onset of temporal lobe epilepsy and/or point towards a delay in hippocampal maturation in a subgroup of patients with TLE. Using Smart Source Parsing},
	Author = {Blumcke, I. and Schewe, J. C. and Normann, S. and Brustle, O. and Schramm, J. and Elger, C. E. and Wiestler, O. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Hippocampus},
	Keywords = {D abstr},
	Number = {3},
	Organization = {Department of Neuropathology, University of Bonn Medical Center, Germany.},
	Pages = {311-21},
	Title = {Increase of nestin-immunoreactive neural precursor cells in the dentate gyrus of pediatric patients with early-onset temporal lobe epilepsy},
	Uuid = {AD8B01B1-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {11},
	Year = {2001}}

@article{Blumenthal:1987,
	Abstract = {We have studied fusion between membranes of vesicular stomatitis virus (VSV) and Vero cells using an assay for lipid mixing based on the relief of self-quenching of octadecylrhodamine (R18) fluorescence. We could identify the two pathways of fusion by the kinetics of R18 dequenching, effects of inhibitors, temperature dependence, and dependence on osmotic pressure. Fusion at the plasma membrane began immediately after lowering the pH below 6 and showed an approximately exponential time course, whereas fusion via the endocytic pathway (pH 7.4) became apparent after a time delay of about 2 min. Fusion via the endocytic pathway was attenuated by treating cells with metabolic inhibitors and agents that raise the pH of the endocytic vesicle. A 10-fold excess of unlabeled virus arrested R18VSV entry via the endocytic pathway, whereas R18 dequenching below pH 6 (fusion at the plasma membrane) was not affected by the presence of unlabeled virus. The temperature dependence for fusion at pH 7.4 (in the endosome) was much steeper than that for fusion at pH 5.9 (with the plasma membrane). Fusion via the endocytic pathway was attenuated at hypo-osmotic pressures, whereas fusion at the plasma membrane was not affected by this treatment. The pH profile of Vero-VSV fusion at the plasma membrane, as measured by the dequenching method, paralleled that observed for VSV-induced cell-cell fusion. Fusion was blocked by adding neutralizing antibody to the Vero-VSV complexes. Activation of the fusion process by lowering the pH was reversible, in that the rate of fusion was arrested by raising the pH back to 7.4. The observation that pH-dependent fusion occurred at similar rates with fragments and with intact cells indicates that pH, voltage, or osmotic gradients are not required for viral fusion.},
	Author = {Blumenthal, R. and Bali-Puri, A. and Walter, A. and Covell, D. and Eidelman, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {Rhodamines;Cell Membrane;Spectrometry, Fluorescence;Vero Cells;Kinetics;Fluorescent Dyes;Receptors, Virus;Thermodynamics;Vesicular stomatitis-Indiana virus;15 Retrovirus mechanism;Humans;Hydrogen-Ion Concentration;Animals;24 Pubmed search results 2008},
	Medline = {88007587},
	Month = {10},
	Nlm_Id = {2985121R},
	Number = {28},
	Organization = {Section of Membrane Structure and Function, National Cancer Institute, Bethesda, Maryland 20892.},
	Pages = {13614-9},
	Pubmed = {2820977},
	Title = {pH-dependent fusion of vesicular stomatitis virus with Vero cells. Measurement by dequenching of octadecyl rhodamine fluorescence},
	Uuid = {7D65D6AF-EE2C-11DA-8605-000D9346EC2A},
	Volume = {262},
	Year = {1987}}

@article{Bock:2000,
	Abstract = {The human genome is rife with the proviral remains of many ancient retroviruses. The past year has seen significant progress in understanding the structure, distribution and potential function of many of these elements. Although hypotheses concerning the potential effects of these elements are common, however, incisive experiments to test any functions remain much less so.},
	Author = {Bock, M. and Stoye, J. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0959-437X},
	Journal = {Curr Opin Genet Dev},
	Keywords = {15 ERVs retroelements;Endogenous Retroviruses;24 Pubmed search results 2008;Phylogeny;Evolution, Molecular;Genetic Code;Genome, Human;15 Retrovirus mechanism;Humans;Proviruses;Germ-Line Mutation;review;Animals},
	Medline = {20541599},
	Month = {12},
	Nlm_Id = {9111375},
	Number = {6},
	Organization = {Division of Virology, National Institute for Medical Research, The Ridgeway, London NW7 1AA, UK.},
	Pages = {651-5},
	Pii = {S0959437X00001386},
	Pubmed = {11088016},
	Title = {Endogenous retroviruses and the human germline},
	Uuid = {DF06D492-3F8A-46B8-90AA-EB6FC4B1A00A},
	Volume = {10},
	Year = {2000}}

@article{Bodick:1982,
	Abstract = {A previous report details morphological alterations in dendritic structure of cortical neurons in severe neurobehavioral retardation of unknown etiology. Using computer graphic techniques, the present study describes perturbations in the 3-dimensional character of the microtubular array, which correspond to degenerative change in dendritic geometry. In large proximal processes, two types of array have been reconstructed. Segmented microtubules may form a continuous helical swirl which underlies a bulge in the dendritic cylinder. Alternatively, small groups of microtubules, while maintaining orderly internal organization, may be disoriented with respect to the long axis of the process. In varicose regions of the dendrite the microtubular array is discontinuous. Microtubules course side by side through constructed regions, only to splay out and terminate within expanded regions. These pathological alterations in the microtubular array contrast sharply with the cortical dendritic microtubular array reconstructed from the normal adult mouse. Perturbation in those parameters which determine packing of microtubules within the dendritic process is also documented. In the pathological condition, microtubules lose the ability to exclude one another from close approach. The role of cross-linking molecules in maintaining the integrity of the microtubular array, and the role of microtubules in maintaining the geometry of the dendrite, are considered.},
	Author = {Bodick, N. and Stevens, J. K. and Sasaki, S. and Purpura, D. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {10 Development;Golgi Apparatus;Humans;10 Structural plasticity;Female;Infant;Staining and Labeling;Get paper from library;Male;Dendrites;Microtubules;Research Support, U.S. Gov't, P.H.S.;Computers;Developmental Disabilities;Cerebral Cortex;Microscopy, Electron;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {83102363},
	Month = {11},
	Nlm_Id = {0045503},
	Number = {3},
	Pages = {299-309},
	Pubmed = {6185183},
	Title = {Microtubular disarray in cortical dendrites and neurobehavioral failure. II. Computer reconstruction of perturbed microtubular arrays},
	Uuid = {1C1714B3-F0FA-451A-B744-3A9EC141AD3D},
	Volume = {281},
	Year = {1982}}

@article{Boehm:1997,
	Abstract = {Interferons are cytokines that play a complex and central role in the resistance of mammalian hosts to pathogens. Type I interferon (IFN-alpha and IFN-beta) is secreted by virus-infected cells. Immune, type II, or gamma-interferon (IFN-gamma) is secreted by thymus-derived (T) cells under certain conditions of activation and by natural killer (NK) cells. Although originally defined as an agent with direct antiviral activity, the properties of IFN-gamma include regulation of several aspects of the immune response, stimulation of bactericidal activity of phagocytes, stimulation of antigen presentation through class I and class II major histocompatibility complex (MHC) molecules, orchestration of leukocyte-endothelium interactions, effects on cell proliferation and apoptosis, as well as the stimulation and repression of a variety of genes whose functional significance remains obscure. The implementation of such a variety of effects by a single cytokine is achieved by complex patterns of cell-specific gene regulation: Several IFN-gamma-regulated genes are themselves components of transcription factors. The IFN-gamma response is itself regulated by interaction with responses to other cytokines including IFN-alpha/beta, TNF-alpha, and IL-4. Over 200 genes are now known to be regulated by IFN-gamma and they are listed in a World Wide Web document that accompanies this review. However, much of the cellular response to IFN-gamma can be described in terms of a set of integrated molecular programs underlying well-defined physiological systems, for example the induction of efficient antigen processing for MHC-mediated antigen presentation, which play clearly defined roles in pathogen resistance. A promising approach to the complexity of the IFN-gamma response is to extend the analysis of the less understood IFN-gamma-regulated genes in terms of molecular programs functional in pathogen resistance.},
	Author = {Boehm, U. and Klamp, T. and Groot, M. and Howard, J. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0732-0582},
	Journal = {Annu Rev Immunol},
	Keywords = {Models, Biological;Antigen Presentation;Interferon Type I;Antiviral Agents;Respiratory Burst;Gene Expression Regulation;Signal Transduction;research support, non-u.s. gov't ;14 Immune;Tumor Necrosis Factor-alpha;Apoptosis;Interferon Type II;Animals;Humans;24 Pubmed search results 2008;review;Tryptophan},
	Nlm_Id = {8309206},
	Organization = {Institute for Genetics, University of Cologne, K{\"o}ln, Germany. UBOEHM\@GENETIK.UNI-KOELN.DE},
	Pages = {749-95},
	Pubmed = {9143706},
	Title = {Cellular responses to interferon-gamma},
	Uuid = {53DA529F-9CC9-4695-996E-301370A9D6A1},
	Volume = {15},
	Year = {1997},
	url = {papers/Boehm_AnnuRevImmunol1997.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1146/annurev.immunol.15.1.749}}

@article{Bohatschek:2001,
	Abstract = {Changes in the morphology of ramified microglia are a common feature in brain pathology and culminate in the appearance of small, rounded, microglia-derived phagocytes in the presence of neural debris. Here, we explored the effect of adding brain cell membranes on the morphology of alphaMbeta2-integrin (CD11b/CD18, CR3) positive microglia cultured on a confluent astrocyte substrate as an in vitro model of deramification. Addition of brain membranes led to a loss of microglial ramification, with full transformation to small, rounded, macrophages at 20-40 microg/ml. Time course studies showed a rapid response, with first effects at 1-3 hours, and full transformation at 24-48 hours. Removal of cell membranes and exchange of the culture medium led to a similarly rapid process of reramification. Comparison of cell membranes from different tissues at 20 microg/ml showed strong transforming effect for the brain, more moderate for kidney and liver, and very weak for spleen and skeletal muscle. Fluorescent labeling of brain membranes revealed uptake by almost all rounded macrophages, by a subpopulation of glial fibrillary acidic protein (GFAP)-positive astrocytes, but not by ramified microglia. Phagocytosis of inert fluorobeads did not lead to a transformation into macrophages but their phagocytosis was inhibited by brain membranes, pointing to a saturable uptake mechanism. In summary, addition of brain cell membranes and their phagocytosis leads to a rapid and reversible loss of ramification. The differences in transforming activity from different tissues and the absence of effect from phagocytosed fluorobeads suggest, however, the need for a second stimulus following the phagocytosis of cell debris.},
	Author = {Bohatschek, M. and Kloss, C. U. and Kalla, R. and Raivich, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Dose-Response Relationship, Drug;Cell Differentiation;Animals;Astrocytes;Cells, Cultured;Coculture Techniques;Viscera;Microglia;Models, Biological;Cell Membrane;Cell Movement;11 Glia;Phagocytes;Brain Diseases;Time Factors;Microspheres;Animals, Newborn;Macrophage-1 Antigen;Cell Size;Gliosis;Mice;Immunohistochemistry;Membrane Proteins;Microscopy, Electron;Research Support, Non-U.S. Gov't},
	Medline = {21286590},
	Month = {6},
	Nlm_Id = {7600111},
	Number = {5},
	Organization = {Department of Neuromorphology, Max-Planck Institute for Neurobiology, Martinsried, Germany.},
	Pages = {508-22},
	Pubmed = {11391706},
	Title = {In vitro model of microglial deramification: ramified microglia transform into amoeboid phagocytes following addition of brain cell membranes to microglia-astrocyte cocultures},
	Uuid = {CD0337AF-3415-418B-947B-1E742A854CF3},
	Volume = {64},
	Year = {2001}}

@article{Boire:2005,
	Abstract = {The laminar distribution of several distinct populations of neurofilament protein containing neurons has been used as a criterion for the delineation of cortical areas in hamsters. SMI-32 is a monoclonal antibody that recognizes a non-phosphorylated epitope on the medium- and high-molecular weight subunits of neurofilament proteins. As in carnivores and primates, SMI-32 immunoreactivity in the hamster neocortex was present in cell bodies, proximal dendrites and axons of some medium and large pyramidal neurons located in cortical layers III, V and VI. A small population of labeled multipolar cells was also found in layer IV. Neurofilament protein immunoreactive neurons were found throughout isocortical areas. Very few labeled cells were encountered in supplemental motor area, insular cortex, medial portion of associative visual cortex and in parietal association cortex. Our data indicate that SMI-32 immunoreactive cells can be efficiently used to trace boundaries between neocortical areas in the hamster's brain. The regional distribution SMI-32 immunoreactivity in the hamster cortex corresponds quite closely with cortical areas as defined by their cytoarchitecture and myeloarchitecture. The primary sensory cortical areas contain the most intense of SMI-32 immunoreactivity and are also those with the highest density of myelinated axons. Very low SMI-32 immunoreactivity was found in orbital, insular, perirhinal, cingulate and infralimbic cortices, which are also poor in myelinated axons. This supports the association between SMI-32 immunoreactivity and myelin contents.},
	Author = {Boire, Denis and Desgent, S{\'e}bastien and Matteau, Isabelle and Ptito, Maurice},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0891-0618},
	Journal = {J Chem Neuroanat},
	Keywords = {23 Technique},
	Month = {5},
	Nlm_Id = {8902615},
	Number = {3},
	Organization = {Ecole d'optom{\'e}trie, Universit{\'e} de Montr{\'e}al, CP 6128 succ Centre-Ville, Montr{\'e}al, Quebec, Canada H3C 3J7.},
	Pages = {193-208},
	Pii = {S0891-0618(05)00017-7},
	Pubmed = {15820621},
	Title = {Regional analysis of neurofilament protein immunoreactivity in the hamster's cortex},
	Uuid = {FC813E7F-D31C-11D9-A0E9-000D9346EC2A},
	Volume = {29},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jchemneu.2005.01.003}}

@article{Bolz:2004,
	Abstract = {The functional architecture of the cerebral cortex is based on intrinsic connections that precisely link neurons from distinct cortical laminae as well as layer-specific afferent and efferent projections. Experimental strategies using in vitro assays originally developed by Friedrich Bonhoeffer have suggested that positional cues confined to individual layers regulate the assembly of local cortical circuits and the formation of thalamocortical projections. One of these wiring molecules is ephrinA5, a ligand for Eph receptor tyrosine kinases. EphrinA5 and Eph receptors exhibit highly dynamic expression patterns in distinct regions of the cortex and thalamus during early and late stages of thalamocortical and cortical circuit formation. In vitro assays suggest that ephrinA5 is a multifunctional wiring molecule for different populations of cortical and thalamic axons. Additionally, the expression patterns of ephrinA5 during cortical development are consistent with this molecule regulating, in alternative ways, specific components of thalamic and cortical connectivity. To test this directly, the organization of thalamocortical projections was examined in mice lacking ephrinA5 gene expression. The anatomical studies in ephrinA5 knockout animals revealed a miswiring of limbic thalamic projections and changes in neocortical circuits that were predicted from the expression pattern and the in vitro analysis of ephrinA5 function.},
	Author = {Bolz, J{\"u}rgen and Uziel, Daniela and M{\"u}hlfriedel, Sven and G{\"u}llmar, Andr{\'e} and Peuckert, Christiane and Zarbalis, Konstantionos and Wurst, Wolfgang and Torii, Masaaki and Levitt, Pat},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Embryo, Mammalian;Neurons;24 Pubmed search results 2008;10 Development;research support, non-u.s. gov't;Embryo, Nonmammalian;Ephrin-A5;Neural Pathways;10 circuit formation;in vitro;Receptor, EphA1;research support, u.s. gov't, p.h.s.;Animals;Thalamus;Cerebral Cortex;review;Axons},
	Month = {4},
	Nlm_Id = {0213640},
	Number = {1},
	Organization = {Universit{\"a}t Jena, Institut f{\"u}r Allgemeine Zoologie und Tierphysiologie, Erberstrasse 1, 07743 Jena, Germany. bolz\@pan.zoo.uni-jena.de},
	Pages = {82-94},
	Pubmed = {15007829},
	Title = {Multiple roles of ephrins during the formation of thalamocortical projections: maps and more},
	Uuid = {C6FFBF29-2055-4EB3-8D8B-CFC457E294FB},
	Volume = {59},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.10346}}

@article{Bondolfi:2002,
	Abstract = {APP23 transgenic mice express mutant human amyloid precursor protein and develop amyloid plaques predominantly in neocortex and hippocampus progressively with age, similar to Alzheimer's disease. We have previously reported neuron loss in the hippocampal CA1 region of 14- to 18-month-old APP23 mice. In contrast, no neuron loss was found in neocortex. In the present study we have reinvestigated neocortical neuron numbers in adult and aged APP23 mice. Surprisingly, results revealed that 8-month-old APP23 mice have 13 and 14\%more neocortical neurons compared with 8-month-old wild-type and 27-month-old APP23 mice, respectively. In 27-month-old APP23 mice we found an inverse correlation between amyloid load and neuron number. These results suggest that APP23 mice have more neurons until they develop amyloid plaques but then lose neurons in the process of cerebral amyloidogenesis. Supporting this notion, we found more neurons with a necrotic-apoptotic phenotype in the neocortex of 24-month-old APP23 mice compared with age-matched wild-type mice. Stimulated by recent reports that demonstrated neurogenesis after targeted neuron death in the mouse neocortex, we have also examined neurogenesis in APP23 mice. Strikingly, we found a fourfold to sixfold increase in newly produced cells in 24-month-old APP23 mice compared with both age-matched wild- type mice and young APP23 transgenic mice. However, subsequent cellular phenotyping revealed that none of the newly generated cells in neocortex had a neuronal phenotype. The majority were microglial and to a lesser extent astroglial cells. We conclude that cerebral amyloidosis in APP23 mice causes a modest neuron loss in neocortex and induces marked gliogenesis.},
	Author = {Bondolfi, L. and Calhoun, M. and Ermini, F. and Kuhn, H. G. and Wiederhold, K. H. and Walker, L. and Staufenbiel, M. and Jucker, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Neocortex/*metabolism/pathology;Human;Amyloidosis/*metabolism/pathology;Neurons/*metabolism/pathology;Alzheimer Disease/metabolism/pathology;G;Phenotype;Female;Cell Count;Animal;Mice, Transgenic;Neuroglia/*metabolism/pathology;11 Glia;Mice, Inbred C57BL;Male;Amyloid beta-Protein Precursor/*genetics;Support, Non-U.S. Gov't;In Situ Nick-End Labeling;Mice;Aging/metabolism/pathology;Cell Division;Bromodeoxyuridine;Cell Death},
	Number = {2},
	Organization = {Department of Neuropathology, Institute of Pathology, University of Basel, CH-4003 Basel, Switzerland.},
	Pages = {515-22.},
	Title = {Amyloid-associated neuron loss and gliogenesis in the neocortex of amyloid precursor protein transgenic mice},
	Uuid = {BF2CAC95-97F5-4657-B001-863B64C3C59B},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11784797%20http://www.jneurosci.org/cgi/content/full/22/2/515%20http://www.jneurosci.org/cgi/content/abstract/22/2/515}}

@article{Bonfanti:2006,
	Abstract = {Polysialic acid (PSA) is a linear homopolymer of alpha2-8-N acetylneuraminic acid whose major carrier in vertebrates is the neural cell adhesion molecule (NCAM). PSA serves as a potent negative regulator of cell interactions via its unusual biophysical properties. PSA on NCAM is developmentally regulated thus playing a prominent role in different forms of neural plasticity spanning from embryonic to adult nervous system, including axonal growth, outgrowth and fasciculation, cell migration, synaptic plasticity, activity-induced plasticity, neuronal-glial plasticity, embryonic and adult neurogenesis. The cellular distribution, developmental changes and possible function(s) of PSA-NCAM in the central nervous system of mammals here are reviewed, along with recent findings and theories about the relationships between NCAM protein and PSA as well as the role of different polysialyltransferases. Particular attention is focused on postnatal/adult neurogenesis, an issue which has been deeply investigated in the last decade as an example of persisting structural plasticity with potential implications for brain repair strategies. Adult neurogenic sites, although harbouring all subsequent steps of cell differentiation, from stem cell division to cell replacement, do not faithfully recapitulate development. After birth, they undergo morphological and molecular modifications allowing structural plasticity to adapt to the non-permissive environment of the mature nervous tissue, that are paralled by changes in the expression of PSA-NCAM. The use of PSA-NCAM as a marker for exploring differences in structural plasticity and neurogenesis among mammalian species is also discussed.},
	Author = {Bonfanti, Luca},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0301-0082},
	Journal = {Prog Neurobiol},
	Keywords = {24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {0370121},
	Number = {3},
	Organization = {Department of Veterinary Morphophysiology, University of Turin, Via Leonardo da Vinci 44, 10095 Grugliasco, Italy; Rita Levi Montalcini Center for Brain Repair, Turin, Italy.},
	Pages = {129-64},
	Pii = {S0301-0082(06)00108-0},
	Pubmed = {17029752},
	Title = {PSA-NCAM in mammalian structural plasticity and neurogenesis},
	Uuid = {CCE82151-1E30-4A24-99CB-36C03A706EFA},
	Volume = {80},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.pneurobio.2006.08.003}}

@article{Bonneau:2007,
	Abstract = {The environment significantly influences the dynamic expression and assembly of all components encoded in the genome of an organism into functional biological networks. We have constructed a model for this process in Halobacterium salinarum NRC-1 through the data-driven discovery of regulatory and functional interrelationships among approximately 80\%of its genes and key abiotic factors in its hypersaline environment. Using relative changes in 72 transcription factors and 9 environmental factors (EFs) this model accurately predicts dynamic transcriptional responses of all these genes in 147 newly collected experiments representing completely novel genetic backgrounds and environments-suggesting a remarkable degree of network completeness. Using this model we have constructed and tested hypotheses critical to this organism's interaction with its changing hypersaline environment. This study supports the claim that the high degree of connectivity within biological and EF networks will enable the construction of similar models for any organism from relatively modest numbers of experiments.},
	Author = {Bonneau, Richard and Facciotti, Marc T. and Reiss, David J. and Schmid, Amy K. and Pan, Min and Kaur, Amardeep and Thorsson, Vesteinn and Shannon, Paul and Johnson, Michael H. and Bare, J. Christopher and Longabaugh, William and Vuthoori, Madhavi and Whitehead, Kenia and Madar, Aviv and Suzuki, Lena and Mori, Tetsuya and Chang, Dong-Eun E. and Diruggiero, Jocelyne and Johnson, Carl H. and Hood, Leroy and Baliga, Nitin S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Transcription, Genetic;Transcription Factors;Systems Biology;Databases, Genetic;20 Networks;Models, Genetic;RNA, Messenger;Time Factors;Gene Expression Regulation, Archaeal;Adaptation, Physiological;Environment;research support, n.i.h., extramural;Archaeal Proteins;Reproducibility of Results;24 Pubmed search results 2008;Gene Regulatory Networks;research support, u.s. gov't, non-p.h.s.;Sodium Chloride;Halobacterium salinarum},
	Month = {12},
	Nlm_Id = {0413066},
	Number = {7},
	Organization = {Center for Genomics & Systems Biology, New York University, New York, NY 10003, USA; Courant Institute of Mathematical Sciences, Department of Computer Science, New York University, New York, NY 10003, USA.},
	Pages = {1354-65},
	Pii = {S0092-8674(07)01416-X},
	Pubmed = {18160043},
	Title = {A predictive model for transcriptional control of physiology in a free living cell},
	Uuid = {674AADE6-FC75-4A51-B28C-E639F8F691FC},
	Volume = {131},
	Year = {2007},
	url = {papers/Bonneau_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2007.10.053}}

@article{Bordey:2006,
	Abstract = {Findings over the past decades demonstrating persistent neurogenesis in the adult brain have challenged the view of a fixed circuitry in normally functioning brain and raised hopes for self-renewal following brain injury. In addition to providing insights for repair, studying adult neurogenesis may improve our understanding of embryonic development assuming that fundamental mechanisms are similar. It is argued here, using examples of cell:cell communication, that parallels can be drawn between adult and embryonic neurogenesis. Paradoxically, cell:cell communication in neurogenic regions resembles that in a mature neuroglial network. This suggests that differences in the integrative properties of cells and the extracellular matrix molecules may constitute a neurogenic environment or "niche". While reasons for persistent adult neurogenesis in humans remains obscure, recent findings regarding the environmental and activity-driven control of neurogenesis reinforce the original concept of a role for neurogenesis in motor memory formation and refinement of information processing.},
	Author = {Bordey,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {1551-4005},
	Journal = {Cell Cycle},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {101137841},
	Number = {7},
	Pii = {2614},
	Pubmed = {16582623},
	Title = {Adult Neurogenesis: Basic Concepts of Signaling},
	Uuid = {6321DE64-188A-4C4C-A4D7-BAD0AF248B82},
	Volume = {5},
	Year = {2006}}

@article{Borlongan:1998,
	Abstract = {This study was designed to explore the efficacy of a human clone cell line as an alternative neural graft source and to validate the practice of cryopreservation and xenografting as logistical approaches toward conducting neural transplantation. We investigated the biological effects of transplanting cultured human neurons (NT2N cells) derived from a well-characterized embryonal carcinoma cell line into the brains of rats subjected to transient, focal cerebral ischemia induced by embolic occlusion of the middle cerebral artery. At 1 month and extending throughout the 6-month posttransplantation test period, ischemic animals that were transplanted with NT2N cells and treated with an immunosuppressive drug displayed a significant improvement in a passive avoidance task as well as a normalization of asymmetrical motor behavior compared to ischemic animals that received rat fetal cerebellar cell grafts or vehicle alone. Remarkably, cryopreserved NT2N cell grafts compared with fresh NT2N cell grafts, remained viable in the immunosuppressed rat brain and effective in producing behavioral recovery in immunosuppressed ischemic animals. The long-term viability of cryopreserved NT2N cell xenografts in vivo and their sustained effectiveness in promoting behavioral recovery suggest potential utilization of xenografting and cryopreservation as useful protocols for establishing clone cell lines as graft source in neural transplantation therapies for central nervous system disorders. 0014-4886 Journal Article},
	Author = {Borlongan, C. V. and Tajima, Y. and Trojanowski, J. Q. and Lee, V. M. and Sanberg, P. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Exp Neurol},
	Keywords = {*Graft Survival;Human;Cerebral Arteries;Motor Activity;Immunosuppressive Agents/therapeutic use;Animals;Carcinoma, Embryonal/*pathology;*Cryopreservation;Rats;Comparative Study;Rats, Sprague-Dawley;Brain/pathology;Avoidance Learning;Ischemic Attack, Transient/pathology/*physiopathology/*surgery;Fetal Tissue Transplantation;17 Transplant Regeneration;Male;Neurons/cytology/pathology/*transplantation;Cell Line;Support, Non-U.S. Gov't;*Transplantation, Heterologous;L abstr;Tumor Cells, Cultured;Cerebellum/transplantation;Support, U.S. Gov't, P.H.S.;Reproducibility of Results;*Brain Tissue Transplantation},
	Number = {2},
	Organization = {Department of Surgery, University of South Florida College of Medicine, Tampa 33612, USA.},
	Pages = {310-21},
	Title = {Transplantation of cryopreserved human embryonal carcinoma-derived neurons (NT2N cells) promotes functional recovery in ischemic rats},
	Uuid = {EEEEDFE7-44E2-41E2-B8AF-082CB5047BB5},
	Volume = {149},
	Year = {1998},
	url = {papers/Borlongan_ExpNeurol1998.pdf}}

@article{Borlongan:1998a,
	Abstract = {Stroke mortality has declined over recent decades, prompting a demand for the development of effective rehabilitative therapies for stroke survivors. This effort has been facilitated by significant progress in replicating the behavioral and neuropathological changes of authentic human cerebral ischemia using relevant animal models. Since the rodent model of middle cerebral artery occlusion mimics several motor abnormalities seen in clinical cerebral ischemia, we have utilized this model to investigate treatment strategies for stroke. The present study explored the potential benefits of neural transplantation of fetal rat striatal cells or human neurons derived from a clonal embryonal carcinoma cell line to correct the abnormalities associated with cerebral ischemia. We report here that ischemia-induced behavioral dysfunctions were ameliorated by the neural grafts as early as 1 month post-transplantation. Of note, transplantation of human neurons induced a significantly more robust recovery than fetal rat striatal grafts. Thus, the logistical and ethical concerns about the use of fetal striatal cells for transplantation therapy can be eliminated by exploiting cell line-derived human neurons as alternative graft sources. Transplantation of human neurons has a therapeutic potential for treatment of behavioral deficits associated with cerebral ischemia. 0959-4965 Journal Article},
	Author = {Borlongan, C. V. and Tajima, Y. and Trojanowski, J. Q. and Lee, V. M. and Sanberg, P. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neuroreport},
	Keywords = {Human;Animals;Clone Cells/chemistry/transplantation;Rats;Cerebrovascular Disorders/surgery;*Fetal Tissue Transplantation;Brain Ischemia/*physiopathology/surgery;Rats, Sprague-Dawley;Motor Activity/physiology;Neurons/chemistry/*transplantation;17 Transplant Regeneration;Male;Corpus Striatum/blood supply/*transplantation;Support, Non-U.S. Gov't;L abstr;Graft Survival/physiology;Behavior, Animal/physiology;Avoidance Learning/physiology;Cell Adhesion Molecules, Neuronal/analysis;Locomotion/physiology;*Brain Tissue Transplantation},
	Number = {16},
	Organization = {National Institutes of Health, National Institute on Drug Abuse, Intramural Research Program, Cellular Neurophysiology, Baltimore, MD 21224, USA.},
	Pages = {3703-9},
	Pubmed = {9858383},
	Title = {Cerebral ischemia and CNS transplantation: differential effects of grafted fetal rat striatal cells and human neurons derived from a clonal cell line},
	Uuid = {82E239B6-7AB1-4AFE-8F2E-FA6D89B0273B},
	Volume = {9},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9858383}}

@article{Borrell:2006,
	Abstract = {Cajal-Retzius cells are critical in the development of the cerebral cortex, but little is known about the mechanisms controlling their development. Three focal sources of Cajal-Retzius cells have been identified in mice-the cortical hem, the ventral pallium and the septum-from where they migrate tangentially to populate the cortical surface. Using a variety of tissue culture assays and in vivo manipulations, we demonstrate that the tangential migration of cortical hem-derived Cajal-Retzius cells is controlled by the meninges. We show that the meningeal membranes are a necessary and sufficient substrate for the tangential migration of Cajal-Retzius cells. We also show that the chemokine CXCL12 secreted by the meninges enhances the dispersion of Cajal-Retzius cells along the cortical surface, while retaining them within the marginal zone in a CXCR4-dependent manner. Thus, the meningeal membranes are fundamental in the development of Cajal-Retzius cells and, hence, in the normal development of the cerebral cortex.},
	Author = {Borrell, V{\'\i}ctor and Mar{\'\i}n, Oscar},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {research support, non-u.s. gov't ;Epithelial Cells;Green Fluorescent Proteins;Laminin;Heterocyclic Compounds;24 Pubmed search results 2008;Cerebral Cortex;Animals;Cells, Cultured;Receptors, CXCR4;comparative study ;Cell Movement;Signal Transduction;Meninges;Organ Culture Techniques;Extracellular Matrix Proteins;Calcium-Binding Protein, Vitamin D-Dependent;In Situ Hybridization;Transplants;Serine Endopeptidases;Chemokines, CXC;Fluorescent Antibody Technique;Indoles;Embryo;Cell Adhesion Molecules, Neuronal;Mice, Inbred ICR;Mice;Neurons;Mice, Transgenic;in vitro ;Nerve Tissue Proteins},
	Month = {10},
	Nlm_Id = {9809671},
	Number = {10},
	Organization = {Instituto de Neurociencias de Alicante, Consejo Superior de Investigaciones Cient{\'\i}ficas & Universidad Miguel Hern{\'a}ndez, 03550 Sant Joan d'Alacant, Spain.},
	Pages = {1284-93},
	Pii = {nn1764},
	Pubmed = {16964252},
	Title = {Meninges control tangential migration of hem-derived Cajal-Retzius cells via CXCL12/CXCR4 signaling},
	Uuid = {735C9844-69E2-4069-9467-0E08874F69F7},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1764}}

@article{Boss:1985,
	Abstract = {We have estimated the number of dentate granule cells in Sprague-Dawley and Wistar rats at 1, 4 and 12 months of age. In Sprague-Dawley rats the number of granule cells is relatively constant throughout this period at about 1 million. In Wistar rats, on the other hand, there is a progressive increase in the number from about 700,000 at 1 month to 1 million at 4 months; thereafter the number declines to about 800,000 at 1 year. Estimates of the numbers of cells in the polymorphic zone that can be stained immunohistochemically for somatostatin, cholecystokinin, vasoactive-intestinal peptide, and glutamic acid decarboxylase show no appreciable differences in the two strains.},
	Author = {Boss, B. D. and Peterson, G. M. and Cowan, W. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {10 Development;10 Hippocampus;Animals;Rats;Comparative Study;Immunoenzyme Techniques;Female;Cell Count;Hippocampus;Rats, Inbred Strains;Vasoactive Intestinal Peptide;Cholecystokinin;Male;Brain Chemistry;Glutamate Decarboxylase;Neurons;Age Factors;Nerve Tissue Proteins;Serotonin},
	Medline = {85281338},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {1},
	Pages = {144-50},
	Pubmed = {3896391},
	Title = {On the number of neurons in the dentate gyrus of the rat},
	Uuid = {6EE3FE21-446E-437E-8E5D-E63C232E678B},
	Volume = {338},
	Year = {1985}}

@article{Boucsein:2000,
	Abstract = {Microglial cells serve as pathologic sensors of the brain. They are highly abundant in all regions of the central nervous system (CNS) and are characterized by a ramified morphology within the normal tissue. In the present study, we have developed a procedure to study the membrane properties of identified, in situ microglia in acutely isolated brain slices from rat cortex, striatum and facial nucleus. Unlike the well characterized cultured microglial cells, ramified microglia of the slice are characterized by little, if any, voltage-gated membrane currents and a very low membrane potential. They are thus distinct from neurons, other glial cells and nonbrain macrophages. To study the consequences of microglial activation on the membrane channel pattern, we compared cells in the normal facial nucleus and at defined times after facial nerve axotomy. Within 12 h of axotomy, microglial cells expressed a prominent inward rectifier current and thus acquired the physiological properties of cultured microglia. Within 24 h of the lesion, the cells expressed an additional outward current, which is typical for lipopolysaccharide (LPS)-activated microglia in vitro. Seven days after the lesion, at a time of major regenerative processes in the facial nucleus, the physiological properties of microglial cells had reverted to those present prior to the pathological event. In conclusion: (i) ramified microglial cells represent a physiologically unique population of cells in the brain; (ii) are distinct from their cultured counterparts; and (iii), undergo a defined pattern of physiological states in the course of pathologic events.},
	Author = {Boucsein, C. and Kettenmann, H. and Nolte, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Plant Lectins;Animals;Cells, Cultured;Rats;Microglia;Female;Patch-Clamp Techniques;Lipopolysaccharides;Rats, Wistar;11 Glia;Animals, Newborn;Support, Non-U.S. Gov't;Potassium Channels;Cerebral Cortex;Cell Size;Membrane Potentials;Axotomy;Facial Nerve;Lectins},
	Medline = {20345454},
	Month = {6},
	Nlm_Id = {8918110},
	Number = {6},
	Organization = {Max Delbr{\"u}ck Center for Molecular Medicine, Cellular Neuroscience, Robert-R{\"o}ssle-Strabetae 10, D-13092 Berlin, Germany.},
	Pages = {2049-58},
	Pii = {ejn100},
	Pubmed = {10886344},
	Title = {Electrophysiological properties of microglial cells in normal and pathologic rat brain slices},
	Uuid = {19AEDB8C-0300-4182-91A3-20C255DF94F5},
	Volume = {12},
	Year = {2000}}

@article{Bourne:2005,
	Abstract = {The maturation of pyramidal neurons in the primary visual cortex (V1) of marmoset monkeys was investigated using an antibody (SMI-32) to non-phosphorylated neurofilament protein (NNF). Analysis of animals aged between birth and postnatal day 91 (PD 91, which corresponds approximately to the peak of synaptogenesis in this species) revealed discrete changes in both the laminar and the areal distribution of NNF. At PD 0, the upper part of layer 6 contained darkly labelled neurons and associated neuropil, including axons. In this layer a centroperipheral gradient, with more labelled cells in the foveal representation, was apparent at PD 0. This topographic gradient gradually disappeared, and by PD 91 a similar density of labelled layer 6 cells was observed throughout V1. Labelled cells were not apparent in layer 3C until PD 7, and were not distributed according to a topographic gradient. Labelled cells were first observed in layer 3B(alpha) at PD 28, when they formed a centroperipheral gradient similar to that seen in layer 6. This gradient was still evident in an adult animal. These results demonstrate an inside-out profile of postnatal cortical development, with the topographic pattern of maturation of V1 mimicking the centroperipheral gradient of maturation in the retina.},
	Author = {Bourne, James A. and Warner, Claire E. and Rosa, Marcello G. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {23 Technique},
	Month = {6},
	Nlm_Id = {9110718},
	Number = {6},
	Organization = {Department of Physiology and Monash University Centre for Brain and Behaviour, Monash University, Victoria 3800, Australia. james.bourne\@med.monash.edu.au},
	Pages = {740-8},
	Pii = {bhh175},
	Pubmed = {15342427},
	Title = {Topographic and laminar maturation of striate cortex in early postnatal marmoset monkeys, as revealed by neurofilament immunohistochemistry},
	Uuid = {A447C9C8-A27C-4B24-BD38-6B78C473BFB5},
	Volume = {15},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhh175}}

@article{Bouzioukh:2001,
	Abstract = {Here we report that synapses in the adult dorsal vagal complex, a gateway for many primary afferent fibers, express a high level of the polysialylated neural cell adhesion molecule (PSA-NCAM). We show that electrical stimulation of the vagal afferents causes a rapid decrease of PSA-NCAM expression both in vivo and in acute slices. Inhibition of NMDA receptor activity completely prevented the decrease. Blockade of calmodulin activation, neuronal nitric oxide (NO) synthase, or soluble guanylyl cyclase and chelation of extracellular NO mimicked this inhibition. Our data provide a mechanistic framework for understanding how activity-linked stimulation of the NMDA-NO-cGMP pathway induces rapid changes in PSA-NCAM expression, which may be associated with long- term depression.},
	Author = {Bouzioukh, F. and Tell, F. and Jean, A. and Rougon, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Vagus Nerve/physiology;Nitric-Oxide Synthase/antagonists &inhibitors/*metabolism;Electric Stimulation;Guanylate Cyclase/antagonists &inhibitors/metabolism;Neural Cell Adhesion Molecules/*biosynthesis;In Vitro;Rats;Nitric Oxide/antagonists &inhibitors/metabolism;Neuronal Plasticity/physiology;Receptors, N-Methyl-D-Aspartate/antagonists &inhibitors/*metabolism;Chelating Agents/pharmacology;Animal;Rats, Sprague-Dawley;Enzyme Inhibitors/pharmacology;Brain Stem/*metabolism;Synapses/*metabolism;Support, Non-U.S. Gov't;Neurons, Afferent/physiology;Cyclic GMP/metabolism;C;04 Adult neurogenesis factors;Neural Inhibition/physiology;Calmodulin/antagonists &inhibitors/metabolism;Sialic Acids/*biosynthesis;Signal Transduction/physiology;GAP-43 Protein/biosynthesis},
	Number = {13},
	Organization = {Faculte de Saint Jerome, Centre National de la Recherche Scientifique (CNRS) Formation de Recherche en Evolution 2132-Unite Sous Contrat Institut National de la Recherche Agronomique 1147, 13397 Marseille, Cedex 20, France.},
	Pages = {4721-30.},
	Title = {NMDA receptor and nitric oxide synthase activation regulate polysialylated neural cell adhesion molecule expression in adult brainstem synapses},
	Uuid = {299175EC-6366-44F0-8FF0-B61D5C83C861},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11425899%20http://www.jneurosci.org/cgi/content/full/21/13/4721%20http://www.jneurosci.org/cgi/content/abstract/21/13/4721}}

@article{Brainard:2002,
	Abstract = {Bird fanciers have known for centuries that songbirds learn their songs. This learning has striking parallels to speech acquisition: like humans, birds must hear the sounds of adults during a sensitive period, and must hear their own voice while learning to vocalize. With the discovery and investigation of discrete brain structures required for singing, songbirds are now providing insights into neural mechanisms of learning. Aided by a wealth of behavioural observations and species diversity, studies in songbirds are addressing such basic issues in neuroscience as perceptual and sensorimotor learning, developmental regulation of plasticity, and the control and function of adult neurogenesis. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Brainard, M. S. and Doupe, A. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Nature},
	Keywords = {Prosencephalon/cytology/growth &development/*physiology;01 Adult neurogenesis general;Hearing/physiology;Learning/*physiology;Motor Cortex/cytology/growth &development/physiology;Human;Female;Neuronal Plasticity;Synapses/physiology;Aging/physiology;Auditory Cortex/cytology/growth &development/physiology;Support, U.S. Gov't, P.H.S.;Songbirds/*physiology;Vocalization, Animal/*physiology;Animals;Support, Non-U.S. Gov't;A pdf},
	Number = {6886},
	Organization = {W.M Keck Center for Integrative Neuroscience, University of California, San Francisco 94143, USA. msb\@phy.ucsf.edu},
	Pages = {351-8},
	Title = {What songbirds teach us about learning},
	Uuid = {9399E62F-21B2-40AA-AD00-F71704628300},
	Volume = {417},
	Year = {2002},
	url = {papers/Brainard_Nature2002}}

@article{Brauer:1982,
	Abstract = {Perineuronal nets could be visualized with some Golgi methods in the rat's brain. Nets were seen in telencephalic, diencephalic and mesencephalic structures covering somata and proximal dendrites of different neuronal types. Some nets could be found originating from microglia cells. In most cases their origin is not recognizable. These perineuronal nets seem to be identical with "Golgi nets" of late anatomists, which played an important role in the discussion between recticularists and neuronists. Some aspects of their possible functional significance are discussed.},
	Author = {Brauer, K. and Werner, L. and Leibnitz, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0021-8359},
	Journal = {J Hirnforsch},
	Keywords = {10 Development;Research Support, Non-U.S. Gov't;Dendrites;Golgi Apparatus;Telencephalon;Rats;Mesencephalon;Get paper from library;Neuroglia;Diencephalon;11 Glia;Nervous System;Nerve Net;Animals;10 Structural plasticity;24 Pubmed search results 2008;Neurons},
	Medline = {83187585},
	Nlm_Id = {0421521},
	Number = {6},
	Pages = {701-8},
	Pubmed = {7169530},
	Title = {Perineuronal nets of glia},
	Uuid = {6C3CFCD5-8E12-4EEE-8600-084388DB2328},
	Volume = {23},
	Year = {1982},
	url = {papers/Brauer_JHirnforsch1982.PDF}}

@article{Bray:1998,
	Abstract = {Chemotactic bacteria such as Escherichia coli can detect and respond to extremely low concentrations of attractants, concentrations of less than 5 nM in the case of aspartate. They also sense gradients of attractants extending over five orders of magnitude in concentration (up to 1 mM aspartate). Here we consider the possibility that this combination of sensitivity and range of response depends on the clustering of chemotactic receptors on the surface of the bacterium. We examine what will happen if ligand binding changes the activity of a receptor, propagating this change in activity to neighbouring receptors in a cluster. Calculations based on these assumptions show that sensitivity to extracellular ligands increases with the extent of spread of activity through an array of receptors, but that the range of concentrations over which the array works is severely diminished. However, a combination of low threshold of response and wide dynamic range can be attained if the cell has both clusters and single receptors on its surface, particularly if the extent of activity spread can adapt to external conditions. A mechanism of this kind can account quantitatively for the sensitivity and response range of E. coli to aspartate.},
	Author = {Bray, D. and Levin, M. D. and Morton-Firth, C. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Models, Biological;24 Pubmed search results 2008;Ligands;21 Neurophysiology;Aspartic Acid;Membrane Proteins;Receptor Aggregation;Receptors, Amino Acid;Chemotactic Factors;Chemotaxis;Bacterial Proteins;Escherichia coli},
	Month = {5},
	Nlm_Id = {0410462},
	Number = {6680},
	Organization = {Department of Zoology, University of Cambridge, UK. d.bray\@zoo.cam.ac.uk},
	Pages = {85-8},
	Pubmed = {9590695},
	Title = {Receptor clustering as a cellular mechanism to control sensitivity},
	Uuid = {FD4BB318-4BA3-4F47-B7BF-30748611FA95},
	Volume = {393},
	Year = {1998},
	url = {papers/Bray_Nature1998.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/30018}}

@article{Braz:2002,
	Abstract = {Systems neuroscience addresses the complex circuits made by populations of neurons in the CNS and the cooperative function of these neurons. Improved approaches to the neuroanatomical analysis of CNS circuits are thus of great interest. In fact, significant advances in tract-tracing methods have recently been made by using transgenic mice that express transneuronal lectin tracers under the control of neuron-specific promoters. The utility of those animals, however, is limited to the CNS circuit influenced by the particular promoter. Here, we describe a new transgenic mouse that can be used for transneuronal tracing analysis of circuits in any region of the brain or spinal cord. The transgene in these mice results in expression of LacZ in neurons throughout the CNS. Excision of the LacZ gene by Cre-mediated recombination initiates expression of the lectin, wheat germ agglutinin (WGA). To illustrate the diverse uses of these ZW (LacZ-WGA) mice, we triggered WGA expression either by crossing the mice with two Cre-expressing transgenic mouse lines or by microinjecting a Cre-expressing adeno-associated virus into the cerebellum or cerebral cortex. Both approaches resulted in extensive WGA expression in the cell bodies and dendrites of neurons in which the recombination event occurred, as well as anterograde and transneuronal transport of the lectin to second and third order neurons. Because the lectin can be induced in developing and adult animals, and in all regions of the brain and spinal cord, these ZW may prove extremely valuable for numerous studies of CNS circuit analysis. 0027-8424 Journal Article},
	Author = {Braz, J. M. and Rico, B. and Basbaum, A. I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {beta-Galactosidase/genetics;Neurons/*physiology;Support, Non-U.S. Gov't;Brain/*physiology;Protein Transport;Recombinant Proteins/metabolism;Promoter Regions (Genetics);T pdf;Mice, Transgenic;Support, U.S. Gov't, P.H.S.;Dependovirus/genetics;Wheat Germ Agglutinins/*genetics/metabolism;Mice;Animals;Integrases/*metabolism;23 Technique;Viral Proteins/*metabolism},
	Number = {23},
	Organization = {Department of Anatomy and Physiology and W. M. Keck Foundation Center for Integrative Neuroscience, University of California, San Francisco 94143, USA.},
	Pages = {15148-53},
	Title = {Transneuronal tracing of diverse CNS circuits by Cre-mediated induction of wheat germ agglutinin in transgenic mice},
	Uuid = {5B619A33-A209-4996-A942-F9D6B5355F1E},
	Volume = {99},
	Year = {2002},
	url = {papers/Braz_ProcNatlAcadSciUSA2002.pdf}}

@article{Brazelton:2000,
	Abstract = {After intravascular delivery of genetically marked adult mouse bone marrow into lethally irradiated normal adult hosts, donor-derived cells expressing neuronal proteins (neuronal phenotypes) developed in the central nervous system. Flow cytometry revealed a population of donor-derived cells in the brain with characteristics distinct from bone marrow. Confocal microscopy of individual cells showed that hundreds of marrow-derived cells in brain sections expressed gene products typical of neurons (NeuN, 200-kilodalton neurofilament, and class III beta-tubulin) and were able to activate the transcription factor cAMP response element-binding protein (CREB). The generation of neuronal phenotypes in the adult brain 1 to 6 months after an adult bone marrow transplant demonstrates a remarkable plasticity of adult tissues with potential clinical applications.},
	Author = {Brazelton, T. R. and Rossi, F. M. and Keshet, G. I. and Blau, H. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Cell Differentiation;Animals;Phosphorylation;Bone Marrow Transplantation;Microscopy, Confocal;Phenotype;Brain;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Male;Olfactory Bulb;Bone Marrow Cells;DNA-Binding Protein, Cyclic AMP-Responsive;Research Support, U.S. Gov't, P.H.S.;Cell Size;Neurons;Flow Cytometry;Mice;Luminescent Proteins;Biological Markers;Gene Expression;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {20553649},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5497},
	Organization = {Department of Molecular Pharmacology, CCSR 4215, 269 Campus Drive, Stanford University, Stanford, CA 94305-5175, USA.},
	Pages = {1775-9},
	Pii = {9028},
	Pubmed = {11099418},
	Title = {From marrow to brain: expression of neuronal phenotypes in adult mice},
	Uuid = {20DD63EE-E9D5-11DA-920C-000D9346EC2A},
	Volume = {290},
	Year = {2000},
	url = {papers/Brazelton_Science2000.pdf}}

@article{Bregman:2002,
	Abstract = {Earlier studies suggested that while after spinal cord lesions and transplants at birth, the transplants serve both as a bridge and as a relay to restore supraspinal input caudal to the injury (Bregman, 1994), after injury in the adult the spinal cord transplants serve as a relay, but not as a bridge. We show here, that after complete spinal cord transection in adult rats, delayed spinal cord transplants and exogenous neurotrophic factors, the transplants can also serve as a bridge to restore supraspinal input (Fig. 9). We demonstrate here that when the delivery of transplants and neurotrophins are delayed until 2 weeks after spinal cord transection, the amount of axonal growth and the amount of recovery of function are dramatically increased. Under these conditions, both supraspinal and propriospinal projections to the host spinal cord caudal to the transection are reestablished. The growth of supraspinal axons across the transplant and back into the host spinal cord caudal to the lesion was dependent upon the presence of exogenous neurotrophic support. Without the neurotrophins, only propriospinal axons were able to re-establish connections across the transplant. Studies using peripheral nerve or Schwann cell grafts have shown that some anatomical connectivity can be restored across the injury site, particularly under the influence of neurotrophins (Xu et al., 1995a,b; Cheng et al., 1996; Ye and Houle, 1997). Without neurotrophin treatment, brainstem axons do not enter [figure: see text] the graft (Xu et al., 1995a,b; Cheng et al., 1996; Ye and Houle, 1997). Similarly, cells genetically modified to secrete neurotrophins and transplanted into the spinal cord influence the axonal growth of specific populations of spinally projecting neurons (Tuszynski et al., 1996, 1997; Grill et al., 1997; Blesch and Tuszynski, 1997). Taken together, these studies support a role for neurotrophic factors in the repair of the mature CNS. The regrowth of supraspinal and propriospinal input across the transection site was associated with consistent improvements in hindlimb locomotor function. Animals performed alternating and reciprocal hindlimb stepping with plantar foot contact to the treadmill or stair during ascension. Furthermore, they acquired hindlimb weight support and demonstrated appropriate postural control for balance and equilibrium of all four limbs. After spinal cord injury in the adult, the circuitry underlying rhythmic alternating stepping movements is still present within the spinal cord caudal to the lesion, but is now devoid of supraspinal control. We show here that restoring even relatively small amounts of input allows supraspinal neurons to access the spinal cord circuitry. Removing the re-established supraspinal input after recovery (by retransection rostral to the transplant) abolished the recovery and abolished the serotonergic fibers within the transplant and spinal cord caudal to the transplant. This suggests that at least some of the recovery observed is due to re-establishing supraspinal input across the transplant, rather than a diffuse influence of the transplant on motor recovery. It is unlikely, however, that the greater recovery of function in animals that received delayed transplant and neurotrophins is due solely to the restoration of supraspinal input. Recent work by Ribotta et al. (2000) suggests that segmental plasticity within the spinal cord contributes to weight support and bilateral foot placement after spinal cord transection. This recovery of function occurs after transplants of fetal raphe cells into the adult spinal cord transected at T11. Recovery of function appears to require innervation of the L1-L2 segments with serotonergic fibers, and importantly, animals require external stimulation (tail pinch) to elicit the behavior. In the current study, animals with transection only did not develop stepping overground or on the treadmill without tail pinch, although the transplant and neurotrophin-treated groups did so without external stimuli. Therefore both reorganization of the segmental circuitry and partial restoration of supraspinal input presumably interact to yield the improvements in motor function observed. It is unlikely that the recovery of skilled forelimb movement observed can be mediated solely by reorganization of segmental spinal cord circuitry. We suggest that the restoration of supraspinal input contributes to the recovery observed. It is likely that after CNS injury, reorganization occurs both within the spinal cord and at supraspinal levels, and together contribute to the recovery of automatic and skilled forelimb function and of locomotion. In summary, the therapeutic intervention of tissue transplantation and exogenous neurotrophin support leads to improvements in supraspinal and propriospinal input across the transplant into the host caudal cord and a concomitant improvement in locomotor function. Paradoxically, delaying these interventions for several weeks after a spinal cord transection leads to dramatic improvements in recovery of function and a concomitant restoration of supraspinal input into the host caudal spinal cord. These findings suggest that opportunity for intervention after spinal cord injury may be far greater than originally envisioned, and that CNS neurons with long-standing injuries may be able to re-initiate growth leading to improvement in motor function.},
	Author = {Bregman, Barbara S. and Coumans, Jean-Valery V. and Dai, Hai Ning and Kuhn, Penelope L. and Lynskey, James and McAtee, Marietta and Sandhu, Faheem},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0079-6123},
	Journal = {Prog Brain Res},
	Keywords = {Axons;Research Support, Non-U.S. Gov't;Neuroprotective Agents;Cell Transplantation;Nerve Regeneration;Spinal Cord Injuries;Neuronal Plasticity;Mammals;Research Support, U.S. Gov't, P.H.S.;Forelimb;Locomotion;Animals;24 Pubmed search results 2008;Neurons;review},
	Medline = {22328364},
	Nlm_Id = {0376441},
	Organization = {Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA. bregmanb\@georgetown.edu},
	Pages = {257-73},
	Pubmed = {12440372},
	Title = {Transplants and neurotrophic factors increase regeneration and recovery of function after spinal cord injury},
	Uuid = {30EF16BD-52DD-46D7-AEE7-341B5FCC8679},
	Volume = {137},
	Year = {2002}}


@article{Brewer:1999,
	Abstract = {Adult mammalian CNS neurons appear to be terminally differentiated and postmitotic. However, this conclusion may be due to nonpermissive conditions in the brain or in culture media. If embryonic rat hippocampal neurons are cultured in Neurobasal/B27 with FGF2, nearly all neurons proliferated until a maximum density was reached. Similarly, adult neurons can be cultured that fire action potentials and display immunoreactivity for neurofilament, MAP2, tau, and glutamate. Seventy percent of the 3000 isolated adult cells per milligram of brain tissue began to proliferate after 3 days in culture and incorporated BrdU. By 4 days of regeneration in culture, virtually all neuron-like cells with asymmetric processes were glutamate positive and immunoreactive for neurofilament. Immunoreactivity of the intermediate filament stem cell marker nestin increased in adult cells to levels present in freshly isolated embryonic neurons. These are the first studies to demonstrate that over 50\%of adult CNS cells with neuron-like characteristics retain regenerative and proliferative potential.},
	Author = {Brewer, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Fetus;Animals;Cells, Cultured;Rats;Fluorescent Antibody Technique;Glutamic Acid;Rats, Sprague-Dawley;Hippocampus;Neurofilament Proteins;Antimetabolites;Fibroblast Growth Factor 2;Nerve Regeneration;Antibodies;Research Support, U.S. Gov't, P.H.S.;Intermediate Filament Proteins;Neurons;Age Factors;Cell Division;24 Pubmed search results 2008;Bromodeoxyuridine;Culture Media;Stem Cells;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {99417615},
	Month = {9},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Medical Microbiology and Immunology, Southern Illinois University School of Medicine, Springfield, Illinois, 62794-9626, USA.},
	Pages = {237-47},
	Pii = {S0014488699971236},
	Pubmed = {10486191},
	Title = {Regeneration and proliferation of embryonic and adult rat hippocampal neurons in culture},
	Uuid = {FC745F52-BE49-4EE2-ACEA-7E52DF4C526E},
	Volume = {159},
	Year = {1999},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.1999.7123}}

@article{Breunig:2007,
	Author = {Breunig, Joshua J. and Arellano, Jon I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Organogenesis;01 Adult neurogenesis general;Cell Fusion;Cell Communication;Neocortex;Microglia;comment;Green Fluorescent Proteins;Animals;24 Pubmed search results 2008;review;Neurons},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {7},
	Organization = {Department of Neurobiology, Yale University School of Medicine, 333 Cedar Street, Sterling Hall of Medicine C300, P.O. Box 208001, New Haven, CT 06520, USA. joshua.breunig\@yale.edu},
	Pages = {1507-8},
	Pubmed = {17304702},
	Title = {Glowing green pyramids: a false positive for neocortical neurogenesis reveals a novel neuronal-microglial fusion in the postnatal brain},
	Uuid = {4A76BE6B-12E3-43AD-859D-42A23A62C45B},
	Volume = {27},
	Year = {2007},
	url = {papers/Breunig_JNeurosci2007.pdf}}

@article{Brewer:1993,
	Abstract = {We have systematically optimized the concentrations of 20 components of a previously published serum-free medium (Brewer and Cotman, Brain Res 494: 65-74, 1989) for survival of rat embryonic hippocampal neurons after 4 days in culture. This serum-free medium supplement, B27, produced neuron survival above 60\%, independent of plating density above 160 plated cells/mm2. For isolated cells (< 100 cells/mm2), survival at 4 days was still above 45\%, but could be rescued to the 60\%level at 40 cells/mm2 by simply applying a coverslip on top of the cells. This suggests a need for additional trophic factors. High survival was achieved with osmolarity lower than found in Dulbecco's Modified Eagle's Medium (DMEM), and by reducing cysteine and glutamine concentrations and by the elimination of toxic ferrous sulphate found in DME/F12. Neurobasal is a new medium that incorporates these modifications to DMEM. In B27/Neurobasal, glial growth is reduced to less than 0.5\%of the nearly pure neuronal population, as judged by immunocytochemistry for glial fibrillary acidic protein and neuron-specific enolase. Excellent long-term viability is achieved after 4 weeks in culture with greater than 90\%viability for cells plated at 640/mm2 and greater than 50\%viability for cells plated at 160/mm2. Since the medium also supports the growth of neurons from embryonic rat striatum, substantia nigra, septum, and cortex, and neonatal dentate gyrus and cerebellum (Brewer, in preparation), support for other neuron types is likely. B27/Neurobasal should be useful for in vitro studies of neuronal toxicology, pharmacology, electrophysiology, gene expression, development, and effects of growth factors and hormones.},
	Author = {Brewer, G. J. and Torricelli, J. R. and Evege, E. K. and Price, P. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Embryo;Rats, Sprague-Dawley;Neuroglia;Culture Media, Serum-Free;Kinetics;Rats;Culture Media, Conditioned;Hippocampus;Time Factors;Cell Division;Asparagine;Glial Fibrillary Acidic Protein;Cell Survival;Animals;Cells, Cultured;23 Technique;Neurons},
	Medline = {93389779},
	Month = {8},
	Nlm_Id = {7600111},
	Number = {5},
	Organization = {Southern Illinois University School of Medicine, Springfield 62794.},
	Pages = {567-76},
	Pubmed = {8377226},
	Title = {Optimized survival of hippocampal neurons in B27-supplemented Neurobasal, a new serum-free medium combination},
	Uuid = {8FA42730-F0CF-11DA-83A9-000D9346EC2A},
	Volume = {35},
	Year = {1993},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.490350513}}

@article{Briellmann:2006,
	Abstract = {Double cortex is a neuronal migration disorder, associated with impaired cognitive function and seizures, and characterized by a subcortical band of neurons. Using functional MRI, we assessed the involvement of the subcortical band in language function and with interictal discharges. In both girls assessed, language-associated activation was in typical cortical areas, as well as in parts of the subcortical band. Interictal discharges were associated with deactivation in the subcortical band. This suggests involvement of the subcortical neurons in physiologic and pathologic functions.},
	Author = {Briellmann, R. S. and Little, T. and Harvey, A. S. and Abbott, D. F. and Jacobs, R. and Waites, A. B. and Jackson, G. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1526-632X},
	Journal = {Neurology},
	Keywords = {21 Dysplasia-heterotopia;21 Neurophysiology;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {0401060},
	Number = {6},
	Organization = {Brain Research Institute, Neurosciences Building, Austin Health, Heidelberg Heights, Victoria 3081, Australia.},
	Pages = {1090-3},
	Pii = {67/6/1090},
	Pubmed = {17000988},
	Title = {Pathologic and physiologic function in the subcortical band of double cortex},
	Uuid = {1AE40BC2-78E9-4D81-BE93-DD3E9E836B36},
	Volume = {67},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1212/01.wnl.0000237554.39283.6b}}

@article{Brill:2008,
	Abstract = {Distinct olfactory bulb (OB) interneurons are thought to become specified depending on from which of the different subregions lining the lateral ventricle wall they originate, but the role of region-specific transcription factors (TFs) in the generation of OB interneurons diversity is still poorly understood. Despite the crucial roles of the Dlx family of TFs for patterning and neurogenesis in the ventral telencephalon during embryonic development, their role in adult neurogenesis has not yet been addressed. Here we show that in the adult brain, Dlx 1 and Dlx2 are expressed in progenitors of the lateral but not the dorsal subependymal zone (SEZ), thus exhibiting a striking regional specificity. Using retroviral vectors to examine the function of Dlx2 in a cell-autonomous manner, we demonstrate that this TF is necessary for neurogenesis of virtually all OB interneurons arising from the lateral SEZ. Beyond its function in generic neurogenesis, Dlx2 also plays a crucial role in neuronal subtype specification in the OB, promoting specification of adult-born periglomerular neurons (PGNs) toward a dopaminergic fate. Strikingly, Dlx2 requires interaction with Pax6, because Pax6 deletion blocks Dlx2-mediated PGN specification. Thus, Dlx2 wields a dual function by first instructing generic neurogenesis from adult precursors and subsequently specifying PGN subtypes in conjunction with Pax6.},
	Author = {Brill, Monika S. and Snapyan, Marina and Wohlfrom, Hilde and Ninkovic, Jovica and Jawerka, Melanie and Mastick, Grant S. and Ashery-Padan, Ruth and Saghatelyan, Armen and Berninger, Benedikt and G{\"o}tz, Magdalena},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Pregnancy;Cell Differentiation;Paired Box Transcription Factors;Animals;Cells, Cultured;Humans;comparative study;Transcription Factors;Female;Homeodomain Proteins;Eye Proteins;Mice, Inbred C57BL;research support, non-u.s. gov't;Olfactory Bulb;Cell Lineage;Neurons;Age Factors;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Repressor Proteins;Transcription, Genetic},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {25},
	Organization = {Department of Physiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, D-80336 Munich, Germany.},
	Pages = {6439-52},
	Pii = {28/25/6439},
	Pubmed = {18562615},
	Title = {A dlx2- and pax6-dependent transcriptional code for periglomerular neuron specification in the adult olfactory bulb},
	Uuid = {C8856377-ADBB-4681-B5D9-04E7CB582507},
	Volume = {28},
	Year = {2008},
	url = {papers/Brill_JNeurosci2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0700-08.2008}}

@article{Brinon:1999,
	Abstract = {The distribution patterns of four calcium-binding proteins (CaBPs)- calbindin D-28k (CB), calretinin (CR), neurocalcin (NC), and parvalbumin (PV)-in the rat main olfactory bulb were compared, and the degrees ofcolocalization of NC with the other CaBPs were determined by using double immunocytochemical techniques. All investigated CaBPs were detected in groups of periglomerular cells and Van Gehuchten cells, whereas other cell types expressed some of the investigated proteins but not all four. Double-labeling techniques demonstrated the colocalization of NC with CB, CR, or PV in periglomerular cells, whereas each neurochemical group constituted entirely segregated populations in the remaining neuronal types. This is evident in granule cells that demonstrated large but segregated populations immunoreactive to either NC or CR. This study provides a further biochemical characterization of interneuronal types in the rat main olfactory bulb. On the basis of the distinct calcium-binding affinities, each neurochemically defined population may have different responses to calcium influx that would result in the existence of distinct functional subgroups within morphologically defined neuronal types. The expression of the investigated CaBPs in periglomerular cells with both single and colocalized patterns suggests that the local circuits in the glomerular layer are constituted by a complex network of elements with particular calcium requirements.},
	Author = {Brinon, J. G. and Martinez-Guijarro, F. J. and Bravo, I. G. and Arevalo, R. and Crespo, C. and Okazaki, K. and Hidaka, H. and Aijon, J. and Alonso, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Comp Neurol},
	Keywords = {I;Nerve Tissue Proteins/*metabolism;Immunohistochemistry;Calcium-Binding Proteins/*metabolism;Rats, Wistar;Tissue Distribution/physiology;Animal;Calcium-Binding Protein, Vitamin D-Dependent/metabolism;Rats/*metabolism;Neurons/metabolism;Support, Non-U.S. Gov't;Male;Parvalbumins/metabolism;Olfactory Bulb/cytology/*metabolism;13 Olfactory bulb anatomy},
	Number = {3},
	Organization = {Departamento de Biologia Celular y Patologia, Universidad de Salamanca, Spain.},
	Pages = {404-14.},
	Title = {Coexpression of neurocalcin with other calcium-binding proteins in the rat main olfactory bulb},
	Uuid = {52C72484-46FE-4B19-A627-DF054EDF01FC},
	Volume = {407},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10320220}}

@article{Brionne:2003,
	Abstract = {TGF-beta1 is a key regulator of diverse biological processes in many tissues and cell types, but its exact function in the developing and adult mammalian CNS is still unknown. We report that lack of TGF-beta1 expression in neonatal Tgfb1(-/-) mice results in a widespread increase in degenerating neurons accompanied by reduced expression of synaptophysin and laminin and a prominent microgliosis. Lack of TGF-beta1 also strongly reduces survival of primary neurons cultured from Tgfb1(-/-) mice. TGF-beta1 deficiency in adult Tgfb1(-/+) mice results in increased neuronal susceptibility to excitotoxic injury, whereas astroglial overexpression of TGF-beta1 protects adult mice against neurodegeneration in acute, excitotoxic and chronic injury paradigms. This study reveals a nonredundant function for TGF-beta1 in maintaining neuronal integrity and survival of CNS neurons and in regulating microglial activation. Because individual TGF-beta1 expression levels in the brain vary considerably between humans, this finding could have important implications for susceptibility to neurodegeneration.},
	Author = {Brionne, Thomas C. and Tesseur, Ina and Masliah, Eliezer and Wyss-Coray, Tony},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Mice, Transgenic;Cell Survival;Mice, Inbred BALB C;Comparative Study;Gliosis;Mice, Inbred C57BL;Not relevant;11 Glia;Microglia;Cell Death;Transforming Growth Factor beta;Support, U.S. Gov't, P.H.S.;Animals;Brain;Mice;Neurons;Cells, Cultured},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.},
	Pages = {1133-45},
	Pii = {S0896627303007669},
	Pubmed = {14687548},
	Title = {Loss of TGF-beta 1 leads to increased neuronal cell death and microgliosis in mouse brain},
	Uuid = {17617A48-818E-4D48-B28C-5752F29172ED},
	Volume = {40},
	Year = {2003}}

@article{Britanova:2006,
	Abstract = {Projection neurons of the developing cerebral cortex are generated in the cerebral ventricular zone and subsequently move to the developing cortical plate via radial migration. Conversely, most inhibitory interneurons originate in the ganglionic eminences and enter the developing cortical plate by tangential migration. Using immunohistochemical analysis together with tracer labeling experiments in organotypic brain slices, we show that a portion of cortical projection neurons migrates tangentially over long distances. Lineage analysis revealed that these neurons are derived from Emx1+ cortical progenitors and express the transcription factor Satb2 but do not express GABA or Olig1. In vitro and in vivo analysis of reeler mutant brains demonstrated that although reeler mutation does not influence tangential migration of interneurons, it affects the tangential migration of cortical projection neurons.},
	Author = {Britanova, and Alifragis, and Junek, and Jones, and Gruss, and Tarabykin,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {0372762},
	Organization = {Department of Molecular Biology of Neuronal Signals, Max-Plank-Institute for Experimental Medicine, 37075 G{\"o}ttingen, Germany; Laboratory of Molecular Technologies, Shemiakin and Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16/10, 117871 Moscow, Russia.},
	Pii = {S0012-1606(06)00964-X},
	Pubmed = {16901480},
	Title = {A novel mode of tangential migration of cortical projection neurons},
	Uuid = {0E6B1D9F-1547-4526-B23A-E0FAB448EA8D},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2006.06.040}}

@article{Britanova:2008,
	Abstract = {Pyramidal neurons of the neocortex can be subdivided into two major groups: deep- (DL) and upper-layer (UL) neurons. Here we report that the expression of the AT-rich DNA-binding protein Satb2 defines two subclasses of UL neurons: UL1 (Satb2 positive) and UL2 (Satb2 negative). In the absence of Satb2, UL1 neurons lose their identity and activate DL- and UL2-specific genetic programs. UL1 neurons in Satb2 mutants fail to migrate to superficial layers and do not contribute to the corpus callosum but to the corticospinal tract, which is normally populated by DL axons. Ctip2, a gene required for the formation of the corticospinal tract, is ectopically expressed in all UL1 neurons in the absence of Satb2. Satb2 protein interacts with the Ctip2 genomic region and controls chromatin remodeling at this locus. Satb2 therefore is required for the initiation of the UL1-specific genetic program and for the inactivation of DL- and UL2-specific genes.},
	Author = {Britanova, Olga and de Juan Romero, Camino and Cheung, Amanda and Kwan, Kenneth Y. and Schwark, Manuela and Gyorgy, Andrea and Vogel, Tanja and Akopov, Sergey and Mitkovski, Miso and Agoston, Denes and Sestan, Nenad and Moln{\'a}r, Zolt{\'a}n and Tarabykin, Victor},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Max-Planck-Institute for Experimental Medicine, Hermann-Rein Strasse 3, 37075 G{\"o}ttingen, Germany; Shemiakin and Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16 / 10, 117871 Moscow, Russia.},
	Pages = {378-92},
	Pii = {S0896-6273(08)00033-0},
	Pubmed = {18255031},
	Title = {Satb2 is a postmitotic determinant for upper-layer neuron specification in the neocortex},
	Uuid = {FD82BD13-9494-469D-85CE-CC4BD6577418},
	Volume = {57},
	Year = {2008},
	url = {papers/Britanova_Neuron2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.12.028}}

@article{Britz:2006,
	Abstract = {We showed previously that the proneural genes Neurogenin1 (Ngn1) and Ngn2 are required to specify the phenotypes of early- and not late-born neurons in the neocortex, acting in part through repression of Mash1, a third cortically expressed proneural gene. The precise timing of Ngn1/2 specification activity was unexpected given these genes are expressed throughout cortical development, prompting us to search for a later function. Here we reveal that Ngn2 and Mash1 are expressed in a dynamic fashion, acquiring a cell cycle-biased, nonoverlapping distribution, with preferential expression in prospective basal progenitors, during mid corticogenesis. We also identified a new function for Ngn2 during this latter period, demonstrating that it is required to regulate the transit of cortical progenitors from the ventricular zone (VZ) to the subventricular zone. Notably, Ngn2 regulates progenitor maturation at least in part through repression of Mash1 as misexpression of Mash1 strongly enhanced progenitor cell exit from the VZ. Significantly, the ability of Mash1 to promote progenitor cell maturation occurred independently of its ability to respecify cortical cells and is thus a novel function for Mash1. Taken together, these data support a model whereby Ngn2 and Mash1 function together to regulate the zonal distribution of progenitors in the developing neocortex.},
	Author = {Britz, Olivier and Mattar, Pierre and Nguyen, Laurent and Langevin, Lisa-Marie M. and Zimmer, C{\'e}line and Alam, Sharmila and Guillemot, Fran\c{c}ois and Schuurmans, Carol},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {Animals;Aging;Cell Differentiation;Research Support, Non-U.S. Gov't;Neurons;Cells, Cultured;24 Pubmed search results 2008;Basic Helix-Loop-Helix Transcription Factors;Nerve Tissue Proteins;Stem Cells;In Vitro;Cell Aggregation;Male;Cell Movement;Mice;Cerebral Cortex;Organogenesis},
	Month = {7},
	Nlm_Id = {9110718},
	Organization = {Division of Molecular Neurobiology, National Institute for Medical Research, The Ridgeway, Mill Hill, London, UK.},
	Pages = {i138-51},
	Pii = {16/suppl_1/i138},
	Pubmed = {16766700},
	Title = {A role for proneural genes in the maturation of cortical progenitor cells},
	Uuid = {67FDB250-8AC2-4895-A535-3777F7F63663},
	Volume = {16 Suppl 1},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhj168}}

@article{Broadwell:1993,
	Abstract = {Extracellular pathways circumventing the mammalian blood-brain fluid barriers (e.g., blood-brain and blood-CSF barriers) have been investigated in the rat by immunohistochemical localization of the endogenous serum proteins albumin, IgG, complement C-9, and IgM and by the exogenous tracer protein horseradish peroxidase (HRP). A demonstrable extracellular pathway into the central nervous system (CNS) is evident at the level of the subarachnoid space/pial surface. Immunoreaction products for the serum proteins and reaction product of intravenously administered HRP are identified over the entire pial surface, in the Virchow-Robin spaces and subpial cortical grey matter, and within phagocytes occupying the subarachnoid space/pial surface and perivascular clefts throughout the CNS. From specific circumventricular organs (e.g., median eminence, area postrema, subfornical organ), well known to lie outside the blood-brain barrier (BBB), each of the blood-borne proteins readily enters adjacent white and grey matter and the ventricular system for subsequent rostrocaudal labeling of the ependymal cell lining. Similar immunohistochemical and blood-borne HRP results are obtained in the CNS of the neonatal rat. Peroxidase delivered into the aorta of postmortem adult rats confirms the presence of a BBB in brain sites containing blood vessels impermeable to blood-borne HRP and the absence of a BBB in sites revealed as leaky to blood-borne HRP in the live rat. The results suggest blood-borne macromolecules, including those of the immune and complement systems, have potential widespread, extracellular distribution within the CNS and cerebrospinal fluid from sites deficient in a BBB (e.g., subarachnoid space/pial surface, circumventricular organs). These observations may have important clinical implications regarding experimental and pathologic autoimmune dysfunction within the CNS and impact on the interpretation of potential transcytosis of blood-borne peptides and proteins through the cerebral endothelium in vivo. A summary diagram of suspected extracellular and intracellular pathways circumventing the blood-brain fluid barriers is provided.},
	Author = {Broadwell, R. D. and Sofroniew, M. V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Immunoglobulin M;Animals;Models, Cardiovascular;Humans;Blood Proteins;Rats;Immunoglobulin G;Serum Albumin;Brain;Female;Extracellular Space;Rats, Wistar;Complement 9;11 Glia;Cerebrovascular Circulation;Rats, Inbred WF;Blood-Brain Barrier;Male;Animals, Newborn;Research Support, U.S. Gov't, P.H.S.;Neurons;Horseradish Peroxidase;Artifacts;Immunohistochemistry;Microscopy, Electron;Models, Neurological;Research Support, Non-U.S. Gov't},
	Medline = {93259273},
	Month = {4},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Surgery, University of Maryland School of Medicine, Baltimore 21201.},
	Pages = {245-63},
	Pii = {S0014488683710599},
	Pubmed = {8491281},
	Title = {Serum proteins bypass the blood-brain fluid barriers for extracellular entry to the central nervous system},
	Uuid = {91116093-779F-4B3F-B875-669A9DC56C53},
	Volume = {120},
	Year = {1993}}

@article{Broccardo:2006,
	Abstract = {The notion that the ATP-binding cassette transporter-A2 (ABCA2) may be involved in brain sterol homeostasis and is associated with early onset Alzheimer's disease led us to explore its neural expression. Our data support and extend the previous reports on ABCA2 expression by oligodendrocytes. They evidence that ABCA2 (i) is located in intracellular vesicles, identified in transfected cells as lysosome-related organelles only partially overlapping with classical endolysosomes; (ii) is a marker of neural progenitors as it is expressed in the subventricular zone of the lateral ventricle and the dentate gyrus of the hippocampal formation, sites of continual neurogenesis in the adult brain, and in nestin(+) cells differentiated in vitro from embryonic stem cells; (iii) persists, in the adult rodent brain, in a subset of GABAergic and glutamatergic neurons. Considering that the latter are targets of Alzheimer's lesions, these data provide a new rationale to explore the neuropathological consequences of ABCA2 functional dysregulations.},
	Author = {Broccardo, and Nieoullon, and Amin, and Masmejean, and Carta, and Tassi, and Pophillat, and Rubartelli, and Pierres, and Rougon, and Nieoullon, and Chazal, and Chimini,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {2985190R},
	Organization = {Centre d'Immunologie de Marseille Luminy INSERM CNRS, Universit{\'e} de la M{\'e}diterran{\'e}e Marseille, France.},
	Pii = {JNC3714},
	Pubmed = {16539677},
	Title = {ABCA2 is a marker of neural progenitors and neuronal subsets in the adult rodent brain},
	Uuid = {E396159E-C1ED-4E5C-A4D3-A7905F147129},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1471-4159.2006.03714.x}}

@article{Brooks:2002,
	Abstract = {As one part of a distinguished scientific career, Dr. Bryn Bridges focused his attention on the issue of DNA damage and repair in stationary phase bacteria. His work in this area led to his interest in DNA repair and mutagenesis in another non-dividing cell population, the neurons in the mammalian nervous system. He has specifically taken an interest in the magnocellular neurons of the central nervous system, and the possibility that somatic mutations may be occurring in these neurons. As part of this special issue dedicated to Bryn Bridges upon his retirement, I will discuss the various DNA repair pathways known to be active in the nervous system. The importance of DNA repair to the nervous system is most graphically illustrated by the neurological abnormalities observed in patients with hereditary diseases associated with defects in DNA repair. I will consider the mechanisms underlying the neurological abnormalities observed in patients with four of these diseases: xeroderma pigmentosum (XP), Cockayne's syndrome (CS), ataxia telangectasia (AT) and AT-like disorder (ATLD). I will also propose a mechanism for one of the observations indicating that somatic mutation can occur in the magnocellular neurons of the aging rat brain. Finally, as a parallel to Bridges inquiry into how much DNA synthesis is going on in stationary phase bacteria, I will address the question of how much DNA synthesis in going on in neurons, and the implications of the answer to this question for recent studies of neurogenesis in adult mammals. 0027-5107 Journal Article Review Review, Academic},
	Author = {Brooks, P. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Mutat Res},
	Keywords = {Nervous System Malformations/*etiology;Mutation;Neurons/*physiology;Aging/genetics;EE pdf;Human;Cockayne Syndrome/genetics;08 Aberrant cell cycle;*DNA Repair;Xeroderma Pigmentosum/genetics;Brain/abnormalities/cytology;Ataxia Telangiectasia/genetics;Heredodegenerative Disorders, Nervous System/etiology},
	Number = {1-2},
	Organization = {Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 12420 Parklawn Drive, MSC 8110, Bethesda, MD 20892-8110, USA. pjbrooks\@mail.nih.gov},
	Pages = {93-108},
	Title = {DNA repair in neural cells: basic science and clinical implications},
	Uuid = {6D9D62F3-DC9B-4854-B692-886058B75248},
	Volume = {509},
	Year = {2002},
	url = {papers/Brooks_MutatRes2002}}

@article{Brown:1979,
	Abstract = {Cultured Friend murine erythroleukemia cells (Friend cells) are induced to undergo erythroid differentiation when grown in the presence of dimethylsulfoxide (DMSO) and other compounds. The effects of unifilar substitution of bromouracil (BU) for thymidine in the DNA (BU-DNA) of Friend cells were examined. Cells were grown in the presence of 5-bromodeoxy-uridine (BrdU) for one generation, then centrifuged and resuspended in medium containing DMSO without BrdU. These cells exhibited a delay in the appearance of heme-producing, benzidine-reative (B+) cells and a decreased rate of cell proliferation in comparison to the control not containing BU-DNA. A transient inhibition of entry into S phase was observed when control cells or cells containing BU-DNA were grown in the presence of DMSO) for 10 to 20 hours. This transient inhibition was increased in the BrdU culture. Thus BU-substitution in Friend cells alters other cellular functions in addition to erythroid differentiation. The rate of increase in the percent of cells committed to differentiate (those forming B+ colonies in plasma clots) was similar in the BrdU and control cultures until 40 to 50 hours. After this time, a delay in the appearance of committed cells was observed in the BrdU culture. The effect of BrdU on the appearance of B+ cells was more pronounced and occurred earlier than its effect on the rate of commitment. Therefore, the delay in the appearance of B+ cells in the BrdU culture was due primarily to perturbation of post-commitment events such as the accumulation of hemoglobin. We also examined the effect on growth and differentiation after BrdU was incorporated during different intervals of S phase in cells synchronized by centrifugal elutriation or by double thymidine block and hydroxyurea treatment. The delay in the appearance of B+ cells and inhibition of cell proliferation were only observed when BrdU was incorporated in the first half of S phase. BrdU (10 muM) had no effect on growth or differentiation when present during late S or G1 and G2. These results, using two very different methods to achieve cell synchrony, indicate that the effects of BrdU on growth and differentiation described above are due to its incorporation into DNA sequences replicating during early S.},
	Author = {Brown, E. H. and Schildkraut, C. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0021-9541},
	Journal = {J Cell Physiol},
	Keywords = {23 Technique;01 Adult neurogenesis general;Cell Differentiation;Research Support, U.S. Gov't, P.H.S.;Cell Division;Leukemia, Experimental;DNA Replication;15 Retrovirus mechanism;Animals;Interphase;Bromodeoxyuridine;Leukemia, Erythroblastic, Acute;24 Pubmed search results 2008},
	Medline = {79216625},
	Month = {5},
	Nlm_Id = {0050222},
	Number = {2},
	Pages = {261-78},
	Pubmed = {287673},
	Title = {Perturbation of growth and differentiation of Friend murine erythroleukemia cells by 5-bromodeoxyuridine incorporation in early S phase},
	Uuid = {E9E269A5-5129-4317-B241-7233CE046A42},
	Volume = {99},
	Year = {1979}}

@article{Brown:2003a,
	Abstract = {During development of the central nervous system, expression of the microtubule binding protein doublecortin (DCX) is associated with migration of neuroblasts. In addition to this developmental role, expression of DCX remains high within certain areas of the adult mammalian brain. These areas, mainly the dentate gyrus and the lateral ventricle wall in conjunction with the rostral migratory stream and olfactory bulb, retain the capacity to generate new neurons into adulthood. Adult neurogenesis is typically detected by incorporation of bromodeoxyuridine (BrdU) into dividing cells and colabeling of BrdU-positive cells with markers for mature neurons. To elucidate whether DCX could act as an alternative indicator for adult neurogenesis, we investigated the temporal expression pattern of DCX in neurogenic regions of the adult brain. Analysis of newly generated cells showed that DCX is transiently expressed in proliferating progenitor cells and newly generated neuroblasts. As the newly generated cells began expressing mature neuronal markers, DCX immunoreactivity decreased sharply below the level of detection and remained undetectable thereafter. The transient expression pattern of DCX in neuronal committed progenitor cells/neuroblasts indicates that DCX could be developed into a suitable marker for adult neurogenesis and may provide an alternative to BrdU labeling. This assumption is further supported by our observation that the number of DCX-expressing cells in the dentate gyrus was decreased with age according to the reduction of neurogenesis in the aging dentate gyrus previously reported.},
	Author = {Brown, Jason P. and Couillard-Despr{\'e}s, S{\'e}bastien and Cooper-Kuhn, Christiana M. and Winkler, J{\"u}rgen and Aigner, Ludwig and Kuhn, H. Georg},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Electrophoresis, Polyacrylamide Gel;Cell Differentiation;Animals;Microtubule-Associated Proteins;Aging;Rats;Fluorescent Antibody Technique;Mitosis;Female;Cell Movement;02 Adult neurogenesis migration;Hippocampus;Rats, Wistar;Time Factors;Neuropeptides;Olfactory Bulb;Blotting, Western;Neurons;Dentate Gyrus;Central Nervous System;Stem Cells;Bromodeoxyuridine;Lateral Ventricles;Research Support, Non-U.S. Gov't},
	Medline = {22935334},
	Month = {12},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Neurology, University of Regensburg, 93053 Regensburg, Germany.},
	Pages = {1-10},
	Pubmed = {14574675},
	Title = {Transient expression of doublecortin during adult neurogenesis},
	Uuid = {2D30F285-6D12-11DA-A4FE-000D9346EC2A},
	Volume = {467},
	Year = {2003},
	url = {papers/Brown_JCompNeurol2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10874}}

@article{Bruccoleri:2000,
	Abstract = {The osteopetrotic (op/op) mouse, deficient in biologically active colony stimulating factor 1 (CSF-1), was used to examine the role of microglia in chemical-induced trauma. Op/op mice and normal phenotype littermates (non-op/op) received an acute i.p. injection of the hippocampal toxicant, trimethyltin hydroxide (TMT; 1.5 or 2.0 mg/kg). At 2.0 mg/kg, both mice displayed severe degeneration of dentate granule neurons. At 1.5 mg/kg, non-op/op mice showed a limited punctate pattern of neuronal death while op/op mice showed prominent neuronal death. TMT-induced astrocyte reactivity was similar in both groups. RNase protection assays were conducted on hippocampal tissue at 24 hr post-TMT. Elevations were seen in mRNA levels for the host response genes: intercellular cell adhesion molecule (ICAM-1; non-op/op 80\%, op/op 85\%), the protease inhibitor EB22 (non-op/op 60\%, op/op 300\%), and glial fibrillary acidic protein (GFAP; non-op/op 300\%, op/op 480\%) within 24 hr. Macrophage-1 antigen (Mac-1) mRNA levels were lower in all op/op mice and were not induced by TMT exposure. Macrophage inflammatory protein (MIP)-1alpha and MIP-1beta mRNA levels were elevated in non-op/op mice while mRNA levels for interferon inducible protein (IP-10) and monocyte chemoattractant protein (MCP-1) were elevated in op/op mice. Tumor necrosis factor alpha (TNFalpha) mRNA levels were significantly elevated in both non-op/op (100\%) and op/op (600\%) mice. TNFbeta mRNA levels in op/op mice were elevated 200\%and interleukin 1alpha (IL-1alpha) 150\%. Reverse transcriptase polymerase chain reaction (RT-PCR) showed a TMT-induced elevation in INFalpha and INFbeta mRNA levels and no elevation of INFgamma. mRNA levels of the CSF-1 receptor, c-fms, were unaltered.},
	Author = {Bruccoleri, A. and Harry, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cytokines;Dose-Response Relationship, Drug;Tumor Necrosis Factor;Animals;Astrocytes;Osteopetrosis;Intercellular Adhesion Molecule-1;Mice, Mutant Strains;Cell Survival;Receptor, Macrophage Colony-Stimulating Factor;Trimethyltin Compounds;Female;Microglia;Lymphotoxin;Hippocampus;RNA, Messenger;11 Glia;Male;Reverse Transcriptase Polymerase Chain Reaction;Ribonucleases;Chemokines, CXC;Neurons;Interleukin-1;Neurodegenerative Diseases;Mice;Monocyte Chemoattractant Protein-1;Glial Fibrillary Acidic Protein},
	Medline = {20459227},
	Month = {10},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Neurotoxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.},
	Pages = {146-55},
	Pii = {10.1002/1097-4547(20001001)62:1<146::AID-JNR15>3.0.CO;2-L},
	Pubmed = {11002296},
	Title = {Chemical-induced hippocampal neurodegeneration and elevations in TNFalpha, TNFbeta, IL-1alpha, IP-10, and MCP-1 mRNA in osteopetrotic (op/op) mice},
	Uuid = {3FDFF91B-4807-4558-8B55-C39CC230736F},
	Volume = {62},
	Year = {2000}}

@article{Brummelkamp:2002,
	Abstract = {Mammalian genetic approaches to study gene function have been hampered by the lack of tools to generate stable loss-of-function phenotypes efficiently. We report here a new vector system, named pSUPER, which directs the synthesis of small interfering RNAs (siRNAs) in mammalian cells. We show that siRNA expression mediated by this vector causes efficient and specific down-regulation of gene expression, resulting in functional inactivation of the targeted genes. Stable expression of siRNAs using this vector mediates persistent suppression of gene expression, allowing the analysis of loss-of-function phenotypes that develop over longer periods of time. Therefore, the pSUPER vector constitutes a new and powerful system to analyze gene function in a variety of mammalian cell types. 1095-9203 Journal Article},
	Author = {Brummelkamp, T. R. and Bernards, R. and Agami, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Science},
	Keywords = {RNA, Untranslated/chemistry/*genetics/metabolism;Human;Transfection;Phenotype;Mutation;23 Technique;Genes, p53;RNA, Small Interfering;Nucleic Acid Conformation;RNA, Messenger/chemistry/*genetics/metabolism;*Gene Silencing;Support, Non-U.S. Gov't;Ligases/genetics;Tumor Cells, Cultured;T abstr;Protein Kinases/genetics/metabolism;Down-Regulation;*Ubiquitin-Protein Ligase Complexes;Protein p53/metabolism;*Genetic Techniques;*Genetic Vectors},
	Number = {5567},
	Organization = {Division of Molecular Carcinogenesis, Division of Tumor Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands.},
	Pages = {550-3},
	Pubmed = {11910072},
	Title = {A system for stable expression of short interfering RNAs in mammalian cells},
	Uuid = {E29548BF-8B2D-4094-95A9-A2A9034DD07A},
	Volume = {296},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11910072}}

@article{Brunet:2007,
	Abstract = {Homeogenes encode homeoprotein transcription factors that have fundamental roles in development. They are key players in genetic networks that lay out the body plan and also determine morphology and physiology at the cellular and multicellular level. However, homeoproteins share activities that extend beyond transcription, including translation regulation and signalling. For example, homeoproteins participate in the definition of territories in the neuroepithelium and also have a function in axonal guidance. Based on these examples, we propose that homeoproteins are not only morphogenetic transcription factors, but also morphogens themselves.},
	Author = {Brunet, Isabelle and Di Nardo, Ariel A. and Sonnier, Laure and Beurdeley, Marine and Prochiantz, Alain},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Neurons;Transcription Factors;24 Pubmed search results 2008;Central Nervous System;Morphogenesis;Animals;Humans;Homeodomain Proteins;review;Axons},
	Month = {6},
	Nlm_Id = {7808616},
	Number = {6},
	Organization = {Unit{\'e} Mixte de Recherche 8542, Development and Evolution of the Nervous System (Development and Neuropharmacology Group), Ecole normale sup{\'e}rieure, 46 rue d'Ulm, 75005 Paris, France.},
	Pages = {260-7},
	Pii = {S0166-2236(07)00075-6},
	Pubmed = {17418905},
	Title = {The topological role of homeoproteins in the developing central nervous system},
	Uuid = {5E1B6B83-E759-4A6D-BA92-8F66734C1861},
	Volume = {30},
	Year = {2007},
	url = {papers/Brunet_TrendsNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tins.2007.03.010}}

@article{Brussel:2004,
	Abstract = {The integrated form of human immunodeficiency virus type 1 (HIV-1) DNA is classically considered to be the sole template for viral gene expression. However, several studies have suggested that unintegrated viral DNA species could also support transcription. To determine the contribution of the different species of HIV-1 DNA to viral expression, we first monitored intracellular levels of various HIV-1 DNA and RNA species in a single-round infection assay. We observed that, in comparison to the precocity of HIV-1 DNA synthesis, viral expression was delayed, suggesting that only the HIV-1 DNA species that persist for a sufficient period of time would be transcribed efficiently. We next evaluated the transcriptional activity of the circular forms of HIV-1 DNA bearing two long terminal repeats, since these episomes were reported to exhibit an intrinsic molecular stability. Our results support the notion that these circular species of HIV-1 DNA are naturally transcribed during HIV-1 infection, thereby participating in virus replication.},
	Author = {Brussel, Audrey and Sonigo, Pierre},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Research Support, Non-U.S. Gov't;DNA, Circular;HIV-1;Cell Line;Gene Expression;DNA, Viral;Transcription, Genetic;RNA, Viral;HIV Integrase;Humans;HIV Long Terminal Repeat;15 Retrovirus mechanism;24 Pubmed search results 2008;Virus Integration},
	Month = {10},
	Nlm_Id = {0113724},
	Number = {20},
	Organization = {D{\'e}partement des Maladies Infectieuses, Institut Cochin, INSERM U567, CNRS UMR 8104, Universit{\'e} Ren{\'e} Descartes, 22 rue M{\'e}chain, 75014 Paris, France.},
	Pages = {11263-71},
	Pii = {78/20/11263},
	Pubmed = {15452245},
	Title = {Evidence for gene expression by unintegrated human immunodeficiency virus type 1 DNA species},
	Uuid = {B12A0D8F-3EE8-49FD-AFC2-15F723FB16D4},
	Volume = {78},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.78.20.11263-11271.2004}}

@article{Brustle:1995,
	Abstract = {The stereotyped positions occupied by individual classes of neurons are a fundamental characteristic of CNS cytoarchitecture. To study the regulation of neuronal positioning, we injected genetically labeled neural precursors derived from dorsal and ventral mouse forebrain into the telencephalic vesicles of embryonic rats. Cells from both areas were found to participate in the generation of telencephalic, diencephalic, and mesencephalic brain regions. Donor-derived neurons populated the host brain in distinct patterns and acquired phenotypic features appropriate for their final location. These observations indicate that neuronal migration and differentiation are predominantly regulated by non-cell-autonomous signals. Exploiting this phenomenon, intrauterine transplantation allows generation of controlled chimerism in the mammalian brain.},
	Author = {Brustle, O. and Maskos, U. and McKay, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neuron},
	Keywords = {02 Adult neurogenesis migration;Cell Differentiation;Transplantation, Heterologous;Rats, Sprague-Dawley;Brain/cytology/*embryology;Rats;Embryo/cytology/*physiology;Mice, Inbred C57BL;Animal;Neurons/cytology/physiology/*transplantation;B abstr;Stem Cells/cytology/physiology/transplantation;Support, Non-U.S. Gov't;Mice;Cell Movement},
	Number = {6},
	Organization = {Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-4092, USA.},
	Pages = {1275-85.},
	Title = {Host-guided migration allows targeted introduction of neurons into the embryonic brain},
	Uuid = {270994A3-2101-40F7-9ACD-E59296800DC4},
	Volume = {15},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8845152}}

@article{Budd:2000,
	Abstract = {In cultured cerebrocortical neurons, mild excitotoxic insults or staurosporine result in apoptosis. We show here that N-methyl-d- aspartate (NMDA) receptor-mediated, but not staurosporine-mediated, apoptosis is preceded by depolarization of the mitochondrial membrane potential (Deltapsi(m)) and ATP loss. Both insults, however, release cytochrome c (Cyt c) into the cytoplasm. What prompts mitochondria to release Cyt c and the mechanism of release are as yet unknown. We examined the effect of inhibition of the adenine nucleotide translocator (ANT), a putative component of the mitochondrial permeability transition pore. Inhibition of the mitochondrial ANT with bongkrekic acid (BA) prevented NMDA receptor-mediated apoptosis of cerebrocortical neurons. Concomitantly, BA prevented Deltapsi(m) depolarization, promoted recovery of cellular ATP content, and blocked caspase-3 activation. However, in the presence of BA, Cyt c was still released. Because BA prevented NMDA-induced caspase-3 activation and apoptosis, the presence of Cyt c in the neuronal cytoplasm is not sufficient for the induction of caspase activity or apoptosis. In contrast to these findings, BA was ineffective in preventing staurosporine-induced activation of caspases or apoptosis. Additionally, staurosporine-induced, but not NMDA-induced, apoptosis was associated with activation of caspase-8. These results indicate that, in cerebrocortical cultures, excessive NMDA receptor activation precipitates neuronal apoptosis by means of mitochondrial dysfunction, whereas staurosporine utilizes a distinct pathway.},
	Author = {Budd, S. L. and Tenneti, L. and Lishnak, T. and Lipton, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Caspases/metabolism;Cerebral Cortex/*cytology;Staurosporine/pharmacology;Nerve Tissue Proteins/antagonists &inhibitors/physiology;Adenine Nucleotide Translocase/antagonists &inhibitors/physiology;Bongkrekic Acid/pharmacology;07 Excitotoxicity Apoptosis;Apoptosis/drug effects/*physiology;Cytochrome c/physiology;Animal;Protein Kinases/antagonists &inhibitors;Adenosine Triphosphate/metabolism;Enzyme Activation/drug effects;E-10;Enzyme Inhibitors/pharmacology;Receptors, N-Methyl-D-Aspartate/physiology;Support, Non-U.S. Gov't;Mitochondria/enzymology/*physiology;Support, U.S. Gov't, P.H.S.;Intracellular Membranes/metabolism;Permeability;Neurons/*cytology/drug effects},
	Number = {11},
	Organization = {Center for Neuroscience and Aging Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.},
	Pages = {6161-6.},
	Title = {Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons},
	Uuid = {C0F9BA2F-AF1D-4C0B-8B9A-8295AB68E8DA},
	Volume = {97},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10811898}}

@article{Bulfone:2005,
	Abstract = {The vertebrate telencephalon is composed of many architectonically and functionally distinct areas and structures, with billions of neurons that are precisely connected. This complexity is fine-tuned during development by numerous genes. To identify genes involved in the regulation of telencephalic development, a specific subset of differentially expressed genes was characterized. Here, we describe a set of cDNAs encoded by genes preferentially expressed during development of the mouse telencephalon that was identified through a functional genomics approach. Of 832 distinct transcripts found, 223 (27\%) are known genes. Of the remaining, 228 (27\%) correspond to expressed sequence tags of unknown function, 58 (7\%) are homologs or orthologs of known genes, and 323 (39\%) correspond to novel rare transcripts, including 48 (14\%) new putative noncoding RNAs. As an example of this latter group of novel precursor transcripts of micro-RNAs, telencephalic embryonic subtractive sequence (TESS) 24.E3 was functionally characterized, and one of its targets was identified: the zinc finger transcription factor ZFP9. The TESS transcriptome has been annotated, mapped for chromosome loci, and arrayed for its gene expression profiles during neural development and differentiation (in Neuro2a and neural stem cells). Within this collection, 188 genes were also characterized on embryonic and postnatal tissue by in situ hybridization, demonstrating that most are specifically expressed in the embryonic CNS. The full information has been organized into a searchable database linked to other genomic resources, allowing easy access to those who are interested in the dissection of the molecular basis of telencephalic development.},
	Author = {Bulfone, Alessandro and Carotenuto, Pietro and Faedo, Andrea and Aglio, Veruska and Garzia, Livia and Bello, Anna Maria and Basile, Andrea and Andr\`{e}, Alessandra and Cocchia, Massimo and Guardiola, Ombretta and Ballabio, Andrea and Rubenstein, John L. R. and Zollo, Massimo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-13 09:45:17 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;MicroRNAs; microRNAs; development},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {33},
	Organization = {Stem Cell Research Institute-Hospital San Raffaele, Istituto Scientifico San Raffaele, 20132 Milan, Italy. bulfone.alessandro\@hsr.it},
	Pages = {7586-600},
	Pii = {25/33/7586},
	Pubmed = {16107646},
	Title = {Telencephalic embryonic subtractive sequences: a unique collection of neurodevelopmental genes},
	Uuid = {22B5E9A9-A103-4318-9BBF-EFF41456ABB9},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0522-05.2005}}

@article{Burns:1992,
	Abstract = {Comparison of the beta-tubulin sequences with the equilibrium colchicine Ka and the Ki for inhibition by podophyllotoxin suggests that residue beta:316 is directly involved in binding the common trimethoxyphenyl-(or A-) ring. By contrast, the analysis indicates that the local hydrophobicity affects the rate of one of the two conformational changes associated with colchicine binding but does not determine the affinity of the colchicine-binding site. 0014-5793 Journal Article Review Review, Tutorial},
	Author = {Burns, R. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {FEBS Lett},
	Keywords = {Colchicine/chemistry/*metabolism;EE, T abstr;Binding Sites;Molecular Sequence Data;Sequence Alignment;08 Aberrant cell cycle;Tubulin/*metabolism;Amino Acid Sequence;Animals},
	Number = {3},
	Organization = {Biophysics Section, Blackett Laboratory, Imperial College of Science, Technology and Medicine, London, UK.},
	Pages = {205-8},
	Pubmed = {1544399},
	Title = {Analysis of the colchicine-binding site of beta-tubulin},
	Uuid = {08D3BE1F-F49D-4EF0-A6C4-14CE23DA14C0},
	Volume = {297},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1544399}}

@article{Burns:1993,
	Abstract = {The restricted host-cell range and low titer of retroviral vectors limit their use for stable gene transfer in eukaryotic cells. To overcome these limitations, we have produced murine leukemia virus-derived vectors in which the retroviral envelope glycoprotein has been completely replaced by the G glycoprotein of vesicular stomatitis virus. Such vectors can be concentrated by ultracentrifugation to titers >10(9) colony-forming units/ml and can infect cells, such as hamster and fish cell lines, that are ordinarily resistant to infection with vectors containing the retroviral envelope protein. The ability to concentrate vesicular stomatitis virus G glycoprotein pseudotyped vectors will facilitate gene therapy model studies and other gene transfer experiments that require direct delivery of vectors in vivo. The availability of these pseudotyped vectors will also facilitate genetic studies in nonmammalian species, including the important zebrafish developmental system, through the efficient introduction and expression of foreign genes. 0027-8424 Journal Article},
	Author = {Burns, J. C. and Friedmann, T. and Driever, W. and Burrascano, M. and Yee, J. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Hamsters;Human;Animals;Kidney;Transfection;J;Helper Viruses/genetics/metabolism;Cell Line, Transformed;Adenoviruses, Human/*genetics;Moloney murine leukemia virus/*genetics;15 Retrovirus mechanism;Restriction Mapping;Vesicular stomatitis-Indiana virus/*genetics/metabolism;Cytomegalovirus/genetics;*Membrane Glycoproteins;Genes, gag;Genes, pol;Genetic Vectors;Viral Envelope Proteins/*biosynthesis/genetics;Cell Line;Plasmids;Support, U.S. Gov't, P.H.S.;Promoter Regions (Genetics);Dogs},
	Number = {17},
	Organization = {Department of Pediatrics, University of California, San Diego School of Medicine, La Jolla 92093.},
	Pages = {8033-7},
	Pubmed = {8396259},
	Title = {Vesicular stomatitis virus G glycoprotein pseudotyped retroviral vectors: concentration to very high titer and efficient gene transfer into mammalian and nonmammalian cells},
	Uuid = {E6FD4BE5-DFA9-4A2C-86A6-6F8570800528},
	Volume = {90},
	Year = {1993},
	url = {papers/Burns_ProcNatlAcadSciUSA1993.pdf}}

@article{Burns:2006,
	Abstract = {Thymidine analogs, including bromodeoxyuridine, chlorodeoxyuridine, iododeoxyuridine, and tritiated thymidine, label dividing cells by incorporating into DNA during S phase of cell division and are widely employed to identify cells transplanted into the central nervous system. However, the potential for transfer of thymidine analogs from grafted cells to dividing host cells has not been thoroughly tested. We here demonstrate that graft-derived thymidine analogs can become incorporated into host neural precursors and glia. Large numbers of labeled neurons and glia were found 3-12 weeks after transplantation of thymidine analog-labeled live stem cells, suggesting differentiation of grafted cells. Remarkably, however, similar results were obtained after transplantation of dead cells or labeled fibroblasts. Our findings reveal for the first time that thymidine analog labeling may not be a reliable means of identifying transplanted cells, particularly in highly proliferative environments such as the developing, neurogenic, or injured brain.},
	Author = {Burns, Terry C. and Ortiz-Gonz{\'a}lez, Xilma R. and Guti{\'e}rrez-P{\'e}rez, Mar{\'\i}a and Keene, C. Dirk and Sharda, Rohit and Demorest, Zachary L. and Jiang, Yuehua and Nelson-Holte, Molly and Soriano, Mario and Nakagawa, Yasushi and Luquin, Mar{\'\i}a Rosario and Garcia-Verdugo, Jose Manuel and Pr{\'o}sper, Felipe and Low, Walter C. and Verfaillie, Catherine M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {Pregnancy;research support, n.i.h., extramural ;Animals;Biological Transport, Active;Stem Cell Transplantation;Rats;Rats, Inbred SHR;Brain;Thymidine;Female;Rats, Sprague-Dawley;in vitro ;Mice, Transgenic;Cell Proliferation;research support, non-u.s. gov't ;Animals, Newborn;Neuroglia;Neurons;Mice;24 Pubmed search results 2008;Central Nervous System;Bromodeoxyuridine},
	Month = {4},
	Nlm_Id = {9304532},
	Number = {4},
	Organization = {Stem Cell Institute, University of Minnesota, 420 Delaware Street, Minneapolis, Minnesota 55455, USA.},
	Pages = {1121-7},
	Pii = {2005-0463},
	Pubmed = {16373692},
	Title = {Thymidine analogs are transferred from prelabeled donor to host cells in the central nervous system after transplantation: a word of caution},
	Uuid = {43CB330D-9013-402B-A3F4-B9A655F036A3},
	Volume = {24},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1634/stemcells.2005-0463}}

@article{Burrone:2006,
	Abstract = {Genetically encoded fluorescent probes have become indispensable tools in the biological sciences. Studies of synaptic vesicle recycling have been facilitated by a group of GFP-derived probes called pHluorins. These probes exploit changes in pH that accompany exocytosis and recapture of synaptic vesicles. Here we describe how these synaptic tracers can be used in rodent hippocampal neurons to monitor the synaptic vesicle cycle in real time and to obtain mechanistic insights about it. Synapses can be observed in living samples using a wide-field fluorescence microscope and a cooled charge-coupled device camera. A simple specimen chamber allows electrical stimulation of synapses to evoke exocytosis in a precisely controlled manner. We present protocols to measure various parameters of the synaptic vesicle cycle. This technique can be easily adapted to study different classes of synapses from wild-type and mutant mice. Once cultured neurons expressing synaptopHluorin are available, the whole procedure should take about 2 h.},
	Author = {Burrone, Juan and Li, Zhiying and Murthy, Venkatesh N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1750-2799},
	Journal = {Nat Protoc},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008},
	Nlm_Id = {101284307},
	Number = {6},
	Organization = {MRC Center for Developmental Neurobiology, King's College London, London SE1 1UL, UK.},
	Pages = {2970-8},
	Pii = {nprot.2006.449},
	Pubmed = {17406557},
	Title = {Studying vesicle cycling in presynaptic terminals using the genetically encoded probe synaptopHluorin},
	Uuid = {9DAA57D0-6FA5-4743-8B02-E4ED6503D192},
	Volume = {1},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nprot.2006.449}}

@article{Bush:1999,
	Abstract = {Reactive astrocytes adjacent to a forebrain stab injury were selectively ablated in adult mice expressing HSV-TK from the Gfap promoter by treatment with ganciclovir. Injured tissue that was depleted of GFAP-positive astrocytes exhibited (1) a prolonged 25-fold increase in infiltration of CD45-positive leukocytes, including ultrastructurally identified monocytes, macrophages, neutrophils, and lymphocytes, (2) failure of blood-brain barrier (BBB) repair, (3) substantial neuronal degeneration that could be attenuated by chronic glutamate receptor blockade, and (4) a pronounced increase in local neurite outgrowth. These findings show that genetic targeting can be used to ablate scar-forming astrocytes and demonstrate roles for astrocytes in regulating leukocyte trafficking, repairing the BBB, protecting neurons, and restricting nerve fiber growth after injury in the adult central nervous system. 0896-6273 Journal Article},
	Author = {Bush, T. G. and Puvanachandra, N. and Horner, C. H. and Polito, A. and Ostenfeld, T. and Svendsen, C. N. and Mucke, L. and Johnson, M. H. and Sofroniew, M. V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neuron},
	Keywords = {G;Nerve Degeneration/*pathology;Ganciclovir/pharmacology;Animals;Leukocytes/metabolism/*pathology;Gene Expression Regulation;Wounds, Stab/*pathology;Brain Injuries/*pathology;Hippocampus/pathology;Female;Cell Count;Mice, Transgenic;Astrocytes/metabolism/*pathology;11 Glia;Simplexvirus/enzymology/genetics;Blood-Brain Barrier;*Cell Movement;Neurons/metabolism/pathology;Support, Non-U.S. Gov't;Histocytochemistry;Thymidine Kinase/biosynthesis/genetics;Mice;Glial Fibrillary Acidic Protein/biosynthesis/genetics;Neurites/metabolism/*pathology},
	Number = {2},
	Organization = {Medical Research Council Cambridge Centre for Brain Repair, and Department of Anatomy, University of Cambridge, United Kingdom.},
	Pages = {297-308},
	Pubmed = {10399936},
	Title = {Leukocyte infiltration, neuronal degeneration, and neurite outgrowth after ablation of scar-forming, reactive astrocytes in adult transgenic mice},
	Uuid = {AB05AF8E-19E9-42A5-A73D-F0845BDBB6FD},
	Volume = {23},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10399936}}

@article{Bushey:2007,
	Abstract = {In mammals, sleep is thought to be important for health, cognition, and memory. Fruit flies share most features of mammalian sleep, and a recent study found that Drosophila lines carrying loss-of-function mutations in Shaker (Sh) are short sleeping, suggesting that the Sh current plays a major role in regulating daily sleep amount. The Sh current is potentiated by a beta modulatory subunit coded by Hyperkinetic (Hk). Here, we demonstrate that severe loss-of-function mutations of Hk reduce sleep and do so primarily by affecting the Sh current. Moreover, we prove, using a transgenic approach, that a wild-type copy of Hk is sufficient to restore normal sleep. Furthermore, we show that short-sleeping Hk mutant lines have a memory deficit, whereas flies carrying a weaker hypomorphic Hk allele have normal sleep and normal memory. By comparing six short-sleeping Sh lines with two normal sleeping ones, we also found that only alleles that reduce sleep also impair memory. These data identify a gene, Hk, which is necessary to maintain normal sleep, and provide genetic evidence that short sleep and poor memory are linked.},
	Author = {Bushey, Daniel and Huber, Reto and Tononi, Giulio and Cirelli, Chiara},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008;Mutation;research support, non-u.s. gov't;21 Neurophysiology;Animals, Genetically Modified;Drosophila Proteins;Shaker Superfamily of Potassium Channels;research support, u.s. gov't, non-p.h.s.;Drosophila;research support, n.i.h., extramural;Animals;Memory Disorders;Potassium Channels;Sleep;Hyperkinesis},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {20},
	Organization = {Department of Psychiatry, University of Wisconsin-Madison, Madison, Wisconsin 53719, USA.},
	Pages = {5384-93},
	Pii = {27/20/5384},
	Pubmed = {17507560},
	Title = {Drosophila Hyperkinetic mutants have reduced sleep and impaired memory},
	Uuid = {959C6B25-B7D8-4899-B222-4314087047EB},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0108-07.2007}}

@article{Bushong:2002,
	Abstract = {Protoplasmic astrocytes are increasingly thought to interact extensively with neuronal elements in the brain and to influence their activity. Recent reports have also begun to suggest that physiologically, and perhaps functionally, diverse forms of these cells may be present in the CNS. Our current understanding of astrocyte form and distribution is based predominantly on studies that used the astrocytic marker glial fibrillary acidic protein (GFAP) and on studies using metal-impregnation techniques. The prevalent opinion, based on studies using these methods, is that astrocytic processes overlap extensively and primarily share the underlying neuropil. However, both of these techniques have serious shortcomings for visualizing the interactions among these structurally complex cells. In the present study, intracellular injection combined with immunohistochemistry for GFAP show that GFAP delineates only approximately 15\%of the total volume of the astrocyte. As a result, GFAP-based images have led to incorrect conclusions regarding the interaction of processes of neighboring astrocytes. To investigate these interactions in detail, groups of adjacent protoplasmic astrocytes in the CA1 stratum radiatum were injected with fluorescent intracellular tracers of distinctive emissive wavelengths and analyzed using three-dimensional (3D) confocal analysis and electron microscopy. Our findings show that protoplasmic astrocytes establish primarily exclusive territories. The knowledge of how the complex morphology of protoplasmic astrocytes affects their 3D relationships with other astrocytes, oligodendroglia, neurons, and vasculature of the brain should have important implications for our understanding of nervous system function.},
	Author = {Bushong, E. A. and Martone, M. E. and Jones, Y. Z. and Ellisman, M. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;Cytoplasm/ultrastructure;G;Rats;Microscopy, Confocal;Iontophoresis;Animal;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein/analysis/metabolism;11 Glia;Male;Oxidation-Reduction;Photochemistry;Cell Size;Isoquinolines;Astrocytes/*cytology/metabolism/ultrastructure;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Microscopy, Electron;Hippocampus/*anatomy &histology/metabolism/ultrastructure},
	Number = {1},
	Organization = {National Center for Microscopy and Imaging Research, University of California, San Diego, La Jolla, California 92093-0608, USA.},
	Pages = {183-92.},
	Title = {Protoplasmic astrocytes in CA1 stratum radiatum occupy separate anatomical domains},
	Uuid = {C7BA755F-4027-437E-B857-9E5A925E61D1},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11756501%20http://www.jneurosci.org/cgi/content/full/22/1/183%20http://www.jneurosci.org/cgi/content/abstract/22/1/183}}

@article{Butovsky:2007,
	Abstract = {Microglia are resident cells in the central nervous system (CNS), of hematopoietic origin with a high plasticity. In this study, we examined whether adaptive immune system, involving in CNS maintenance and repair, can induce microglia to express markers of neural cells. We show that long exposure (above 10 days) of microglia to low doses (10 ng/ml) of the 'proinflammatory' T-cell derived cytokine, IFN-gamma, induced them to express neuronal markers including gamma-aminobutyric acid (GABA) and glutamic acid decarboxylase (GAD-67). In contrast, exposure of microglia to low doses (10 ng/ml) of the 'anti-inflammatory' T-cell derived cytokine, IL-4, induced the expression of oligodendrocyte markers and dendritic cell (DC) marker, CD11c. The microglial origin of the neural-like cells was confirmed using microglia from transgenic mice expressing GFP under promoter of the chemokine fractalkine receptor CX(3)CR1, and diphtheria toxin receptor, under CD11c promoter. This study emphasizes that microglial plasticity includes their ability to give rise to neural-like cells and shows that cytokines produced by the adaptive immune system are involved in these processes.},
	Author = {Butovsky, Oleg and Bukshpan, Shay and Kunis, Gilad and Jung, Steffen and Schwartz, Michal},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {gamma-Aminobutyric Acid;Animals;Interleukin-4;Brain;Interferon Type II;Microglia;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;research support, non-u.s. gov't;08 Aberrant cell cycle;Time Factors;14 Immune;Green Fluorescent Proteins;Animals, Newborn;Glutamate Decarboxylase;Receptors, Chemokine;Mice;24 Pubmed search results 2008;Isoenzymes;Nerve Tissue Proteins;Antigens, CD11c},
	Month = {7},
	Nlm_Id = {9100095},
	Number = {3},
	Organization = {Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel.},
	Pages = {490-500},
	Pii = {S1044-7431(07)00105-4},
	Pubmed = {17560122},
	Title = {Microglia can be induced by IFN-gamma or IL-4 to express neural or dendritic-like markers},
	Uuid = {5CD8DEDC-DE31-4955-83F6-2BFA5BA36E85},
	Volume = {35},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2007.04.009}}

@article{Butt:1996,
	Abstract = {The glia response to Wallerian degeneration was studied in optic nerves 21 days after unilateral enucleation (PED21) of immature rats, 21 days old (P21), using immunohistochemical labelling. Nerves from normal P21 and P42 nerves were also studied for comparison. At PED21, there was a virtual loss of axons apart from a few solitary fibres of unknown origin. The nerve comprised a homogeneous glial scar tissue formed by dense astrocyte processes, oriented parallel to the long axis of the nerve along the tracks of degenerated axons. Astrocytes were almost perfectly co-labelled by antibodies to glial fibrillary acid protein and vimentin in both normal and transected nerves. However, there was a small population of VIM+GFAP- cells in normal P21 and P42 nerves, and we discuss the possibility that they correspond to O-2A progenitor cells described in vitro. Significantly, double immunofluorescence labelling in transected nerves revealed a distinct population of hypertrophic astrocytes which were GFAP+VIM-. These cells represented a novel morphological and antigenic subtype of reactive astrocyte. It was also noted that the number of oligodendrocytes in transected nerves did not appear to be less than in normal nerves, on the basis of double immunofluorescence staining for carbonic anhydrase II, myelin oligodendrocyte glycoprotein, myelin basic protein, glial fibrillary acid protein and ED-1 (for macrophages), although it was not excluded that a small proportion may have been microglia. A further prominent feature of transected nerves was that they contained a substantial amount of myelin debris, notwithstanding that OX-42 and ED1 immunostaining showed that there were abundant microglia and macrophages, sufficient for the rapid and almost complete removal of axonal debris. In conclusion, glial cells in the immature P21 rat optic nerve reacted to Wallerian degeneration in a way equivalent to the adult CNS, i.e. astrocytes underwent pronounced reactive changes and formed a dense glial scar, oligodendrocytes persisted and were not dependent on axons for their continued survival, and there was ineffective phagocytosis of myelin possibly due to incomplete activation of microglia/macrophages.},
	Author = {Butt, A. M. and Kirvell, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Fluorescent Dyes;Animals;Astrocytes;In Vitro;Rats;Myelin Basic Proteins;Myelin-Associated Glycoprotein;Microglia;Oligodendroglia;Optic Nerve;Vimentin;Axons;Rats, Wistar;Not relevant;11 Glia;Animals, Newborn;Eye Enucleation;Support, Non-U.S. Gov't;Wallerian Degeneration;Neuroglia;Age Factors;Immunohistochemistry;Glial Fibrillary Acidic Protein},
	Medline = {96432734},
	Month = {6},
	Nlm_Id = {0364620},
	Number = {6},
	Organization = {Division of Physiology, UMDS, St. Thomas' Hospital, London, UK.},
	Pages = {381-92},
	Pubmed = {8835786},
	Title = {Glial cells in transected optic nerves of immature rats. II. An immunohistochemical study},
	Uuid = {682A5121-D491-42E1-A5D5-623F1EA087AC},
	Volume = {25},
	Year = {1996}}

@article{Butt:2002,
	Abstract = {In the adult CNS, antibodies to the NG2 chondroitin sulphate proteoglycan (CSPG) label a large population of glia that have the antigenic phenotype of oligodendrocyte progenitor cells (OPC). However, NG2 expressing glia have the morphological phenotype of astrocytes, not OPC. We propose adult NG2 expressing glia are a distinct mature glial type, which we have called syantocytes or synantoglia after the Greek 'to contact', because they specifically contact neurons and axons at synapses and nodes of Ranvier, respectively. Synantocytes are highly complex cells that elaborate multiple branching processes and are an equally significant population in both white and grey matter. We provide evidence that phenotypically distinct synantocytes develop postnatally and that neither postnatal nor adult synantocytes depend on axons for their survival, indicating they respond with markedly different behaviours to the environmental cues and axonal signals that control the differentiation of OPC into oligodendrocytes. The primary response of synantocytes to changes in the CNS environment is a rapid and localised reactive gliosis. Reactive synantocytes interact intimately with astrocytes and macrophages at lesion sites, consistent with them playing a key role in the orchestration of scar formation that protects the underlying neural tissue. It is our hypothesis that synantocytes are specialised to monitor and respond to changes in the integrity of the CNS, by way of their cellular contacts, repertoire of plasmalemmal receptors and the NG2 molecule itself. To paraphrase Del Rio Hortega, we propose that synantocytes are the fifth element in the CNS, in addition to neurons, astrocytes, oligodendrocytes and microglia. 0300-4864 Journal Article},
	Author = {Butt, A. M. and Kiff, J. and Hubbard, P. and Berry, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurocytol},
	Keywords = {11 Glia;G pdf},
	Number = {6-7},
	Organization = {Centre for Neuroscience Research, GKT School of Biomedical Sciences, King's College, London SE1 1UL, United Kingdom. arthur.butt\@kcl.ac.uk},
	Pages = {551-65},
	Pubmed = {14501223},
	Title = {Synantocytes: new functions for novel NG2 expressing glia},
	Uuid = {C7E35671-6B78-44CF-A13F-205760E9C08B},
	Volume = {31},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14501223}}

@article{Buttery:2006,
	Abstract = {The morphological and functional differentiation of neuronal dendrites is controlled through transcriptional programs and cell-cell signaling. Synaptic activity is thought to play an important role in the maturation of dendritic arbors, but the signaling pathways that couple neuronal activity and morphological changes in dendrites are not well understood. We explored the function of alpha1-chimaerin, a neuronal diacylglycerol-binding protein with a Rho GTPase-activating protein domain that inactivates Rac1. We find that stimulation of phospholipase Cbeta-coupled cell surface receptors recruits alpha1-chimaerin to the plasma membrane of cultured hippocampal neurons. We further show that alpha1-chimaerin protein levels are controlled by synaptic activity and that increased alpha1-chimaerin expression results in the pruning of dendritic spines and branches. This pruning activity requires both the diacylglycerol-binding and Rac GTPase-activating protein activity of alpha1-chimaerin. Suppression of alpha1-chimaerin expression resulted in increased process growth from the dendritic shaft and from spine heads. Our data suggest that alpha1-chimaerin is an activity-regulated Rho GTPase regulator that is activated by phospholipase Cbeta-coupled cell surface receptors and contributes to pruning of dendritic arbors.},
	Author = {Buttery, Philip and Beg, Asim A. and Chih, Ben and Broder, Arkady and Mason, Carol A. and Scheiffele, Peter},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {10 Development;research support, n.i.h., extramural ;Signal Transduction;Animals;Gene Expression Regulation;Humans;Tissue Culture Techniques;10 Structural plasticity;Diglycerides;Protein Transport;Cell Membrane;Hippocampus;Phospholipase C;Dendrites;research support, non-u.s. gov't ;Cell Line;Cell Shape;Mice;24 Pubmed search results 2008;Isoenzymes;Chimerin 1},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {6},
	Organization = {Department of Pathology and Cell Biology, Center for Neurobiology and Behavior, Columbia University, College of Physicians and Surgeons, P&S 14-509, 630 West 168th Street, New York, NY 10032, USA.},
	Pages = {1924-9},
	Pii = {0510655103},
	Pubmed = {16446429},
	Title = {The diacylglycerol-binding protein alpha1-chimaerin regulates dendritic morphology},
	Uuid = {AB641F84-3317-45C5-A46E-8364491CC8C8},
	Volume = {103},
	Year = {2006},
	url = {papers/Buttery_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0510655103}}

@article{Buttner:2002,
	Abstract = {Sialylation is essential for development and regeneration in mammals. Using N-propanoylmannosamine, a novel precursor of sialic acid, we were able to incorporate unnatural sialic acids with a prolonged N-acyl side chain (e.g., N-propanoylneuraminic acid) into cell surface glycoconjugates. Here we report that this biochemical engineering of sialic acid leads to a stimulation of neuronal cells. Both PC12 cells and cerebellar neurons showed a significant increase in neurite outgrowth after treatment with this novel sialic acid precursor. Furthermore, also the reestablishment of the perforant pathway was stimulated in brain slices. In addition, we surprisingly identified several cytosolic proteins with regulatory functions, which are differentially expressed after treatment with N-propanoylmannosamine. Because sialic acid is the only monosaccharide that is activated in the nucleus, we hypothesize that transcription could be modulated by the unnatural CMP-N-propanoylneuraminic acid and that sialic acid activation might be a general tool to regulate cellular functions, such as neurite outgrowth. 1529-2401 Journal Article},
	Author = {Buttner, B. and Kannicht, C. and Schmidt, C. and Loster, K. and Reutter, W. and Lee, H. Y. and Nohring, S. and Horstkorte, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:43 -0400},
	Journal = {J Neurosci},
	Keywords = {Axons/drug effects/*physiology;Mice, Inbred BALB C;Cell Differentiation/drug effects;Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization;Neuraminic Acids/metabolism/pharmacology;Animals;Cells, Cultured;Rats;T pdf;Cerebellum/cytology;Female;23 Technique;Sialic Acids/*chemistry/*metabolism;Hexosamines/metabolism/pharmacology;PC12 Cells;Male;Perforant Pathway/cytology/drug effects;Support, Non-U.S. Gov't;Electrophoresis, Gel, Two-Dimensional;Neurons/cytology/drug effects/*metabolism;Membrane Glycoproteins/metabolism;Mice;Neurites/drug effects/physiology;Cell Membrane/chemistry/*metabolism;Nerve Regeneration/drug effects/physiology;Proteome/analysis},
	Number = {20},
	Organization = {Institut fur Molekularbiologie und Biochemie, Fachbereich Humanmedizin, Freie Universitat Berlin, D-14195 Berlin-Dahlem, Germany.},
	Pages = {8869-75},
	Title = {Biochemical engineering of cell surface sialic acids stimulates axonal growth},
	Uuid = {DD96ACA2-2490-4576-AD4E-0467ADCCDFFC},
	Volume = {22},
	Year = {2002},
	url = {papers/Buttner_JNeurosci2002.pdf}}

@article{Butz:2006,
	Abstract = {We describe a strongly biologically motivated artificial neural network approach to model neurogenesis and synaptic turnover as it naturally occurs for example in the hippocampal dentate gyrus (DG) of the developing and adult mammalian and human brain. The results suggest that cell proliferation (CP) has not only a functional meaning for computational tasks and learning but is also relevant for maintaining homeostatic stability of the neural activity. Moderate rates of CP buffer disturbances in input activity more effectively than networks without or very high CP. Up to a critical mark an increase of CP enhances synaptogenesis which might be beneficial for learning. However, higher rates of CP are rather ineffective as they destabilize the network: high CP rates and a disturbing input activity effect a reduced cell survival. By these results the simulation model sheds light on the recurrent interdependence of structure and function in biological neural networks especially in hippocampal circuits and the interacting morphogenetic effects of neurogenesis and synaptogenesis.},
	Author = {Butz, Markus and Lehmann, Konrad and Dammasch, Ingolf E. and Teuchert-Noodt, Gertraud},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:18 -0400},
	Issn = {0893-6080},
	Journal = {Neural Netw},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {8805018},
	Number = {10},
	Organization = {Department for Neuroanatomy, University of Bielefeld, Germany.},
	Pages = {1490-505},
	Pii = {S0893-6080(06)00186-9},
	Pubmed = {17014989},
	Title = {A theoretical network model to analyse neurogenesis and synaptogenesis in the dentate gyrus},
	Uuid = {82370F89-32EE-43B6-94E5-487492C72B04},
	Volume = {19},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neunet.2006.07.007}}

@article{Cabantous:2005,
	Abstract = {Existing protein tagging and detection methods are powerful but have drawbacks. Split protein tags can perturb protein solubility or may not work in living cells. Green fluorescent protein (GFP) fusions can misfold or exhibit altered processing. Fluorogenic biarsenical FLaSH or ReASH substrates overcome many of these limitations but require a polycysteine tag motif, a reducing environment and cell transfection or permeabilization. An ideal protein tag would be genetically encoded, would work both in vivo and in vitro, would provide a sensitive analytical signal and would not require external chemical reagents or substrates. One way to accomplish this might be with a split GFP, but the GFP fragments reported thus far are large and fold poorly, require chemical ligation or fused interacting partners to force their association, or require coexpression or co-refolding to produce detectable folded and fluorescent GFP. We have engineered soluble, self-associating fragments of GFP that can be used to tag and detect either soluble or insoluble proteins in living cells or cell lysates. The split GFP system is simple and does not change fusion protein solubility.},
	Author = {Cabantous, St{\'e}phanie and Terwilliger, Thomas C. and Waldo, Geoffrey S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {23 Technique},
	Month = {1},
	Nlm_Id = {9604648},
	Number = {1},
	Organization = {Bioscience Division, MS-M888, Los Alamos National Laboratory, PO Box 1663, Los Alamos, New Mexico 87545, USA.},
	Pages = {102-7},
	Pii = {nbt1044},
	Pubmed = {15580262},
	Title = {Protein tagging and detection with engineered self-assembling fragments of green fluorescent protein},
	Uuid = {7FCDFD7D-101A-4310-B293-05E0F72C7158},
	Volume = {23},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt1044}}

@article{Calaora:2001,
	Abstract = {Neuregulin 1 (Nrg-1) isoforms have been shown to influence the emergence and growth of oligodendrocytes, the CNS myelin-forming cells. We have investigated how Nrg-1 signaling of ErbB receptors specifically controls the early stages of oligodendrocyte generation from multipotential neural precursors (NPs). We show here that embryonic striatal NPs express multiple Nrg-1 transcripts and proteins as well as their specific receptors, ErbB2 and ErbB4, but not ErbB3. The major isoform synthesized by striatal NPs is a transmembrane type III isoform called cysteine-rich domain Nrg-1. To examine the biological effect of Nrg-1, we added soluble ErbB3 (sErbB3) to growing neurospheres. This inhibitor of Nrg-1 bioactivity decreased mitosis of NPs and increased their apoptosis, resulting in a significant reduction in neurosphere size and number. When NPs were induced to migrate and differentiate by adhesion of neurospheres to the substratum, the level of type III isoforms detected by RT-PCR and Western blot decreased in parallel with a reduction in Nrg-1 fluorescence intensity in differentiating astrocytes, neurons, and oligodendrocytes. Pretreatment of growing neurospheres with sErbB3 induced a threefold increase in the proportion of oligodendrocytes generated from NPs migrating out of the neurosphere. This effect was not observed with an unrelated soluble receptor. Addition of sErbB3 during NP growth and differentiation enhanced oligodendrocyte maturation as shown by expression of galactocerebroside and myelin basic protein. We propose that both type III Nrg-1 signaling and soluble ErbB receptors modulate oligodendrocyte development from NPs.},
	Author = {Calaora, V. and Rogister, B. and Bismuth, K. and Murray, K. and Brandt, H. and Leprince, P. and Marchionni, M. and Dubois-Dalcq, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Protein Isoforms/antagonists &inhibitors/metabolism/pharmacology;Cell Survival/drug effects;Cells, Cultured;Neurons/cytology/*metabolism;Rats;Signal Transduction/*physiology;Apoptosis;Receptor, erbB-3/metabolism;Chromones;Animal;Cell Division/drug effects/physiology;Mice, Inbred C57BL;Neuregulin-1/antagonists &inhibitors/*metabolism/pharmacology;Receptor, Epidermal Growth Factor/metabolism;Spinal Cord/cytology/embryology/metabolism;Support, Non-U.S. Gov't;Oligodendroglia/cytology/*metabolism;Astrocytes/cytology/metabolism;Glycosides;C;04 Adult neurogenesis factors;Stem Cells/cytology/drug effects/*metabolism;Cell Differentiation/drug effects/physiology;Mice;Cell Adhesion/physiology;Receptor, erbB-2/metabolism;Corpus Striatum/cytology/embryology/metabolism;Cell Movement/physiology;Mitosis/drug effects},
	Number = {13},
	Organization = {Neurovirologie et Regeneration du Systeme Nerveux, Institut Pasteur, 75724 Paris, France.},
	Pages = {4740-51.},
	Title = {Neuregulin signaling regulates neural precursor growth and the generation of oligodendrocytes in vitro},
	Uuid = {E93154B8-830A-4369-A314-2820FBBB3370},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11425901%20http://www.jneurosci.org/cgi/content/full/21/13/4740%20http://www.jneurosci.org/cgi/content/abstract/21/13/4740}}

@article{Calegari:2005,
	Abstract = {During embryonic development of the mammalian brain, the average cell-cycle length of progenitor cells in the ventricular zone is known to increase. However, for any given region of the developing cortex and stage of neurogenesis, the length of the cell cycle is thought to be similar in the two coexisting subpopulations of progenitors [i.e., those undergoing (symmetric) proliferative divisions and those undergoing (either asymmetric or symmetric) neuron-generating divisions]. Using cumulative bromodeoxyuridine labeling of Tis21-green fluorescent protein knock-in mouse embryos, in which these two subpopulations of progenitors can be distinguished in vivo, we now show that at the onset as well as advanced stages of telencephalic neurogenesis, progenitors undergoing neuron-generating divisions are characterized by a significantly longer cell cycle than progenitors undergoing proliferative divisions. In addition, we find that the recently characterized neuronal progenitors dividing at the basal side of the ventricular zone and in the subventricular zone have a longer G(2) phase than those dividing at the ventricular surface. These findings are consistent with the hypothesis (Calegari and Huttner, 2003) that cell-cycle lengthening can causally contribute to neural progenitors switching from proliferative to neuron-generating divisions and may have important implications for the expansion of somatic stem cells in general.},
	Author = {Calegari, Federico and Haubensak, Wulf and Haffner, Christiane and Huttner, Wieland B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {28},
	Organization = {Max Planck Institute of Molecular Cell Biology and Genetics, D-01307 Dresden, Germany.},
	Pages = {6533-8},
	Pii = {25/28/6533},
	Pubmed = {16014714},
	Title = {Selective lengthening of the cell cycle in the neurogenic subpopulation of neural progenitor cells during mouse brain development},
	Uuid = {129C72CB-6B43-45CB-86BC-137755F1CD36},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0778-05.2005}}

@article{Calmels:2005,
	Abstract = {Recent reports linking insertional activation of LMO2 following gene therapy for X-linked severe combined immunodeficiency (X-SCID) have led to a re-evaluation of risks following gene therapy with retroviral vectors. In our analysis of 702 integration sites in rhesus macaques that underwent transplantation up to 7 years earlier with autologous CD34+ cells transduced with amphotropic murine leukemia virus (MLV)-derived retroviral vectors containing marker genes, we detected insertion into one locus, the Mds1/Evi1 region, a total of 14 times in 9 animals. Mds1/Evi1 integrations were observed stably long term, primarily in myeloid cells. We hypothesize that this over-representation likely results from an impact on the self-renewal and engraftment potential of CD34+ progenitor cells via insertional mutagenesis at this specific locus. There is no evidence of ongoing in vivo clonal expansion of the Mds1/Evi1 populations, and all animals are hematologically normal without evidence for leukemia. Characterization of integration sites in this relevant preclinical model provides critical information for gene therapy risk assessment as well as identification of genes controlling hematopoiesis.},
	Author = {Calmels, Boris and Ferguson, Cole and Laukkanen, Mikko O. and Adler, Rima and Faulhaber, Marion and Kim, Hyeoung-Joon J. and Sellers, Stephanie and Hematti, Peiman and Schmidt, Manfred and von Kalle, Christof and Akagi, Keiko and Donahue, Robert E. and Dunbar, Cynthia E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Transcription Factors;Disease Progression;Animals;DNA-Binding Proteins;Humans;Granulocytes;Leukemia;15 Retrovirus mechanism;Antigens, CD34;Retroviridae;Time Factors;Genetic Vectors;Leukocytes, Mononuclear;Leukemia Virus, Murine;Macaca mulatta;Hematopoiesis;Gene Therapy;Risk;Proto-Oncogenes;Hematopoietic Stem Cells;22 Stem cells;24 Pubmed search results 2008;Stem Cells;Primates;Mutagenesis, Insertional},
	Month = {10},
	Nlm_Id = {7603509},
	Number = {7},
	Organization = {Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD, USA.},
	Pages = {2530-3},
	Pii = {2005-03-1115},
	Pubmed = {15933056},
	Title = {Recurrent retroviral vector integration at the Mds1/Evi1 locus in nonhuman primate hematopoietic cells},
	Uuid = {FCBDF24F-9ED2-4AC9-85ED-ACDF048F06FF},
	Volume = {106},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2005-03-1115}}

@article{Calof:1998,
	Abstract = {The vertebrate olfactory epithelium (OE) is a system in which behavior of neuronal progenitor cells can be observed and manipulated easily. It is morphologically and functionally similar to embryonic germinal neuroepithelia, but is simpler in that it produces large numbers of a single type of neuron, the olfactory receptor neuron (ORN). The OE is amenable to tissue culture, gene transfer, and in vivo surgical approaches, and these have been exploited in experiments aimed at understanding the characteristics of OE neuronal progenitor cells. This has led to the realization that the ORN lineage contains at least three distinct stages of proliferating neuronal progenitor cells (including a stem cell), each of which represents a point at which growth control can be exerted. Neurogenesis proceeds continually in the OE, and studies in vivo have shown that this is a regulated process that serves to maintain the number of ORNs at a particular level. These studies suggest that OE neuronal progenitors-which are in close physical proximity to ORNs-can "read"the number of differentiated neurons in their environment and regulate production of new neurons accordingly. Putative neuronal stem cells of the OE have been identified in vitro, and studies of these cells indicate that ORNs produce a signal that feeds back to inhibit neurogenesis. This inhibitory signal may be exerted at the level of the stem cell itself. Recent studies to identify this signal, as well as endogenous stimulatory signals that may be important in regulating OE neurogenesis, are also discussed.},
	Author = {Calof, A. L. and Mumm, J. S. and Rim, P. C. and Shou, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurobiol},
	Keywords = {Neurons/*physiology;I;Cell Division/physiology;Cell Line/physiology;Animal;Cell Communication/physiology;Support, U.S. Gov't, P.H.S.;Olfactory Mucosa/*cytology;Support, Non-U.S. Gov't;13 Olfactory bulb anatomy;Stem Cells/*physiology},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology and the Developmental Biology Center, University of California, Irvine, College of Medicine, 92697- 1275, USA.},
	Pages = {190-205.},
	Title = {The neuronal stem cell of the olfactory epithelium},
	Uuid = {7E0CB235-A148-44E4-9157-E74A14050C75},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9712304}}

@article{Calvo:2000,
	Abstract = {The immunohistochemical detection of bromodeoxyuridine (BrdU) was used to study the cell proliferation in the developing rat pineal gland, from the appearance of pineal primordium in the embryonic day 15 (E15) until 30 days after birth. The results showed three different proliferative phases. From E15 to E21, the pineal gland shows a phase of rapid proliferation. The second phase corresponds to the first postnatal week, in which the number of labeled cells per surface unit decreases suddenly to values between 20\%to 10\%of those of embryonic period. From the second postnatal week onwards, the number of BrdU-positive cells progressively decreases.},
	Author = {Calvo, J. L. and Boya, J. and Carbonell, A. L. and Garc{\'\i}a-Mauri\~{n}o, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0213-3911},
	Journal = {Histol Histopathol},
	Keywords = {Thymidine;Research Support, Non-U.S. Gov't;Pineal Gland;Rats;Immunohistochemistry;DNA;Female;Rats, Wistar;Cell Division;Antimetabolites;Animals;24 Pubmed search results 2008;Bromodeoxyuridine},
	Medline = {20458233},
	Month = {10},
	Nlm_Id = {8609357},
	Number = {4},
	Organization = {Department of Histology, Faculty of Medicine, Complutense University, Madrid, Spain.},
	Pages = {1005-10},
	Pubmed = {11005223},
	Title = {Cell proliferation in the developing rat pineal gland. A bromodeoxyuridine immunohistochemical study},
	Uuid = {A5D89977-6DBD-4E18-901F-AD1BC3B6740D},
	Volume = {15},
	Year = {2000}}

@article{Cam:2008,
	Abstract = {Transposable elements and their remnants constitute a substantial fraction of eukaryotic genomes. Host genomes have evolved defence mechanisms, including chromatin modifications and RNA interference, to regulate transposable elements. Here we describe a genome surveillance mechanism for retrotransposons by transposase-derived centromeric protein CENP-B homologues of the fission yeast Schizosaccharomyces pombe. CENP-B homologues of S. pombe localize at and recruit histone deacetylases to silence Tf2 retrotransposons. CENP-Bs also repress solo long terminal repeats (LTRs) and LTR-associated genes. Tf2 elements are clustered into 'Tf' bodies, the organization of which depends on CENP-Bs that display discrete nuclear structures. Furthermore, CENP-Bs prevent an 'extinct' Tf1 retrotransposon from re-entering the host genome by blocking its recombination with extant Tf2, and silence and immobilize a Tf1 integrant that becomes sequestered into Tf bodies. Our results reveal a probable ancient retrotransposon surveillance pathway important for host genome integrity, and highlight potential conflicts between DNA transposons and retrotransposons, major transposable elements believed to have greatly moulded the evolution of genomes.},
	Author = {Cam, Hugh P. and Noma, Ken-ichi and Ebina, Hirotaka and Levin, Henry L. and Grewal, Shiv I. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Cell Cycle Proteins;Centromere Protein B;DNA-Binding Proteins;Schizosaccharomyces pombe Proteins;Genomic Instability;Genes, Mating Type, Fungal;Protein Transport;Evolution, Molecular;Histone Deacetylases;research support, n.i.h., intramural;15 Retrovirus mechanism;Heterochromatin;Gene Expression Regulation, Fungal;Oxidative Stress;DNA Transposable Elements;Genome, Fungal;21 Neurophysiology;Gene Silencing;21 Activity-development;Retroelements;24 Pubmed search results 2008;Genes, Fungal;Terminal Repeat Sequences;15 ERVs retroelements;Schizosaccharomyces},
	Month = {1},
	Nlm_Id = {0410462},
	Number = {7177},
	Organization = {Laboratory of Biochemistry and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892, USA.},
	Pages = {431-6},
	Pii = {nature06499},
	Pubmed = {18094683},
	Title = {Host genome surveillance for retrotransposons by transposon-derived proteins},
	Uuid = {D7343506-EFD6-4B88-AEEB-C552C324D4DD},
	Volume = {451},
	Year = {2008},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06499}}

@article{Cameron:1998,
	Abstract = {The generation of neurons and glia in the developing nervous system is likely to be regulated by extrinsic factors, including growth factors and neurotransmitters. Evidence from in vivo and/or in vitro systems indicates that basic fibroblast growth factor, transforming growth factor (TGF)-alpha, insulin-like growth factor-1, and the monoamine neurotransmitters act to increase proliferation of neural precursors. Conversely, glutamate, gamma-aminobutyric acid, and opioid peptides are likely to play a role in down-regulating proliferation in the developing nervous system. Several other factors, including the neuropeptides vasoactive intestinal peptide and pituitary adenylate cyclase-activating peptide, as well as the growth factors platelet- derived growth factor, ciliary neurotrophic factor, and members of the TGF-beta family, have different effects on proliferation and differentiation depending on the system examined. Expression of many of these factors and their receptors in germinal regions of the central nervous system suggests that they can act directly on precursor populations to control their proliferation. Together, the findings discussed here indicate that proliferation and cell fate determination in the developing brain are regulated extrinsically by complex interactions between a relatively large number of growth factors and neurotransmitters.},
	Author = {Cameron, H. A. and Hazel, T. G. and McKay, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurobiol},
	Keywords = {C;Human;Brain/*growth &development;Growth Substances/*physiology;Aging/physiology;Animal;04 Adult neurogenesis factors;Neurotransmitters/*physiology;Animals, Newborn/growth &development},
	Number = {2},
	Organization = {Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892, USA.},
	Pages = {287-306.},
	Title = {Regulation of neurogenesis by growth factors and neurotransmitters},
	Uuid = {D6B56B84-061B-4CD1-82D2-10EB4D0B952E},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9712310}}

@article{Cameron:1995,
	Abstract = {The effects of afferent input and N-methyl-D-aspartate (NMDA) receptor activation on neurogenesis were examined in an intact system, the rat dentate gyrus, where neurons are naturally born in the adult. In the adult dentate gyrus, activation of NMDA receptors rapidly decreased the number of cells synthesizing DNA, whereas blockade of NMDA receptors rapidly increased the number of cells in the S phase identified with 3H- thymidine. Acute treatment with NMDA receptor antagonists increased the birth of neurons and increased the overall density of neurons in the granule cell layer. Lesion of the entorhinal cortex, the main excitatory afferent population to the granule neurons, also increased the birth of cells in the dentate gyrus. These results suggest that adult neurogenesis in the dentate gyrus of the rat is altered by afferent input, via NMDA receptors, and may be regulated naturally by endogenous excitatory amino acids.},
	Author = {Cameron, H. A. and McEwen, B. S. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {J Neurosci},
	Keywords = {Hippocampus/cytology/drug effects/*physiology;Dizocilpine Maleate/pharmacology;Cell Survival/drug effects;Neurons/cytology/drug effects/*physiology;Rats;Thymidine/metabolism;2-Amino-5-phosphonovalerate/analogs &derivatives/pharmacology;Receptors, N-Methyl-D-Aspartate/antagonists &inhibitors/*physiology;Homeostasis;Rats, Sprague-Dawley;Animal;Male;Time Factors;D-3;DNA/biosynthesis;Support, Non-U.S. Gov't;Afferent Pathways/*physiology;06 Adult neurogenesis injury induced;*Cell Division/drug effects;Support, U.S. Gov't, P.H.S.;S Phase;N-Methylaspartate/*pharmacology},
	Number = {6},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021, USA.},
	Pages = {4687-92.},
	Title = {Regulation of adult neurogenesis by excitatory input and NMDA receptor activation in the dentate gyrus},
	Uuid = {B2B080AD-6774-44C6-9A10-29B531BCEE8D},
	Volume = {15},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7790933}}

@article{Cameron:1999,
	Abstract = {The production of hippocampal granule neurons continues throughout adulthood but dramatically decreases in old age. Here we show that reducing corticosteroid levels in aged rats restored the rate of cell proliferation, resulting in increased numbers of new granule neurons. This result indicates that the neuronal precursor population in the dentate gyrus remains stable into old age, but that neurogenesis is normally slowed by high levels of corticosteroids. The findings further suggest that decreased neurogenesis may contribute to age-related memory deficits associated with high corticosteroids, and that these deficits may be reversible.},
	Author = {Cameron, H. A. and McKay, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Neurons/*physiology;DNA/biosynthesis;Rats, Sprague-Dawley;Hippocampus/cytology/*physiology;Cell Division/physiology;Cell Survival/physiology;Rats;Adrenal Glands/physiology;Adrenal Cortex Hormones/physiology;Biological Markers;Animal;Aging/*physiology;04 Adult neurogenesis factors;Bromodeoxyuridine;Adrenalectomy;C abstr},
	Number = {10},
	Organization = {Laboratory of Molecular Biology, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA. cameron\@codon.nih.gov},
	Pages = {894-7.},
	Title = {Restoring production of hippocampal neurons in old age},
	Uuid = {7DC9E7B6-4ED4-46F0-A2A5-8B59E943237F},
	Volume = {2},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10491610%20http://library.neurosci.nature.com/server-java/Propub/neuro/nn1099_894.fulltext%20http://library.neurosci.nature.com/server-java/Propub/neuro/nn1099_894.abstract}}

@article{Cameron:1993,
	Abstract = {In order to determine whether newly born cells in the dentate gyrus of the adult rat express the neuronal marker, neuron-specific enolase, or the glial marker, glial fibrillary acidic protein, we performed combined immunohistochemistry and autoradiography on brains from adult rats perfused at various times ranging from 1 h to four weeks following [3H]thymidine administration. Light-microscopic examination revealed a negligible number of [3H]thymidine-labeled cells showing neuron- specific enolase immunoreactivity during mitosis. However, by two weeks after [3H]thymidine administration, a significant increase in the density of [3H]thymidine-labeled neuron-specific enolase-immunoreactive cells was detected. Three weeks following [3H]thymidine injection the majority of [3H]thymidine-labeled cells (>70\%) were immunoreactive for the neuronal marker. At the four-week time-point, [3H]thymidine-labeled neuron-specific enolase-immunoreactive cells were indistinguishable from neighboring granule cells. In contrast, glial fibrillary acidic protein immunoreactivity was observed in a small but significant number of [3H]thymidine cells at the 1-h time-point and the proportion of labeled cells that were immunoreactive for this cell marker did not increase with time. [3H]Thymidine-labeled cells that were immunoreactive for glial fibrillary acidic protein typically showed morphologic characteristics of radial glia at all time-points. At the 1- h time-point, the majority of [3H]thymidine-labeled cells were observed in the hilus (>60\%) with the remainder being located in the granule cell layer. However, with a four-week survival-time most [3H]thymidine- labeled cells (>85\%) were located in the granule cell layer. The majority of newly born cells in the adult dentate gyrus differentiate into neurons.(ABSTRACT TRUNCATED AT 250 WORDS)},
	Author = {Cameron, H. A. and Woolley, C. S. and McEwen, B. S. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neuroscience},
	Keywords = {Cell Aging;Rats;Comparative Study;A-5;Neuroglia/chemistry/*cytology;Animal;Cell Movement;Rats, Sprague-Dawley;Phosphopyruvate Hydratase/*analysis;Neurons/*cytology/enzymology;Male;Support, Non-U.S. Gov't;Glial Fibrillary Acidic Protein/*analysis;Support, U.S. Gov't, P.H.S.;Cell Division;Biological Markers;Hippocampus/*cytology;Nerve Tissue Proteins/*analysis},
	Number = {2},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.},
	Pages = {337-44.},
	Title = {Differentiation of newly born neurons and glia in the dentate gyrus of the adult rat},
	Uuid = {9FB6E0A6-67A7-11DA-A4B6-000D9346EC2A},
	Volume = {56},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8247264}}

@article{Cameron:1994,
	Abstract = {The dentate gyrus of the rat produces new granule neurons well into adulthood. In the adult, newly born granule neurons migrate from the hilus to the granule cell layer, receive synaptic input, extend axons into the mossy fiber pathway, and express a neuronal marker. No previous studies have identified factors that regulate neuronal birth in the adult dentate gyrus. In order to determine whether glucocorticoids control neurogenesis in the adult dentate gyrus, the effects of adrenal steroid manipulations on neuronal birth were assessed using [3H]thymidine autoradiography and immunohistochemistry for the neuronal marker neuron specific enolase. Acute treatment with corticosterone produced a significant decrease in the density of [3H]thymidine-labeled cells in the hilus of the dentate gyrus. In contrast, removal of endogenous adrenal steroids stimulated increased neuronal birth; adrenalectomy resulted in a significant increase in the number of neuron specific enolase-immunoreactive [3H]thymidine labeled cells in the granule cell layer compared to sham operation. Replacement of corticosterone to adrenalectomized rats after [3H]thymidine injection did not substantially alter the increase in neurogenesis observed following adrenalectomy, even though this replacement protects cells from adrenalectomy-induced cell death. These results indicate that the rate of neurogenesis in the dentate gyrus of the adult rat is dependent upon the levels of circulating adrenal steroids.},
	Author = {Cameron, H. A. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {Neuroscience},
	Keywords = {Hippocampus/cytology/drug effects/*physiology;Cell Differentiation;Corticosterone/pharmacology/*physiology;Rats;Apoptosis/*physiology;Animal;Rats, Sprague-Dawley;Stem Cells/*cytology/drug effects;DNA Replication;C abstr;Male;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Phosphopyruvate Hydratase/analysis;*Adrenalectomy;Biological Markers;Neurons/*cytology/drug effects;Cell Division/drug effects},
	Number = {2},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.},
	Pages = {203-9.},
	Title = {Adult neurogenesis is regulated by adrenal steroids in the dentate gyrus},
	Uuid = {E67201A2-2FA3-4A82-B5D9-F28E4425C54B},
	Volume = {61},
	Year = {1994},
	url = {papers/Cameron_Neuroscience1994}}

@article{Cameron:1998a,
	Abstract = {Adrenal steroids and N-methyl-D-aspartate receptor activation have both been shown to regulate the rate of proliferation of granule neuron progenitor cells in the dentate gyrus of adult rats [Cameron H. A. and Gould E. (1994) Neuroscience 61, 203-209; Cameron H. A. et al. (1995) J. Neurosci. 15, 46874692]. Parallels between the actions of these two factors suggest that they may regulate cell division through a common pathway. This hypothesis was tested by altering both of the factors simultaneously and determining whether the effects were additive. The results of this study demonstrate that alterations in N-methyl-D- aspartate receptor activation block the effects of corticosterone level on cell proliferation; N-methyl-D-aspartate blocks the adrenalectomy- induced increase in [3H]thymidine-labelled cell density in the dentate gyrus, whereas the N-methyl-D-aspartate receptor antagonist dizocilpine maleate (MK-801) prevents the corticosterone-induced decrease in proliferating cells. This finding suggests that adrenal steroids and N- methyl-D-aspartate receptor activation regulate granule cell production in the adult rat dentate gyrus through a common pathway and that N- methyl-D-aspartate receptor activation operates downstream of corticosterone in this pathway.},
	Author = {Cameron, H. A. and Tanapat, P. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neuroscience},
	Keywords = {Dizocilpine Maleate/pharmacology;Rats;Corticosterone/metabolism;Excitatory Amino Acid Antagonists/pharmacology;Animal;Adrenalectomy;Rats, Sprague-Dawley;C abstr;Biotransformation/physiology;Male;Adrenal Cortex Hormones/*physiology;Support, Non-U.S. Gov't;inhibitors/*physiology;Cell Division/physiology;Dentate Gyrus/*cytology/*physiology;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Receptors, N-Methyl-D-Aspartate/agonists/antagonists &;Neurons/physiology},
	Number = {2},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021, USA.},
	Pages = {349-54.},
	Title = {Adrenal steroids and N-methyl-D-aspartate receptor activation regulate neurogenesis in the dentate gyrus of adult rats through a common pathway},
	Uuid = {60B3B25D-3B50-4114-9F6F-6A2F75310409},
	Volume = {82},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9466447}}

@article{Cammer:1996,
	Abstract = {In the brains of adult rodents carbonic anhydrase II (CA) immunoreactivity has been observed in the choroid plexus and in oligodendrocytes, astrocytes, and myelin. Localization and functions of CA in the neonatal brain, however, have been controversial. One issue is whether the CAII-immunopositive round and ameboid cells in the corpus callosum and cingulum in the rat CNS during the first postnatal week are oligodendrocytes or microglia. Colocalization of CAII with the microglial antigen, ED1, and the microglia-specific isolectin, BSI-B4, suggested that most (approx. 60\%) of the CAII-positive round and ameboid cells in rat brain during the first postnatal week were, indeed, macrophages and microglia. During that initial week, some CAII-positive protoplasmic astrocytes (approx. 40\%) were observed as well. At the end of the first postnatal week smooth-surfaced CAII-positive cells began to appear in the corpus callosum. Those cells also bound MAbO4, a marker for the oligodendrocyte cell line. We conclude that during the first postnatal week most of the CAII-positive cells are macrophages and microglia, and that some are protoplasmic astrocytes. During the second postnatal week CAII-positive cells in the oligodendrocyte lineage become apparent, and by the end of that week there are few CAII-positive microglia. Confocal microscopy suggests that in brains of three-day-old rats the ameboid microglia are associated with nerve fibers, where they may perform phagocytosis of axons, directional guidance of axons, or disinhibition of axonal growth.},
	Author = {Cammer, W. and Zhang, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Prosencephalon;Microscopy, Confocal;Rats;Neurofilament Proteins;Not relevant;Rats, Wistar;11 Glia;Antibody Specificity;Animals, Newborn;Support, U.S. Gov't, P.H.S.;Microglia;Animals;Support, Non-U.S. Gov't;Carbonic Anhydrases;Neurons;Axons},
	Medline = {96337181},
	Month = {7},
	Nlm_Id = {8109498},
	Number = {2},
	Organization = {Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.},
	Pages = {131-6},
	Pii = {S0165572896000677},
	Pubmed = {8765336},
	Title = {Carbonic anhydrase II in microglia in forebrains of neonatal rats},
	Uuid = {A1B54073-2C96-4DE7-BA9C-35554083F979},
	Volume = {67},
	Year = {1996}}

@article{Campbell:2005a,
	Abstract = {Cortical neurogenesis is a highly stereotyped process in which progenitor cells generate neurons destined for specific cortical layers depending on the timing of cell cycle exit. Previous work has shown that during corticogenesis, progenitors become progressively restricted in their developmental potential. Recent work has uncovered some of the intrinsic mechanisms that underlie this fate restriction. In addition to timing, new studies suggest that the location of cell cycle exit in the cortical germinal zone may also contribute to cortical neuron specification.},
	Author = {Campbell, Kenneth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development},
	Month = {5},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA. kenneth.campbell\@chmcc.org},
	Pages = {373-6},
	Pii = {S0896-6273(05)00350-8},
	Pubmed = {15882634},
	Title = {Cortical neuron specification: it has its time and place},
	Uuid = {8C13F59D-C13A-42E1-A833-0BD37DC04DB4},
	Volume = {46},
	Year = {2005},
	url = {papers/Campbell_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.04.014}}

@article{Canaple:2003,
	Abstract = {Biological clocks are intrinsic time-keeping systems that regulate behavior and physiological functions in most living organisms. Recent works in this area have addressed possible molecular links between the endogenous circadian clock and cell cycle regulation. In this review, by addressing how circadian clocks can interfere with the cell cycle and how the disruption of the circadian rhythm may cause defects in regulation of cell proliferation, we highlight this potential connection between circadian rhythm and cell cycle. We also discuss how the acquisition of recent data in circadian clock mechanism may help chronotherapy, which takes into account the biological time to improve cancer treatments, and may open new therapeutic avenues for treating circadian-related diseases. 0008-5472 Journal Article Review Review, Tutorial},
	Author = {Canaple, L. and Kakizawa, T. and Laudet, V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Cancer Res},
	Keywords = {Neoplasms/*pathology/therapy;Cell Division/physiology;10 Development;Cell Cycle/physiology;F abstr;Human;Circadian Rhythm/*physiology;Support, Non-U.S. Gov't;Animals},
	Number = {22},
	Organization = {Structure and Evolution of Nuclear Hormone Receptors, UMR 5665 Centre National de la Recherche Scientifique, Ecole Normale Superieure de Lyon, 46 allee d'Italie, 69364 Lyon Cedex 07, France.},
	Pages = {7545-52},
	Pubmed = {14633665},
	Title = {The days and nights of cancer cells},
	Uuid = {D8434813-7B45-4D69-9E37-5B5001DB608B},
	Volume = {63},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14633665}}

@article{Canki:2000,
	Abstract = {Human immunodeficiency virus type 1 (HIV-1) has been found in the vitreous of persons with AIDS. Here we investigated the susceptibility of human retinal pigment epithelial (RPE) cells to HIV-1 infection in culture and the effects of HIV-1 on the phagocytic function of the RPE. We found that 10 of 11 populations of RPE cells isolated from different fetal or adult eyes were susceptible to low-level replication of HIV-1/NL4-3 as determined by the detection of viral DNA and spliced viral RNA encoding envelope. HIV-1 infection was not inhibited by recombinant soluble CD4, suggesting that CD4 is not required for virus entry into RPE cells. RPE cells fused with target cells constitutively expressing HIV-1 envelope glycoproteins, indicating that HIV-1 enters cells by receptor-mediated fusion. Exposure to HIV-1 or recombinant gp120 caused a two- to four-fold increase in the binding and uptake of isolated rod outer segments by RPE cells. These findings introduce a new cell target of HIV-1 replication in the eye and indicate that RPE cells function aberrantly when exposed to HIV-1 or its envelope glycoprotein.},
	Author = {Canki, M. and Sparrow, J. R. and Chao, W. and Potash, M. J. and Volsky, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0889-2229},
	Journal = {AIDS Res Hum Retroviruses},
	Keywords = {Fetus;Human;Phagocytosis;Animals;HIV-1;Cells, Cultured;Hamsters;RNA, Viral;Comparative Study;Epithelial Cells;Recombinant Proteins;CHO Cells;15 Retrovirus mechanism;Cell Fusion;Antigens, CD4;11 Glia;Pigment Epithelium of Eye;Support, Non-U.S. Gov't;Adult;Support, U.S. Gov't, P.H.S.;Polymerase Chain Reaction;DNA, Viral;Virus Replication;Rod Outer Segments;HIV Envelope Protein gp120},
	Medline = {20233485},
	Month = {3},
	Nlm_Id = {8709376},
	Number = {5},
	Organization = {Molecular Virology Laboratory, St. Luke's/Roosevelt Hospital Center, Columbia University, New York, New York 10019, USA.},
	Pages = {453-63},
	Pubmed = {10772531},
	Title = {Human immunodeficiency virus type 1 can infect human retinal pigment epithelial cells in culture and alter the ability of the cells to phagocytose rod outer segment membranes},
	Uuid = {49EDF80E-68CB-4EB5-B2EE-219AF6D10C70},
	Volume = {16},
	Year = {2000},
	url = {papers/Canki_AIDSResHumRetroviruses2000.pdf}}

@article{Capela:2006,
	Abstract = {LeX/SSEA1/CD15 is an extracellular matrix-associated carbohydrate expressed by ES cells and by adult neural and bone marrow stem cells. It is important for cell adhesion, compaction and FGF2 responses of early embryonic stem cells; however, its function at later stages is not clear. We now show that LeX is expressed by primary mouse neural progenitor cells, including neural stem cells, neuroblasts and glioblasts, but not by their more differentiated products. LeX distinguishes highly proliferative cells even in the primitive neuroepithelium, demonstrating heterogeneity in cell potential before radial glia arise. At later stages, LeX expressing progenitors are frequently radial in morphology. Surface LeX expression can be used to enrich neural stem and progenitor cells from different CNS regions throughout development by FACS. We found that LeX expression is particularly strong in neural regions with prolonged neurogenesis, e.g., the olfactory epithelium, hippocampus, basal forebrain and cerebellum. These regions also express high levels of the growth factors FGF8 and/or Wnt-1. We show here that LeX-containing molecules in the developing nervous system bind Wnt-1. Our findings suggest that LeX, which is present on the surface of principle neural progenitors and secreted into their extracellular niche, may bind and present growth factors important for their proliferation and self-renewal.},
	Author = {Capela, and Temple,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {10 Development;03 Adult neurogenesis progenitor source;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0372762},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA.},
	Pii = {S0012-1606(05)00909-7},
	Pubmed = {16458284},
	Title = {LeX is expressed by principle progenitor cells in the embryonic nervous system, is secreted into their environment and binds Wnt-1},
	Uuid = {92AF7DFD-C8DF-4738-9413-31C50398EF83},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2005.12.030}}

@article{Capela:2002,
	Abstract = {Adult neural stem cells are rare, and little is known about their unique characteristics, leaving their in vivo identity enigmatic. We show that Lewis X (LeX), a carbohydrate expressed by embryonic pluripotent stem cells, is made by adult mouse subventricular zone (SVZ) stem cells and shed into their environment. Only 4\%of acutely isolated SVZ cells are LeX(+); this subpopulation, purified by FACS, contains the SVZ stem cells. Ependymal cells are LeX(-), and purified ependymal cells do not make neurospheres, resolving the controversial claim that these are stem cells. Thus, LeX expression by adult CNS stem cells aids their in vivo identification, allows their enrichment, and raises new questions about the role of this unusual carbohydrate in stem cell biology. 22260733 0896-6273 Journal Article},
	Author = {Capela, A. and Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {Neuron},
	Keywords = {02 Adult neurogenesis migration;Antigens, CD15/*biosynthesis;Female;Central Nervous System/cytology/*metabolism;Ependyma/cytology/*metabolism;Animal;B-23;Support, U.S. Gov't, P.H.S.;Stem Cells/cytology/*metabolism;Support, Non-U.S. Gov't;Cells, Cultured;Mice;Brain/cytology/metabolism},
	Number = {5},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA. alexandra.capela\@stemcellsinc.com},
	Pages = {865-75},
	Title = {LeX/ssea-1 is expressed by adult mouse CNS stem cells, identifying them as nonependymal},
	Uuid = {1E680164-BC67-44B2-99B8-49383C94419B},
	Volume = {35},
	Year = {2002},
	url = {papers/Capela_Neuron2002.pdf}}

@article{Cara:1997,
	Abstract = {During infection with different retroviruses, high levels of unintegrated extrachromosomal DNA accumulate in infected cells. While extrachromosomal linear DNA is the immediate precursor of the integrated provirus, the function, if any, of extrachromosomal circular DNA has been unclear. Several groups have attempted to address the possible function, activity, and importance of this unintegrated DNA during the life cycle of retroviruses and the course of retroviral-associated diseases. This review summarizes recent work in this field and tries to analyze some aspects of extrachromosomal forms of retroviral DNA and their possible application as a molecular biological tool.},
	Author = {Cara, A. and Reitz, M. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0887-6924},
	Journal = {Leukemia},
	Keywords = {DNA, Circular;Virus Replication;Retroviridae;Transcription, Genetic;DNA, Viral;review, tutorial;15 Retrovirus mechanism;Extrachromosomal Inheritance;Humans;Animals;Retroviridae Infections;review;24 Pubmed search results 2008},
	Medline = {97449094},
	Month = {9},
	Nlm_Id = {8704895},
	Number = {9},
	Organization = {Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.},
	Pages = {1395-9},
	Pubmed = {9305590},
	Title = {New insight on the role of extrachromosomal retroviral DNA},
	Uuid = {C15AE1AF-DF22-4017-B443-A4EC54C092B8},
	Volume = {11},
	Year = {1997}}

@article{Carbonell:2005,
	Abstract = {Microglia rapidly become reactive in response to diverse stimuli and are thought to be prominent participants in the pathophysiology of both acute injury and chronic neurological diseases. However, mature microglial reactions to a focal lesion have not been characterized dynamically in adult vertebrate tissue. Here, we present a detailed analysis of long-distance perilesional microglial migration using time-lapse confocal microscopy in acutely isolated living slices from adult brain-injured mice. Extensive migration of perilesional microglia was apparent by 24 h after injury and peaked at 3 d. Average instantaneous migration speeds of approximately 5 microm/min and peak speeds >10 microm/min were observed. Collective, directed migration toward the lesion edge was not observed as might be expected in the presence of chemoattractive gradients. Rather, migration was autonomous and could be modeled as a random walk. Pharmacological blockade of the cysteine-cysteine chemokine receptor 5 reduced migration velocity and the number of perilesional migratory microglia without affecting directional persistence, suggesting a novel role for chemokines in modulation of discrete migratory parameters. Finally, activated microglia in the denervated hippocampal stratum oriens did not migrate extensively, whereas human immunodeficiency virus-1 tat-activated microglia migrated nearly twice as fast as those at the stab lesion, indicating a nonuniform microglial response to different stimuli. Understanding the characteristics and specific molecular mechanisms underlying microglial migration after neural injury could reveal novel targets for therapeutic strategies for modulating neuroinflammation in human diseases.},
	Author = {Carbonell, W. Shawn and Murase, Shin-Ichi and Horwitz, Alan F. and Mandell, James W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Alpha;11 Glia},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {30},
	Organization = {Medical Scientist Training Program, Division of Neuropathology, University of Virginia Health System, Charlottesville, Virginia 22908, USA.},
	Pages = {7040-7},
	Pii = {25/30/7040},
	Pubmed = {16049180},
	Title = {Migration of perilesional microglia after focal brain injury and modulation by CC chemokine receptor 5: an in situ time-lapse confocal imaging study},
	Uuid = {66AD9FD0-5414-4591-8028-BD02718578CE},
	Volume = {25},
	Year = {2005},
	url = {papers/Carbonell_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5171-04.2005}}

@article{Cardona:2006,
	Abstract = {Microglia, the resident inflammatory cells of the CNS, are the only CNS cells that express the fractalkine receptor (CX3CR1). Using three different in vivo models, we show that CX3CR1 deficiency dysregulates microglial responses, resulting in neurotoxicity. Following peripheral lipopolysaccharide injections, Cx3cr1-/- mice showed cell-autonomous microglial neurotoxicity. In a toxic model of Parkinson disease and a transgenic model of amyotrophic lateral sclerosis, Cx3cr1-/- mice showed more extensive neuronal cell loss than Cx3cr1+ littermate controls. Augmenting CX3CR1 signaling may protect against microglial neurotoxicity, whereas CNS penetration by pharmaceutical CX3CR1 antagonists could increase neuronal vulnerability.},
	Author = {Cardona, Astrid E. and Pioro, Erik P. and Sasse, Margaret E. and Kostenko, Volodymyr and Cardona, Sandra M. and Dijkstra, Ineke M. and Huang, Deren and Kidd, Grahame and Dombrowski, Stephen and Dutta, RanJan and Lee, Jar-Chi C. and Cook, Donald N. and Jung, Steffen and Lira, Sergio A. and Littman, Dan R. and Ransohoff, Richard M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Neurotoxicity Syndromes;research support, n.i.h., extramural ;Animals;Cells, Cultured;Microglia;Lipopolysaccharides;Mice, Transgenic;Parkinson Disease;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;comparative study ;Disease Models, Animal;research support, non-u.s. gov't ;Analysis of Variance;Receptors, Chemokine;Neurons;Calcium-Binding Proteins;Flow Cytometry;Mice;Motor Neuron Disease;24 Pubmed search results 2008;Central Nervous System;Immunohistochemistry;Cell Death;Nerve Tissue Proteins;Cytokines},
	Month = {7},
	Nlm_Id = {9809671},
	Number = {7},
	Organization = {Neuroinflammation Research Center and Department of Neurosciences, Lerner Research Institute, Cleveland, Ohio 44195, USA.},
	Pages = {917-24},
	Pii = {nn1715},
	Pubmed = {16732273},
	Title = {Control of microglial neurotoxicity by the fractalkine receptor},
	Uuid = {46AFD8D0-8775-4F51-B487-D873A909F8EE},
	Volume = {9},
	Year = {2006},
	url = {papers/Cardona_NatNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1715}}

@article{Caric:2001,
	Abstract = {Epidermal growth factor receptors (EGFRs) have been implicated in the control of migration in the telencephalon, but the mechanism underlying their contribution is unclear. We show that expression of a threshold level of EGFRs confers chemotactic competence in stem cells, neurons and astrocytes in cortical explants. This level of receptor expression is normally achieved by a subpopulation of cells during mid-embryonic development. Cells that express high levels of EGFR are located in migration pathways, including the tangential pathway to the olfactory bulb via the rostral migratory stream (RMS), the lateral cortical stream (LCS) leading to ventrolateral cortex and the radial pathway from proliferative zones to cortical plate. The targets of these pathways express the ligands HB-EGF and/or TGFalpha. To test the idea that EGFRs mediate chemotactic migration these pathways, we increased the size of the population of cells expressing threshold levels of EGFRs in vivo by viral transduction. Our results suggest that EGFRs mediate migration radially to the cortical plate and ventrolaterally in the LCS, but not tangentially in the RMS. Within the bulb, however, EGFRs also mediate radial migration. Our findings suggest that developmental changes in EGFR expression, together with changes in ligand expression regulate the migration of specific populations of cells in the telencephalon by a chemoattractive mechanism.},
	Author = {Caric, D. and Raphael, H. and Viti, J. and Feathers, A. and Wancio, D. and Lillien, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Development},
	Keywords = {Chemotaxis/*physiology;Rats, Sprague-Dawley;Transplants;Female;Epidermal Growth Factor/genetics/immunology/metabolism;Rats;Transforming Growth Factor alpha/metabolism;Embryonic Induction;Animal;Receptor, Epidermal Growth Factor/genetics/*metabolism;Pregnancy;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Telencephalon/*embryology/metabolism/transplantation;C abstr},
	Number = {21},
	Organization = {Department of Neurobiology and Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, W1454 Biomedical Science Tower, Pittsburgh, PA 15261, USA.},
	Pages = {4203-16.},
	Title = {EGFRs mediate chemotactic migration in the developing telencephalon},
	Uuid = {3C24400D-2EF2-4FDB-B5A0-81385F4F4314},
	Volume = {128},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11684657%20http://dev.biologists.org/cgi/content/full/128/21/4203%20http://dev.biologists.org/cgi/content/abstract/128/21/4203}}

@article{Carlen:2002,
	Abstract = {Over the past decade, it has become clear that neural stem cells in the adult mammalian brain continuously generate new neurons, predominantly in the hippocampus and olfactory bulb. However, the central issue of whether these new neurons participate in functional synaptic circuitry has yet to be resolved. Here, we use virus-based transsynaptic neuronal tracing and c-Fos mapping of odor-induced neuronal activity to demonstrate that neurons generated in the adult functionally integrate into the synaptic circuitry of the brain.},
	Author = {Carlen, M. and Cassidy, R. M. and Brismar, H. and Smith, G. A. and Enquist, L. W. and Frisen, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {Curr Biol},
	Keywords = {01 Adult neurogenesis general;A both},
	Number = {7},
	Organization = {Department of Cell and Molecular Biology, Medical Nobel Institute, Stockholm, Sweden},
	Pages = {606-8.},
	Title = {Functional integration of adult-born neurons},
	Uuid = {258B37FE-8387-4DD0-AF08-FD776A092463},
	Volume = {12},
	Year = {2002},
	url = {papers/Carlen_CurrBiol2002}}

@article{Carleton:2002,
	Abstract = {Olfaction was long considered to belong more to the realm of art than to that of science. As a result, how the brain perceives, discriminates, and recognizes odorant molecules is still a mystery. Recent progress has nonetheless been made at early stages of the olfactory pathway when olfactory studies entered into the molecular era to elucidate the first contact of an odor molecule with a receptor. Our group focuses on the analysis of odor information in the olfactory bulb, the first processing relay in the mammalian brain. Using this model, we are attempting to decipher the code for odorant information. Furthermore, the olfactory bulb also provides an attractive model to investigate neuronal proliferation, differentiation, migration, and neuronal death, processes involving an interplay between genetic and epigenetic influences. Finally, our goal is to explore the possible consequences of the olfactory bulb plasticity, in olfactory performance. For these purposes, we aim to combine morphological, electrophysiological and behavioral approaches to investigate: (1) how the olfactory bulb processes odor molecule information, (2) how neural precursors differentiate into olfactory bulb interneurons, (3) how these newly-generated neurons integrate into an operational neural network, (4) what role they play in the adult olfactory bulb, and (5) how are basic olfactory functions maintained in such a sensory system subjected to continuous renewal of a large percentage of its neuronal population. These questions should provide new fuel for the molecular and cellular bases of sensory perception and shed light onto cellular bases of learning and memory.},
	Author = {Carleton, A. and Rochefort, C. and Morante-Oria, J. and Desmaisons, D. and Vincent, J. D. and Gheusi, G. and Lledo, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:43 -0400},
	Journal = {J Physiol Paris},
	Keywords = {B both;02 Adult neurogenesis migration},
	Number = {1-2},
	Organization = {C.N.R.S., UPR 2197, Unite "Developpement, Evolution, Plasticite du Systeme Nerveux", Avenue de la Terrasse, 91198 Cedex, Gif-sur-Yvette, France},
	Pages = {115-22.},
	Title = {Making scents of olfactory neurogenesis},
	Uuid = {F0986BA5-FF8E-4E45-8F60-22033BB48238},
	Volume = {96},
	Year = {2002},
	url = {papers/Carleton_JPhysiolParis2002.pdf}}

@article{Carleton:2003,
	Abstract = {New neurons are continually recruited throughout adulthood in certain regions of the adult mammalian brain. How these cells mature and integrate into preexisting functional circuits remains unknown. Here we describe the physiological properties of newborn olfactory bulb interneurons at five different stages of their maturation in adult mice. Patch-clamp recordings were obtained from tangentially and radially migrating young neurons and from neurons in three subsequent maturation stages. Tangentially migrating neurons expressed extrasynaptic GABA(A) receptors and then AMPA receptors, before NMDA receptors appeared in radially migrating neurons. Spontaneous synaptic activity emerged soon after migration was complete, and spiking activity was the last characteristic to be acquired. This delayed excitability is unique to cells born in the adult and may protect circuits from uncontrolled neurotransmitter release and neural network disruption. Our results show that newly born cells recruited into the olfactory bulb become neurons, and a unique sequence of events leads to their functional integration. 1097-6256 Journal Article},
	Author = {Carleton, A. and Petreanu, L. T. and Lansford, R. and Alvarez-Buylla, A. and Lledo, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Synaptic Transmission/drug effects/physiology;Cell Differentiation;Neurons/*cytology/drug effects/*physiology;Animals;In Vitro;Synaptic Transmission;Cell Movement;Mice, Inbred C57BL;Male;Olfactory Bulb;Animals, Newborn;Support, Non-U.S. Gov't;Cell Movement/drug effects/physiology;Research Support, U.S. Gov't, P.H.S.;Neurons;Olfactory Bulb/*cytology/drug effects/*growth &development;Support, U.S. Gov't, P.H.S.;Mice;Cell Differentiation/physiology;A pdf;Research Support, Non-U.S. Gov't},
	Medline = {22600675},
	Month = {5},
	Nlm_Id = {9809671},
	Number = {5},
	Organization = {Pasteur Institute, Laboratory of Perception and Memory, CNRS UMR 2182, 25 Rue du Dr Roux, 75015 Paris, France.},
	Pages = {507-18},
	Pii = {nn1048},
	Pubmed = {12704391},
	Title = {Becoming a new neuron in the adult olfactory bulb},
	Uuid = {3C8CAB4B-CDEF-11D9-B244-000D9346EC2A},
	Volume = {6},
	Year = {2003},
	url = {papers/Carleton_NatNeurosci2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1048}}

@article{Carmeliet:2005,
	Abstract = {The growth of blood vessels (a process known as angiogenesis) is essential for organ growth and repair. An imbalance in this process contributes to numerous malignant, inflammatory, ischaemic, infectious and immune disorders. Recently, the first anti-angiogenic agents have been approved for the treatment of cancer and blindness. Angiogenesis research will probably change the face of medicine in the next decades, with more than 500 million people worldwide predicted to benefit from pro- or anti-angiogenesis treatments.},
	Author = {Carmeliet, Peter},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Drug Resistance, Neoplasm;10 Development;Research Support, Non-U.S. Gov't;Bone Marrow Cells;14 Immune;Neovascularization, Physiologic;Neoplasms;Blood Vessels;Animals;Humans;24 Pubmed search results 2008;review;Neovascularization, Pathologic},
	Month = {12},
	Nlm_Id = {0410462},
	Number = {7070},
	Organization = {Center of Transgene Technology and Gene Therapy, University of Leuven, Flanders Interuniversity Institute for Biotechnology (VIB), B-3000 Leuven, Belgium. peter.carmeliet\@med.kuleuven.be},
	Pages = {932-6},
	Pii = {nature04478},
	Pubmed = {16355210},
	Title = {Angiogenesis in life, disease and medicine},
	Uuid = {94D2D284-F69B-43E0-B269-EE327AF32ED3},
	Volume = {438},
	Year = {2005},
	url = {papers/Carmeliet_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature04478}}

@article{Carmichael:2002,
	Abstract = {The ability of the adult brain to form new connections in areas denervated by a lesion (axonal sprouting) is more widespread than previously thought, but mechanisms remain unknown. We have previously demonstrated an unexpected, robust axonal sprouting of contralateral corticostriatal neurons into the denervated striatum after ischemic cortical lesions. We now take advantage of marked differences in the degree of axonal sprouting from contralateral homotypic cortex after two types of cortical lesions to define the role of neuronal activity in this response. Thermal-ischemic lesions (TCL) of sensorimotor cortex, which induce axonal sprouting, produced two sequential patterns of low-frequency, synchronized neuronal activity that are not seen after similarly sized aspiration lesions, which do not induce axonal sprouting. An early rhythm of synchronous neuronal activity occurred in perilesion cortex on day 1 after lesion, with a frequency range of 0.2-2 Hz. A later pattern of activity occurred on days 2 and 3 after lesion, with a frequency range of 0.1-0.4 Hz. This second rhythm synchronized neuronal activity across widespread areas, including the cortical areas that contain the cell bodies of the sprouting axons. TTX was used to block this patterned neuronal activity and determine whether axonal sprouting was prevented. Chronic TTX infusion into the lesion site blocked the synchronous neuronal activity after TCL as well as axonal sprouting. Thus, both after different types of lesions and in the blockade experiments axonal sprouting was strongly correlated with synchronous neuronal activity, suggesting a role for this activity in anatomical reorganization after brain lesion in the adult.},
	Author = {Carmichael, S. Thomas and Chesselet, Marie-Fran\c{c}oise F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Corpus Striatum;Rats;Neuronal Plasticity;research support, u.s. gov't, p.h.s. ;Synaptic Transmission;Cell Communication;Rats, Sprague-Dawley;Periodicity;Axons;Tetrodotoxin;Male;Nerve Regeneration;research support, non-u.s. gov't ;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;21 Neurophysiology;Neurons;Somatosensory Cortex;21 Cortical oscillations;24 Pubmed search results 2008;Cerebral Decortication;Electroencephalography;Electrodes, Implanted;Electrocoagulation},
	Medline = {22117911},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {Department of Neurology, University of California Los Angeles, Los Angeles, California 90095, USA. scarmichael\@mednet.ucla.edu},
	Pages = {6062-70},
	Pii = {22/14/6062},
	Pubmed = {12122067},
	Title = {Synchronous neuronal activity is a signal for axonal sprouting after cortical lesions in the adult},
	Uuid = {49D83BE0-4483-4AAC-A898-6437A2B8C3D5},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/20026605}}

@article{Carmona:2006,
	Abstract = {Patterned intrinsic network activity plays a central role in shaping immature neuronal networks into functional circuits. However, the long-lasting signals that regulate spontaneous activity of developing circuits have not been identified. Here we study the net impact of TrkB signaling on early network activity of identified neuronal populations by analyzing postnatal hippocampi from trkB null mice. Ca2+ imaging showed that pyramidal neurons of trkB-/- mice displayed a decrease in intrinsic synchronous activity in neonatal animals but an increase in juveniles. Strikingly, alterations in network activity in trkB-/- hippocampus were associated with an aberrant induction of the transcription factor Fos. In contrast to pyramidal neurons, spontaneous [Ca2+]i oscillations in trkB-/- interneurons were consistently impaired throughout postnatal development. Moreover, the number of GABAergic synapses and the expression levels of GAD65 and KCC2 were decreased in mutant hippocampi, indicating that pre- and post-synaptic GABAergic components were impaired in trkB-/- mice. Finally, the partial blockade of GABA(A) receptor in postnatal slices revealed that mutant hippocampi displayed an increased susceptibility to network hyperexcitability. These results indicate that the lack of TrkB signaling during development impairs GABAergic neurotransmission, thereby leading to an age-dependent decrease followed by an increase in the intrinsic excitability of neuronal circuits. Furthermore, the present study indicates that long-lasting TrkB signaling may contribute to the construction of CNS circuits by modulating patterns of spontaneous [Ca2+]i oscillations.},
	Author = {Carmona, Maria A. and Pozas, Esther and Mart{\'\i}nez, Albert and Espinosa-Parrilla, Juan F. and Soriano, Eduardo and Aguado, Fernando},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {gamma-Aminobutyric Acid;10 Development;Signal Transduction;Calcium Signaling;Animals;Aging;Neuronal Plasticity;Synaptic Transmission;Hippocampus;Mice, Inbred C57BL;Biological Clocks;research support, non-u.s. gov't;Animals, Newborn;Nerve Net;Mice, Knockout;Receptor, trkB;10 genetics malformation;Mice;Interneurons;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {9110718},
	Number = {1},
	Organization = {Department of Cell Biology and IRBB-Barcelona Science Park, University of Barcelona, Barcelona E-08028, Spain.},
	Pages = {47-63},
	Pii = {bhi083},
	Pubmed = {15829735},
	Title = {Age-dependent spontaneous hyperexcitability and impairment of GABAergic function in the hippocampus of mice lacking trkB},
	Uuid = {CD196995-D831-420D-A249-2065EDC07B70},
	Volume = {16},
	Year = {2006},
	url = {papers/Carmona_CerebCortex2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhi083}}

@article{Carneiro:2006,
	Abstract = {The entry of enveloped animal viruses into their host cells always depends on membrane fusion triggered by conformational changes in viral envelope glycoproteins. Vesicular stomatitis virus (VSV) infection is mediated by virus spike glycoprotein G, which induces membrane fusion between the viral envelope and the endosomal membrane at the acidic environment of this compartment. In this work, we evaluated VSV interactions with membranes of different phospholipid compositions, at neutral and acidic pH, using atomic force microscopy (AFM) operating in the force spectroscopy mode, isothermal calorimetry (ITC) and molecular dynamics simulation. We found that the binding forces differed dramatically depending on the membrane phospholipid composition, revealing a high specificity of G protein binding to membranes containing phosphatidylserine (PS). In a previous work, we showed that the sequence corresponding amino acid 164 of VSV G protein was as efficient as the virus in catalyzing membrane fusion at pH 6.0. Here, we used this sequence to explore VSV-PS interaction using ITC. We found that peptide binding to membranes was exothermic, suggesting the participation of electrostatic interactions. Peptide-membrane interaction at pH 7.5 was shown to be specific to PS and dependent on the presence of His residues in the fusion peptide. The application of the simplified continuum Gouy-Chapman theory to our system predicted a pH of 5.0 at membrane surface, suggesting that the His residues should be protonated when located close to the membrane. Molecular dynamics simulations suggested that the peptide interacts with the lipid bilayer through its N-terminal residues, especially Val(145) and His(148).},
	Author = {Carneiro, Fabiana A. and Lapido-Loureiro, Pedro A. and Cordo, Sandra M. and Stauffer, Fausto and Weissm{\"u}ller, Gilberto and Bianconi, M. Lucia and Juliano, Maria A. and Juliano, Luiz and Bisch, Paulo M. and Poian, Andrea T. Da},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0175-7571},
	Journal = {Eur Biophys J},
	Keywords = {15 PS VSVG receptor;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8409413},
	Number = {2},
	Organization = {Instituto de Bioqu\`{i}mica M{\'e}dica, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-590, Brazil.},
	Pages = {145-54},
	Pubmed = {16184389},
	Title = {Probing the interaction between vesicular stomatitis virus and phosphatidylserine},
	Uuid = {108FA85E-F7CC-43F8-A9DD-EA7CC4218326},
	Volume = {35},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00249-005-0012-z}}

@article{Carneiro:2002,
	Abstract = {Vesicular stomatitis virus (VSV) infection depends on the fusion of viral and cellular membranes, which is mediated by virus spike glycoprotein G at the acidic environment of the endosomal compartment. VSV G protein does not contain a hydrophobic amino acid sequence similar to the fusion peptides found among other viral glycoproteins, suggesting that membrane recognition occurs through an alternative mechanism. Here we studied the interaction between VSV G protein and liposomes of different phospholipid composition by force spectroscopy, isothermal titration calorimetry (ITC), and fluorescence spectroscopy. Force spectroscopy experiments revealed the requirement for negatively charged phospholipids for VSV binding to membranes, suggesting that this interaction is electrostatic in nature. In addition, ITC experiments showed that VSV binding to liposomes is an enthalpically driven process. Fluorescence data also showed the lack of VSV interaction with the vesicles as well as inhibition of VSV-induced membrane fusion at high ionic strength. Intrinsic fluorescence measurements showed that the extent of G protein conformational changes depends on the presence of phosphatidylserine (PS) on the target membrane. Although the increase in PS content did not change the binding profile, the rate of the fusion reaction was remarkably increased when the PS content was increased from 25 to 75\%. On the basis of these data, we suggest that G protein binding to the target membrane essentially depends on electrostatic interactions, probably between positive charges on the protein surface and negatively charged phospholipids in the cellular membrane. In addition, the fusion is exothermic, indicating no entropic constraints to this process.},
	Author = {Carneiro, Fabiana A. and Bianconi, M. Lucia and Weissm{\"u}ller, Gilberto and Stauffer, Fausto and Da Poian, Andrea T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Electrostatics;Animals;Vesicular stomatitis-Indiana virus;Spectrometry, Fluorescence;Microscopy, Atomic Force;Thermodynamics;Cell Membrane;Liposomes;15 Retrovirus mechanism;Calorimetry;Viral Envelope Proteins;Cell Line;Membrane Glycoproteins;Membrane Fusion;Phospholipids;Cricetinae;24 Pubmed search results 2008;15 PS VSVG receptor;Research Support, Non-U.S. Gov't},
	Medline = {21904718},
	Month = {4},
	Nlm_Id = {0113724},
	Number = {8},
	Organization = {Departamento de Bioqu{\'\i}mica M{\'e}dica, Instituto de Ci\^{e}ncias Biom{\'e}dicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21941-590, Brazil.},
	Pages = {3756-64},
	Pubmed = {11907215},
	Title = {Membrane recognition by vesicular stomatitis virus involves enthalpy-driven protein-lipid interactions},
	Uuid = {9EC4BC91-5941-4C88-B3D1-91C530C801F5},
	Volume = {76},
	Year = {2002}}

@article{Carp:2002,
	Abstract = {A series of inbred strains of mice have been developed that are either prone (SAMP) or resistant (SAMR) to accelerated senescence. All of these strains originated from an inadvertent cross or crosses between the AKR/J mouse strain and an unknown strain(s). The characteristics of the nine senescence-prone lines differ, with all strains showing generalized aspects of accelerated aging but with each line having a specific aging-related change that is emphasized, e.g. learning and memory deficits, osteoporosis and senile amyloidosis. The senescence-resistant strains have normal patterns of aging and do not show the specific aging-related changes seen in SAMP strains. The fact that AKR mice have high levels of endogenous, ecotropic murine leukemia virus (MuLV) prompted an examination of the expression levels of MuLV in SAM strains. Analysis of brain, spleen and thymus samples revealed that seven of nine SAMP strains had high levels of MuLV and contained the Emv11 provirus (previously termed Akv1) that encodes the predominant MuLV found in AKR mice. In contrast, none of the SAMR strains had Emv11 or significant amounts of virus. The current findings represent an initial step in determining the role of MuLV in the accelerated senescence seen in SAMP strains.},
	Author = {Carp, R. I. and Meeker, H. C. and Chung, R. and Kozak, C. A. and Hosokawa, M. and Fujisawa, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0047-6374},
	Journal = {Mech Ageing Dev},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Aging;Brain;Female;15 Retrovirus mechanism;Crosses, Genetic;Male;Proviruses;Cell Line;Animals, Newborn;Leukemia Virus, Murine;Thymus Gland;Mice;24 Pubmed search results 2008;15 ERVs retroelements;Spleen;Mice, Inbred AKR},
	Medline = {21839529},
	Month = {3},
	Nlm_Id = {0347227},
	Number = {6},
	Organization = {New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA. richard.carp\@omr.state.ny.us},
	Pages = {575-84},
	Pii = {S0047637401003773},
	Pubmed = {11850021},
	Title = {Murine leukemia virus in organs of senescence-prone and -resistant mouse strains},
	Uuid = {833A211C-4326-11DB-A5D2-000D9346EC2A},
	Volume = {123},
	Year = {2002}}

@article{Carr:1992,
	Abstract = {Young adult rats were unilaterally bulbectomized and tritiated thymidine ([3H]TdR) was injected at variable times following surgery to determine the effect of bulbectomy on the rates of cell proliferation and cell death in the olfactory epithelium. Removal of the olfactory bulb elicits a two- to fourfold increase in the proliferation rate of ipsilateral olfactory epithelial cells 7-50 days following surgery. On the contralateral side, there was a temporary twofold increase in the proliferation rate during the second week after surgery, but this returned to control values at 3 weeks. This temporary increase was in parallel with the response on the ipsilateral side so that the ratio between operated and unoperated sides remained at two. Cell death in olfactory epithelium is also up-regulated following bulbectomy. Death of cells can occur as early as 1 day following incorporation of [3H]TdR, i.e., well before the sensory neurons become mature. This means there is an over-production of sensory cells, and they die at all stages of their life cycle. The number of cells dying is greater after bulbectomy, indicating that the overproduction of olfactory cells is more pronounced after surgery.},
	Author = {Carr, V. M. and Farbman, A. I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Exp Neurol},
	Keywords = {Support, U.S. Gov't, P.H.S.;Tritium;Neurons, Afferent/physiology;Nerve Degeneration;Rats;Autoradiography;Thymidine/metabolism;Neurons/cytology/*physiology;Animal;Cell Death;DNA Replication;I abstr;Olfactory Bulb/*physiology;Olfactory Mucosa/cytology/innervation/*physiology;13 Olfactory bulb anatomy;Epithelium/cytology/physiology;*Nerve Regeneration},
	Number = {1},
	Organization = {Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208-3520.},
	Pages = {55-9.},
	Title = {Ablation of the olfactory bulb up-regulates the rate of neurogenesis and induces precocious cell death in olfactory epithelium},
	Uuid = {E149A3D1-A46D-4253-9399-F28482F8D432},
	Volume = {115},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1728573}}

@article{Carroll:2008,
	Abstract = {Biologists have long sought to understand which genes and what kinds of changes in their sequences are responsible for the evolution of morphological diversity. Here, I outline eight principles derived from molecular and evolutionary developmental biology and review recent studies of species divergence that have led to a genetic theory of morphological evolution, which states that (1) form evolves largely by altering the expression of functionally conserved proteins, and (2) such changes largely occur through mutations in the cis-regulatory sequences of pleiotropic developmental regulatory loci and of the target genes within the vast networks they control.},
	Author = {Carroll, Sean B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008;research support, non-u.s. gov't;Evolution, Molecular;Evolution;Animals;Humans;Proteins;Developmental Biology;Gene Regulatory Networks},
	Month = {7},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Howard Hughes Medical Institute, Laboratory of Molecular Biology, University of Wisconsin-Madison, Madison, WI 53706, USA. sbcarrol\@wisc.edu},
	Pages = {25-36},
	Pii = {S0092-8674(08)00817-9},
	Pubmed = {18614008},
	Title = {Evo-devo and an expanding evolutionary synthesis: a genetic theory of morphological evolution},
	Uuid = {15AA6C3C-CCF7-443F-88B2-8D1FF0DC4A23},
	Volume = {134},
	Year = {2008},
	url = {papers/Carroll_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.06.030}}

@article{Carson:2006,
	Abstract = {Central nervous system (CNS) immune privilege is an experimentally defined phenomenon. Tissues that are rapidly rejected by the immune system when grafted in sites, such as the skin, show prolonged survival when grafted into the CNS. Initially, CNS immune privilege was construed as CNS isolation from the immune system by the blood-brain barrier (BBB), the lack of draining lymphatics, and the apparent immunoincompetence of microglia, the resident CNS macrophage. CNS autoimmunity and neurodegeneration were presumed automatic consequences of immune cell encounter with CNS antigens. Recent data have dramatically altered this viewpoint by revealing that the CNS is neither isolated nor passive in its interactions with the immune system. Peripheral immune cells can cross the intact BBB, CNS neurons and glia actively regulate macrophage and lymphocyte responses, and microglia are immunocompetent but differ from other macrophage/dendritic cells in their ability to direct neuroprotective lymphocyte responses. This newer view of CNS immune privilege is opening the door for therapies designed to harness autoreactive lymphocyte responses and also implies (i) that CNS autoimmune diseases (i.e. multiple sclerosis) may result as much from neuronal and/or glial dysfunction as from immune system dysfunctions and (ii) that the severe neuronal and glial dysfunction associated with neurodegenerative disorders (i.e. Alzheimer's disease) likely alters CNS-specific regulation of lymphocyte responses affecting the utility of immune-based therapies (i.e. vaccines).},
	Author = {Carson, Monica J. and Doose, Jonathan M. and Melchior, Benoit and Schmid, Christoph D. and Ploix, Corinne C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0105-2896},
	Journal = {Immunol Rev},
	Keywords = {14 Immune;11 Glia;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {7702118},
	Organization = {Division of Biomedical Sciences, University of California, Riverside, Riverside, CA, USA.},
	Pages = {48-65},
	Pii = {IMR441},
	Pubmed = {16972896},
	Title = {CNS immune privilege: hiding in plain sight},
	Uuid = {93DE4D67-E9D3-47D5-818D-DFB3FACC695C},
	Volume = {213},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1600-065X.2006.00441.x}}

@article{Carson:2005,
	Abstract = {Olfactory receptor neurons (ORNs) undergo caspase-mediated retrograde apoptosis after target removal (bulbectomy), in which axonal caspase-9 and caspase-3 activation leads to terminal apoptosis in ORN soma of the olfactory epithelium. Here, we show that caspase-8 can act as an initiator of ORN apoptosis after bulbectomy and also after synaptic instability is induced by NMDA-mediated excitotoxic death of ORN target neurons in the olfactory bulb. Caspase-8 and caspase-3 are sequentially activated within ORN presynaptic terminals, and caspase-8 complexes with dynactin p150Glued, (a retrograde motor protein) and is transported retrogradely, preceding axonal caspase-3 activation and apoptosis of ORN cell bodies. Focal in vivo inhibition of initiator caspase activation or microtubule-dependent transport (with Taxol) at the lesioned axon terminus results in a significant reduction in retrograde axonal caspase-8 and caspase-3 activation and inhibition of retrograde ORN death. Caspase-8 activation and retrograde transport after NMDA lesion is similarly reduced in mice null for p75, the low-affinity nerve growth factor receptor. The retrograde apoptosis of ORNs thus involves a novel mechanism that used p75 in the local activation of caspase-8. Once caspase-8 is maximally activated in the presynaptic terminal, it is transported retrogradely by the motor complex dynactin/dynein, a process that can be inhibited focally to inhibit ORN apoptosis after acute axonal lesion. These data have revealed a novel mechanism of retrograde apoptosis, in which caspase-8 complexes directly with axonal dynactin p150Glued to reveal a differential vulnerability of subpopulations of ORNs to undergo apoptosis after axonal damage and the loss of olfactory bulb target neurons.},
	Author = {Carson, Christine and Saleh, Maya and Fung, France W. and Nicholson, Donald W. and Roskams, A. Jane},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {26},
	Organization = {Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.},
	Pages = {6092-104},
	Pii = {25/26/6092},
	Pubmed = {15987939},
	Title = {Axonal dynactin p150Glued transports caspase-8 to drive retrograde olfactory receptor neuron apoptosis},
	Uuid = {C1422DF8-8C94-4B6C-9A45-B45A7503AC05},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0707-05.2005}}

@article{Castejon:2005,
	Abstract = {The inflammatory reaction surrounding hemorrhagic and perihematomal brain parenchyma has been studied by means of light and transmission electron microscopy in 12 patients with severe traumatic head injuries complicated with subdural or extradural hematoma or hygroma. Perivascular cells, ameboid phagocytic microglial cells, and infiltrated macrophage/monocyte system were observed surrounding perivascular and intraparenchymal hemorrhagic foci. They showed phagocytic activity of degenerated nerve cell processes, and organized proteinaceous edema fluid present in the enlarged extracellular space. Endocytosis by means of clathrin coated vesicles also was observed. Facultative and professional phagocytes exhibited a full repertoire of lysosomes, phagosomes containing nerve cell debris, lipid droplets, and lipofucsin granules. Phagocytic pericytes remaining within the capillary basement membrane were also observed around perivascular hemorrhages. The inflammatory reaction was examined in young and old patients with an evolution time of brain injury ranging from 1 day to 2 years. The inflammatory process developed according to the intensity of traumatic insult, patient age, associated hematoma or hygroma, severity of vasogenic and cytotoxic oedema, and anoxic-ischemic conditions of brain parenchyma.},
	Author = {Castej{\'o}n, O. J. and Castellano, A. and Arismendi, G. J. and Medina, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {1122-9497},
	Journal = {J Submicrosc Cytol Pathol},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Medline = {102464197},
	Month = {4},
	Nlm_Id = {8804312},
	Number = {1},
	Organization = {Institute of Biological Investigations, Faculty of Medicine, University of Zulia, Maracaibo, Venezuela. ocastejo\@cantv.net},
	Pages = {43-52},
	Pubmed = {16136727},
	Title = {The inflammatory reaction in human traumatic oedematous cerebral cortex},
	Uuid = {E17FB550-B18D-49DD-8B99-52B57FDED32A},
	Volume = {37},
	Year = {2005}}

@article{Catapano:2004,
	Abstract = {Cellular repair of neuronal circuitry affected by neurodegenerative disease or injury may be approached in the adult neocortex via transplantation of neural precursors ("neural stem cells") or via molecular manipulation and recruitment of new neurons from endogenous precursors in situ. A major challenge for potential future approaches to neuronal replacement will be to specifically direct and control progressive differentiation, axonal projection and connectivity of neural precursors along a specific neuronal lineage. This goal will require a progressively more detailed understanding of the molecular controls over morphologic differentiation of specific neuronal lineages, including neurite outgrowth and elongation, in order to accurately permit and direct proper neuronal integration and connectivity. Here, we investigate controls over the morphologic differentiation of a specific prototypical lineage of cortical neurons: callosal projection neurons (CPN). We highly enriched CPN to an essentially pure population, and cultured them at three distinct stages of development from embryonic and postnatal mouse cortex by retrograde fluorescence labelling, followed by fluorescence-activated cell sorting. We find that specific peptide growth factors exert direct stage-specific positive and negative effects over the morphologic differentiation and process outgrowth of CPN. These effects are distinct from the effects of these growth factors on CPN survival [Catapano et al. (2001)J. Neurosci., 21, 8863-8872]. These data may be critical for the future goal of directing lineage-specific neuronal differentiation of transplanted or endogenous precursors/"stem cells" toward cellular repair of complex cortical circuitry.},
	Author = {Catapano, Lisa A. and Arlotta, Paola and Cage, Tene A. and Macklis, Jeffrey D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Differentiation;Apoptosis;Cell Survival;Immunohistochemistry;Male;Animals;Cells, Cultured;Flow Cytometry;Research Support, U.S. Gov't, P.H.S.;Proto-Oncogene Proteins;Bromodeoxyuridine;Fibroblast Growth Factor 2;Pregnancy;Cell Polarity;Neurofilament Proteins;Dendrites;Neocortex;Brain-Derived Neurotrophic Factor;Axons;Laterality;Comparative Study;Aging;Corpus Callosum;17 Transplant Regeneration;Proto-Oncogene Proteins c-bcl-2;Neurotrophin 3;Female;Embryo;Time Factors;Animals, Newborn;Cell Size;01 Adult neurogenesis general;Mice, Knockout;Mice;Neurons;Polymerase Chain Reaction;Research Support, Non-U.S. Gov't},
	Month = {5},
	Nlm_Id = {8918110},
	Number = {9},
	Organization = {Departments of Neurosurgery and Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.},
	Pages = {2421-34},
	Pii = {EJN3303},
	Pubmed = {15128396},
	Title = {Stage-specific and opposing roles of BDNF, NT-3 and bFGF in differentiation of purified callosal projection neurons toward cellular repair of complex circuitry},
	Uuid = {24C8BB7C-71A6-44C1-AA77-C87F3C0481E4},
	Volume = {19},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.0953-816X.2004.03303.x}}

@article{Catapano:2001,
	Abstract = {Repair of specific neuronal circuitry in the neocortex may be possible via neural precursor transplantation or manipulation of endogenous precursors in situ. These approaches will almost certainly require a detailed understanding of the mechanisms that control survival and differentiation of specific neuronal lineages. Such analysis has been hampered by the overwhelming diversity of neuronal types intermixed in neocortex and the inability to isolate individual lineages. To elucidate stage-specific controls over the survival of individual lineages of cortical neurons, we purified immature callosal projection neurons (CPN) at distinct stages of development from embryonic and postnatal mouse cortex by retrograde fluorescence labeling, followed by fluorescence-activated cell sorting. Purified CPN survive well in culture, acquire stage-specific projection neuron morphologies, and express appropriate neurotransmitters and growth factor receptors. Purified CPN are dependent on exogenous trophic support for survival in a stage-specific manner. Survival of postnatal day 2 (P2) to P3 and P6-P7 CPN is promoted by overlapping but distinct sets of neurotrophic factors, whereas embryonic day 19 CPN show less specificity of dependence on peptide factors. These studies demonstrate for the first time the stage-specific control by peptide growth factors over the survival of a specific cortical neuronal lineage. Such information may be critical for the future goal of directed differentiation of transplanted or endogenous precursors toward cellular repair of complex cortical circuitry. 1529-2401 Journal Article},
	Author = {Catapano, L. A. and Arnold, M. W. and Perez, F. A. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;10 Development;Cell Separation;Animals;Cells, Cultured;Cell Lineage/drug effects/physiology;Nerve Growth Factors/*metabolism/pharmacology;Cell Survival/drug effects/physiology;Cerebral Cortex/drug effects/*embryology/*metabolism;Mice, Inbred C57BL;Microspheres;Support, Non-U.S. Gov't;Culture Media, Conditioned/pharmacology;Axons/metabolism;D, F pdf;06 Adult neurogenesis injury induced;Cell Differentiation/drug effects/physiology;Flow Cytometry;Support, U.S. Gov't, P.H.S.;Mice;Neurons/cytology/drug effects/*metabolism;Immunohistochemistry},
	Number = {22},
	Organization = {Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {8863-72},
	Title = {Specific neurotrophic factors support the survival of cortical projection neurons at distinct stages of development},
	Uuid = {6DD121C9-AC6C-4A8C-8FED-2AFD352DFA2D},
	Volume = {21},
	Year = {2001},
	url = {papers/Catapano_JNeurosci2001.pdf}}

@article{Catapano:1999,
	Abstract = {In the current experiments, we address the emerging hypothesis that transplanted neural precursor cells can respond to local microenvironmental signals in the post-developmental brain and exhibit patterns of differentiation that depend critically on specific location within the brain. HiB5 precursor cells were transplanted into adult mouse cortex, corpus callosum, and multiple positions in striatum, and assessed for differentiation by morphology and immunocytochemistry. Our results indicate that the likelihood of both neuronal and glial differentiation of transplanted precursors depends on proximity to the medial striatum or subventricular zone of the adult host, supporting the concept that microenvironmental signals can critically affect the differentiation fate of neural precursors, and suggesting the potential to manipulate such signals in the adult brain.},
	Author = {Catapano, L. A. and Sheen, V. L. and Leavitt, B. R. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Neuroreport},
	Keywords = {Cell Differentiation;Transplantation, Heterologous;17 Transplant Regeneration;Neurons/*cytology/physiology/*transplantation;Immunohistochemistry;Rats;Human;L abstr;Autoradiography;Animal;Corpus Striatum/*physiology;Stem Cells/*cytology/physiology/*transplantation;Support, U.S. Gov't, P.H.S.;Cell Line, Transformed;Support, Non-U.S. Gov't;Mice;Cell Movement/physiology},
	Number = {18},
	Organization = {Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.},
	Pages = {3971-7.},
	Title = {Differentiation of transplanted neural precursors varies regionally in adults striatum},
	Uuid = {A1E361A1-0A65-4F03-BFA3-3E03098DDCF4},
	Volume = {10},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10716243}}

@article{Cayouette:2003,
	Abstract = {Asymmetric segregation of cell-fate determinants during cell division plays an important part in generating cell diversity in invertebrates. We showed previously that cells in the neonatal rat retina divide at various orientations and that some dividing cells asymmetrically distribute the cell-fate determinant Numb to the two daughter cells. Here, we test the possibility that such asymmetric divisions contribute to retinal cell diversification. We have used long-term videomicroscopy of green-fluorescent-protein (GFP)-labeled retinal explants from neonatal rats to visualize the plane of cell division and follow the differentiation of the daughter cells. We found that cells that divided with a horizontal mitotic spindle, where both daughter cells should inherit Numb, tended to produce daughters that became the same cell type, whereas cells that divided with a vertical mitotic spindle, where only one daughter cell should inherit Numb, tended to produce daughters that became different. Moreover, overexpression of Numb in the dividing cells promoted the development of photoreceptor cells at the expense of interneurons and Muller glial cells. These findings indicate that the plane of cell division influences cell-fate choice in the neonatal rat retina and support the hypothesis that the asymmetric segregation of Numb normally influences some of these choices. 22588265 0950-1991 Journal Article},
	Author = {Cayouette, M. and Raff, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:51 -0400},
	Journal = {Development},
	Keywords = {Microscopy, Video;Cell Differentiation;Tissue Culture;10 Development;Rats;Photoreceptors, Vertebrate/cytology;Mitosis;Recombinant Proteins/genetics;Models, Biological;Animal;Rats, Sprague-Dawley;Nerve Tissue Proteins/genetics;Animals, Newborn;Support, Non-U.S. Gov't;Interneurons/cytology;Eye Proteins/genetics;Retina/*cytology/*growth &development/metabolism;Cell Division;Luminescent Proteins/genetics;F},
	Number = {11},
	Organization = {MRC Laboratory for Molecular Cell Biology and Cell Biology Unit, University College London, London WC1E 6BT, UK. m.cayouette\@stanford.edu},
	Pages = {2329-39},
	Pubmed = {12702648},
	Title = {The orientation of cell division influences cell-fate choice in the developing mammalian retina},
	Uuid = {ABBAC658-12A9-4D86-9EF9-012C878D715D},
	Volume = {130},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12702648}}

@article{Cayouette:2002,
	Abstract = {It is a major challenge to understand how the neuroepithelial cells of the developing CNS choose between alternative cell fates to generate cell diversity. In invertebrates such as Drosophila melanogaster and Caenorhabditis elegans, asymmetric segregation of cell-fate determining proteins or mRNAs to the two daughter cells during precursor cell division plays a crucial part in cell diversification. There is increasing evidence that this mechanism also operates in vertebrate neural development and that Numb proteins, which function as cell-fate determinants during Drosophila development, may also function in this way in vertebrates. Recent studies on mouse cortical progenitor cells have provided the strongest evidence yet that this is the case. Here, we review these and other findings that suggest an important role for the asymmetric segregation of Numb proteins in vertebrate neural development. 22337315 1097-6256 Journal Article Review Review, Tutorial},
	Author = {Cayouette, M. and Raff, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Drosophila/embryology/metabolism;10 Development;Mammals/embryology/metabolism;Human;Neurons/*cytology/metabolism;Animal;Membrane Proteins/genetics/*metabolism;Cell Lineage/*genetics;F;Nerve Tissue Proteins/genetics/*metabolism;Central Nervous System/cytology/*embryology/metabolism;Support, Non-U.S. Gov't;Cell Division/*genetics;Cell Differentiation/*genetics;Stem Cells/*cytology/metabolism},
	Number = {12},
	Organization = {MRC Laboratory for Molecular Cell Biology and Cell Biology Unit, University College London, Gower Street, London WC1E 6BT, UK. m.cayouette\@stanford.edu},
	Pages = {1265-9},
	Pubmed = {12447381},
	Title = {Asymmetric segregation of Numb: a mechanism for neural specification from Drosophila to mammals},
	Uuid = {3E581062-C6E6-4E1C-8264-294F0876AD5D},
	Volume = {5},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12447381}}

@article{Cayre:2001,
	Abstract = {In the house cricket (Acheta domesticus) mushroom bodies, neurogenesis still occurs during adulthood. Using in vitro approaches, the respective roles of natural polyamines in neurogenesis were examined. Mushroom body neuroblast proliferation was assayed in organotypic culture using 5-bromo, 2'-deoxyuridine labeling. The number of labeled cells was significantly increased when putrescine was added to culture medium, whereas spermidine and spermine supplementation did not alter cell proliferation. Conversely, in vitro morphometric studies on mushroom body neurons cultured in a defined medium showed that putrescine addition failed to alter any morphological character of these interneurons, whereas addition of the long-chain polyamines, spermidine and spermine, stimulated neuron differentiation. These two polyamines significantly increased total neurite length; moreover, spermidine-treated cells exhibited more branches than the controls. The present data demonstrate that putrescine has a mitogenic effect on mushroom body neuronal precursors, and that spermidine and spermine, which failed to induce neuroblast proliferation, act on neuronal differentiation, inducing neurite outgrowth. Our results indicate that short- and long-chain polyamines play specific roles during neurogenesis, and provide a basis for further studies on neuronal precursor proliferation and differentiation. Copyright 2001 John Wiley &Sons, Inc.},
	Author = {Cayre, M. and Malaterre, J. and Strambi, C. and Charpin, P. and Ternaux, J. P. and Strambi, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:43 -0400},
	Journal = {J Neurobiol},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {4},
	Organization = {Laboratoire de Neurobiologie, CNRS, 31 Chemin Joseph Aiguier, 13402 Marseille cedex 20, France.},
	Pages = {315-24.},
	Title = {Short- and long-chain natural polyamines play specific roles in adult cricket neuroblast proliferation and neuron differentiation in vitro},
	Uuid = {94AA8BE7-E491-44C5-8FD1-C7E78FDE069F},
	Volume = {48},
	Year = {2001},
	url = {papers/Cayre_JNeurobiol2001.pdf}}

@article{Cayre:2006,
	Abstract = {Adult neural stem cells in the subventricular zone (SVZ) produce neuronal progenitors that migrate along the rostral migratory stream (RMS) and generate olfactory interneurons. Here, we evaluate the migratory potential of SVZ cells outside the RMS and their capacity to generate oligodendrocytes in the adult brain. We show that SVZ cells migrate long distances when grafted into white matter tracts such as the cingulum (Ci) and corpus callosum (CC). Furthermore, 22 days postinjection, most present morphologic and phenotypic characteristics of cells committed to the oligodendrocyte lineage. Cells grafted in shiverer CC and Ci become MBP-positive oligodendrocytes, abundantly myelinating these white matter tracts. Type A progenitors are involved in this myelinating process. Altogether, this study reveals the migrating and myelinating potential of SVZ cells in a new environmental context. Therefore, SVZ cells stand as interesting candidates for the development of novel therapeutic strategies for demyelinating diseases.},
	Author = {Cayre, Myriam and Bancila, Mircea and Virard, Isabelle and Borges, Ana and Durbec, Pascale},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {9100095},
	Number = {4},
	Organization = {UMR 6216, Institut de Biologie du D{\'e}veloppement de Marseille Luminy, Case 907, 13288 Marseille Cedex 9, France.},
	Pages = {748-58},
	Pii = {S1044-7431(06)00006-6},
	Pubmed = {16481195},
	Title = {Migrating and myelinating potential of subventricular zone neural progenitor cells in white matter tracts of the adult rodent brain},
	Uuid = {A699B43E-148A-4F14-BE99-7DC3468E5468},
	Volume = {31},
	Year = {2006},
	url = {papers/Cayre_MolCellNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2006.01.004}}

@article{Cecchi:2001,
	Abstract = {Adult neurogenesis has long been documented in the vertebrate brain and recently even in humans. Although it has been conjectured for many years that its functional role is related to the renewing of memories, no clear mechanism as to how this can be achieved has been proposed. Using the mammalian olfactory bulb as a paradigm, we present a scheme in which incorporation of new neurons proceeds at a constant rate, while their survival is activity-dependent and thus contingent on new neurons establishing suitable connections. We show that a simple mathematical model following these rules organizes its activity so as to maximize the difference between its responses and can adapt to changing environmental conditions in unsupervised fashion, in agreement with current neurophysiological data.},
	Author = {Cecchi, G. A. and Petreanu, L. T. and Alvarez-Buylla, A. and Magnasco, M. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Comput Neurosci},
	Keywords = {01 Adult neurogenesis general;A abstr},
	Number = {2},
	Organization = {Laboratory of Mathematical Physics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, U.S.A.; Functional Neuroimaging Laboratory, Weill Medical College of Cornell University, New York, NY 10021 and Biometaphorical Computing Group, TJ Watson Center, IBM Research, Yorktown Heights, NY 10598, USA. Email: gcecchi\@us.ibm.com},
	Pages = {175-182.},
	Title = {Unsupervised Learning and Adaptation in a Model of Adult Neurogenesis},
	Uuid = {E50C2E4C-B5D4-4595-99F4-F5F323B517A6},
	Volume = {11},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11717533}}

@article{Cernak:2002,
	Abstract = {Few studies have characterised apoptosis in a brain injury model that causes a significant degree of diffuse axonal injury. Such characterisation is essential from a clinical viewpoint since diffuse axonal injury is a major component of human head injury. The present study therefore, examines the expression of active and proactive caspase-3, and the bax, bcl-2 and bcl-x members of the bcl-2 family, to characterise the temporal profile of apoptosis in a model of traumatic brain injury in rats that produces significant diffuse axonal injury. Pentobarbital anaesthetised male Sprague-Dawley rats were injured using the 2m impact-acceleration model of diffuse traumatic brain injury. After injury, diffuse trauma resulted in an increased bax expression followed by induction of caspase-3. The increase in caspase-3 was simultaneous with an increase in anti-apoptotic bcl-2 expression. Bcl-x levels were increased after induction of caspase-3 and the increased levels of bcl-x were sustained to the end of the 5-day observation period. Increased active caspase-3 expression was associated with the appearance of TUNEL positive cells. These cells were detected in different brain regions at different times, with some regions showing no apoptotic cells until 3 days after injury. No TUNEL positive cells were detected at 7 and 14 days after injury. DNA electrophoresis confirmed that DNA fragmentation was maximal at 3 days after injury. Increased active caspase-3 levels were also significantly correlated with increased bcl-2 levels (r=0.80; P<0.001) suggesting that the apoptotic cascade after diffuse traumatic brain injury is a carefully controlled cellular homeostatic response. Pharmacological manipulation of this balance may offer a therapeutic approach for preventing cell death and improving outcome after diffuse traumatic brain injury. 0967-5868 Journal Article},
	Author = {Cernak, I. and Chapman, S. M. and Hamlin, G. P. and Vink, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Clin Neurosci},
	Keywords = {Proto-Oncogene Proteins c-bcl-2/biosynthesis;Animals;Neurons/pathology;Brain Injuries/*pathology;Rats;Electrophoresis, Agar Gel;Apoptosis/*physiology;D pdf;Rats, Sprague-Dawley;Male;Immunoblotting;Proto-Oncogene Proteins/biosynthesis;Support, Non-U.S. Gov't;In Situ Nick-End Labeling;06 Adult neurogenesis injury induced;Immunohistochemistry;Caspases/biosynthesis;DNA Fragmentation},
	Number = {5},
	Organization = {Department of Neuroscience, Georgetown University, Washington, DC, USA.},
	Pages = {565-72},
	Pubmed = {12383417},
	Title = {Temporal characterisation of pro- and anti-apoptotic mechanisms following diffuse traumatic brain injury in rats},
	Uuid = {70775058-6D6C-4E7F-A9F5-6BA58738903B},
	Volume = {9},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12383417}}

@article{Chae:1997,
	Abstract = {The adult mammalian cortex is characterized by a distinct laminar structure generated through a well-defined pattern of neuronal migration. Successively generated neurons are layered in an "inside-out" manner to produce six cortical laminae. We demonstrate here that p35, the neuronal-specific activator of cyclin-dependent kinase 5, plays a key role in proper neuronal migration. Mice lacking p35, and thus p35/cdk5 kinase activity, display severe cortical lamination defects and suffer from sporadic adult lethality and seizures. Histological examination reveals that the mutant mice lack the characteristic laminated structure of the cortex. Neuronal birth-dating experiments indicate a reversed packing order of cortical neurons such that earlier born neurons reside in superficial layers and later generated neurons occupy deep layers. The phenotype of p35 mutant mice thus demonstrates that the formation of cortical laminar structure depends on the action of the p35/cdk5 kinase.},
	Author = {Chae, T. and Kwon, Y. T. and Bronson, R. and Dikkes, P. and Li, E. and Tsai, L. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Animals;Humans;Seizures;Open Reading Frames;Protein-Serine-Threonine Kinases;Gene Deletion;Genomic Library;Mice, Neurologic Mutants;Embryonic and Fetal Development;Crosses, Genetic;Cerebral Cortex;Neurons;Recombination, Genetic;Mice, Knockout;10 genetics malformation;Polymerase Chain Reaction;research support, u.s. gov't, p.h.s.;Mice;Cyclin-Dependent Kinase 5;Cyclin-Dependent Kinases;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {29-42},
	Pii = {S0896-6273(01)80044-1},
	Pubmed = {9010203},
	Title = {Mice lacking p35, a neuronal specific activator of Cdk5, display cortical lamination defects, seizures, and adult lethality},
	Uuid = {94101B09-067D-436C-ABB9-3F910F8A9A29},
	Volume = {18},
	Year = {1997}}

@article{Chaisuksunt:2000,
	Abstract = {Some neurons in the brain and spinal cord will regenerate axons into a living peripheral nerve graft inserted at the site of injury, others will not. We have examined the patterns of expression of four molecules thought to be involved in developmental and regenerative axonal growth, in the cerebellum and brainstem of adult rats, following the implantation into the cerebellum of peripheral nerve grafts. We also determined how the expression patterns observed correlate with the abilities of neurons in these regions to regenerate axons. Three days to 16 weeks after insertion of living tibial nerve autografts, neurons which had regenerated axons into the graft were retrogradely labelled from the distal extremity of the graft with cholera toxin conjugated to horseradish peroxidase, and sections through the cerebellum and brainstem were processed for visualization of transported tracer and/or hybridized with riboprobes to detect messenger RNAs for the cell recognition molecules L1 and CHL1 (close homologue of L1), growth-associated protein-43 and the cellular oncogene c-jun. Retrogradely labelled neurons were present in cerebellar deep nuclei close to the graft and in brainstem nuclei known to project to the cerebellum. Neurons in these same nuclei were found to have up-regulated expression of all four messenger RNAs. Individual retrogradely labelled neurons also expressed high levels of L1, CHL1, c-jun or growth-associated protein-43 messenger RNAs (and vice versa), and every messenger RNA investigated was co-localized with at least one other messenger RNA. Purkinje cells did not regenerate axons into the graft or up-regulate L1, CHL1 or growth-associated protein-43 messenger RNAs, but there was increased expression of c-jun messenger RNA in some Purkinje cells close to the graft. Freeze-killed grafts produced no retrograde labelling of neurons, and resulted in only transient and low levels of up-regulation of the tested molecules, mainly L1 and CHL1.These findings show that cerebellar deep nucleus neurons and precerebellar brainstem neurons, but not Purkinje cells, have a high propensity for axon regeneration, and that axonal regeneration by these neurons is accompanied by increased expression of L1, CHL1, c-jun and growth-associated protein-43. Furthermore, although the patterns of expression of the four molecules investigated are not identical in regenerating neuronal populations, it is probable that all four are up-regulated in all neurons whose axons regenerate into the grafts and that their up-regulation may be required for axon regeneration to occur. Finally, because c-jun up-regulation is seen in Purkinje cells close to the graft, unaccompanied by up-regulation of the other molecules investigated, c-jun up-regulation alone cannot be taken to reliably signify a regenerative response to axotomy.},
	Author = {Chaisuksunt, V. and Zhang, Y. and Anderson, P. N. and Campbell, G. and Vaudano, E. and Schachner, M. and Lieberman, A. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Tibial Nerve;Neural Cell Adhesion Molecules;GAP-43 Protein;Purkinje Cells;Tissue Distribution;Animals;Leukocyte L1 Antigen Complex;Rats;Female;Axons;Rats, Sprague-Dawley;Reference Values;RNA, Messenger;Proto-Oncogene Proteins c-jun;Nerve Regeneration;Membrane Glycoproteins;Neurons;Cerebellum;Neural Cell Adhesion Molecule L1;24 Pubmed search results 2008;Brain Stem;Research Support, Non-U.S. Gov't},
	Medline = {20453519},
	Nlm_Id = {7605074},
	Number = {1},
	Organization = {Department of Anatomy and Developmental Biology, University College London, Gower Street, WC1E 6BT, London, UK.},
	Pages = {87-108},
	Pii = {S0306452200002542},
	Pubmed = {10996461},
	Title = {Axonal regeneration from CNS neurons in the cerebellum and brainstem of adult rats: correlation with the patterns of expression and distribution of messenger RNAs for L1, CHL1, c-jun and growth-associated protein-43},
	Uuid = {0FD521FA-93BA-4F19-9D61-3EB8543E7667},
	Volume = {100},
	Year = {2000}}

@article{Chambers:2001,
	Abstract = {The olfactory bulb, neocortex and archicortex arise from a common pool of progenitors in the dorsal telencephalon. We studied the consequences of supplying excess Notch1 signal in vivo on the cellular and regional destinies of telencephalic precursors using bicistronic replication defective retroviruses. After ventricular injections mid-neurogenesis (E14.5), activated Notch1 retrovirus markedly inhibited the generation of neurons from telencephalic precursors, delayed the emergence of cells from the subventricular zone (SVZ), and produced an augmentation of glial progeny in the neo- and archicortex. However, activated Notch1 had a distinct effect on the progenitors of the olfactory bulb, markedly reducing the numbers of cells of any type that migrated there. To elucidate the mechanism of the cell fate changes elicited by Notch1 signals in the cortical regions, short- and long-term cultures of E14.5 telencephalic progenitors were examined. These studies reveal that activated Notch1 elicits a cessation of proliferation that coincides with an inhibition of the generation of neurons. Later, during gliogenesis, activated Notch1 triggers a rapid cellular proliferation with a significant increase in the generation of cells expressing GFAP. To examine the generation of cells destined for the olfactory bulb, we used stereotaxic injections into the early postnatal anterior subventricular zone (SVZa). We observed that precursors of the olfactory bulb responded to Notch signals by remaining quiescent and failing to give rise to differentiated progeny of any type, unlike cortical precursor cells, which generated glia instead of neurons. These data show that forebrain precursors vary in their response to Notch signals according to spatial and temporal cues, and that Notch signals influence the composition of forebrain regions by modulating the rate of proliferation of neural precursor cells.},
	Author = {Chambers, C. B. and Peng, Y. and Nguyen, H. and Gaiano, N. and Fishell, G. and Nye, J. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Development},
	Keywords = {10 Development;Signal Transduction;Recombinant Fusion Proteins/metabolism;Embryo/cytology/metabolism;Cells, Cultured;Rats;Animal;Neurons/*metabolism;Retroviridae/genetics/metabolism;Prosencephalon/cytology/*embryology/metabolism;Microscopy, Fluorescence;Membrane Proteins/*metabolism;Genetic Vectors;Support, Non-U.S. Gov't;Cell Size;Support, U.S. Gov't, P.H.S.;Olfactory Bulb/cytology/embryology;Mice;Cell Division;Immunohistochemistry;Neuroglia/metabolism;Stem Cells/*metabolism;F;Genes, Reporter},
	Number = {5},
	Organization = {Departments of Molecular Pharmacology &Biological Chemistry, Northwestern University Medical School, Chicago, IL 60611, USA.},
	Pages = {689-702.},
	Title = {Spatiotemporal selectivity of response to Notch1 signals in mammalian forebrain precursors},
	Uuid = {66DE6081-0136-48E7-B54A-97C295730010},
	Volume = {128},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11171394%20http://www.biologists.com/Development/128/05/dev9653.html}}

@article{Chan:2006,
	Abstract = {Despite intense study, the precise origin and cell lineage of microglia, the resident mononuclear phagocytes of the nervous system, are still a matter for debate. Unlike macroglia (astrocytes and oligodendrocytes) and neurons, which are derived from neuroectoderm, microglial progenitors arise from peripheral mesodermal (myeloid) tissue. The view still commonly held is that tissue-resident mononuclear phagocytes (including microglia) are derived from circulating blood monocytes and these take up residence late in gestation and postnatally. However, microglial progenitors colonise the nervous system primarily during embryonic and fetal periods of development. Recent evidence indicates differences between the lineage of mononuclear phagocytes during the embryonic and fetal period from that in the neonate and adult-mononuclear phagocytes that take up residence within tissues are derived from a lineage of myeloid cells that is independent of the monocyte lineage. Our own findings on the development and differentiation of microglial progenitors, taken together with findings by other investigators, and in the context of the heterogeneity between myeloid differentiation in the fetus and in the adult, support the view that microglia are derived prenatally from mesodermal progenitors that are distinct from monocytes. Furthermore, microglial progenitors colonise the nervous system via extravascular routes initially. These findings challenge the concept that resident microglia in the nervous system are derived from circulating blood monocytes. Work is still underway to establish the tissue of origin and lineage of microglial progenitors in vivo. This information is critical not only from a developmental perspective, but significantly from a therapeutic viewpoint, as (i) the unique property of microglial progenitors to colonise the nervous system from the periphery allows these cells to be exploited as a biological and non-invasive means for cell therapy by delivering genes to the nervous system (microglial engraftment), and (ii) there are indications that microglial progenitors are specifically able to home to the nervous system. Use of microglial progenitors for therapeutic purposes becomes feasible only if the origin and cell lineage of these microglial progenitors are known and these cells can be isolated and manipulated in vitro (i.e., to express specific trophic factors) prior to therapeutic transfer (e.g., intravenously) in vivo. In this paper, we shall briefly consider the existing concepts on the origin and lineage of microglial progenitors and discuss new hypotheses in the light of emerging data that suggest clear differences between fetal and adult ontogeny of myeloid cells.},
	Author = {Chan, and Kohsaka, and Rezaie,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0165-0173},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {8908638},
	Organization = {Department of Anatomy, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.},
	Pii = {S0165-0173(06)00118-4},
	Pubmed = {17188751},
	Title = {The origin and cell lineage of microglia-New concepts},
	Uuid = {FCE99306-B317-4A82-8B42-AEBC3C1860F9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainresrev.2006.11.002}}

@article{Chanas-Sacre:2000,
	Abstract = {Radial glial cells play a major guidance role for migrating neurons during central nervous system (CNS) histogenesis but also play many other crucial roles in early brain development. Being among the earliest cells to differentiate in the early CNS, they provide support for neuronal migration during embryonic brain development; provide instructive and neurotrophic signals required for the survival, proliferation, and differentiation of neurons; and may be multipotential progenitor cells that give rise to various cell types, including neurons. Radial glial cells constitute a major cell type of the developing brain in numerous nonmammalian and mammalian vertebrates, increasing in complexity in parallel with the organization of the nervous tissue they help to build. In mammalian species, these cells transdifferentiate into astrocytes when neuronal migration is completed, whereas, in nonmammalian species, they persist into adulthood as a radial component of astroglia. Thus, our perception of radial glia may have to change from that of path-defining cells to that of specialized precursor cells transiently fulfilling a guidance role during brain histogenesis. In that respect, their apparent change of phenotype from radial fiber to astrocyte probably constitutes one of the most common transdifferentiation events in mammalian development.},
	Author = {Chanas-Sacre, G. and Rogister, B. and Moonen, G. and Leprince, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Cell Differentiation;Neuroglia/*physiology;Human;Phenotype;Animal;Cell Lineage/physiology;11 Glia;Signal Transduction/*physiology;Cell Movement/*physiology;Support, Non-U.S. Gov't;Astrocytes/physiology;G;Cell Adhesion Molecules, Neuron-Glia/*physiology},
	Number = {4},
	Organization = {Center for Cellular and Molecular Neurobiology, University of Liege, Liege, Belgium.},
	Pages = {357-63.},
	Title = {Radial glia phenotype: origin, regulation, and transdifferentiation},
	Uuid = {9F6E2B37-DC23-4D53-8D92-0CF33C1E4C56},
	Volume = {61},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10931521}}

@article{Chang:2000,
	Abstract = {Cerebral inflammation often originates in a region where neuronal death occurs and thereafter slowly spreads outward. This study aimed to elucidate the roles of neurons in modulating the production of inflammatory factors stimulated by the bacterial endotoxin lipopolysaccharide (LPS). Culturing neurons with mixed glia reduced nitrite and tumor necrosis factor-alpha (TNF-alpha) production compared to cultures with only mixed glia, and shifted the dose-response curve to the right. The decreased nitrite and TNF-alpha production were not due to the cytotoxicity of LPS. Immunocytochemical analysis of glia-neuron co-cultures revealed the morphological changes in the activated microglia. Culturing PC12 cells with rat mixed-glia also reduced nitrite production. The influence of neurons on glial inflammation was partly due to the cell-cell contacts between neurons and glia via neural cell adhesion molecules (NCAM) because NCAM significantly reduced LPS-stimulated nitrite production. These results demonstrate that neurons reduce the production of inflammatory factors by glia. Since cerebral inflammation is important in many neurological disorders, this study might provide insight about the role of glia-neuron interactions in inflammatory responses in the brain.},
	Author = {Chang, R. C. and Hudson, P. and Wilson, B. and Haddon, L. and Hong, J. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Dose-Response Relationship, Drug;Tumor Necrosis Factor;Animals;Cells, Cultured;Rats;Lipopolysaccharides;Cell Communication;Nitric-Oxide Synthase;L-Lactate Dehydrogenase;11 Glia;PC12 Cells;Rats, Inbred F344;Animals, Newborn;Coculture;Cell Size;Neurons;Neuroglia;Down-Regulation;Mice;Inflammation;Nitric Oxide;Neural Cell Adhesion Molecules},
	Medline = {20108612},
	Month = {1},
	Nlm_Id = {0045503},
	Number = {2},
	Organization = {Neuropharmacology Section, MD F1-01, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.},
	Pages = {236-44},
	Pii = {S0006899399022556},
	Pubmed = {10640621},
	Title = {Influence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-alpha by cultured glia},
	Uuid = {6FF741D3-0ED0-4F06-B988-CDA6AE2E7927},
	Volume = {853},
	Year = {2000}}

@article{Chang:2001,
	Abstract = {The microenvironment of the CNS has been considered to tonically inhibit glial activities. It has been shown that glia become activated where neuronal death occurs in the aging brain. We have previously demonstrated that neurons tonically inhibit glial activities including their responses to the bacterial endotoxin lipopolysaccharide (LPS). It is not clear whether activation of glia, especially microglia in the aging brain, is the consequence of disinhibition due to neuronal death. This study was designed to determine if glia regain their responsiveness to LPS once the neurons have died in aged cultures. When cultured alone, glia from postnatal day one rat mesencephalons stimulated with LPS (0.1-1000 ng/mL) produced both nitric oxide (NO) and tumor necrosis factor alpha (TNFalpha), yielding a sigmoid and a bell-shaped curve, respectively. When neuron-containing cultures were prepared from embryonic day 14/15 mesencephalons, the shape of the dose-response curve for NO was monotonic and the bell-shaped curve for TNFalpha production was shifted to the right. After 1 month of culture under conditions where neurons die, the production curves for NO and TNFalpha in LPS-stimulated glia shifted back to the left compared to mixed neuron-glia cultures. Immunostaining of rat microglia for the marker CR3 (the receptor for complement component C3) demonstrated that high concentrations of LPS (1 microg/mL) reduced the number of microglia in mixed-glial cultures. In contrast, reduction of CR3 immunostaining was not observed in LPS-stimulated mixed neuron-glia cultures. Taken together, the results demonstrate that disinhibition of the glial response to LPS occurs after neurons die in aged cultures. Once neurons have died, the responsiveness of glia to LPS is restored. Neurons prevented injury to microglia by reducing their responsiveness to LPS. This study broadens our understanding of the ways in which the CNS microenvironment affects cerebral inflammation.},
	Author = {Chang, R. C. and Chen, W. and Hudson, P. and Wilson, B. and Han, D. S. and Hong, J. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Cell Survival;Dose-Response Relationship, Drug;Tumor Necrosis Factor;Animals;Cells, Cultured;Rats;Microglia;Lipopolysaccharides;Cell Count;11 Glia;Time Factors;Rats, Inbred F344;Membrane Glycoproteins;Coculture;Neuroglia;Mesencephalon;Neurons;Nitric Oxide},
	Medline = {21103903},
	Month = {2},
	Nlm_Id = {2985190R},
	Number = {4},
	Organization = {Neuropharmacology section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, North Carolina, USA. rccchang\@hkucc.hku.hk},
	Pages = {1042-9},
	Pubmed = {11181823},
	Title = {Neurons reduce glial responses to lipopolysaccharide (LPS) and prevent injury of microglial cells from over-activation by LPS},
	Uuid = {E040697E-CEC9-4B02-AE9E-81BE0BC1FDD6},
	Volume = {76},
	Year = {2001},
	url = {papers/Chang_JNeurochem2001.pdf}}

@article{Chang:2008,
	Abstract = {Phenotypic cell-to-cell variability within clonal populations may be a manifestation of 'gene expression noise', or it may reflect stable phenotypic variants. Such 'non-genetic cell individuality' can arise from the slow fluctuations of protein levels in mammalian cells. These fluctuations produce persistent cell individuality, thereby rendering a clonal population heterogeneous. However, it remains unknown whether this heterogeneity may account for the stochasticity of cell fate decisions in stem cells. Here we show that in clonal populations of mouse haematopoietic progenitor cells, spontaneous 'outlier' cells with either extremely high or low expression levels of the stem cell marker Sca-1 (also known as Ly6a; ref. 9) reconstitute the parental distribution of Sca-1 but do so only after more than one week. This slow relaxation is described by a gaussian mixture model that incorporates noise-driven transitions between discrete subpopulations, suggesting hidden multi-stability within one cell type. Despite clonality, the Sca-1 outliers had distinct transcriptomes. Although their unique gene expression profiles eventually reverted to that of the median cells, revealing an attractor state, they lasted long enough to confer a greatly different proclivity for choosing either the erythroid or the myeloid lineage. Preference in lineage choice was associated with increased expression of lineage-specific transcription factors, such as a >200-fold increase in Gata1 (ref. 10) among the erythroid-prone cells, or a >15-fold increased PU.1 (Sfpi1) (ref. 11) expression among myeloid-prone cells. Thus, clonal heterogeneity of gene expression level is not due to independent noise in the expression of individual genes, but reflects metastable states of a slowly fluctuating transcriptome that is distinct in individual cells and may govern the reversible, stochastic priming of multipotent progenitor cells in cell fate decision.},
	Author = {Chang, Hannah H. and Hemberg, Martin and Barahona, Mauricio and Ingber, Donald E. and Huang, Sui},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Transcription, Genetic;Cell Differentiation;Animals;Trans-Activators;GATA1 Transcription Factor;Antigens, Ly;Myeloid Cells;research support, non-u.s. gov't;Gene Expression Profiling;Cell Line;Erythroid Cells;Cell Lineage;research support, n.i.h., extramural;Hematopoietic Stem Cells;Mice;Proto-Oncogene Proteins;Membrane Proteins;24 Pubmed search results 2008;Clone Cells;research support, u.s. gov't, non-p.h.s.;Stochastic Processes},
	Month = {5},
	Nlm_Id = {0410462},
	Number = {7194},
	Organization = {Vascular Biology Programme, Department of Pathology and Surgery, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {544-7},
	Pii = {nature06965},
	Pubmed = {18497826},
	Title = {Transcriptome-wide noise controls lineage choice in mammalian progenitor cells},
	Uuid = {0E2B7A0C-09AC-498D-ABF3-CF4A2E10D507},
	Volume = {453},
	Year = {2008},
	url = {papers/Chang_Nature2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06965}}

@article{Chang:2005,
	Abstract = {OBJECTIVE: To define the behavioral profile of periventricular nodular heterotopia (PNH), a malformation of cortical development that is associated with seizures but reportedly normal intelligence, and to correlate the results with anatomic and clinical features of this disorder. METHODS: Ten consecutive subjects with PNH, all with epilepsy and at least two periventricular nodules, were studied with structural MRI and neuropsychological testing. Behavioral results were statistically analyzed for correlation with other features of PNH. RESULTS: Eight of 10 subjects had deficits in reading skills despite normal intelligence. Processing speed and executive function were also impaired in some subjects. More marked reading difficulties were seen in subjects with more widely distributed heterotopia. There was no correlation between reading skills and epilepsy severity or antiepileptic medication use. CONCLUSION: The neuronal migration disorder of periventricular nodular heterotopia is associated with an impairment in reading skills despite the presence of normal intelligence.},
	Author = {Chang, B. S. and Ly, J. and Appignani, B. and Bodell, A. and Apse, K. A. and Ravenscroft, R. S. and Sheen, V. L. and Doherty, M. J. and Hackney, D. B. and O'Connor, M. and Galaburda, A. M. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1526-632X},
	Journal = {Neurology},
	Keywords = {Neuropsychological Tests;Research Support, Non-U.S. Gov't;Magnetic Resonance Imaging;Humans;Middle Aged;21 Epilepsy;Female;Epilepsy;Predictive Value of Tests;Cell Movement;Dyslexia;Male;Intelligence;Research Support, U.S. Gov't, P.H.S.;Nervous System Malformations;Cerebral Cortex;Neurons;21 Neurophysiology;Adult;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Choristoma;Adolescent},
	Month = {3},
	Nlm_Id = {0401060},
	Number = {5},
	Organization = {Division of Neurogenetics, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. bchang\@bidmc.harvard.edu},
	Pages = {799-803},
	Pii = {64/5/799},
	Pubmed = {15753412},
	Title = {Reading impairment in the neuronal migration disorder of periventricular nodular heterotopia},
	Uuid = {396B8700-7587-4BEE-8EF0-47A5E7E0E31F},
	Volume = {64},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1212/01.WNL.0000152874.57180.AF}}

@article{Chang:2006,
	Abstract = {Mutations in the MECP2 gene cause Rett syndrome (RTT). Bdnf is a MeCP2 target gene; however, its role in RTT pathogenesis is unknown. We examined Bdnf conditional mutant mice for RTT-relevant pathologies and observed that loss of BDNF caused smaller brain size, smaller CA2 neurons, smaller glomerulus size, and a characteristic hindlimb-clasping phenotype. BDNF protein level was reduced in Mecp2 mutant mice, and deletion of Bdnf in Mecp2 mutants caused an earlier onset of RTT-like symptoms. To assess whether this interaction was functional and potentially therapeutically relevant, we increased BDNF expression in the Mecp2 mutant brain with a conditional Bdnf transgene. BDNF overexpression extended the lifespan, rescued a locomotor defect, and reversed an electrophysiological deficit observed in Mecp2 mutants. Our results provide in vivo evidence for a functional interaction between Mecp2 and Bdnf and demonstrate the physiological significance of altered BDNF expression/signaling in RTT disease progression.},
	Author = {Chang, Qiang and Khare, Gargi and Dani, Vardhan and Nelson, Sacha and Jaenisch, Rudolf},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {research support, non-u.s. gov't ;Methyl-CpG-Binding Protein 2;Disease Models, Animal;24 Pubmed search results 2008;Immunohistochemistry;Male;Animals;Brain;comparative study ;Rett Syndrome;Electric Stimulation;RNA, Messenger;research support, n.i.h., extramural ;Motor Activity;Disease Progression;Behavior, Animal;Brain-Derived Neurotrophic Factor;Mutation;Gene Expression Regulation;Organ Size;Action Potentials;Patch-Clamp Techniques;Female;Enzyme-Linked Immunosorbent Assay;Animals, Newborn;Mice, Knockout;21 Neurophysiology;Mice;Neurons;Humans;in vitro ;Reverse Transcriptase Polymerase Chain Reaction},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA.},
	Pages = {341-8},
	Pii = {S0896-6273(06)00010-9},
	Pubmed = {16446138},
	Title = {The disease progression of Mecp2 mutant mice is affected by the level of BDNF expression},
	Uuid = {6853FBC3-7D8A-46E7-9960-4036757111F7},
	Volume = {49},
	Year = {2006},
	url = {papers/Chang_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.12.027}}

@article{Chao:2007,
	Abstract = {MeCP2 is a transcriptional repressor critical for normal neurological function. Prior studies demonstrated that either loss or doubling of MeCP2 results in postnatal neurodevelopmental disorders. To understand the impact of MeCP2 expression on neuronal function, we studied the synaptic properties of individual neurons from mice that either lack or express twice the normal levels of MeCP2. Hippocampal glutamatergic neurons that lack MeCP2 display a 46\%reduction in synaptic response, whereas neurons with doubling of MeCP2 exhibit a 2-fold enhancement in synaptic response. Further analysis shows that these changes were primarily due to the number of synapses formed. These results reveal that MeCP2 is a key rate-limiting factor in regulating glutamatergic synapse formation in early postnatal development and that changes in excitatory synaptic strength may underlie global network alterations in neurological disorders due to altered MeCP2 levels.},
	Author = {Chao, Hsiao-Tuan T. and Zoghbi, Huda Y. and Rosenmund, Christian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.},
	Pages = {58-65},
	Pii = {S0896-6273(07)00647-2},
	Pubmed = {17920015},
	Title = {MeCP2 controls excitatory synaptic strength by regulating glutamatergic synapse number},
	Uuid = {CE053998-14BC-4E10-A1FB-D81D0E212059},
	Volume = {56},
	Year = {2007},
	url = {papers/Chao_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.08.018}}

@article{Charlton:2000,
	Abstract = {Considerable evidence points to an involvement of neural cell adhesion molecule (NCAM) in myoblast fusion. Changes in the level of NCAM expression, isoform specificity, and localization in muscle cells and tissues correspond to key morphogenetic events during muscle differentiation and repair. Furthermore, anti-NCAM antibodies have been shown by others to reduce the rate of myoblast fusion, whereas overexpression of NCAM cDNAs increases the rate of myoblast fusion compared to controls. In this study we have used a novel fusion assay based on intracistronic complementation of lacZ, in combination with fluorescent X-gal histochemistry and immunocytochemistry to assess levels of NCAM expression in individual muscle cells. Our results indicate that a substantial proportion of newly fused myoblasts have NCAM expression levels unchanged from the levels of the surrounding unfused population suggesting that increased expression of NCAM is not required for wild-type myoblasts to fuse. Moreover, pure populations of primary myoblasts isolated from mice homozygous null for NCAM and therefore lacking the molecule, when placed in differentiation medium, consistently fused to form contractile myotubes with kinetics equivalent to wild-type primary myoblasts. We conclude that the increase in expression of NCAM, although typically observed during myogenesis, is not essential to myoblast fusion to form myotubes.},
	Author = {Charlton, C. A. and Mohler, W. A. and Blau, H. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {Transfection;Gene Expression Regulation, Developmental;Neural Cell Adhesion Molecules;Cell Adhesion;Research Support, Non-U.S. Gov't;Cell Differentiation;Kinetics;Muscles;Mice, Knockout;Cell Fusion;Research Support, U.S. Gov't, P.H.S.;Microscopy, Fluorescence;Animals;Cells, Cultured;Mice;Genes, Reporter;24 Pubmed search results 2008},
	Medline = {20237581},
	Month = {5},
	Nlm_Id = {0372762},
	Number = {1},
	Organization = {Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, California 94305, USA.},
	Pages = {112-9},
	Pii = {S0012-1606(00)99654-4},
	Pubmed = {10772795},
	Title = {Neural cell adhesion molecule (NCAM) and myoblast fusion},
	Uuid = {9AD35254-3357-40B1-B7A2-EA463B1B955A},
	Volume = {221},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/dbio.2000.9654}}

@article{Chavez:2002,
	Abstract = {Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that regulates the adaptive response to hypoxia in mammalian cells. It consists of a regulatory subunit HIF-1alpha, which accumulates under hypoxic conditions, and a constitutively expressed subunit HIF-1beta. In this study we analyzed HIF-1alpha expression in the rat cerebral cortex after transient global ischemia induced by cardiac arrest and resuscitation. Our results showed that HIF-1alpha accumulates as early as 1 hr of recovery and persists for at least 7 d. In addition, the expression of HIF-1 target genes, erythropoietin and Glut-1, were induced at 12 hr to 7d of recovery. A logical explanation for HIF-1alpha accumulation might be that the brain remained hypoxic for prolonged periods after resuscitation. By using the hypoxic marker 2-(2-nitroimidazole-1[H]-y1)-N-(2,2,3,3,3-pentafluoropropyl)-acetamide (EF5), we showed that the brain is hypoxic during the first hours of recovery from cardiac arrest, but the tissue is no longer hypoxic at 2 d. Thus, the initial ischemic episode must have activated other nonhypoxic mechanisms that maintain prolonged HIF-1alpha accumulation. One such mechanism might be initiated by insulin-like growth factor-1 (IGF-1). Our results showed that IGF-1 expression was upregulated after cardiac arrest and resuscitation. In addition, we showed that IGF-1 was able to induce HIF-1alpha in pheochromocytoma cells and cultured neurons as well as in the brain of rats that received intracerebroventricular and systemic IGF-1 infusion. Moreover, infusion of a selective IGF-1 receptor antagonist abrogates HIF-1alpha accumulation after cardiac arrest and resuscitation. Our study suggest that activation of HIF-1 might be part of the mechanism by which IGF-1 promotes cell survival after cerebral ischemia. 1529-2401 Journal Article},
	Author = {Chavez, J. C. and LaManna, J. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:43 -0400},
	Journal = {J Neurosci},
	Keywords = {Receptor, IGF Type 1/antagonists &inhibitors/biosynthesis;Animals;Insulin-Like Growth Factor I/*metabolism/pharmacology;Hydrocarbons, Fluorinated;Rats;Up-Regulation;Neurons/drug effects/metabolism;Nuclear Proteins/genetics/*metabolism;Etanidazole/*analogs &derivatives;Rats, Wistar;*Ubiquitin-Protein Ligases;Male;*Tumor Suppressor Proteins;Disease Models, Animal;PC12 Cells;DNA-Binding Proteins/genetics/*metabolism;Cardiopulmonary Resuscitation;Ligases/metabolism;Cerebral Cortex/cytology/drug effects/*metabolism;Heart Arrest, Induced;Support, U.S. Gov't, P.H.S.;04 Adult neurogenesis factors;Peptide Hydrolases/metabolism;Immunohistochemistry;C pdf;Hypoxia, Brain/metabolism;Ischemic Attack, Transient/*metabolism},
	Number = {20},
	Organization = {Department of Anatomy, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4938, USA.},
	Pages = {8922-31},
	Title = {Activation of hypoxia-inducible factor-1 in the rat cerebral cortex after transient global ischemia: potential role of insulin-like growth factor-1},
	Uuid = {D94490D2-8822-4D78-9657-C40647686904},
	Volume = {22},
	Year = {2002},
	url = {papers/Chavez_JNeurosci2002.pdf}}

@article{Chazal:2000,
	Abstract = {In vertebrates, interneurons of the olfactory bulb (OB) are generated postnatally and throughout life at the subventricular zone of the forebrain. The neuronal precursors migrate tangentially through the forebrain using a well defined pathway, the rostral migratory stream (RMS), and a particular mode of migration in a chain-like organization. A severe size reduction of the OB represents the most striking morphological phenotype in neural cell adhesion molecule (NCAM)- deficient mice. This defect has been traced back to a migration deficit of the precursors in the RMS and linked to the lack of the polysialylated form of NCAM. In this study we investigate the morphological alterations and functional properties of the RMS in mice totally devoid of all isoforms of NCAM and polysialic acid (PSA). We show that a morphologically altered, but defined and continuous pathway exists in mutants, and we present in vivo and in vitro evidence that PSA-NCAM in the RMS is not essential for the formation and migration of chains. Instead, we find a massive gliosis associated with the formation of membrane specializations in a heterotypic manner, linking precursors to astrocytes. This finding and the over-representation and defasciculation of axons in the pathway suggest that important interactions between migrating cells and their stationary environment are perturbed in the mutants. Finally, we used transplantation experiments to demonstrate that lack of PSA-NCAM leads to a decrease but not a total blockade of migration and demonstrate that the mutant RMS is functional in transporting normal neuronal precursors to the OB.},
	Author = {Chazal, G. and Durbec, P. and Jankovski, A. and Rougon, G. and Cremer, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Movement/*physiology;Stem Cells/physiology;Olfactory Bulb/abnormalities/*physiology/ultrastructure;Animal;Neurons/cytology/*physiology/ultrastructure;Mice, Inbred C57BL;Sialic Acids/genetics;Axons/physiology/ultrastructure;Crosses, Genetic;Neuroglia/cytology/physiology/ultrastructure;Neural Cell Adhesion Molecules/chemistry/genetics/*physiology;Support, Non-U.S. Gov't;Cerebral Ventricles/cytology/physiology;Mice, Knockout;Olfactory Pathways/cytology/physiology;04 Adult neurogenesis factors;Mice;Prosencephalon/cytology/*physiology/ultrastructure;C pdf;Protein Isoforms/deficiency/genetics/physiology;Organ Culture},
	Number = {4},
	Organization = {Laboratoire de Genetique et Physiologie du Developpement, Institut de Biologie du Developpement de Marseille, Centre National de la Recherche Scientifique/ Universite de la Sante et de la Recherche Medicale, INSERM, Paris Cedex, France.},
	Pages = {1446-57.},
	Title = {Consequences of neural cell adhesion molecule deficiency on cell migration in the rostral migratory stream of the mouse},
	Uuid = {32A22AA6-9886-45E0-A8D8-82C41C0B6E64},
	Volume = {20},
	Year = {2000},
	url = {papers/Chazal_JNeurosci2000.pdf}}

@article{Chen:2006,
	Abstract = {An important issue in stem cell biology relates to mechanisms of cellular plasticity. Specifically, could any observed multipotency of, e.g., adult stem cells arise from true transdifferentiation or as a result of cell-cell fusion? We studied this issue using a culture paradigm of astrocyte monolayers and multipotent neurospheres generated from neonatal cerebellar cortex and the subventricular zone (SVZ). Based on fluorescence in situ hybridization (FISH), cells from these cultures were found to contain an abnormal number of sex chromosomes, suggesting that cellular fusion is a common in vitro occurrence. A Cre/lox recombination method was also exploited to further confirm the evidence of fusion. Next, we assessed the potential of fusogenic microglial involvement by combining CD11b immunolabeling with FISH sex chromosome analysis. Differentiating neurospheres were also studied from the PU.1 knockout mouse that lacks cells of myeloid origin, presumed to be a source of central nervous system microglia. Very few cells immunopositive for the microglial marker CD11b were found to be aneuploid, and there was no difference in fusion frequency between PU.1+/+ and PU.1-/- neurospheres. These results, together, suggest that stem and/or progenitor cells that generate neurons and glia in culture possess the ability to generate fused polyploidal cells, but microglial participation is not a requirement for fusion to occur. In addition to caution that should be exerted during the interpretation of in vitro neural cell plasticity, the data also suggest that novel therapeutic treatments could be designed that exploit cellular fusion in rescue paradigms for degenerating neuronal populations.},
	Author = {Chen, and Laywell, and Marshall, and Walton, and Zheng, and Steindler,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {03 Adult neurogenesis progenitor source;08 Aberrant cell cycle;11 Glia;22 Stem cells;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {0370712},
	Organization = {Department of Neuroscience, The McKnight Brain Institute of the University of Florida, PO Box 100244, Gainesville, FL 32610, USA.},
	Pii = {S0014-4886(05)00421-8},
	Pubmed = {16406350},
	Title = {Fusion of neural stem cells in culture},
	Uuid = {B751DF09-7CD8-4F49-B996-3AC5A6132D5E},
	Year = {2006},
	url = {papers/Chen_ExpNeurol2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2005.11.016}}

@article{Chen:2000a,
	Abstract = {Increasing evidence suggests that mood disorders are associated with a reduction in regional CNS volume and neuronal and glial cell atrophy or loss. Lithium, a mainstay in the treatment of mood disorders, has recently been demonstrated to robustly increase the levels of the cytoprotective B-cell lymphoma protein-2 (bcl-2) in areas of rodent brain and in cultured cells. In view of bcl-2's antiapoptotic and neurotrophic effects, the present study was undertaken to determine if lithium affects neurogenesis in the adult rodent hippocampus. Mice were chronically treated with lithium, and 5-bromo-2-deoxyuridine (BrdU) labeling of dividing cells was conducted over 12 days. Immunohistochemical analysis was undertaken 1 day after the last injection, and three-dimensional stereological cell counting revealed that lithium produced a significant 25\%increase in the BrdU-labeled cells in the dentate gyrus. Double-labeling immunofluorescence studies were undertaken to co-localize BrdU-positive cells with neuron-specific nuclear protein and showed that approximately 65\%of the cells were double-labeled. These results add to the growing body of evidence suggesting that mood stabilizers and antidepressants exert neurotrophic effects and may therefore be of use in the long-term treatment of other neuropsychiatric disorders.},
	Author = {Chen, G. and Rajkowska, G. and Du, F. and Seraji-Bozorgzad, N. and Manji, H. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {J Neurochem},
	Keywords = {Proto-Oncogene Proteins c-bcl-2/metabolism;Antigens, Differentiation/metabolism;Phenotype;Lithium/*pharmacology;Animal;Hippocampus/cytology/*drug effects/metabolism;Mice, Inbred C57BL;Nerve Regeneration/drug effects;Male;Neurons/cytology/*drug effects/metabolism;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice;Immunohistochemistry;C pdf;Bromodeoxyuridine;Cell Division/drug effects},
	Number = {4},
	Organization = {Laboratory of Molecular Pathophysiology, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. gchen\@med.wayne.edu},
	Pages = {1729-34.},
	Title = {Enhancement of hippocampal neurogenesis by lithium},
	Uuid = {8B65E5FC-0B7D-421D-A472-DDA53AF94D85},
	Volume = {75},
	Year = {2000},
	url = {papers/Chen_JNeurochem2000}}

@article{Chen:1999,
	Abstract = {Qualitative and quantitative changes were found in the cerebellar circuitry of old as compared to young rats. The old group had a reduced number of synapses (at least 30\%), however, there was an increase in the size of remaining synaptic components (13.5\%for spine head volume, 66\%for bouton volume, and 17\%for the area of synaptic contact zones). Furthermore, there were pronounced morphological changes in the older group appearing as: 1) prominent lipofuscin bodies in Purkinje cell somata, 2) numerous myelinated fibers in the lower part of the molecular layer, 3) tortuous Purkinje cell dendrites in a thinned molecular layer, and 4) abundant vacuolar profiles and membrane swirls in small and intermediate-sized dendrites. Our findings suggest that Purkinje cell dendrites are dying-back reducing the target field for granule cells and that remaining synaptic sites compensate by increasing synaptic contact area as well as the size of pre- and postsynaptic structures.},
	Author = {Chen, S. and Hillman, D. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Purkinje Cells;Myelin Sheath;Synapses;Animals;Aging;Rats;Neuronal Plasticity;Vacuoles;Female;Axons;Endoplasmic Reticulum;Not relevant;Calcium-Binding Protein, Vitamin D-Dependent;11 Glia;Dendrites;Rats, Inbred F344;Lipofuscin;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Nerve Tissue Proteins},
	Medline = {20085219},
	Month = {3},
	Nlm_Id = {0364620},
	Number = {3},
	Organization = {Departments of Otolaryngology and Physiology/Biophysics, New York University Medical Center, 550 First Avenue, New York, NY 10016, USA.},
	Pages = {187-96},
	Pubmed = {10617901},
	Title = {Dying-back of Purkinje cell dendrites with synapse loss in aging rats},
	Uuid = {4E0D75B6-63B9-4441-9C49-0056C2F7F20B},
	Volume = {28},
	Year = {1999},
	url = {papers/Chen_JNeurocytol1999.pdf}}

@article{Chen:2000,
	Abstract = {PURPOSE: Misplaced (heterotopic) cortical neurons are a common feature of developmental epilepsies. To better understand seizure disorders associated with cortical heterotopia, the sites of aberrant discharge activity were investigated in vivo and in vitro in a seizure-prone mutant rat (tish) exhibiting subcortical band heterotopia. METHODS: Depth electrode recordings and postmortem assessment of regional c-fos mRNA levels were used to characterize the distribution of aberrant discharge activity during spontaneous seizures in vivo. Electrophysiologic recordings of spontaneous and evoked activity also were performed by using in vitro brain slices from the tish rat treated with proconvulsant drugs (penicillin and 4-aminopyridine). RESULTS: Depth electrode recordings demonstrate that seizure activity begins almost simultaneously in the normotopic and heterotopic areas of the tish neocortex. Spontaneous seizures induce c-fos mRNA in normotopic and heterotopic neocortical areas, and limbic regions. The threshold concentrations of proconvulsant drugs for inducing epileptiform spiking were similar in the normotopic and heterotopic areas of tish brain slices. Manipulations that blocked communication between the normotopic and heterotopic areas of the cortex inhibited spiking in the heterotopic, but not the normotopic, area of the cortex. CONCLUSIONS: These findings indicate that aberrant discharge activity occurs in normotopic and heterotopic areas of the neocortex, and in certain limbic regions during spontaneous seizures in the tish rat. Normotopic neurons are more prone to exhibit epileptiform activity than are heterotopic neurons in the tish cortex, and heterotopic neurons are recruited into spiking by activity initiated in normotopic neurons. The findings indicate that seizures in the tish brain primarily involve telencephalic structures, and suggest that normotopic neurons are responsible for initiating seizures in the dysplastic neocortex.},
	Author = {Chen, Z. F. and Schottler, F. and Bertram, E. and Gall, C. M. and Anzivino, M. J. and Lee, K. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:45:42 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Electrophysiology;Animals;In Vitro;Evoked Potentials;Rats;Seizures;Brain;21 Epilepsy;Epilepsy;Genes, fos;RNA, Messenger;Tetrodotoxin;Get paper from library;In Situ Hybridization;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;21 Neurophysiology;24 Pubmed search results 2008;Autoradiography;Penicillin G;Electrodes, Implanted;Rats, Mutant Strains},
	Medline = {20264387},
	Month = {5},
	Nlm_Id = {2983306R},
	Notes = {have print},
	Number = {5},
	Organization = {Department of Neuroscience, University of Virginia Health Science Center, Charlottesville, Virginia 22908, USA.},
	Pages = {493-501},
	Pubmed = {10802753},
	Title = {Distribution and initiation of seizure activity in a rat brain with subcortical band heterotopia},
	Uuid = {B46F43C4-D4ED-4291-89DF-09E8AF188F37},
	Volume = {41},
	Year = {2000},
	url = {papers/Chen_Epilepsia2000.pdf}}

@article{Chen:2002,
	Abstract = {Following peripheral nerve transection, CX3CR1 and TGF-beta1 are increased in a time-dependent manner within the injured facial motor nucleus. To explore the relationship between TGF-beta1 and CX3CR1 in the CNS, the effects of TGF-beta1 on CX3CR1 mRNA, protein and fractalkine-dependent stimulation of signal transduction cascades in primary cultures of rat microglia were examined. TGF-beta1 increased steady state levels of CX3CR1 mRNA, 125I-fractalkine binding sites and blunted fractalkine-stimulated ERK1/2 phosphorylation. The half-life of CX3CR1 mRNA was unaltered by TGF-beta1 and two potential Smad binding elements (SBEs) were identified in the rat CX3CR1 promoter. TGF-beta1 may shift fractalkine-dependent signaling away from activation of ERK1/2 towards other pathways and/or may provide a mechanism for microglia to more strongly adhere to neurons.},
	Author = {Chen, Shuzhen and Luo, Defang and Streit, Wolfgang J. and Harrison, Jeffrey K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Dose-Response Relationship, Drug;Signal Transduction;Nerve Degeneration;Animals;Gene Expression Regulation;Up-Regulation;Rats;Transforming Growth Factor beta;Cells, Cultured;Microglia;Rats, Sprague-Dawley;RNA, Messenger;Not relevant;11 Glia;Time Factors;Chemokines, CX3C;Animals, Newborn;Receptors, Interleukin-8A;Support, U.S. Gov't, P.H.S.;Membrane Proteins;Mitogen-Activated Protein Kinases;Transcription, Genetic},
	Medline = {22336839},
	Month = {12},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Pharmacology and Therapeutics, College of Medicine, University of Florida, Gainesville, FL 32610-0267, USA.},
	Pages = {46-55},
	Pii = {S0165572802003545},
	Pubmed = {12446007},
	Title = {TGF-beta1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia},
	Uuid = {CCAE918A-039B-4AA5-BE97-F22835215BF3},
	Volume = {133},
	Year = {2002}}

@article{Chen:2003a,
	Abstract = {Neuronal heterotopia has a strong association with epilepsy, but the mechanisms that underlie this relationship are largely unknown. We have utilized the in utero irradiated rat model to study circuit abnormalities in experimentally induced subcortical heterotopic gray matter. Spontaneous and miniature inhibitory (IPSCs) and excitatory (EPSCs) postsynaptic currents were recorded from visualized heterotopic pyramidal neurons in in vitro hemispheric slices and compared with control neocortical pyramidal neurons using the whole cell patch-clamp technique. The frequency of spontaneous and miniature IPSCs was significantly reduced in pyramidal neurons from heterotopic cortex. Amplitude and kinetics of IPSCs were not different between the two groups. Spontaneous and miniature EPSCs were not different between the two groups. Short-term synaptic plasticity of stimulus-evoked EPSCs showed depression in heterotopic neurons and facilitation in control pyramidal neurons. This study shows a selective impairment of the GABAergic circuitry in experimental heterotopic gray matter. We have reported similar findings in normotopic dysplastic cortex from this model. Taken together, these studies demonstrate a pervasive defect in inhibition throughout the cortex of irradiated rats with cortical dysplasia and neuronal heterotopia. This may have important implications regarding cortical development and function following in utero injuries.},
	Author = {Chen, Huan-Xin X. and Roper, Steven N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:45:42 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {10 Development;Pregnancy;Animals;Rats;Neuronal Plasticity;Synaptic Transmission;Patch-Clamp Techniques;Female;Epilepsy;Pyramidal Cells;Organ Culture Techniques;Brain Diseases;10 genetics malformation;research support, u.s. gov't, p.h.s.;Cerebral Cortex;24 Pubmed search results 2008;Choristoma;Neural Inhibition;Excitatory Postsynaptic Potentials},
	Month = {1},
	Nlm_Id = {0375404},
	Number = {1},
	Organization = {Department of Neurological Surgery, University of Florida, Gainesville 32610, USA.},
	Pages = {150-8},
	Pubmed = {12522167},
	Title = {Reduction of spontaneous inhibitory synaptic activity in experimental heterotopic gray matter},
	Uuid = {778E5A90-1ADA-421B-8E3C-12276A53930B},
	Volume = {89},
	Year = {2003},
	url = {papers/Chen_JNeurophysiol2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1152/jn.00325.2002}}

@article{Chen:2001a,
	Abstract = {The Slit proteins are a new family of secreted guidance cues involved in axon guidance and neuronal migration. Each mammalian Slit protein contains >1400 amino acid residues, with four leucine-rich regions (LRRs), nine epidermal growth factor repeats, a laminin G domain, and a C-terminal cysteine-rich domain. A receptor for Slit is the transmembrane protein Roundabout (Robo), whose extracellular part contains five Ig domains and three fibronectin type III repeats. We report here that the LRRs in Slit are sufficient for binding to the Ig domains of Robo. Mutant forms of Slit containing only the LRRs function as chemorepellents for axons projecting from the olfactory bulb both in vitro and in the telencephalon. The LRRs can repel neurons migrating from the anterior subventricular zone (SVZa) to the olfactory bulb in brain slices isolated from neonatal rodents. However, the LRRs do not show repulsive effects on the SVZa neurons migrating in collagen gels. Our results indicate that the same LRRs are sufficient for guiding both axon projection and neuronal migration and suggest that the other regions in the Slit proteins may be involved in regulating the diffusion and distribution of the Slit proteins. The fact that the same domains are involved in guiding axon projection and neuronal migration further strengthens the idea of a conserved guidance mechanism for these important processes.},
	Author = {Chen, J. H. and Wen, L. and Dupuis, S. and Wu, J. Y. and Rao, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {J Neurosci},
	Keywords = {Axons/drug effects/*physiology;Human;Peptide Fragments/pharmacology;Receptors, Immunologic/genetics/metabolism;In Vitro;Rats;Transfection;Nerve Tissue Proteins/genetics/*metabolism/pharmacology;Cell Movement/drug effects;Protein Binding/physiology;Animal;Repetitive Sequences, Amino Acid/physiology;Cell Line;Support, Non-U.S. Gov't;Protein Structure, Tertiary/physiology;Kidney/cytology/metabolism;Coculture;Neurons/cytology/drug effects/*metabolism;Olfactory Bulb/cytology/drug effects/*metabolism;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Leucine/genetics/*metabolism;Amino Acid Motifs;C pdf;Cerebral Ventricles/cytology},
	Number = {5},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.},
	Pages = {1548-56.},
	Title = {The N-terminal leucine-rich regions in Slit are sufficient to repel olfactory bulb axons and subventricular zone neurons},
	Uuid = {35E6014A-0541-441F-B978-7AFD4166BB4C},
	Volume = {21},
	Year = {2001},
	url = {papers/Chen_JNeurosci2001}}

@article{Chen:2007,
	Abstract = {Previous studies using dominant-mutant constructs have implicated Rac1 GTPase in neuritogenesis and neuronal migration. However, overexpression of dominant mutants generally blocks Rho-GTPase activity; thus, it may not reveal the specific or physiological functions of Rac1. To address this issue, we have applied a conditional gene-targeting strategy, using Foxg1-Cre mice to delete Rac1 in the ventricular zone (VZ) of telencephalon and Dlx5/6-Cre-IRES (internal ribosomal entry site)-EGFP (enhanced green fluorescent protein) (Dlx5/6-CIE) in the subventricular zone (SVZ) of ventral telencephalon, respectively. Surprisingly, the deletion of Rac1 in VZ progenitors did not prevent axonal outgrowth of telencephalic neurons. However, the anterior commissure was absent, and the corpus callosal as well as hippocampal commissural axons failed to cross the midline in Rac1/Foxg1-Cre knock-out embryos. The thalamocortical and corticothalamic axons also showed defasciculation or projection defects. These results suggest that Rac1 controls axon guidance rather than neuritogenesis. In addition, although Rac1/Foxg1-Cre knock-out embryos showed delayed radial migration of cortical projection neurons and severe impairment of tangential migration by the ventral telencephalon-derived interneurons, deletion of Rac1 in the SVZ by Dlx5/6-CIE mice produced no discernible defects in tangential migration. These contrasting effects of Rac1 deletion on tangential migration suggest that Rac1 is dispensable for cellular motility per se during neuronal migration. Together, these results underscore the challenge of deciphering the biological functions of Rac1, and Rho-GTPases in general, during mammalian brain development. Moreover, they indicate that Rac1 has a critical role in axon guidance and in acquisition of migratory competency during differentiation of the progenitors for the ventral telencephalon-derived interneurons.},
	Author = {Chen, Lei and Liao, Guanghong and Waclaw, Ronald R. and Burns, Kevin A. and Linquist, Diana and Campbell, Kenneth and Zheng, Yi and Kuan, Chia-Yi Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.},
	Pages = {3884-93},
	Pii = {27/14/3884},
	Pubmed = {17409253},
	Title = {Rac1 controls the formation of midline commissures and the competency of tangential migration in ventral telencephalic neurons},
	Uuid = {B7885DB6-4930-401A-82E8-E3A267F96573},
	Volume = {27},
	Year = {2007},
	url = {papers/Chen_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3509-06.2007}}

@article{Chen:2001,
	Abstract = {OBJECT: The management of intractable epilepsy remains a challenge, despite advances in its surgical and nonsurgical treatment. The identification of low-risk, low-cost therapeutic strategies that lead to improved outcome is therefore an important ongoing goal of basic and clinical research. Single-dose focal ionizing beam radiation delivered at necrosis-inducing and subnecrotic levels was investigated for its effects on seizure activity by using an established model of chronic recurrent spontaneous limbic seizures in rats. METHODS: A single 90-minute period of repetitive electrical stimulation (inducing stimulus) of the hippocampus in rats elicited a single episode of status epilepticus, followed by a 2- to 4-week seizure-free period. Spontaneous recurrent seizures developed subsequently and persisted for the duration of monitoring (2-10 months). Simultaneous computerized electroencephalography and video recording were used to monitor the animals. After the establishment of spontaneous recurrent seizures, bilateral radiation centered in the ventral hippocampal formation was administered with the Leksell gamma knife, aided by a stereotactic device custom made for small animals. A center dose of 10, 20, or 40 Gy was administered using a 4-mm collimator. Control animals were subjected to the same seizure-inducing stimulus but underwent a sham treatment instead of gamma irradiation. In a second experiment, the authors examined the effects of gamma irradiation on the proclivity of hippocampal neurons to display epileptiform discharges. Naive animals were irradiated with a single 40-Gy dose, as already described. Slices of the hippocampus were prepared from animals killed between 1 and 178 days postirradiation. Sensitivity to penicillin-induced epileptiform spiking was examined in vitro in slices prepared from control and irradiated rat brains. CONCLUSIONS: In the first experiment, single doses of 20 or 40 Gy (but not 10 Gy) reduced substantially, and in some cases eliminated, behaviorally and electrographically recognized seizures. Significant reductions in both the frequency and duration of spontaneous seizures were observed during a follow-up period of up to 10 months postradiation. Histological examination of the targeted region did not reveal signs of necrosis. These findings indicate that single-dose focal ionizing beam irradiation at subnecrotic dosages reduces or eliminates repetitive spontaneous seizures in a rat model of temporal lobe epilepsy. In the second experiment, synaptically driven neuronal firing was shown to be intact in hippocampal neurons subjected to 40-Gy doses. However, the susceptibility to penicillin-induced epileptiform activity was reduced in the brain slices of animals receiving 40-Gy doses, compared with those from control rats that were not irradiated. The results provide rational support for the utility of subnecrotic gamma irradiation as a therapeutic strategy for treating epilepsy. These findings also provide evidence that a functional increase in the seizure threshold of hippocampal neurons contributes to the anticonvulsant influence of subnecrotic gamma irradiation.},
	Author = {Chen, Z. F. and Kamiryo, T. and Henson, S. L. and Yamamoto, H. and Bertram, E. H. and Schottler, F. and Patel, F. and Steiner, L. and Prasad, D. and Kassell, N. F. and Shareghis, S. and Lee, K. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0022-3085},
	Journal = {J Neurosurg},
	Keywords = {Epilepsy;21 Epilepsy;Treatment Outcome;Research Support, Non-U.S. Gov't;21 Neurophysiology;Rats;Hippocampus;Research Support, U.S. Gov't, P.H.S.;Evoked Potentials;Animals;Male;24 Pubmed search results 2008;Radiosurgery;Neurons},
	Medline = {21081721},
	Month = {2},
	Nlm_Id = {0253357},
	Number = {2},
	Organization = {Department of Neuroscience, University of Virginia Health Sciences Center, Charlottesville 22908, USA.},
	Pages = {270-80},
	Pubmed = {11213965},
	Title = {Anticonvulsant effects of gamma surgery in a model of chronic spontaneous limbic epilepsy in rats},
	Uuid = {2862ADFF-F71C-4449-ADC8-286763E5BA97},
	Volume = {94},
	Year = {2001}}

@article{Chen:2003b,
	Abstract = {We developed a rat model of epidural plastic bead implantation to study the effect of physical compression on the cerebral cortex. Epidural implantation of a bead of appropriate size compressed the underlying sensorimotor cortex without apparent ischemia, since the capillary density of the cortex was increased. Although the thickness of all layers of the compressed cortex was significantly decreased, no apparent changes in the number of NADPH-diaphorase reactive neurons, reactive astrocytes, or microglial cells were observed, nor were apoptotic neurons observed. In fact, the densities of the neurons in most cortical layers apparently increased. To determine how epidural compression affects neuronal morphology, the dendritic arbors of layer III and V pyramidal neurons were evaluated using a fixed tissue intracellular dye injection technique. Neurons in both layers remained pyramidal in shape and their somatic sizes remained unaltered for at least a month after compression. On the other hand, their total dendritic length was significantly reduced beginning at 3 days post implantation. These analyses showed that apical dendrites were affected sooner than basal ones. The reduction of dendritic length was associated with a drop in the number of dendritic branches rather than dendritic trunks, suggesting the trimming of the peripheral part of the dendritic arbor. Detailed analysis showed that dendritic spines on all dendrites were reduced as early as 3 days following implantation. These results suggest that cortical neurons remodel their structures substantially within 3 days after being subjected to epidural compression.},
	Author = {Chen, Jeng-Rung R. and Wang, Yueh-Jan J. and Tseng, Guo-Fang F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0897-7151},
	Journal = {J Neurotrauma},
	Keywords = {Laterality;10 Development;NADPH Dehydrogenase;Rats;Female;Astrocytes;Rats, Wistar;Microglia;Epidural Space;10 Structural plasticity;Support, Non-U.S. Gov't;Animals;Cerebral Cortex;Neurons;Beta},
	Medline = {22846858},
	Month = {8},
	Nlm_Id = {8811626},
	Number = {8},
	Organization = {Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.},
	Pages = {767-80},
	Pubmed = {12965055},
	Title = {The effect of epidural compression on cerebral cortex: a rat model},
	Uuid = {8711D255-748A-4F13-A902-25B2876A8B2E},
	Volume = {20},
	Year = {2003},
	url = {papers/Chen_JNeurotrauma2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/089771503767869999}}

@article{Chen:2005c,
	Abstract = {Caspase activation occurs within 1h of reperfusion in discrete cell populations of the adult rat brain following transient forebrain ischemia. Based on the proximity of these cells to regions of adult neurogenesis and the known susceptibility of developing neurons to apoptosis, we tested the hypothesis that rapidly triggered post-ischemic caspase activation occurs in immature neurons or neuroprogenitor cells. Adult male Long Evans rats were injected with BrdU to label mitotic cells 1, 7, or 28 days prior to being studied. Rats were then subjected to either sham surgery or 10-min transient forebrain ischemia. At 1h after reperfusion, rats underwent perfusion fixation and brains prepared for immunohistochemical analysis. Immunolabeling for caspase-substrate cleavage, using an antibody directed at the caspase derived fragment of alpha-spectrin, was observed in discrete cell populations of the rostral dentate gyrus, dorsal striatum, extreme paramedian CA1 hippocampus, indusium gresium, olfactory tubercle, and thalamus. No cells double-labeled for caspase-substrate cleavage and BrdU at any time point after BrdU injection. Furthermore, cells immunolabeled for caspase-substrate cleavage did not double-label for markers of immature neurons (doublecortin) or progenitor cells (nestin), but did double-label for the mature neuronal marker NeuN. These results indicate that the phenomenon of rapidly triggered caspase activation in the adult rat brain after transient forebrain ischemia is specific to mature neurons and does not occur in neuroprogenitor cells or immature neurons.},
	Author = {Chen, Zhaoming and Kontonotas, Diana and Friedmann, Daniel and Pitts-Kiefer, Alex and Frederick, James R. and Siman, Robert and Neumar, Robert W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7600130},
	Number = {3},
	Organization = {Department of Emergency Medicine, University of Pennsylvania School of Medicine, 3400 Spruce Street, Philadelphia, PA 19104-4283, USA.},
	Pages = {166-70},
	Pii = {S0304-3940(04)01462-4},
	Pubmed = {15721215},
	Title = {Developmental status of neurons selectively vulnerable to rapidly triggered post-ischemic caspase activation},
	Uuid = {BDFF59EE-50B4-4B31-B92F-ACDDD8F34947},
	Volume = {376},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neulet.2004.11.051}}

@article{Chen:2004,
	Abstract = {The adult mammalian CNS shows a very limited capacity to regenerate after injury. However, endogenous precursors, or stem cells, provide a potential source of new neurons in the adult brain. Here, we induce the birth of new corticospinal motor neurons (CSMN), the CNS neurons that die in motor neuron degenerative diseases, including amyotrophic lateral sclerosis, and that cause loss of motor function in spinal cord injury. We induced synchronous apoptotic degeneration of CSMN and examined the fates of newborn cells arising from endogenous precursors, using markers for DNA replication, neuroblast migration, and progressive neuronal differentiation, combined with retrograde labeling from the spinal cord. We observed neuroblasts entering the neocortex and progressively differentiating into mature pyramidal neurons in cortical layer V. We found 20-30 new neurons per mm(3) in experimental mice vs. 0 in controls. A subset of these newborn neurons projected axons into the spinal cord and survived >56 weeks. These results demonstrate that endogenous precursors can differentiate into even highly complex long-projection CSMN in the adult mammalian brain and send new projections to spinal cord targets, suggesting that molecular manipulation of endogenous neural precursors in situ may offer future therapeutic possibilities for motor neuron degenerative disease and spinal cord injury.},
	Author = {Chen, Jinhui and Magavi, Sanjay S. P. and Macklis, Jeffrey D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {01 Adult neurogenesis general;Research Support, Non-U.S. Gov't;17 Transplant Regeneration;Motor Neurons;Nerve Regeneration;Female;Apoptosis;Research Support, U.S. Gov't, P.H.S.;Neural Pathways;Mice, Inbred C57BL;Stem Cells;06 Adult neurogenesis injury induced;Spinal Cord;Animals;Mice;Cerebral Cortex;Neurons},
	Month = {11},
	Nlm_Id = {7505876},
	Number = {46},
	Organization = {Department of Neurosurgery and Program in Neuroscience, Massachusetts General Hospital-Harvard Medical School Center for Nervous System Repair, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.},
	Pages = {16357-62},
	Pii = {0406795101},
	Pubmed = {15534207},
	Title = {Neurogenesis of corticospinal motor neurons extending spinal projections in adult mice},
	Uuid = {5196DFAF-E740-41F8-A7C2-2E9C4D92C43A},
	Volume = {101},
	Year = {2004},
	url = {papers/Chen_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0406795101}}

@article{Chen:2005,
	Abstract = {Pyramidal neurons of the cerebral cortex display marked layer- and subtype-specific differences in their axonal projections and dendritic morphologies. Here we show that transcription factor Zfp312 is selectively expressed by layer V and VI subcortical projection pyramidal neurons and their progenitor cells. Knocking down Zfp312 with small interfering RNAs dramatically reduced the number of subcortical axonal projections from deep-layer pyramidal neurons and altered their dendritic morphology. In contrast, misexpression of Zfp312 in cortically projecting pyramidal neurons of layers II and III induced the expression of Tbr1, a transcription factor enriched in deep-layer neurons, and the formation of ectopic subcortical axonal projections. Thus, our results indicate that transcription factor Zfp312 plays a critical role in layer- and neuronal subtype-specific patterning of cortical axonal projections and dendritic morphologies.},
	Author = {Chen, and Rasin, and Kwan, and Sestan,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {10 Development},
	Month = {11},
	Nlm_Id = {7505876},
	Organization = {Department of Neurobiology and Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06510.},
	Pii = {0509032102},
	Pubmed = {16314561},
	Title = {Zfp312 is required for subcortical axonal projections and dendritic morphology of deep-layer pyramidal neurons of the cerebral cortex},
	Uuid = {9347FA49-9ED5-4438-B495-8DE8D24EE662},
	Year = {2005},
	url = {papers/Chen_ProcNatlAcadSciUSA2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0509032102}}

@article{Chen:2005a,
	Abstract = {During the development of the cerebral cortex, progenitor cells produce neurons that migrate to laminar positions appropriate for their birth dates, adopt specific neuronal identities, and form appropriate local and long-distance axonal connections. Here, we report that forebrain embryonic zinc-finger-like protein (Fezl), a putative zinc-finger transcriptional repressor, is required for the differentiation of projection neurons in cortical layer 5. In Fezl-deficient mice, these neurons display molecular, morphological, and axonal targeting defects. The corticospinal tract was absent in Fezl(-/-) mice, corticotectal and pontine projections were severely reduced, and Fezl-expressing neurons formed aberrant axonal projections. The expression of many molecular markers for deep-layer neurons was reduced or absent in the Fezl(-/-) cerebral cortex. Most strikingly, Ctip2, a transcription factor required for the formation of the corticospinal tract, was not expressed in the Fezl-deficient cortex. These results suggest that Fezl regulates the differentiation of layer 5 subcortical projection neurons.},
	Author = {Chen, Bin and Schaevitz, Laura R. and McConnell, Susan K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {10 Development;Cell Differentiation;Heterozygote;Animals;DNA-Binding Proteins;Humans;Neural Pathways;Axons;Staining and Labeling;Zinc Fingers;Mice, Knockout;Cerebral Cortex;Motor Neurons;Mice;research support, n.i.h., extramural;Genes, Reporter;24 Pubmed search results 2008;Nerve Tissue Proteins;Repressor Proteins;Genetic Markers},
	Month = {11},
	Nlm_Id = {7505876},
	Number = {47},
	Organization = {Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA.},
	Pages = {17184-9},
	Pii = {0508732102},
	Pubmed = {16284245},
	Title = {Fezl regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex},
	Uuid = {47027172-2F0E-4655-9C93-9F865549D39A},
	Volume = {102},
	Year = {2005},
	url = {papers/Chen_ProcNatlAcadSciUSA2005a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0508732102}}

@article{Chen:2005b,
	Abstract = {Cell-cell fusion is fundamental to the development and physiology of multicellular organisms, but little is known of its mechanistic underpinnings. Recent studies have revealed that many proteins involved in cell-cell fusion are also required for seemingly unrelated cellular processes such as phagocytosis, cell migration, axon growth, and synaptogenesis. We review advances in understanding cell-cell fusion by contrasting it with virus-cell and intracellular vesicle fusion. We also consider how proteins involved in general aspects of membrane dynamics have been co-opted to control fusion of diverse cell types by coupling with specialized proteins involved in cell-cell recognition, adhesion, and signaling.},
	Author = {Chen, Elizabeth H. and Olson, Eric N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {08 Aberrant cell cycle;11 Glia;15 Retrovirus mechanism},
	Month = {4},
	Nlm_Id = {0404511},
	Number = {5720},
	Organization = {Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. echen\@jhmi.edu},
	Pages = {369-73},
	Pii = {308/5720/369},
	Pubmed = {15831748},
	Title = {Unveiling the mechanisms of cell-cell fusion},
	Uuid = {13A0E6EF-EE5E-11DA-8605-000D9346EC2A},
	Volume = {308},
	Year = {2005},
	url = {papers/Chen_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1104799}}

@article{Chen:2000b,
	Abstract = {Lentiviral vectors efficiently transduce human CD34(+) cells that mediate long-term engraftment of nonobese diabetic/severe combined immunodeficient mice. However, hematopoiesis in these animals is abnormal. Typically, 95\%of the human cells in peripheral blood are B lymphocytes. To determine whether lentiviral vectors efficiently transduce stem cells that maintain normal hematopoiesis in vivo, we isolated Sca-1(+)c-Kit(+)Lin(-) bone marrow cells from mice without 5-fluorouracil treatment, and transduced these cells in the absence of cytokine stimulation with a novel lentiviral vector containing a GFP (green flourescent protein) reporter gene. These cells were transplanted into lethally irradiated C57Bl/6 mice. In fully reconstituted animals, GFP expression was observed in 8.0\%of peripheral blood mononuclear cells for 20 weeks posttransplantation. Lineage analysis demonstrated that a similar percentage (approximately 8.0\%) of GFP-positive cells was detected in peripheral blood B cells, T cells, granulocytes and monocytes, bone marrow erythroid precursor cells, splenic B cells, and thymic T cells. In secondary transplant recipients, up to 20\%of some lineages expressed GFP. Our results suggest that quiescent, hematopoietic stem cells are efficiently transduced by lentiviral vectors without impairing self-renewal and normal lineage specification in vivo. Efficient gene delivery into murine stem cells with lentiviral vectors will allow direct tests of genetic therapies in mouse models of hematopoietic diseases such as sickle cell anemia and thalassemia, in which corrected cells may have a selective survival advantage.},
	Author = {Chen, W. and Wu, X. and Levasseur, D. N. and Liu, H. and Lai, L. and Kappes, J. C. and Townes, T. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {T-Lymphocytes;Cell Differentiation;Animals;Humans;Whole-Body Irradiation;Transfection;Lentivirus;B-Lymphocytes;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Hematopoietic Stem Cell Transplantation;Genetic Vectors;Research Support, U.S. Gov't, P.H.S.;Thymus Gland;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Genes, Reporter;Spleen;Research Support, Non-U.S. Gov't},
	Medline = {20465652},
	Nlm_Id = {9304532},
	Number = {5},
	Organization = {Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Alabama, USA.},
	Pages = {352-9},
	Pubmed = {11007919},
	Title = {Lentiviral vector transduction of hematopoietic stem cells that mediate long-term reconstitution of lethally irradiated mice},
	Uuid = {97EFD9CA-4768-4FA2-826D-729DE3E23B96},
	Volume = {18},
	Year = {2000}}

@article{Chen:2003c,
	Abstract = {In the course of normal embryogenesis, embryonic stem (ES) cells differentiate along different lineages in the context of complex three-dimensional (3D) tissue structures. In order to study this phenomenon in vitro under controlled conditions, 3D culture systems are necessary. Here, we studied in vitro differentiation of rhesus monkey ES cells in 3D collagen matrixes (collagen gels and porous collagen sponges). Differentiation of ES cells in these 3D systems was different from that in monolayers. ES cells differentiated in collagen matrixes into neural, epithelial, and endothelial lineages. The abilities of ES cells to form various structures in two chemically similar but topologically different matrixes were different. In particular, in collagen gels ES cells formed gland-like circular structures, whereas in collagen sponges ES cells were scattered through the matrix or formed aggregates. Soluble factors produced by feeder cells or added to the culture medium facilitated ES cell differentiation into particular lineages. Coculture with fibroblasts in collagen gel facilitated ES cell differentiation into cells of a neural lineage expressing nestin, neural cell adhesion molecule, and class III beta-tubulin. In collagen sponges, keratinocytes facilitated ES cell differentiation into cells of an endothelial lineage expressing factor VIII. Exogenous granulocyte-macrophage colony-stimulating factor further enhanced endothelial differentiation. Thus, both soluble factors and the type of extracellular matrix seem to be critical in directing differentiation of ES cells and the formation of tissue-like structures. Three-dimensional culture systems are a valuable tool for studying the mechanisms of these phenomena.},
	Author = {Chen, Silvia S. and Revoltella, Roberto P. and Papini, Sandra and Michelini, Monica and Fitzgerald, Wendy and Zimmerberg, Joshua and Margolis, Leonid},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {Cytokines;Cell Differentiation;Cell Culture Techniques;Animals;Cells, Cultured;Research Support, U.S. Gov't, Non-P.H.S.;Diffusion Chambers, Culture;Culture Media, Conditioned;Extracellular Matrix;Gelatin Sponge, Absorbable;Macaca mulatta;Gels;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Pluripotent Stem Cells;Cell Division;Immunohistochemistry;22 Stem cells;Biological Markers;Collagen;Research Support, Non-U.S. Gov't},
	Medline = {22628933},
	Nlm_Id = {9304532},
	Number = {3},
	Organization = {NASA/NIH Center for Three Dimensional Tissue Culture, Laboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development (NICHD), NIH, Bethesda, Maryland 20892, USA.},
	Pages = {281-95},
	Pubmed = {12743323},
	Title = {Multilineage differentiation of rhesus monkey embryonic stem cells in three-dimensional culture systems},
	Uuid = {3F3C87F1-217B-4784-BAB4-0A543614B6A4},
	Volume = {21},
	Year = {2003},
	url = {papers/Chen_StemCells2003.pdf}}

@article{Cheng:2005,
	Abstract = {The complexity and cellular diversity of the adult brain arises from the proliferation and differentiation of a small number of stem cells. The intrinsic state of stem cells depends on their spatial and temporal history and affects their responsiveness to extrinsic signals from the microenvironment. Stem cell self-renewal and differentiation along neuronal and glial lineages are defined by the dynamic interplay between transcription, epigenetic control, and posttranscriptional regulators, including microRNAs, whose key role in stem cell biology is just emerging.},
	Author = {Cheng, Li-Chun C. and Tavazoie, Masoud and Doetsch, Fiona},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-13 09:45:17 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development; MicroRNAs; microRNAs; development},
	Month = {5},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Pathology, Columbia University, 630 West 168th Street, New York, New York 10032, USA.},
	Pages = {363-7},
	Pii = {S0896-6273(05)00363-6},
	Pubmed = {15882632},
	Title = {Stem cells: from epigenetics to microRNAs},
	Uuid = {F81A60FF-D4D9-4208-82AE-E0615BC1F841},
	Volume = {46},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.04.027}}

@article{Chenn:2005,
	Abstract = {Asymmetric cell division plays a major role in the generation of cell diversity during development. In this issue of Neuron, Sun and colleagues present evidence that the epidermal growth factor receptor is asymmetrically distributed in mitotic cerebral cortical precursors, and the resulting unequal inheritance generates offspring with different responsiveness to growth factor and unique cell fates.},
	Author = {Chenn, Anjen},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {review;Cell Differentiation;10 Development;Neuroglia;Receptor, Epidermal Growth Factor;Stem Cells;Cell Division;review, tutorial;comment;Brain Neoplasms;Humans;Animals;Cerebral Cortex;Cell Lineage;Neurons},
	Month = {3},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA.},
	Pages = {817-9},
	Pii = {S0896-6273(05)00193-5},
	Pubmed = {15797541},
	Title = {The simple life (of cortical progenitors)},
	Uuid = {0BDA0140-672B-4098-ADC5-BE62EFE32763},
	Volume = {45},
	Year = {2005},
	url = {papers/Chenn_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.03.001}}

@article{Chernoff:1996,
	Abstract = {Studies of neuronal survival and axonal regeneration in birds and mammals have made it clear that the microenvironment of the CNS is critical to the failure of CNS regeneration in these animals. This environment includes growth and trophic factors, ECM components and matrix turnover enzymes, cytokines and other immune system contributions. Urodele amphibians (salamanders and newts) can regenerate spinal cord even as adults, and environmental contributions of glial populations are a major part of the difference between urodele and higher vertebrate spinal cord regeneration. In particular, the behavior of injury-reactive ependymal cells (radial glia) is critical to the regenerative capacity of urodele spinal cord. In this review we examine what is known about cell-cell interactions between ependymal cells and neurons and between ependymal cells and other glial populations. The known contributions of ependymal cell products such as matrix metalloproteinases and trophic factors are discussed. There is evidence in the literature that an ependymal response occurs during embryonic or fetal development in birds and mammals following spinal cord transection, and this review discusses the implications of such a process for future studies of spinal cord injury. 0214-6282 Journal Article Review Review, Tutorial},
	Author = {Chernoff, E. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {Int J Dev Biol},
	Keywords = {17 Transplant Regeneration;Cell Communication;Rats;Chick Embryo;Growth Substances/physiology;Spinal Cord/*physiology;L pdf;Urodela/*physiology;Animals;*Regeneration;Ependyma/cytology;Intermediate Filament Proteins/physiology},
	Number = {4},
	Organization = {Department of Biology, Indiana University-Purdue University at Indianapolis, 46202-5132, USA. echernof\@indyvax.iupui.edu},
	Pages = {823-31},
	Title = {Spinal cord regeneration: a phenomenon unique to urodeles?},
	Uuid = {4A5D455E-59DB-4472-9185-E50FD648CE80},
	Volume = {40},
	Year = {1996},
	url = {papers/Chernoff_IntJDevBiol1996.pdf}}

@article{Cheynet:2006,
	Abstract = {The cellular HERV-W envelope/syncytin-1 protein, encoded by the envelope gene of the ERVWE1 proviral locus is a fusogenic glycoprotein probably involved in the formation of the placental syncytiotrophoblast layer. Syncytin-1-induced in vitro cell-cell fusion is dependent on the interaction with hASCT2. As no receptor binding domain has been clearly defined in the SU of neither the HERV-W Env nor the retroviruses of the same interference group, we designed an in vitro binding assay to evaluate the interaction of the HERV-W envelope with the hASCT2 receptor. Using truncated HERV-W SU subunits, a region consisting of the N-terminal 124 amino acids of the mature SU glycoprotein was determined as the minimal receptor-binding domain. This domain contains several sub-domains which are poorly conserved among retroviruses of this interference group but a region of 18 residus containing the SDGGGX2DX2R conserved motif was proved to be essential for syncytin-1-hASCT2 interaction.},
	Author = {Cheynet, Val{\'e}rie and Oriol, Guy and Mallet, Fran\c{c}ois},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1742-4690},
	Journal = {Retrovirology},
	Keywords = {15 ERVs retroelements;Endogenous Retroviruses;Cell Fusion;Hela Cells;Gene Products, env;Cell Line;Amino Acid Transport System ASC;14 Immune;Receptors, Virus;15 Retrovirus mechanism;Humans;24 Pubmed search results 2008;Pregnancy Proteins},
	Nlm_Id = {101216893},
	Organization = {UMR 2714 CNRS-bioM{\'e}rieux, IFR128 BioSciences Lyon-Gerland, Ecole Normale Sup{\'e}rieure de Lyon, 69364 Lyon Cedex 07, France. valerie.cheynet\@ens-lyon.fr},
	Pages = {41},
	Pii = {1742-4690-3-41},
	Pubmed = {16820059},
	Title = {Identification of the hASCT2-binding domain of the Env ERVWE1/syncytin-1 fusogenic glycoprotein},
	Uuid = {02106ACC-67D0-4A6B-9388-6A7209A24F08},
	Volume = {3},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1742-4690-3-41}}

@article{Chiasson:1999,
	Abstract = {The adult derivatives of the embryonic forebrain germinal zones consist of two morphologically distinct cell layers surrounding the lateral ventricles: the ependyma and the subependyma. Cell cycle analyses have revealed that at least two proliferating populations exist in this region, one that is constitutively proliferating and one that is relatively quiescent and thought to include the endogenous adult neural stem cells. Earlier studies demonstrated that specific dissection of the region surrounding the lateral ventricles was necessary for the in vitro isolation of multipotent, self-renewing neural stem cells. However, in these studies, the ependymal layer was not physically separated from the subependymal layer to identify the specific adult laminar localization of the neural stem cells around the lateral ventricles. To determine which cellular compartment in the adult forebrain contained the neural stem cells, we isolated and cultured the ependyma separately from the subependyma and tested for the presence of neural stem cells using the in vitro neurosphere assay. We demonstrate that the ependymal cells can proliferate in vitro to form sphere-like structures. However, the ependymal cells generating spheres do not have the ability to self-renew (proliferate to form secondary spheres after dissociation) nor to produce neurons, but rather only seem to generate glial fibrillary acidic protein-positive ependymal cells when plated under differentiation conditions in culture. On the other hand, a subpopulation of subependymal cells do possess the self-renewing and multipotential characteristics of neural stem cells. Therefore, the adult forebrain neural stem cell resides within the subependymal compartment.},
	Author = {Chiasson, B. J. and Tropepe, V. and Morshead, C. M. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {J Neurosci},
	Keywords = {02 Adult neurogenesis migration;Prosencephalon/*cytology/drug effects;Cerebral Ventricles/cytology/drug effects;Neurons/*cytology/drug effects;Comparative Study;B-14;Ependyma/*cytology/drug effects;Stem Cells/*cytology/drug effects;Cell Division/drug effects/physiology;Fibroblast Growth Factor, Basic/pharmacology;Animal;Nerve Growth Factors/pharmacology;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Mice;Male},
	Number = {11},
	Organization = {Neurobiology Research Group, Department of Anatomy and Cell Biology, University of Toronto, Toronto, Canada, M5S 1A8.},
	Pages = {4462-71.},
	Title = {Adult mammalian forebrain ependymal and subependymal cells demonstrate proliferative potential, but only subependymal cells have neural stem cell characteristics},
	Uuid = {C00389AC-EC80-11DA-8605-000D9346EC2A},
	Volume = {19},
	Year = {1999},
	url = {papers/Chiasson_JNeurosci1999.pdf}}

@article{Chikada:1999,
	Abstract = {Gene therapy is a therapeutic strategy in treating cardiovascular disease. Vein graft failure, the major limitation on coronary artery bypass surgery, may be amenable to gene approaches. Some studies describe gene therapies using functioning genes to prevent vein graft stenosis. Gene transfer efficiency remains a major issue. In this rabbit vein graft model, we studied gene delivery using a replication-deficit recombinant adenovirus to improve gene transfer efficiency into vein grafts. The adenovirus vector that contains the E.coli lacZ gene encoding beta gal was used because this vector is widely used and thought to be effective. Gene transfer was detected by X-gal staining. We hypothesized that dimethylsulfoxide and hyaluronidase, both drug delivery enhancers, would improve efficiency and that, in transfer to adventitia, direct injection would be more effective than dwelling. We studied 3 gene delivery methods to intima and media (controls, using dimethylsulfoxide and using hyaluronidase before transfection) and 2 delivery methods to adventitia (direct injection and dwelling). We used 6 rabbits per delivery method. X-gal stained positive cell rates were counted using light microscopy. Our findings indicate that (1) dimethylsulfoxide increased the efficiency of transfection to media and intima, (2) hyaluronidase increased intimal transfection efficiency, (3) direct injection to adventitia was more effective than dwelling. These findings suggest that in vein grafting, our methods are feasible for improving gene transfer efficiency. 1344-4964 Journal Article},
	Author = {Chikada, M. and Jones, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Jpn J Thorac Cardiovasc Surg},
	Keywords = {Genetic Vectors;Gene Therapy/*methods;Graft Occlusion, Vascular/prevention &control;EE, DMSO, abstr;08 Aberrant cell cycle;Hyaluronoglucosaminidase;Transfection/*methods;Adenoviridae;Rabbits;Animals;Disease Models, Animal;Dimethyl Sulfoxide;Veins/*transplantation},
	Number = {5},
	Organization = {Department of Cardiovascular Surgery, National Children's Hospital, Tokyo, Japan.},
	Pages = {204-9},
	Pubmed = {10402767},
	Title = {Study of gene delivery in a rabbit vein graft model. Improvement of the efficiency of gene transfer into vein grafts},
	Uuid = {0992A834-9446-4397-B41D-35A118C2EF61},
	Volume = {47},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10402767}}

@article{Chittajallu:2002,
	Abstract = {Proliferative oligodendrocyte progenitor cells (OPs) express large, delayed outward-rectifying K(+) currents (I(K)), whereas nondividing immature and mature oligodendrocytes display much smaller I(K). Here, we show that up-regulation of I(K) occurs in G(1) phase of the cell cycle in purified cultured OPs and is the result of an RNA synthesis-dependent, selective increase of the K(+) channel subunit proteins Kv1.3 and Kv1.5. In oligodendrocyte cells acutely isolated from developing rat brain, a decrease of cyclin D expression is observed as these cells mature along their lineage. This is accompanied by a decrease in Kv1.3 and Kv1.5 subunit expression, suggesting a role for these subunits in the proliferative potential of OPs in situ. I(K) expressed in OPs in subventricular zone and developing white matter in acutely isolated slice preparations were selectively blocked by antagonists of Kv1.3, illustrating the functional presence of this subunit in situ. Interestingly, Kv1.3 block inhibited S-phase entry of both purified OPs in culture and in tissue slice cultures. Thus, we employ both in vitro and in situ experimental approaches to show that (i) RNA-dependent synthesis of Kv1.3 and Kv1.5 subunit proteins occurs in G(1) phase of the OP cell cycle and is responsible for the observed increase in I(K), and (ii) currents through Kv1.3-containing channels play a crucial role in G(1)/S transition of proliferating OPs. 0027-8424 Journal Article},
	Author = {Chittajallu, R. and Chen, Y. and Wang, H. and Yuan, X. and Ghiani, C. A. and Heckman, T. and McBain, C. J. and Gallo, V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Human;Electrophysiology;Animals;Cells, Cultured;Up-Regulation;Rats;*G1 Phase;Rats, Sprague-Dawley;11 Glia;G abstr;Oligodendroglia/*cytology/metabolism;Time Factors;Dimerization;Support, Non-U.S. Gov't;Cell Lineage;Blotting, Western;Brain/embryology/metabolism/physiology;Lysine/*analogs &derivatives/metabolism;Cell Division;Cyclins/biosynthesis;Immunohistochemistry;*S Phase;Potassium Channels/*biosynthesis;Platelet-Derived Growth Factor/metabolism;RNA/metabolism},
	Number = {4},
	Organization = {Laboratory of Cellular and Synaptic Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4495, USA.},
	Pages = {2350-5},
	Pubmed = {11854528},
	Title = {Regulation of Kv1 subunit expression in oligodendrocyte progenitor cells and their role in G1/S phase progression of the cell cycle},
	Uuid = {8B0AB717-A368-4304-B620-61D9316F8005},
	Volume = {99},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11854528}}

@article{Chiu:1996,
	Abstract = {Several lines of evidence suggest an important role for glia in establishing boundaries during development of mammalian cortex and insect olfactory lobe. In the adult rat olfactory bulb distinct morphological categories of astroglial cells with clear laminar specificity are easily recognized following immunocytochemical staining of glial fibrillary acidic protein (GFAP). To explore the developmental distribution of olfactory bulb astrocytes and their possible role in establishing the segregation of neurons in specific olfactory bulb laminae, we used immunocytochemical localization of GFAP in rats at 0, 6, 9, 12, 15 and 21 days postnatal plus the adult. In the adult we confirmed prior observations and identified five morphological categories of astrocytes: linear, wedge, elongate, semicircular, and circular. Each category had a unique sublaminar distribution across the olfactory bulb, although categories could occur in more than one lamina. Between 0 and 21 days postnatal a 6th category was apparent, radial glial cells. The mature astrocyte morphologies did not emerge uniformly. Astrocytes found in the outermost glomerular layer developed first with the appearance of the linear, wedge and elongate morphologies. Deeper laminate of the olfactory bulb followed in a successive fashion until the adult pattern was evident around 15 days postnatal. As radial glia disappeared, the mature morphologies assumed their final position. The data suggest that the maturation of olfactory bulb astrocytes may be linked to the final migration and maturation of olfactory bulb neurons.},
	Author = {Chiu, K. and Greer, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Glial Fibrillary Acidic Protein/metabolism;Rats, Sprague-Dawley;G abstr;Immunohistochemistry;Rats;Animals, Newborn/physiology;Animal;11 Glia;Support, U.S. Gov't, P.H.S.;Olfactory Bulb/*cytology/*growth &development/metabolism;Astrocytes/metabolism/*physiology/ultrastructure},
	Number = {1},
	Organization = {Section of Neurosurgery, Yale University School of Medicine, New Haven, CT 06510, USA.},
	Pages = {28-37.},
	Title = {Immunocytochemical analyses of astrocyte development in the olfactory bulb},
	Uuid = {720A4690-540F-457D-A195-166571380D9F},
	Volume = {95},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8873973}}

@article{Chmielnicki:2004,
	Abstract = {Neurogenesis from endogenous progenitor cells in the adult forebrain ventricular wall may be induced by the local viral overexpression of cognate neuronal differentiation agents, in particular BDNF. Here, we show that the overexpression of noggin, by acting to inhibit glial differentiation by subependymal progenitor cells, can potentiate adenoviral BDNF-mediated recruitment of new neurons to the adult rat neostriatum. The new neurons survive at least 2 months after their genesis in the subependymal zone and are recruited primarily as GABAergic DARPP-32+ medium spiny neurons in the caudate-putamen. The new medium spiny neurons successfully project to the globus pallidus, their usual developmental target, extending processes over several millimeters of the normal adult striatum. Thus, concurrent suppression of subependymal glial differentiation and promotion of neuronal differentiation can mobilize endogenous subependymal progenitor cells to achieve substantial neuronal addition to otherwise non-neurogenic regions of the adult brain. 1529-2401 Journal Article},
	Author = {Chmielnicki, E. and Benraiss, A. and Economides, A. N. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {J Neurosci},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {9},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA.},
	Pages = {2133-42},
	Title = {Adenovirally expressed noggin and brain-derived neurotrophic factor cooperate to induce new medium spiny neurons from resident progenitor cells in the adult striatal ventricular zone},
	Uuid = {602A11ED-D3D4-4BA0-82A3-EDF31E266AA6},
	Volume = {24},
	Year = {2004},
	url = {papers/Chmielnicki_JNeurosci2004.pdf}}

@article{Cho:2003,
	Abstract = {Transection of the medial forebrain bundle caused apoptosis of dopamine neurons in the rat substantia nigra. Immunohistochemical localization of activated microglia and tyrosine hydroxylase in the axotomized substantia nigra showed that activation of microglia was rapid and OX-6 (MHC-II marker)-positive and ED1 (lysosomal phagocytic marker)-positive microglia were apposed to structurally intact tyrosine hydroxylase-positive dopamine neurons, indicating microglial phagocytosis of degenerating dopamine neurons. The occurrence of microglial phagocytosis at early stages of apoptosis may indicate the evolution of apoptosis into an irreversible state. Alternatively, interventions that suppress early activation of microglia might lead to novel mechanisms for neuron protection.},
	Author = {Cho, Byung Pil and Sugama, Shuei and Shin, Dong Hoon and DeGiorgio, Lorraine A. and Kim, Sung Soo and Kim, Yoon Seong and Lim, So Young and Park, Key Chung and Volpe, Bruce T. and Cho, Sunghee and Joh, Tong H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0272-4340},
	Journal = {Cell Mol Neurobiol},
	Keywords = {Dopamine;Nerve Degeneration;Animals;Phagocytosis;Rats;Medial Forebrain Bundle;Apoptosis;Microglia;Reaction Time;Substantia Nigra;Rats, Wistar;Not relevant;11 Glia;Male;Neurons;Axotomy;Tyrosine 3-Monooxygenase;Biological Markers;Membrane Proteins;Histocompatibility Antigens Class II},
	Medline = {22875838},
	Month = {10},
	Nlm_Id = {8200709},
	Number = {4-5},
	Organization = {The Burke Medical Research Institute, Department of Neurology and Neuroscience, Weill Medical College, Graduate School of Medical Sciences of Cornell University, White Plains, New York 10605, USA.},
	Pages = {551-60},
	Pubmed = {14514015},
	Title = {Microglial phagocytosis of dopamine neurons at early phases of apoptosis},
	Uuid = {4916D88B-13F5-4847-8B85-07B3D6678D21},
	Volume = {23},
	Year = {2003}}

@article{Choi:2003,
	Abstract = {AIMS/HYPOTHESIS: Bone marrow cells contain at least two distinct types of stem cells which are haematopoietic stem cells and mesenchymal stem cells. Both cells have the ability to differentiate into a variety of cell types derived from all three germ layers. Thus, bone marrow stem cells could possibly be used to generate new pancreatic beta cells for the treatment of diabetes. In this study, we investigated the feasibility of bone marrow-derived cells to differentiate into beta cells in pancreas. METHODS: Using green fluorescent protein transgenic mice as donors, the distribution of haematogenous cells in the pancreas was studied after bone marrow transplantation. RESULTS: In the pancreas of green fluorescent protein chimeric mice, green fluorescent protein-positive cells were found in the islets, but none of these cells expressed insulin. Previous data has suggested that tissue injury can recruit haematopoietic stem cells or their progeny to a non-haematopietic cell fate. Therefore, low-dose streptozotocin (30 or 50 mg/kg on five consecutive days) was injected into the mice 5 weeks after bone marrow transplantation, but no green fluorescent protein-positive cells expressing insulin were seen in the islets or around the ducts of the pancreas. CONCLUSIONS/INTERPRETATION: Our data suggests that bone marrow-derived cells are a distinct cell population from islet cells and that transdifferentiation from bone marrow-derived cells to pancreatic beta cells is rarely observed.},
	Author = {Choi, J. B. and Uchino, H. and Azuma, K. and Iwashita, N. and Tanaka, Y. and Mochizuki, H. and Migita, M. and Shimada, T. and Kawamori, R. and Watada, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0012-186X},
	Journal = {Diabetologia},
	Keywords = {Indicators and Reagents;Cell Differentiation;Research Support, Non-U.S. Gov't;Luminescent Proteins;Chimera;Bone Marrow Cells;Streptozocin;Islets of Langerhans;Bone Marrow Transplantation;11 Glia;Mice, Transgenic;Pancreas;Insulin;Green Fluorescent Proteins;Mice;Animals;Feasibility Studies},
	Medline = {22892238},
	Month = {10},
	Nlm_Id = {0006777},
	Number = {10},
	Organization = {Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.},
	Pages = {1366-74},
	Pubmed = {12898006},
	Title = {Little evidence of transdifferentiation of bone marrow-derived cells into pancreatic beta cells},
	Uuid = {BACB0482-2E63-46D3-A64B-050727B8FFA6},
	Volume = {46},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00125-003-1182-9}}

@article{Choi:2003a,
	Abstract = {The present study examined whether thrombin-induced microglial activation could contribute to death of dopaminergic neurons in the rat substantia nigra (SN) in vivo. Seven days after thrombin injection into the SN, tyrosine hydroxylase immunohistochemistry showed a significant loss of nigral dopaminergic neurons. In parallel, thrombin-activated microglia, visualized by immunohistochemical staining using antibodies against the complement receptor type 3 (OX-42) and the major histocompatibility complex class II antigens were also observed in the SN, where degeneration of nigral neurons was found. Reverse transcription PCR at various time points demonstrated that activated microglia in vivo exhibited an early and transient expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and several proinflammatory cytokines, including interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor alpha. Western blot analysis and double-label immunohistochemistry showed an increase in the expression of iNOS and COX-2 and the colocalization of these proteins within microglia. The thrombin-induced loss of SN dopaminergic neurons was partially inhibited by NG-nitro-L-arginine methyl ester hydrochloride, an NOS inhibitor, and by DuP-697, a COX-2 inhibitor. Additional studies demonstrated that extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) were activated in the SN as early as 30 min after thrombin injection, and that these kinases were localized within microglia. Inhibition of ERK1/2 and p38 MAPK reduced iNOS and COX-2 mRNA expression and rescued dopaminergic neurons in the SN. The present results strongly suggest that microglial activation triggered by endogenous compound(s) such as thrombin may be involved in the neuropathological processes of dopaminergic neuronal cell death that occur in Parkinson's disease.},
	Author = {Choi, Sang-H H. and Joe, Eun H. and Kim, Seung U. and Jin, Byung K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Prostaglandin-Endoperoxide Synthase;Dopamine;Animals;Disease Progression;Stereotaxic Techniques;Microinjections;Rats;Enzyme Inhibitors;07 Excitotoxicity Apoptosis;Microglia;Female;Cell Count;Nitric-Oxide Synthase;Rats, Sprague-Dawley;Substantia Nigra;Not relevant;11 Glia;Support, Non-U.S. Gov't;Neurons;Thrombin;Tyrosine 3-Monooxygenase;Parkinsonian Disorders;Immunohistochemistry;Isoenzymes;Mitogen-Activated Protein Kinases;Cytokines},
	Medline = {22727329},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {13},
	Organization = {Brain Disease Research Center, Neuroscience Graduate Program, Ajou University School of Medicine, Suwon 442-749, Korea.},
	Pages = {5877-86},
	Pii = {23/13/5877},
	Pubmed = {12843292},
	Title = {Thrombin-induced microglial activation produces degeneration of nigral dopaminergic neurons in vivo},
	Uuid = {CD6E53EB-9EE0-4988-AEBC-A1E9A802B3E6},
	Volume = {23},
	Year = {2003},
	url = {papers/Choi_JNeurosci2003}}

@article{Choi:2005,
	Abstract = {To better understand the pathophysiological role of Src protein, a non-receptor protein tyrosine kinase of 60kDa, in the ischemic brain, we investigated the time course and regional distribution of active Src expression by using a specific antibody against Tyr416 phosphorylated Src (phospho-Src) in the rat hippocampus after transient forebrain ischemia. In the hippocampus of the control animals, active Src expression was too low to be detected by immunolabeling. Beginning 4h after reperfusion, active Src expression became evident and, after 1 day, had increased preferentially in the CA field of the hippocampus proper and the dentate gyrus. By day 3, active Src expression markedly increased in the pyramidal cell layer of CA1 and the dentate hilar region in temporal correlation with neuronal cell death occurring in these areas, where cells typical of phagocytic microglia showed phospho-Src immunoreactivity. Double-labeling experiments revealed that cells expressing active Src were microglia that stained for biotinylated lectin derived from Griffonia simplicifolia (GSI-B4). Active Src expression began to decline at day 7 and returned to the basal level by day 14 after reperfusion. These results demonstrate increased phosphorylation of Src in activated microglia of the post-ischemic hippocampus, indicating that Src signaling may be involved in the microglial reaction to an ischemic insult.},
	Author = {Choi, Jeong-Sun S. and Kim, Ha-Young Y. and Chung, Jin-Woong W. and Chun, Myung-Hoon H. and Kim, Seong Yun and Yoon, Shin-Hee H. and Lee, Mun-Yong Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Animals;Rats;Comparative Study;src-Family Kinases;Microglia;Rats, Sprague-Dawley;Hippocampus;Pyramidal Cells;Gene Expression Regulation, Enzymologic;11 Glia;Time Factors;Disease Models, Animal;Male;Antigens;Immunohistochemistry;Ischemic Attack, Transient;Lectins;Research Support, Non-U.S. Gov't},
	Nlm_Id = {7600130},
	Number = {1-2},
	Organization = {Department of Anatomy, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, Korea.},
	Pages = {1-5},
	Pii = {S0304-3940(05)00029-7},
	Pubmed = {15854740},
	Title = {Activation of Src tyrosine kinase in microglia in the rat hippocampus following transient forebrain ischemia},
	Uuid = {144F8DED-B473-4749-8A8B-6C154CD8A590},
	Volume = {380},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neulet.2005.01.015}}

@article{Chugani:1991,
	Abstract = {The developmental appearance of ameboid and ramified microglia in the rat brain has been examined by immunofluorescent localization of vaults, recently described ribonucleoprotein particles (Kedersha and Rome, 1986a). Vaults are distinct, multiarched structures of unknown function expressed by higher and lower eukaryotic species. Although vaults have been detected in all mammalian cells examined to date, they are highly enriched in macrophages. In the brain, vault antisera is highly specific for both ameboid and ramified microglia. The developmental profile of vault immunoreactivity in rat brain slices suggests that microglia enter the brain at 2 locations, with different time scales for each. The first migration, which begins before embryonic day 15 and subsides between postnatal days 7 and 14, was identified by vault immunoreactivity and Bandeiraea simplicifolia B4-isolectin (a microglia marker) staining. The cells appear to enter from blood vessels and display a ramified morphology as soon as they are detected in the brain. The second microglial migration occurs in the first postnatal week, when ameboid microglia appear in the corpus callosum and other large fiber tracts. Ameboid microglia appear to differentiate into ramified microglia between postnatal days 4 and 14. Vault immunoreactivity, as a very early microglial marker, provides new insight regarding the much-debated origin of the ramified microglia. It is quite clear that ameboid cells are not the sole source of ramified microglia because ramified cells can be detected before the influx of ameboid microglia. Colocalization studies with monocyte/macrophage markers ED1 and OX42 demonstrate that both ramified and ameboid microglia originate from monocyte lineage.},
	Author = {Chugani, D. C. and Kedersha, N. L. and Rome, L. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:28 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Aging;Cells, Cultured;Embryo;Neuroglia;Rats;Not relevant;11 Glia;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Mesoderm;Fluorescent Antibody Technique;Animals;Brain;Immune Sera;Macrophages;Organelles},
	Medline = {91093747},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {1},
	Organization = {Department of Radiological Sciences, UCLA School of Medicine 90024.},
	Pages = {256-68},
	Pubmed = {1986066},
	Title = {Vault immunofluorescence in the brain: new insights regarding the origin of microglia},
	Uuid = {4FF36366-73EF-4915-A2A7-E731849C9193},
	Volume = {11},
	Year = {1991}}

@article{Ciaroni:1999,
	Abstract = {Neurogenesis occurs throughout adult life in rat dentate gyrus. Factors and mechanisms of adult neurogenesis regulation are not well known. Vitamin E deficiency has been found to deliver a neurogenetic potential in rat dorsal root ganglia. To determine whether the role of tocopherols in adult neurogenesis may be generalized to the central nervous system, changes in adult rat dentate gyrus neurogenesis were investigated in vitamin E deficiency. Neurogenesis was quantitatively studied by determination of the density of 5-bromo-2'-deoxyuridine (BrdU)-labeled cells and by determination of the total number of cells in the granule cell layer. The BrdU-labeled cells were immunocytochemically characterized by demonstration of neuronal marker calbindin D28K. The following results were found: (1) the volume of the granule layer increased in controls from 1 to 5 months of age, mainly due to cell density decrease; (2) the volume increased by a similar amount in vitamin E-deficient rats, mainly because of an increase in cell number; (3) BrdU-positive cells were more numerous in vitamin E- deficient rats in comparison to age-matched controls; (4) the increase in proliferated cells was located in the hilus and in the plexiform layer. This study confirms that neurogenesis occurs within adult dentate gyrus and demonstrates that this process is enhanced in vitamin E deficiency. This finding indicates that vitamin E may be an exogenous factor regulating adult neurogenesis.},
	Author = {Ciaroni, S. and Cuppini, R. and Cecchini, T. and Ferri, P. and Ambrogini, P. and Cuppini, C. and Del Grande, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Rats, Sprague-Dawley;C-12;Rats/*anatomy &histology;Cell Division;Cell Count;Animal;Vitamin E Deficiency/*pathology;DNA Replication;04 Adult neurogenesis factors;Male;Neurons/*pathology;Dentate Gyrus/*pathology},
	Number = {3},
	Organization = {Istituto di Scienze Morfologiche, University of Urbino, I-61029 Urbino, Italy. s.ciaroni\@uniurb.it},
	Pages = {495-502.},
	Title = {Neurogenesis in the adult rat dentate gyrus is enhanced by vitamin E deficiency},
	Uuid = {E46723EB-6EF3-424B-8414-F8D8D533A99F},
	Volume = {411},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10413782}}

@article{Ciaroni:2002,
	Abstract = {In order to investigate the role of postnatal neurogenesis in granule cell number control in the rat dentate gyrus, we administered Methylazoxymethanol (MAM), a drug able to prevent cells from dividing, on P3, P5, P7, P9, when the most granule cells are produced. The effect of MAM on the number of proliferating precursors and of granule cells was examined at P16 and P90. We used 5-bromo-2'-deoxyuridine administration to label proliferating cells and immunohistochemistry to characterize the cell phenotype using neuron markers TUC 4, PSA-NCAM, Calbindin D28K and glial marker GFAP. At 16 days of age in MAM-treated rats we observed a significant decrease of BrdU-positive cells. Consistently, a decrease in density and number of granule cells was found compared to the controls. At 90 days the dentate gyrus of treated rats showed a complete recovery: no differences in the density, total number of neurons, the BrdU- and TUC 4-positive cells were revealed with respect to the controls. No deficits were evident in performance on the water maze in MAM-treated rats. These data suggest that the dentate gyrus is able to re-establish the proliferative zone and to rebuild the granule cell layer following neonatal MAM administration.},
	Author = {Ciaroni, S. and Cecchini, T. and Ferri, P. and Ambrogini, P. and Cuppini, R. and Lombardelli, G. and Peruzzi, G. and Del Grande, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:19 -0400},
	Journal = {Mech Ageing Dev},
	Keywords = {D;06 Adult neurogenesis injury induced},
	Number = {5},
	Organization = {Institute of Morphological Sciences, University of Urbino, loc. Crocicchia, I-61029 (PS), Urbino, Italy},
	Pages = {499-509.},
	Title = {Postnatal development of rat dentate gyrus: effects of methylazoxymethanol administration},
	Uuid = {DA923AC9-6C2B-4C62-BB2B-7A10E8B1A3B1},
	Volume = {123},
	Year = {2002},
	url = {papers/Ciaroni_MechAgeingDev2002}}

@article{Clay:1999,
	Abstract = {The purpose of this review is to illustrate some of the technical and biological hurdles that need to be addressed when developing new gene therapy based clinical trials. Gene transfer approaches can be used to "mark" cells to monitor their persistence in vivo in patients, to protect cells from toxic chemotherapeutic agents, correct a genetic defect within the target cell, or to confer a novel function on the target cell. Selection of the most suitable vector for gene transfer depends upon a number of factors such as the target cell itself and whether gene expression needs to be sustained or transient. The TCR gene transfer approach described here represents one innovative strategy being pursued as a potential therapy for metastatic melanoma. Tumor reactive T cells can be isolated from the tumor infiltrating lymphocytes (TIL) of melanoma patients. A retroviral vector has been constructed containing the T cell receptor (TCR) alpha and beta chain genes from a MART-1-specific T cell clone (TIL 5). Jurkat cells transduced with this virus specifically release cytokine in response to MART-1 peptide pulsed T2 cells, showing that the virus can mediate expression of a functional TCR. HLA-A2 transgenic mice are being used to examine whether transduced bone marrow progenitor cells will differentiate in vivo into mature CD8+ T cells expressing the MART-1-specific TCR. Expression of the human TCR alpha and beta chain genes has been detected by RT-PCR in the peripheral blood of HLA-A2 transgenic mice reconstituted with transduced mouse bone marrow. Expression of the TIL 5 TCR genes in the peripheral blood of these mice was maintained for greater than 40 weeks after bone marrow reconstitution. TIL 5 TCR gene expression was also maintained following transfer of bone marrow from mice previously reconstituted with transduced bone marrow to secondary mouse recipients, suggesting that a pluripotent progenitor or lymphocyte progenitor cell has been transduced.},
	Author = {Clay, T. M. and Custer, M. C. and Spiess, P. J. and Nishimura, M. I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {1219-4956},
	Journal = {Pathol Oncol Res},
	Keywords = {Cell Differentiation;Jurkat Cells;Genetic Vectors;Receptors, Antigen, T-Cell, alpha-beta;Melanoma;T-Lymphocytes, Cytotoxic;Gene Therapy;Epitopes;Animals;Lymphocytes, Tumor-Infiltrating;Gene Expression;Transfection;Mice, Inbred C57BL;Hematopoietic Stem Cells;Neoplasm Metastasis;11 Glia;Hematopoietic Stem Cell Transplantation;Neoplasm Proteins;HLA-A2 Antigen;Lymphokines;Retroviridae;Graft Survival;COS Cells;review;Radiation Chimera;Mice, Inbred C3H;Mice;review, tutorial;Humans;Mice, Transgenic;Reverse Transcriptase Polymerase Chain Reaction},
	Medline = {99180734},
	Nlm_Id = {9706087},
	Number = {1},
	Organization = {National Cancer Institute, National Institutes of Health, Surgery Branch, Bethesda, MD 20892, USA. Tim\_Clay\@nih.gov.usa},
	Pages = {3-15},
	Pubmed = {10079371},
	Title = {Potential use of T cell receptor genes to modify hematopoietic stem cells for the gene therapy of cancer},
	Uuid = {D8E5848C-F90F-40F7-AFE7-7DC3E697EB67},
	Volume = {5},
	Year = {1999}}

@article{Cobos:2005,
	Abstract = {Dlx homeodomain transcription factors are essential during embryonic development for the production of forebrain GABAergic interneurons. Here we show that Dlx1 is also required for regulating the functional longevity of cortical and hippocampal interneurons in the adult brain. We demonstrate preferential Dlx1 expression in a subset of cortical and hippocampal interneurons which, in postnatal Dlx1 mutants, show a time-dependent reduction in number. This reduction preferentially affects calretinin(+) (bipolar cells) and somatostatin(+) subtypes (for example, bitufted cells), whereas parvalbumin(+) subpopulations (basket cells and chandelier cells) seem to be unaffected. Cell transplantation analysis demonstrates that interneuron loss reflects cell-autonomous functions of Dlx1. The decrease in the number of interneurons was associated with a reduction of GABA-mediated inhibitory postsynaptic current in neocortex and hippocampus in vitro and cortical dysrhythmia in vivo. Dlx1 mutant mice show generalized electrographic seizures and histological evidence of seizure-induced reorganization, linking the Dlx1 mutation to delayed-onset epilepsy associated with interneuron loss.},
	Author = {Cobos, Inma and Calcagnotto, Maria Elisa and Vilaythong, Alex J. and Thwin, Myo T. and Noebels, Jeffrey L. and Baraban, Scott C. and Rubenstein, John L. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {gamma-Aminobutyric Acid;Animals;Synapses;Aging;Brain;Apoptosis;Homeodomain Proteins;Epilepsy;Cell Count;21 Epilepsy;Gene Deletion;Behavior, Animal;Research Support, U.S. Gov't, P.H.S.;Mice, Knockout;Neurons;21 Neurophysiology;Cerebral Cortex;Mice;Interneurons;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Neural Inhibition;12 Interneuron development;Research Support, Non-U.S. Gov't},
	Month = {8},
	Nlm_Id = {9809671},
	Number = {8},
	Organization = {Nina Ireland Laboratory of Developmental Neurobiology, Department of Psychiatry, University of California San Francisco, San Francisco, California 94158, USA. icobos\@itsa.ucsf.edu},
	Pages = {1059-68},
	Pii = {nn1499},
	Pubmed = {16007083},
	Title = {Mice lacking Dlx1 show subtype-specific loss of interneurons, reduced inhibition and epilepsy},
	Uuid = {890F4BC0-8C79-47AD-BCC2-76565AB7090D},
	Volume = {8},
	Year = {2005},
	url = {papers/Cobos_NatNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1499}}

@article{Cogle:2004,
	Abstract = {Background End-organ repair by adult haemopoietic stem cells is under great scrutiny with investigators challenging the notion of these cells'plasticity. Some investigations of animals and short-term human bone marrow transplants suggest that bone marrow can repair brain. We looked for evidence of clinically relevant marrow-derived restorative neurogenesis: long-term, multilineage, neural engraftment that is not the result of cell-fusion events. Methods We examined autopsy brain specimens from three sex-mismatched female bone-marrow-transplantation patients, a female control, and a male control. We did immunohistochemistry, fluorescence in-situ hybridisation, and tissue analysis to look for multilineage, donor-derived neurogenesis. Findings Hippocampal cells containing a Y chromosome were present up to 6 years post-transplant in all three patients. Transgender neurons accounted for 1\%of all neurons; there was no evidence of fusion events since only one X chromosome was present. Moreover, transgender astrocytes and microglia made up 1-2\%of all glial cells. Interpretation Postnatal human neuropoiesis happens, and human haemopoietic cells can transdifferentiate into neurons, astrocytes, and microglia in a long-term setting without fusing. Transplantable human haemopoietic cells could serve as a therapeutic source for long-term regenerative neuropoiesis. 1474-547x Journal Article},
	Author = {Cogle, C. R. and Yachnis, A. T. and Laywell, E. D. and Zander, D. S. and Wingard, P. J. and Steindler, P. D. and Scott, E. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {Lancet},
	Keywords = {EE, L pdf},
	Number = {9419},
	Organization = {Program in Stem Cell Biology and Regenerative Medicine, University of Florida Shands Cancer Center, Gainesville, FL, USA.},
	Pages = {1432-7},
	Title = {Bone marrow transdifferentiation in brain after transplantation: a retrospective study},
	Uuid = {794DD876-D3AF-11D9-A0E9-000D9346EC2A},
	Volume = {363},
	Year = {2004},
	url = {papers/Cogle_Lancet2004.pdf}}

@article{Cogswell:1998,
	Abstract = {A recently discovered, spontaneous, autosomal recessive mutation in rats, flathead (fh), results in greatly reduced brain growth beginning in late fetal development. In this study we have mapped the fh mutation by determining the pattern of segregation of polymorphic microsatellite markers with respect to fh in 51 affected F2 offspring from a single interstrain intercross. Two markers on chromosome 12, D12Rat80 and D12Mgh6, cosegregated with the fh mutation in all 51 affected animals. The distribution of six additional markers in 40 informative meioses further localizes fh approximately 2 cM teleomeric to nos1. There are no known mutations in homologous regions of either mouse or human genomes that result in deficits in late neurodevelopment similar to that observed in fh/fh animals. The unique phenotype of fh/fh animals and the location of fh suggests the presence of a novel gene essential to normal brain development on the distal end of rat chromosome 12.},
	Author = {Cogswell, C. A. and Sarkisian, M. R. and Leung, V. and Patel, R. and D'Mello, S. R. and LoTurco, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Genetic Markers;Rats, Mutant Strains;Animals;Genes, Recessive;Humans;Aging;Rats;Phenotype;Brain;Female;Lod Score;Rats, Wistar;Embryonic and Fetal Development;Crosses, Genetic;Male;Homozygote;Mice;Chromosome Mapping;Genes, Essential},
	Medline = {98378253},
	Month = {7},
	Nlm_Id = {7600130},
	Number = {1},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, Storrs 06269-4156, USA.},
	Pages = {5-8},
	Pii = {S0304394098004789},
	Pubmed = {9714451},
	Title = {A gene essential to brain growth and development maps to the distal arm of rat chromosome 12},
	Uuid = {B85E5D54-69B0-11DA-A4B6-000D9346EC2A},
	Volume = {251},
	Year = {1998},
	url = {papers/Cogswell_NeurosciLett1998.pdf}}

@article{Coil:2004,
	Abstract = {The envelope protein from vesicular stomatitis virus (VSV) has become an important tool for gene transfer and gene therapy. It is widely used mainly because of its ability to mediate virus entry into all cell types tested to date. Consistent with the broad tropism of the virus, the receptor for VSV is thought to be a ubiquitous membrane lipid, phosphatidylserine (PS). However, the evidence for this hypothesis is indirect and incomplete. Here, we have examined the potential interaction of VSV and PS at the plasma membrane in more detail. Measurements of cell surface levels of PS show a wide range across cell types from different organisms. We demonstrate that there is no correlation between the cell surface PS levels and VSV infection or binding. We also demonstrate that an excess of annexin V, which binds specifically and tightly to PS, does not inhibit infection or binding by VSV. While the addition of PS to cells does allow increased virus entry, we show that this effect is not specific to the VSV envelope. We conclude that PS is not the cell surface receptor for VSV, although it may be involved in a postbinding step of virus entry.},
	Author = {Coil, David A. and Miller, A. Dusty},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {15 PS VSVG receptor;Cell Membrane;Phosphatidylserines;Receptors, Cell Surface;Cricetinae;Cell Line;Annexin A5;Research Support, U.S. Gov't, P.H.S.;Receptors, Virus;Vesicular stomatitis-Indiana virus;Dogs;15 Retrovirus mechanism;Animals;Humans;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {0113724},
	Number = {20},
	Organization = {Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N., Room C2-105, P.O. Box 19024, Seattle, WA 98109-1024, USA.},
	Pages = {10920-6},
	Pii = {78/20/10920},
	Pubmed = {15452212},
	Title = {Phosphatidylserine is not the cell surface receptor for vesicular stomatitis virus},
	Uuid = {D0F5469D-DDC6-42E6-8510-0D78677E7ABE},
	Volume = {78},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.78.20.10920-10926.2004}}

@article{Coil:2005,
	Abstract = {Enveloped virus vectors are used in a wide variety of applications. We have discovered that treatment of cultured cells with phosphatidylserine (PS) liposomes can increase virus vector infection by up to 20-fold. This effect does not abrogate virus receptor requirements, is specific to PS compared to other phospholipids, and is limited to enveloped viruses. Furthermore, the enhancement of infection does not occur through increases in virus receptor levels or virus binding, indicating that virus fusion is enhanced. The liposomes are easily generated, store well, and allow enhanced infection with a variety of virus vectors and cell types.},
	Author = {Coil, David A. and Miller, A. Dusty},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {15 PS VSVG receptor;Phosphatidylserines;Virus Replication;Cell Line;Retroviridae;Research Support, U.S. Gov't, P.H.S.;Research Support, N.I.H., Extramural;15 Retrovirus mechanism;Humans;Animals;24 Pubmed search results 2008;Genetic Vectors},
	Month = {9},
	Nlm_Id = {0113724},
	Number = {17},
	Organization = {Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA.},
	Pages = {11496-500},
	Pii = {79/17/11496},
	Pubmed = {16103200},
	Title = {Enhancement of enveloped virus entry by phosphatidylserine},
	Uuid = {EFC78F89-375C-4D53-B511-2B695B95C59D},
	Volume = {79},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.79.17.11496-11500.2005}}

@article{Coil:2005a,
	Abstract = {BACKGROUND: A major determinant of retrovirus host range is the presence or absence of appropriate cell-surface receptors required for virus entry. Often orthologs of functional receptors are present in a wide range of species, but amino acid differences can render these receptors non-functional. In some cases amino acid differences result in additional N-linked glycosylation that blocks virus infection. The latter block to retrovirus infection can be overcome by treatment of cells with compounds such as tunicamycin, which prevent the addition of N-linked oligosaccharides. RESULTS: We have discovered that treatment of cells with liposomes composed of phosphatidylserine (PS) can also overcome the block to infection mediated by N-linked glycosylation. Importantly, this effect occurs without apparent change in the glycosylation state of the receptors for these viruses. This effect occurs with delayed kinetics compared to previous results showing enhancement of virus infection by PS treatment of cells expressing functional virus receptors. CONCLUSION: We have demonstrated that PS treatment can relieve the block to retrovirus infection of cells expressing retroviral receptors that have been rendered non-functional by glycosylation. These findings have important implications for the current model describing inhibition of virus entry by receptor glycosylation.},
	Author = {Coil, David A. and Miller, A. Dusty},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1742-4690},
	Journal = {Retrovirology},
	Keywords = {15 PS VSVG receptor;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {101216893},
	Organization = {Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA. coild\@u.washington.edu},
	Pages = {49},
	Pii = {1742-4690-2-49},
	Pubmed = {16091143},
	Title = {Phosphatidylserine treatment relieves the block to retrovirus infection of cells expressing glycosylated virus receptors},
	Uuid = {19DFEABE-41DC-47BB-84FB-A7D9D942B230},
	Volume = {2},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1742-4690-2-49}}

@article{Colavincenzo:2000,
	Abstract = {We have examined the clearance of myelin debris from the visual pathways of the goldfish during Wallerian degeneration. Both the rate and pattern of myelin disappearance from the optic nerve and tract were determined using immunohistochemistry on frozen sections, as well as plastic sections and electron microscopy. Animals with and without regenerating optic axons were examined in order to determine whether the axons play a role in myelin clearance. We found that myelin is cleared at different rates along the visual paths. Thus, virtually all myelin debris is gone in the optic tract and distal optic nerve stump by 4 weeks after surgery, while in the cranial nerve segment, myelin clearance is still incomplete at 6 weeks postoperative. These temporal and spatial patterns of myelin clearance are the same in animals with and without regenerating axons, thus indicating that growing axons do not influence this process. Finally, ultrastructural observations revealed that both astrocytes and microglia participate in phagocytosing myelin debris in the optic nerve, while in the tract, the vast majority of debris is removed by microglia alone. These data are discussed with regard to possible mechanisms controlling the differential expression of myelin clearance.},
	Author = {Colavincenzo, J. and Levine, R. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Wallerian Degeneration;Goldfish;Cytokines;Nerve Regeneration;Myelin Sheath;Astrocytes;Microscopy, Electron;Not relevant;11 Glia;Optic Nerve;Animals;Visual Pathways;Phagocytosis;Support, Non-U.S. Gov't},
	Medline = {20121686},
	Month = {1},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Biology, McGill University, Montr{\'e}al, Qu{\'e}bec, Canada.},
	Pages = {47-62},
	Pii = {10.1002/(SICI)1097-4547(20000101)59:1<47::AID-JNR7>3.0.CO;2-P},
	Pubmed = {10658185},
	Title = {Myelin debris clearance during Wallerian degeneration in the goldfish visual system},
	Uuid = {657F374F-2CEE-4454-9C85-C99DF6D0095A},
	Volume = {59},
	Year = {2000}}

@article{Colombo:1997,
	Abstract = {Long astroglial processes traversing several cortical laminae appear to be characteristic of primate brains. Whether interlaminar processes develop as a modification of radial glia or are truly postnatal elements stemming from stellate astroglia, could be assessed by analyzing their early developmental stages. A survey of glial fibrillar acidic protein immunoreactive (GFAP-IR) astroglial interlaminar processes in the cerebral cortex of Ceboidea monkeys at various postnatal developmental ages, and in human cortical samples of a ten day and a seven year old child disclosed that such processes develop postnatally. At one month of age GFAP-IR interlaminar processes in monkeys were scarce and short in most frontal, parietal or occipital (striate) cortical areas, except for sulcal (principal and orbital sulci) and temporal cortical areas. Some processes were weakly positive for vimentin, and these were most abundant in ventral temporal cortical areas. At two months of age processes were present in all these areas, albeit in restricted patches and significantly shorter than in adults. The expression of this pattern was increased at seven months of age. At three years of age almost every area showed abundant processes and with lengths comparable to the adult Ceboidea individuals. In humans, at 10 days of age long interlaminar processes were readily apparent in a frontal cortex sample, becoming most apparent at the age of seven years although not reaching yet the adult characteristics as described previously. CONCLUSIONS: (1) GFAP-IR interlaminar processes develop postnatally, thus typifying a subtype of the classical stellate forms; (2) they bear no obvious direct relationship with radial glia; (3) their development is not contemporary among the various cortical regions. These long cellular processes represent an addition to those already described for other astroglial cell types in the adult mammalian brain (Golgi-Bergmann glia, tanicytes, Muller cells).},
	Author = {Colombo, J. A. and Lipina, S. and Yanez, A. and Puissant, V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Int J Dev Neurosci},
	Keywords = {Species Specificity;Cerebral Cortex/*growth &development;Human;Immunohistochemistry;Glial Fibrillary Acidic Protein/analysis;Astrocytes/*physiology/ultrastructure;11 Glia;Animal;Cebus;Saimiri;Support, Non-U.S. Gov't;G;Child;Infant, Newborn},
	Number = {7},
	Organization = {Programa Unidad de Neurobiologia Aplicada (PRUNA) (CEMIC-CONICET), Buenos Aires, Argentina. colombo\@pruna.gov.ar},
	Pages = {823-33.},
	Title = {Postnatal development of interlaminar astroglial processes in the cerebral cortex of primates},
	Uuid = {8CEFFDC9-AA39-435F-AA95-8B8F75A40614},
	Volume = {15},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9580494}}

@article{Colombo:2007,
	Abstract = {ARX loss-of-function mutations cause X-linked lissencephaly with ambiguous genitalia (XLAG), a severe neurological condition that results in profound brain malformations, including microcephaly, absence of corpus callosum, and impairment of the basal ganglia. Despite such dramatic defects, their nature and origin remain largely unknown. Here, we used Arx mutant mice as a model to characterize the cellular and molecular mechanisms underlying the basal ganglia alterations. In these animals, the early differentiation of this tissue appeared normal, whereas subsequent differentiation was impaired, leading to the periventricular accumulation of immature neurons in both the lateral ganglionic eminence and medial ganglionic eminence (MGE). Both tangential migration toward the cortex and striatum and radial migration to the globus pallidus and striatum were greatly reduced in the mutants, causing a periventricular accumulation of NPY+ or calretinin+ neurons in the MGE. Arx mutant neurons retained their differentiation potential in vitro but exhibited deficits in morphology and migration ability. These findings imply that cell-autonomous defects in migration underlie the neuronal localization defects. Furthermore, Arx mutants lacked a large fraction of cholinergic neurons and displayed a strong impairment of thalamocortical projections, in which major axon fiber tracts failed to traverse the basal ganglia. Altogether, these results highlight the critical functions of Arx in promoting neural migration and regulating basal ganglia differentiation in mice, consistent with the phenotype of XLAG patients.},
	Author = {Colombo, Elena and Collombat, Patrick and Colasante, Gaia and Bianchi, Marta and Long, Jason and Mansouri, Ahmed and Rubenstein, John L. R. and Broccoli, Vania},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;Cell Differentiation;Animals;Basal Ganglia;Cells, Cultured;Genitalia;Mice, Mutant Strains;Transcription Factors;Pregnancy;Homeodomain Proteins;Cell Movement;Female;Substantia Nigra;Mice, Inbred C57BL;Organ Culture Techniques;research support, non-u.s. gov't;Male;Septal Nuclei;Animals, Newborn;Thalamus;X Chromosome;Cerebral Cortex;Globus Pallidus;research support, n.i.h., extramural;Mice;Interneurons;24 Pubmed search results 2008;12 Interneuron development},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Stem Cell Research Department, San Raffaele Scientific Institute, 20132 Milan, Italy.},
	Pages = {4786-98},
	Pii = {27/17/4786},
	Pubmed = {17460091},
	Title = {Inactivation of Arx, the murine ortholog of the X-linked lissencephaly with ambiguous genitalia gene, leads to severe disorganization of the ventral telencephalon with impaired neuronal migration and differentiation},
	Uuid = {18F33651-D0F0-40F7-8416-D4522CB63A37},
	Volume = {27},
	Year = {2007},
	url = {papers/Colombo_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0417-07.2007}}

@article{Combs:1999,
	Abstract = {Microglial interaction with amyloid fibrils in the brains of Alzheimer's and prion disease patients results in the inflammatory activation of these cells. We observed that primary microglial cultures and the THP-1 monocytic cell line are stimulated by fibrillar beta-amyloid and prion peptides to activate identical tyrosine kinase-dependent inflammatory signal transduction cascades. The tyrosine kinases Lyn and Syk are activated by the fibrillar peptides and initiate a signaling cascade resulting in a transient release of intracellular calcium that results in the activation of classical PKC and the recently described calcium-sensitive tyrosine kinase PYK2. Activation of the MAP kinases ERK1 and ERK2 follows as a subsequent downstream signaling event. We demonstrate that PYK2 is positioned downstream of Lyn, Syk, and PKC. PKC is a necessary intermediate required for ERK activation. Importantly, the signaling response elicited by beta-amyloid and prion fibrils leads to the production of neurotoxic products. We have demonstrated in a tissue culture model that conditioned media from beta-amyloid- and prion-stimulated microglia or from THP-1 monocytes are neurotoxic to mouse cortical neurons. This toxicity can be ameliorated by treating THP-1 cells with specific enzyme inhibitors that target various components of the signal transduction pathway linked to the inflammatory responses.},
	Author = {Combs, C. K. and Johnson, D. E. and Cannady, S. B. and Lehman, T. M. and Landreth, G. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Signal Transduction;Protein Kinase C;Neurotoxins;Enzyme Activation;Amyloid beta-Protein;Enzyme Precursors;Tyrosine;Animals;Cells, Cultured;src-Family Kinases;Microglia;Amyloid;Phosphorylation;Not relevant;Ca(2+)-Calmodulin Dependent Protein Kinase;11 Glia;Calcium;Peptide Fragments;Support, U.S. Gov't, P.H.S.;Mice;Prions;Intracellular Membranes;Protein-Tyrosine Kinase},
	Medline = {99119437},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {3},
	Organization = {Alzheimer Research Laboratory, Departments of Neurology and Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4928, USA.},
	Pages = {928-39},
	Pubmed = {9920656},
	Title = {Identification of microglial signal transduction pathways mediating a neurotoxic response to amyloidogenic fragments of beta-amyloid and prion proteins},
	Uuid = {6158C12B-0F22-4645-A708-B24421D117C1},
	Volume = {19},
	Year = {1999},
	url = {papers/Combs_JNeurosci1999.pdf}}

@article{Combs:2001,
	Abstract = {Reactive microglia associated with the beta-amyloid plaques in Alzheimer's disease (AD) brains initiate a sequence of inflammatory events integral to the disease process. We have observed that fibrillar beta-amyloid peptides activate a tyrosine kinase-based signaling response in primary mouse microglia and the human monocytic cell line, THP-1, resulting in production of neurotoxic secretory products, proinflammatory cytokines, and reactive oxygen species. We report that most of the amyloid-induced tyrosine kinase activity was stimulated after activation of Src family members such as Lyn. However, transduction of the signaling response required for increased production of the cytokines TNFalpha and IL1-beta was mediated by the nonreceptor tyrosine kinase, Syk. Additionally, beta-amyloid stimulated an NFkappaB-dependent pathway in parallel that was required for cytokine production. Importantly, TNFalpha generated by the monocytes and microglia was responsible for the majority of the neuorotoxic activity secreted by these cells after beta-amyloid stimulation but must act in concert with other factors elaborated by microglia to elicit neuronal death. Moreover, we observed that the neuronal loss was apoptotic in nature and involved increased neuronal expression of inducible nitric oxide synthase and subsequent peroxynitrite production. Selective inhibitors of inducible nitric oxide synthase effectively protected cells from toxicity associated with the microglial and monocytic secretory products. This study demonstrates a functional linkage between beta-amyloid-dependent activation of microglia and several characteristic markers of neuronal death occurring in Alzheimer's disease brains.},
	Author = {Combs, C. K. and Karlo, J. C. and Kao, S. C. and Landreth, G. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Human;Tumor Necrosis Factor;Signal Transduction;Animals;Monocytes;Amyloid beta-Protein;Enzyme Precursors;Cells, Cultured;NF-kappa B;Transcription Factors;src-Family Kinases;Apoptosis;Microglia;Nitric-Oxide Synthase;Mice, Inbred C57BL;11 Glia;Not relevant;Support, Non-U.S. Gov't;Peptide Fragments;Alzheimer Disease;Neurons;Support, U.S. Gov't, P.H.S.;Mice;Inflammation;Protein-Tyrosine Kinase},
	Medline = {21114081},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {4},
	Organization = {Alzheimer Research Laboratory, Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.},
	Pages = {1179-88},
	Pii = {21/4/1179},
	Pubmed = {11160388},
	Title = {beta-Amyloid stimulation of microglia and monocytes results in TNFalpha-dependent expression of inducible nitric oxide synthase and neuronal apoptosis},
	Uuid = {12F137BE-A9B3-4A7C-8517-95AFAC432C19},
	Volume = {21},
	Year = {2001},
	url = {papers/Combs_JNeurosci2001.pdf}}

@article{Condeelis:2006,
	Abstract = {Macrophages within the tumor microenvironment facilitate angiogenesis and extracellular-matrix breakdown and remodeling and promote tumor cell motility. Recent studies reveal that direct communication between macrophages and tumor cells leads to invasion and egress of tumor cells into the blood vessels (intravasation). Thus, macrophages are at the center of the invasion microenvironment and are an important drug target for cancer therapy.},
	Author = {Condeelis, John and Pollard, Jeffrey W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {2},
	Organization = {Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. condeeli\@aecom.yu.edu},
	Pages = {263-6},
	Pii = {S0092-8674(06)00055-9},
	Pubmed = {16439202},
	Title = {Macrophages: obligate partners for tumor cell migration, invasion, and metastasis},
	Uuid = {B67276BD-D36B-4702-A039-E339D50A1D40},
	Volume = {124},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.01.007}}

@article{Condic:2001,
	Abstract = {In a variety of adult CNS injury models, embryonic neurons exhibit superior regenerative performance when compared with adult neurons. It is unknown how young neurons extend axons in the injured adult brain, in which adult neurons fail to regenerate. This study shows that cultured adult neurons do not adapt to conditions that are characteristic of the injured adult CNS: low levels of growth-promoting molecules and the presence of inhibitory proteoglycans. In contrast, young neurons readily adapt to these same conditions, and adaptation is accompanied by an increase in the expression of receptors for growth- promoting molecules (receptors of the integrin family). Surprisingly, the regenerative performance of adult neurons can be restored to that of young neurons by gene transfer-mediated expression of a single alpha- integrin.},
	Author = {Condic, M. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Neurosci},
	Keywords = {Fibronectins/metabolism/pharmacology;Cells, Cultured;Receptors, Fibronectin/biosynthesis/genetics;Rats;Transfection;Neurons, Afferent/cytology/drug effects/*metabolism;Adenoviridae/genetics;Animal;Laminin/metabolism/pharmacology;Cell Division/drug effects/genetics;Ganglia, Spinal/cytology/metabolism;Animals, Newborn;Nerve Regeneration/drug effects/*genetics;C;04 Adult neurogenesis factors;Integrins/*biosynthesis/*genetics;Support, U.S. Gov't, P.H.S.;*Transgenes;Aging/metabolism;Gene Expression;Ligands},
	Number = {13},
	Organization = {Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, Utah 84132-0002, USA. maureen.condic\@hsc.utah.edu},
	Pages = {4782-8.},
	Title = {Adult neuronal regeneration induced by transgenic integrin expression},
	Uuid = {5F2A9C4B-445F-4DFF-9C72-F832F4D69B64},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11425905%20http://www.jneurosci.org/cgi/content/full/21/13/4782%20http://www.jneurosci.org/cgi/content/abstract/21/13/4782}}

@article{Conover:2000,
	Abstract = {The subventricular zone (SVZ) of the lateral ventricles, the largest remaining germinal zone of the adult mammalian brain, contains an extensive network of neuroblasts migrating rostrally to the olfactory bulb. Little is known about the endogenous proliferation signals for SVZ neural stem cells or guidance cues along the migration pathway. Here we show that the receptor tyrosine kinases EphB1-3 and EphA4 and their transmembrane ligands, ephrins-B2/3, are expressed by cells of the SVZ. Electron microscopy revealed ephrin-B ligands associated with SVZ astrocytes, which function as stem cells in this germinal zone. A three-day infusion of the ectodomain of either EphB2 or ephrin-B2 into the lateral ventricle disrupted migration of neuroblasts and increased cell proliferation. These results suggest that Eph/ephrin signaling is involved in the migration of neuroblasts in the adult SVZ and in either direct or indirect regulation of cell proliferation.},
	Author = {Conover, J. C. and Doetsch, F. and Garcia-Verdugo, J. M. and Gale, N. W. and Yancopoulos, G. D. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Lateral Ventricles/drug effects/*metabolism;Receptor Protein-Tyrosine Kinases/*metabolism;02 Adult neurogenesis migration;Cell Movement/drug effects/*physiology;Human;B-18;Signal Transduction/drug effects/physiology;Animal;Cell Division/drug effects/physiology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Fetal Proteins/*metabolism;Membrane Proteins/*metabolism/pharmacology;Mice;Astrocytes/cytology/drug effects/*metabolism},
	Number = {11},
	Organization = {The Rockefeller University, 1230 York Avenue, New York, New York 10021, USA. jcc\@jax.org},
	Pages = {1091-7.},
	Title = {Disruption of Eph/ephrin signaling affects migration and proliferation in the adult subventricular zone},
	Uuid = {7F310AFC-04E9-4B6F-9438-DCFE7B128042},
	Volume = {3},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11036265%20http://www.nature.com/cgi-taf/DynaPage.taf?file=/neuro/journal/v3/n11/full/nn1100_1091.html%20http://www.nature.com/cgi-taf/DynaPage.taf?file=/neuro/journal/v3/n11/abs/nn1100_1091.html}}

@article{Cook:1978,
	Abstract = {Localized Wallerian degeneration was induced in cat optic nerves by the gentle scratching of the exposed retinas. At intervals ranging up to 103 days after operation, the cats were killed and microscopic examination of the optic nerves showed, in addition to axonal degeneration, the presence of both demyelinating and demyelinated normal axons. The tongues of oligodendroglial cytoplasm were still associated with these demyelinated axons. This phenomenon is considered to reflect a change in the homeostasis of the oligodendroglial cell imposed by degeneration of a few axons from a state of maintaining the myelin sheath to one of resorption from adjacent normal axons. No evidence for the involvement of microglia in this process was found. It is concluded also that oligodendrocytes alone can be responsible for the removal of myelin debris during Wallerian degeneragion. This observation may be important to the understanding of certain demyelinating diseases of the central nervous system.},
	Author = {Cook, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Neuroglia;Wallerian Degeneration;Nerve Degeneration;Lipids;Cats;Myelin Sheath;Astrocytes;Not relevant;11 Glia;Optic Nerve;Animals;Oligodendroglia;Phagocytosis},
	Medline = {79073355},
	Nlm_Id = {7609829},
	Number = {5},
	Pages = {357-68},
	Pubmed = {724091},
	Title = {Primary demyelination in cat optic nerves associated with surgically induced axonal degeneration},
	Uuid = {123A0A17-63F4-4CC9-B7A9-D6A323B513C9},
	Volume = {4},
	Year = {1978}}

@article{Cooper:1986,
	Abstract = {Plant lectins were used to examine the disposition of glycosylated molecules in vibratome sections through the barrel subfield of mouse somatosensory cortex at selected times during postnatal development. The peroxidase conjugates of peanut agglutinin (PNA, specific for N-acetylgalactosamine), concanavalin A (specific for mannose), and wheat germ agglutinin (specific for N-acetylglucosamine and N-acetylneuraminic acid) were used to study lectin binding in aldehyde-fixed tissue sections of cortex. Following peroxidase cytochemistry and light microscopy, it was found that all three lectins bound in the region of the barrel subfield as early as postnatal day 3 (day of birth = postnatal day 1). The lectins bound to the prospective sides and/or septae of individual barrels in preference to the prospective hollows. This lectin demarcation of the barrel field occurred prior to the detection of this region with cresyl violet staining and was still demonstrable on postnatal day 6, when the individual barrels became discernible with cresyl violet. This suggests that the lectin binding material is present before the barrel field becomes a fully formed and organized region. A decrease in lectin affinity for binding sites in these tissue sections occurs during postnatal development (Cooper and Steindler: Soc. Neurosci. (Abstr.) 10: 43a, '84) and this study demonstrates that lectins do not delineate the barrel field of more mature animals (2-3 months old), whereas barrels can be detected with cresyl violet at this time. A preliminary electron microscope analysis of the postnatal day 6 somatosensory cortex demonstrates that the lectin PNA binds to elements of the forming neuropil and also to Golgi apparatus intermediate saccules in neuronal cells. The prospective barrel field can be detected with lectins during a critical period in development in which alterations can occur in the barrel field in response to peripheral deprivation (Jeanmonod et al: Neuroscience 6:1503-35, '81) and therefore we suggest that the glycans visualized with lectin-peroxidase conjugates denote possible candidates for molecules involved in shaping barrel structure. 0021-9967 Journal Article},
	Author = {Cooper, N. G. and Steindler, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Comp Neurol},
	Keywords = {16 Barrels;K abstr;Binding Sites;Somatosensory Cortex/*metabolism;Peanut Agglutinin;Mice, Inbred ICR;Concanavalin A/metabolism;Support, U.S. Gov't, P.H.S.;Animals, Newborn;Lectins/*metabolism;Animals;Wheat Germ Agglutinins;Support, Non-U.S. Gov't;Mice;Vibrissae},
	Number = {2},
	Pages = {157-69},
	Pubmed = {3755448},
	Title = {Lectins demarcate the barrel subfield in the somatosensory cortex of the early postnatal mouse},
	Uuid = {71D090A0-A3BE-46E8-AF47-485F4A96AD1C},
	Volume = {249},
	Year = {1986},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3755448}}

@article{Cooper-Kuhn:2002,
	Abstract = {Since the early 1960s, in vivo observations have shown the generation of new neurons from dividing precursor cells. Nevertheless, these experiments suffered from skepticism, suggesting that the prevailing labeling method, which incorporates tagged thymidine analogs, such as [3H]-thymidine or bromodeoxyuridine (BrdU), may not be detecting a proliferative event, but could rather mark DNA repair in postmitotic neurons. Even today many scientists outside the field are still skeptical, because the question of specificity for thymidine labeling has not been sufficiently answered. This current paper aims at evaluating the arguments that are used by proponents and skeptics of this method by (i) presenting histological evidence of specificity of BrdU labeling for neural stem cell/progenitor activity in the adult brain; (ii) validating and comparing BrdU labeling with other histological methods; and (iii) combining BrdU and labeling methods for apoptosis to argue against DNA repair being a major contribution of BrdU-positive cells. 0165-3806 Journal Article},
	Author = {Cooper-Kuhn, C. M. and Kuhn, H. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Animals;Neurology/methods;Rats;Apoptosis/physiology;Neurons/*cytology;Cell Cycle/physiology;Fluorescent Antibody Technique;Brain/*cytology;Female;Rats, Wistar;Time Factors;Cell Aging/physiology;In Situ Nick-End Labeling;Cell Division;Microscopy, Electron;Bromodeoxyuridine;A both;*DNA Repair},
	Number = {1-2},
	Organization = {Department of Neurology, University of Regensburg, Universitaetsstrasse 84, Regensburg, Germany.},
	Pages = {13-21},
	Title = {Is it all DNA repair? Methodological considerations for detecting neurogenesis in the adult brain},
	Uuid = {0688DF66-CDF1-11D9-B244-000D9346EC2A},
	Volume = {134},
	Year = {2002},
	url = {papers/Cooper-Kuhn_BrainResDevBrainRes2002}}

@article{Corbo:2002,
	Abstract = {Doublecortin (DCX) is a microtubule-associated protein that is required for normal neocortical and hippocampal development in humans. Mutations in the X-linked human DCX gene cause gross neocortical disorganization (lissencephaly or "smooth brain") in hemizygous males, whereas heterozygous females show a mosaic phenotype with a normal cortex as well as a second band of misplaced (heterotopic) neurons beneath the cortex ("double cortex syndrome"). We created a mouse carrying a targeted mutation in the Dcx gene. Hemizygous male Dcx mice show severe postnatal lethality; the few that survive to adulthood are variably fertile. Dcx mutant mice show neocortical lamination that is largely indistinguishable from wild type and show normal patterns of neocortical neurogenesis and neuronal migration. In contrast, the hippocampus of both heterozygous females and hemizygous males shows disrupted lamination that is most severe in the CA3 region. Behavioral tests show defects in context and cued conditioned fear tests, suggesting that deficits in hippocampal learning accompany the abnormal cytoarchitecture. 1529-2401 Journal Article},
	Author = {Corbo, J. C. and Deuel, T. A. and Long, J. M. and LaPorte, P. and Tsai, E. and Wynshaw-Boris, A. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {J Neurosci},
	Keywords = {Motor Activity;Heterozygote;Hippocampus/abnormalities/pathology/*physiopathology;Gene Targeting;Animals;Fear;Memory;Mice, Mutant Strains;10 Development;Phenotype;10 Hippocampus;Female;Neocortex/abnormalities/pathology/*physiopathology;F pdf;Reaction Time;Disease Models, Animal;Behavior, Animal;Male;Crosses, Genetic;Neurons/metabolism/pathology;Neuropeptides/deficiency/genetics/*metabolism;Learning;Support, U.S. Gov't, P.H.S.;Mice;Fetal Viability;Microtubule-Associated Proteins/metabolism;Genes, Reporter;Nervous System Malformations/*metabolism/pathology},
	Number = {17},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {7548-57},
	Title = {Doublecortin is required in mice for lamination of the hippocampus but not the neocortex},
	Uuid = {C2063D4B-DF58-4196-BAEE-2EB2A32353B1},
	Volume = {22},
	Year = {2002},
	url = {papers/Corbo_JNeurosci2002.pdf}}

@article{Coronas:2002,
	Abstract = {Previous experiments have established that grafts of embryonic day (E) 16 frontal cortex placed into the occipital cortex of postnatal day (P) 0-P1 rats selectively attract axons from the ventrolateral and ventromedial (VL/VM) thalamic nuclei (Frapp{\'e} et al., Exp. Neurol. 169 (2001) 264). The present study was therefore undertaken to identify any possible maturation-promoting activity of the cortex on VL/VM thalamic cells. In a first step, a primary culture of VL/VM thalamic cells taken from P0-P1 rats was developed. Neurons, glial cells and a few immature, nestin immunoreactive cells were identified in the culture. In a second step, VL/VM thalamic cells that had been maintained in vitro for 4-5 days were cultured for 7 additional days in isolation (control condition) or with an E16 or P5 explant of frontal or occipital cortex placed on a microporous membrane. In control conditions, the total cell population and the percentage of MAP-2 immunoreactive neurons were not modified with time. In contrast, the percentage of MAP-2 immunoreactive neurons was increased in E16 cortex co-cultures whereas the total cell population was unchanged and the proliferative activity remained very low. Also, the mean number of neurites per neuron was increased but no effect was found on neuritic length. Similar effects on neuronal maturation were found with E16 frontal or occipital cortex explants, indicating a lack of areal specificity. P5 cortex also produced, but to a lesser extent, an increase in percentage of MAP-2 immunoreactive neurons. Further, P5 cortex had no effect on mean number of neurites per neuron but substantially promoted elongation of neuronal processes. We propose that in addition to their well-established survival promoting effect, diffusible molecules released by embryonic and early postnatal cortex can promote in vitro the maturation of thalamic neurons.},
	Author = {Coronas, Val{\'e}rie and Arnault, Patricia and Roger, Michel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0168-0102},
	Journal = {Neurosci Res},
	Keywords = {Microtubule-Associated Proteins;Cell Differentiation;Animals;Pregnancy;Cells, Cultured;Coculture Techniques;Rats;Neural Pathways;Frontal Lobe;Female;Cell Communication;Neurites;Rats, Wistar;Animals, Newborn;Thalamus;Cerebral Cortex;Neurons;Occipital Lobe;Body Patterning;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Diffusion;Growth Substances},
	Medline = {22070432},
	Month = {5},
	Nlm_Id = {8500749},
	Number = {1},
	Organization = {CNRS-UMR 6558, Laboratoire des Biomembranes et Signalisation Cellulaire, Universit{\'e} de Poitiers, Facult{\'e} des Sciences, Poitiers, France. valerie.coronas\@univ-poitiers.fr},
	Pages = {57-67},
	Pii = {S0168010202000202},
	Pubmed = {12074841},
	Title = {Cortical diffusible factors increase MAP-2 immunoreactive neuronal population in thalamic cultures},
	Uuid = {55D37F41-652C-4379-A566-047270D1E02A},
	Volume = {43},
	Year = {2002}}

@article{Corotto:1993,
	Abstract = {Neurogenesis of olfactory bulb granule cells is known to persist in adult rats where, in some strains, the bulbs grow throughout life. In mice, bulb growth ceases early in adulthood and here we ask if granule cell neurogenesis persists after the bulbs have stopped growing. By injecting adult mice with bromodeoxyuridine (BrdU) and allowing short and long survival times, we found that new cells form in the subependymal layer and that they migrate subsequently into the olfactory bulbs where they acquire the nuclear morphology of granule cells and express neuron-specific markers. Using [3H]thymidine, we found that most of these adult-generated granule neurons persist within the bulbs for at least 16 weeks. This shows the persistence of neurogenesis and neuronal migration in adult animals in which the olfactory bulbs have stopped growing.},
	Author = {Corotto, F. S. and Henegar, J. A. and Maruniak, J. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Neurosci Lett},
	Keywords = {Neurons/*physiology;02 Adult neurogenesis migration;Cell Differentiation;Olfactory Bulb/cytology/growth &development;Cell Survival/physiology;Female;Immunohistochemistry;03 Adult neurogenesis progenitor source;Thymidine/metabolism;Bromodeoxyuridine/pharmacology;Cytoplasmic Granules/ultrastructure;Calcium-Binding Protein, Vitamin D-Dependent/immunology/metabolism;Animal;BB;Brain/anatomy &histology/cytology/*growth &development;Mice},
	Number = {2},
	Organization = {Division of Biological Sciences, University of Missouri, Columbia 65211.},
	Pages = {111-4.},
	Title = {Neurogenesis persists in the subependymal layer of the adult mouse brain},
	Uuid = {69B14899-B1BF-483C-9C23-E0088B22B32D},
	Volume = {149},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8474679}}

@article{Corral:2001,
	Abstract = {Embryologists have long used morphological characteristics, and more recently marker genes, to identify neural tissue and to test the neural- inducing activity of specific cell populations and signalling molecules. These markers are also used to assess the function(s) of neural genes themselves. Progression from neural induction to terminal differentiation of neurons is a multistep process, and each step involves the activation and/or repression of genes that can be used as molecular markers for these different events. Here we briefly review these key steps in neurogenesis within the vertebrate central nervous system, and evaluate the markers used to define them. We emphasize the importance of cellular context and an understanding of gene function for interpreting the significance of marker genes.},
	Author = {Corral, R. D. and Storey, K. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {10 Development;F pdf},
	Number = {11},
	Organization = {Kate G. Storey and Ruth Diez del Corral are both at the Division of Cell and Developmental Biology, Wellcome Trust Building, University of Dundee, Dow Street, Dundee DD1 5EH, UK.},
	Pages = {835-9.},
	Title = {Markers in vertebrate neurogenesis},
	Uuid = {A50ED16D-C2C2-43D8-9D95-638346F4DE4A},
	Volume = {2},
	Year = {2001},
	url = {papers/Corral_NatRevNeurosci2001.pdf}}

@article{Corti:2002,
	Abstract = {The aim of the present study is to determine whether the expansion and mobilization of circulating bone marrow (BM) stem cells by in vivo treatment with granulocyte-colony stimulating factor (G-CSF) and stem cell factor (SCF) increase the amount of BM-derived neuronal cells in mouse brain. The presence of BM-derived cells in the brain was traced by transplanting into lethally irradiated adults and newborns adult BM from transgenic mice that ubiquitously expressed enhanced green fluorescent protein (GFP). GFP+ and Y-chromosome+ donor-derived cells were present in several brain areas of all treated mice (cortical and subcortical areas, cerebellum, olfactory bulb). The presence of GFP+ cells expressing nuclear neural specific antigen (NeuN), neurofilament, and beta-III tubulin in cortical forebrain and olfactory bulb (OB) was higher in G-CSF-SCF treated groups (P <0.05, analysis of variance, Fisher post hoc). We observed that overall the amount of double positive cells was higher in animals treated at birth than in adults and in OB than in forebrain areas (P <0.05). Temporal cortical areas of cytokine-treated adult animals revealed a mean threefold increase in the number of GFP+ cells expressing the nuclear neural specific antigen (211 +/- 86 GFP+NeuN+/mm(3) in G-CSF + SCF treated mice and 66 +/- 33 GFP+NeuN+/mm(3) in control animals). GFP+ cells coexpressing neuronal markers contain only one nucleus and have a DNA index (a measure of DNA ploidy) identical to that of surrounding neurons, thus excluding donor cell fusion with endogenous cells as a relevant phenomenon under these experimental conditions. Our results indicate that G-CSF and SCF administration modulates the availability of GFP+ cells in the brain and enhances their capacity to acquire neuronal characteristics. Cytokine stimulation of autologous stem cells might be seen as a new strategy for neuronal repair in neurodegenerative diseases.},
	Author = {Corti, S. and Locatelli, F. and Strazzer, S. and Salani, S. and Del Bo, R. and Soligo, D. and Bossolasco, P. and Bresolin, N. and Scarlato, G. and Comi, G. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cytokines;Cell Differentiation;Animals;Bone Marrow Transplantation;Brain;Antigens, Differentiation;Female;Cell Count;Mice, Transgenic;Granulocyte Colony-Stimulating Factor;Mice, Inbred C57BL;11 Glia;Cell Movement;Male;Bone Marrow Cells;Animals, Newborn;Neurons;Age Factors;Mice;Stem Cell Factor;Luminescent Proteins;Y Chromosome;Stem Cells;Genes, Reporter;Research Support, Non-U.S. Gov't},
	Medline = {22316816},
	Month = {10},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Centro Dino Ferrari, Dipartimento di Scienze Neurologiche, Universit\`{a} degli Studi di Milano, I.R.C.C.S. Ospedale Maggiore Policlinico, 20122, Milan, Italy.},
	Pages = {443-52},
	Pii = {S0014488602980040},
	Pubmed = {12429190},
	Title = {Modulated generation of neuronal cells from bone marrow by expansion and mobilization of circulating stem cells with in vivo cytokine treatment},
	Uuid = {0A7E0CD4-D220-42EA-9CD3-F13E52734429},
	Volume = {177},
	Year = {2002}}

@article{Corti:2002a,
	Abstract = {There is now evidence that bone marrow (BM) can generate cells expressing neuronal antigens in adult mouse brain. In the present study, we examined the spinal cord and dorsal root ganglia (DRG) of adult mice 3 months after BM cell transplantation from transgenic donor mice expressing the enhanced green fluorescent protein (GFP). To determine whether GFP(+) cells acquire neuroectodermal phenotypes, we tested, by immunocytochemistry followed by confocal analysis, the coexpression of the astrocytic marker glial fibrillary acidic protein (GFAP) and the neuronal markers NeuN, neurofilament (NF), and class III beta-tubulin (TuJ1). Rare GFP(+) cells coexpressing TuJ1, NF, and NeuN were found both in spinal cord and in sensory ganglia. These cells have small dimensions and short cytoplasmic processes, probably reflecting an immature phenotype. Double GFP and GFAP positivity was found only in spinal cord. To determine whether cell fusion with endogenous cells occurred, we investigated the nuclear content of cells coexpressing GFP and neuronal or astrocytic markers, demonstrating that these cells have only one nucleus and a DNA ploidy that it is not different from that of surrounding neurons and astrocytes. Large numbers of GFP(+) cells are also positively stained for F4/80, a microglial-recognizing antibody, and present a characteristic microglial-like morphology both in spinal cord and, with a higher frequency, in sensory ganglia. These data support a potential role for BM-derived stem cells in spinal cord neuroneogenesis. They also confirm that the microglial compartment within the CNS and in DRG undergoes a relatively fast turnover, with the contribution of hematopoietic stem cells. Both these findings might prove useful for the development of treatments for spinal cord neurodegenerative and acquired disorders.},
	Author = {Corti, S. and Locatelli, F. and Donadoni, C. and Strazzer, S. and Salani, S. and Del Bo, R. and Caccialanza, M. and Bresolin, N. and Scarlato, G. and Comi, G. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Glial Fibrillary Acidic Protein;Cell Differentiation;Animals;Stem Cell Transplantation;Ectoderm;Ganglia, Spinal;Bone Marrow Transplantation;Microscopy, Confocal;Microglia;Mice, Transgenic;11 Glia;Green Fluorescent Proteins;Male;Spinal Cord;Bone Marrow Cells;Neurons;Mice;Immunohistochemistry;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22331219},
	Month = {12},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {Centro Dino Ferrari, Dipartimento di Scienze Neurologiche, Universit\`{a} degli Studi di Milano, IRCCS Ospedale Maggiore Policlinico, Milano, Italy. stcorti\@yahoo.it},
	Pages = {721-33},
	Pubmed = {12444594},
	Title = {Neuroectodermal and microglial differentiation of bone marrow cells in the mouse spinal cord and sensory ganglia},
	Uuid = {2D57F590-D3B1-11D9-A0E9-000D9346EC2A},
	Volume = {70},
	Year = {2002},
	url = {papers/Corti_JNeurosciRes2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10455}}

@article{Corvetti:2005,
	Abstract = {Chondroitin sulfate proteoglycans are major constituents of the extracellular matrix and form perineuronal nets. Information regarding the growth-inhibitory activity of these molecules after injury is rapidly expanding. However, less is known about their physiological role in the adult undamaged CNS. Here, we investigated the function of chondroitin sulfate proteoglycans in maintaining the proper structure of Purkinje axons in the cerebellum of adult rats. To this end, we examined the morphology and distribution of intracortical Purkinje neurites after intraparenchymal injection of chondroitinase ABC. Staining with the lectin Wisteria floribunda agglutinin or 2B6 antibodies showed that this treatment efficiently removed chondroitin sulfate proteoglycans from wide areas of the cerebellar cortex. In the same sites, there was a profuse outgrowth of terminal branches from the Purkinje infraganglionic plexus, which invaded the deeper regions of the granular layer. In contrast, myelinated axon segments were not affected and maintained their normal relationship with oligodendroglial sheaths. Purkinje axon sprouting was first evident at 4 d and increased further at 7 d after enzyme application. Within 42 d, the expression pattern of chondroitin sulfate proteoglycans gradually recovered, whereas axonal modifications progressively regressed. Our results show that, in the absence of injury or novel external stimuli, degradation of chondroitin sulfate proteoglycans is sufficient to induce Purkinje axon sprouting but not the formation of long-lasting synaptic contacts. Together with other growth-inhibitory molecules, such as myelin-associated proteins, chondroitin sulfate proteoglycans restrict structural plasticity of intact Purkinje axons to maintain normal wiring patterns in the adult cerebellar cortex.},
	Author = {Corvetti, Luigi and Rossi, Ferdinando},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;11 Glia;10 Structural plasticity;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {31},
	Organization = {Department of Neuroscience, Rita Levi Montalcini Center for Brain Repair, University of Turin, I-10125 Turin, Italy. luigi.corvetti\@unito.it},
	Pages = {7150-8},
	Pii = {25/31/7150},
	Pubmed = {16079397},
	Title = {Degradation of chondroitin sulfate proteoglycans induces sprouting of intact purkinje axons in the cerebellum of the adult rat},
	Uuid = {EC668BA2-4CD0-4B9A-9C8A-3B88CF2E44BF},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0683-05.2005}}

@article{Coskun:2001,
	Abstract = {Bone morphogenetic proteins (BMPs), a group of cytokines in the TGF- beta superfamily, have complex regulatory roles in the control of neural proliferation and cell fate decision. In this study, we analyzed the potential role(s) of BMP signaling on the regulation of the proliferation and differentiation of the unique progenitor cells of the neonatal anterior subventricular zone (SVZa). Unlike other progenitor cells of the brain, SVZa progenitor cells have the capacity to divide even though they express a neuronal phenotype. In order to augment or inhibit endogenous BMP signaling, we injected into the neonatal rat SVZa replication-deficient retroviruses encoding for either the wild- type BMP receptor subtype Ia (wt-BMPR-Ia) or a mutated dominant- negative version of BMPR-Ia (dn-BMPR-Ia) in conjunction with a reporter gene, human alkaline phosphatase (AP) and perfused the pups 1, 4 and 7 days post injection. We analyzed whether changing the expression of BMPR-Ia has an effect on the spatial-temporal expression pattern of the cyclin dependent kinase inhibitor, p19(INK4d), or on the phenotype of SVZa derived cells. The results of our study confirmed and extended our previous findings that in control (non injected) animals, the rostral migratory stream (RMS), traversed by the SVZa-derived cells en route to the olfactory bulb, exhibits an anterior(high)-posterior(low) gradient of p19(INK4d) expression; p19(INK4d) expression is essentially absent in the SVZa and highest in the subependymal zone in the middle of the olfactory bulb. However, SVZa progenitor cells encoding the wt-BMPR-Ia gene express p19(INK4d) within the SVZa, suggesting that the BMPs induce SVZa cells to ectopically undergo cell cycle exit within the SVZa. Furthermore, unlike striatal SVZ progenitor cells, which acquire an astrocytic phenotype when exposed to BMPs, SVZa progenitor cells retain their neuronal commitment under augmented BMP signaling.},
	Author = {Coskun, V. and Venkatraman, G. and Yang, H. and Rao, M. S. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Int J Dev Neurosci},
	Keywords = {Human;Cell Differentiation;Genetic Vectors/genetics;Recombinant Fusion Proteins/biosynthesis/genetics;Transfection;Rats;Receptors, Growth Factor/genetics/*physiology;Olfactory Bulb/*cytology/embryology;Alkaline Phosphatase/biosynthesis/genetics;Cell Movement;Animal;Protein-Serine-Threonine Kinases/genetics/*physiology;Cerebral Ventricles/embryology;Bone Morphogenetic Proteins/*physiology;Animals, Newborn;Neurons, Afferent/*cytology;Morphogenesis;Defective Viruses/genetics;Cell Lineage;C;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Retroviridae/genetics;Carrier Proteins/*biosynthesis/genetics;Genes, Reporter;*Gene Expression Regulation},
	Number = {2},
	Organization = {Department of Cell Biology, Emory University School of Medicine, 1648 Pierce Drive, Atlanta, GA 30322, USA.},
	Pages = {219-27.},
	Title = {Retroviral manipulation of the expression of bone morphogenetic protein receptor Ia by SVZa progenitor cells leads to changes in their p19(INK4d) expression but not in their neuronal commitment},
	Uuid = {BD0149DF-395B-466B-92C3-7723A276A87E},
	Volume = {19},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11255035}}

@article{Coskun:2001a,
	Abstract = {In this study we investigated whether the pattern of expression of the cyclin-dependent kinase inhibitor p19(INK4d) by the unique progenitor cells of the neonatal anterior subventricular zone (SVZa) can account for their ability to divide even though they express phenotypic characteristics of differentiated neurons. p19(INK4d) was chosen for analysis because it usually acts to block permanently the cell cycle at the G(1) phase. p19(INK4d) immunoreactivity and the incorporation of bromodeoxyuridine (BrdU) by SVZa cells were compared with that of the more typical progenitor cells of the prenatal telencephalic ventricular zone. In the developing telencephalon, p19(INK4d) is expressed by postmitotic cells and has a characteristic perinuclear distribution depending on the laminar position and state of differentiation of a cell. Moreover, the laminar-specific staining of the developing cerebral cortex revealed that the ventricular zone (VZ) is divided into p19(INK4d)(+) and p19(INK4d)(-) sublaminae, indicating that the VZ has a previously unrecognized level of functional organization. Furthermore, the rostral migratory stream, traversed by the SVZa- derived cells, exhibits an anterior(high)-posterior(low) gradient of p19(INK4d) expression. On the basis of the p19(INK4d) immunoreactivity and BrdU incorporation, SVZa-derived cells appear to exit and reenter the cell cycle successively. Thus, in contrast to telencephalic VZ cells, SVZa cells continue to undergo multiple rounds of division and differentiation before becoming postmitotic.},
	Author = {Coskun, V. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation/genetics;Carrier Proteins/*biosynthesis;Rats;Telencephalon/cytology/embryology/*metabolism;Cell Cycle;*Gene Expression Regulation, Developmental;Animal;Cell Movement;Rats, Sprague-Dawley;Enzyme Inhibitors/pharmacology;Stem Cells/cytology/*metabolism;Animals, Newborn;Cell Division/genetics;Cell Lineage;Cyclin-Dependent Kinases/antagonists &inhibitors;C;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Neurons/cytology/metabolism;Cerebral Cortex/cytology/embryology/metabolism;Cerebral Ventricles/cytology/embryology/metabolism;Bromodeoxyuridine},
	Number = {9},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {3092-103.},
	Title = {The expression pattern of the cell cycle inhibitor p19(INK4d) by progenitor cells of the rat embryonic telencephalon and neonatal anterior subventricular zone},
	Uuid = {57686C2E-DF32-45CB-A205-F5B6754A631A},
	Volume = {21},
	Year = {2001},
	url = {papers/Coskun_JNeurosci2001}}

@article{Coskun:2002,
	Abstract = {An overriding principle of development is that neurons become permanently postmitotic once they initiate differentiation. Work in our laboratory, however, has provided evidence for a population of progenitor cells in mammalian forebrain that express properties of differentiated neurons, even though they continue to divide. These neuronal progenitor cells are situated in the rostral migratory stream (RMS), which extends from a specialized portion of the subventricular zone surrounding the anterior tip of the lateral ventricle, referred to as the SVZa, to the middle of the olfactory bulb. As SVZa-derived cells migrate to the olfactory bulb, they undergo cell division, and they never deviate from the RMS. Once they reach their final destinations, they become terminally postmitotic interneurons. This Mini-Review concerns findings from our recent experiments designed to reveal the intrinsic and extrinsic mechanisms governing the proliferation and differentiation of the unique SVZa neuronal progenitor cells. We have investigated the role(s) of cell cycle regulatory proteins, in particular, the cell cycle inhibitor p19(INK4d), in the control of SVZa cell proliferation. Several studies have indicated that cells withdraw from the cell cycle once they express p19(INK4d). To begin to investigate whether p19(INK4d)(+) SVZa-derived cells are postmitotic, we analyzed the pattern of p19(INK4d) expression by the cells of the RMS. A pronounced gradient of p19(INK4d) expression was demonstrated; progressively more cells are p19(INK4d) immunoreactive as the olfactory bulb is approached. In addition, the capacity of p19(INK4d)(+) cells to incorporate bromodeoxyuridine was investigated. From the results of these studies, we conclude that SVZa cells in the RMS can successively down-regulate their expression of p19(INK4d) as they migrate and that they repeatedly exit and reenter the cell cycle while en route to the olfactory bulb. These studies led us to investigate whether bone morphogenetic proteins (BMPs) are involved in the regulation of SVZa cell proliferation and p19(INK4d) expression, because, elsewhere in the CNS, BMPs modulate cell proliferation and influence cell fate decisions. To determine the effects of BMP signaling on SVZa cell proliferation and differentiation, we altered the expression of the BMP receptor Ia (BMPR-Ia) using retrovirally mediated gene transfer. The cells in the SVZa encoding the wild-type BMPR-Ia exit the cell cycle and do not appear to migrate through the RMS. Conversely, both within the SVZa and along the RMS, the majority of SVZa-derived cells encoding a dominant-negative BMPR-Ia gene do not express p19(INK4d). These findings indicate that p19(INK4d) expression is suppressed when BMP signaling is inhibited. Furthermore, SVZa-derived cells with both augmented and inhibited BMP signaling retain their neuronal commitment. Collectively, these studies have revealed that SVZa cell proliferation and differentiation is under the control of several interacting intrinsic and extrinsic factors.},
	Author = {Coskun, Volkan and Luskin, Marla B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Rodentia;02 Adult neurogenesis migration;Cell Differentiation;03 Adult neurogenesis progenitor source;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Cell Division;Animals;Brain;Cell Movement;Neurons;review},
	Medline = {22194568},
	Month = {9},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {795-802},
	Pubmed = {12205673},
	Title = {Intrinsic and extrinsic regulation of the proliferation and differentiation of cells in the rodent rostral migratory stream},
	Uuid = {B67306E0-6850-4BE3-B0AB-614623359CAD},
	Volume = {69},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10336}}

@article{Couillard-Despres:2005,
	Abstract = {Progress in the field of neurogenesis is currently limited by the lack of tools enabling fast and quantitative analysis of neurogenesis in the adult brain. Doublecortin (DCX) has recently been used as a marker for neurogenesis. However, it was not clear whether DCX could be used to assess modulations occurring in the rate of neurogenesis in the adult mammalian central nervous system following lesioning or stimulatory factors. Using two paradigms increasing neurogenesis levels (physical activity and epileptic seizures), we demonstrate that quantification of DCX-expressing cells allows for an accurate measurement of modulations in the rate of adult neurogenesis. Importantly, we excluded induction of DCX expression during physiological or reactive gliogenesis and excluded also DCX re-expression during regenerative axonal growth. Our data validate DCX as a reliable and specific marker that reflects levels of adult neurogenesis and its modulation. We demonstrate that DCX is a valuable alternative to techniques currently used to measure the levels of neurogenesis. Importantly, in contrast to conventional techniques, analysis of neurogenesis through the detection of DCX does not require in vivo labelling of proliferating cells, thereby opening new avenues for the study of human neurogenesis under normal and pathological conditions.},
	Author = {Couillard-Despres, Sebastien and Winner, Beate and Schaubeck, Susanne and Aigner, Robert and Vroemen, Maurice and Weidner, Norbert and Bogdahn, Ulrich and Winkler, J{\"u}rgen and Kuhn, Hans-Georg G. and Aigner, Ludwig},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration},
	Month = {1},
	Nlm_Id = {8918110},
	Number = {1},
	Organization = {Volkswagen-Foundation Junior Group, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany.},
	Pages = {1-14},
	Pii = {EJN3813},
	Pubmed = {15654838},
	Title = {Doublecortin expression levels in adult brain reflect neurogenesis},
	Uuid = {AE708C23-95D4-44C3-924F-2A8E153194EA},
	Volume = {21},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2004.03813.x}}

@article{Cowan:2001,
	Abstract = {Caspase-9, an initiator caspase, and caspase-3, an effector caspase, have been suggested to mediate the terminal stages of neuronal apoptosis, but little is known about their activation in vivo. We examined temporal and spatial aspects of caspase-9 and -3 activation in olfactory receptor neurons (ORNs) undergoing apoptosis after target removal in vivo. After removal of the olfactory bulb, enhanced expression of procaspase-9 and -3 is observed in ORNs, followed by activation initially at the level of the lesion, then in axons, and only later in the ORN soma. We established the amyloid precursor-like protein-2 (APLP2) as a caspase substrate that is cleaved in an identical spatiotemporal pattern, suggesting its cleavage is the result of retrograde propagation of a pro-apoptotic signal in a caudorostral wave from the synapse through the axon to the ORN cell body. A null mutation in caspase-3 causes a change in axonal patterning indicative of an overall developmental expansion of the ORN population, and mature ORNs of caspase-3 knock-outs do not undergo caspase-dependent terminal dUTP nick end labeling-positive apoptosis after olfactory bulb removal. These results demonstrate that ORNs require caspase-3 activation to undergo normal developmental and mature target-deprived apoptosis. In addition, we demonstrate an axonal site of action for caspase-3 and -9 and show that regulation and activation of caspase-3 and -9 leading to apoptosis is a highly ordered process that occurs initially at the presynaptic level and only later at the cell body after deafferentation.},
	Author = {Cowan, C. M. and Thai, J. and Krajewski, S. and Reed, J. C. and Nicholson, D. W. and Kaufmann, S. H. and Roskams, A. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:44 -0400},
	Journal = {J Neurosci},
	Keywords = {I pdf;13 Olfactory bulb anatomy},
	Number = {18},
	Organization = {Centre for Molecular Medicine and Therapeutics, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.},
	Pages = {7099-109.},
	Title = {Caspases 3 and 9 send a pro-apoptotic signal from synapse to cell body in olfactory receptor neurons},
	Uuid = {6B9B5E48-2D76-4E7D-B9D1-089855113E38},
	Volume = {21},
	Year = {2001},
	url = {papers/Cowan_JNeurosci2001.pdf}}

@article{Cowan:2005,
	Abstract = {We have explored the use of embryonic stem cells as an alternative to oocytes for reprogramming human somatic nuclei. Human embryonic stem (hES) cells were fused with human fibroblasts, resulting in hybrid cells that maintain a stable tetraploid DNA content and have morphology, growth rate, and antigen expression patterns characteristic of hES cells. Differentiation of hybrid cells in vitro and in vivo yielded cell types from each embryonic germ layer. Analysis of genome-wide transcriptional activity, reporter gene activation, allele-specific gene expression, and DNA methylation showed that the somatic genome was reprogrammed to an embryonic state. These results establish that hES cells can reprogram the transcriptional state of somatic nuclei and provide a system for investigating the underlying mechanisms.},
	Author = {Cowan, Chad A. and Atienza, Jocelyn and Melton, Douglas A. and Eggan, Kevin},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Cell Differentiation;22 Stem cells;Cell Line;24 Pubmed search results 2008;Mice, Nude;Male;Animals;Pluripotent Stem Cells;Transcription, Genetic;Gene Expression Regulation, Developmental;Phenotype;Polyploidy;Transfection;Cell Transplantation;Chromosomes, Human;Hybrid Cells;Cell Cycle;08 Aberrant cell cycle;Biological Markers;Gene Expression Profiling;Epigenesis, Genetic;Teratoma;Embryo;Female;Cell Nucleus;Fibroblasts;Adult;Mice;Research Support, Non-U.S. Gov't;Cell Fusion;Humans;Cell Shape},
	Month = {8},
	Nlm_Id = {0404511},
	Number = {5739},
	Organization = {Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.},
	Pages = {1369-73},
	Pii = {309/5739/1369},
	Pubmed = {16123299},
	Title = {Nuclear reprogramming of somatic cells after fusion with human embryonic stem cells},
	Uuid = {FF6AA2E1-D3AD-41BE-94CA-9C48153A5D54},
	Volume = {309},
	Year = {2005},
	url = {papers/Cowan_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1116447}}

@article{Craig:1996,
	Abstract = {The lateral ventricle subependyma in the adult mammalian forebrain contains both neural stem and progenitor cells. This study describes the in situ modulation of these subependymal neural precursor populations after intraventricular administration of exogenous growth factors. In vivo infusion of epidermal growth factor (EGF) into adult mouse forebrain for 6 consecutive days resulted in a dramatic increase in the proliferation and total number of subependymal cells and induced their migration away from the lateral ventricle walls into adjacent parenchyma. Immediately after EGF infusion, immunohistochemical characterization of the EGF-expanded cell population demonstrated that >95\%of these cells were EGF receptor- and nestin-positive, whereas only 0.9\%and 0.2\%labeled for astrocytic and neuronal markers, respectively. Seven weeks after EGF withdrawal, 25\%of the cells induced to proliferate after 6d of EGF were still detectable; 28\%of these cells had differentiated into new astrocytes and 3\%into new neurons in the cortex, striatum, and septum. Newly generated oligodendrocytes were also observed. These in vivo results (1) confirm the existence of EGF-responsive subependymal neural precursor cells in the adult mouse forebrain and (2) suggest that EGF acts directly as a proliferation, survival, and migration factor for subependymal precursor cells to expand these populations and promote the movement of these cells into normal brain parenchyma. Thus, in situ modulation of endogenous forebrain precursor cells represents a novel model for studying neural development in the adult mammalian brain and may provide insights that will achieve adult replacement of neurons and glia lost to disease or trauma.},
	Author = {Craig, C. G. and Tropepe, V. and Morshead, C. M. and Reynolds, B. A. and Weiss, S. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Neurosci},
	Keywords = {Ependyma/*drug effects;Time Factors;Dose-Response Relationship, Drug;Brain/*drug effects;Animal;Astrocytes/metabolism;Epidermal Growth Factor/*pharmacology;04 Adult neurogenesis factors;Neurons/metabolism;Support, Non-U.S. Gov't;C-5;Mice;Cell Count/drug effects;Mice, Inbred Strains},
	Number = {8},
	Organization = {Deparment of Anatomy and Cell Biology, University of Toronto, Ontario, Canada.},
	Pages = {2649-58.},
	Title = {In vivo growth factor expansion of endogenous subependymal neural precursor cell populations in the adult mouse brain},
	Uuid = {1D9DB226-AA0D-453C-9BD6-EF04A1C6B966},
	Volume = {16},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8786441}}

@article{Craig:1999,
	Abstract = {Initial experiments to evaluate the in vivo fate(s) of constitutively proliferating subependymal cells determined that, following in vivo labeling of this population by infection with a retrovirus containing a beta-galactosidase reporter gene, there was a progressive and eventually complete loss of histochemically beta-galactosidase-positive cells within the lateral ventricle subependyma with increasing survival times of up to 28 days after retroviral infection. Subsequent experiments were designed to ascertain the potential contributions of: (i) the migration of subependymal cells away from the forebrain lateral ventricles; and (ii) the down-regulation of the retroviral reporter gene expression. Retroviral lineage tracing experiments demonstrate that a major in vivo fate for constitutively proliferating subependymal cells is their rostral migration away from the walls of the lateral ventricle to the olfactory bulb. Although down-regulation of retroviral reporter gene expression does not contribute to the loss of detection of beta-galactosidase-labeled cells from the lateral ventricle subependyma, it does result in an underestimation of the absolute number of retrovirally labeled cells in the olfactory bulb at longer survival times. Furthermore, a temporal decrease in the double labeling of beta-galactosidase-labeled cells with [3H]thymidine was observed, indicating that only a subpopulation of the migratory subependymal- derived cells continue to actively proliferate en route to the olfactory bulb. These two events may contribute to the lack of a significant increase in the total number of retrovirally labeled subependymal cells during rostral migration. Evidence from separately published studies suggests that cell death is also an important regulator of the size of the constitutively proliferating subependymal population. In summary, in vivo studies utilizing retroviral reporter gene labeling demonstrate that constitutively proliferating subependymal cells born in the lateral ventricle migrate rostrally to the olfactory bulb. Loss of proliferation potential and retroviral reporter gene down-regulation contribute to the lack of any significant increase in the total number of labeled cells recovered in the olfactory bulb. Using Smart Source Parsing},
	Author = {Craig, C. G. and D'sa, R. and Morshead, C. M. and Roach, A. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Neuroscience},
	Keywords = {Prosencephalon/*cytology;Genetic Vectors/analysis/genetics;Animal;Stem Cells/cytology;02 Adult neurogenesis migration;Cell Movement;Ependyma/*cytology;beta-Galactosidase/genetics;DNA Replication;Male;Support, Non-U.S. Gov't;Retroviridae/genetics;B;Cell Lineage;Olfactory Bulb/cytology;Mice;Cell Division;Genes, Reporter;Gene Expression;Cerebral Ventricles/cytology},
	Number = {3},
	Organization = {Department of Anatomy and Cell Biology, University of Toronto, Ontario, Canada.},
	Pages = {1197-206},
	Title = {Migrational analysis of the constitutively proliferating subependyma population in adult mouse forebrain},
	Uuid = {3F782E5C-A0C0-4A00-BE5E-778280DFE379},
	Volume = {93},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10473285}}

@article{Cramer:2005,
	Abstract = {Many kinds of information are carried in the acoustic signal that reaches auditory receptor cells in the cochlea. The analysis of this information is possible in large part because of the neuronal architecture of the auditory system. The mechanisms that establish the precise circuitry that underlies auditory processing have not yet been identified. The Eph receptor tyrosine kinases and their ligands are proteins that regulate axon guidance and have been shown to contribute to the establishment of topographic projections in several areas of the nervous system. Several studies have begun to investigate whether these proteins are involved in the formation of auditory system connections. Studies of gene expression show that Eph proteins are extensively expressed in structures of the inner ear as well as in neurons in the peripheral and central components of the auditory system. Functional studies have demonstrated that Eph signaling influences the assembly of auditory pathways. These studies suggest that Eph protein signaling has a significant role in the formation of auditory circuitry.},
	Author = {Cramer, Karina S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0378-5955},
	Journal = {Hear Res},
	Keywords = {Ephrins;Humans;24 Pubmed search results 2008;10 Development;research support, non-u.s. gov't;Mammals;10 circuit formation;Receptor, EphA1;research support, n.i.h., extramural;Birds;research support, u.s. gov't, p.h.s.;Animals;Auditory Pathways;Cochlear Nerve;review;Axons},
	Month = {8},
	Nlm_Id = {7900445},
	Number = {1-2},
	Organization = {Department of Neurobiology and Behavior, University of California, 2205 McGaugh Hall, Irvine, CA 92697-4550, USA. cramerk\@uci.edu},
	Pages = {42-51},
	Pii = {S0378-5955(05)00086-9},
	Pubmed = {16080997},
	Title = {Eph proteins and the assembly of auditory circuits},
	Uuid = {A87DAD9C-54DC-47A2-B178-47D1265AAE81},
	Volume = {206},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.heares.2004.11.024}}

@article{Cremer:1997,
	Abstract = {The neural cell adhesion molecule (NCAM), probably the best characterized and most abundant cell adhesion molecule on neurons, is thought to be a major regulator of axonal growth and pathfinding. Here we present a detailed analysis of these processes in mice deficient for all NCAM isoforms, generated by gene targeting. The hippocampal mossy fiber tract shows prominent expression of polysialylated NCAM and the generation of new axonal projections throughout life. Focusing on this important intrahippocampal connection, we demonstrate that in the absence of NCAM, fasciculation and pathfinding of these axons are strongly affected. In addition we show alterations in the distribution of mossy fiber terminals. The phenotype is more severe in adult than in young animals, suggesting an essential role for NCAM in the maintenance of plasticity in the mature nervous system.},
	Author = {Cremer, H. and Chazal, G. and Goridis, C. and Represa, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Aging;Staining and Labeling;Nerve Fibers;Research Support, Non-U.S. Gov't;Mice, Knockout;Golgi Apparatus;Neural Cell Adhesion Molecules;Hippocampus;Nerve Endings;Neurons;Mice, Inbred C57BL;Animals;Mice;24 Pubmed search results 2008;Mice, Inbred Strains;Axons},
	Medline = {97230486},
	Nlm_Id = {9100095},
	Number = {5},
	Organization = {IBDM, CNRS/INSERM/Universit{\'e} de la M{\'e}diterran{\'e}e, Marseille Cedex 9, France.},
	Pages = {323-35},
	Pii = {S1044-7431(96)90588-6},
	Pubmed = {9073395},
	Title = {NCAM is essential for axonal growth and fasciculation in the hippocampus},
	Uuid = {03980902-0C78-46F9-96A9-D66C2B5E40A7},
	Volume = {8},
	Year = {1997},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/mcne.1996.0588}}

@article{Cremer:1994,
	Abstract = {Neural-cell adhesion molecules (N-CAMs) are members of the immunoglobulin superfamily mediating homo- and heterophilic cell-cell interactions. N-CAM exists in various isoforms which are generated by alternative splicing. During embryonic development, N-CAMs are expressed in derivatives of all three germ layers, whereas in the adult animal they are predominantly present in neural tissue. Processes like neurulation, axonal outgrowth, histogenesis of the retina and development of the olfactory system are correlated with the regulated expression of N-CAMs. We show here that N-CAM-deficient mice generated by gene targeting appear healthy and fertile, but adult mutants show a 10\%reduction in overall brain weight and a 36\%decline in size of the olfactory bulb. N-CAM deficiency coincides with almost total loss of protein-bound alpha-(2,8)-linked polysialic acid, a carbohydrate structure thought to be correlated with neural development and plasticity. The animals showed deficits in spatial learning when tested in the Morris water maze, whereas activity and motor abilities appeared normal.},
	Author = {Cremer, H. and Lange, R. and Christoph, A. and Plomann, M. and Vopper, G. and Roes, J. and Brown, R. and Baldwin, S. and Kraemer, P. and Scheff, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Embryo;Mutation;Base Sequence;Research Support, Non-U.S. Gov't;DNA Primers;Molecular Sequence Data;Heterozygote;Homozygote;Cell Line;Mice, Inbred C57BL;Spatial Behavior;Olfactory Bulb;Mice;Animals;24 Pubmed search results 2008;Cell Adhesion Molecules, Neuronal;Sialic Acids},
	Medline = {94150622},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {6462},
	Organization = {Institute for Genetics, University of Cologne, Germany.},
	Pages = {455-9},
	Pubmed = {8107803},
	Title = {Inactivation of the N-CAM gene in mice results in size reduction of the olfactory bulb and deficits in spatial learning},
	Uuid = {4189DF3B-70FF-498F-BFAB-295496647134},
	Volume = {367},
	Year = {1994},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/367455a0}}

@article{Cremer:1998,
	Abstract = {Cell adhesion molecules (CAMs) are known to be involved in a variety of developmental processes that play key roles in the establishment of synaptic connectivity during embryonic development, but recent evidence implicates the same molecules in synaptic plasticity of the adult. In the present study, we have used neural CAM (NCAM)-deficient mice, which have learning and behavioral deficits, to evaluate NCAM function in the hippocampal mossy fiber system. Morphological studies demonstrated that fasciculation and laminar growth of mossy fibers were strongly affected, leading to innervation of CA3 pyramidal cells at ectopic sites, whereas individual mossy fiber boutons appeared normal. Electrophysiological recordings performed in hippocampal slice preparations revealed that both basal synaptic transmission and two forms of short-term plasticity, i.e., paired-pulse facilitation and frequency facilitation, were normal in mice lacking all forms of NCAM. However, long-term potentiation of glutamatergic excitatory synapses after brief trains of repetitive stimulation was abolished. Taken together, these results strongly suggest that in the hippocampal mossy fiber system, NCAM is essential both for correct axonal growth and synaptogenesis and for long-term changes in synaptic strength.},
	Author = {Cremer, H. and Chazal, G. and Carleton, A. and Goridis, C. and Vincent, J. D. and Lledo, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Research Support, Non-U.S. Gov't;Neural Cell Adhesion Molecules;Long-Term Potentiation;Animals;Synapses;In Vitro;Neuronal Plasticity;Synaptic Transmission;Synaptophysin;Axons;Hippocampus;Mice, Inbred C57BL;Mental Disorders;Mice, Knockout;Mice;24 Pubmed search results 2008;Nerve Fibers;Learning Disorders},
	Medline = {99007299},
	Month = {10},
	Nlm_Id = {7505876},
	Number = {22},
	Organization = {Developmental Biology Institute of Marsaille, Centre National de la Recherche Scientifique, Marseille Cedex 9, France.},
	Pages = {13242-7},
	Pubmed = {9789073},
	Title = {Long-term but not short-term plasticity at mossy fiber synapses is impaired in neural cell adhesion molecule-deficient mice},
	Uuid = {C071967B-1786-48FE-B370-C62AF5EC7042},
	Volume = {95},
	Year = {1998}}

@article{Crespel:2005,
	Abstract = {An increased neurogenesis is reported in animal models of mesial temporal lobe epilepsy (MTLE) but the fate of newborn cells is unknown. Here, we attempted to demonstrate neurogenesis in adult epileptic tissue obtained after hippocampectomy. MTLE hippocampi showed increased expression of division markers and of Musashi-1, a marker of neural progenitors, compared to control hippocampi. Large quantities of Musashi-1(+) cells were obvious in the subgranular layer and the subventricular zone, both known neurogenic areas, and in the fissura hippocampi. Musashi-1 was expressed by small cells that were mainly vimentin(+) or nestin(+), rarely Dcx(+) or PSA-NCAM(+) and negative for markers of mature neurons or astrocytes. Some of them are present in the granular layer, the hilus, and CA1 area resembling the ectopic positions described in rodents. These findings demonstrate that neural progenitors proliferate in chronic epilepsy and suggest that the fissura hippocampi behaves like another neurogenic area.},
	Author = {Crespel, Arielle and Rigau, Val{\'e}rie and Coubes, Philippe and Rousset, Marie Claude and de Bock, Fr{\'e}d{\'e}ric and Okano, Hideyuki and Baldy-Moulinier, Michel and Bockaert, Jo{\"e}l and Lerner-Natoli, Mireille},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0969-9961},
	Journal = {Neurobiol Dis},
	Keywords = {24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {9500169},
	Number = {3},
	Organization = {Institut de G{\'e}nomique Fonctionnelle, CNRS UMR 5023-INSERM U661, UM1-UM2, 141 rue de la Cardonille, F-34094 Montpellier Cedex 5, France; Unit{\'e} M{\'e}dico-chirurgicale de l'Epilepsie, H\^{o}pital Gui de Chauliac, 80 av Fliche, 34295 Montpellier Cedex 05, France.},
	Pages = {436-50},
	Pii = {S0969-9961(05)00035-5},
	Pubmed = {16023586},
	Title = {Increased number of neural progenitors in human temporal lobe epilepsy},
	Uuid = {12A24875-FBC8-4B22-9D78-430DAD66B199},
	Volume = {19},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.nbd.2005.01.020}}

@article{Crocker:2001,
	Abstract = {Siglecs are members of the Ig superfamily that bind to sialic acid (Sia) and are mainly expressed by cells of the hematopoietic system. Until three years ago, only four Siglecs were known, namely sialoadhesin, CD22, myelin-associated glycoprotein and CD33. Since then, a further six human CD33-related Siglecs with features of inhibitory receptors have been identified and shown to be expressed by discrete subsets of leukocytes. Recognition of Sia by these Siglecs could play a role in the regulation of the innate immune system.},
	Author = {Crocker, P. R. and Varki, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1471-4906},
	Journal = {Trends Immunol},
	Keywords = {Animals;Antigens, Differentiation, B-Lymphocyte;Antigens, Differentiation, Myelomonocytic;Humans;Antigens, CD22;Myelin-Associated Glycoprotein;review;Antigens, CD;Models, Immunological;11 Glia;Receptors, Immunologic;Immune System;Research Support, U.S. Gov't, P.H.S.;Membrane Glycoproteins;Sialic Acids;Amino Acid Sequence;Cell Adhesion Molecules;Molecular Sequence Data;Lectins;Research Support, Non-U.S. Gov't},
	Medline = {21273599},
	Month = {6},
	Nlm_Id = {100966032},
	Number = {6},
	Organization = {The Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, DD1 5EH, Dundee, UK. p.r.crocker\@dundee.ac.uk},
	Pages = {337-42},
	Pii = {S1471490601019305},
	Pubmed = {11377294},
	Title = {Siglecs, sialic acids and innate immunity},
	Uuid = {974B49A6-3332-45F2-98DD-12F39E16CFC8},
	Volume = {22},
	Year = {2001},
	url = {papers/Crocker_TrendsImmunol2001.pdf}}

@article{Croquelois:2008,
	Abstract = {In human, neuronal migration disorders are commonly associated with developmental delay, mental retardation, and epilepsy. We describe here a new mouse mutant that develops a heterotopic cortex (HeCo) lying in the dorsolateral hemispheric region, between the homotopic cortex (HoCo) and subcortical white matter. Cross-breeding demonstrated an autosomal recessive transmission. Birthdating studies and immunochemistry for layer-specific markers revealed that HeCo formation was due to a transit problem in the intermediate zone affecting both radially and tangentially migrating neurons. The scaffold of radial glial fibers, as well as the expression of doublecortin is not altered in the mutant. Neurons within the HeCo are generated at a late embryonic age (E18) and the superficial layers of the HoCo have a correspondingly lower cell density and layer thickness. Parvalbumin immunohistochemistry showed the presence of gamma-aminobutyric acidergic cells in the HeCo and the mutant mice have a lowered threshold for the induction of epileptic seizures. The mutant showed a developmental delay but, in contrast, memory function was relatively spared. Therefore, this unique mouse model resembles subcortical band heterotopia observed in human. This model represents a new and rare tool to better understand cortical development and to investigate future therapeutic strategies for refractory epilepsy.},
	Author = {Croquelois, and Giuliani, and Savary, and Kielar, and Amiot, and Schenk, and Welker,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1460-2199},
	Journal = {Cereb Cortex},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {9110718},
	Organization = {Service de Neuropsychologie et de Neuror{\'e}habilitation, Centre Hospitalier Universitaire Vaudois (CHUV), Avenue Pierre Decker 5, 1011 Lausanne, Switzerland.},
	Pii = {bhn106},
	Pubmed = {18562329},
	Title = {Characterization of the HeCo Mutant Mouse: A New Model of Subcortical Band Heterotopia Associated with Seizures and Behavioral Deficits},
	Uuid = {590E78D6-E64D-4866-9EC5-8941E9D316DE},
	Year = {2008},
	url = {papers/Croquelois_CerebCortex2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhn106}}

@article{Crowe:1995,
	Abstract = {There are a number of machanisms by which HIV-infected macrophages contribute to the pathogenesis of the Acquired Immunodeficiency Syndrome (AIDS). Macrophage-tropic strains of HIV are present at the time of infection, and persist throughout the course of infection, despite the emergence of T cell tropic quasispecies. As HIV causes chronic infection of macrophages with only minimal cytopathology, these cells can provide an important viral reservoir in HIV-infected persons. Macrophages are more susceptible to HIV infection than freshly isolated monocytes. HIV-infected macrophages can contribute to CD4 T lymphocyte depletion through a gp120-CD4 dependent fusion process with uninfected CD4-expressing T cells. Increasing data support the role of HIV-infected macrophages and microglia in the pathogenesis of HIV-related encephalopathy and AIDS-related dementia through the production of neurotoxins. HIV infection of macrophages in vitro results in impairment of many aspects of their function. Reduced phagocytic capacity for certain opportunistic pathogens, including Toxoplasma gondii and Candida albicans, may be responsible for reactivation of these pathogens in persons with advanced HIV infection, although the mechanisms underlying reactivation of infections and susceptibility to disease from new infections are likely to be multifactorial. Our studies showing defective phagocytosis and killing provide additional information that contribute to our understanding of the pathogenesis of AIDS. Studies of in vitro efficacy of potential antiretroviral therapies should be performed in both primary lymphocyte and monocyte cultures, given the importance of both of these cell populations to HIV pathogenesis and their differing biology.},
	Author = {Crowe, S. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0004-8291},
	Journal = {Aust N Z J Med},
	Keywords = {Research Support, Non-U.S. Gov't;HIV Infections;AIDS-Related Opportunistic Infections;AIDS Dementia Complex;CD4 Lymphocyte Count;CD4-Positive T-Lymphocytes;11 Glia;review, tutorial;Macrophages;Humans;HIV;Phagocytosis;review},
	Medline = {96366176},
	Month = {12},
	Nlm_Id = {1264322},
	Number = {6},
	Organization = {AIDS Pathogenesis Research Unit, Macfarlane Burnet Centre for Medical Research, Melbourne.},
	Pages = {777-83},
	Pubmed = {8770353},
	Title = {Role of macrophages in the pathogenesis of human immunodeficiency virus (HIV) infection},
	Uuid = {A2D09029-1D9D-4721-BF46-C2FBE6A3D4BD},
	Volume = {25},
	Year = {1995}}

@article{Cubells:1994,
	Abstract = {Methamphetamine (MA) produces selective degeneration of dopamine (DA) neuron terminals without cell body loss. While excitatory amino acids (EAAs) contribute to MA toxicity, terminal loss is not characteristic of excitotoxic lesions nor is excitotoxicity selective for DA fibers; rather, EAAs may modulate MA-induced DA turnover, suggesting that DA-dependent events play a key role in MA neurotoxicity. To examine this possibility, we used postnatal ventral midbrain DA neuron cultures maintained under continuous EAA blockade. As in vivo, MA caused neurite degeneration but minimal cell death. We found that MA is a vacuologenic weak base that induces swelling of endocytic compartments; MA also induces blebbing of the plasma membrane. However, these morphological changes occurred in MA-treated cultures lacking DA neurons. Therefore, while collapse of endosomal and lysosomal pH gradients and vacuolation may contribute to MA neurotoxicity, this does not explain selective DA terminal degeneration. Alternatively, MA could exert its neurotoxic effects by collapsing synaptic vesicle proton gradients and redistributing DA from synaptic vesicles to the cytoplasm. This could cause the formation of DA-derived free radicals and reactive metabolites. To test whether MA induces oxidative stress within living DA neurons, we used 2,7-dichlorofluorescin diacetate (DCF), an indicator of intracellular hydroperoxide production. MA dramatically increased the number of DCF-labeled cells in ventral midbrain cultures, which contain about 30\%DA neurons, but not in nucleus accumbens cultures, which do not contain DA neurons. In the DA neuron cultures, intracellular DDF labeling was localized to axonal varicosities, blebs, and endocytic organelles. These results suggest that MA redistributes DA from the reducing environment within synaptic vesicles to extravesicular oxidizing environments, thus generating oxygen radicals and reactive metabolites within DA neurons that may trigger selective DA terminal loss.},
	Author = {Cubells, J. F. and Rayport, S. and Rajendran, G. and Sulzer, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;Methamphetamine;Dopamine;Neurotoxins;Astrocytes;Organelles;Animals;Rats;Vacuoles;Oxygen;Cells, Cultured;Biological Transport;Fluoresceins;Free Radicals;Synaptic Vesicles;Neurites;Ventral Tegmental Area;Not relevant;Substantia Nigra;Kinetics;Time Factors;11 Glia;Animals, Newborn;Endocytosis;Neurons;Support, U.S. Gov't, P.H.S.;Cell Death},
	Medline = {94210059},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {4},
	Organization = {Department of Psychiatry, Columbia University, New York, New York 10032.},
	Pages = {2260-71},
	Pubmed = {8158268},
	Title = {Methamphetamine neurotoxicity involves vacuolation of endocytic organelles and dopamine-dependent intracellular oxidative stress},
	Uuid = {2E5F4322-E0F2-4960-AE30-4397822F9357},
	Volume = {14},
	Year = {1994},
	url = {papers/Cubells_JNeurosci1994.pdf}}

@article{Cucchiarini:2003,
	Abstract = {Microglia represent a crucial cell population in the central nervous system, participating in the regulation and surveillance of physiological processes as well as playing key roles in the etiologies of several major brain disorders. The ability to target gene transfer vehicles selectively to microglia would provide a powerful new approach to investigations of mechanisms regulating brain pathologies, as well as enable the development of novel therapeutic strategies. In this study, we evaluate the feasibility of specifically and efficiently targeting microglia relative to other brain cells, using vectors based on two different serotypes of adeno-associated virus (AAV) carrying cell-type-specific transcriptional elements to regulate gene expression. Among a set of promoter choices examined, an element derived from the gene for the murine macrophage marker F4/80 was the most discriminating for microglia. Gene expression from vectors controlled by this element was highly selective for microglia, both in vitro and in vivo. To our knowledge, this is the first demonstration of selective expression of transferred genes in microglia using AAV-derived vectors, as well as the first utilization of recombinant AAV-5 vectors in any macrophage lineage. These results provide strong encouragement for the application of these vectors and this approach for delivering therapeutic and other genes selectively to microglia.},
	Author = {Cucchiarini, M. and Ren, X. L. and Perides, G. and Terwilliger, E. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;Macrophages, Alveolar;Gene Targeting;Humans;Rats;Animals;Dependovirus;Brain;Microglia;Rats, Sprague-Dawley;11 Glia;Brain Diseases;Male;Genetic Vectors;Research Support, U.S. Gov't, P.H.S.;Genetic Engineering;Gene Therapy;Serotyping;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {22578074},
	Month = {4},
	Nlm_Id = {9421525},
	Number = {8},
	Organization = {Harvard Institutes of Medicine and Beth Israel Deaconess Medical Center, Boston, MA, USA.},
	Pages = {657-67},
	Pii = {3301925},
	Pubmed = {12692594},
	Title = {Selective gene expression in brain microglia mediated via adeno-associated virus type 2 and type 5 vectors},
	Uuid = {D994EFAD-7149-4A9B-A442-02A4EAFC7BD8},
	Volume = {10},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3301925}}

@article{Cui:2002,
	Abstract = {Hematopoietic stem cells (HSCs) represent an important target for the treatment of various blood disorders. As the source of critical cells within the immune system, genetic modification of HSCs can also be used to modulate immune responses. The effectiveness of HSC-mediated gene therapy largely depends on efficient gene delivery into long-term repopulating progenitors and targeted transgene expression in an appropriate progeny of the transduced pluripotent HSCs. Self-inactivating (SIN) lentiviral vectors have been demonstrated to be capable of transducing mitotically inactive cells, including HSCs, and accommodating a nonviral promoter to control the transgene expression in transduced cells. In this study, we constructed 2 SIN lentiviral vectors, EF.GFP and DR.GFP, to express the green fluorescent protein (GFP) gene controlled solely by the promoter of either a housekeeping gene EF-1alpha or the human HLA-DRalpha gene, which is selectively expressed in antigen-presenting cells (APCs). We demonstrated that both vectors efficiently transduced human pluripotent CD34+ cells capable of engrafting nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice. When the EF.GFP vector was used, constitutive high-level GFP expression was obtained in all the human HSC progeny detectable in NOD/SCID mice and in subsequent in vitro differentiation assays, indicating that engrafting human HSCs have been transduced. In contrast, the DR.GFP vector mediated transgene expression specifically in human HLA-DR+ cells and highly in differentiated dendritic cells (DCs), which are critical in regulating immunity. Furthermore, human DCs derived from transduced and engrafted human cells potently stimulated allogeneic T-cell proliferation. This study demonstrated successful targeting of transgene expression to APCs/DCs after stable gene transduction of pluripotent HSCs.},
	Author = {Cui, Yan and Golob, Jonathan and Kelleher, Erin and Ye, Zhaohui and Pardoll, Drew and Cheng, Linzhao},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Cell Differentiation;Mice, SCID;Genetic Vectors;Green Fluorescent Proteins;HLA-DR Antigens;Luminescent Proteins;Feasibility Studies;Animals;Lymphocyte Activation;Genes, Synthetic;Research Support, U.S. Gov't, P.H.S.;Peptide Elongation Factor 1;Transgenes;Genes, Reporter;Promoter Regions (Genetics);Transfection;Isoantigens;Hematopoietic Stem Cells;Dendritic Cells;Spleen;Macrophages;T-Lymphocytes;11 Glia;Hematopoietic Stem Cell Transplantation;Leukocytes, Mononuclear;Gene Expression Regulation;Mice, Inbred NOD;Graft Survival;Bone Marrow Cells;Mice;Research Support, Non-U.S. Gov't;Lentivirus;Humans},
	Medline = {21640012},
	Month = {1},
	Nlm_Id = {7603509},
	Number = {2},
	Organization = {Division of Immunology and Hematopoiesis, Johns Hopkins Oncology Center, Johns Hopkins University, Baltimore, MD 21231, USA.},
	Pages = {399-408},
	Pubmed = {11781219},
	Title = {Targeting transgene expression to antigen-presenting cells derived from lentivirus-transduced engrafting human hematopoietic stem/progenitor cells},
	Uuid = {A69D80D5-4118-40DC-9311-36C314F36E6C},
	Volume = {99},
	Year = {2002}}

@article{Culic:1994,
	Abstract = {Experiments were performed to investigate the effects of cerebellar stimulation on epilepsy induced by parenteral administration of penicillin, in rats without or with the lesion of sensorimotor cortex. There were no differences in the EEG activity of the same experimental animal after the first and subsequent penicillin treatments (at least 7 days later). The electrical stimulation (duration of 5-10 min) of the lateral cerebellar nucleus was applied repetitively 135-315 min after penicillin administration, when the EEG power spectra markedly increased. The cerebellar stimulation evoked the decrease of the mean total EEG power spectra, but the effects were temporary. The EEG power spectra were significantly lower (P < 0.05) during the period of 150-330 min after penicillin treatment in experimental sessions with applied cerebellar stimulation in comparison to the experimental sessions without such stimulation. The residual effects (if any) of cerebellar stimulation on the EEG activity in the later period, 345-600 after penicillin treatment were not significant (P > 0.05). Cerebellar stimulation had the same effect among unlesioned animals and animals with prior cortical lesion in the acute model of epilepsy.},
	Author = {Culic, M. and Saponjic, J. and Jankovic, B. and Rakic, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0971-5916},
	Journal = {Indian J Med Res},
	Keywords = {Electric Stimulation;Penicillins;Electroencephalography;Research Support, Non-U.S. Gov't;Epilepsy;21 Neurophysiology;24 Pubmed search results 2008;Rats;21 Epilepsy;Rats, Wistar;Animals;Disease Models, Animal;Cerebral Cortex;Cerebellar Nuclei;Male},
	Medline = {95048604},
	Month = {9},
	Nlm_Id = {0374701},
	Organization = {Institute for Biological Research, Center for Multidisciplinary Studies, Belgrade, Yugoslavia.},
	Pages = {135-9},
	Pubmed = {7959970},
	Title = {Effect of cerebellar stimulation on EEG power spectra in the acute model of epilepsy},
	Uuid = {54CAFF0B-98E9-4626-A7FE-8B7AE58D65C3},
	Volume = {100},
	Year = {1994}}

@article{Culic:1995,
	Abstract = {The experiments were performed in order to investigate the sparing of function following early postnatal cortical lesion in the acute rat model of epilepsy. Sensorimotor cortex was unilaterally removed at 9 and 10 days of postnatal age in lesioned animals, while control animals were only sham operated (at the same early stage of life) or non-operated (before implantation of the electrodes). Seizure activity was recorded by means of electroencephalograms at adult stage of life induced by parenteral administration of penicillin (1,000,000 I.U./kg, i.p.). Our results showed that when the cortical lesion was performed in infancy (on the contrary to the lesion performed in adulthood) there was no prolongation of seizure activity in an acute model of epilepsy.},
	Author = {Culi\'{c}, M. and Saponji\'{c}, J. and Jankovi\'{c}, B. and Pekovi\'{c}, S. and Stojiljkovi\'{c}, M. and Udovi\'{c}, S. and Raki\'{c}, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0736-5748},
	Journal = {Int J Dev Neurosci},
	Keywords = {Penicillins;Aging;Prognosis;Research Support, Non-U.S. Gov't;Neuroprotective Agents;Epilepsy;Electroencephalography;Rats;21 Neurophysiology;24 Pubmed search results 2008;21 Epilepsy;Rats, Wistar;Male;Injections, Intraperitoneal;Cerebral Cortex;Animals;Disease Models, Animal},
	Medline = {96104002},
	Month = {10},
	Nlm_Id = {8401784},
	Number = {6},
	Organization = {Institute for Biological Research, University of Belgrade, Serbia Montenegro.},
	Pages = {655-8},
	Pii = {0736574895000218},
	Pubmed = {8553901},
	Title = {Effect of early cortical lesion on the acute model of epilepsy},
	Uuid = {3A325323-445A-4004-A9E9-0F264B2F3F11},
	Volume = {13},
	Year = {1995}}

@article{Cunto:2002,
	Abstract = {During spermatogenesis, the first morphological indication of spermatogonia differentiation is incomplete cytokinesis, followed by the assembly of stable intercellular cytoplasmic communications. This distinctive feature of differentiating male germ cells has been highly conserved during evolution, suggesting that regulation of the cytokinesis endgame is a crucial aspect of spermatogenesis. However, the molecular mechanisms underlying testis-specific regulation of cytokinesis are still largely unknown. Citron kinase is a myotonin-related protein acting downstream of the GTPase Rho in cytokinesis control. We previously reported that Citron kinase knockout mice are affected by a complex neurological syndrome caused by cytokinesis block and apoptosis of specific neuronal precursors. In this report we show that, in addition, these mice display a dramatic testicular impairment, with embryonic and postnatal loss of undifferentiated germ cells and complete absence of mature spermatocytes. By contrast, the ovaries of mutant females appear essentially normal. Developmental analysis revealed that the cellular depletion observed in mutant testes is caused by increased apoptosis of undifferentiated and differentiating precursors. The same cells display a severe cytokinesis defect, resulting in the production of multinucleated cells and apoptosis. Our data indicate that Citron kinase is specifically required for cytokinesis of the male germ line. 0021-9533 Journal Article},
	Author = {Cunto, F. D. and Imarisio, S. and Camera, P. and Boitani, C. and Altruda, F. and Silengo, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Cell Sci},
	Keywords = {Spermatocytes/*cytology;In Situ Nick-End Labeling;Testis/cytology/enzymology/growth &development;05 Citron Kinase flathead;Mice, Knockout;Immunohistochemistry;Cell Cycle/*physiology;CK;Protein-Serine-Threonine Kinases/genetics/*physiology;Support, Non-U.S. Gov't;Animals;Male;Mice},
	Number = {Pt 24},
	Organization = {Department of Genetics, Biology and Biochemistry, Via Santena 5 bis, Torino, Italy. ferdinando.dicunto\@unito.it},
	Pages = {4819-26},
	Pubmed = {12432070},
	Title = {Essential role of citron kinase in cytokinesis of spermatogenic precursors},
	Uuid = {831222AB-90D7-4800-A0EE-E566CA5A25A2},
	Volume = {115},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12432070}}

@article{Curtis:2007,
	Abstract = {During brain development, one of the most important structures is the subventricular zone (SVZ), from which most neurons are generated. In adulthood the SVZ maintains a pool of progenitor cells that continuously replace neurons in the olfactory bulb. Neurodegenerative diseases induce a substantial upregulation or downregulation of SVZ progenitor cell proliferation, depending on the type of disorder. Far from being a dormant layer, the SVZ responds to neurodegenerative disease in a way that makes it a potential target for therapeutic intervention.},
	Author = {Curtis, Maurice A. and Faull, Richard L. M. and Eriksson, Peter S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1471-003X},
	Journal = {Nat Rev Neurosci},
	Keywords = {research support, non-u.s. gov't;Neurodegenerative Diseases;Lateral Ventricles;Animals;Humans;24 Pubmed search results 2008;Neurons;review},
	Month = {9},
	Nlm_Id = {100962781},
	Number = {9},
	Organization = {Institute of Neuroscience and Physiology at Sahlgrenska Academy, Medicinaregat 11, Box 432, s-40530 G{\"o}teborg, Sweden. maurice.curtis\@neuro.gu.se},
	Pages = {712-23},
	Pii = {nrn2216},
	Pubmed = {17704813},
	Title = {The effect of neurodegenerative diseases on the subventricular zone},
	Uuid = {2B9851EE-8704-4BD0-9FD1-C31C21DF7D35},
	Volume = {8},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrn2216}}

@article{Curtis:2003,
	Abstract = {Neurogenesis has recently been observed in the adult human brain, suggesting the possibility of endogenous neural repair. However, the augmentation of neurogenesis in the adult human brain in response to neuronal cell loss has not been demonstrated. This study was undertaken to investigate whether neurogenesis occurs in the subependymal layer (SEL) adjacent to the caudate nucleus in the human brain in response to neurodegeneration of the caudate nucleus in Huntington's disease (HD). Postmortem control and HD human brain tissue were examined by using the cell cycle marker proliferating cell nuclear antigen (PCNA), the neuronal marker beta III-tubulin, and the glial cell marker glial fibrillary acidic protein (GFAP). We observed a significant increase in cell proliferation in the SEL in HD compared with control brains. Within the HD group, the degree of cell proliferation increased with pathological severity and increasing CAG repeats in the HD gene. Most importantly, PCNA+ cells were shown to coexpress beta III-tubulin or GFAP, demonstrating the generation of neurons and glial cells in the SEL of the diseased human brain. Our results provide evidence of increased progenitor cell proliferation and neurogenesis in the diseased adult human brain and further indicate the regenerative potential of the human brain.},
	Author = {Curtis, Maurice A. and Penney, Ellen B. and Pearson, Andree G. and van Roon-Mom, Willeke M. C. and Butterworth, Niqi J. and Dragunow, Michael and Connor, Bronwen and Faull, Richard L. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Minisatellite Repeats;Trinucleotide Repeats;Glial Fibrillary Acidic Protein;Aged;Research Support, Non-U.S. Gov't;Case-Control Studies;Nerve Regeneration;Tubulin;Adult;Proliferating Cell Nuclear Antigen;06 Adult neurogenesis injury induced;Cell Division;Middle Aged;Huntington Disease;Humans;Brain},
	Medline = {22758992},
	Month = {7},
	Nlm_Id = {7505876},
	Number = {15},
	Organization = {Department of Anatomy with Radiology, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand.},
	Pages = {9023-7},
	Pii = {1532244100},
	Pubmed = {12853570},
	Title = {Increased cell proliferation and neurogenesis in the adult human Huntington's disease brain},
	Uuid = {CE947B36-E6A7-4BBF-A6A8-936CF6E73020},
	Volume = {100},
	Year = {2003},
	url = {papers/Curtis_ProcNatlAcadSciUSA2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.1532244100}}

@article{Czeh:2001,
	Abstract = {Stress-induced structural remodeling in the adult hippocampus, involving debranching and shortening of dendrites and suppression of neurogenesis, provides a cellular basis for understanding the impairment of neural plasticity in the human hippocampus in depressive illness. Accordingly, reversal of structural remodeling may be a desirable goal for antidepressant therapy. The present study investigated the effect of tianeptine, a modified tricyclic antidepressant, in the chronic psychosocial stress model of adult male tree shrews (Tupaia belangeri), a model with high validity for research on the pathophysiology of major depression. Animals were subjected to a 7-day period of psychosocial stress to elicit stress-induced endocrine and central nervous alterations before the onset of daily oral administration of tianeptine (50 mg/kg). The psychosocial stress continued throughout the treatment period of 28 days. Brain metabolite concentrations were determined in vivo by proton magnetic resonance spectroscopy, cell proliferation in the dentate gyrus was quantified by using BrdUrd immunohistochemistry, and hippocampal volume was measured post mortem. Chronic psychosocial stress significantly decreased in vivo concentrations of N-acetyl-aspartate (-13\%), creatine and phosphocreatine (-15\%), and choline-containing compounds (-13\%). The proliferation rate of the granule precursor cells in the dentate gyrus was reduced (-33\%). These stress effects were prevented by the simultaneous administration of tianeptine yielding normal values. In stressed animals treated with tianeptine, hippocampal volume increased above the small decrease produced by stress alone. These findings provide a cellular and neurochemical basis for evaluating antidepressant treatments with regard to possible reversal of structural changes in brain that have been reported in depressive disorders.},
	Author = {Czeh, B. and Michaelis, T. and Watanabe, T. and Frahm, J. and de Biurrun, G. and van Kampen, M. and Bartolomucci, A. and Fuchs, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:44 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {22},
	Organization = {Division of Neurobiology, German Primate Center, 37077 Gottingen, Germany; and Biomedizinische NMR Forschungs GmbH am Max-Planck-Institut fur biophysikalische Chemie, 37070 Gottingen, Germany.},
	Pages = {12796-801.},
	Title = {Stress-induced changes in cerebral metabolites, hippocampal volume, and cell proliferation are prevented by antidepressant treatment with tianeptine},
	Uuid = {5E856E0C-82FD-4BC6-BFBE-2E722CFBF907},
	Volume = {98},
	Year = {2001},
	url = {papers/Czeh_ProcNatlAcadSciUSA2001.pdf}}

@article{DAmour:2003,
	Abstract = {Stem cells (SCs) are functionally defined by their abilities to self-renew and generate differentiated cells. Although much effort has been focused on defining the common characteristics among various types of SCs, the genetic and functional differences between multipotent and pluripotent SCs have garnered less attention. We report a direct genetic and functional comparison of molecularly defined and clonally related populations of neural SCs (NSCs) and embryonic SCs (ESCs), using the Sox2 promoter for isolation of purified populations by fluorescence-activated cell sorting. A stringent expression profile comparison of promoter-defined NSCs and ESCs revealed a striking dissimilarity, and subsequent chimera analyses confirmed the fundamental differences in cellular potency between these populations. This direct comparison elucidates the molecular basis for the functional differences in pluripotent ESCs and multipotent NSCs. 0027-8424 Journal Article},
	Author = {D'Amour, K. A. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {DNA, Complementary/genetics;DNA-Binding Proteins/genetics;Animals;Base Sequence;Comparative Study;Chimeric Proteins/genetics;Mice, Transgenic;Pluripotent Stem Cells/*cytology/*physiology;Nuclear Proteins/genetics;Gene Expression Profiling;Reverse Transcriptase Polymerase Chain Reaction;04 Adult neurogenesis factors;Multipotent Stem Cells/*cytology/*physiology;Neurons/*chemistry/*physiology;Promoter Regions (Genetics);Mice;C pdf;Luminescent Proteins/genetics},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.},
	Pages = {11866-72},
	Pubmed = {12923297},
	Title = {Genetic and functional differences between multipotent neural and pluripotent embryonic stem cells},
	Uuid = {57AEB715-82A8-441F-9D56-7AF4A8745939},
	Volume = {100 Suppl 1},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12923297}}

@article{DAntuono:2004,
	Abstract = {Patients with Taylor's type focal cortical dysplasia (FCD) present with seizures that are often medically intractable. Here, we attempted to identify the cellular and pharmacological mechanisms responsible for this epileptogenic state by using field potential and K+-selective recordings in neocortical slices obtained from epileptic patients with FCD and, for purposes of comparison, with mesial temporal lobe epilepsy (MTLE), an epileptic disorder that, at least in the neocortex, is not characterized by any obvious structural aberration of neuronal networks. Spontaneous epileptiform activity was induced in vitro by applying 4-aminopyridine (4AP)-containing medium. Under these conditions, we could identify in FCD slices a close temporal relationship between ictal activity onset and the occurrence of slow interictal-like events that were mainly contributed by GABAA receptor activation. We also found that in FCD slices, pharmacological procedures capable of decreasing or increasing GABAA receptor function abolished or potentiated ictal discharges, respectively. In addition, the initiation of ictal events in FCD tissue coincided with the occurrence of GABAA receptor-dependent interictal events leading to [K+]o elevations that were larger than those seen during the interictal period. Finally, by testing the effects induced by baclofen on epileptiform events generated by FCD and MTLE slices, we discovered that the function of GABAB receptors (presumably located at presynaptic inhibitory terminals) was markedly decreased in FCD tissue. Thus, epileptiform synchronization leading to in vitro ictal activity in the human FCD tissue is initiated by a synchronizing mechanism that paradoxically relies on GABAA receptor activation causing sizeable increases in [K+]o. This mechanism may be facilitated by the decreased ability of GABAB receptors to control GABA release from interneuron terminals.},
	Author = {D'Antuono, M. and Louvel, J. and K{\"o}hling, R. and Mattia, D. and Bernasconi, A. and Olivier, A. and Turak, B. and Devaux, A. and Pumain, R. and Avoli, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0006-8950},
	Journal = {Brain},
	Keywords = {Adolescent;10 Development;in vitro;Electrophysiology;Epilepsies, Partial;Humans;Neocortex;Female;Homeostasis;Child;Baclofen;research support, non-u.s. gov't;Male;Analysis of Variance;Potassium;Receptors, GABA-A;Potassium Channel Blockers;Epilepsy, Temporal Lobe;10 genetics malformation;Adult;24 Pubmed search results 2008;4-Aminopyridine;Receptors, N-Methyl-D-Aspartate;GABA Agonists},
	Month = {7},
	Nlm_Id = {0372537},
	Number = {Pt 7},
	Organization = {Dipartimento di Fisiologia Umana e Farmacologia V. Erspamer, Universit\`{a} degli Studi di Roma La Sapienza, Italy.},
	Pages = {1626-40},
	Pii = {awh181},
	Pubmed = {15175227},
	Title = {GABAA receptor-dependent synchronization leads to ictogenesis in the human dysplastic cortex},
	Uuid = {1447F7E2-27E5-49A4-B844-C8BEF0797B4F},
	Volume = {127},
	Year = {2004},
	url = {papers/D'Antuono_Brain2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/brain/awh181}}

@article{Dal-Canto:1997,
	Abstract = {In many patients with AIDS, severe neurologic deficits develop that have been designated the cf2HIV-associated cognitive-motor complex. cf1 Pathologically, these symptoms correlate with a low-grade inflammatory condition, referred to as cf2HIV encephalitis,cf1 in which the most characteristic change is the presence of multinucleated giant cells. Cortical changes include neuronal loss and alterations of dendrites and synapses. There is pallor of white matter generally associated with the mononuclear inflammatory infiltrates. The only cells that seem to be directly infected by HIV are the microglia/monocyte and the giant cells derived from fusion of monocytes. It is hypothesized, therefore, that cortical and white matter alterations in patients with this syndrome depend on the production of injurious soluble factors liberated by these cells and by astrocytes under the influence of many of these same factors. This article reviews recent advances in the understanding of these secondary effects and discusses pathogenetic mechanisms of tissue injury.},
	Author = {Dal Canto, M. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {1052-5149},
	Journal = {Neuroimaging Clin N Am},
	Keywords = {HIV Infections;Central Nervous System;AIDS Dementia Complex;11 Glia;Humans;HIV;review},
	Medline = {97268964},
	Month = {5},
	Nlm_Id = {9211377},
	Number = {2},
	Organization = {Division of Neuropathology, Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611, USA.},
	Pages = {231-41},
	Pubmed = {9113688},
	Title = {Mechanisms of HIV infection of the central nervous system and pathogenesis of AIDS-dementia complex},
	Uuid = {0A3F7B00-D7A7-4315-9C58-8228F5BBB4F1},
	Volume = {7},
	Year = {1997}}

@article{Dalmau:1998,
	Abstract = {During the prenatal development of the hippocampus, microglial cell precursors progressively occur in all subfields in accordance with known ontogenetic gradients of the region (Dalmau et al., J. Comp. Neurol. 1997a;377:70-84). The present study follows the regional distribution of these microglial cell precursors and their morphological differentiation in the rat hippocampus from birth to postnatal (P) day 18. The results demonstrate that the cellular differentiation and the subregional distribution of microglia follow the specific developmental gradients of the different parts of Ammon's horn and the dentate gyrus. Microglial cell distribution in the dentate gyrus is thus delayed compared with that in Ammon's horn. The appearance of microglia in the hippocampal subregions and differentiation of cell precursors into adult microglia occur earlier at temporal levels than at septal levels. Distribution of microglial cells follows an outside-to-inside pattern from the hippocampal fissure to the main cell layers in either Ammon's horn or the dentate gyrus. Meanwhile, the resident microglial cells located in the stratum oriens and dentate hilus at birth also increase in number and gradually disperse throughout the whole tissue of the two layers with age. In Ammon's horn, microglial differentiation occurs earlier in CA3 than in CA1. In the dentate gyrus, microglia appear earlier in relation to the external limb than to the internal limb, largely following a lateral-to-medial gradient. The differentiation and appearance of microglia in the various hippocampal and dentate subregions often correspond to the developmental stage of intrinsic and extrinsic afferent nerve fiber projections. Finally, in both Ammon's horn and the dentate gyrus, cells resembling reactive microglia are also observed and, in particular, in the perforant path projections from P9 to P18, suggesting their participation not only in phagocytosis of dead cells but also in axonal elimination and/or fiber reorganization.},
	Author = {Dalmau, I. and Finsen, B. and Zimmer, J. and Gonz{\'a}lez, B. and Castellano, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {1050-9631},
	Journal = {Hippocampus},
	Keywords = {Acid Anhydride Hydrolases;Cell Differentiation;Female;Hippocampus;Cell Aging;Not relevant;Rats, Wistar;Time Factors;11 Glia;Microglia;Animals, Newborn;Histocytochemistry;Rats;Animals;Male;Support, Non-U.S. Gov't;Dentate Gyrus},
	Medline = {99041331},
	Nlm_Id = {9108167},
	Number = {5},
	Organization = {Department of Cell Biology and Physiology, Universitat Aut\`{o}noma de Barcelona, Spain. i.dalmau\@cc.uab.es},
	Pages = {458-74},
	Pubmed = {9825958},
	Title = {Development of microglia in the postnatal rat hippocampus},
	Uuid = {BBAFE0C6-F320-485A-9BE5-6D809607E8B0},
	Volume = {8},
	Year = {1998}}

@article{Dalmau:2003,
	Abstract = {Entrance of mesodermal precursors into the developing CNS is the most well-accepted origin of microglia. However, the contribution of proliferation and death of recruited microglial precursors to the final microglial cell population remains to be elucidated. To investigate microglial proliferation and apoptosis during development, we combined proliferating cell nuclear antigen (PCNA) immunohistochemistry, in situ detection of nuclear DNA fragmentation (TUNEL), and caspase-3 immunohistochemistry with tomato lectin histochemistry, a selective microglial marker. The study was carried out in Wistar rats from embryonic day (E) 16 to postnatal day (P) 18 in cerebral cortex, subcortical white matter, and hippocampus. Proliferating microglial cells were found at all ages in the three brain regions and represented a significant fraction of the total microglial cell population. The percentage of microglia expressing PCNA progressively increased from the embryonic period (25-51\%at E16) to a maximum at P9, when the great majority of microglia expressed PCNA (92-99\%) in all the brain regions analyzed. In spite of the remarkable proliferation and expansion of the microglial population with time, the density of microglia remained quite constant in most brain regions because of the considerable growth of the brain during late prenatal and early postnatal periods. In contrast, apoptosis of microglia was detected only at certain times and was restricted to some ameboid cells in white matter and primitive ramified cells in gray matter, representing a small fraction of the microglial population. Therefore, our results point to proliferation of microglial precursors in the developing brain as a physiological mechanism contributing to the acquisition of the adult microglial cell population. In contrast, microglial apoptosis occurs only locally at certain developmental stages and thus seems less crucial for the establishment of the final density of microglia.},
	Author = {Dalmau, Ishar and Vela, Jos{\'e} Miguel and Gonz{\'a}lez, Berta and Finsen, Bente and Castellano, Bernardo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Caspases;In Situ Nick-End Labeling;Rats;Proliferating Cell Nuclear Antigen;Rats, Wistar;Cell Count;11 Glia;Microglia;Cell Division;Not relevant;Support, Non-U.S. Gov't;Brain;Phagocytosis;Animals;DNA Fragmentation},
	Medline = {22483863},
	Month = {3},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Departmet of Histology, Faculty of Medicine, Autonomous University of Barcelona, E-08193-Bellaterra, Spain.},
	Pages = {144-57},
	Pubmed = {12596255},
	Title = {Dynamics of microglia in the developing rat brain},
	Uuid = {40B43435-EC28-11DA-8617-000D9346EC2A},
	Volume = {458},
	Year = {2003},
	url = {papers/Dalmau_JCompNeurol2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10572}}

@article{Daneman:2005,
	Abstract = {Despite the importance of the blood-brain barrier (BBB), little is known about the molecular mechanisms that control its integrity. The identification of moody, a gene required for the formation and maintenance of the Drosophila BBB, provides new insight into how paracellular junctions are formed at the barrier. Meanwhile, moody also has been identified in a screen for fly mutants with altered sensitivity to cocaine, remarkably implicating the BBB in the physiological response to narcotics.},
	Author = {Daneman, Richard and Barres, Ben A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008;10 Development;Neuroglia;Blood-Brain Barrier;Cell Adhesion Molecules;Drosophila Proteins;Signal Transduction;Tight Junctions;Animals;Endothelial Cells;Humans;Receptors, G-Protein-Coupled;review},
	Month = {10},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Department of Neurobiology, Stanford University School of Medicine, CA 94305, USA. rdaneman\@stanford.edu},
	Pages = {9-12},
	Pii = {S0092-8674(05)00970-0},
	Pubmed = {16213208},
	Title = {The blood-brain barrier--lessons from moody flies},
	Uuid = {9F1CE65B-675C-4D6C-94E8-C981493AA296},
	Volume = {123},
	Year = {2005},
	url = {papers/Daneman_Cell2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.09.017}}

@article{Darbinian-Sarkissian:2006,
	Abstract = {Transcription of the HIV-1 genome is controlled by the cooperation of viral regulatory proteins and several host factors which bind to specific DNA sequences within the viral promoter spanning the long terminal repeat, (LTR). Here, we describe the identification of a novel protein, p27(SJ), present in a laboratory callus culture of Hypericum perforatum (St John's Wort) that suppresses transcription of the HIV-1 genome in several human cell types including primary culture of microglia and astrocytes. p27(SJ) associates with C/EBPbeta, a transcription factor that regulates expression of the HIV-1 genome in macrophages and monocytic cells, and the viral transactivator, Tat. The association of p27(SJ) with C/EBPbeta and Tat alters their subcellular localization, causing their accumulation in the perinuclear cytoplasmic compartment of the cells. Fusion of a nuclear localization signal to p27(SJ) forces its entry into the nucleus and diminishes the capacity of p27(SJ) to suppress Tat activity, but does not alter its ability to suppress C/EBPbeta activation of the LTR. Results from binding assays showed the inhibitory effect of p27(SJ) on C/EBPbeta interaction with DNA. Finally, our results demonstrate that expression of p27(SJ) decreases the level of viral replication in HIV-1-infected cells. These observations suggest the potential for the development of a therapeutic advance based on p27(SJ) protein to control HIV-1 transcription and replication in cells associated with HIV-1 infection in the brain.},
	Author = {Darbinian-Sarkissian, N. and Darbinyan, A. and Otte, J. and Radhakrishnan, S. and Sawaya, B. E. and Arzumanyan, A. and Chipitsyna, G. and Popov, Y. and Rappaport, J. and Amini, S. and Khalili, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Phytotherapy;Gene Expression Regulation, Viral;HIV-1;Astrocytes;Base Sequence;U937 Cells;Transfection;Cells, Cultured;Humans;Microglia;Plant Proteins;Hypericum;Depression, Chemical;11 Glia;HIV Infections;Gene Therapy;Genome, Viral;Virus Replication;Research Support, N.I.H., Extramural;Terminal Repeat Sequences;Molecular Sequence Data},
	Month = {2},
	Nlm_Id = {9421525},
	Number = {4},
	Organization = {Department of Neuroscience, Center for Neurovirology, Temple University School of Medicine, Philadelphia, PA, USA.},
	Pages = {288-95},
	Pii = {3302649},
	Pubmed = {16251997},
	Title = {p27(SJ), a novel protein in St John's Wort, that suppresses expression of HIV-1 genome},
	Uuid = {2F05D204-EA51-4D43-92A8-A678BC28D40F},
	Volume = {13},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3302649}}

@article{Dasgupta:2005,
	Abstract = {Females are more susceptible than males to multiple sclerosis (MS). However, the underlying mechanism behind this gender difference is poorly understood. Because the presence of neuroantigen-primed T cells within the CNS is necessary for the development of MS, the present study was undertaken to investigate the activation of microglia by myelin basic protein (MBP)-primed T cells of male, female and castrated male mice. Interestingly, MBP-primed T cells isolated from female and castrated male but not from male mice induced the expression of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines (IL-1b, IL-1a, IL-6 and TNF-a) in microglia by cell-cell contact. Again there was no apparent defect in male microglia because MBP-primed T cells isolated from female and castrated male but not male mice were capable of inducing the production of NO in male primary microglia. Inhibition of female T cell contact-mediated microglial expression of proinflammatory molecules by dominant-negative mutants of p65 and C/EBPb suggest that female MBP-primed T cells induce microglial expression of proinflammatory molecules through the activation of NF-kB and C/EBPb. Interestingly, MBP-primed T cells of male, female and castrated male mice were able to induce microglial activation of NF-kB. However, MBP-primed T cells of female and castrated male but not male mice induced microglial activation of C/EBPb. These studies suggest that microglial activation of C/EBPb but not NF-kB by T cell:microglial contact is a gender-specific event and that male MBP-primed T cells are not capable of inducing microglial expression of proinflammatory molecules due to their inability to induce the activation of C/EBPb in microglia. This novel gender-sensitive activation of microglia by neuroantigen-primed T cell contact could be one of the mechanisms behind the female-loving nature of MS.},
	Author = {Dasgupta, and Jana, and Liu, and Pahan,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {Castration;Research Support, N.I.H., Extramural;NF-kappa B;Male;Animals;Transcription, Genetic;Research Support, U.S. Gov't, P.H.S.;Myelin Basic Proteins;Central Nervous System;CCAAT-Enhancer-Binding Protein-beta;Interleukin-1;T-Lymphocytes;11 Glia;Mutation;Multiple Sclerosis;Tumor Necrosis Factor-alpha;Cell Membrane;Nitric Oxide;Oligonucleotide Array Sequence Analysis;Female;Sex Factors;Microglia;Cell Nucleus;Interleukin-6;Mice;Inflammation;Research Support, Non-U.S. Gov't;RNA;Genes, Dominant;Cytokines;Immunoblotting},
	Month = {7},
	Nlm_Id = {2985121R},
	Number = {38},
	Organization = {Section of Neuroscience, Oral Biology, University of Nebraska Medical Center, Lincoln, NE 68583-0740.},
	Pages = {32609-17},
	Pii = {M500299200},
	Pubmed = {16046404},
	Title = {Myelin basic protein-primed T cells of female but not male mice induce nitric oxide synthase and proinflammatory cytokines in microglia: Implications for gender bias in multiple sclerosis},
	Uuid = {9B3B99B6-9F0F-11DA-8D49-000D9346EC2A},
	Volume = {280},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1074/jbc.M500299200}}

@article{Daval:2004,
	Abstract = {Continuous generation of new neurons has been demonstrated in the adult mammalian brain, and this process was shown to be stimulated by various pathologic conditions, including cerebral ischemia. Because brain oxygen deprivation is particularly frequent in neonates and represents the primary event of asphyxia, we analyzed long-term consequences of transient hypoxia in the newborn rat. Within 24 h after birth, animals were exposed to 100\%N2 for 20 min at 36 degrees C, and temporal changes in the vulnerable CA1 hippocampus were monitored. Cell density measurements revealed delayed cell death in the pyramidal cell layer reflecting apoptosis, as shown by characteristic nuclear morphology and expression levels of Bcl-2, Bax, and caspase-3. Neuronal loss was confirmed by reduced density of neuron-specific enolase (NSE)-labeled cells, and peaked by 1 wk post insult, to reach 27\%of total cells. A gradual recovery then occurred, and no significant difference in cell density could be detected between controls and hypoxic rats at postnatal d 21. Repeated injections of bromodeoxyuridine (50 mg/kg) showed that newly divided cells expressing neuronal markers increased by 225\%in the germinative subventricular zone, and they tended to migrate along the posterior periventricle toward the hippocampus. Therefore, transient hypoxia in the newborn rat triggered apoptosis in the CA1 hippocampus followed by increased neurogenesis and apparent anatomical recovery, suggesting that the developing brain may have a high capacity for self-repair. 0031-3998 Journal article},
	Author = {Daval, J. L. and Pourie, G. and Grojean, S. and Lievre, V. and Strazielle, C. and Blaise, S. and Vert, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {Pediatr Res},
	Keywords = {06 Adult neurogenesis injury induced;D pdf},
	Organization = {INSERM EMI 0014, Faculte de Medecine, UHP, 54500 Vandoeuvre-les-Nancy, France, and Medecine et Reanimation Neonatales, Maternite Regionale, 54000 Nancy, France.},
	Title = {Neonatal Hypoxia Triggers Transient Apoptosis Followed by Neurogenesis in the Rat CA1 Hippocampus},
	Uuid = {66B9D124-96A0-48AA-A35C-608EC802180A},
	Year = {2004},
	url = {papers/Daval_PediatrRes2004.pdf}}

@article{Davalos:2005,
	Abstract = {Parenchymal microglia are the principal immune cells of the brain. Time-lapse two-photon imaging of GFP-labeled microglia demonstrates that the fine termini of microglial processes are highly dynamic in the intact mouse cortex. Upon traumatic brain injury, microglial processes rapidly and autonomously converge on the site of injury without cell body movement, establishing a potential barrier between the healthy and injured tissue. This rapid chemotactic response can be mimicked by local injection of ATP and can be inhibited by the ATP-hydrolyzing enzyme apyrase or by blockers of G protein-coupled purinergic receptors and connexin channels, which are highly expressed in astrocytes. The baseline motility of microglial processes is also reduced significantly in the presence of apyrase and connexin channel inhibitors. Thus, extracellular ATP regulates microglial branch dynamics in the intact brain, and its release from the damaged tissue and surrounding astrocytes mediates a rapid microglial response towards injury.},
	Author = {Davalos, Dimitrios and Grutzendler, Jaime and Yang, Guang and Kim, Jiyun V. and Zuo, Yi and Jung, Steffen and Littman, Dan R. and Dustin, Michael L. and Gan, Wen-Biao B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Signal Transduction;Animals;Astrocytes;Phagocytosis;Brain;Microglia;Chemotaxis;Cell Communication;Mice, Transgenic;Reaction Time;Connexins;11 Glia;Green Fluorescent Proteins;Adenosine Triphosphate;Brain Injuries;Research Support, U.S. Gov't, P.H.S.;Apyrase;Gliosis;Mice;Research Support, N.I.H., Extramural;Receptors, Purinergic P2;Research Support, Non-U.S. Gov't},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Organization = {Molecular Neurobiology Program, Department of Physiology and Neuroscience, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.},
	Pages = {752-8},
	Pii = {nn1472},
	Pubmed = {15895084},
	Title = {ATP mediates rapid microglial response to local brain injury in vivo},
	Uuid = {3E2D7CA0-FFAF-11DA-9E68-000D9346EC2A},
	Volume = {8},
	Year = {2005},
	url = {papers/Davalos_NatNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1472}}

@article{Davidoff:2001,
	Abstract = {Inhibition of tumor-induced neovascularization appears to be an effective anticancer approach, although long-term angiogenesis inhibition may be required. An alternative to chronic drug administration is a gene therapy-mediated approach in which long-term in vivo protein expression is established. We have tested this approach by modifying murine bone marrow-derived cells with a gene encoding an angiogenesis inhibitor: a soluble, truncated form of the vascular endothelial growth factor receptor-2, fetal liver kinase-1 (Flk-1). Murine bone marrow cells were transduced with a retroviral vector encoding either truncated, soluble Flk-1 (tsFlk-1) together with green fluorescent protein (GFP) or GFP alone. Tumor growth in mice challenged 3 months after transplantation with tsFlk-1-expressing bone marrow cells was significantly inhibited when compared with tumor growth in control-transplanted mice. Immunohistochemical analysis of tumors in each group demonstrated colocalization of GFP expression in cells staining with endothelial cell markers, suggesting that the endothelial cells of the tumor-induced neovasculature were derived, at least in part, from bone marrow precursors. These results suggest that long-term expression of a functional angiogenesis inhibitor can be generated through gene-modified, bone marrow-derived stem cells, and that this approach can have significant anticancer efficacy. Modifying these cells seems to have the added potential benefit of targeting transgene expression to the tumor neovasculature, because bone marrow-derived endothelial cell precursors seem to be recruited in the process of tumor-induced angiogenesis.},
	Author = {Davidoff, A. M. and Ng, C. Y. and Brown, P. and Leary, M. A. and Spurbeck, W. W. and Zhou, J. and Horwitz, E. and Vanin, E. F. and Nienhuis, A. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {1078-0432},
	Journal = {Clin Cancer Res},
	Keywords = {Receptors, Growth Factor;Angiogenesis Inhibitors;Gene Expression Regulation;Animals;Fluorescent Antibody Technique;Transfection;Humans;Female;Mice, SCID;11 Glia;Green Fluorescent Proteins;Xenograft Model Antitumor Assays;Genetic Vectors;Hematopoietic Stem Cell Transplantation;Neovascularization, Pathologic;Mice, Inbred Strains;Bone Marrow Cells;Gene Therapy;Receptors, Vascular Endothelial Growth Factor;Tumor Cells, Cultured;Research Support, U.S. Gov't, P.H.S.;Receptor Protein-Tyrosine Kinases;Mice;Cell Division;Luminescent Proteins;Neoplasms, Experimental;Research Support, Non-U.S. Gov't},
	Medline = {21439142},
	Month = {9},
	Nlm_Id = {9502500},
	Number = {9},
	Organization = {Department of Surgery, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. andrew.davidoff\@stjude.org},
	Pages = {2870-9},
	Pubmed = {11555605},
	Title = {Bone marrow-derived cells contribute to tumor neovasculature and, when modified to express an angiogenesis inhibitor, can restrict tumor growth in mice},
	Uuid = {9B91A181-0D94-454C-8CE9-136E4447B9FC},
	Volume = {7},
	Year = {2001}}

@article{Davidson:2007,
	Abstract = {RNA interference (RNAi), a mediator of gene silencing, has swiftly become one of the most exciting and applicable biological discoveries. There has been rapid progress in identifying RNAi pathway components and elucidating the mechanisms of microRNA (miRNA) biogenesis and gene suppression. As a result, RNAi technologies have been successfully employed in a variety of systems as biological tools, and studies are underway to test the therapeutic utility of RNAi. In the span of several years, significant advances in the delivery of inhibitory RNAs in the nervous system have been made. We have glimpses into how endogenous miRNAs interface with neuronal development and function; in addition, RNAi has shown therapeutic efficacy in several mouse models of human neurological conditions. In this review, we summarize the current state-of-the-art of RNAi and its utility to neuroscientists.},
	Author = {Davidson, Beverly L. and Boudreau, Ryan L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-13 09:45:17 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Models, Biological;24 Pubmed search results 2008;research support, non-u.s. gov't;Nervous System Physiology;RNA Interference;research support, n.i.h., extramural;Gene Therapy;Animals;Humans;Nervous System Diseases;review;RNA, Small Interfering; microRNAs; development},
	Month = {3},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA. beverly-davidson\@uiowa.edu},
	Pages = {781-8},
	Pii = {S0896-6273(07)00140-7},
	Pubmed = {17359914},
	Title = {RNA interference: a tool for querying nervous system function and an emerging therapy},
	Uuid = {CD2A927F-B4B2-497B-99A4-18E233194F3A},
	Volume = {53},
	Year = {2007},
	url = {papers/Davidson_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.02.020}}

@article{Davy:2005,
	Abstract = {Eph receptors and ephrins have captured the interest of the developmental biology community in recent years for their pleiotropic functions during embryogenesis. Loss-of-function studies using various animal models have demonstrated the involvement of Ephs and ephrins in many aspects of embryogenesis including segmentation, neural crest cells migration, angiogenesis, and axon guidance. An essential property of this signaling pathway is the ability of both Ephs and ephrins to behave as receptors or ligands and their consequent cell autonomous and nonautonomous mode of action. While many reports did not discriminate between Eph autonomous signaling (forward) and ephrin autonomous signaling (reverse), recent genetic and in vivo studies have shown that both forward and reverse signaling play important roles during embryogenesis.},
	Author = {Davy, Alice and Soriano, Philippe},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1058-8388},
	Journal = {Dev Dyn},
	Keywords = {10 Development;Signal Transduction;Animals;Xenopus;Humans;Ephrins;Neural Crest;review;Receptors, Eph Family;Models, Biological;Cell Movement;Axons;research support, non-u.s. gov't;10 circuit formation;Neovascularization, Physiologic;research support, u.s. gov't, p.h.s.;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Ligands},
	Month = {1},
	Nlm_Id = {9201927},
	Number = {1},
	Organization = {Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.},
	Pages = {1-10},
	Pubmed = {15580616},
	Title = {Ephrin signaling in vivo: look both ways},
	Uuid = {F497D3B7-A87F-4D82-9ABC-5D3F0169C242},
	Volume = {232},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/dvdy.20200}}

@article{Dawson:2003a,
	Abstract = {Glial progenitor cells of the developing CNS committed to the oligodendrocyte lineage (OPCs) express the chondroitin sulfate proteoglycan, NG2. A proportion of OPCs fail to differentiate past the stage at which they express NG2 and the lipid antigen O4 and persist in the adult CNS in a phenotypically immature form. However, the physiological function of NG2(+) cells in the adult CNS is unknown. Using antibodies against NG2 we show that NG2 is expressed by a distinct cell population in the mature CNS with the homogeneous antigenic phenotype of oligodendrocyte progenitors. The morphology of NG2(+) OPCs varies from region to region, reflecting the different structural environments, but they appear to represent a homogeneous population within any one gray or white matter region. A study of nine CNS regions showed that NG2(+) OPCs are numerous throughout the CNS and numbers in the white matter are only 1.5 times that in the gray. Whereas the ratio of OPCs to myelinating oligodendrocytes in the spinal cord gray and white matter approximates 1:4, gray matter regions of the forebrain have a 1:1 ratio, a phenomenon that will have consequences for oligodendrocyte replacement following demyelination. BrdU incorporation experiments showed that NG2(+) cells are the major dividing cell population of the adult rat CNS. Since very little apoptosis was detected and BrdU became increasingly present in oligodendrocytes after a 10-day pulse chase, with a concomitant decrease in NG2(+) BrdU incorporating cells, we suggest that the size of the oligodendrocyte population may actually increase during adult life. 1044-7431 Journal Article},
	Author = {Dawson, M. R. and Polito, A. and Levine, J. M. and Reynolds, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Rats, Sprague-Dawley;Cell Cycle/physiology;Comparative Study;Central Nervous System/cytology/*metabolism;Antigens/*biosynthesis/genetics;Rats;Neuroglia/cytology/*metabolism;Proteoglycans/*biosynthesis/genetics;11 Glia;Stem Cells/cytology/*metabolism;Support, Non-U.S. Gov't;Animals;Male;G pdf;Gene Expression Regulation/physiology},
	Number = {2},
	Organization = {Department of Neuroinflammation, Imperial College London, Charing Cross Hospital Campus, UK.},
	Pages = {476-88},
	Pubmed = {14572468},
	Title = {NG2-expressing glial progenitor cells: an abundant and widespread population of cycling cells in the adult rat CNS},
	Uuid = {1C48BD05-8B72-4C7E-A5AF-57DF4A2F6EF0},
	Volume = {24},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14572468}}

@article{Dawson:2003,
	Abstract = {Parkinson's disease (PD) is a complex disorder with many different causes, yet they may intersect in common pathways, raising the possibility that neuroprotective agents may have broad applicability in the treatment of PD. Current evidence suggests that mitochondrial complex I inhibition may be the central cause of sporadic PD and that derangements in complex I cause alpha-synuclein aggregation, which contributes to the demise of dopamine neurons. Accumulation and aggregation of alpha-synuclein may further contribute to the death of dopamine neurons through impairments in protein handling and detoxification. Dysfunction of parkin (a ubiquitin E3 ligase) and DJ-1 could contribute to these deficits. Strategies aimed at restoring complex I activity, reducing oxidative stress and alpha-synuclein aggregation, and enhancing protein degradation may hold particular promise as powerful neuroprotective agents in the treatment of PD.},
	Author = {Dawson, Ted M. and Dawson, Valina L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:45 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Human;Dopamine;Nerve Degeneration;Animals;review, tutorial;Brain;Mitochondria;review;Mutation;21 Neurodegenerative;Animals, Genetically Modified;Cysteine Endopeptidases;Parkinson Disease;Ubiquitin;Multienzyme Complexes;Support, Non-U.S. Gov't;Oxidative Stress;21 Neurophysiology;Neurons;Ubiquitin-Protein Ligases;Support, U.S. Gov't, P.H.S.;Parkinsonian Disorders;Nerve Tissue Proteins;Electron Transport Complex I},
	Medline = {22954844},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5646},
	Organization = {Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. tdawson\@jhmi.edu},
	Pages = {819-22},
	Pii = {302/5646/819},
	Pubmed = {14593166},
	Title = {Molecular pathways of neurodegeneration in Parkinson's disease},
	Uuid = {BA7EF0AB-446A-4D65-ADA7-0DBAA6258E6E},
	Volume = {302},
	Year = {2003},
	url = {papers/Dawson_Science2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1087753}}

@article{Dayer:2005,
	Abstract = {Ongoing neurogenesis in the adult mammalian dentate gyrus and olfactory bulb is generally accepted, but its existence in other adult brain regions is highly controversial. We labeled newly born cells in adult rats with the S-phase marker bromodeoxyuridine (BrdU) and used neuronal markers to characterize new cells at different time points after cell division. In the neocortex and striatum, we found BrdU-labeled cells that expressed each of the eight neuronal markers. Their size as well as staining for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase 67, calretinin and/or calbindin, suggest that new neurons in both regions are GABAergic interneurons. BrdU and doublecortin-immunoreactive (BrdU+/DCX+) cells were seen within the striatum, suggesting migration of immature neurons from the subventricular zone. Surprisingly, no DCX+ cells were found within the neocortex. NG2 immunoreactivity in some new neocortical neurons suggested that they may instead be generated from the NG2+ precursors that reside within the cortex itself.},
	Author = {Dayer, Alexandre G. and Cleaver, Kathryn M. and Abouantoun, Thamara and Cameron, Heather A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {01 Adult neurogenesis general},
	Month = {1},
	Nlm_Id = {0375356},
	Number = {3},
	Organization = {Unit on Neuroplasticity, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892.},
	Pages = {415-27},
	Pii = {jcb.200407053},
	Pubmed = {15684031},
	Title = {New GABAergic interneurons in the adult neocortex and striatum are generated from different precursors},
	Uuid = {09F42FC2-CE44-11D9-B244-000D9346EC2A},
	Volume = {168},
	Year = {2005},
	url = {papers/Dayer_JCellBiol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200407053}}

@article{DeFazio:2000,
	Abstract = {Recent studies have demonstrated an important role for the N-methyl-D-aspartate receptor (NMDAR) in epilepsy. NMDARs have also been shown to play a critical role in hyperexcitability associated with several animal models of human epilepsy. Using whole-cell voltage clamp recordings in brain slices, we studied evoked paroxysmal discharges in the freeze-lesion model of neocortical microgyria. The voltage dependence of epileptiform discharges indicated that these paroxysmal events were produced by a complex pattern of excitatory and inhibitory inputs. We examined the effect of the NMDAR antagonist D-2-amino-5-phosphopentanoic acid (APV) and the NMDA receptor subunit type 2B (NR2B)-selective antagonist ifenprodil on the threshold, peak amplitude, and area of evoked epileptiform discharges in brain slices from lesioned animals. Both compounds consistently raised the threshold for evoking the discharge but had modest effects on the discharge peak and amplitude. For comparison with nonlesioned cortex, we examined the effects of ifenprodil on the epileptiform discharge evoked in the presence of 2 microM bicuculline (partial disinhibition). In slices from nonlesioned cortex, 10 microM ifenprodil had little effect on the threshold whereas 71\%of the recordings in bicuculline-treated lesioned cortex showed a >25\%increase in threshold. These results suggest that NR2B-containing receptors are functionally enhanced in freeze-lesioned cortex and may contribute to the abnormal hyperexcitability observed in this model of neocortical microgyria.},
	Author = {DeFazio, R. A. and Hablitz, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {Excitatory Amino Acid Antagonists;Pregnancy;Piperidines;Animals;In Vitro;Evoked Potentials;Rats;Humans;Brain;21 Epilepsy;Female;Epilepsy;Rats, Sprague-Dawley;2-Amino-5-phosphonovalerate;Pyramidal Cells;Patch-Clamp Techniques;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;21 Neurophysiology;24 Pubmed search results 2008;Receptors, N-Methyl-D-Aspartate;Research Support, Non-U.S. Gov't},
	Medline = {20102988},
	Month = {1},
	Nlm_Id = {0375404},
	Number = {1},
	Organization = {Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.},
	Pages = {315-21},
	Pubmed = {10634874},
	Title = {Alterations in NMDA receptors in a rat model of cortical dysplasia},
	Uuid = {33B5F443-E433-4FA8-9DFF-36CADF518E15},
	Volume = {83},
	Year = {2000}}

@article{DeKosky:2003,
	Abstract = {Early detection of neurodegenerative disorders would provide clues to the underlying pathobiology of these diseases and would enable more effective diagnosis and treatment of patients. Recent advances in molecular neuroscience have begun to provide the tools to detect diseases like Alzheimer's disease, Parkinson's disease, and others early in their course and potentially even before the development of clinical manifestations of disease. These genetic, imaging, clinical, and biochemical tools are being validated in a number of studies. Early detection of these slowly progressive diseases offers the promise of presymptomatic diagnosis and, ultimately, of disease-modifying medications for use early in disease and during the presymptomatic period.},
	Author = {DeKosky, Steven T. and Marek, Kenneth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:45 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Human;Dopamine;Aging;Memory;review, tutorial;Brain;Diagnostic Imaging;review;Mutation;21 Neurodegenerative;Parkinson Disease;Time Factors;Genetic Predisposition to Disease;Support, Non-U.S. Gov't;Alzheimer Disease;21 Neurophysiology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Huntington Disease;Neurodegenerative Diseases;Biological Markers;Cognition Disorders;Genetic Markers},
	Medline = {22954847},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5646},
	Organization = {Department of Neurology and Alzheimer Disease Research Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. DeKoskyST\@upmc.edu},
	Pages = {830-4},
	Pii = {302/5646/830},
	Pubmed = {14593169},
	Title = {Looking backward to move forward: early detection of neurodegenerative disorders},
	Uuid = {E4C1673C-8A27-429C-841D-B89E2B0FF1B4},
	Volume = {302},
	Year = {2003},
	url = {papers/DeKosky_Science2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1090349}}

@article{De-Marchis:2001,
	Abstract = {Continual neurogenesis in the subventricular zone (SVZ) of postnatal and adult mammalian forebrain has been well documented, but the mechanisms underlying cell migration and differentiation in this region are poorly understood. We have developed novel in vivo and in vitro methods to investigate these processes. Using stereotaxic injections of a variety of tracers/tracker [Cholera Toxin beta subunit (CTb-), Fluorogold (FG), and Cell Tracker Green (CTG)], we could efficiently label SVZ cells. Over several days, labeled cells migrate along the rostral migratory stream (RMS) to their final differentiation site in the olfactory bulb (OB). The compatibility of these tracers/trackers with immunohistochemistry allows for cell labeling with multiple dyes (e.g., CTb and CTG) and/or specific cell antigens. To investigate the dynamics of migration we labeled SVZ progenitor cells with small injections of CTG and monitored the movements of individual cells in fresh parasagittal brain slices over several hours using time-lapse confocal microscopy. Our observations suggest that tangential cell migration along the RMS occurs more rapidly than radial cell migration into the OB granule cell layer. To investigate migration over longer time periods, we developed an in vitro organotypic slice in which labeled SVZ progenitors migrate along the RMS and differentiate within the OB. The phenotypic characteristics of these cells in vitro were equivalent to those observed in vivo. Taken together, these methods provide useful tools investigating cell migration and differentiation in a preparation that maintains the anatomical organization of the RMS. 0022-3034 Journal Article},
	Author = {De Marchis, S. and Fasolo, A. and Shipley, M. and Puche, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {J Neurobiol},
	Keywords = {Fluorescent Dyes;Neurons/*physiology;B both;Animals;Stereotaxic Techniques;Dextrans;Microscopy, Confocal;02 Adult neurogenesis migration;*Stilbamidines;Stem Cells/*physiology;Olfactory Bulb/cytology/*physiology;Animals, Newborn;Prosencephalon/cytology/*physiology;Support, Non-U.S. Gov't;Biotin/*analogs &derivatives;Support, U.S. Gov't, P.H.S.;Cell Movement/physiology;Mice;Cell Differentiation/physiology;Immunohistochemistry;Organ Culture},
	Number = {4},
	Organization = {Department of Human and Animal Biology, University of Torino, 10123 Torino, Italy.},
	Pages = {326-38},
	Title = {Unique neuronal tracers show migration and differentiation of SVZ progenitors in organotypic slices},
	Uuid = {3324AFE4-DD35-4E07-A1BA-67889EB89C7B},
	Volume = {49},
	Year = {2001},
	url = {papers/DeMarchis_JNeurobiol2001}}

@article{De-Palma:2003,
	Abstract = {Angiogenic tumor vessels are promising targets for the activity and the selective delivery of cancer therapeutics. The bone marrow contributes different cell types to the tumor stroma, including hematopoietic cells and, as recently suggested, vascular endothelial cells (ECs). Thus, transplantation of genetically modified bone marrow progenitors may represent a vehicle for the transport of gene therapy to tumors. We transduced bone marrow progenitors with lentiviral vectors expressing genes from transcription-regulatory elements of Tie2/Tek gene. When tumors were grown in the transplanted mice, the new vector marked a distinct hematopoietic population that 'homed' to the tumor and closely interacted with vascular ECs at the tumor periphery. These Tie2-expressing mononuclear (TEM) cells had a distinguishable phenotype and were present selectively at angiogenic sites. Unexpectedly, we did not find bone marrow-derived ECs in tumor vessels when we transplanted bone marrow progenitors constitutively expressing a marker gene from the Tie2 or ubiquitously active promoters. By delivering a 'suicide' gene, we selectively eliminated the TEM cells and achieved substantial inhibition of angiogenesis and slower tumor growth without systemic toxicity. Thus, TEM cells may account for the proangiogenic activity of bone marrow-derived cells in tumors, may represent a new target for drug development and may provide the means for selective gene delivery and targeted inhibition of tumor angiogenesis.},
	Author = {De Palma, Michele and Venneri, Mary Anna and Roca, Cristina and Naldini, Luigi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1078-8956},
	Journal = {Nat Med},
	Keywords = {Transduction, Genetic;Gene Targeting;Animals;Humans;Bone Marrow Transplantation;Phenotype;Receptor, TIE-2;Female;11 Glia;Male;Mice, Nude;Hematopoietic Stem Cell Transplantation;Neovascularization, Pathologic;Mice, Inbred Strains;Genetic Vectors;Gene Therapy;Tumor Cells, Cultured;Receptor Protein-Tyrosine Kinases;Mice;Genes, Reporter;Biological Markers;Neoplasms, Experimental;Hematopoietic Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {22662628},
	Month = {6},
	Nlm_Id = {9502015},
	Number = {6},
	Organization = {Laboratory for Gene Transfer and Therapy, IRCC, Institute for Cancer Research and Treatment, University of Torino Medical School, Strada Provinciale 142, 10060 Candiolo, Torino, Italy.},
	Pages = {789-95},
	Pii = {nm871},
	Pubmed = {12740570},
	Title = {Targeting exogenous genes to tumor angiogenesis by transplantation of genetically modified hematopoietic stem cells},
	Uuid = {F530D3BE-FD2C-477F-8C5A-1025F3D97FD8},
	Volume = {9},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nm871}}

@article{De-Simone:2004,
	Abstract = {In the central nervous system (CNS), apoptosis plays an important role during development and is a primary pathogenic mechanism in several adult neurodegenerative diseases. A main feature of apoptotic cell death is the efficient and fast removal of dying cells by macrophages and nonprofessional phagocytes, without eliciting inflammation in the surrounding tissue. Apoptotic cells undergo several membrane changes, including the externalization of so-called "eat me" signals whose cognate receptors are present on professional phagocytes. Among these signals, the aminophospholipid phosphatidylserine (PS) appears to have a crucial and unique role in preventing the classical pro-inflammatory activation of macrophages, thus ensuring the silent and safe removal of apoptotic cells. Although extensively studied in the peripheral organs, the process of recognition and removal of apoptotic cells in the brain has only recently begun to be unraveled. Here, we summarize the evidence suggesting that upon interaction with PS-expressing apoptotic neurons, microglia may no longer promote the inflammatory cascade, but rather facilitate the elimination of damaged neurons through antiinflammatory and neuroprotective functions. We propose that the anti-inflammatory microglial phenotype induced through the activation of the specific PS receptor (PtdSerR), expressed by resting and activated microglial cells, could be relevant to the final outcome of neurodegenerative diseases, in which apoptosis seems to play a crucial role.},
	Author = {De Simone, Roberta and Ajmone-Cat, Maria Antonietta and Minghetti, Luisa},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0893-7648},
	Journal = {Mol Neurobiol},
	Keywords = {Alpha;Human;Inflammation;Apoptosis;Not relevant;11 Glia;Microglia;review, tutorial;Support, Non-U.S. Gov't;Animals;review;Neurons},
	Month = {4},
	Nlm_Id = {8900963},
	Number = {2},
	Organization = {Department of Cell Biology and Neurosciences, Istituto Superiore di Sanit\`{a}, Viale Regina Elena 299, 00161 Italy.},
	Pages = {197-212},
	Pii = {MN:29:2:197},
	Pubmed = {15126686},
	Title = {Atypical antiinflammatory activation of microglia induced by apoptotic neurons: possible role of phosphatidylserine-phosphatidylserine receptor interaction},
	Uuid = {4BEEB42C-8AF9-4DF5-AC9E-6A98906FD8A7},
	Volume = {29},
	Year = {2004}}

@article{Deacon:1994,
	Abstract = {In order to determine whether the lateral ganglionic eminence (LGE) of the fetal telencephalon is the primary source of striatal precursors in striatal transplants and tissue cultures, cells derived exclusively from the LGE of fetal rat brains were transplanted into the quinolinic-acid-lesioned striatum of adult rats. After 2-3 months they produced grafts that were almost entirely AChE-positive as well as DARPP-32-, TH-, and calbindin-immunoreactive. The grafts were integrated into the host striatum so that host corticofugal fiber tracts interdigitated with graft tissues similar to the way they penetrate the gray matter of the normal striatum. Fast Blue dye injected into the ipsilateral globus pallidus of LGE grafted produced retrogradely labeled neurons within the grafts, but Fluorogold dye injected into the ipsilateral substantia nigra did not. In a separate experiment using DARPP-32-immunohistochemstry as a striatal marker, fetal (E16) and neonatal (P2) rat brains showed DARPP-32 immunoreactivity in the LGE but not in the adjacent medial ganglionic eminence (MGE). In summary, both fetal LGE cells and LGE grafts express specific striatal markers, and LGE grafts integrate into the host striatum and innervate the major striatal efferent target within the host brain. These data suggest that the LGE is the origin of cells committed to striatal phenotypes in the developing brain. 0006-8993 Journal Article},
	Author = {Deacon, T. W. and Pakzaban, P. and Isacson, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Brain Res},
	Keywords = {Animals;Acetylcholinesterase/analysis;Efferent Pathways;Rats;Fluorescent Antibody Technique;*Fetal Tissue Transplantation;Tyrosine 3-Monooxygenase/analysis;Rats, Sprague-Dawley;Nerve Tissue Proteins/analysis;Male;*Phosphoproteins;N;Amidines;Support, Non-U.S. Gov't;19 Neocortical evolution;Calcium-Binding Protein, Vitamin D-Dependent/analysis;Telencephalon/*cytology/embryology/transplantation;Dopamine/analysis;Neostriatum/chemistry/*cytology/transplantation;Support, U.S. Gov't, P.H.S.;Immunohistochemistry},
	Number = {1-2},
	Organization = {Neuroregeneration Laboratory, McLean Hospital, Belmont, MA 02178, USA.},
	Pages = {211-9},
	Pubmed = {7704606},
	Title = {The lateral ganglionic eminence is the origin of cells committed to striatal phenotypes: neural transplantation and developmental evidence},
	Uuid = {7EE40E68-A56C-4FC8-A88A-7471EF4E819B},
	Volume = {668},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7704606}}

@article{Debassio:1985,
	Abstract = {Although there is extensive literature documenting the effects of undernutrition on brain development, most studies have been concerned with cell differentiation with little attention given to neuronal migration. In a rat model we have investigated the effect of chronic protein deprivation on cell migration from the anterior lateral ventricle to the olfactory bulb. By using standard autoradiographic techniques and comparing the position of heavily labeled cells within the migratory stream, we estimated the migration rate to be 100 microns/h in 25\%-casein-diet rats and between 33 and 70 microns/h in 8\%-casein-diet rats. We therefore conclude that migration is slowed in chronically protein-deprived rats and this slowed migration may be related to subsequent abnormalities of cell differentiation seen in protein-deprived rats. eng Journal Article},
	Author = {Debassio, W. A. and Kemper, T. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Journal = {Brain Res},
	Keywords = {Protein Deficiency/*embryology;Female;Rats;Animal;Caseins/administration &dosage;Pregnancy;Mitosis;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Cell Movement;Rats, Inbred Strains;C abstr;Olfactory Bulb/*embryology},
	Number = {2},
	Pages = {191-6.},
	Title = {The effects of protein deprivation on neuronal migration in rats},
	Uuid = {9352DEA3-22BA-4E05-BCEA-CEED4C301A58},
	Volume = {352},
	Year = {1985}}

@article{Decherchi:2000,
	Abstract = {The present work investigates the extent to which mature central neurons acutely or chronically axotomized by a spinal lesion still maintained the potential to regenerate an axon following post-traumatic nerve grafting within supra-lesional spinal structures. In adult rats, a C3 cervical hemisection (injury) was made and an autologous segment of the peroneal nerve was implanted 2mm rostrally into the ventrolateral part of the ipsilateral C2 spinal cord. Nerve graft implantations were carried out acutely at the time of injury (group I, acute conditions) or chronically, three weeks post-injury (group II, chronic conditions). Central neurons axotomized by the spinal lesion were labeled by True Blue injected at the lesion site at the time of trauma. Central neurons regenerating axons within the nerve grafts were labeled with either horseradish peroxidase (only in group I, n=4) or Nuclear Yellow (group I, n=3 and group II, n=6) applied two to four months post-grafting to the distal cut end of the nerve grafts. Neurons with dual staining (True Blue/Nuclear Yellow) represented central regenerating neurons which were previously axotomized by the spinal lesion and which had retained the capacity for axonal regeneration for a delayed period after injury. In group I (acute injury conditions), all types of labeled cells were found to be scattered with a clear bimodal distribution within the spinal cord and the brainstem. No labeled cells were found within the motor cortex. There was no statistically significant difference between horseradish peroxidase and all cells containing Nuclear Yellow (Nuclear Yellow and True Blue/Nuclear Yellow). In group II (chronic injury conditions), Nuclear Yellow- and True Blue/Nuclear Yellow-labeled cells had a similar dual distribution to that of group I, but were found to be significantly less represented (P=0.019). These differences are discussed in terms of capacity for cell survival and axonal regrowth after acute and chronic injury. The main conclusion is based on the evidence of dual staining of central neurons in both groups, which demonstrates that brainstem and spinal neurons involved in acute and chronic axotomy after spinal C3 lesion can survive the trauma and still maintain the capacity to regenerate lesioned axons within nerve grafts inserted rostrally (C2 spinal cord) to the primary site of injury. Although exhibited to a lesser extent in chronic than in acute conditions, this capacity was found to occur for as long as three weeks post-injury.These results indicate that supra-lesional post-traumatic nerve grafts may constitute an efficient delayed strategy for inducing axonal regrowth of chronically axotomized adult central neurons. We suggest that surgical intervention, which is not always possible immediately after a spinal cord injury, may be satisfactorily carried out after an appropriate delay.},
	Author = {Decherchi, P. and Gauthier, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Fluorescent Dyes;Animals;Cervical Vertebrae;Rats;Neural Pathways;Postoperative Complications;Recovery of Function;Peroneal Nerve;Female;Axons;Rats, Sprague-Dawley;Tissue Transplantation;Spinal Cord;Nerve Regeneration;Spinal Cord Injuries;Survival Rate;Axotomy;Horseradish Peroxidase;24 Pubmed search results 2008;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {20521983},
	Nlm_Id = {7605074},
	Number = {1},
	Organization = {Laboratoire des D{\'e}terminants Physiologiques de l'Activit{\'e} Physique, Facult{\'e} des Sciences du Sport de Marseille-Luminy, Universit{\'e} de la M{\'e}diterran{\'e}e (Aix-Marseille II), Case courrier 910, 163, avenue de Luminy, 13288 Marseille Cedex 09, France.},
	Pages = {197-210},
	Pii = {S0306452200003432},
	Pubmed = {11068148},
	Title = {Regrowth of acute and chronic injured spinal pathways within supra-lesional post-traumatic nerve grafts},
	Uuid = {FA676BA0-BC33-42E6-835A-2C0A91409872},
	Volume = {101},
	Year = {2000}}

@article{Dedesma:2006,
	Abstract = {The identity and biology of stem cells and progenitors in the adult brain are of considerable interest, because these cells hold great promise for the development of novel therapies for damaged brain tissue in human diseases. This research field critically needs biological markers that specifically identify the resident precursors in the germinal zones of the adult central nervous system so that the discovery of regulatory influences for adult neurogenesis may be facilitated. In this study, by using a combination of in situ hybridization, bromodeoxyuridine incorporation, immunocolocalization, and ultrastructural studies, we show that in rodents Tctex-1, a cytoplasmic dynein light chain, is selectively enriched in almost all cycling progenitors and young neuronal progeny, but not in mature granular cells and astrocytes, in the subgranular zone of the adult dentate gyrus. Tctex-1 is also selectively abundant in cells closely resembling previously described immature progenitors and migrating neuroblasts at the subventricular zone of the lateral ventricle. Our results suggest that Tctex-1 serves as a novel marker for the identification of neural progenitors of the adult brain. J. Comp. Neurol. 496:773-786, 2006. (c) 2006 Wiley-Liss, Inc.},
	Author = {Dedesma, Carlos and Chuang, Jen-Zen Z. and Alfinito, Peter D. and Sung, Ching-Hwa H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {0406041},
	Number = {6},
	Organization = {Graduate Program in Neuroscience, Weill Medical College of Cornell University, New York, New York 10021.},
	Pages = {773-86},
	Pubmed = {16628620},
	Title = {Dynein light chain Tctex-1 identifies neural progenitors in adult brain},
	Uuid = {018A3A9E-A204-4074-B44F-DD4198EDFFDB},
	Volume = {496},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20958}}

@article{Deisseroth:2004,
	Abstract = {A wide variety of in vivo manipulations influence neurogenesis in the adult hippocampus. It is not known, however, if adult neural stem/progenitor cells (NPCs) can intrinsically sense excitatory neural activity and thereby implement a direct coupling between excitation and neurogenesis. Moreover, the theoretical significance of activity-dependent neurogenesis in hippocampal-type memory processing networks has not been explored. Here we demonstrate that excitatory stimuli act directly on adult hippocampal NPCs to favor neuron production. The excitation is sensed via Ca(v)1.2/1.3 (L-type) Ca(2+) channels and NMDA receptors on the proliferating precursors. Excitation through this pathway acts to inhibit expression of the glial fate genes Hes1 and Id2 and increase expression of NeuroD, a positive regulator of neuronal differentiation. These activity-sensing properties of the adult NPCs, when applied as an "excitation-neurogenesis coupling rule" within a Hebbian neural network, predict significant advantages for both the temporary storage and the clearance of memories.},
	Author = {Deisseroth, Karl and Singla, Sheela and Toda, Hiroki and Monje, Michelle and Palmer, Theo D. and Malenka, Robert C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Microtubule-Associated Proteins;Cell Differentiation;Animals;Transcription Factors;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Rats;Neuronal Plasticity;Cells, Cultured;Synaptic Transmission;Female;Homeodomain Proteins;Rats, Sprague-Dawley;Hippocampus;03 Adult neurogenesis progenitor source;Rats, Inbred F344;Animals, Newborn;Support, Non-U.S. Gov't;Nerve Net;Neurons;Support, U.S. Gov't, P.H.S.;Calcium Channels, L-Type;Receptors, N-Methyl-D-Aspartate;Nerve Tissue Proteins;Stem Cells;Excitatory Postsynaptic Potentials},
	Month = {5},
	Nlm_Id = {8809320},
	Notes = {there is a supplement for this in omega data},
	Number = {4},
	Organization = {Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.},
	Pages = {535-52},
	Pii = {S0896627304002661},
	Pubmed = {15157417},
	Title = {Excitation-neurogenesis coupling in adult neural stem/progenitor cells},
	Uuid = {84F3AFEA-DB36-4E3C-BFF0-88E9825110F8},
	Volume = {42},
	Year = {2004},
	url = {papers/Deisseroth_Neuron2004.pdf}}

@article{Del-Turco:2004,
	Abstract = {The dentate gyrus of rodents is characterized by a highly laminar organization: above a compact granule cell layer, commissural/associational (C/A) fibers terminate on proximal granule cell dendrites and entorhinal fibers terminate on distal granule cell dendrites in a nonoverlapping manner. To gain insights into mechanisms that underlie the formation of this laminar structure, we studied mice deficient for BETA2/NeuroD, a basic helix-loop-helix transcription factor essential for granule cell differentiation. Anterograde tracing was used to label C/A and entorhinal fibers and combined with confocal double immunofluorescence for calbindin, calretinin, parvalbumin, and reelin to visualize putative target cells. The dentate gyrus of mutant mice contained only few granule cells, which formed a cap-like structure adjacent to area CA3. Despite the severe hypoplasia of the dentate gyrus, the remaining BETA2/NeuroD-deficient granule cells expressed mature markers, extended dendrites into the molecular layer, and extended mossy fibers into area CA3. Entorhinal and C/A fibers terminated in a nonoverlapping manner in the dendritic field overlying the rudiment. Entorhinal fibers terminated in the outermost portion of the dentate gyrus where they surrounded reelin-positive Cajal-Retzius cells, and C/A fibers terminated above and within the dentate rudiment. The laminar termination of C/A fibers was closest to normal in zones of the rudiment in which granule cells were densely packed. These data indicate that granule cells are able to differentiate in the absence of BETA2/NeuroD and suggest that the signals underlying the laminar anatomy of the dentate gyrus are present in the absence of most target cells.},
	Author = {Del Turco, Domenico and Gebhardt, Carl and Burbach, Guido J. and Pleasure, Samuel J. and Lowenstein, Daniel H. and Deller, Thomas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {gamma-Aminobutyric Acid;Research Support, Non-U.S. Gov't;Animals;DNA-Binding Proteins;Trans-Activators;Mice, Mutant Strains;Neural Pathways;Phosphopyruvate Hydratase;Female;Pyramidal Cells;Calcium-Binding Protein, Vitamin D-Dependent;Research Support, U.S. Gov't, P.H.S.;Parvalbumins;Dentate Gyrus;Mice;Immunohistochemistry;Nerve Tissue Proteins;Phytohemagglutinins},
	Month = {9},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Clinical Neuroanatomy, J.W. Goethe University, D-60590 Frankfurt/Main, Germany.},
	Pages = {81-95},
	Pubmed = {15281081},
	Title = {Laminar organization of the mouse dentate gyrus: insights from BETA2/Neuro D mutant mice},
	Uuid = {AD8B17DF-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {477},
	Year = {2004},
	url = {papers/DelTurco_JCompNeurol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20239}}

@article{Deloulme:1996,
	Abstract = {We have examined the regulation of neuron-specific gamma-enolase gene (NSE) expression in oligodendrocytes at various steps of their differentiation/maturation. We have demonstrated for the first time that NSE is expressed in oligodendroglial cells in vitro and in vivo, and only at a certain stage of differentiation. A heterogeneity of the gamma subunit was observed in cultured oligodendrocytes and the same one was found in adult rat brain. The level of gamma mRNA increased when precursor cells differentiated into oligodendrocytes. By contrast, no significant change in alpha-enolase gene expression was observed. High NSE (gamma gamma and alpha gamma) enolase activity was detected in cultured oligodendrocytes. Treatment with basic fibroblast growth factor, which stimulates the proliferation of oligodendrocyte precursor cells and reversibly blocks their differentiation, resulted in lower alpha gamma- and gamma gamma-enolase activities in these cells, but it enhanced alpha alpha-enolase activity slightly. These data indicate that gamma-enolase gene expression is associated with the differentiation of the oligodendrocytes and that it is repressed in adult fully mature cells.},
	Author = {Deloulme, J. C. and Lucas, M. and Gaber, C. and Bouillon, P. and Keller, A. and Eclancher, F. and Sensenbrenner, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Isoenzymes;01 Adult neurogenesis general;Aging;Tissue Distribution;Research Support, Non-U.S. Gov't;Molecular Sequence Data;Cell Differentiation;Rats;24 Pubmed search results 2008;Phosphopyruvate Hydratase;Gene Expression;Amino Acid Sequence;Animals;Brain;Oligodendroglia;Cells, Cultured;Fibroblast Growth Factor 2},
	Medline = {96365675},
	Month = {3},
	Nlm_Id = {2985190R},
	Number = {3},
	Organization = {Laboratoire de Neurobiologie Ontog{\'e}nique, Centre de Neurochimie du CNRS, Strasbourg, France.},
	Pages = {936-45},
	Pubmed = {8769852},
	Title = {Expression of the neuron-specific enolase gene by rat oligodendroglial cells during their differentiation},
	Uuid = {200C7D62-081D-4B01-B703-FD2C7D8034B7},
	Volume = {66},
	Year = {1996}}

@article{Dememes:1975,
	Abstract = {The macrophagic and neuroglial reactions occurring in the corpus callosum following transection were studied by radioautography and electron microscopy in adult rats. The animals were killed at intervals ranging from two days to three months after operation. In the lesion itself and the immediately surrounding tissues an important proliferation of hematogenous macrophages was observed. Further away from the point of severance no significant numerical increase in the neuroglia could be noted. However the accumulation of glial filaments, lipid droplets and fragments of myelin sheath in the astrocytes seems to indicate that this type of cell plays a phagocytic role. As for the oligodendrocytes, there is no evidence of their participation in phagocytosis, whereas the microglia plays an important part. In the removal of the tissue debris the role and the origin of the macrophages and the microglia are discussed, as is the share of each type of cell in the phagocytic response depending on the extent of the lesion and the degree of axonal degeneration.},
	Author = {Dem\^{e}mes, D. and Marty, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0044-3107},
	Journal = {Z Mikrosk Anat Forsch},
	Keywords = {Neuroglia;Wallerian Degeneration;Nerve Degeneration;Rats;Microscopy, Electron;Autoradiography;English Abstract;Not relevant;Astrocytes;11 Glia;Macrophages;Animals;Oligodendroglia;Phagocytosis;Corpus Callosum},
	Medline = {77083555},
	Nlm_Id = {0413637},
	Number = {6},
	Pages = {1104-17},
	Pubmed = {1234813},
	Title = {[Macrophagic and neuroglial reactions during axonic degeneration following transection of corpus callosum: a radioautographic and ultrastructural study]},
	Uuid = {B819D836-9629-46E1-8CF3-697BB1C4FDA2},
	Volume = {89},
	Year = {1975}}

@article{Demyanenko:2004,
	Abstract = {We show that the neural cell recognition molecule Close Homolog of L1 (CHL1) is required for neuronal positioning and dendritic growth of pyramidal neurons in the posterior region of the developing mouse neocortex. CHL1 was expressed in pyramidal neurons in a high-caudal to low-rostral gradient within the developing cortex. Deep layer pyramidal neurons of CHL1-minus mice were shifted to lower laminar positions in the visual and somatosensory cortex and developed misoriented, often inverted apical dendrites. Impaired migration of CHL1-minus cortical neurons was suggested by strikingly slower rates of radial migration in cortical slices, failure to potentiate integrin-dependent haptotactic cell migration in vitro, and accumulation of migratory cells in the intermediate and ventricular/subventricular zones in vivo. The restriction of CHL1 expression and effects of its deletion in posterior neocortical areas suggests that CHL1 may regulate area-specific neuronal connectivity and, by extension, function in the visual and somatosensory cortex.},
	Author = {Demyanenko, Galina P. and Schachner, Melitta and Anton, Eva and Schmid, Ralf and Feng, Guoping and Sanes, Joshua and Maness, Patricia F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.},
	Pages = {423-37},
	Pii = {S0896627304006464},
	Pubmed = {15504324},
	Title = {Close homolog of L1 modulates area-specific neuronal positioning and dendrite orientation in the cerebral cortex},
	Uuid = {C1B3DFF6-882C-4F93-9D65-D89109BCB19A},
	Volume = {44},
	Year = {2004},
	url = {papers/Demyanenko_Neuron2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2004.10.016}}

@article{Deng:2003,
	Abstract = {Although the existence of the hepatic oval cell (HOC), the liver stem cell has been known for almost 70 years, little is known about the potential for this adult stem cell to trans-differentiate into cells of other tissues. While their origin remains enigmatic, HOCs share many similarities with hematopoietic stem cells. Recent studies have revealed that a small percentage of HOCs can arise from a bone marrow-derived stem cell source. Here we report that, like bone marrow stem cells, HOCs can survive transplantation to the neonatal mouse brain and show signs of trans-differentiation by adopting the morphology and antigenic phenotype of both macro- and microglia cells. Trans-differentiated microglia cells were functional, showing active phagocytosis when cotransplanted with latex microbeads in vivo. In addition to glial markers, a small number of transplanted HOCs were immunopositive for neuronal markers, but displayed ambiguous phenotype, making their characterization difficult.},
	Author = {Deng, Jie and Steindler, Dennis A. and Laywell, Eric D. and Petersen, Bryon E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cell Survival;Cell Differentiation;Animals;Stem Cell Transplantation;Cells, Cultured;Antigens, Ly;Brain;Antigens, Differentiation;Microglia;Mice, Transgenic;Liver;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Neurons;Immunomagnetic Separation;Dicarbethoxydihydrocollidine;Mice;Luminescent Proteins;Stem Cells;Membrane Proteins;Lateral Ventricles;Graft Survival},
	Medline = {22777802},
	Month = {8},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32610, USA.},
	Pages = {373-82},
	Pii = {S001448860300058X},
	Pubmed = {12895448},
	Title = {Neural trans-differentiation potential of hepatic oval cells in the neonatal mouse brain},
	Uuid = {BCB07045-79CF-43D5-B38A-1C64660013B6},
	Volume = {182},
	Year = {2003},
	url = {papers/Deng_ExpNeurol2003.pdf}}

@article{Dennis:2004,
	Author = {Dennis, Carina},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Odors;Olfactory Pathways;Smell;Olfactory Receptor Neurons;Human;Gene Expression Regulation;Neurosciences;Receptors, Odorant;Animals;13 Olfactory bulb anatomy;news},
	Month = {3},
	Nlm_Id = {0410462},
	Number = {6981},
	Pages = {362-4},
	Pii = {428362a},
	Pubmed = {15042058},
	Title = {Neuroscience: the sweet smell of success},
	Uuid = {BD1835BD-9C93-4A24-B2BE-EBC345780C96},
	Volume = {428},
	Year = {2004},
	url = {papers/Dennis_Nature2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/428362a}}

@article{Depaepe:2005,
	Abstract = {Mechanisms controlling brain size include the regulation of neural progenitor cell proliferation, differentiation, survival and migration. Here we show that ephrin-A/EphA receptor signalling plays a key role in controlling the size of the mouse cerebral cortex by regulating cortical progenitor cell apoptosis. In vivo gain of EphA receptor function, achieved through ectopic expression of ephrin-A5 in early cortical progenitors expressing EphA7, caused a transient wave of neural progenitor cell apoptosis, resulting in premature depletion of progenitors and a subsequent dramatic decrease in cortical size. In vitro treatment with soluble ephrin-A ligands similarly induced the rapid death of cultured dissociated cortical progenitors in a caspase-3-dependent manner, thereby confirming a direct effect of ephrin/Eph signalling on apoptotic cascades. Conversely, in vivo loss of EphA function, achieved through EphA7 gene disruption, caused a reduction in apoptosis occurring normally in forebrain neural progenitors, resulting in an increase in cortical size and, in extreme cases, exencephalic forebrain overgrowth. Together, these results identify ephrin/Eph signalling as a physiological trigger for apoptosis that can alter brain size and shape by regulating the number of neural progenitors.},
	Author = {Depaepe, Vanessa and Suarez-Gonzalez, Nathalie and Dufour, Audrey and Passante, Lara and Gorski, Jessica A. and Jones, Kevin R. and Ledent, Catherine and Vanderhaeghen, Pierre},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {10 Development;Signal Transduction;Animals;Caspase 3;Ephrins;Brain;Receptors, Eph Family;Ephrin-A5;Mutation;Apoptosis;Mice, Transgenic;Caspases;research support, non-u.s. gov't;10 circuit formation;research support, u.s. gov't, p.h.s.;Neurons;Organ Size;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Stem Cells},
	Month = {6},
	Nlm_Id = {0410462},
	Number = {7046},
	Organization = {Institut de Recherches Interdisciplinaires en Biologie Humaine et Mol{\'e}culaire (IRIBHM), University of Brussels, Campus Erasme, 808 Route de Lennik, B-1070 Brussels, Belgium.},
	Pages = {1244-50},
	Pii = {nature03651},
	Pubmed = {15902206},
	Title = {Ephrin signalling controls brain size by regulating apoptosis of neural progenitors},
	Uuid = {FEC22ED6-D1D8-4AF0-B632-65B1AE92207A},
	Volume = {435},
	Year = {2005},
	url = {papers/Depaepe_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03651}}

@article{Deuel:2006,
	Abstract = {Although mutations in the human doublecortin gene (DCX) cause profound defects in cortical neuronal migration, a genetic deletion of Dcx in mice produces a milder defect. A second locus, doublecortin-like kinase (Dclk), encodes a protein with similar "doublecortin domains" and microtubule stabilization properties that may compensate for Dcx. Here, we generate a mouse with a Dclk mutation that causes no obvious migrational abnormalities but show that mice mutant for both Dcx and Dclk demonstrate perinatal lethality, disorganized neocortical layering, and profound hippocampal cytoarchitectural disorganization. Surprisingly, Dcx(-/y);Dclk(-/-) mutants have widespread axonal defects, affecting the corpus callosum, anterior commissure, subcortical fiber tracts, and internal capsule. Dcx/Dclk-deficient dissociated neurons show abnormal axon outgrowth and dendritic structure, with defects in axonal transport of synaptic vesicle proteins. Dcx and Dclk may directly or indirectly regulate microtubule-based vesicle transport, a process critical to both neuronal migration and axon outgrowth.},
	Author = {Deuel, Thomas A. S. and Liu, Judy S. and Corbo, Joseph C. and Yoo, Seung-Yun Y. and Rorke-Adams, Lucy B. and Walsh, Christopher A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Microtubule-Associated Proteins;Animals;Mice, Mutant Strains;Congenital Abnormalities;Embryo, Mammalian;Neocortex;Synaptic Vesicles;Brain;Cell Movement;Protein-Serine-Threonine Kinases;RNA, Messenger;Axons;Embryo;Dendrites;Neuropeptides;Animals, Newborn;Mice, Knockout;Neurons;Abnormalities;Mice;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Nerve Tissue Proteins;Tissue Survival;Research Support, Non-U.S. Gov't},
	Month = {1},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {41-53},
	Pii = {S0896-6273(05)00962-1},
	Pubmed = {16387638},
	Title = {Genetic interactions between doublecortin and doublecortin-like kinase in neuronal migration and axon outgrowth},
	Uuid = {D094E506-D974-4AC6-9162-4FB60B50D377},
	Volume = {49},
	Year = {2006},
	url = {papers/Deuel_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.10.038}}

@article{Dexter:1977,
	Abstract = {0092-8674 Journal Article},
	Author = {Dexter, T. M. and Scott, D. and Teich, N. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Cell},
	Keywords = {Clone Cells;Temperature;Friend murine leukemia virus/*growth &development;Hematopoietic Stem Cells/*cytology;Erythropoietin/pharmacology;EE, DMSO, abstr;Dimethyl Sulfoxide/pharmacology;08 Aberrant cell cycle;Moloney murine leukemia virus/*growth &development;Cell Division;Cell Adhesion;Leukemia, Experimental/*etiology;Cells, Cultured;Animals;Mice;*Hematopoiesis},
	Number = {2},
	Pages = {355-64},
	Pubmed = {912746},
	Title = {Infection of bone marrow cells in vitro with FLV: effects on stem cell proliferation, differentiation and leukemogenic capacity},
	Uuid = {955E9C42-635D-4A42-9C31-DC345181A089},
	Volume = {12},
	Year = {1977},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=912746}}

@article{Dheen:1994,
	Abstract = {This study describes the ultrastructural changes in the cuneate nucleus of the streptozotocin-induced diabetic rats at 3, 6, 9, and 12 months post-induction. At 3 and 6 months, post-diabetes, a marked atrophy was observed in the myelinated axons. The atrophic axons showed delamination of myelin sheath, tightly arranged lamellar whorls, vesicular elements and degenerating debris within the electron-lucent axoplasm. At 9 and 12 months post-diabetes, a variety of dystrophic and degenerating axonal profiles and dendrites were seen in neuropil. The dystrophic axonal profiles containing tubulovesicular elements, slit-like clefts, vacuoles, swollen mitochondria, membranous and multigranular bodies appeared to be hypertrophied. The degenerating axon terminals contained swollen mitochondria and clustered spherical agranular vesicles in their electron-dense granular axoplasm. The degenerating dendrites were identified by the presence of swollen mitochondria, dilated ER in the electron-dense cytoplasm and they often formed the synaptic glomeruli with central axon terminals. Macrophages containing lipid bodies and electron-dense elements in their cytoplasm were in the process of phagocytosis. In all the time intervals studied, the somata appeared to be normal and the number of dystrophic and degenerating axonal profiles in the cuneate nucleus of diabetic rats was significantly increased in comparison with age-matched saline injected control rats.},
	Author = {Dheen, S. T. and Tay, S. S. and Wong, W. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0021-8359},
	Journal = {J Hirnforsch},
	Keywords = {Dendrites;Nerve Degeneration;Rats;Presynaptic Terminals;Myelin Sheath;Medulla Oblongata;Not relevant;Rats, Wistar;Mitochondrial Swelling;Microglia;11 Glia;Blood Glucose;Male;Animals;Support, Non-U.S. Gov't;Diabetes Mellitus, Experimental;Axons},
	Medline = {94342733},
	Nlm_Id = {0421521},
	Number = {2},
	Organization = {Department of Anatomy, Faculty of Medicine, National University of Singapore, Kent Ridge.},
	Pages = {253-62},
	Pubmed = {8064142},
	Title = {Ultrastructure of the cuneate nucleus in the streptozotocin-induced diabetic rat},
	Uuid = {5219A600-F8CC-4D37-BBCB-715E2F23C909},
	Volume = {35},
	Year = {1994}}

@article{Dhillon:2007,
	Abstract = {There is increasing cumulative evidence that activated mononuclear phagocytes (macrophages/microglia) releasing inflammatory mediators in the CNS are a better correlate of HIV-associated dementia (HAD) than the actual viral load in the brain. Earlier studies on simian HIV/rhesus macaque model of NeuroAIDS confirmed that pathological changes in brains of macaques with encephalitis were associated with up-regulation of platelet-derived growth factor (PDGF) and the chemokine, CXCL10. Because the complex interplay of inflammatory mediators released by macrophages often leads to the induction of neurotoxins in HAD, we hypothesized that PDGF could interact with IFN-gamma to modulate the expression of CXCL10 in these primary virus target cells. Although PDGF alone had no effect on the induction of CXCL10 in human macrophages, in conjunction with IFN-gamma, it significantly augmented the expression of CXCL10 RNA & protein through transcriptional and posttranscriptional mechanisms. Signaling molecules, such as JAK and STATs, PI3K, MAPK, and NF-kappaB were found to play a role in the synergistic induction of CXCL10. Furthermore, PDGF via its activation of p38 MAPK was able to increase the stability of IFN-gamma-induced CXCL10 mRNA. Understanding the mechanisms involved in the synergistic up-regulation of CXCL10 could aid in the development of therapeutic modalities for HAD.},
	Author = {Dhillon, Navneet Kaur and Peng, Fuwang and Ransohoff, Richard M. and Buch, Shilpa},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {21 Neurophysiology;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {2985117R},
	Number = {5},
	Organization = {Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.},
	Pages = {2722-30},
	Pii = {179/5/2722},
	Pubmed = {17709485},
	Title = {PDGF synergistically enhances IFN-gamma-induced expression of CXCL10 in blood-derived macrophages: implications for HIV dementia},
	Uuid = {A43DA349-9E9C-4793-9E1E-0AF6D31CB9BB},
	Volume = {179},
	Year = {2007}}

@article{Di-Cunto:1998,
	Abstract = {We have identified a novel serine/threonine kinase belonging to the myotonic dystrophy kinase family. The kinase can be produced in at least two different isoforms: a approximately 240-kDa protein (Citron Rho-interacting kinase, CRIK), in which the kinase domain is followed by the sequence of Citron, a previously identified Rho/Rac binding protein; a approximately 54-kDa protein (CRIK-short kinase (SK)), which consists mostly of the kinase domain. CRIK and CRIK-SK proteins are capable of phosphorylating exogenous substrates as well as of autophosphorylation, when tested by in vitro kinase assays after expression into COS7 cells. CRIK kinase activity is increased severalfold by coexpression of costitutively active Rho, while active Rac has more limited effects. Kinase activity of endogenous CRIK is indicated by in vitro kinase assays after immunoprecipitation with antibodies recognizing the Citron moiety of the protein. When expressed in keratinocytes, full-length CRIK, but not CRIK-SK, localizes into corpuscular cytoplasmic structures and elicits recruitment of actin into these structures. The previously reported Rho-associated kinases ROCK I and II are ubiquitously expressed. In contrast, CRIK exhibits a restricted pattern of expression, suggesting that this kinase may fulfill a more specialized function in specific cell types. 99009084 0021-9258 Journal Article},
	Author = {Di Cunto, F. and Calautti, E. and Hsiao, J. and Ong, L. and Topley, G. and Turco, E. and Dotto, G. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {J Biol Chem},
	Keywords = {Keratinocytes/enzymology;Protein Binding;Protein-Serine-Threonine Kinases/genetics/*metabolism;Base Sequence;Molecular Sequence Data;Sequence Homology, Amino Acid;CK;Animal;Amino Acid Sequence;Support, U.S. Gov't, P.H.S.;Proteins/*metabolism;Fluorescent Antibody Technique;Support, Non-U.S. Gov't;COS Cells;Cloning, Molecular;Mice;DNA, Complementary},
	Number = {45},
	Organization = {Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.},
	Pages = {29706-11},
	Title = {Citron rho-interacting kinase, a novel tissue-specific ser/thr kinase encompassing the Rho-Rac-binding protein Citron},
	Uuid = {AD8AF79E-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {273},
	Year = {1998},
	url = {papers/DiCunto_JBiolChem1998.pdf}}

@article{Di-Cunto:2000,
	Abstract = {Citron-kinase (Citron-K) has been proposed by in vitro studies as a crucial effector of Rho in regulation of cytokinesis. To further investigate in vivo its biologic functions, we have inactivated Citron-K gene in mice by homologous recombination. Citron-K-/- mice grow at slower rates, are severely ataxic, and die before adulthood as a consequence of fatal seizures. Their brains display defective neurogenesis, with depletion of specific neuronal populations. These abnormalities arise during development of the central nervous system due to altered cytokinesis and massive apoptosis. Our results indicate that Citron-K is essential for cytokinesis in vivo but only in specific neuronal precursors. Moreover, they suggest a novel molecular mechanism for a subset of human malformative syndromes of the CNS. 20537823 0896-6273 Journal Article},
	Author = {Di Cunto, F. and Imarisio, S. and Hirsch, E. and Broccoli, V. and Bulfone, A. and Migheli, A. and Atzori, C. and Turco, E. and Triolo, R. and Dotto, G. P. and Silengo, L. and Altruda, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {Neuron},
	Keywords = {Protein-Serine-Threonine Kinases/biosynthesis/deficiency/*genetics;Neurons/*metabolism/pathology;Stem Cells/metabolism/pathology;Neurodegenerative Diseases/complications/*genetics/pathology;Animal;CK;DNA/biosynthesis;Support, Non-U.S. Gov't;Ataxia/etiology;Mice, Knockout;Cell Division/*genetics;Support, U.S. Gov't, P.H.S.;Seizures/etiology;Polyploidy;Apoptosis/*genetics;Cyclin D1/metabolism;Mice;Brain/embryology/pathology},
	Number = {1},
	Organization = {Department of Genetics, Biology and Biochemistry, University of Torino, Italy. dicunto\@molinette.unito.it},
	Pages = {115-27},
	Title = {Defective neurogenesis in citron kinase knockout mice by altered cytokinesis and massive apoptosis},
	Uuid = {F54293FA-69B4-11DA-A4B6-000D9346EC2A},
	Volume = {28},
	Year = {2000},
	url = {papers/DiCunto_Neuron2000}}

@article{Di-Stefano:1996,
	Abstract = {The most frequent neurological complication of AIDS is a dementia-like syndrome. Power and collaborators (J Virol 1994; 68:4643-4649) have reported an association between the clinical signs of AIDS dementia and the amino acid composition of two positions (305 and 329) within the V3 region of HIV-1 strains amplified from brain tissue. Similarly, we analyzed position 305 in the V3 region of HIV-1 present in the brain or cerebrospinal fluid of 25 nondemented subjects at different clinical stages of HIV-1 infection. Our results are, however, at variance with the findings presented by Power and colleagues. Histidine, found to be common among sequences derived from demented patients, was also present in the majority (16 of 25) of nondemented patients analyzed by us. In the hands of Power and colleagues, sequences derived from nondemented patients contained proline at position 305. None of our patients had proline in this position. We also asked the question whether the presence of a specific amino acid at position 305 of the V3 loop is linked to an increased capacity of HIV-1 isolates to infect primary microglial cells, the major target cell for HIV-1 infection in the brain. Primary HIV-1 isolates derived from blood and cerebrospinal fluid of five patients, two asymptomatic and three AIDS patients, were used to infect microglia cell cultures. Infection was monitored by syncytium formation and by p24 antigen release in the culture supernatant. All but one of the paired blood/CSF isolates replicated in human brain cultures. Replication occurred independently from the amino acid present at position 305 of the V3 region of the viral envelope. Our results indicate that the majority of HIV-1 isolates, even derived during the asymptomatic stage, have the capacity to infect microglial cells. The relevance of viral envelope sequences in determining tropism for microglial cells and development of neurological symptoms remains an open question.},
	Author = {Di Stefano, M. and Wilt, S. and Gray, F. and Dubois-Dalcq, M. and Chiodi, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0889-2229},
	Journal = {AIDS Res Hum Retroviruses},
	Keywords = {Giant Cells;Research Support, Non-U.S. Gov't;Molecular Sequence Data;Adult;HIV Core Protein p24;Human;AIDS Dementia Complex;HIV-1;11 Glia;Microglia;Amino Acid Sequence;Acquired Immunodeficiency Syndrome;Cells, Cultured;Support, Non-U.S. Gov't;Humans;HIV Envelope Protein gp120},
	Medline = {96296958},
	Month = {4},
	Nlm_Id = {8709376},
	Number = {6},
	Organization = {Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden.},
	Pages = {471-6},
	Pubmed = {8679301},
	Title = {HIV type 1 V3 sequences and the development of dementia during AIDS},
	Uuid = {0771BF68-089F-47BF-80C0-1575449044BE},
	Volume = {12},
	Year = {1996}}

@article{Dietz:2005,
	Abstract = {The mitral-granule reciprocal synapse shapes the response of the olfactory bulb to odour stimuli by mediating lateral and reciprocal inhibition. We investigated the short-term plasticity of both the mitral-to-granule excitatory synapse and the granule-to-mitral inhibitory synapse in rat olfactory bulb slices, using whole-cell patch clamp recordings. The granule-to-mitral inhibitory synapse invariably exhibited paired-pulse depression at interstimulus intervals of less than a second, while the mitral-to-granule excitatory synapse showed heterogeneous responses, which on average yielded a moderate facilitation. Trains of stimuli led to a much greater depression at the granule-to-mitral synapse than at the mitral-to-granule synapse. Since mitral cells commonly respond to odours by burst firing with each inhalation cycle, we used bursts of stimuli to study recovery from depression. We found that recovery from depression induced by fast trains of stimuli was more rapid at the mitral-to-granule synapse than at the granule-to-mitral synapse. In addition, depression was enhanced by higher calcium concentrations, suggesting at least partial contribution of presynaptic mechanisms to short-term depression. The observed short-term plasticity could enable mitral cells to overcome autoinhibition and increase action potential propagation along lateral dendrites by burst firing.},
	Author = {Dietz, Shelby B. and Murthy, Venkatesh N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0022-3751},
	Journal = {J Physiol},
	Keywords = {gamma-Aminobutyric Acid;research support, n.i.h., extramural ;Animals;Synapses;Rats;Neuronal Plasticity;Synaptic Transmission;research support, u.s. gov't, non-p.h.s. ;Patch-Clamp Techniques;Calcium;Time Factors;Odors;Dendrites;research support, non-u.s. gov't ;Temperature;Action Potentials;Olfactory Bulb;Neurons;21 Neurophysiology;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {0266262},
	Number = {Pt 2},
	Organization = {Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA. vnmurthy\@fas.harvard.edu.},
	Pages = {475-88},
	Pii = {jphysiol.2005.095844},
	Pubmed = {16166156},
	Title = {Contrasting short-term plasticity at two sides of the mitral-granule reciprocal synapse in the mammalian olfactory bulb},
	Uuid = {563CAD52-0C7D-4B04-A2C9-B1A7012D3098},
	Volume = {569},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1113/jphysiol.2005.095844}}

@article{Dietz:2003,
	Abstract = {Human institutions--ways of organizing activities--affect the resilience of the environment. Locally evolved institutional arrangements governed by stable communities and buffered from outside forces have sustained resources successfully for centuries, although they often fail when rapid change occurs. Ideal conditions for governance are increasingly rare. Critical problems, such as transboundary pollution, tropical deforestation, and climate change, are at larger scales and involve nonlocal influences. Promising strategies for addressing these problems include dialogue among interested parties, officials, and scientists; complex, redundant, and layered institutions; a mix of institutional types; and designs that facilitate experimentation, learning, and change.},
	Author = {Dietz, Thomas and Ostrom, Elinor and Stern, Paul C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5652},
	Organization = {Environmental Science and Policy Program and Departments of Sociology and Crop and Soil Sciences, Michigan State University, East Lansing, MI 48824, USA.},
	Pages = {1907-12},
	Pii = {302/5652/1907},
	Pubmed = {14671286},
	Title = {The struggle to govern the commons},
	Uuid = {1E2A77E3-6E60-45C6-ABF0-E7DED5662DD9},
	Volume = {302},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1091015}}

@article{Dijkstra:2001,
	Abstract = {CD81 (TAPA), a member of the tetraspanin family of proteins, is upregulated by astrocytes and microglia after traumatic injury to the rat central nervous system (CNS). To further understand the role of CD81 in the microglial response to injury, we analysed the functional effects of a CD81 antibody, AMP1, on cultured rat microglia. We found that AMP1 suppressed microglial proliferation in a dose-dependent manner. Furthermore, AMP1 stimulated myelin phagocytosis, probably by opsonizing the myelin. The phagocytosis of latex beads, as well as the production of nitric oxide, were not significantly influenced by AMP1. These data indicate that CD81 is involved in an important subset of microglial effector functions after CNS injury.},
	Author = {Dijkstra, S. and Geisert, E. E. and Dijkstra, C. D. and B{\"a}r, P. R. and Joosten, E. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Membrane Proteins;Rats;Myelin Sheath;Spinal Cord Injuries;Antigens, CD;Rats, Wistar;11 Glia;Microglia;Cell Division;Nitric Oxide;Microspheres;Cells, Cultured;Animals;Phagocytosis;Antibodies;In Vitro},
	Medline = {21136064},
	Month = {3},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Experimental Neurology, UMC Utrecht, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands. s.dijkstra\@neuro.azu.nl},
	Pages = {151-9},
	Pii = {S0165572801002405},
	Pubmed = {11240026},
	Title = {CD81 and microglial activation in vitro: proliferation, phagocytosis and nitric oxide production},
	Uuid = {74EC884A-DA5D-4FB3-83F7-30FCD60E0D42},
	Volume = {114},
	Year = {2001}}

@article{Dill:1981,
	Author = {Dill, R. C. and Scott, M. C. and Porter, R. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Epilepsy;24 Pubmed search results 2008;Electroencephalography;21 Epilepsy;21 Neurophysiology;Cats;Action Potentials;Pressure;Penicillin G;Research Support, U.S. Gov't, Non-P.H.S.;Blood Pressure;Animals;Cerebral Cortex;Freezing;Stomach},
	Medline = {81261112},
	Month = {8},
	Nlm_Id = {0370712},
	Number = {2},
	Pages = {534-41},
	Pubmed = {7262253},
	Title = {Changes in the rate of cortical epileptiform activity by increased intragastric pressure in cats},
	Uuid = {39F46E2E-1757-44FC-BA55-E7FC694259A5},
	Volume = {73},
	Year = {1981}}

@article{Dingli:2007,
	Abstract = {Many tumors derive from the transformation of normal stem cells into cancer stem cells that retain their self-renewal capacity. This modern view of cancer has provided a natural explanation for the striking parallels which exist between these two different types of self-renewing cells. Here we develop a simple mathematical model to investigate the implications of this concept regarding the evolution of tumors in the hematopoietic system. Our results unequivocally demonstrate that stochastic effects related to the finite size of the active stem cell population have a profound influence on the dynamics of cancer evolution. For input parameters compatible with both the natural history of human cancer and mouse models, our results show how stochastic dynamics alone may lead to both remission in some cases and rapid expansion in others.},
	Author = {Dingli, David and Traulsen, Arne and Pacheco, Jorge M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1551-4005},
	Journal = {Cell Cycle},
	Keywords = {Models, Biological;Hematologic Neoplasms;Cell Differentiation;research support, non-u.s. gov't;Hematopoietic Stem Cells;Neoplastic Stem Cells;Cell Proliferation;Stochastic Processes;09 Evolutionary dynamics;Computer Simulation;22 Stem cells;22 Cancer;Animals;Disease Progression;Humans;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {101137841},
	Number = {4},
	Organization = {Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts 02138, USA. dingli\@fas.harvard.edu},
	Pages = {461-6},
	Pii = {3853},
	Pubmed = {17329969},
	Title = {Stochastic dynamics of hematopoietic tumor stem cells},
	Uuid = {9D99B9F2-FC34-4B50-93A4-EE13CB1B7EF6},
	Volume = {6},
	Year = {2007},
	url = {papers/Dingli_CellCycle2007.pdf}}

@article{Dingli:2007a,
	Abstract = {Most tissues in metazoans undergo continuous turnover due to cell death or epithelial shedding. Since cellular replication is associated with an inherent risk of mutagenesis, tissues are maintained by a small group of stem cells (SCs) that replicate slowly to maintain their own population and that give rise to differentiated cells. There is increasing evidence that many tumors are also maintained by a small population of cancer stem cells that may arise by mutations from normal SCs. SC replication can be either symmetric or asymmetric. The former can lead to expansion of the SC pool. We describe a simple model to evaluate the impact of (a)symmetric SC replication on the expansion of mutant SCs and to show that mutations that increase the probability of asymmetric replication can lead to rapid mutant SC expansion in the absence of a selective fitness advantage. Mutations in several genes can lead to this process and may be at the root of the carcinogenic process.},
	Author = {Dingli, David and Traulsen, Arne and Michor, Franziska},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {1553-7358},
	Journal = {PLoS Comput Biol},
	Keywords = {Models, Biological;Mutation;Cell Transformation, Neoplastic;Cell Proliferation;Stem Cells;Evolution;Neoplasms;Animals;Humans;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {101238922},
	Number = {3},
	Organization = {Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts, United States of America. dingli\@fas.harvard.edu},
	Pages = {e53},
	Pii = {06-PLCB-RA-0506R1},
	Pubmed = {17367205},
	Title = {(A)symmetric stem cell replication and cancer},
	Uuid = {D6FFEE19-53E1-4881-833A-EAAC782C2669},
	Volume = {3},
	Year = {2007},
	url = {papers/Dingli_PLoSComputBiol2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.0030053}}

@article{Dityatev:2003,
	Abstract = {1471-003x Journal Article Review Review, Academic},
	Author = {Dityatev, A. and Schachner, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {Human;11 Glia;Neuronal Plasticity/*physiology;Neurons/physiology;Support, Non-U.S. Gov't;Animals;G pdf;Extracellular Matrix Proteins/*physiology;Neuroglia/physiology},
	Number = {6},
	Organization = {Zentrum fur Molekulare Neurobiologie, University of Hamburg, Martinistr. 52, 20246 Hamburg, Germany. dityatev\@zmnh.uni-hamburg.de},
	Pages = {456-68},
	Pubmed = {12778118},
	Title = {Extracellular matrix molecules and synaptic plasticity},
	Uuid = {28BF6648-0F35-4557-8869-B34C151B8CC2},
	Volume = {4},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12778118}}

@article{Dobrenis:2005,
	Abstract = {Microglia, the tissue macrophages of the central nervous system (CNS), intimately interact with neurons physically and through soluble factors that can affect microglial activation state and neuronal survival and physiology. We report here a new mechanism of interaction between these cells, provided by the formation of gap junctions composed of connexin (Cx) 36. Among eight Cxs tested, expression of Cx36 mRNA and protein was found in microglial cultures prepared from human and mouse, and Cx45 mRNA was found in mouse microglial cultures. Electrophysiological measurements found coupling between one-third of human or mouse microglial pairs that averaged below 30 pico-Siemens and displayed electrical properties consistent with Cx36 gap junctions. Importantly, similar frequency of low-strength electrical coupling was also obtained between microglia and neurons in cocultures prepared from neocortical or hippocampal rodent tissue. Lucifer yellow dye coupling between neurons and microglia was observed in 4\%of pairs tested, consistent with the low strength and incidence of electrical coupling. Cx36 expression level and/or the degree of coupling between microglia did not significantly change in the presence of activating agents, including lipopolysaccharide, granulocyte-macrophage colony-stimulating factor, interferon-gamma, and tumor necrosis factor-alpha, except for some reduction of Cx36 protein when exposed to the latter two agents. Our findings that intercellular coupling occurs between neuronal and microglial populations through Cx36 gap junctions have potentially important implications for normal neural physiology and microglial responses in neuronopathology in the mammalian CNS. (c) 2005 Wiley-Liss, Inc.},
	Author = {Dobrenis, K. and Chang, H-Y Y. and Pina-Benabou, M. H. and Woodroffe, A. and Lee, S. C. and Rozental, R. and Spray, D. C. and Scemes, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Fluorescent Dyes;Animals;Humans;Encephalitis;Rats;Coculture Techniques;Cells, Cultured;Microglia;Patch-Clamp Techniques;Cell Communication;Rats, Sprague-Dawley;Telencephalon;Mice, Inbred C57BL;Connexins;11 Glia;RNA, Messenger;Animals, Newborn;Neurons;Inflammation Mediators;Isoquinolines;Membrane Potentials;Gliosis;Mice;Research Support, N.I.H., Extramural;Research Support, Non-U.S. Gov't},
	Month = {11},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York.},
	Pages = {306-15},
	Pubmed = {16211561},
	Title = {Human and mouse microglia express connexin36, and functional gap junctions are formed between rodent microglia and neurons},
	Uuid = {070598CF-CEF5-11DA-8A64-000D9346EC2A},
	Volume = {82},
	Year = {2005},
	url = {papers/Dobrenis_JNeurosciRes2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20650}}

@article{Dobreva:2006,
	Abstract = {Vertebrate skeletogenesis involves two processes, skeletal patterning and osteoblast differentiation. Here, we show that Satb2, encoding a nuclear matrix protein, is expressed in branchial arches and in cells of the osteoblast lineage. Satb2-/- mice exhibit both craniofacial abnormalities that resemble those observed in humans carrying a translocation in SATB2 and defects in osteoblast differentiation and function. Multiple osteoblast-specific genes were identified as targets positively regulated by SATB2. In addition, SATB2 was found to repress the expression of several Hox genes including Hoxa2, an inhibitor of bone formation and regulator of branchial arch patterning. Molecular analysis revealed that SATB2 directly interacts with and enhances the activity of both Runx2 and ATF4, transcription factors that regulate osteoblast differentiation. This synergy was genetically confirmed by bone formation defects in Satb2/Runx2 and Satb2/Atf4 double heterozygous mice. Thus, SATB2 acts as a molecular node in a transcriptional network regulating skeletal development and osteoblast differentiation.},
	Author = {Dobreva, Gergana and Chahrour, Maria and Dautzenberg, Marcel and Chirivella, Laura and Kanzler, Benoit and Fari\~{n}as, Isabel and Karsenty, Gerard and Grosschedl, Rudolf},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {10 Development;Cell Differentiation;Animals;Transcription Factors;Gene Expression Regulation, Developmental;Skull;Osteogenesis;Homeodomain Proteins;Mutation;Activating Transcription Factor 4;Facial Bones;Branchial Region;research support, non-u.s. gov't;Matrix Attachment Region Binding Proteins;Osteoblasts;Genes, Homeobox;Core Binding Factor Alpha 1 Subunit;Craniofacial Abnormalities;Mice, Knockout;Body Patterning;Mice;24 Pubmed search results 2008;Repressor Proteins},
	Month = {6},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Max-Planck Institute of Immunobiology, Department of Cellular and Molecular Immunology, 79108 Freiburg, Germany.},
	Pages = {971-86},
	Pii = {S0092-8674(06)00578-2},
	Pubmed = {16751105},
	Title = {SATB2 is a multifunctional determinant of craniofacial patterning and osteoblast differentiation},
	Uuid = {02DBF595-3EE5-4B90-AFF2-ABA5737F4186},
	Volume = {125},
	Year = {2006},
	url = {papers/Dobreva_Cell2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.05.012}}

@article{Dobyns:1993,
	Abstract = {OBJECTIVE--We review the clinical phenotype, pathological changes, and results of cytogenetic and molecular genetic studies in 90 probands with lissencephaly (smooth brain) with emphasis on patients with the classical form (type I). We also describe the recent discovery of the lissencephaly gene (LIS1), deletions of which have been implicated as the cause of this disorder in many patients. DATA SOURCES--We have performed clinical, cytogenetic, and molecular genetic studies of 25 probands with Miller-Dieker syndrome and 65 probands with isolated lissencephaly sequence (ILS). We have further subdivided patients with ILS into those with classical lissencephaly and those with lissencephaly variants. STUDY SELECTION--We consider primarily our own published and unpublished data, but include references to studies of other series of patients with lissencephaly. DATA SYNTHESIS--Visible cytogenetic deletions of 17p13.3 were detected in 14 of 25 Miller-Dieker syndrome probands, and either visible cytogenetic or submicroscopic deletions in 23 (92\%) of 25. Submicroscopic deletions were detected in eight of 45 patients with all types of ILS. If only ILS patients with the classical form are considered, we detected deletions in eight (38\%) of 21. CONCLUSIONS--Deletions of the lissencephaly critical region in chromosome 17p13.3, including LIS1, appear to be the most frequent cause of classical lissencephaly. Molecular cytogenetic studies, particularly fluorescence in situ hybridization, should be performed in all such patients. LIS1 shows homology to genes involved in signal transduction, which may be its function in development of the telencephalon. Other genetic causes of classical lissencephaly and genetic and nongenetic causes of other types of lissencephaly exist and are under study.},
	Author = {Dobyns, W. B. and Reiner, O. and Carrozzo, R. and Ledbetter, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0098-7484},
	Journal = {JAMA},
	Keywords = {Chromosomes, Human, Pair 17;Chromosome Deletion;Brain Diseases;10 Development;In Situ Hybridization, Fluorescence;24 Pubmed search results 2008;DNA;Gene Expression;Polymorphism, Restriction Fragment Length;Congenital Abnormalities;10 genetics malformation;research support, u.s. gov't, p.h.s.;Humans;Brain;Chromosome Mapping;review;Neurons},
	Month = {12},
	Nlm_Id = {7501160},
	Number = {23},
	Organization = {Department of Neurology, University of Minnesota Medical School, Minneapolis.},
	Pages = {2838-42},
	Pubmed = {7907669},
	Title = {Lissencephaly. A human brain malformation associated with deletion of the LIS1 gene located at chromosome 17p13},
	Uuid = {167AC304-50C4-4A35-A1E6-79CAD55BF12E},
	Volume = {270},
	Year = {1993}}

@article{Doetsch:1999,
	Abstract = {Neural stem cells reside in the subventricular zone (SVZ) of the adult mammalian brain. This germinal region, which continually generates new neurons destined for the olfactory bulb, is composed of four cell types: migrating neuroblasts, immature precursors, astrocytes, and ependymal cells. Here we show that SVZ astrocytes, and not ependymal cells, remain labeled with proliferation markers after long survivals in adult mice. After elimination of immature precursors and neuroblasts by an antimitotic treatment, SVZ astrocytes divide to generate immature precursors and neuroblasts. Furthermore, in untreated mice, SVZ astrocytes specifically infected with a retrovirus give rise to new neurons in the olfactory bulb. Finally, we show that SVZ astrocytes give rise to cells that grow into multipotent neurospheres in vitro. We conclude that SVZ astrocytes act as neural stem cells in both the normal and regenerating brain.},
	Author = {Doetsch, F. and Caille, I. and Lim, D. A. and Garcia-Verdugo, J. M. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Cell},
	Keywords = {Brain/cytology/physiology;Glial Fibrillary Acidic Protein/genetics/metabolism;02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;Cerebral Ventricles/*cytology/physiology;Regeneration;Chick Embryo;Animal;Olfactory Bulb;Support, U.S. Gov't, P.H.S.;Astrocytes/*cytology;Support, Non-U.S. Gov't;Male;B-10a;Mice;Stem Cells/*cytology},
	Number = {6},
	Organization = {The Rockefeller University, New York, New York 10021, USA.},
	Pages = {703-16.},
	Title = {Subventricular zone astrocytes are neural stem cells in the adult mammalian brain},
	Uuid = {7710ED33-68D7-11DA-A4B6-000D9346EC2A},
	Volume = {97},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10380923}}

@article{Doetsch:2005,
	Abstract = {Adult neurogenesis occurs in most species and is regulated by a wide variety of environmental and pharmacological challenges. The functional integration of neurons generated in the adult was first demonstrated in songbirds more than two decades ago. In the adult mammalian brain, neurons are continuously generated in two structures, the olfactory bulb and the hippocampus. Current evidence suggests that adult-born immature neurons have distinct electrophysiological properties from old neurons, and proposed roles in a variety of functions including olfaction, learning and mood regulation.},
	Author = {Doetsch, Fiona and Hen, Rene},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Departments of Pathology, Neurology and Center for Neurobiology and Behavior, Columbia University, 630W 168(th) Street, NYC, NY 10032, USA.},
	Pages = {121-8},
	Pii = {S0959-4388(05)00019-X},
	Pubmed = {15721754},
	Title = {Young and excitable: the function of new neurons in the adult mammalian brain},
	Uuid = {BC296855-C811-491D-823A-45CA9CB0A72C},
	Volume = {15},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.01.018}}

@article{Doetsch:1997,
	Abstract = {The adult mammalian subventricular zone (SVZ) contains stem cells that give rise to neurons and glia. In vivo, SVZ progeny migrate 3-8 mm to the olfactory bulb, where they form neurons. We show here that the SVZ of the lateral wall of the lateral ventricles in adult mice is composed of neuroblasts, glial cells, and a novel putative precursor cell. The topographical organization of these cells suggests how neurogenesis and migration are integrated in this region. Type A cells had the ultrastructure of migrating neuronal precursors. These cells were arranged as chains parallel to the walls of the ventricle and were polysialylated neural adhesion cell molecule- (PSA-NCAM), TuJ1- (beta- tubulin), and nestin-positive but GFAP- and vimentin-negative. Chains of Type A cells were ensheathed by two ultrastructurally distinct astrocytes (Type B1 and B2) that were GFAP-, vimentin-, and nestin- positive but PSA-NCAM- and TuJ1-negative. Type A and B2 (but not B1) cells incorporated [3H]thymidine. The most actively dividing cell in the SVZ corresponded to Type C cells, which had immature ultrastructural characteristics and were nestin-positive but negative to the other markers. Type C cells formed focal clusters closely associated with chains of Type A cells. Whereas Type C cells were present throughout the SVZ, they were not found in the rostral migratory stream that links the SVZ with the olfactory bulb. These results suggest that chains of migrating neuroblasts in the SVZ may be derived from Type C cells. Our results provide a topographical model for the adult SVZ and should serve as a basis for the in vivo identification of stem cells in the adult mammalian brain.},
	Author = {Doetsch, F. and Garcia-Verdugo, J. M. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Neurosci},
	Keywords = {02 Adult neurogenesis migration;Image Processing, Computer-Assisted;Female;Microscopy, Electron;Immunohistochemistry;B-7;Thymidine/metabolism;Autoradiography;Animal;Support, U.S. Gov't, P.H.S.;Male;Mice;Cerebral Ventricles/*cytology/metabolism/ultrastructure},
	Number = {13},
	Organization = {The Rockefeller University, New York, New York 10021, USA.},
	Pages = {5046-61.},
	Title = {Cellular composition and three-dimensional organization of the subventricular germinal zone in the adult mammalian brain},
	Uuid = {8EFAF554-4A23-4404-A7AE-C1B72245A2A8},
	Volume = {17},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9185542}}

@article{Doetsch:2002,
	Abstract = {The subventricular zone (SVZ) is the largest germinal layer in the adult mammalian brain and comprises stem cells, transit-amplifying progenitors, and committed neuroblasts. Although the SVZ contains the highest concentration of dividing cells in the adult brain, the intracellular mechanisms controlling their proliferation have not been elucidated. We show here that loss of the cyclin-dependent kinase inhibitor p27Kip1 has very specific effects on a population of CNS progenitors responsible for adult neurogenesis. Using bromodeoxyuridine and [(3)H]thymidine incorporation to label cells in S phase and cell- specific markers and electron microscopy to identify distinct cell types, we compared the SVZ structure and proliferation characteristics of wild-type and p27Kip1-null mice. Loss of p27Kip1 had no effect on the number of stem cells but selectively increased the number of the transit-amplifying progenitors concomitantly with a reduction in the number of neuroblasts. We conclude that cell-cycle regulation of SVZ adult progenitors is remarkably cell-type specific, with p27Kip1 being a key regulator of the cell division of the transit-amplifying progenitors.},
	Author = {Doetsch, F. and Verdugo, J. M. and Caille, I. and Alvarez-Buylla, A. and Chao, M. V. and Casaccia-Bonnefil, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Neurosci},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {6},
	Organization = {Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.},
	Pages = {2255-64.},
	Title = {Lack of the cell-cycle inhibitor p27Kip1 results in selective increase of transit-amplifying cells for adult neurogenesis},
	Uuid = {B5B7BC68-2BD1-460A-81AA-D2CFE5B72B16},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11896165%20http://www.jneurosci.org/cgi/content/full/22/6/2255%20http://www.jneurosci.org/cgi/content/abstract/22/6/2255}}

@article{Doetsch:2003,
	Abstract = {Glia are the most numerous cells in the brain, and their many diverse functions highlight their essential role in the nervous system. Recent studies have revealed an unexpected new role for glia in a wide variety of species, that of stem cells/progenitors in the adult and embryonic brain. Differentiation along the glial lineage may be a default state of development reflected in the progression of stem cells along the neuroepithelial-->radial glia-->astrocyte lineage. 1097-6256 Journal Article Review Review, Academic},
	Author = {Doetsch, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Nat Neurosci},
	Keywords = {01 Adult neurogenesis general;Astrocytes/cytology;Cell Differentiation/*physiology;Neurons/*cytology/physiology;Epithelial Cells;Neuroglia/classification/*cytology/physiology;Stem Cells/*metabolism;Central Nervous System/cytology/embryology/physiology;Lateral Ventricles;Animals;Support, Non-U.S. Gov't;Cell Lineage;A pdf},
	Number = {11},
	Organization = {Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA. fkd2101\@columbia.edu},
	Pages = {1127-34},
	Pubmed = {14583753},
	Title = {The glial identity of neural stem cells},
	Uuid = {BD1FCAC8-A894-4D21-88A9-AF2E36777177},
	Volume = {6},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14583753}}

@article{Doetsch:1996,
	Abstract = {Cells in the brains of adult mammals continue to proliferate in the subventricular zone (SVZ) throughout the lateral wall of the lateral ventricle. Here we show, using whole mount dissections of this wall from adult mice, that the SVZ is organized as an extensive network of chains of neuronal precursors. These chains are immunopositive to the polysialylated form of NCAM, a molecule present at sites of plasticity, and TuJ1, an early neuronal marker. The majority of the chains are oriented along the rostrocaudal axis and many join the rostral migratory stream that terminates in the olfactory bulb. Using focal microinjections of DII and transplantation of SVZ cells carrying a neuron-specific reporter gene, we demonstrate that cells originating at different rostrocaudal levels of the SVZ migrate rostrally and reach the olfactory bulb where they differentiate into neurons. Our results reveal an extensive network of pathways for the tangential chain migration of neuronal precursors throughout the lateral wall of the lateral ventricle in the adult mammalian brain.},
	Author = {Doetsch, F. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Brain/cytology/*physiology;02 Adult neurogenesis migration;Mammals;B-6a;*Nerve Net;Neurons/cytology/*physiology;Animal;Support, U.S. Gov't, P.H.S.;Cell Movement/*physiology;Mice},
	Number = {25},
	Organization = {Rockefeller University, New York, NY 10021, USA.},
	Pages = {14895-900.},
	Title = {Network of tangential pathways for neuronal migration in adult mammalian brain},
	Uuid = {2DC83B8E-2080-46BA-981F-8176CE0F119E},
	Volume = {93},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8962152}}

@article{Doetsch:1999a,
	Abstract = {Neuronal precursors reside in the subventricular zone (SVZ) of adult mammals. This region is composed of a network of chains of migrating neuroblasts ensheathed by astrocytes and juxtaposed by clusters of immature precursors (type C cells). Here we show that after antimitotic treatment with cytosine-beta-D-arabinofuranoside, neuroblasts and type C cells are eliminated but some astrocytes remain. Remarkably, the SVZ network rapidly regenerates. Soon after cytosine-beta-D- arabinofuranoside treatment astrocytes divide. Two days later, type C cells reappear, followed at 4.5 days by migrating neuroblasts. By 10 days the SVZ network is fully regenerated, and the orientation and organization of chains of migrating neuroblasts resemble that of normal mice. This regeneration reveals an unexpected plasticity in the adult central nervous system and should provide a model system to study the early stages of neurogenesis in the adult brain.},
	Author = {Doetsch, F. and Garcia-Verdugo, J. M. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Neural Cell Adhesion Molecules/analysis;02 Adult neurogenesis migration;Cytarabine/pharmacology;Cell Communication;Immunohistochemistry;Microscopy, Electron;B-10;Thymidine/metabolism;Brain/*cytology/drug effects/physiology;Regeneration;Glial Fibrillary Acidic Protein/analysis;Animal;Support, U.S. Gov't, P.H.S.;Mice;Male},
	Number = {20},
	Organization = {The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.},
	Pages = {11619-24.},
	Title = {Regeneration of a germinal layer in the adult mammalian brain},
	Uuid = {7710F2B3-68D7-11DA-A4B6-000D9346EC2A},
	Volume = {96},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10500226%20http://www.pnas.org/cgi/content/full/96/20/11619%20http://www.pnas.org/cgi/content/abstract/96/20/11619}}

@article{Dogusan:2004,
	Abstract = {It has been hypothesized that B cell precursors that undergo programmed cell death due to nonproductive Ig gene rearrangements are cleared from the bone marrow by macrophages. However, a role for macrophages in this process is supported only by micrographs showing their association with apoptotic-appearing, B lineage cells. Functional data demonstrating phagocytosis of apoptotic, bone marrow lymphocytes by macrophages have not been presented, nor have receptors potentially involved in that process been identified. The data in this report demonstrate that macrophages isolated from murine bone marrow efficiently phagocytose apoptotic murine B lineage cells using multiple receptors that include CD14, integrins, class A scavenger receptor, and CD31 (PECAM-1). In addition, the results further reveal a new role for the hemopoietic microenvironment in B cell development in view of data demonstrating that murine bone marrow stromal cells are also capable of clearing apoptotic cells via an integrin-dependent mechanism.},
	Author = {Dogusan, Zeynep and Montecino-Rodriguez, Encarnacion and Dorshkind, Kenneth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Mice, Inbred BALB C;Phagocytosis;Animals;Cells, Cultured;Coculture Techniques;Macrophages;Integrins;Lymphoid Tissue;Apoptosis;B-Lymphocytes;11 Glia;Antigens, CD14;Antigens, CD31;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Antigens, CD36;Mice;Stromal Cells},
	Month = {4},
	Nlm_Id = {2985117R},
	Number = {8},
	Organization = {Department of Pathology and Laboratory Medicine and the Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.},
	Pages = {4717-23},
	Pubmed = {15067047},
	Title = {Macrophages and stromal cells phagocytose apoptotic bone marrow-derived B lineage cells},
	Uuid = {FD895052-A713-44CC-AF32-FDFA20C6C7E6},
	Volume = {172},
	Year = {2004}}

@article{Dolnikov:2003,
	Abstract = {In this study, the cell cycle modulation of retrovirus vector production and transduction was analysed. Retrovirus vector expression was found to be similar in all phases of the cell cycle and, in contrast to some other virus promoters shown previously to be upregulated by G(2)/M arrest, Moloney murine leukaemia virus LTR-driven expression was upregulated neither by G(2)/M growth arrest nor by G(1)/S growth arrest. In contrast, cultures enriched for S phase cells produced more infectious virions, apparently by modulation of stages consequent to provirus expression. In terms of retrovirus transduction, limitations appear to be slow progression through the cell cycle and short half-life of the virus. Synchronization of cells prior to mitosis can increase transduction efficiency. Cell cycle modulation can be used to modify retrovirus vector production and transduction and can allow short transduction periods. 0022-1317 Journal Article},
	Author = {Dolnikov, A. and Wotherspoon, S. and Millington, M. and Symonds, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:20 -0400},
	Journal = {J Gen Virol},
	Keywords = {*Transduction, Genetic;*Genetic Vectors;*Cell Cycle;Human;EE, J pdf;Cell Line;08 Aberrant cell cycle;Retroviridae/*genetics/*growth &development;G2 Phase;Mitosis;Animals;Support, Non-U.S. Gov't;*Virus Cultivation;Virus Integration},
	Number = {Pt 11},
	Organization = {Department of Clinical Pharmacology and Toxicology, St Vincent's Hospital, Darlinghurst, NSW 2010, Australia.},
	Pages = {3131-41},
	Title = {Retrovirus vector production and transduction: modulation by the cell cycle},
	Uuid = {B16F0C6C-CA28-4C3C-BDFB-1A089AA6B02F},
	Volume = {84},
	Year = {2003},
	url = {papers/Dolnikov_JGenVirol2003.pdf}}

@article{Domaradzka-Pytel:2000,
	Abstract = {The present study investigates the development of microglial and astroglial cells in the postnatal rat striatum, using immunohistochemical methods with panel antibodies that recognize macrophage antigens of unknown function--ED 1, complement type 3 receptor--OX-42 (for microglia) and glial fibrillary acidic protein (for astrocytes). On the day of birth, ED1/OX-42- immunoreactive microglial cells present in the striatum represent ameboid microglia. Between P0 and P10 we could observe the migration of ameboid microglial cells from neuroepithelial ventricular zone through internal and external capsules into the striatum. During the second postnatal week (P10, P14) a considerable decline of ameboid ED1-immunoreactive microglial cells and an increase of the number of OX-42 positive ramified cells was observed. At P21 only OX-42 positive ramified cells were observed in the whole striatum. On the day of birth, only a few GFAP-positive cells resembling radial glia were observed in the striatum. During the first postnatal week, the number of GFAP-positive cells increased significantly; they showed typical morphology of the astrocytes present in the adult animals. After P21 the final striatal population of astroglia was formed. Using Smart Source Parsing},
	Author = {Domaradzka-Pytel, B. and Ludkiewicz, B. and Jagalska-Majewska, H. and Morys, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Folia Morphol},
	Keywords = {Aging;Rats;Immunohistochemistry;Rats, Wistar;Animal;11 Glia;Animals, Newborn;Astrocytes/*cytology;Support, Non-U.S. Gov't;G;Corpus Striatum/cytology/*growth &development;Microglia/*cytology},
	Number = {4},
	Organization = {Department of Anatomy and Neurobiology, Medical University of Gdansk.},
	Pages = {315-23},
	Title = {Immunohistochemical study of microglial and astroglial cells during postnatal development of rat striatum},
	Uuid = {012F55BF-F9B5-4783-BACE-8E937F1C6592},
	Volume = {58},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11000888}}

@article{Domaradzka-Pytel:1999,
	Abstract = {The distribution of microglia during the early stages of postnatal development in the rat was studied on rat brain from day of birth to postnatal day 90 (P90), using immunohistochemical methods with a panel of monoclonal antibodies that recognized the complement type 3 receptor (OX-42), macrophage antigen of unknown function (ED1), and the major histocompatibility complex (MHC) class I (OX-18) or class II (OX-6) antigens. Starting from the day of birth, ameboid microglia can be differentiated with positive immunoreactivity to OX-42, OX-18, and ED1. Labeled cells were localized mainly in the developing white matter. After P21, only positive reaction to OX-42 was present, and those cells had the typical morphology of the resting microglial cells that were located either in the white or grey matter. The changes in the appearance of different antigens are correlated with the morphological differentiation and transformation of ameboid microglial cells that are to become ramified microglia, present in the adult animals.},
	Author = {Domaradzka-Pytel, B. and Ludkiewicz, B. and Mory\'{s}, J. and Wisniewski, H. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0021-8359},
	Journal = {J Hirnforsch},
	Keywords = {Aging;Cell Differentiation;Receptors, Complement;Telencephalon;Immunohistochemistry;Antibodies, Monoclonal;Histocompatibility Antigens Class II;Not relevant;Rats;Biological Markers;11 Glia;Microglia;Animals, Newborn;Rats, Wistar;Histocompatibility Antigens Class I;Animals;Support, Non-U.S. Gov't},
	Medline = {20005253},
	Nlm_Id = {0421521},
	Number = {3},
	Organization = {Department of Anatomy and Neurobiology, Medical University of Gda\'{n}sk, Poland.},
	Pages = {283-91},
	Pubmed = {10536861},
	Title = {Expression and distribution of various antigens of developing microglial cells in the rat telencephalon},
	Uuid = {F731D3F7-138E-4F6C-B3AD-29B1E784E551},
	Volume = {39},
	Year = {1999},
	url = {papers/Domaradzka-Pytel_JHirnforsch1999.pdf}}

@article{Doms:1987,
	Abstract = {We have characterized the process by which the vesicular stomatitis virus (VSV) G protein acquires its final oligomeric structure using density-gradient centrifugation in mildly acidic sucrose gradients. The mature wild-type VSV G protein is a noncovalently associated trimer. Trimers are assembled from newly synthesized G monomers with a t1/2 of 6-8 min. To localize the site of trimerization and to correlate trimer formation with steps in transport between the endoplasmic reticulum (ER) and Golgi complex, we examined the kinetics of assembly of the temperature-sensitive mutant VSV strain, ts045. At the nonpermissive temperature (39 degrees C), ts045 G protein is not transported from the ER. The phenotypic defect that inhibited export from the ER at the nonpermissive temperature was found to be the accumulation of ts045 G protein in an aggregate. After being shifted to the permissive temperature (32 degrees C), the ts045 G protein aggregate rapidly dissociated (t1/2 less than 1 min) to monomeric G protein which subsequently trimerized with the same kinetics as the wild-type G protein. Only trimers were transported to the Golgi complex. Kinetic studies, as well as the finding that trimerization occurred under conditions which block ER to Golgi transport (at both 15 and 4 degrees C), showed that trimers were formed in the ER. Depletion of cellular ATP inhibited both the dissociation of the aggregated intermediate of ts045 G protein as well as the formation of stable trimers. The results indicate that oligomerization of G protein occurs in several steps, is sensitive to cellular ATP, and is required for transport from the ER.},
	Author = {Doms, R. W. and Keller, D. S. and Helenius, A. and Balch, W. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {Adenosine Triphosphate;Macromolecular Substances;Research Support, Non-U.S. Gov't;Membrane Glycoproteins;Membrane Proteins;Kinetics;Cell Line;Research Support, U.S. Gov't, P.H.S.;Viral Matrix Proteins;Vesicular stomatitis-Indiana virus;Protein Processing, Post-Translational;15 Retrovirus mechanism;Animals;24 Pubmed search results 2008;Viral Envelope Proteins},
	Medline = {88059229},
	Month = {11},
	Nlm_Id = {0375356},
	Number = {5},
	Organization = {Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06510.},
	Pages = {1957-69},
	Pubmed = {2824524},
	Title = {Role for adenosine triphosphate in regulating the assembly and transport of vesicular stomatitis virus G protein trimers},
	Uuid = {481808F9-EE2C-11DA-8605-000D9346EC2A},
	Volume = {105},
	Year = {1987}}

@article{Donaldson:1994,
	Abstract = {The distribution, cell tropism, and cytopathology in vivo of human immunodeficiency virus (HIV) was investigated in postmortem tissue samples from a series of HIV-infected individuals who died either of complications associated with AIDS or for unrelated reasons while they were asymptomatic. Proviral sequences were detected at a high copy number in lymphoid tissue of both presymptomatic patients and patients with AIDS, whereas significant infection of nonlymphoid tissue such as that from brains, spinal cords, and lungs were confined to those with AIDS. V3 loop sequences from both groups showed highly restricted sequence variability and a low overall positive charge of the encoded amino acid sequence compared with those of standard laboratory isolates of HIV type 1 (HIV-1). The low charge and the restriction in sequence variability were comparable to those observed with isolates showing a non-syncytium-inducing (NSI) and macrophage-tropic phenotype in vitro. All patients were either exclusively infected (six of seven cases) or predominantly infected (one case) with variants with a predicted NSI/macrophage-tropic phenotype, irrespective of the degree of disease progression. p24 antigen was detected by immunocytochemical staining of paraffin-fixed sections in the germinal centers within lymphoid tissue, although little or no antigen was found in areas of lymph node or spleen containing T lymphocytes from either presymptomatic patients or patients with AIDS. The predominant p24 antigen-expressing cells in the lungs and brains of the patients with AIDS were macrophages and microglia (in brains), frequently forming multinucleated giant cells (syncytia) even though the V3 loop sequences of these variants resembled those of NSI isolates in vitro. These studies indicate that lack of syncytium-forming ability in established T-cell lines does not necessarily predict syncytium-forming ability in primary target cells in vivo. Furthermore, variants of HIV with V3 sequences characteristic of NSI/macrophage-tropic isolates form the predominant population in a range of lymphoid and nonlymphoid tissues in vivo, even in patients with AIDS.},
	Author = {Donaldson, Y. K. and Bell, J. E. and Holmes, E. C. and Hughes, E. S. and Brown, H. K. and Simmonds, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {T-Lymphocytes;Human;HIV-1;Humans;Base Sequence;Sequence Homology, Amino Acid;Macrophages;Comparative Study;Variation (Genetics);Acquired Immunodeficiency Syndrome;Sequence Alignment;Phylogeny;11 Glia;Genes, pol;Proviruses;HIV Infections;DNA Primers;Support, Non-U.S. Gov't;Amino Acid Sequence;Molecular Sequence Data;HIV Envelope Protein gp120;Research Support, Non-U.S. Gov't},
	Medline = {94335116},
	Month = {9},
	Nlm_Id = {0113724},
	Number = {9},
	Organization = {Department of Medical Microbiology, University of Edinburgh, Medical School, United Kingdom.},
	Pages = {5991-6005},
	Pubmed = {7545945},
	Title = {In vivo distribution and cytopathology of variants of human immunodeficiency virus type 1 showing restricted sequence variability in the V3 loop},
	Uuid = {C0DBE78A-5A3F-4CD5-B329-1D42F72212A1},
	Volume = {68},
	Year = {1994}}

@article{Donovan:2001,
	Abstract = {Pluripotent stem cells can be expanded seemingly indefinitely in culture, maintain a normal karyotype and have the potential to generate any cell type in the body. As such they represent an incredible resource for the repair of diseased or damaged tissues in our bodies. These cells also promise to open a new window into the embryonic development of our species. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Donovan, P. J. and Gearhart, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Nature},
	Keywords = {F abstr;Embryo/cytology;10 Development;Models, Animal;Forecasting;Consumer Product Safety;Human;Cell Culture;Cell Line;*Stem Cells;*Cell Differentiation;Animals;Mice;Stem Cell Transplantation},
	Number = {6859},
	Organization = {Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. pdonovan\@lac.jci.tju.edu},
	Pages = {92-7},
	Pubmed = {11689953},
	Title = {The end of the beginning for pluripotent stem cells},
	Uuid = {8B0449FD-C616-4FE6-AB74-7B79951C09DF},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689953}}

@article{Doucette:1993,
	Abstract = {There are two morphologically distinct types of glial cells (i.e., ensheathing cells and astrocytes) in the nerve fiber layer (NFL) of the adult mammalian olfactory bulb. Ensheathing cells provide ensheathment for olfactory axons, whereas astrocytes occupy the interfascicular spaces of the olfactory NFL. During embryonic development, however, only one type of glial cell is found in this layer of the olfactory bulb, namely, the ensheathing cell. Even though ensheathing cells take up residence within the CNS, they are actually derived from the olfactory placode. Far less is known about the developmental origin of interfascicular astrocytes, which arise either from the glial progenitor cells that give rise to ensheathing cells or from astrocyte precursor cells that migrate into the NFL from deeper layers of the bulb primordium. In the present study, enriched populations of ensheathing cells were grown in vitro in media known to promote the growth and differentiation of astrocytes to determine whether ensheathing cell progenitors could differentiate into astrocytes. These media failed to induce the appearance of astrocytes in the ensheathing cell cultures. It was concluded that the astrocytes of the NFL most likely arise from progenitor cells that migrate into this layer from deeper parts of the developing bulb.},
	Author = {Doucette, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Pregnancy;Rats;Phenotype;Neuroglia/*physiology;Olfactory Bulb/*cytology/embryology;Female;Animal;Astrocytes/physiology;Rats, Wistar;G abstr;11 Glia;Stem Cells/*physiology;Support, Non-U.S. Gov't;Mice;Animals, Newborn/physiology;Immunohistochemistry;Cell Differentiation/physiology;Nerve Fibers/*physiology;Culture Media},
	Number = {3},
	Organization = {Department of Anatomy, College of Medicine, University of Saskatchewan, Saskatoon, Canada.},
	Pages = {274-87.},
	Title = {Glial progenitor cells of the nerve fiber layer of the olfactory bulb: effect of astrocyte growth media},
	Uuid = {4F6013D5-580C-4F9F-940F-DB6CF96525CE},
	Volume = {35},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8350389}}

@article{Douen:2004,
	Abstract = {During embryogenesis, transient expression of nestin in proliferating neuroepithelial stem cells signals the commitment of progenitor cells to differentiate. Although adult mammalian brain contains very little nestin, significant upregulation of nestin has been reported following cerebral injury, leading to speculation that nestin may be involved in brain repair. In this study, we assessed the temporal profile of nestin expression following ablation injury of the sensory barrel cortex and investigated the influence of contralateral whisker stimulation on nestin expression. Since the adult mammalian brain contains proliferating neuronal progenitor cells that can be labeled with bromodeoxyuridine (BrdU), we also determined the association of nestin reexpression with BrdU-labeled cells. Nestin reexpression was detected predominantly in the ipsilateral cortex 3 days post-ablation. There was no significant nestin upregulation in the subcortical region. Nestin reexpression was most marked surrounding the lesion, but also extended throughout the entire lateral cortex. Nestin in the ipsilateral cortex subsided by day 7, although perilesional nestin expression was still apparent 28 days post-injury. Western blot analysis of nestin expression 3 days post-ablation confirmed a significant two-fold increase in nestin expression (p<0.05). Double immunofluorescence labeling demonstrated that the majority of nestin expression occurred in astrocytes. We were unable to detect any colocalization with neuronal makers. However, BrdU-labeled cells, which were readily detected in the subventricular zone prior to injury, were readily detected in the perilesional area 3 days post-ablation, concomitant with nestin in this area. Confocal microscopy detected several BrdU-positive cells expressing nestin. Taken together, the data support a potential role for nestin reexpression in brain repair.},
	Author = {Douen, A. G. and Dong, Li and Vanance, S. and Munger, R. and Hogan, M. J. and Thompson, C. S. and Hakim, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Animals;Rats;Fluorescent Antibody Technique;Microscopy, Confocal;Indicators and Reagents;Vibrissae;Rats, Wistar;Physical Stimulation;Motor Cortex;Deoxyglucose;Antimetabolites;Nerve Regeneration;Male;Brain Chemistry;Blotting, Western;Intermediate Filament Proteins;Cerebral Cortex;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine;Nerve Tissue Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {5},
	Nlm_Id = {0045503},
	Number = {2},
	Organization = {Trillium Medical Centre, Mississauga, Ontario, Canada.},
	Pages = {139-46},
	Pii = {S0006899304002331},
	Pubmed = {15145750},
	Title = {Regulation of nestin expression after cortical ablation in adult rat brain},
	Uuid = {325FE1FE-40BE-4EEA-8094-DBED17895ECF},
	Volume = {1008},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainres.2003.08.070}}

@article{Doyle:2001,
	Abstract = {The intermediate filament protein nestin has been widely used as a marker for proliferating neural progenitor cells in the nervous system. The mammalian olfactory neuroepithelium is a region of the nervous system that robustly supports ongoing neurogenesis, yet where nestin has not been reported to mark proliferating progenitors. Using immunohistochemistry, we examined nestin expression in the mature olfactory neuroepithelium and found it to be tightly restricted to the basal compartment where the olfactory neuronal progenitor cell population resides. The pattern of nestin immunoreactivity was consistent with expression by the endfeet and inferior processes of sustentacular cells rather than basal cells. Using a bank of defined antibody markers, we confirmed nestin's pattern of distribution to be different from that of cytokeratin, vimentin, GBC-1, GAP43, and carnosine. It was highly similar to the pattern of SUS-4 immunoreactivity in the basal region of the neuroepithelium. Following surgical bulbectomy, nestin expression was up-regulated and became evident in the cell bodies of sustentacular cells situated more apically in the neuroepithelium. We have shown nestin to be present in the basal region of the adult olfactory neuroepithelium in the zone that supports ongoing neurogenesis in the adult, but its expression is restricted to the inferior parts of sustentacular cells rather than the neuronal progenitor cells. Nestin may play a potential role in the migration of recently proliferated olfactory neurons on the scaffolding of sustentacular cells in a manner analogous to its proposed role in radial glia during embryonic development of the central nervous system. Copyright 2001 Wiley-Liss, Inc. eng Journal Article},
	Author = {Doyle, K. L. and Khan, M. and Cunningham, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Journal = {J Comp Neurol},
	Keywords = {02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;BB abstr},
	Number = {2},
	Organization = {Neurobiology Program, The Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia.},
	Pages = {186-95.},
	Title = {Expression of the intermediate filament protein nestin by sustentacular cells in mature olfactory neuroepithelium},
	Uuid = {45CB9D4B-9A66-4D5F-9FD0-A31B088402E2},
	Volume = {437},
	Year = {2001}}

@article{Dorr:2002,
	Abstract = {Apoptosis mediated by members of the tumor necrosis factor (TNF)-nerve growth factor superfamily plays a crucial role in the interaction of the nervous and the immune system. On the one hand, it is involved in the defense mechanisms of the brain, the immune privilege. On the other hand, it is involved in the induction of glial-neuronal cell death in neuroinflammatory diseases. Here, we show that in contrast to the other known death ligands, TNF-related apoptosis-inducing ligand (TRAIL) is not constitutively expressed in the human brain, whereas both apoptosis-mediating and apoptosis-blocking TRAIL receptors are found on neurons, astrocytes, and oligodendrocytes. Thus, the brain differs from other immune-privileged organs, such as the placenta, with the TRAIL receptor-TRAIL system not being part of the immune privilege of the brain. Conversely, this death receptor-ligand system might well play an important role in T cell-mediated autoimmune diseases of the CNS such as multiple sclerosis.},
	Author = {D{\"o}rr, Jan and Bechmann, Ingo and Waiczies, Sonia and Aktas, Orhan and Walczak, Henning and Krammer, Peter H. and Nitsch, Robert and Zipp, Frauke},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Epilepsy;Brain Chemistry;Membrane Glycoproteins;Research Support, Non-U.S. Gov't;Reverse Transcriptase Polymerase Chain Reaction;Immunohistochemistry;Cell Line;Apoptosis;Placenta;Tumor Necrosis Factor-alpha;Antibody Specificity;11 Glia;Receptors, Tumor Necrosis Factor;RNA, Messenger;Humans;Blotting, Western;Brain},
	Medline = {21839207},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {4},
	Organization = {Department of Neurology, Division of Neuroimmunology, Charit{\'e} Neuroscience Research Center, 10098 Berlin, Germany.},
	Pages = {RC209},
	Pii = {20026087},
	Pubmed = {11844843},
	Title = {Lack of tumor necrosis factor-related apoptosis-inducing ligand but presence of its receptors in the human brain},
	Uuid = {4051B298-6087-40FD-8068-32DBC19A4B0E},
	Volume = {22},
	Year = {2002}}

@article{Drapeau:2003,
	Abstract = {Neurogenesis occurs within the adult dentate gyrus of the hippocampal formation and it has been proposed that the newly born neurons, recruited into the preexistent neuronal circuits, might be involved in hippocampal-dependent learning processes. Age-dependent spatial memory impairments have been related to an alteration in hippocampal plasticity. The aim of the current study was to examine whether cognitive functions in aged rats are quantitatively correlated with hippocampal neurogenesis. To this end, we took advantage of the existence of spontaneous individual differences observed in aged subjects in a hippocampal-dependent task, the water maze. We expected that the spatial memory capabilities of aged rats would be related to the levels of hippocampal neurogenesis. Old rats were trained in the water maze, and, 3 weeks after training, rats were injected with 5-bromo-2'-deoxyuridine (BrdUrd, 50 or 150 mg/kg) to label dividing cells. Cell proliferation was examined one day after the last BrdUrd injection, whereas cell survival and differentiation were determined 3 weeks later. It is shown that a quantitative relationship exists between learning and the number of newly generated neurons. Animals with preserved spatial memory, i.e., the aged-unimpaired rats, exhibited a higher level of cell proliferation and a higher number of new neurons in comparison with rats with spatial memory impairments, i.e., the aged-impaired rats. In conclusion, the extent of memory dysfunction in aged rats is quantitatively related to the hippocampal neurogenesis. These data reinforce the assumption that neurogenesis is involved in memory processes and aged-related cognitive alterations. 0027-8424 Journal Article},
	Author = {Drapeau, E. and Mayo, W. and Aurousseau, C. and Le Moal, M. and Piazza, P. V. and Abrous, D. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:52 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {01 Adult neurogenesis general;A pdf},
	Number = {24},
	Organization = {Institut National de la Santa et de la Recherche Medicale Unite 588, Domaine de Carreire, Rue Camille Saint Saens, University of Bordeaux II, 33077 Bordeaux Cedex, France.},
	Pages = {14385-90},
	Pubmed = {14614143},
	Title = {Spatial memory performances of aged rats in the water maze predict levels of hippocampal neurogenesis},
	Uuid = {2A4E97E2-B7CC-4533-9F1C-24204593AD11},
	Volume = {100},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14614143}}

@article{Drescher:2002,
	Abstract = {Eph receptor tyrosine kinases and ephrins have been identified in organisms ranging from sponges to flies and worms to chick, mice and humans, thus allowing their function to be approached also from an evolutionary perspective. The structural analysis of Eph/ephrin crystals is providing hints for the existence of Eph and ephrin folds in plants and suggests a mechanism for triggering bi-directional signalling.},
	Author = {Drescher, Uwe},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0959-437X},
	Journal = {Curr Opin Genet Dev},
	Keywords = {Retina;Receptors, Eph Family;10 Development;Protein Structure, Tertiary;Phylogeny;Evolution, Molecular;Multigene Family;10 circuit formation;Ephrins;Animals;Superior Colliculi;24 Pubmed search results 2008;review},
	Month = {8},
	Nlm_Id = {9111375},
	Number = {4},
	Organization = {MRC Centre for Developmental Neurobiology, King's College London, New Hunt's House, London, UK. uwe.drescher\@kcl.ac.uk},
	Pages = {397-402},
	Pii = {S0959437X02003167},
	Pubmed = {12100883},
	Title = {Eph family functions from an evolutionary perspective},
	Uuid = {F8A5D055-88E9-4301-A1E9-1AB8FE2A468F},
	Volume = {12},
	Year = {2002},
	url = {papers/Drescher_CurrOpinGenetDev2002.pdf}}

@article{Dromard:2006,
	Abstract = {Neural stem cells cultured with FGF2/EGF generate clonal expansions called neurospheres (NS) which are widely used for therapy in animal models. However, their cellular composition is still poorly defined. Here, we report that NS derived from several embryonic and adult central nervous system (CNS) regions are mainly composed of remarkable cells coexpressing radial glia markers (BLBP, RC2, GLAST), oligodendrogenic/neurogenic factors (Mash1, Olig2, Nkx2.2) and markers which in vivo are typical of the oligodendrocyte lineage (NG2, A2B5, PDGFRalpha). On NS differentiation, the latter remain mostly expressed in neurons, together with Olig2 and Mash1. Using cytometry, we show that in growing NS the small population of multipotential self-renewing NS-forming cells are A2B5(+) and NG2(+). Additionally, we demonstrate that these NS-forming cells in the embryonic spinal cord were initially NG2- and rapidly acquired NG2 in vitro. NG2 and Olig2 were found to be rapidly induced by cell culture conditions in spinal cord neural precursor cells. Olig2 expression was also induced in astrocytes and embryonic peripheral nervous system (PNS) cells in culture following EGF/FGF treatment. These data provide new evidence for profound phenotypic modifications in CNS and PNS neural precursor cells induced by culture conditions.},
	Author = {Dromard, and Bartolami, and Deleyrolle, and Takebayashi, and Ripoll, and Simonneau, and Prome, and Puech, and Tran Van Ba, and Duperray, and Valmier, and Privat, and Hugnot,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {9304532},
	Organization = {INSERM U583, Physiopathologie et Th{\'e}rapie des d{\'e}ficits sensoriels et moteurs, Institut des Neurosciences de Montpellier, H\^{o}pital St ELOI, Montpellier, France.},
	Pii = {2005-0556},
	Pubmed = {17053213},
	Title = {NG2 and olig2 expression provides evidence for phenotypic deregulation of cultured CNS and PNS neural precursor cells},
	Uuid = {7569E901-515A-49F1-A24C-3065E34418DE},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1634/stemcells.2005-0556}}

@article{Duan:2007,
	Abstract = {Adult neurogenesis occurs throughout life in discrete regions of the adult mammalian brain. Little is known about the mechanism governing the sequential developmental process that leads to integration of new neurons from adult neural stem cells into the existing circuitry. Here, we investigated roles of Disrupted-In-Schizophrenia 1 (DISC1), a schizophrenia susceptibility gene, in adult hippocampal neurogenesis. Unexpectedly, downregulation of DISC1 leads to accelerated neuronal integration, resulting in aberrant morphological development and mispositioning of new dentate granule cells in a cell-autonomous fashion. Functionally, newborn neurons with DISC1 knockdown exhibit enhanced excitability and accelerated dendritic development and synapse formation. Furthermore, DISC1 cooperates with its binding partner NDEL1 in regulating adult neurogenesis. Taken together, our study identifies DISC1 as a key regulator that orchestrates the tempo of functional neuronal integration in the adult brain and demonstrates essential roles of a susceptibility gene for major mental illness in neuronal development, including adult neurogenesis.},
	Author = {Duan, Xin and Chang, Jay H. and Ge, Shaoyu and Faulkner, Regina L. and Kim, Ju Young and Kitabatake, Yasuji and Liu, Xiao-bo B. and Yang, Chih-Hao H. and Jordan, J. Dedrick and Ma, Dengke K. and Liu, Cindy Y. and Ganesan, Sundar and Cheng, Hwai-Jong J. and Ming, Guo-li L. and Lu, Bai and Song, Hongjun},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Cell Differentiation;Genetic Vectors;24 Pubmed search results 2008;Genotype;Animals;Hippocampus;Synaptic Transmission;Cell Movement;Morphogenesis;Phenotype;research support, n.i.h., extramural;Synapses;Mice, Inbred C57BL;Dendrites;Carrier Proteins;Schizophrenia;Retroviridae;Action Potentials;Time Factors;RNA, Small Interfering;Cell Lineage;Cell Size;research support, non-u.s. gov't;Cell Proliferation;Recombinant Fusion Proteins;Mice;Neurons;Stem Cells;Nerve Tissue Proteins;RNA Interference;Dentate Gyrus},
	Month = {9},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA.},
	Pages = {1146-58},
	Pii = {S0092-8674(07)00897-5},
	Pubmed = {17825401},
	Title = {Disrupted-In-Schizophrenia 1 regulates integration of newly generated neurons in the adult brain},
	Uuid = {1F52DD1A-ADD4-4B49-942A-F3266E3D31CE},
	Volume = {130},
	Year = {2007},
	url = {papers/Duan_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2007.07.010}}

@article{Duan:2005,
	Abstract = {A major problem for neuroscience has been to find a means to achieve reliable regeneration of synaptic connections following injury to the adult CNS. This problem has been solved by the leech, where identified neurons reconnect precisely with their usual targets following axotomy, re-establishing in the adult the connections formed during embryonic development. It cannot be assumed that once axons regenerate specific synapses, function will be restored. Recent work on the leech has shown following regeneration of the synapse between S-interneurons, which are required for sensitization of reflexive shortening, a form of non-associative learning, the capacity for sensitization is delayed. The steps in repair of synaptic connections in the leech are reviewed, with the aim of understanding general mechanisms that promote successful repair. New results are presented regarding the signals that regulate microglial migration to lesions, a first step in the repair process. In particular, microglia up to 900 microm from the lesion respond within minutes by moving rapidly toward the injury, controlled in part by nitric oxide (NO), which is generated immediately at the lesion and acts via a soluble guanylate cyclase (sGC). The cGMP produced remains elevated for hours after injury. The relationship of microglial migration to axon outgrowth is discussed.},
	Author = {Duan, Yuanli and Panoff, Joseph and Burrell, Brian D. and Sahley, Christie L. and Muller, Kenneth J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0272-4340},
	Journal = {Cell Mol Neurobiol},
	Keywords = {Alpha;11 Glia},
	Medline = {102378122},
	Month = {3},
	Nlm_Id = {8200709},
	Number = {2},
	Organization = {Department of Physiology & Biophysics, University of Miami School of Medicine, Miami, Florida 33136, USA.},
	Pages = {441-50},
	Pubmed = {16047551},
	Title = {Repair and regeneration of functional synaptic connections: cellular and molecular interactions in the leech},
	Uuid = {184D781B-C650-4D31-942A-3B8BC33BBA9E},
	Volume = {25},
	Year = {2005},
	url = {papers/Duan_CellMolNeurobiol2005.pdf}}

@article{Dubeau:1995,
	Abstract = {Grey matter heterotopias, demonstrated by MRI, may present with a broad spectrum of clinical severity. We have studied 33 patients with periventricular nodular heterotopias (PNH); 19 (58\%) had unilateral and 14 (42\%) bilateral lesions. Thirteen of the 19 patients (68\%) with unilateral subependymal nodules of grey matter had, in addition, unilateral focal subcortical heterotopias (SNH), comprising 39\%of the entire group. Most had normal intellectual and motor function but some presented with mild mental retardation and neurological deficits. Recurrent seizures were described in 82\%, mainly partial attacks with temporo-parieto-occipital auras. Nodular heterotopias led to unilateral or bilateral independent temporal epileptic discharges in 47\%of epileptic patients with PNH alone and in 61\%of those who had SNH in addition. Extratemporal or multilobar, unilateral or bilateral interictal spiking was present in 10 other patients (36\%). Two first degree relatives of patients with seizures were affected but had no seizures, three were investigated for other apparently unrelated neurological symptoms: memory impairment, vertigo or transient ischaemic attacks in one person each. Contiguous ovoid nodules of grey matter, symmetrically lining both lateral ventricles, were described in nine patients. Seven of them were female, including four with familial incidence of PNH. Such lesions may explain the familial occurrence of epilepsy in some families. Seven patients underwent anterior temporal resection: two patients with unilateral subependymal and focal subcortical heterotopias were seizure free or significantly improved. Four patients, three with PNH alone and one with additional subcortical nodules, did not improve significantly after surgery. The remaining patient was followed for less than 6 months.},
	Author = {Dubeau, F. and Tampieri, D. and Lee, N. and Andermann, E. and Carpenter, S. and Leblanc, R. and Olivier, A. and Radtke, R. and Villemure, J. G. and Andermann, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0006-8950},
	Journal = {Brain},
	Keywords = {10 Development;Magnetic Resonance Imaging;Child, Preschool;Humans;Middle Aged;Female;Epilepsy;Child;Brain Diseases;Male;Cerebral Ventricles;10 genetics malformation;Cerebral Cortex;Adult;24 Pubmed search results 2008;Choristoma;Data Interpretation, Statistical;Electroencephalography;Adolescent},
	Month = {10},
	Nlm_Id = {0372537},
	Organization = {Department of Neurology and Neurosurgery, Montreal Neurological Hospital, Canada.},
	Pages = {1273-87},
	Pubmed = {7496786},
	Title = {Periventricular and subcortical nodular heterotopia. A study of 33 patients},
	Uuid = {19F63C25-2E09-464A-86A8-5EEDB06ECE0D},
	Volume = {118 ( Pt 5)},
	Year = {1995}}

@article{Dubois-Dalcq:2005,
	Abstract = {Recent studies on adult neural stem cells and the developmental biology of myelination have generated the expectation that neural precursors can repair the damaged central nervous system of multiple sclerosis patients where the endogenous remyelination process has failed. As a result, many laboratories are engaged in translational studies in which the goal is to design ways to promote remyelination and repair. Here we raise issues highlighted by prior experimental and human work that should be considered lest these studies become "lost in translation."},
	Author = {Dubois-Dalcq, Monique and Ffrench-Constant, Charles and Franklin, Robin J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Models, Biological;24 Pubmed search results 2008;Multiple Sclerosis;Central Nervous System;Myelin Sheath;Regeneration;Tissue Therapy;Animals;Oligodendroglia;Disease Models, Animal;review;Humans},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA. dalcqm\@mail.nih.gov},
	Pages = {9-12},
	Pii = {S0896-6273(05)00770-1},
	Pubmed = {16202704},
	Title = {Enhancing central nervous system remyelination in multiple sclerosis},
	Uuid = {F3A0CD50-409A-4704-97A3-079A981BDE00},
	Volume = {48},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.09.004}}

@article{Duelli:2007,
	Abstract = {Chromosomal instability (CIN) underlies malignant properties of many solid cancers and their ability to escape therapy, and it might itself cause cancer [1, 2]. CIN is sustained by deficiencies in proteins, such as the tumor suppressor p53 [3-5], that police genome integrity, but the primary cause of CIN in sporadic cancers remains uncertain [6, 7]. The primary suspects are mutations that deregulate telomere maintenance, or mitosis, yet such mutations have not been identified in the majority of sporadic cancers [6]. Alternatively, CIN could be caused by a transient event that destabilizes the genome without permanently affecting mechanisms of mitosis or proliferation [5, 8]. Here, we show that an otherwise harmless virus rapidly causes massive chromosomal instability by fusing cells whose cell cycle is deregulated by oncogenes. This synergy between fusion and oncogenes "randomizes" normal diploid human fibroblasts so extensively that each analyzed cell has a unique karyotype, and some produce aggressive, highly aneuploid, heterogeneous, and transplantable epithelial cancers in mice. Because many viruses are fusogenic, this study suggests that viruses, including those that have not been linked to carcinogenesis, can cause chromosomal instability and, consequently, cancer by fusing cells.},
	Author = {Duelli, Dominik M. and Padilla-Nash, Hesed M. and Berman, David and Murphy, Kathleen M. and Ried, Thomas and Lazebnik, Yuri},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {Mason-Pfizer monkey virus;Transduction, Genetic;Animals;Humans;Carcinoma;Fibroblasts;Female;research support, n.i.h., intramural;Cell Fusion;Neoplasms;15 Retrovirus mechanism;08 Aberrant cell cycle;Mice, Nude;Oncogenes;Cell Transformation, Viral;research support, n.i.h., extramural;Mice;22 Stem cells;24 Pubmed search results 2008;Chromosomal Instability;Cell Transformation, Neoplastic;22 Cancer},
	Month = {3},
	Nlm_Id = {9107782},
	Number = {5},
	Organization = {Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, NY 11724, USA.},
	Pages = {431-7},
	Pii = {S0960-9822(07)00888-3},
	Pubmed = {17320392},
	Title = {A virus causes cancer by inducing massive chromosomal instability through cell fusion},
	Uuid = {11C9B88B-91FF-48D3-AE3C-F5D8B386BD91},
	Volume = {17},
	Year = {2007},
	url = {papers/Duelli_CurrBiol2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2007.01.049}}

@article{Dugas:2006,
	Abstract = {To better understand the molecular mechanisms governing oligodendrocyte (OL) differentiation, we have used gene profiling to quantitatively analyze gene expression in synchronously differentiating OLs generated from pure oligodendrocyte precursor cells in vitro. By comparing gene expression in these OLs to OLs generated in vivo, we discovered that the program of OL differentiation can progress normally in the absence of heterologous cell-cell interactions. In addition, we found that OL differentiation was unexpectedly prolonged and occurred in at least two sequential stages, each characterized by changes in distinct complements of transcription factors and myelin proteins. By disrupting the normal dynamic expression patterns of transcription factors regulated during OL differentiation, we demonstrated that these sequential stages of gene expression can be independently controlled. We also uncovered several genes previously uncharacterized in OLs that encode transmembrane, secreted, and cytoskeletal proteins that are as highly upregulated as myelin genes during OL differentiation. Last, by comparing genomic loci associated with inherited increased risk of multiple sclerosis (MS) to genes regulated during OL differentiation, we identified several new positional candidate genes that may contribute to MS susceptibility. These findings reveal a previously unexpected complexity to OL differentiation and suggest that an intrinsic program governs successive phases of OL differentiation as these cells extend and align their processes, ensheathe, and ultimately myelinate axons.},
	Author = {Dugas, Jason C. and Tai, Yu Chuan and Speed, Terence P. and Ngai, John and Barres, Ben A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;research support, non-u.s. gov't;Rats, Sprague-Dawley;Rats;Oligonucleotide Array Sequence Analysis;Gene Expression Regulation;Quantitative Trait Loci;comparative study;research support, n.i.h., extramural;Protein Array Analysis;Animals;Cells, Cultured;Oligodendroglia;24 Pubmed search results 2008;Transcription Factors},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {43},
	Organization = {Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA. jcdugas\@alum.mit.edu},
	Pages = {10967-83},
	Pii = {26/43/10967},
	Pubmed = {17065439},
	Title = {Functional genomic analysis of oligodendrocyte differentiation},
	Uuid = {31F1BEC8-9DCC-4A59-B5ED-4071C5EAA46A},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2572-06.2006}}

@article{Duke:2004,
	Abstract = {The cell culture model utilized in this study represents one of the most widely used paradigms of microglia in vitro. After 14 days, microglia harvested from the neonatal rat brain are considered 'mature'. However, it is clear that this represents a somewhat arbitrary definition. In this paper, we provide a transcriptome definition of such microglial cells. More than 7,000 known genes and 1,000 expressed sequence tag clusters were analysed. 'Microglia genes' were defined as sequences consistently expressed in all microglia samples tested. Accordingly, 388 genes were identified as microglia genes. Another 1,440 sequences were detected in a subset of the cultures. Genes consistently expressed by microglia included genes known to be involved in the cellular immune response, brain tissue surveillance, microglial migration as well as proliferation. The expression profile reported here provides a baseline against which changes of microglia in vitro can be examined. Importantly, expression profiling of normal microglia will help to provide the presently purely operational definition of 'microglial activation' with a molecular biological correlate. Furthermore, the data reported here add to our understanding of microglia biology and allow projections as to what functions microglia may exert in vivo, as well as in vitro.},
	Author = {Duke, D. C. and Moran, L. B. and Turkheimer, F. E. and Banati, R. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {11 Glia},
	Nlm_Id = {7809375},
	Number = {1},
	Organization = {Department of Neuropathology, Division of Neuroscience and Psychological Medicine, Faculty of Medicine, Imperial College London, London, UK.},
	Pages = {30-7},
	Pii = {DNE2004026001030},
	Pubmed = {15509896},
	Title = {Microglia in culture: what genes do they express?},
	Uuid = {38D082FA-3AA6-4D7D-B04A-CEEC8B0FE8D2},
	Volume = {26},
	Year = {2004},
	url = {papers/Duke_DevNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000080709}}

@article{Dunlap:2006,
	Abstract = {Endogenous retroviruses (ERVs) are fixed and abundant in the genomes of vertebrates. Circumstantial evidence suggests that ERVs play a role in mammalian reproduction, particularly placental morphogenesis, because intact ERV envelope genes were found to be expressed in the syncytiotrophoblasts of human and mouse placenta and to elicit fusion of cells in vitro. We report here in vivo and in vitro experiments finding that the envelope of a particular class of ERVs of sheep, endogenous Jaagsiekte sheep retroviruses (enJSRVs), regulates trophectoderm growth and differentiation in the periimplantation conceptus (embryo/fetus and associated extraembryonic membranes). The enJSRV envelope gene is expressed in the trophectoderm of the elongating ovine conceptus after day 12 of pregnancy. Loss-of-function experiments were conducted in utero by injecting morpholino antisense oligonucleotides on day 8 of pregnancy that blocked enJSRV envelope protein production in the conceptus trophectoderm. This approach retarded trophectoderm outgrowth during conceptus elongation and inhibited trophoblast giant binucleate cell differentiation as observed on day 16. Pregnancy loss was observed by day 20 in sheep receiving morpholino antisense oligonucleotides. In vitro inhibition of the enJSRV envelope reduced the proliferation of mononuclear trophectoderm cells isolated from day 15 conceptuses. Consequently, these results demonstrate that the enJSRV envelope regulates trophectoderm growth and differentiation in the periimplantation ovine conceptus. This work supports the hypothesis that ERVs play fundamental roles in placental morphogenesis and mammalian reproduction.},
	Author = {Dunlap, Kathrin A. and Palmarini, Massimo and Varela, Mariana and Burghardt, Robert C. and Hayashi, Kanako and Farmer, Jennifer L. and Spencer, Thomas E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Pregnancy;Cell Differentiation;research support, n.i.h., extramural ;Embryo Implantation;Animals;Humans;Female;Sheep;15 Retrovirus mechanism;Trophoblasts;Endogenous Retroviruses;research support, non-u.s. gov't ;Mice;24 Pubmed search results 2008;Jaagsiekte sheep retrovirus;15 ERVs retroelements;Oligonucleotides, Antisense;Viral Proteins},
	Month = {9},
	Nlm_Id = {7505876},
	Number = {39},
	Organization = {Center for Animal Biotechnology and Genomics, Department of Animal Science, Texas A&M University, College Station, TX 77843, USA.},
	Pages = {14390-5},
	Pii = {0603836103},
	Pubmed = {16980413},
	Title = {Endogenous retroviruses regulate periimplantation placental growth and differentiation},
	Uuid = {6B785E0C-2917-47FF-9AD8-146B742B2DA5},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0603836103}}

@article{Dupressoir:2005,
	Abstract = {Recently, we and others have identified two human endogenous retroviruses that entered the primate lineage 25-40 million years ago and that encode highly fusogenic retroviral envelope proteins (syncytin-1 and -2), possibly involved in the formation of the placenta syncytiotrophoblast layer generated by trophoblast cell fusion at the materno-fetal interface. A systematic in silico search throughout mouse genome databases presently identifies two fully coding envelope genes, present as unique copies and unrelated to any known murine endogenous retrovirus, that we named syncytin-A and -B. Quantitative RT-PCR demonstrates placenta-specific expression for both genes, with increasing transcript levels in this organ from 9.5 to 14.5 days postcoitum. In situ hybridization of placenta cryosections further localizes these transcripts in the syncytiotrophoblast-containing labyrinthine zona. Consistently, we show that both genes can trigger cell-cell fusion in ex vivo transfection assays, with distinct cell type specificities suggesting different receptor usage. Genes orthologous to syncytin-A and -B and disclosing a striking conservation of their coding status are found in all Muridae tested (mouse, rat, gerbil, vole, and hamster), dating their entry into the rodent lineage approximately 20 million years ago. Together, these data strongly argue for a critical role of syncytin-A and -B in murine syncytiotrophoblast formation, thus unraveling a rather unique situation where two pairs of endogenous retroviruses, independently acquired by the primate and rodent lineages, would have been positively selected for a convergent physiological role.},
	Author = {Dupressoir, Anne and Marceau, Geoffroy and Vernochet, C{\'e}cile and B{\'e}nit, Laurence and Kanellopoulos, Colette and Sapin, Vincent and Heidmann, Thierry},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Gene Products, env;Placenta;Animals;Base Sequence;Evolution, Molecular;Cell Fusion;Trophoblasts;Endogenous Retroviruses;15 Retrovirus mechanism;RNA, Messenger;Genes, env;Organ Specificity;Pregnancy Proteins;Mice;24 Pubmed search results 2008;Molecular Sequence Data;15 ERVs retroelements;Selection (Genetics);Research Support, Non-U.S. Gov't},
	Month = {1},
	Nlm_Id = {7505876},
	Number = {3},
	Organization = {Unit{\'e} des R{\'e}trovirus Endog\`{e}nes et El{\'e}ments R{\'e}tro{\"\i}des des Eucaryotes Sup{\'e}rieurs, Unit{\'e} Mixte de Recherche, 8122 Centre National de la Recherche Scientifique, Institut Gustave Roussy, 94805 Villejuif, France.},
	Pages = {725-30},
	Pii = {0406509102},
	Pubmed = {15644441},
	Title = {Syncytin-A and syncytin-B, two fusogenic placenta-specific murine envelope genes of retroviral origin conserved in Muridae},
	Uuid = {9DD5EBF2-EE51-11DA-8605-000D9346EC2A},
	Volume = {102},
	Year = {2005},
	url = {papers/Dupressoir_ProcNatlAcadSciUSA2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0406509102}}

@article{Dupret:2007,
	Abstract = {The role of adult hippocampal neurogenesis in spatial learning remains a matter of debate. Here, we show that spatial learning modifies neurogenesis by inducing a cascade of events that resembles the selective stabilization process characterizing development. Learning promotes survival of relatively mature neurons, apoptosis of more immature cells, and finally, proliferation of neural precursors. These are three interrelated events mediating learning. Thus, blocking apoptosis impairs memory and inhibits learning-induced cell survival and cell proliferation. In conclusion, during learning, similar to the selective stabilization process, neuronal networks are sculpted by a tightly regulated selection and suppression of different populations of newly born neurons.},
	Author = {Dupret, David and Fabre, Annabelle and D{\"o}br{\"o}ssy, M\`{a}t\`{e} D\`{a}niel and Panatier, Aude and Rodr{\'\i}guez, Jos{\'e} Julio and Lamarque, St{\'e}phanie and Lemaire, Valerie and Oliet, Stephane H. R. and Piazza, Pier-Vincenzo V. and Abrous, Djoher Nora},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1545-7885},
	Journal = {PLoS Biol},
	Keywords = {research support, non-u.s. gov't;21 Neurophysiology;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {101183755},
	Number = {8},
	Organization = {INSERM U862, Bordeaux Neuroscience Research Center, Bordeaux, France.},
	Pages = {e214},
	Pii = {07-PLBI-RA-0438},
	Pubmed = {17683201},
	Title = {Spatial learning depends on both the addition and removal of new hippocampal neurons},
	Uuid = {897AEE30-1C20-4876-9DCE-D86F09503122},
	Volume = {5},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0050214}}

@article{Durand:2006,
	Abstract = {We have established a quantitative reverse transcriptase-PCR (RT-PCR) approach for the analysis of RNA transcript levels in individual cells of living brain slices. Quantification is achieved by using rapid-cycle, real-time PCR protocols and high-resolution external cDNA standard curves for the gene of interest. The method consists of several procedures, including cell soma harvest, reverse transcription, and an optimized cDNA purification step, which allowed us to quantify transcripts in small types of neurons, like cerebellar granule cells. Thus, we detected in single granule cells an average of 20 transcript copies of the housekeeping gene glyceraldehyde-3-phosphate-dehydrogenase. We combined two-photon calcium imaging and quantitative RT-PCR in single Purkinje and granule cells, respectively, and identified distinct glutamate receptor-dependent Ca(2+) responses in these two cell types. The approach was further tested by profiling the expression of the ionotropic glutamate receptor subunits NR2B and NR2C in the cerebellum. Our study revealed a developmental switch from an average of 15 NR2B copies/cell at postnatal day 8 (P8) to about five NR2C copies/cell after P26. Taken together, our results demonstrate that the new method is rapid, highly sensitive, provides reliable results in neurons of various sizes, and can be used in combination with Ca(2+) imaging.},
	Author = {Durand, and Marandi, and Herberger, and Blum, and Konnerth,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0031-6768},
	Journal = {Pflugers Arch},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {0154720},
	Number = {6},
	Organization = {Institut f{\"u}r Physiologie, Ludwig-Maximilians-Universit{\"a}t, Pettenkofer Stra$\beta$e 12, 80336, Mnchen, Germany, blum\@lrz.uni-muenchen.de.},
	Pages = {716-726},
	Pubmed = {16211366},
	Title = {Quantitative single-cell RT-PCR and Ca(2+) imaging in brain slices},
	Uuid = {0D317B0A-DD4B-4754-A73F-72C7CD76FACC},
	Volume = {451},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00424-005-1514-3}}

@article{Durbec:2001,
	Abstract = {In vertebrates, interneurons of the olfactory bulb are continuously generated postnatally and throughout life at the subventricular zone of the forebrain. From there, the neuronal progenitors migrate tangentially in a typical chain-like structure to the olfactory bulb in which they differentiate as interneurons. We have used a mouse/chick xenograft strategy to explore the migration and differentiation potential of the mouse olfactory progenitors in a heterochronic and heterotypic environment. We compared the migration of primary cells derived from the subventricular zone of adult or newborn lateral ventricule with the behavior of in vitro amplified cells derived from the same structures. We show that in the chick environment, olfactory bulb progenitors from newborn brain tissue perform chain migration along the neural crest cell routes, whereas grafted neurosphere-derived- cells migrate as isolated cells. These results, together with in vitro observations, allow us to propose that neuronal chain migration is a community effect independent of environmental cues but which is closely regulated by the differentiation program of the cells. We established that the progenitor cells performing chain migration are already committed, while neurosphere-derived-cells are able to integrate and differentiate as components of the peripheral nervous system. Copyright 2001 Academic Press.},
	Author = {Durbec, P. and Rougon, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:45 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Interneurons/chemistry/*cytology/*transplantation;Neural Cell Adhesion Molecules/analysis;Olfactory Bulb/*cytology;Tubulin/analysis;Transplantation, Heterologous;Vimentin/analysis;Sialic Acids/analysis;Tyrosine 3-Monooxygenase/analysis;L pdf;Animal;Mammals;17 Transplant Regeneration;Stem Cells/chemistry/*cytology/*transplantation;Support, Non-U.S. Gov't;Chick Embryo;Mice, Inbred Strains;Animals, Newborn;Graft Survival/physiology;Age Factors;Cell Movement/physiology;Intermediate Filament Proteins/analysis;Cell Differentiation/physiology;Mice;*Brain Tissue Transplantation},
	Number = {3},
	Organization = {Laboratoire de Genetique et Physiologie du Developpement, IBDM, CNRS/INSERM/Universite de la Mediterranee/AP de Marseille, Parc Scientifique de Luminy, Marseille Cedex 9, 13288, France.},
	Pages = {561-76.},
	Title = {Transplantation of mammalian olfactory progenitors into chick hosts reveals migration and differentiation potentials dependent on cell commitment},
	Uuid = {E4EFB43A-EE51-437B-A09D-AC7E73D0F14F},
	Volume = {17},
	Year = {2001},
	url = {papers/Durbec_MolCellNeurosci2001.pdf}}

@article{Durbec:2001a,
	Abstract = {Since its first description the polysialylated form of NCAM (PSA-NCAM) is thought to be a major regulator of cell-cell interactions in the nervous system. Over the past few years many crucial questions have been answered concerning PSA biosynthesis and function. Among these are the identification and cloning of the key enzymes that are responsible for its synthesis and the fact that expression of PSA is not restricted to developmental stages but maintained in the adult nervous system. In the adult, PSA has been shown to be not only a marker of structural plasticity but seems to be a major player in these processes. Originally suggested to be a purely anti-adhesive factor, modulating cell-cell interactions in general and by this allowing plasticity, there is now increasing evidence that this might not be the whole story. Instead, it appears possible that PSA-NCAM interacts with secreted signaling molecules and by this fulfills a more instructive function in brain plasticity.},
	Author = {Durbec, P. and Cremer, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0893-7648},
	Journal = {Mol Neurobiol},
	Keywords = {Axons;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Neural Cell Adhesion Molecules;Nervous System Physiology;Cell Communication;Neural Cell Adhesion Molecule L1;Neuronal Plasticity;Humans;Cell Movement;Sialic Acids;review;Animals},
	Medline = {21820121},
	Nlm_Id = {8900963},
	Number = {1-3},
	Organization = {Laboratoire de G{\'e}n{\'e}tique et Physiologie du D{\'e}veloppement, Developmental Biology Institute of Marseille, Universit{\'e} de la M{\'e}diterran{\'e}e, France.},
	Pages = {53-64},
	Pii = {MN:24:1-3:053},
	Pubmed = {11831554},
	Title = {Revisiting the function of PSA-NCAM in the nervous system},
	Uuid = {6938CC3D-DD2B-4AF0-8AED-28A2071DD7E4},
	Volume = {24},
	Year = {2001}}

@article{Dymecki:2007,
	Abstract = {New genetic technologies are transforming nervous system studies in mice, impacting fields from neural development to the neurobiology of disease. Alongside these methodological advances, new concepts are taking shape with respect to both vocabulary and form. Here we review aspects of both burgeoning areas. Presented are technologies which, by co-opting site-specific recombinase systems, enable select genes to be turned on or off in specific brain cells of otherwise undisturbed mouse embryos or adults. Manipulated genes can be endogenous loci or inserted transgenes encoding reporter, sensor, or effector molecules, making it now possible to assess not only gene function, but also cell function, origin, fate, connectivity, and behavioral output. From these methodological advances, a new form of molecular neuroscience is emerging that may be said to lean on the concepts of genetic access, genetic lineage, and genetic anatomy-the three "Gs"-much like a general education rests on the basics of reading, 'riting, and 'rithmetic.},
	Author = {Dymecki, Susan M. and Kim, Jun Chul},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;24 Pubmed search results 2008;23 Technique},
	Month = {4},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.},
	Pages = {17-34},
	Pii = {S0896-6273(07)00205-X},
	Pubmed = {17408575},
	Title = {Molecular Neuroanatomy's "Three Gs": A Primer},
	Uuid = {747622AE-BA34-4963-B9B2-9D41414A30DF},
	Volume = {54},
	Year = {2007},
	url = {papers/Dymecki_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.03.009}}

@article{Dziembowska:2005,
	Abstract = {Oligodendrocyte development is controlled by a number of survival and migratory factors. The present study shows that signaling of CXCR4 receptor by the chemokine CXCL12 regulates survival and migration of neural precursors (NP) as well as oligodendrocyte progenitors (OP). CXCR4 is expressed by E14 striatal NP and OP generated by neurospheres. In CXCR4-defective mice, the number of NP in neurosphere outgrowth was twofold less than in wild-type (WT) mice; NP radial cell migration was also decreased. In contrast, the addition of CXCL12 to WT NP increased radial migration from the sphere in a dose-dependent manner with a maximal response at 200 nM. When oligodendrocytes differentiated in neurosphere outgrowth, CXCR4 was downregulated. OP isolated from newborn brain coexpressed CXCR4 with platelet-derived growth factor receptor-alpha (PDGFR alpha) or chondroitin sulfate proteoglycan; receptor expression also decreased during differentiation in vitro. Neonatal OP showed a peak migratory response to 20 nM of CXCL12 in chemotactic chambers, a migration inhibited by a CXCR4 antagonist and anti-CXCL12 antibody. In the embryonic spinal cord, the number of OP-expressing PDGFR alpha was reduced more than twofold in CXCR4-defective mice compared with WT and the ratio of ventral to dorsal OP was significantly increased. This indicates a defect in OP survival and their dorsal migration from the ventral cord region, probably because CXCR4(-/-) OP are unable to respond to CXCL12 made by vascular endothelia and the pia mater. We propose that CXCR4 signaling regulate survival and outward chemotactic migration of OP during embryonic and postnatal CNS development.},
	Author = {Dziembowska, M. and Tham, T. N. and Lau, P. and Vitry, S. and Lazarini, F. and Dubois-Dalcq, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Cell Survival;Dose-Response Relationship, Drug;Cell Differentiation;Signal Transduction;Animals;Cells, Cultured;Receptors, CXCR4;Spheroids, Cellular;Oligodendroglia;Cell Count;Cell Movement;Mice, Inbred C57BL;Mice, Knockout;Neurons;Chemokines, CXC;Down-Regulation;Mice;Receptor, Platelet-Derived Growth Factor alpha;24 Pubmed search results 2008;Central Nervous System;Stem Cells;Proteochondroitin Sulfates;Research Support, Non-U.S. Gov't},
	Month = {5},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Neuroscience, Pasteur Institute, Paris, France.},
	Pages = {258-69},
	Pubmed = {15756692},
	Title = {A role for CXCR4 signaling in survival and migration of neural and oligodendrocyte precursors},
	Uuid = {72C1ED51-39C7-4BC6-8824-88F22C9D6145},
	Volume = {50},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20170}}

@article{Eagleson:2007,
	Abstract = {The cre/loxP system is used routinely to manipulate gene expression in the mouse nervous system. In order to delete genes specifically from the telencephalon, the Foxg1-cre line was created previously by replacing the intron-less Foxg1 coding region with cre, resulting in a Foxg1 heterozygous mouse. As the telencephalon of heterozygous Foxg1 mice was reported to be normal, this genotype often has been used as the control in subsequent analyses. Here we describe substantial disruption of forebrain development of heterozygous mice in the Foxg1-cre line, maintained on the C57BL/6J background. High resolution magnetic resonance microscopy reveals a significant reduction in the volume of the neocortex, hippocampus and striatum. The alteration in the neocortex results, in part, from a decrease in its tangential dimension, although gross patterning of the cortical sheet appears normal. This decrease is observed in three different Foxg1 heterozygous mouse lines, independent of the method of achieving deletion of the Foxg1 gene. Although Foxg1 is not expressed in the diencephalon, three-dimensional magnetic resonance microscopy revealed that thalamic volume in the adult is reduced. In contrast, at postnatal day 4, thalamic volume is normal, suggesting that interactions between cortex and dorsal thalamus postnatally produce the final adult thalamic phenotype. In the Foxg1-cre line maintained on the C57BL/6J background, the radial domain of the cerebral cortex also is disrupted substantially, particularly in supragranular layers. However, neither Foxg1 heterozygous mice of the Foxg1-tet (tetracycline transactivator) line, nor those of the Foxg1-lacZ and Foxg1-cre lines maintained on a mixed background, displayed a reduced cortical thickness. Thus Cre recombinase contributes to the radial phenotype, although only in the context of the congenic C57BL/6J background. These observations highlight an important role for Foxg1 in cortical development, reveal noteworthy complexity in the invocation of specific mechanisms underlying phenotypes expressed following genetic manipulations and stress the importance of including appropriate controls of all genotypes.},
	Author = {Eagleson, K. L. and Schlueter McFadyen-Ketchum, L. J. and Ahrens, E. T. and Mills, P. H. and Does, M. D. and Nickols, J. and Levitt, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {7605074},
	Number = {2},
	Organization = {Vanderbilt Kennedy Center for Research on Human Development and Department of Pharmacology, Vanderbilt University School of Medicine, 8110B Medical Research Building III, 465 21st Avenue South, Nashville, TN 37232, USA. kathie.eagleson\@vanderbilt.edu},
	Pages = {385-99},
	Pii = {S0306-4522(07)00740-3},
	Pubmed = {17640820},
	Title = {Disruption of Foxg1 expression by knock-in of cre recombinase: effects on the development of the mouse telencephalon},
	Uuid = {4C65A9D2-3581-4242-A2DF-9EC322DA62D5},
	Volume = {148},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2007.06.012}}

@article{Eberwine:2001,
	Author = {Eberwine, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:45 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Human;Alternative Splicing;Gene Expression Regulation;Cells;Molecular Biology;review, tutorial;RNA, Messenger;Animals;Polymerase Chain Reaction;review;23 Technique},
	Medline = {21547535},
	Month = {11},
	Nlm_Id = {9809671},
	Organization = {Department of Pharmacology, University of Pennsylvania Medical Center, 36th Street and Hamilton Walk, Philadelphia, Pennsylvania 19104, USA. eberwine\@pharm.med.upenn.edu},
	Pages = {1155-6},
	Pii = {nn1101-1155},
	Pubmed = {11687821},
	Title = {Single-cell molecular biology},
	Uuid = {F673BD71-8639-4626-84C6-4F7D4E0B9601},
	Volume = {4 Suppl},
	Year = {2001},
	url = {papers/Eberwine_NatNeurosci2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1101-1155}}

@article{Edenfeld:2005,
	Abstract = {In all complex organisms, glial cells are pivotal for neuronal development and function. Insects are characterized by having only a small number of these cells, which nevertheless display a remarkable molecular diversity. An intricate relationship between neurons and glia is initially required for glial migration and during axonal patterning. Recent data suggest that in organisms such as Drosophila, a prime role of glial cells lies in setting boundaries to guide and constrain axonal growth.},
	Author = {Edenfeld, Gundula and Stork, Tobias and Kl{\"a}mbt, Christian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Institut f{\"u}r Neurobiologie, Universit{\"a}t M{\"u}nster, Badestr. 9, 48149 M{\"u}nster, Germany.},
	Pages = {34-9},
	Pii = {S0959-4388(05)00008-5},
	Pubmed = {15721742},
	Title = {Neuron-glia interaction in the insect nervous system},
	Uuid = {34DAFB0E-F2C9-43AA-8AF5-80F58751FF86},
	Volume = {15},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.01.007}}

@article{Eder:1999,
	Abstract = {Morphological, immunophenotypical and electrophysiological properties were investigated in isolated cultured murine microglia before and after exposure to astrocyte-conditioned medium (ACM). Following application of ACM, microglial cells underwent a dramatic shape transformation from an amoeboid appearance to a ramified morphology. In parallel to morphological changes, a downregulation of macrophage surface antigens was observed in microglia exposed to ACM. Staining intensities for major histocompatibility complex (MHC) class II molecules and for the adhesion molecules leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) were significantly decreased in ramified microglia 5 days after exposure to ACM. In microglial cells treated daily with ACM over a period of 5 days, the smallest staining intensities for all surface antigens as well as the smallest ramification index as a measure for the highest degree of ramification were determined. In addition, upregulation of delayed rectifier K + currents was observed in microglia exposed to ACM for 1 day or treated daily with ACM for 5 days. In contrast, untreated amoeboid microglia or ramified microglia analysed 5 days after exposure to ACM did not express delayed rectifier K + currents. Analyses of the resting membrane potential and expression levels and properties of inward rectifier K + currents did not reveal any differences between untreated and ACM-treated microglia. It is suggested that electrophysiological properties of microglia do not strongly correlate with the morphology or the immunophenotype of microglial cells.},
	Author = {Eder, C. and Schilling, T. and Heinemann, U. and Haas, D. and Hailer, N. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Differentiation;Animals;Astrocytes;Cells, Cultured;Coculture Techniques;Microglia;Culture Media, Conditioned;11 Glia;Animals, Newborn;Mice, Inbred Strains;Cell Size;Potassium Channels, Voltage-Gated;Potassium Channels;Membrane Potentials;Barium;Delayed Rectifier Potassium Channels;Mice;24 Pubmed search results 2008;Immunohistochemistry;Potassium Channels, Inwardly Rectifying;Cell Adhesion Molecules;Histocompatibility Antigens Class II;Research Support, Non-U.S. Gov't},
	Medline = {20062492},
	Month = {12},
	Nlm_Id = {8918110},
	Number = {12},
	Organization = {Department of Neurophysiology, Institute of Physiology, Humboldt University, Berlin, Germany. claudia.eder\@charite.de},
	Pages = {4251-61},
	Pii = {ejn852},
	Pubmed = {10594651},
	Title = {Morphological, immunophenotypical and electrophysiological properties of resting microglia in vitro},
	Uuid = {604EEC69-7FA5-44FD-A8E9-1CC86F2EF3F9},
	Volume = {11},
	Year = {1999}}

@article{Eder:2005,
	Abstract = {Microglia play an important role in the central nervous system, where these cells, it is believed, have both neuroprotective and neurotoxic effects. In response to acute brain injury or during neurodegenerative and neuroinflammatory diseases, activated microglial cells undergo shape changes, migrate to the affected sites of neuronal damage, proliferate, and release a variety of substances, such as cytokines and reactive oxygen species (ROS). This review summarizes the physiological mechanisms underlying microglial activation and deactivation processes, with particular focus on the involvement of microglial ion channels. Microglial ion channels have been shown to be capable, by regulating membrane potential, cell volume, and intracellular ion concentrations, of modulating or facilitating proliferation, migration, cytokine secretion, shape changes, and the respiratory burst of microglial cells. (c) 2005 Wiley-Liss, Inc.},
	Author = {Eder,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {11 Glia},
	Month = {5},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Institute of Physiology, Humboldt University, Berlin, Germany.},
	Pages = {314-321},
	Pubmed = {15929071},
	Title = {Regulation of microglial behavior by ion channel activity},
	Uuid = {3E1C9713-6E2B-468D-9F0F-46F0972F6321},
	Volume = {81},
	Year = {2005},
	url = {papers/Eder_JNeurosciRes2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20476}}

@article{Eder:2001,
	Abstract = {Microglia, macrophages that reside in the brain, can express at least 12 different ion channels, including voltage-gated proton channels. The properties of H+ currents in microglia are similar to those in other phagocytes. Proton currents are elicited by depolarizing the membrane potential, but activation also depends strongly on both intracellular pH (pH(i)) and extracellular pH (pH(o)). Increasing pH(o) or lowering pH(i) promotes H+ channel opening by shifting the activation threshold to more negative potentials. H+ channels in microglia open only when the pH gradient is outward, so they carry only outward current in the steady state. Time-dependent activation of H+ currents is slow, with a time constant roughly 1 s at room temperature. Microglial H+ currents are inhibited by inorganic polyvalent cations, which reduce H+ current amplitude and shift the voltage dependence of activation to more positive potentials. Cytoskeletal disruptive agents modulate H+ currents in microglia. Cytochalasin D and colchicine decrease the current density and slow the activation of H+ currents. Similar changes of H+ currents, possibly due to cytoskeletal reorganization, occur in microglia during the transformation from ameboid to ramified morphology. Phagocytes, including microglia, undergo a respiratory burst, in which NADPH oxidase releases bactericidal superoxide anions into the phagosome and stoichiometrically releases protons into the cell, tending to depolarize and acidify the cell. H+ currents may help regulate both the membrane potential and pH(i) during the respiratory burst. By compensating for the efflux of electrons and counteracting intracellular acidification, H+ channels help maintain superoxide anion production.},
	Author = {Eder, C. and DeCoursey, T. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0301-0082},
	Journal = {Prog Neurobiol},
	Keywords = {Ion Channel Gating;Ion Channels;Research Support, Non-U.S. Gov't;Research Support, U.S. Gov't, P.H.S.;11 Glia;Microglia;Electrophysiology;Protons;Humans;Animals;Hydrogen-Ion Concentration;review;Brain Chemistry},
	Medline = {21137604},
	Month = {6},
	Nlm_Id = {0370121},
	Number = {3},
	Organization = {Institut f{\"u}r Physiologie der Charit{\'e}, Humboldt Universit{\"a}t, Tucholskystr. 2, D 10117 Berlin, Germany. claudia.eder\@charite.de},
	Pages = {277-305},
	Pii = {S0301008200000629},
	Pubmed = {11240310},
	Title = {Voltage-gated proton channels in microglia},
	Uuid = {0B567502-EE2F-11DA-8605-000D9346EC2A},
	Volume = {64},
	Year = {2001},
	url = {papers/Eder_ProgNeurobiol2001.pdf}}

@article{Egea:2007,
	Abstract = {Ephrins are cell-surface tethered guidance cues that bind to Eph receptor tyrosine kinases in trans on opposing cells. In the developing nervous system, the Eph-ephrin signaling system controls a large variety of cellular responses including contact-mediated attraction or repulsion, adhesion or de-adhesion, and migration. Eph-ephrin signaling can be bidirectional, and is subject to modulation by ectodomain cleavage of ephrins and by Eph-ephrin endocytosis. Recent work has highlighted the importance of higher-order clustering of functional Eph-ephrin complexes and the requirement for Rho GTPases as signal transducers. Co-expression of Ephs and ephrins within the same cellular membrane can result in Eph-ephrin cis interaction or in lateral segregation into distinct domains from where they signal opposing effects on the axon.},
	Author = {Egea, Joaquim and Klein, R{\"u}diger},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0962-8924},
	Journal = {Trends Cell Biol},
	Keywords = {10 Development;research support, non-u.s. gov't;Signal Transduction;10 circuit formation;Endocytosis;Ephrins;rho GTP-Binding Proteins;Animals;24 Pubmed search results 2008;review;Axons},
	Month = {5},
	Nlm_Id = {9200566},
	Number = {5},
	Organization = {Max-Planck Institute of Neurobiology, D-82152 Martinsried, Germany. jegea\@neuro.mpg.de <jegea\@neuro.mpg.de>},
	Pages = {230-8},
	Pii = {S0962-8924(07)00072-4},
	Pubmed = {17420126},
	Title = {Bidirectional Eph-ephrin signaling during axon guidance},
	Uuid = {6774D901-70BE-4A4B-8CC6-E3BC82745C4D},
	Volume = {17},
	Year = {2007},
	url = {papers/Egea_TrendsCellBiol2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tcb.2007.03.004}}

@article{Egensperger:1998,
	Abstract = {Microglial cells are considered to play an important role in the pathogenesis of Alzheimer disease. Apart from producing the Alzheimer amyloid precursor (APP) as an acute phase protein, microglial cells seem to be involved in the deposition of its amyloidogenic cleavage product, the amyloid-beta peptide (Abeta). Abeta is bound by apolipoprotein E (APOE) in an isoform-specific manner, and it has been demonstrated that inheritance of the AD susceptibility allele, APOE epsilon4, is associated with increased deposition of Abeta in the cerebral cortex. However, the relationship between APOE epsilon4 gene dose and microglial activation is unknown. Using microglial expression of major histocompatibility complex class II molecules as a marker, we have performed a quantitative genotype-phenotype analysis on microglial activation in frontal and temporal cortices of 20 APOE genotyped AD brains. The number of activated microglia and the tissue area occupied by these cells increased significantly with APOE epsilon4 gene dose. When a model of multiple linear regression was used to compare the relative influence of APOE genotype, sex, disease duration, age at death, diffuse and neuritic plaques as well as neurofibrillary tangles on microglial activation, only APOE genotype was found to have a significant effect. Thus, the APOE gene product represents an important determinant of microglial activity in AD. Since microglial activation by APP has been shown to be modulated by apoE in vitro, a direct role of microglia in AD pathogenesis is conceivable.},
	Author = {Egensperger, R. and K{\"o}sel, S. and von Eitzen, U. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {1015-6305},
	Journal = {Brain Pathol},
	Keywords = {Histocompatibility Antigens Class II;Humans;Frontal Lobe;Image Processing, Computer-Assisted;Middle Aged;Immunoenzyme Techniques;Microglia;Female;11 Glia;Male;Aged;Apolipoproteins E;Alzheimer Disease;Linear Models;Temporal Lobe;Senile Plaques;Neurofibrillary Tangles;Research Support, Non-U.S. Gov't},
	Medline = {98332358},
	Month = {7},
	Nlm_Id = {9216781},
	Number = {3},
	Organization = {Molecular Neuropathology Laboratory, Institute of Neuropathology, Hannover Medical School, Germany.},
	Pages = {439-47},
	Pubmed = {9669695},
	Title = {Microglial activation in Alzheimer disease: Association with APOE genotype},
	Uuid = {11359BCB-1C33-4E06-93F8-11A853825610},
	Volume = {8},
	Year = {1998}}

@article{Eggan:2004,
	Abstract = {Cloning by nuclear transplantation has been successfully carried out in various mammals, including mice. Until now mice have not been cloned from post-mitotic cells such as neurons. Here, we have generated fertile mouse clones derived by transferring the nuclei of post-mitotic, olfactory sensory neurons into oocytes. These results indicate that the genome of a post-mitotic, terminally differentiated neuron can re-enter the cell cycle and be reprogrammed to a state of totipotency after nuclear transfer. Moreover, the pattern of odorant receptor gene expression and the organization of odorant receptor genes in cloned mice was indistinguishable from wild-type animals, indicating that irreversible changes to the DNA of olfactory neurons do not accompany receptor gene choice.},
	Author = {Eggan, Kevin and Baldwin, Kristin and Tackett, Michael and Osborne, Joseph and Gogos, Joseph and Chess, Andrew and Axel, Richard and Jaenisch, Rudolf},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Embryo;Gene Expression Regulation, Developmental;Research Support, Non-U.S. Gov't;Totipotent Stem Cells;Embryonic and Fetal Development;Olfactory Receptor Neurons;Research Support, U.S. Gov't, P.H.S.;Oocytes;Cloning, Organism;22 Stem cells;Animals;Receptors, Odorant;Cell Nucleus;Mice;Polyploidy},
	Month = {3},
	Nlm_Id = {0410462},
	Number = {6978},
	Organization = {Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.},
	Pages = {44-9},
	Pii = {nature02375},
	Pubmed = {14990966},
	Title = {Mice cloned from olfactory sensory neurons},
	Uuid = {35D6617F-E354-42DE-A4D7-98D6549C826E},
	Volume = {428},
	Year = {2004},
	url = {papers/Eggan_Nature2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature02375}}

@article{Eggan:2000,
	Abstract = {To study whether cloning resets the epigenetic differences between the two X chromosomes of a somatic female nucleus, we monitored X inactivation in cloned mouse embryos. Both X chromosomes were active during cleavage of cloned embryos, followed by random X inactivation in the embryo proper. In the trophectoderm (TE), X inactivation was nonrandom with the inactivated X of the somatic donor being chosen for inactivation. When female embryonic stem cells with two active X chromosomes were used as donors, random X inactivation was seen in the TE and embryo. These results demonstrate that epigenetic marks can be removed and reestablished on either X chromosome during cloning. Our results also suggest that the epigenetic marks imposed on the X chromosomes during gametogenesis, responsible for normal imprinted X inactivation in the TE, are functionally equivalent to the marks imposed on the chromosomes during somatic X inactivation.},
	Author = {Eggan, K. and Akutsu, H. and Hochedlinger, K. and Rideout, W. and Yanagimachi, R. and Jaenisch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Transgenes;Research Support, Non-U.S. Gov't;Cell Differentiation;Placenta;Animals;Stem Cell Transplantation;Female;Oocytes;Cloning, Organism;Green Fluorescent Proteins;Embryonic and Fetal Development;Embryo;Reverse Transcriptase Polymerase Chain Reaction;Muridae;Research Support, U.S. Gov't, P.H.S.;Male;Alleles;X Chromosome;Gene Silencing;Cell Nucleus;Mice;22 Stem cells;Luminescent Proteins;Stem Cells;Genes, Reporter;Dosage Compensation, Genetic;Genomic Imprinting},
	Medline = {20545826},
	Month = {11},
	Nlm_Id = {0404511},
	Number = {5496},
	Organization = {Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA.},
	Pages = {1578-81},
	Pii = {9012},
	Pubmed = {11090356},
	Title = {X-Chromosome inactivation in cloned mouse embryos},
	Uuid = {0FD6F8F1-C84F-4B8A-A7A1-39552A60064B},
	Volume = {290},
	Year = {2000}}

@article{Egger:2003,
	Abstract = {Granule cells are axonless local interneurons that mediate lateral inhibitory interactions between the principal neurons of the olfactory bulb via dendrodendritic reciprocal synapses. This unusual arrangement may give rise to functional properties different from conventional lateral inhibition. Although granule cells spike, little is known about the role of the action potential with respect to their synaptic output. To investigate the signals that underlie dendritic release in these cells, two-photon microscopy in rat brain slices was used to image calcium transients in granule cell dendrites and spines. Action potentials evoked calcium transients throughout the dendrites, with amplitudes increasing with distance from soma and attaining a plateau level within the external plexiform layer, the zone of granule cell synaptic output. Transient amplitudes were, on average, equal in size in spines and adjacent dendrites. Surprisingly, both spine and dendritic amplitudes were strongly dependent on membrane potential, decreasing with depolarization and increasing with hyperpolarization from rest. Both the current-voltage relationship and the time course of inactivation were consistent with the known properties of T-type calcium channels, and the voltage dependence was blocked by application of the T-type calcium channel antagonists Ni2+ and mibefradil. In addition, mibefradil reduced action potential-mediated synaptic transmission from granule to mitral cells. The implication of a transiently inactivating calcium channel in synaptic release from granule cells suggests novel mechanisms for the regulation of lateral inhibition in the olfactory bulb. 1529-2401 Journal Article},
	Author = {Egger, V. and Svoboda, K. and Mainen, Z. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurosci},
	Keywords = {13 Olfactory bulb anatomy;Calcium/*metabolism;Animals;Cells, Cultured;Rats;Dendrites/metabolism;Synaptic Transmission;Calcium Channels, T-Type/physiology;Rats, Sprague-Dawley;Kinetics;Ion Transport;Olfactory Bulb/*cytology/metabolism/*physiology;*Neural Inhibition;Support, Non-U.S. Gov't;Interneurons/cytology/*metabolism/physiology;Support, U.S. Gov't, P.H.S.;Membrane Potentials;I pdf;*Action Potentials},
	Number = {20},
	Organization = {Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. egger\@cshl.edu},
	Pages = {7551-8},
	Pubmed = {12930793},
	Title = {Mechanisms of lateral inhibition in the olfactory bulb: efficiency and modulation of spike-evoked calcium influx into granule cells},
	Uuid = {13897D52-EF1C-4BA2-9316-A644F10C970F},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12930793}}

@article{Eglitis:1997,
	Abstract = {Glial cells are thought to derive embryologically from either myeloid cells of the hematopoietic system (microglia) or neuroepithelial progenitor cells (astroglia and oligodendrocytes). However, it is unclear whether the glia in adult brains free of disease or injury originate solely from cells present in the brain since the fetal stage of development, or if there is further input into such adult brains from cells originating outside the central nervous system. To test the ability of hematopoietic cells to contribute to the central nervous system, we have transplanted adult female mice with donor bone marrow cells genetically marked either with a retroviral tag or by using male donor cells. Using in situ hybridization histochemistry, a continuing influx of hematopoietic cells into the brain was detected. Marrow-derived cells were already detected in the brains of mice 3 days after transplant, and their numbers increased over the next several weeks, exceeding 14,000 cells per brain in several animals. Marrow-derived cells were widely distributed throughout the brain, including the cortex, hippocampus, thalamus, brain stem, and cerebellum. When in situ hybridization histochemistry was combined with immunohistochemical staining using lineage-specific markers, some bone marrow-derived cells were positive for the microglial antigenic marker F4/80. Other marrow-derived cells surprisingly expressed the astroglial marker glial fibrillary acidic protein. These results indicate that some microglia and astroglia arise from a precursor that is a normal constituent of adult bone marrow.},
	Author = {Eglitis, M. A. and Mezey, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {In Situ Hybridization;Gene Transfer Techniques;Cell Differentiation;Neuroglia;Hematopoietic Stem Cells;Female;Mice, Inbred C57BL;Genetic Markers;11 Glia;Microglia;Hematopoietic Stem Cell Transplantation;Animals;Mice;Male},
	Medline = {97268700},
	Month = {4},
	Nlm_Id = {7505876},
	Number = {8},
	Organization = {Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892, USA.},
	Pages = {4080-5},
	Pubmed = {9108108},
	Title = {Hematopoietic cells differentiate into both microglia and macroglia in the brains of adult mice},
	Uuid = {8481D91C-D3B7-11D9-A0E9-000D9346EC2A},
	Volume = {94},
	Year = {1997}}

@article{Ehninger:2003,
	Abstract = {We here report that voluntary wheel running led to a regional increase in the number of newly generated cortical microglia. We asked how adult cortical cell genesis would respond to environmental enrichment and physical activity, both stimuli that robustly induce adult hippocampal neurogenesis. After labeling proliferating cells with bromodeoxyuridine (BrdU) and immunohistochemical detection of BrdU, we found that both experimental paradigms did not result in general effects on cell proliferation and cell genesis in the neocortex. However, there were regionally and layer specific changes in the number of BrdU marked cells, both 1 day and 4 weeks after BrdU. Environmental enrichment led to a significant increase in the number of new astrocytes in layer 1 of the motor cortex. Voluntary wheel running, in contrast, caused an induction in the proliferation of microglia in superficial cortical layers of several brain regions. Under no condition was the number of new oligodendrocytes measurably enhanced. In contrast to the hippocampus, we did not find any new neurons in the cortex. The physiological 'activation' of microglia adds a new aspect to the question of microglial function in the healthy brain and of how adult brain cells can plastically react to physiological stimuli.},
	Author = {Ehninger, Dan and Kempermann, Gerd},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {01 Adult neurogenesis general;Female;Environment;Cell Division;Neocortex;11 Glia;Microglia;Motor Activity;Mice, Inbred C57BL;06 Adult neurogenesis injury induced;Mice;Animals;Support, Non-U.S. Gov't},
	Medline = {22737282},
	Month = {8},
	Nlm_Id = {9110718},
	Number = {8},
	Organization = {Max Delbr{\"u}ck Center for Molecular Medicine (MDC), Berlin-Buch, Robert-R{\"o}ssle-Strasse 10, 13125 Berlin.},
	Pages = {845-51},
	Pubmed = {12853371},
	Title = {Regional effects of wheel running and environmental enrichment on cell genesis and microglia proliferation in the adult murine neocortex},
	Uuid = {47FF837A-4296-11DB-A5D2-000D9346EC2A},
	Volume = {13},
	Year = {2003},
	url = {papers/Ehninger_CerebCortex2003.pdf}}

@article{Ehring:2003,
	Abstract = {BACKGROUND: An optimal system for the expansion of pluripotent HPCs would ideally eliminate the use of cytokines and animal-derived serum. We have shown previously that a 3D, tantalum-coated porous biomaterial (Cytomatrix) supports the maintenance and expansion of human BM HPCs in the absence of cytokines. METHODS: Umbilical cord blood (UCB) derived HPC were cultured in the Cytomatrix in the absence of exogenous cytokines. Phenotype was determined using FACS. Colony-forming units (CFU) activity was evaluated. Engraftment capacity was evaluated by transplanting the expanded cells into non-obese diabetic (NOD)/SCID mice. RESULTS: We describe the expansion of HPCs from UCB using the Cytomatrix system. When UCB-derived CD34(+) cells were cultured in the Cytomatrix system for 2 weeks we observed an increase in the number of nucleated cells (3-fold) and CFU (2.6-fold). The number of CD45(+) and CD34(+) cells both increased three-fold. Trends demonstrated an increase in the frequency of CD34(+)C38(-) cells, and an increase in both CD34(+)C33(+) cells and CD34(+)C61(+) cells. No expansion of T or B lymphocytes was observed. When expanded UCB cells from the Cytomatrix were injected into sub-lethally irradiated NOD/SCID mice, human cells were detected in the murine peripheral blood and BM 6 weeks post-transplantation. DISCUSSION: This unique approach to the expansion of UCB cells in a serum-free, cytokine-free environment may provide expansion of HPCs with multi-lineage engraftment capability that could be used clinically.},
	Author = {Ehring, B. and Biber, K. and Upton, T. M. and Plosky, D. and Pykett, M. and Rosenzweig, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1465-3249},
	Journal = {Cytotherapy},
	Keywords = {Mice, SCID;Antigens, CD45;Animals;Flow Cytometry;Receptors, CXCR4;Integrin beta3;ADP-ribosyl Cyclase;Cell Count;Cell Division;Antigens, CD;Hematopoietic Stem Cells;Research Support, U.S. Gov't, Non-P.H.S.;Antigens, CD3;Antigens, Differentiation, Myelomonocytic;Macrophages;Granulocytes;Transplantation, Heterologous;11 Glia;Hematopoietic Stem Cell Transplantation;Coated Materials, Biocompatible;Antigens, CD19;Fetal Blood;Integrin alpha4beta1;Antigens, CD34;Mice, Inbred NOD;Colony-Forming Units Assay;Bone Marrow Cells;Mice;Cell Culture Techniques;Humans},
	Nlm_Id = {100895309},
	Number = {6},
	Organization = {Cytomatrix, Woburn, MA 01801, USA.},
	Pages = {490-9},
	Pii = {4K0GEY9DGFC1EAGM},
	Pubmed = {14660045},
	Title = {Expansion of HPCs from cord blood in a novel 3D matrix},
	Uuid = {42B8FF9D-377A-446C-845B-563E002076EF},
	Volume = {5},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1080/14653240310003585}}

@article{Eichhoff:2008,
	Abstract = {PURPOSE: Over the last decade, in vivo calcium imaging became a powerful tool for studying brain function. With the use of two-photon microscopy and modern labelling techniques, it allows functional studies of individual living cells, their processes and their interactions within neuronal networks. In vivo calcium imaging is even more important for studying the aged brain, which is hard to investigate in situ due to the fragility of neuronal tissue. METHODS: In this article, we give a brief overview of the techniques applicable to image aged rodent brain at cellular resolution. RESULTS: We use multicolor imaging to visualize specific cell types (neurons, astrocytes, microglia) as well as the autofluorescence of the "aging pigment" lipofuscin. CONCLUSIONS: Further, we illustrate an approach for simultaneous imaging of cortical cells and senile plaques in mouse models of Alzheimer's disease.},
	Author = {Eichhoff, and Busche, and Garaschuk,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1619-7070},
	Journal = {Eur J Nucl Med Mol Imaging},
	Keywords = {21 Neurophysiology;21 Calcium imaging;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {101140988},
	Organization = {Institute of Neuroscience, Technical University of Munich, Biedersteinerstr. 29, 80802, Munich, Germany, olga.garaschuk\@lrz.tum.de.},
	Pubmed = {18193219},
	Title = {In vivo calcium imaging of the aging and diseased brain},
	Uuid = {55FE76AA-34C2-44D6-9435-515179756E74},
	Year = {2008},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00259-007-0709-6}}

@article{Eidelman:1984,
	Abstract = {Purified G-protein from vesicular stomatitis virus was reconstituted into egg phosphatidylcholine vesicles by detergent dialysis of octyl glucoside. A homogeneous population of reconstituted vesicles could be obtained, provided the protein to lipid ratio was high (about 0.3 mol \%protein) and the detergent removal was slow. The reconstituted vesicles were assayed for fusion activity using electron microscopy and fluorescence energy transfer. The fusion activity mediated by the viral envelope protein was dependent upon pH, temperature, and target membrane lipid composition. Incubation of reconstituted vesicles at low pH with small unilamellar vesicles containing negatively charged lipids resulted in the appearance of large cochleate structures, as shown by electron microscopy using negative stain. This process did not cause leakage of a vesicle-encapsulated aqueous marker. The rate of fusion was pH-dependent with a pK of about 4 and the apparent energy of activation for the fusion was 16 +/- 1 kcal/mol. G-protein-mediated fusion showed a large preference for target membranes which contain phosphatidylserine or phosphatidic acid. Inclusion of 36\%cholesterol in any of the lipid compositions had no effect on the rate of fusion. These reconstituted vesicles provide a system to study the mechanism of pH-dependent fusion induced by a viral spike protein.},
	Author = {Eidelman, O. and Schlegel, R. and Tralka, T. S. and Blumenthal, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {24 Pubmed search results 2008;Membrane Glycoproteins;Research Support, Non-U.S. Gov't;Kinetics;Microscopy, Electron;Liposomes;Cell Line;Cercopithecus aethiops;Viral Proteins;Vesicular stomatitis-Indiana virus;Glucosides;Phosphatidylcholines;Animals;Hydrogen-Ion Concentration;Kidney;Viral Envelope Proteins;15 Retrovirus mechanism},
	Medline = {84162177},
	Month = {4},
	Nlm_Id = {2985121R},
	Number = {7},
	Pages = {4622-8},
	Pubmed = {6323480},
	Title = {pH-dependent fusion induced by vesicular stomatitis virus glycoprotein reconstituted into phospholipid vesicles},
	Uuid = {68302A7A-EE2C-11DA-8605-000D9346EC2A},
	Volume = {259},
	Year = {1984}}

@article{Ekdahl:2001,
	Abstract = {The dentate gyrus (DG) is one of the few regions in the brain that continues to produce new neurons throughout adulthood. Seizures not only increase neurogenesis, but also lead to death of DG neurons. We investigated the relationship between cell death and neurogenesis following seizures in the DG of adult rats by blocking caspases, which are key components of apoptotic cell death. Multiple intracerebroventricular infusions of caspase inhibitors (pancaspase inhibitor zVADfmk, and caspase 3 and 9 inhibitor) prior to, just after, 1 day after, and 1 week following 2 h of lithium-pilocarpine-induced status epilepticus reduced the number of terminal deoxynucleotidyl transferase-mediated fluorescein-dUTP nick-end labelled (TUNEL) cells and increased the number of bromodeoxyuridine (BrdU) -stained proliferated cells in the subgranular zone at 1 week. The caspase inhibitor-treated group did not differ from control at 2 days or 5 weeks following the epileptic insult. Our findings suggest that caspases modulate seizure-induced neurogenesis in the DG, probably by regulating apoptosis of newly born neurons, and that this action can be suppressed transiently by caspase inhibitors. Furthermore, although previous studies have indicated that increased neuronal death can trigger neurogenesis, we show here that reduction in apoptotic death may be associated with increased neurogenesis.},
	Author = {Ekdahl, C. T. and Mohapel, P. and Elmer, E. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {06 Adult neurogenesis injury induced;D pdf},
	Number = {6},
	Organization = {Section of Restorative Neurology, Wallenberg Neuroscience Center, BMC A11, SE-221 84 Lund, Sweden; Section of Experimental Brain Research, Wallenberg Neuroscience Center, BMC A13, SE-221 84 Lund, Sweden.},
	Pages = {937-45.},
	Title = {Caspase inhibitors increase short-term survival of progenitor-cell progeny in the adult rat dentate gyrus following status epilepticus},
	Uuid = {44A1F12E-393A-4C39-8495-F4D1CC64EB6C},
	Volume = {14},
	Year = {2001},
	url = {papers/Ekdahl_EurJNeurosci2001}}

@article{Ekdahl:2003,
	Abstract = {New hippocampal neurons are continuously generated in the adult brain. Here, we demonstrate that lipopolysaccharide-induced inflammation, which gives rise to microglia activation in the area where the new neurons are born, strongly impairs basal hippocampal neurogenesis in rats. The increased neurogenesis triggered by a brain insult is also attenuated if it is associated with microglia activation caused by tissue damage or lipopolysaccharide infusion. The impaired neurogenesis in inflammation is restored by systemic administration of minocycline, which inhibits microglia activation. Our data raise the possibility that suppression of hippocampal neurogenesis by activated microglia contributes to cognitive dysfunction in aging, dementia, epilepsy, and other conditions leading to brain inflammation. 0027-8424 Journal Article},
	Author = {Ekdahl, C. T. and Claasen, J. H. and Bonde, S. and Kokaia, Z. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Hippocampus/metabolism;Neurons/*physiology;Animals;*Inflammation;Bromodeoxyuridine/pharmacology;Rats;Microglia/metabolism;D pdf;Rats, Sprague-Dawley;Minocycline/pharmacology;Lipopolysaccharides/metabolism/pharmacology;Male;Support, Non-U.S. Gov't;Anti-Bacterial Agents/pharmacology;Antimetabolites/pharmacology;06 Adult neurogenesis injury induced;Brain/*metabolism;Immunohistochemistry},
	Number = {23},
	Organization = {Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, Wallenberg Neuroscience Center, Biomedical Center A-11, Lund, Sweden.},
	Pages = {13632-7},
	Title = {Inflammation is detrimental for neurogenesis in adult brain},
	Uuid = {D7A5FFDD-B724-49AD-9C19-F5627372966F},
	Volume = {100},
	Year = {2003},
	url = {papers/Ekdahl_ProcNatlAcadSciUSA2003.pdf}}

@article{Ekstrand:1996,
	Abstract = {A non-radioactive 96-well microtitre plate reverse transcriptase (RT) assay, based on the use of covalently bound riboadenosine homopolymer in the wells and 5-bromodeoxyuridined 5'-triphosphate (BrdUTP) as dNTP, is described. The whole assay is performed in a single well, including the quantitative detection of incorporated BrdU, which is performed immunologically using alkaline phosphatase-conjugated anti-BrdU antibody and colorometric reading. The system also allows the use of variable amounts of primer. The kinetics and characteristics of the assay using BrdUTP is similar to the use of [3H]dTTP. The sensitivity of the assay can be varied either by altering the duration of RT assay time and/or by prolonging the alkaline phosphatase reaction. Thus the assay can detect < 0.02 pg of recombinant human-immunodeficiency-virus (HIV) type I RT, < 0.005 m unit of avian-myeloblastosis-virus RT or < 0.02 m unit of recombinant Moloney-murine-leukaemia-virus RT. The assay was found to be useful with various types of cell-culture material, and a comparative study of 16 HIV-infected lymphocyte cultures, using 10 microliters of supernatant medium for RT assay and 22.5 microliters for p24 antigen assay showed that the new RT assay was at least 25-fold more sensitive than the p24 antigen assay. The results also show a good correlation between the RT activities found and the p24-antigen level detected, with exception for HIV2 isolates, as they only became positive in the RT assay. The technical performance and the capacity of the test compared with other available RT kits is discussed, as well as its use for other applications.},
	Author = {Ekstrand, D. H. and Awad, R. J. and K{\"a}llander, C. F. and Gronowitz, J. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0885-4513},
	Journal = {Biotechnol Appl Biochem},
	Keywords = {Thymine Nucleotides;Reference Standards;Titrimetry;RNA-Directed DNA Polymerase;HIV Infections;Research Support, Non-U.S. Gov't;Deoxyuracil Nucleotides;DNA;Subcellular Fractions;Sensitivity and Specificity;15 Retrovirus mechanism;Humans;HIV;Cells, Cultured;Templates, Genetic;24 Pubmed search results 2008},
	Medline = {96206778},
	Month = {4},
	Nlm_Id = {8609465},
	Organization = {Department of Medical Genetics, Uppsala University, Sweden.},
	Pages = {95-105},
	Pubmed = {8639277},
	Title = {A sensitive assay for the quantification of reverse transcriptase activity based on the use of carrier-bound template and non-radioactive-product detection, with special reference to human-immunodeficiency-virus isolation},
	Uuid = {3CAB3E90-F035-426D-9260-48A8AF34429C},
	Volume = {23 ( Pt 2)},
	Year = {1996}}

@article{El-Maarouf:2006,
	Abstract = {Polysialic acid (PSA), a large cell-surface carbohydrate that regulates cell interactions, is used during vertebrate development to promote precursor cell migration and axon path-finding. The induction of PSA expression in damaged adult CNS tissues could help them to rebuild by creating conditions permissive for architectural remodeling. This possibility has been explored in two contexts, the regeneration of axons and the recruitment of endogenous neural precursors to a lesion. Glial scars that form at CNS injury sites block axon regeneration. It has been found that transfection of scar astrocytes by a viral vector encoding polysialyltransferase leads to sustained expression of high levels of PSA. With this treatment, a substantial portion of severed corticospinal tract axon processes were able to grow through a spinal injury site. In the studies of precursor cell migration to a cortical lesion, it was found that induced PSA expression in a path extending from the subventricular zone to a lesion near the cortical surface increased recruitment of BrdU/nestin-positive cells along the path and into the injury site. These displaced precursors were able to differentiate in a regionally appropriate manner. These findings suggest that induced PSA expression can be used as a strategy for promoting tissue repair involving both replacement of cells and rebuilding of neural connections.},
	Author = {El Maarouf, Abderrahman and Petridis, Athanasios K. and Rutishauser, Urs},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Mice;Sialic Acids;Transfection;24 Pubmed search results 2008;Central Nervous System;Nerve Regeneration;Sialyltransferases;Astrocytes;Recombinant Proteins;Stem Cells;Mice, Transgenic;Animals;Cell Movement;Male;Brain Injuries;Axons},
	Month = {11},
	Nlm_Id = {7505876},
	Number = {45},
	Organization = {Laboratory of Cellular and Developmental Neuroscience, Department of Cell Biology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA. a-el-maarouf\@ski.mskcc.org},
	Pages = {16989-94},
	Pii = {0608036103},
	Pubmed = {17075041},
	Title = {Use of polysialic acid in repair of the central nervous system},
	Uuid = {1AC1BB78-AB09-481E-8887-BFE7D5CF8CF2},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0608036103}}

@article{ElShamy:1998,
	Abstract = {More than half of the dorsal root ganglion (DRG) neurons are lost by excessive cell death coinciding with precursor proliferation and cell cycle exit in neurotrophin-3 null mutant (NT-3-/-) mice. We find that in the absence of NT-3, sensory precursor cells fail to arrest the cell cycle, override the G1 phase restriction point, and die by apoptosis in S phase, which can be prevented in vivo by a cell cycle blocker. Uncoordinated cell cycle reentry is preceded by a failure of nuclear N-myc downregulation and is paralleled by the activation of the full repertoire of G1 and S phase cell cycle proteins required for cell cycle entry. Our results provide evidence for novel activity of neurotrophins in cell cycle control and point toward an N-myc sensitization to cell death in the nervous system that is under the control of NT-3. 0896-6273 Journal Article},
	Author = {ElShamy, W. M. and Fridvall, L. K. and Ernfors, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {Neuron},
	Keywords = {Neurotrophin 3;EE pdf;Mice, Inbred BALB C;Mice, Knockout;Nerve Growth Factors/*deficiency/*genetics;Cell Division/genetics;Neurons, Afferent/*pathology;08 Aberrant cell cycle;G1 Phase/*genetics;Animals;Support, Non-U.S. Gov't;Mice;S Phase/*genetics;Stem Cells/*pathology},
	Number = {5},
	Organization = {Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.},
	Pages = {1003-15},
	Pubmed = {9856457},
	Title = {Growth arrest failure, G1 restriction point override, and S phase death of sensory precursor cells in the absence of neurotrophin-3},
	Uuid = {ED2AF5FF-B3D0-4632-8AF4-2A38059275FC},
	Volume = {21},
	Year = {1998},
	url = {papers/ElShamy_Neuron1998.pdf}}

@article{Elias:2007,
	Abstract = {Radial glia, the neuronal stem cells of the embryonic cerebral cortex, reside deep within the developing brain and extend radial fibres to the pial surface, along which embryonic neurons migrate to reach the cortical plate. Here we show that the gap junction subunits connexin 26 (Cx26) and connexin 43 (Cx43) are expressed at the contact points between radial fibres and migrating neurons, and acute downregulation of Cx26 or Cx43 impairs the migration of neurons to the cortical plate. Unexpectedly, gap junctions do not mediate neuronal migration by acting in the classical manner to provide an aqueous channel for cell-cell communication. Instead, gap junctions provide dynamic adhesive contacts that interact with the internal cytoskeleton to enable leading process stabilization along radial fibres as well as the subsequent translocation of the nucleus. These results indicate that gap junction adhesions are necessary for glial-guided neuronal migration, raising the possibility that the adhesive properties of gap junctions may have an important role in other physiological processes and diseases associated with gap junction function.},
	Author = {Elias, Laura A. B. and Wang, Doris D. and Kriegstein, Arnold R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Gap Junctions;research support, non-u.s. gov't;Cell Adhesion;Rats, Sprague-Dawley;Rats;Gene Expression Regulation;Neocortex;research support, n.i.h., extramural;Connexin 43;Animals;Cell Movement;Connexins;Neurons;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {0410462},
	Number = {7156},
	Organization = {Neuroscience Graduate Program, University of California San Francisco, 513 Parnassus Avenue, San Francisco, California 94143, USA. EliasL\@stemcell.ucsf.edu},
	Pages = {901-7},
	Pii = {nature06063},
	Pubmed = {17713529},
	Title = {Gap junction adhesion is necessary for radial migration in the neocortex},
	Uuid = {74F7A21E-43F8-432B-8A34-92B102A01079},
	Volume = {448},
	Year = {2007},
	url = {papers/Elias_Nature2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06063}}

@article{Eliopoulos:2002,
	Abstract = {Naturally occurring drug resistance genes of human origin can be exploited for selection of genetically engineered cells co-expressing a desired therapeutic transgene. Their non-immunogenicity in clinical applications would be a major asset. Human cytidine deaminase (hCD) is a chemoresistance gene that inactivates cytotoxic cytosine nucleoside analogs, such as cytosine arabinoside (Ara-C). The aim of this study was to establish if the hCD gene can serve as an ex vivo dominant selectable marker in engineered bone marrow stromal cells (MSCs). A bicistronic retrovector comprising the hCD cDNA and the green fluorescent protein (GFP) reporter gene was generated and used for transduction of A549 cells and primary murine MSCs. Analysis of transduced cells demonstrated stable integration of proviral DNA, more than 1000-fold increase in CD enzyme activity, and drug resistance to cytosine nucleoside analogs. In a mixture of transduced and untransduced MSCs, the percentage of retrovector-expressing cells could be increased to virtual purity (>99.5\%) through in vitro drug selection with 1 microM Ara-C. Increased selective pressure with 2.5 microM Ara-C allowed for enrichment of a mixed population of MSCs expressing approximately six-fold higher levels of GFP and of CD activity when compared with unmanipulated engineered MSCs. Moreover, engraftment and endothelial differentiation of these in vitro selected and enriched gene-modified marrow stromal cells was demonstrated by Matrigel assay in vivo. In conclusion, these findings outline the potential of human CD as an ex vivo selection and enrichment marker of genetically engineered MSCs for transgenic cell therapy applications.},
	Author = {Eliopoulos, N. and Al-Khaldi, A. and Beaus{\'e}jour, C. M. and Momparler, R. L. and Momparler, L. F. and Galipeau, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;Cytidine Deaminase;Humans;Animals;Cell Separation;Antimetabolites, Antineoplastic;Female;Neoplasms;Mice, Inbred C57BL;Retroviridae;11 Glia;Green Fluorescent Proteins;Genetic Vectors;Bone Marrow Cells;Cytarabine;Gene Therapy;Tumor Cells, Cultured;Mice;Drug Resistance;Biological Markers;Luminescent Proteins;Stromal Cells;Research Support, Non-U.S. Gov't},
	Medline = {21935229},
	Month = {4},
	Nlm_Id = {9421525},
	Number = {7},
	Organization = {Lady Davis Institute for Medical Research, Department of Experimental Medicine, McGill University, Montreal, Canada.},
	Pages = {452-62},
	Pubmed = {11938460},
	Title = {Human cytidine deaminase as an ex vivo drug selectable marker in gene-modified primary bone marrow stromal cells},
	Uuid = {4D3B7275-F873-4EB8-8E96-48B2CF717790},
	Volume = {9},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301675}}

@article{Elliot:1981,
	Abstract = {Nerve injury that severs axons also disrupts ensheathing glial cells. Specifically, crushing or cutting the leech nerve cord separates the glial cell's nucleated portion from an anucleate recording, by intracellular injection of Lucifer Yellow dye and horseradish peroxidase (HRP) as tracers, and by electron microscopy. The nucleated portion of the glial cell did not divide, degenerate, or grow appreciably. The severed glial stump remained isolated from the nucleated portion but maintained its resting potential and normal morphology for months. Stumps typically began to deteriorate after 3 months. Small macrophage-like cells, or 'microglia' increased in number after injury and ensheathed axons, thus partially replacing the atrophying glial stump. Some axons in the nerve cord degenerated; the remainder appeared morphologically and physiologically normal. Thus, both nucleated and anucleate glial segments persisted throughout the one to two months required for axons to regenerate functional connections. Glial cells in the leech are therefore available to guide physically the growing axons or to contribute in other ways to nerve regeneration.},
	Author = {Elliot, E. J. and Muller, K. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Research Support, Non-U.S. Gov't;Neuroglia;Nerve Regeneration;Microscopy, Electron;Research Support, U.S. Gov't, P.H.S.;Leeches;11 Glia;Immunoenzyme Techniques;Animals;24 Pubmed search results 2008;Axons},
	Medline = {82001443},
	Month = {8},
	Nlm_Id = {0045503},
	Number = {1-2},
	Pages = {99-113},
	Pubmed = {7023608},
	Title = {Long-term survival of glial segments during nerve regeneration in the leech},
	Uuid = {D70A0965-8D59-4AE2-A4EC-F5F375183090},
	Volume = {218},
	Year = {1981}}

@article{Elliott:2008,
	Abstract = {During embryonic development, large numbers of apoptotic cells are rapidly cleared by phagocytes. In this issue, Kurant et al. (2008) describe a new phagocytic receptor, called six-microns-under (SIMU), that promotes engulfment of apoptotic neurons by glial cells in the developing nervous system of Drosophila.},
	Author = {Elliott, Michael R. and Ravichandran, Kodi S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {Neuroglia;Central Nervous System;Membrane Proteins;Apoptosis;Drosophila Proteins;Drosophila;comment;Animals;Phagocytosis;Neurons;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {3},
	Organization = {Carter Immunology Center and the Department of Microbiology, University of Virginia, Charlottesville, VA 22908, USA.},
	Pages = {393-5},
	Pii = {S0092-8674(08)00505-9},
	Pubmed = {18455977},
	Title = {Death in the CNS: six-microns-under},
	Uuid = {73346BAF-FEA0-47BD-95FB-57CCB3663DA9},
	Volume = {133},
	Year = {2008},
	url = {papers/Elliott_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.04.014}}

@article{Elliott:2001,
	Abstract = {In various chemoconvulsant models of human temporal lobe epilepsy, the induction of epileptogenesis by a prolonged period of continuous seizure activity is accompanied by significant changes in hippocampal structure. These changes include an increase in neurogenesis within the proliferative subgranular zone (SGZ) of the dentate gyrus and induction of mossy fiber sprouting in mature dentate granule cells. As dentate granule cell neurogenesis and axon outgrowth are also hallmarks of hippocampal development, we hypothesized that molecules involved in normal development may also play a role in similar changes associated with epileptogenesis. To begin to test this hypothesis, we have analyzed the expression patterns of multiple members of the basic helix- loop-helix (bHLH) family of transcription factors in both normal and epileptic adult rats. bHLH protein expression has been found recently in dentate granule cells at specific developmental stages, and analysis of developmental models suggests specific neural differentiation functions for these molecules. We show that mRNA expression of all seven bHLH family members examined in this study, as well as the divergent homeobox protein Prox1, is present in the adult. Patterns of expression varied considerably between family members, ranging from the limited expression of Mash1 in the neurogenic SGZ of the dentate gyrus to the scattered, widespread profile of Hes5 throughout the dentate gyrus and the hippocampus proper. Moreover, these varied profiles of expression were differentially regulated following status epilepticus, with some increasing (Mash1, Id2), some falling (Hes5, Prox1), and others remaining mostly unchanged (NeuroD/BETA2, NeuroD2/NDRF, Id3, Rath2/Nex1).While the function of these molecules in the adult brain remains to be characterized, our findings support the idea that molecules controlling cell-fate decisions in the developing dentate gyrus are also operative during seizure-induced neurogenesis and plasticity. Using Smart Source Parsing},
	Author = {Elliott, R. C. and Khademi, S. and Pleasure, S. J. and Parent, J. M. and Lowenstein, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Neuroscience},
	Keywords = {Epilepsy, Temporal Lobe/*genetics/metabolism/physiopathology;Neuropeptides/genetics;DNA-Binding Proteins/genetics;RNA, Messenger/*metabolism;Gene Expression Regulation/*physiology;Rats;Muscarinic Agonists/pharmacology;Neuronal Plasticity/physiology;Helminth Proteins/genetics;Repressor Proteins/genetics;Status Epilepticus/*genetics/metabolism/physiopathology;Animal;Rats, Sprague-Dawley;Nerve Tissue Proteins/genetics;C abstr;Male;Transcription Factors/*genetics;Dentate Gyrus/*metabolism/pathology/physiopathology;Pilocarpine/pharmacology;Annexins/genetics;Homeodomain Proteins/genetics;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Bromodeoxyuridine/pharmacokinetics;Helix-Loop-Helix Motifs/*physiology},
	Number = {1},
	Organization = {Program in Brain Plasticity and Epilepsy, Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA.},
	Pages = {79-88},
	Title = {Differential regulation of basic helix-loop-helix mRNAs in the dentate gyrus following status epilepticus},
	Uuid = {6A812D74-81A7-4FC8-80A3-035878E0551A},
	Volume = {106},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11564418}}

@article{Emerman:2006,
	Author = {Emerman, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {7505876},
	Number = {14},
	Organization = {Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.},
	Pages = {5249-50},
	Pii = {0601373103},
	Pubmed = {16567650},
	Title = {How TRIM5\{alpha\}defends against retroviral invasions},
	Uuid = {22C64505-DC86-4B54-A851-40AF2FC4D659},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0601373103}}

@article{Emery:1987,
	Abstract = {Cultured mouse spinal neurons were fixed at three different intervals after dendrite amputation: within the first 15 min, at 2 h and at 24 h. Dendrites were amputated at lesion distance of either 50 microns (31\%probability of cell survival) or 100 microns (53\%probability of cell survival) from the edge of their perikarya. When fixed within 15 min, operated neurons showed a two-phase gradient of ultrastructural damage which spread from the transection site towards the perikaryon. At 2 h after dendrite amputation all neurons operated close to their perikarya were categorized as either viable, moribund or dead, based on their appearance with phase contrast microscopy. These categories of response to physical trauma corresponded to distinctly different ultrastructural changes. Moribund neurons were filled with membrane-bound vesicles which were derived from swollen mitochondria and grossly dilated cisternae of the smooth endoplasmic reticulum. The cytoplasm of dead neurons contained large clear areas and many condensed, dark mitochondria. Both moribund and dead neurons lacked cytoskeletal elements. All of these ultrastructural changes are hypothesized to be the result of an increase in the intracellular concentrations of free calcium. Although evidence of residual mitochondrial swelling was present in some surviving neurons at 24 h, the ultrastructure of others was comparable to that of control cells. Some surviving neurons had terminal swellings at the ends of the severed neurites which were very similar to retraction balls of transected axons after CNS trauma.},
	Author = {Emery, D. G. and Lucas, J. H. and Gross, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0014-4819},
	Journal = {Exp Brain Res},
	Keywords = {G;10 Development;Cell Survival;Nerve Degeneration;Animals;Cells, Cultured;Lasers;10 Structural plasticity;11 Glia;Get paper from library;Time Factors;Spinal Cord;Dendrites;Research Support, U.S. Gov't, P.H.S.;Neurons;Mice;Microscopy, Electron;24 Pubmed search results 2008},
	Medline = {87304679},
	Nlm_Id = {0043312},
	Number = {1},
	Pages = {41-51},
	Pubmed = {3622681},
	Title = {The sequence of ultrastructural changes in cultured neurons after dendrite transection},
	Uuid = {6E1737C2-EA48-4EB8-BCB9-E4E780E971AD},
	Volume = {67},
	Year = {1987}}

@article{Emsley:2004a,
	Author = {Emsley, Jason G. and Arlotta, Paola and Macklis, Jeffrey D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Neurons;Glial Fibrillary Acidic Protein;Central Nervous System;17 Transplant Regeneration;Wound Healing;Nerve Regeneration;Astrocytes;11 Glia;review, tutorial;Cells, Cultured;Animals;Vimentin;review},
	Month = {5},
	Nlm_Id = {7808616},
	Number = {5},
	Organization = {MGH-HMS Center for Nervous System Repair, Departments of Neurosurgery and Neurology, and Program in Neuroscience, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.},
	Pages = {238-40},
	Pii = {S0166223604000657},
	Pubmed = {15111002},
	Title = {Star-cross'd neurons: astroglial effects on neural repair in the adult mammalian CNS},
	Uuid = {F93781DE-26A1-4F84-95C2-A3D3FFF0C99C},
	Volume = {27},
	Year = {2004},
	url = {papers/Emsley_TrendsNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tins.2004.02.008}}

@article{Englund:2002,
	Abstract = {Here we examined the ability of human neural progenitors from the embryonic forebrain, expanded for up to a year in culture in the presence of growth factors, to respond to environmental signals provided by the developing rat brain. After survival times of up to more than a year after transplantation into the striatum, the hippocampus, and the subventricular zone, the cells were analyzed using human-specific antisera and the reporter gene green fluorescent protein (GFP). From grafts implanted in the striatum, the cells migrated extensively, especially within white matter structures. Neuronal differentiation was most pronounced at the striatal graft core, with axonal projections extending caudally along the internal capsule into mesencephalon. In the hippocampus, cells migrated throughout the entire hippocampal formation and into adjacent white matter tracts, with differentiation into neurons both in the dentate gyrus and in the CA1-3 regions. Directed migration along the rostral migratory stream to the olfactory bulb and differentiation into granule cells were observed after implantation into the subventricular zone. Glial differentiation occurred at all three graft sites, predominantly at the injection sites, but also among the migrating cells. A lentiviral vector was used to transduce the cells with the GFP gene prior to grafting. The reporter gene was expressed for at least 15 weeks and the distribution of the gene product throughout the entire cytoplasmic compartment of the expressing cells allowed for a detailed morphological analysis of a portion of the grafted cells. The extensive integration and differentiation of in vitro-expanded human neural progenitor cells indicate that multipotent progenitors are capable of responding in a regionally specific manner to cues present in the developing rat brain. 0014-4886 Journal Article},
	Author = {Englund, U. and Fricker-Gates, R. A. and Lundberg, C. and Bjorklund, A. and Wictorin, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {Exp Neurol},
	Keywords = {Human;Animals;Neuroglia/cytology/metabolism/ultrastructure;Rats;Cell Movement/*physiology;*Fetal Tissue Transplantation;*Stem Cell Transplantation;J pdf;Cell Count;Corpus Striatum/cytology/metabolism;15 Retrovirus mechanism;Lateral Ventricles/cytology/metabolism;*Axons/ultrastructure;Rats, Sprague-Dawley;Cell Differentiation/*physiology;Cell Line;Animals, Newborn;Stem Cells/cytology/metabolism;Support, Non-U.S. Gov't;Prosencephalon/cytology/embryology/transplantation;Hippocampus/cytology/metabolism;Genes, Reporter;Neurons/cytology/metabolism/ultrastructure;Graft Survival;*Brain Tissue Transplantation;Luminescent Proteins/biosynthesis/genetics},
	Number = {1},
	Organization = {Wallenberg Neuroscience Center, Division of Neurobiology, Lund University, S-221 84 Lund, Sweden.},
	Pages = {1-21},
	Title = {Transplantation of human neural progenitor cells into the neonatal rat brain: extensive migration and differentiation with long-distance axonal projections},
	Uuid = {1F8EB7E3-E335-46E3-81E8-3B971DC928BB},
	Volume = {173},
	Year = {2002},
	url = {papers/Englund_ExpNeurol2002}}

@article{Englund:2000,
	Abstract = {A major obstacle in ex vivo gene transfer has been the loss of transgene expression soon after implantation of the grafted transduced cells. Recently, a lentiviral vector system has been developed which has proven to express high levels of transgenes in vivo after direct injection into the tissue. In this study, we have investigated the use of such a vector for ex vivo gene transfer to the brain. A number of neural cell types were found to be permissive to transduction by the lentiviral vector in vitro and a majority of them expressed the transgene after transplantation to the rat brain. Transgene expression was detected up to 8 weeks post-grafting. These findings suggest that recombinant lentiviral vectors may be used for further development of ex vivo gene therapy protocols to the CNS. 0959-4965 Journal Article},
	Author = {Englund, U. and Ericson, C. and Rosenblad, C. and Mandel, R. J. and Trono, D. and Wictorin, K. and Lundberg, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Issn = {0959-4965},
	Journal = {Neuroreport},
	Keywords = {Cell Differentiation;Gene Therapy/trends;Cells, Cultured/cytology/metabolism/transplantation;Genetic Vectors;Green Fluorescent Proteins;Luminescent Proteins;Gene Therapy;Transduction, Genetic;Stem Cells/cytology/metabolism;Animals;*Gene Transfer Techniques;DNA, Recombinant;Brain;Cells, Cultured;Stem Cell Transplantation;Transgenes;Brain Tissue Transplantation;15 Retrovirus mechanism;Genetic Vectors/*genetics;Gene Expression Regulation, Viral/physiology;11 Glia;Luminescent Proteins/genetics;Brain/*virology;Gene Expression Regulation, Viral;DNA, Recombinant/genetics;Gene Transfer Techniques;Rats;Cell Differentiation/genetics;J;Stem Cells;Mice;Lentivirus/*genetics;Research Support, Non-U.S. Gov't;Lentivirus;Humans;Transgenes/*genetics;Human;Support, Non-U.S. Gov't},
	Medline = {21033203},
	Month = {12},
	Nlm_Id = {9100935},
	Number = {18},
	Organization = {Wallenberg Neuroscience Center, Division of Neurobiology, Lund University, Sweden.},
	Pages = {3973-7},
	Pubmed = {11192612},
	Title = {The use of a recombinant lentiviral vector for ex vivo gene transfer into the rat CNS},
	Uuid = {44C3494F-9934-46CD-B342-F65CB34AFC6B},
	Volume = {11},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11192612}}

@article{Englund:2002a,
	Abstract = {In vitro expanded neural stemprogenitor cells can undergo region-specific differentiation after transplantation to the developing or adult brain, and display morphologies and markers characteristic of mature neurons. Here we have used patch-clamp techniques to explore whether grafted stem cells also can develop physiological properties of mature neurons and become functionally integrated within host neural circuitry. The immortalized neural progenitor cell line, RN33B, prelabeled with GFP by using a lentiviral vector, was transplanted into the cortex or hippocampus of neonatal rats. We found that the grafted GFP-positive cells differentiated into cells with morphological features of cortical or hippocampal pyramidal neurons, and that many of them had established appropriate cortico-thalamic and contralateral hippocampal connections, respectively, as revealed by retrograde tracing. Whole-cell patch-clamp recordings from grafted cells with morphological characteristics of pyramidal neurons showed that they were able to generate action potentials, and received functional excitatory and inhibitory synaptic inputs from neighboring cells. These data provide evidence that grafted neural progenitors can differentiate into morphologically mature pyramidal projection neurons, establish appropriate long-distance axonal projections, exhibit normal electrophysiological properties, and become functionally integrated into host cortical circuitry.},
	Author = {Englund, Ulrica and Bjorklund, Anders and Wictorin, Klas and Lindvall, Olle and Kokaia, Merab},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Stem Cell Transplantation;Synapses;Cell Differentiation;Rats;Action Potentials;Pyramidal Cells;Cell Line;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Hippocampus;22 Stem cells;gamma-Aminobutyric Acid;Receptors, N-Methyl-D-Aspartate;Animals;Cerebral Cortex;Neurons;Axons},
	Medline = {22388235},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {26},
	Organization = {Sections of Neurobiology and Restorative Neurology, Wallenberg Neuroscience Center, BMC A-11, Lund University, S-221 84 Lund, Sweden Europe.},
	Pages = {17089-94},
	Pii = {252589099},
	Pubmed = {12471158},
	Title = {Grafted neural stem cells develop into functional pyramidal neurons and integrate into host cortical circuitry},
	Uuid = {4C875399-689E-4696-BF25-AF9CB57ECDBF},
	Volume = {99},
	Year = {2002},
	url = {papers/Englund_ProcNatlAcadSciUSA2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.252589099}}

@article{Engstrom:2001,
	Abstract = {An iron induced model of posttraumatic chronic focal epilepsy in rats was studied with respect to extracellular amino acids, electrophysiology, and morphology, approx. 6 months after intracortical injection of ferrous chloride. Twenty-six of the twenty-eight (93\%) rats developed spontaneous epileptiform EEG-activity and electrical cortical stimulation done in eight animals evoked seizure activity in five animals (62.5\%). Epileptic brain tissue displayed significantly higher extracellular interictal levels of aspartate (ASP), compared to normal brain, measured with intracerebral microdialysis. The interictal levels of serine (SER) were significantly higher at the lesion side compared to the contralateral cortex in epileptic animals. Spontaneous elevations of ASP and glutamate (GLU) levels up to 8 times the basal level were found in 4/5 (80\%). There was no consistent amino acid pattern following the electrically induced seizures, but in association with more intense seizure activity ASP and GLU were elevated. Histopathologically, the necrotic lesions in the cortex contained small vessels and iron pigment loaded astrocytes. Scattered eosinophilic neurons were found in the hippocampus, bilaterally in 37\%of the animals. The results show that a focal epileptiform activity developed in a high percentage of animals that received an intracortical iron injection. The observed amino acid changes in epileptic animals may be involved in the development of seizures in this model of posttraumatic epilepsy.},
	Author = {Engstr{\"o}m, E. R. and Hillered, L. and Flink, R. and Kihlstr{\"o}m, L. and Lindquist, C. and Nie, J. X. and Olsson, Y. and Silander, H. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0920-1211},
	Journal = {Epilepsy Res},
	Keywords = {Animals;Craniocerebral Trauma;Serine;Rats;Glutamic Acid;Brain;21 Epilepsy;Aspartic Acid;Epilepsy;Extracellular Space;Rats, Sprague-Dawley;Amino Acids;Male;Microdialysis;Cerebral Cortex;21 Neurophysiology;Ferrous Compounds;24 Pubmed search results 2008;Injections;Electroencephalography;Research Support, Non-U.S. Gov't},
	Medline = {21099206},
	Month = {2},
	Nlm_Id = {8703089},
	Number = {2},
	Organization = {Department of Neurosurgery, Uppsala University Hospital, S-751-85, Uppsala, Sweden. elisabeth.ronne-engstrom\@nc.uas.lul.se},
	Pages = {135-44},
	Pii = {S0920121100001911},
	Pubmed = {11164702},
	Title = {Extracellular amino acid levels measured with intracerebral microdialysis in the model of posttraumatic epilepsy induced by intracortical iron injection},
	Uuid = {53BACC36-5EB3-430D-BFE8-91E0CE3C5DBD},
	Volume = {43},
	Year = {2001}}

@article{Ennis:2001,
	Abstract = {Olfactory receptor neurons of the nasal epithelium project via the olfactory nerve (ON) to the glomeruli of the main olfactory bulb, where they form glutamatergic synapses with the apical dendrites of mitral and tufted cells, the output cells of the olfactory bulb, and with juxtaglomerular interneurons. The glomerular layer contains one of the largest population of dopamine (DA) neurons in the brain, and DA in the olfactory bulb is found exclusively in juxtaglomerular neurons. D2 receptors, the predominant DA receptor subtype in the olfactory bulb, are found in the ON and glomerular layers, and are present on ON terminals. In the present study, field potential and single-unit recordings, as well as whole cell patch-clamp techniques, were used to investigate the role of DA and D2 receptors in glomerular synaptic processing in rat and mouse olfactory bulb slices. DA and D2 receptor agonists reduced ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells. Spontaneous and ON-evoked spiking of mitral cells was also reduced by DA and D2 agonists, and enhanced by D2 antagonists. DA did not produce measurable postsynaptic changes in juxtaglomerular cells, nor did it alter their responses to mitral/tufted cell inputs. DA also reduced 1) paired-pulse depression of ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells and 2) the amplitude and frequency of spontaneous, but not miniature, excitatory postsynaptic currents in juxtaglomerular cells. Taken together, these findings are consistent with the hypothesis that activation of D2 receptors presynaptically inhibits ON terminals. DA and D2 agonists had no effect in D2 receptor knockout mice, suggesting that D2 receptors are the only type of DA receptors that affect signal transmission from the ON to the rodent olfactory bulb.},
	Author = {Ennis, M. and Zhou, F. M. and Ciombor, K. J. and Aroniadou-Anderjaska, V. and Hayar, A. and Borrelli, E. and Zimmer, L. A. and Margolis, F. and Shipley, M. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {J Neurophysiol},
	Keywords = {Olfactory Nerve/*physiology;Olfactory Receptor Neurons/*physiology;Receptors, Presynaptic/*physiology;Olfactory Bulb/cytology/physiology;In Vitro;Electrophysiology;Rats;13 Olfactory bulb anatomy;Patch-Clamp Techniques;Animal;Excitatory Postsynaptic Potentials/physiology;Mice, Inbred C57BL;Male;Support, Non-U.S. Gov't;Extracellular Space/physiology;Receptors, Dopamine D2/genetics/*physiology;Synaptic Transmission/physiology;Mice, Knockout;Support, U.S. Gov't, P.H.S.;Nerve Endings/*physiology;I pdf;Mice},
	Number = {6},
	Organization = {Department of Anatomy and Neurobiology and Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. mennis\@umaryland.edu},
	Pages = {2986-97.},
	Title = {Dopamine D2 receptor-mediated presynaptic inhibition of olfactory nerve terminals},
	Uuid = {2D82F0DC-8D85-4D0B-ADEF-955A80999859},
	Volume = {86},
	Year = {2001},
	url = {papers/Ennis_JNeurophysiol2001}}

@article{Epperly:2003,
	Abstract = {There is a rapid onset of organizing alveolitis/fibrosis at 120-140 d after whole lung irradiation of C57BL/6J mice. To test the hypothesis that circulating cells of bone marrow origin contribute to irradiation fibrosis, irradiated chimeric green fluorescent protein (GFP)+ C57BL/6J mice were followed for GFP+ cells in areas of lung fibrosis. In a second experimental model, C57BL/6J female mice received 20 Gy total lung irradiation, and after 60 or 80 d were intravenously injected with cells from a clonal GFP+ male bone marrow stromal cell line or male GFP+ whole bone marrow, respectively. The mice were then followed for the development of pulmonary fibrosis, and the contribution of Y-probe-positive, GFP+ cells to fibrotic areas was quantitated. Bromodeoxyuridine labeling of developing fibrotic areas showed that the cell division occurred predominantly in GFP+, Y-probe-positive, and vimentin-positive cells. Immunohistochemistry demonstrated that these cells were macrophages and fibroblasts, not endothelial cells. Mice that received manganese superoxide dismutase-plasmid/liposome intratracheal injection 24 h before total lung irradiation demonstrated a decrease in GFP+ fibroblastic cells in the lung. Thus, pulmonary irradiation fibrosis contains proliferating cells of bone marrow origin, and gene therapy prevention of this condition acts in part by decreasing the migration and proliferation of marrow origin cells.},
	Author = {Epperly, Michael W. and Guo, Hongliang and Gretton, Joan E. and Greenberger, Joel S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1044-1549},
	Journal = {Am J Respir Cell Mol Biol},
	Keywords = {Animals;Macrophages;Fibroblasts;Myocardium;Female;Superoxide Dismutase;Mice, Transgenic;Fibrosis;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Male;Time Factors;Microscopy, Fluorescence;Cell Line;Pulmonary Fibrosis;Research Support, U.S. Gov't, P.H.S.;Bone Marrow Cells;Bone Marrow;In Situ Hybridization;Mice;Cell Division;Y Chromosome;Luminescent Proteins;Immunohistochemistry;Bromodeoxyuridine;Lung},
	Medline = {22760085},
	Month = {8},
	Nlm_Id = {8917225},
	Number = {2},
	Organization = {Department of Radiation Oncology, University of Pittsburgh Cancer Institute, PA, USA.},
	Pages = {213-24},
	Pii = {2002-0069OC},
	Pubmed = {12649121},
	Title = {Bone marrow origin of myofibroblasts in irradiation pulmonary fibrosis},
	Uuid = {429B97FE-3653-459C-9393-3E96AA740D4C},
	Volume = {29},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1165/rcmb.2002-0069OC}}

@article{Eriksson:1998,
	Abstract = {The genesis of new cells, including neurons, in the adult human brain has not yet been demonstrated. This study was undertaken to investigate whether neurogenesis occurs in the adult human brain, in regions previously identified as neurogenic in adult rodents and monkeys. Human brain tissue was obtained postmortem from patients who had been treated with the thymidine analog, bromodeoxyuridine (BrdU), that labels DNA during the S phase. Using immunofluorescent labeling for BrdU and for one of the neuronal markers, NeuN, calbindin or neuron specific enolase (NSE), we demonstrate that new neurons, as defined by these markers, are generated from dividing progenitor cells in the dentate gyrus of adult humans. Our results further indicate that the human hippocampus retains its ability to generate neurons throughout life.},
	Author = {Eriksson, P. S. and Perfilieva, E. and Bjork-Eriksson, T. and Alborn, A. M. and Nordborg, C. and Peterson, D. A. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {Nat Med},
	Keywords = {Rodentia;Human;Neurons/cytology/pathology/*physiology;Stem Cells/cytology/pathology/physiology;Dentate Gyrus/cytology/pathology/*physiology;Animal;Glial Fibrillary Acidic Protein/analysis;Nerve Tissue Proteins/analysis;01 Adult neurogenesis general;DNA/biosynthesis;Calcium-Binding Protein, Vitamin D-Dependent/analysis;Haplorhini;Support, Non-U.S. Gov't;Hippocampus/cytology/pathology/*physiology;Adult;Support, U.S. Gov't, P.H.S.;*Nerve Regeneration;Phosphopyruvate Hydratase/analysis;Bromodeoxyuridine;Biological Markers/analysis;A-10;Astrocytes/cytology/pathology/physiology},
	Number = {11},
	Organization = {Department of Clinical Neuroscience, Institute of Neurology, Sahlgrenska University Hospital, Goteborg, Sweden.},
	Pages = {1313-7.},
	Title = {Neurogenesis in the adult human hippocampus},
	Uuid = {62B56769-CCDD-11D9-8C77-000D9346EC2A},
	Volume = {4},
	Year = {1998},
	url = {papers/Eriksson_NatMed1998.pdf}}

@article{Espinosa-Heidmann:2003,
	Abstract = {PURPOSE: The pathogenesis of choroidal neovascularization (CNV) is postulated to be driven by angiogenesis, a process in which the cellular components of the new vessel complex are derived from cells resident within an adjacent preexisting capillary. Recently, an alternative paradigm, termed postnatal vasculogenesis, has been shown to contribute to some forms of neovascularization. In vasculogenesis, the cellular components of the new vessel complex are derived from circulating vascular progenitors from bone marrow. In the current study, transplantation of green fluorescent protein (GFP)-labeled bone marrow and laser-induced CNV were combined to examine the contribution of vasculogenesis to the formation of CNV. METHODS: Ten adult C57BL/6 female mice were used as recipients for bone marrow transplantation. Bone marrow was obtained from three C57BL/6 female mice transgenic for the beta-actin promoter GFP. One month after bone marrow transplantation, CNV was induced in recipient mice by making four separate burns in the choroid of each eye with a red diode laser. Four weeks after CNV was induced, eyes of recipient mice were processed for immunohistochemistry to detect GFP and markers for vascular smooth muscle cells (alpha-smooth muscle actin, desmin, and NG2 chondroitin sulfate proteoglycan), endothelial cells (CD31, BS-1 lectin), or macrophages (F4/80). RESULTS: GFP-labeled cells represented 17\%of the total cell population in the lesion. Many of the GFP-labeled cells were immunoreactive for alpha-smooth muscle actin (39\%), desmin, NG2, CD31 (41\%), BS-1 lectin, or F4/80. GFP-labeled cells were morphologically indistinguishable from cells normally present in CNV lesions. CONCLUSIONS: This study is the first to demonstrate that bone marrow-derived progenitor cells are a source of endothelial and smooth musclelike cells in CNV.},
	Author = {Espinosa-Heidmann, Diego G. and Caicedo, Alejandro and Hernandez, Eleut P. and Csaky, Karl G. and Cousins, Scott W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0146-0404},
	Journal = {Invest Ophthalmol Vis Sci},
	Keywords = {Hematopoietic Stem Cells;Fluorescent Antibody Technique, Indirect;Animals;Proteoglycans;Antigens, Differentiation;Female;Indicators and Reagents;Choroidal Neovascularization;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Antigens, CD31;Hematopoietic Stem Cell Transplantation;Research Support, U.S. Gov't, P.H.S.;Antigens;Choroid;Mice;Muscle, Smooth, Vascular;Actins;Luminescent Proteins;Biological Markers;Laser Coagulation;Desmin;Endothelium, Vascular},
	Medline = {22939978},
	Month = {11},
	Nlm_Id = {7703701},
	Number = {11},
	Organization = {Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, Miami, Florida 33136, USA.},
	Pages = {4914-9},
	Pubmed = {14578417},
	Title = {Bone marrow-derived progenitor cells contribute to experimental choroidal neovascularization},
	Uuid = {3A53E54E-4F42-4719-833B-516285066994},
	Volume = {44},
	Year = {2003}}

@article{Estivill-Torrus:2002,
	Abstract = {In the proliferative zone of the developing cerebral cortex, multipotential progenitors predominate early in development and divide to increase the progenitor pool. As corticogenesis progresses, proportionately fewer progenitors are produced and, instead, cell divisions yield higher numbers of postmitotic neurones or glial cells. As the switch from the generation of progenitors to that of differentiated cells occurs, the orientation of cell division alters from predominantly symmetrical to predominantly asymmetrical. It has been hypothesised that symmetrical divisions expand the progenitor pool, whereas asymmetrical divisions generate postmitotic cells, although this remains to be proved. The molecular mechanisms regulating these processes are poorly understood. The transcription factor Pax6 is highly expressed in the cortical proliferative zone and there are morphological defects in the Pax6(Sey/Sey) (Pax6 null) cortex, but little is known about the principal cellular functions of Pax6 in this region. We have analysed the cell-cycle kinetics, the progenitor cleavage orientation and the onset of expression of differentiation markers in Pax6(Sey/Sey) cortical cells in vivo and in vitro. We showed that, early in corticogenesis at embryonic day (E) 12.5, the absence of Pax6 accelerated cortical development in vivo, shortening the cell cycle and the time taken for the onset of expression of neural-specific markers. This also occurred in dissociated culture of isolated cortical cells, indicating that the changes were intrinsic to the cortical cells. From E12.5 to E15.5, proportions of asymmetrical divisions increased more rapidly in mutant than in wild-type embryos. By E15.5, interkinetic nuclear migration during the cell cycle was disrupted and the length of the cell cycle was significantly longer than normal in the Pax6(Sey/Sey) cortex, with a lengthening of S phase. Together, these results show that Pax6 is required in developing cortical progenitors to control the cell-cycle duration, the rate of progression from symmetrical to asymmetrical division and the onset of expression of neural-specific markers. 0950-1991 Journal Article},
	Author = {Estivill-Torrus, G. and Pearson, H. and van Heyningen, V. and Price, D. J. and Rashbass, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Development},
	Keywords = {Pregnancy;10 Development;Animals;Stem Cells/cytology/*physiology;Cells, Cultured;Cell Cycle/physiology;Female;Homeodomain Proteins/*metabolism;Mice, Transgenic;Cerebral Cortex/cytology/*embryology/growth &development;Cell Differentiation/*physiology;Support, Non-U.S. Gov't;Neuroglia/physiology;Cell Division/*physiology;Transcription Factors/*metabolism;Cell Size;Nerve Tissue Proteins/metabolism;Mice;Immunohistochemistry;Biological Markers;Neurons/physiology;F},
	Number = {2},
	Organization = {Department of Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK.},
	Pages = {455-66},
	Pubmed = {11807037},
	Title = {Pax6 is required to regulate the cell cycle and the rate of progression from symmetrical to asymmetrical division in mammalian cortical progenitors},
	Uuid = {141767D5-B5F4-4825-B349-FED10063DB1B},
	Volume = {129},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11807037}}

@article{Estivill-Torrus:2007,
	Abstract = {Lysophosphatidic acid (LPA) is a simple phospholipid with extracellular signaling properties mediated by specific G protein-coupled receptors. At least 2 LPA receptors, LPA(1) and LPA(2), are expressed in the developing brain, the former enriched in the neurogenic ventricular zone (VZ), suggesting a normal role in neurogenesis. Despite numerous studies reporting the effects of exogenous LPA using in vitro neural models, the first LPA(1) loss-of-function mutants reported did not show gross cerebral cortical defects in the 50\%that survived perinatal demise. Here, we report a role for LPA(1) in cortical neural precursors resulting from analysis of a variant of a previously characterized LPA(1)-null mutant that arose spontaneously during colony expansion. These LPA(1)-null mice, termed maLPA(1), exhibit almost complete perinatal viability and show a reduced VZ, altered neuronal markers, and increased cortical cell death that results in a loss of cortical layer cellularity in adults. These data support LPA(1) function in normal cortical development and suggest that the presence of genetic modifiers of LPA(1) influences cerebral cortical development.},
	Author = {Estivill-Torr{\'u}s, and Llebrez-Zayas, and Matas-Rico, and Sant{\'\i}n, and Pedraza, and De Diego, and Del Arco, and Fern{\'a}ndez-Llebrez, and Chun, and De Fonseca,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {9110718},
	Organization = {Unidad de Investigaci{\'o}n, Fundaci{\'o}n IMABIS, Hospital Carlos Haya, E-29010 M{\'a}laga, Spain.},
	Pii = {bhm132},
	Pubmed = {17656621},
	Title = {Absence of LPA1 Signaling Results in Defective Cortical Development},
	Uuid = {F1577208-B96D-4828-A0D0-D894819E6DFF},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhm132}}

@article{Eugenin:2006,
	Abstract = {Encephalitis and dementia associated with acquired immunodeficiency syndrome (AIDS) are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, blood-brain barrier (BBB) disruption, and eventual loss of neurons. Little is known about whether human immunodeficiency virus 1 (HIV-1) infection of leukocytes affects their ability to transmigrate in response to chemokines and to alter BBB integrity. We now demonstrate that HIV infection of human leukocytes results in their increased transmigration across our tissue culture model of the human BBB in response to the chemokine CCL2, as well as in disruption of the BBB, as evidenced by enhanced permeability, reduction of tight junction proteins, and expression of matrix metalloproteinases (MMP)-2 and MMP-9. HIV-infected cells added to our model did not transmigrate in the absence of CCL2, nor did this condition alter BBB integrity. The chemokines CXCL10/interferon-gamma-inducible protein of 10 kDa, CCL3/macrophage inflammatory protein-1alpha, or CCL5/RANTES (regulated on activation normal T-cell expressed and secreted) did not enhance HIV-infected leukocyte transmigration or BBB permeability. The increased capacity of HIV-infected leukocytes to transmigrate in response to CCL2 correlated with their increased expression of CCR2, the chemokine receptor for CCL2. These data suggest that CCL2, but not other chemokines, plays a key role in infiltration of HIV-infected leukocytes into the CNS and the subsequent pathology characteristic of NeuroAIDS.},
	Author = {Eugenin, Eliseo A. and Osiecki, Kristin and Lopez, Lillie and Goldstein, Harris and Calderon, Tina M. and Berman, Joan W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {4},
	Organization = {Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.},
	Pages = {1098-106},
	Pii = {26/4/1098},
	Pubmed = {16436595},
	Title = {CCL2/monocyte chemoattractant protein-1 mediates enhanced transmigration of human immunodeficiency virus (HIV)-infected leukocytes across the blood-brain barrier: a potential mechanism of HIV-CNS invasion and NeuroAIDS},
	Uuid = {4C30E377-CB8B-4604-9218-9A7C4EDEA585},
	Volume = {26},
	Year = {2006},
	url = {papers/Eugenin_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3863-05.2006}}

@article{Ever:2005,
	Abstract = {Cells with radial morphology in the developing brain were first identified more than 100 years ago. These cells, later termed radial glia, have been studied primarily as migratory scaffolds and glial progenitors. However, it has become increasingly clear, on the basis of in vitro studies and more recent in vivo fate mapping experiments, that radial glia also generate neurons during embryonic development. Now the challenge will be to understand the signaling events that regulate the spatial and temporal heterogeneity of these cells and their developmental potential. Recent work has identified the Notch, ErbB, and fibroblast growth factor signaling pathways as central to the regulation of radial 'glial' progenitors.},
	Author = {Ever, Leah and Gaiano, Nicholas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.},
	Pages = {29-33},
	Pii = {S0959-4388(05)00006-1},
	Pubmed = {15721741},
	Title = {Radial 'glial' progenitors: neurogenesis and signaling},
	Uuid = {2E7D982F-150A-488F-921E-FDB861E3C4C6},
	Volume = {15},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.01.005}}

@article{Everhart:2005,
	Abstract = {To facilitate study of alveolar macrophages in vivo, we developed a method to rapidly and efficiently replace resident alveolar macrophages with macrophages of a different (donor) genotype. Chimeric mice were generated by lethal irradiation followed by fetal liver transplantation (FLT) using green fluorescent protein (GFP) transgenic reporter mice as donors. Kinetics of peripheral blood monocyte (PBM) and alveolar macrophage reconstitution was determined 4 and 10 weeks post-FLT by quantifying the percentage of GFP+ cells. To enhance the recruitment of donor monocytes into the lung after FLT, mice were treated with intratracheal administration of liposomal clodronate to deplete host alveolar macrophages at 6 weeks post-FLT. PBM reconstitution occurred by 4 weeks after FLT (85.7+/-1.6\%of CD11b+/Gr-1+ monocytes were GFP+), and minimal alveolar macrophage repopulation was observed (9.5\%GFP+). By 10 weeks following FLT, 48\%of alveolar macrophages were GFP+ by immunostaining of macrophages on lung tissue sections, and 55.1 +/- 1.6\%of lung lavage macrophages were GFP+ by fluorescein-activated cell sorter analysis. Clodronate treatment resulted in a significant increase in GFP+ alveolar macrophages 10 weeks after FLT. By immunostaining, 90\%of macrophages were GFP+ on lung tissue sections and 87.5 +/- 1.1\%GFP+ in lung lavage (compared with GFP-transgenic controls). The ability of newly recruited alveolar macrophages to clear Pseudomonas aeruginosa and activate nuclear factor-kappaB in response to Eschericia coli lipopolysaccharide demonstrated normal macrophage function. Optimizing this methodology provides an important tool for the study of specific genes and their contribution to alveolar macrophage function in vivo.},
	Author = {Everhart, M. Brett and Han, Wei and Parman, Kelly S. and Polosukhin, Vasiliy V. and Zeng, Heng and Sadikot, Ruxana T. and Li, Bo and Yull, Fiona E. and Christman, John W. and Blackwell, Timothy S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0741-5400},
	Journal = {J Leukoc Biol},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {8405628},
	Number = {2},
	Organization = {Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2650, USA.},
	Pages = {173-80},
	Pii = {jlb.1203647},
	Pubmed = {15563581},
	Title = {Intratracheal administration of liposomal clodronate accelerates alveolar macrophage reconstitution following fetal liver transplantation},
	Uuid = {380CDFE2-6F4E-4389-991D-39256CE322C6},
	Volume = {77},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1189/jlb.1203647}}

@article{Eyupoglu:2003,
	Abstract = {Primary neuronal destruction in the central nervous system triggers rapid changes in glial morphology and function, after which activated glial cells contribute to secondary neuronal changes. Here we show that, after entorhinal cortex lesion, activation of microglia, but not other glial cells, leads to massive secondary dendritic changes of deafferentiated hippocampal neurons. Blocking of microglial activation in vivo reduced this secondary neuronal damage and enhanced regenerative axonal sprouting. In contrast, abolishing astrocytes or oligodendroglia did not result in specific neuronal changes. Furthermore, primary damage leads to an interleukin 1beta up-regulation, which is attenuated by the immuno-modulator transforming growth factor beta1, whereas tumor necrosis factor alpha is not affected. Modification of microglial activity following denervation of the hippocampus protects neurons from secondary dendritic alterations and therefore enables their reinnervation. These data render activated microglia a putative therapeutic target during the course of axonal degeneration.},
	Author = {Ey{\"u}poglu, Ilker Y. and Bechmann, Ingo and Nitsch, Robert},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {Dendrites;Cytokines;Rats;Hippocampus;Nerve Regeneration;Anti-Inflammatory Agents;Denervation;Cell Survival;11 Glia;Microglia;Transforming Growth Factor beta;Animals;Neurons;Axons},
	Medline = {22658121},
	Month = {6},
	Nlm_Id = {8804484},
	Number = {9},
	Organization = {Institute of Anatomy, Department of Cell and Neurobiology, Humboldt University Hospital (Charit{\'e}), 10098 Berlin, Germany. robert.nitsch\@charite.de},
	Pages = {1110-1},
	Pii = {02-0825fje},
	Pubmed = {12692086},
	Title = {Modification of microglia function protects from lesion-induced neuronal alterations and promotes sprouting in the hippocampus},
	Uuid = {D91C5624-C402-4F66-AFB3-079CE93905EE},
	Volume = {17},
	Year = {2003},
	url = {papers/Eyüpoglu_FASEBJ2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.02-0825fje}}

@article{Fabel:2003,
	Abstract = {Declining learning and memory function is associated with the attenuation of adult hippocampal neurogenesis. As in humans, chronic stress or depression in animals is accompanied by hippocampal dysfunction, and neurogenesis is correspondingly down regulated, in part, by the activity of the hypothalamic-pituitary-adrenal axis as well as glutamatergic and serotonergic networks. Antidepressants can reverse this effect over time but one of the most clinically effective moderators of stress or depression and robust stimulators of neurogenesis is simple voluntary physical exercise such as running. Curiously, running also elevates circulating stress hormone levels yet neurogenesis is doubled in running animals. In evaluating the signalling that running provides to the central nervous system in mice, we have found that peripheral vascular endothelial growth factor (VEGF) is necessary for the effects of running on adult hippocampal neurogenesis. Peripheral blockade of VEGF abolished running-induced neurogenesis but had no detectable effect on baseline neurogenesis in non-running animals. These data suggest that VEGF is an important element of a 'somatic regulator'of adult neurogenesis and that these somatic signalling networks can function independently of the central regulatory networks that are typically considered in the context of hippocampal neurogenesis. 0953-816x Journal Article},
	Author = {Fabel, K. and Tam, B. and Kaufer, D. and Baiker, A. and Simmons, N. and Kuo, C. J. and Palmer, T. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Bromodeoxyuridine/pharmacokinetics;Extracellular Matrix Proteins/pharmacology;Immunohistochemistry;Male;Mitotic Index/methods;Vascular Endothelial Growth Factor Receptor-2/metabolism;Animals;Blotting, Northern;Vascular Endothelial Growth Factor A/immunology/*physiology;04 Adult neurogenesis factors;Hippocampus/cytology/drug effects/metabolism/*physiology;Cell Count;Stem Cells/metabolism;Mice, Inbred C57BL;Tubulin/metabolism;Behavior, Animal;Support, U.S. Gov't, P.H.S.;Rats, Inbred F344;Comparative Study;Genistein/pharmacology;Running;C pdf;Enzyme Inhibitors/pharmacology;Rats;Dose-Response Relationship, Drug;Enzyme-Linked Immunosorbent Assay;Neurons/drug effects/*physiology;Microscopy, Confocal;Support, Non-U.S. Gov't;Mice;Physical Conditioning, Animal/*physiology;Reverse Transcriptase Polymerase Chain Reaction;Neuropilins/metabolism},
	Number = {10},
	Organization = {Department of Neurosurgery, Mail Code 5487, MSLS P309, 1201 Welch Rd, Stanford University, Stanford, CA 94305-5487, USA.},
	Pages = {2803-12},
	Pubmed = {14656329},
	Title = {VEGF is necessary for exercise-induced adult hippocampal neurogenesis},
	Uuid = {8BF9D87D-B88E-41E5-B025-400F7A76477A},
	Volume = {18},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14656329}}

@article{Fainzilber:2006,
	Abstract = {Wallerian degeneration of distal axons after nerve injury is significantly delayed in the Wlds mutant mouse. The Wlds protein is a fusion of nicotinamide mononucleotide adenyltransferase-1 (Nmnat1), an essential enzyme in the biosynthesis pathway of nicotinamide adenine dinucleotide (NAD), with the N-terminal 70 amino acids of the Ube4b ubiquitination assembly factor. The mechanism of Wlds action is still enigmatic, although recent efforts suggest that it is indirect and requires sequences flanking or linking the two fused open reading frames. Three papers in this issue of Neuron now show that Wlds action is conserved in Drosophila and that a critical role of Wlds may be the suppression of axonal self-destruct signals that induce Draper-mediated clearance of damaged axons by glial cells.},
	Author = {Fainzilber, Mike and Twiss, Jeffery L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;research support, n.i.h., extramural ;Wallerian Degeneration;Membrane Proteins;research support, non-u.s. gov't ;Drosophila Proteins;Nerve Tissue Proteins;Nicotinamide-Nucleotide Adenylyltransferase;research support, u.s. gov't, non-p.h.s. ;comment;Sirtuins;Animals;Humans;10 Structural plasticity;review;24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Biological Chemistry, Weizmann Institute of Science, 76100 Rehovot, Israel. mike.fainzilber\@weizmann.ac.il},
	Pages = {819-21},
	Pii = {S0896-6273(06)00416-8},
	Pubmed = {16772165},
	Title = {Tracking in the Wlds--the hunting of the SIRT and the luring of the Draper},
	Uuid = {B6084E8E-E738-4AAF-85A0-977A0EE98C35},
	Volume = {50},
	Year = {2006},
	url = {papers/Fainzilber_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.05.023}}

@article{Fallon:2000,
	Abstract = {The development of an in vivo procedure for the induction of massive proliferation, directed migration, and neurodifferentiation (PMD) in the damaged adult central nervous system would hold promise for the treatment of human neurodegenerative disorders such as Parkinson's disease. We investigated the in vivo induction of PMD in the forebrain of the adult rat by using a combination of 6-hydroxydopamine lesion of the substantia nigra dopaminergic neurons and infusions of transforming growth factor alpha (TGFalpha) into forebrain structures. Only in animals with both lesion and infusion of TGFalpha was there a rapid proliferation of forebrain stem cells followed by a timed migration of a ridge of neuronal and glial progenitors directed toward the region of the TGFalpha infusion site. Subsequently, increasing numbers of differentiated neurons were observed in the striatum. In behavioral experiments, there was a significant reduction of apomorphine-induced rotations in animals receiving the TGFalpha infusions. These results show that the brain contains stem cells capable of PMD in response to an exogenously administered growth factor. This finding has significant implications with respect to the development of treatments for both acute neural trauma and neurodegenerative diseases.},
	Author = {Fallon, J. and Reid, S. and Kinyamu, R. and Opole, I. and Opole, R. and Baratta, J. and Korc, M. and Endo, T. L. and Duong, A. and Nguyen, G. and Karkehabadhi, M. and Twardzik, D. and Patel, S. and Loughlin, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:46 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Neurons/cytology/drug effects/metabolism/*physiology;Cell Differentiation;Rats, Sprague-Dawley;Transforming Growth Factor alpha/administration &dosage/genetics;Prosencephalon/*cytology/drug effects;Rats;D;06 Adult neurogenesis injury induced;Cell Division;Animal;Support, U.S. Gov't, P.H.S.;Cell Movement/*physiology;Support, Non-U.S. Gov't;Oxidopamine/administration &dosage;Male},
	Number = {26},
	Organization = {Departments of Anatomy and Neurobiology, Medicine, and Pharmacology, University of California, Irvine, CA 92697-1275, USA. jfallon\@uci.edu},
	Pages = {14686-91.},
	Title = {In vivo induction of massive proliferation, directed migration, and differentiation of neural cells in the adult mammalian brain},
	Uuid = {867020E3-202B-4D0E-B995-79138F77F850},
	Volume = {97},
	Year = {2000},
	url = {papers/Fallon_ProcNatlAcadSciUSA2000.pdf}}

@article{Fan:2005,
	Abstract = {Our previous studies have shown that intracerebral administration of endotoxin, lipopolysaccharide (LPS), induces selective white matter injury and hypomyelination in the neonatal rat brain and that the LPS-induced brain injury is associated with activation of microglia. To test the hypothesis that inhibition of microglial activation may protect against LPS-induced white matter injury, we examined roles of minocycline, a putative suppressor of microglial activation, on LPS-induced brain injury in the neonatal rat. A stereotactic intracerebral injection of LPS (1 mg/kg) was performed in postnatal day 5 Sprague-Dawley rats and control rats were injected with sterile saline. Minocycline (45 mg/kg) was administered intraperitoneally 12 h before and immediately after LPS injection and then every 24 h for 3 days. Inflammatory responses, activation of microglia and brain injury were examined 1 and 3 days after LPS injection. LPS injection resulted in brain injury in selective brain areas, including bilateral ventricular enlargement, cell death at the sub- and periventricular areas, loss of O4+ and O1+ oligodendrocyte (OL) immunoreactivity and hypomyelination, as indicated by decreased myelin basic protein immunostaining, in the neonatal rat brain. Minocycline administration significantly attenuated LPS-induced brain injury in these rat brains. The protective effect of minocycline was associated with suppressed microglial activation as indicated by the decreased number of activated microglial cells following LPS stimulation and with consequently decreased elevation of interleukin 1beta and tumor necrosis factor-alpha concentrations induced by LPS and a reduced number of inducible nitric oxide synthase expressing cells. Protection of minocycline was also linked with the reduction in LPS-induced oxidative stress, as indicated by 4-hydroxynonenal positive OLs. The overall results suggest that reduction in microglial activation may protect the neonatal brain from LPS-induced white matter injury and inhibition of microglial activation might be an effective approach for the therapeutic treatment of infection-induced white matter injury.},
	Author = {Fan, L-W W. and Pang, Y. and Lin, S. and Rhodes, P. G. and Cai, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Animals;Rats;Tumor Necrosis Factor-alpha;Brain;Neuroprotective Agents;Female;Microglia;Rats, Sprague-Dawley;Nitric-Oxide Synthase;Macrophage Activation;11 Glia;Lipopolysaccharides;Brain Diseases;Alpha;Male;Cerebral Ventricles;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Oxidative Stress;Interleukin-1;Minocycline;Anti-Bacterial Agents;Immunohistochemistry;Research Support, N.I.H., Extramural;Injections;Enzyme-Linked Immunosorbent Assay},
	Nlm_Id = {7605074},
	Number = {1},
	Organization = {Department of Pediatrics, Division of Newborn Medicine, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.},
	Pages = {159-68},
	Pii = {S0306-4522(05)00213-7},
	Pubmed = {15893639},
	Title = {Minocycline attenuates lipopolysaccharide-induced white matter injury in the neonatal rat brain},
	Uuid = {D270FE50-A024-4A04-8E92-8A4D139EDFDD},
	Volume = {133},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2005.02.016}}

@article{Farbman:1998,
	Abstract = {Olfactory marker protein (OMP) is a phylogenetically conserved, 19-kDa, acidic, soluble protein found abundantly in mature olfactory sensory neurons. Its function has been enigmatic although recent evidence from studies on OMP null mice suggests that neurons lacking OMP exhibit altered physiological activity, including prolonged onset and recovery kinetics following stimulation. We have reported increased expression of OMP in individual surviving sensory neurons that have been deprived of their target, the olfactory bulb. Because olfactory epithelia deprived of their target also exhibit an increased rate of cell division we investigated the effect of recombinant OMP on cell division in organotypic cultures of fetal rat (embryonic day 19) epithelium grown for 3 days in vitro. After 3 days, cultures were given a 1-hr pulse of a mitotic marker, bromodeoxyuridine (BrdU), fixed and prepared for immunohistochemistry to determine the number of proliferating cells. We found a dose-dependent increase in the number of BrdU- positive cells/100-mm length of epithelium. The number of labeled cells increased incrementally, reached a plateau at 25 pM OMP/ml culture medium, 50\%higher than in cultures with no OMP added, and remained at that level at 50 and 100 pM doses. Controls included trypsinized OMP and addition of equivalent volumes of TRIS buffer lacking OMP. These results, taken together with previous studies on several growth factors indicate that regulation of neurogenesis in olfactory tissue is a multifactorial process and that OMP may play a role.},
	Author = {Farbman, A. I. and Buchholz, J. A. and Walters, E. and Margolis, F. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {Recombinant Proteins/pharmacology;Nerve Tissue Proteins/metabolism/*pharmacology;Rats;Olfactory Receptor Neurons/*cytology/metabolism;Dose-Response Relationship, Drug;Animal;Support, U.S. Gov't, P.H.S.;I abstr;Cell Differentiation/drug effects/physiology;Cells, Cultured;Mice;13 Olfactory bulb anatomy},
	Organization = {Northwestern University, Evanston, Illinois 60208, USA. afarbman\@nwu.edu},
	Pages = {248-51.},
	Title = {Does olfactory marker protein participate in olfactory neurogenesis?},
	Uuid = {0036C1E0-BDCA-4514-B1CD-79E6DB9E9BBD},
	Volume = {855},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9929615}}

@article{Fassati:2003,
	Abstract = {Human immunodeficiency virus type 1 (HIV-1), like other lentiviruses, can infect non-dividing cells. This property depends on the active nuclear import of its intracellular reverse transcription complex (RTC). We have studied nuclear import of purified HIV-1 RTCs in primary macrophages and found that importin 7, an import receptor for ribosomal proteins and histone H1, is involved in the process. Nuclear import of RTCs requires, in addition, energy and the components of the Ran system. Depletion of importin 7 from cultured cells by small interfering RNA inhibits HIV-1 infection. These results provide a new insight into the molecular mechanism for HIV-1 nuclear import and reveal potential targets for therapeutic intervention.},
	Author = {Fassati, Ariberto and G{\"o}rlich, Dirk and Harrison, Ian and Zaytseva, Lyubov and Mingot, Jos{\'e}-Manuel M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0261-4189},
	Journal = {EMBO J},
	Keywords = {Transcription, Genetic;HIV-1;Humans;Macrophages;Cells, Cultured;Nuclear Envelope;HIV-1 Reverse Transcriptase;Mutation;Antigens, CD4;Karyopherins;15 Retrovirus mechanism;RNA, Small Interfering;ran GTP-Binding Protein;Hela Cells;HIV Infections;Active Transport, Cell Nucleus;Cell Nucleolus;Cell Nucleus;Receptors, CCR5;DNA, Viral;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {22737498},
	Month = {7},
	Nlm_Id = {8208664},
	Number = {14},
	Organization = {The Wohl Virion Centre, Windeyer Institute, University College London Medical School, 46 Cleveland Street, London W1T 4JF, UK. a.fassati\@ucl.ac.uk},
	Pages = {3675-85},
	Pubmed = {12853482},
	Title = {Nuclear import of HIV-1 intracellular reverse transcription complexes is mediated by importin 7},
	Uuid = {010D180F-E038-4459-BE82-F03C8039C98F},
	Volume = {22},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/emboj/cdg357}}

@article{Faulkner:2000,
	Abstract = {Mutations in the LIS1 gene cause gross histological disorganization of the developing human brain, resulting in a brain surface that is almost smooth. Here we show that LIS1 protein co-immunoprecipitates with cytoplasmic dynein and dynactin, and localizes to the cell cortex and to mitotic kinetochores, which are known sites for binding of cytoplasmic dynein. Overexpression of LIS1 in cultured mammalian cells interferes with mitotic progression and leads to spindle misorientation. Injection of anti-LIS1 antibody interferes with attachment of chromosomes to the metaphase plate, and leads to chromosome loss. We conclude that LIS1 participates in a subset of dynein functions, and may regulate the division of neuronal progenitor cells in the developing brain.},
	Author = {Faulkner, N. E. and Dujardin, D. L. and Tai, C. Y. and Vaughan, K. T. and O'Connell, C. B. and Wang, Y. and Vallee, R. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {10 Development;Microtubule-Associated Proteins;Animals;Humans;Mitosis;research support, u.s. gov't, p.h.s. ;1-Alkyl-2-acetylglycerophosphocholine Esterase;Cercopithecus aethiops;Cytoplasm;COS Cells;research support, non-u.s. gov't ;Microtubules;Cell Line;Kinetochores;Subcellular Fractions;Dynein ATPase;Cell Division;24 Pubmed search results 2008;Dogs;Gene Expression;Precipitin Tests},
	Month = {11},
	Nlm_Id = {100890575},
	Number = {11},
	Organization = {Department of Cell Biology University of Massachusetts Medical School, 377 Plantation Street, Worcester, Massachusetts 01605, USA.},
	Pages = {784-91},
	Pubmed = {11056532},
	Title = {A role for the lissencephaly gene LIS1 in mitosis and cytoplasmic dynein function},
	Uuid = {685D6C43-5E44-441F-A63C-3A62645C2E69},
	Volume = {2},
	Year = {2000},
	url = {papers/Faulkner_NatCellBiol2000.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35041020}}

@article{Faux:2001,
	Abstract = {The differentiation of precursor cells into neurons has been shown to be influenced by both the Notch signaling pathway and growth factor stimulation. In this study, the regulation of neuronal differentiation by these mechanisms was examined in the embryonic day 10 neuroepithelial precursor (NEP) population. By downregulating Notch1 expression and by the addition of a Delta1 fusion protein (Delta Fc), it was shown that signaling via the Notch pathway inhibited neuron differentiation in the NEP cells, in vitro. The expression of two of the Notch receptor homologs, Notch1 and Notch3, and the ligand Delta1 in these NEP cells was found to be influenced by a number of different growth factors, indicating a potential interaction between growth factors and Notch signaling. Interestingly, none of the growth factors examined promoted neuron differentiation; however, the fibroblast growth factors (FGFs) 1 and 2 potently inhibited differentiation. FGF1 and FGF2 upregulated the expression of Notch and decreased expression of Delta1 in the NEP cells. In addition, the inhibitory response of the cells to the FGFs could be overcome by downregulating Notch1 expression and by disrupting Notch cleavage and signaling by the ablation of the Presenilin1 gene. These results indicate that FGF1 and FGF2 act via the Notch pathway, either directly or indirectly, to inhibit differentiation. Thus, signaling through the Notch receptor may be a common regulator of neuronal differentiation within the developing forebrain.},
	Author = {Faux, C. H. and Turnley, A. M. and Epa, R. and Cappai, R. and Bartlett, P. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {J Neurosci},
	Keywords = {10 Development;Receptors, Cell Surface/genetics/metabolism;Neurons/cytology/*metabolism;Cells, Cultured;Mice, Mutant Strains;Down-Regulation (Physiology);Fibroblast Growth Factor, Basic/metabolism/pharmacology;Protein Binding/physiology;Cell Count;Animal;F pdf;Cell Differentiation/drug effects/*physiology;Signal Transduction/drug effects/physiology;Mice, Inbred CBA;Support, Non-U.S. Gov't;Immunoglobulins, Fc/genetics;Proto-Oncogene Proteins/genetics/metabolism;Stem Cells/cytology/drug effects/metabolism;Mice;Gene Expression/drug effects;inhibitors/deficiency/genetics/*metabolism/pharmacology;Blood Proteins/pharmacology;Fibroblast Growth Factor/*metabolism/pharmacology;Recombinant Fusion Proteins/genetics/metabolism;Oligonucleotides, Antisense/pharmacology;Membrane Proteins/antagonists &},
	Number = {15},
	Organization = {The Walter and Eliza Hall Institute of Medical Research, The Royal Melbourne Hospital, Victoria 3050, Australia.},
	Pages = {5587-96.},
	Title = {Interactions between fibroblast growth factors and Notch regulate neuronal differentiation},
	Uuid = {897B8CBE-DBF0-4ADC-9468-6128A7E3ADB7},
	Volume = {21},
	Year = {2001},
	url = {papers/Faux_JNeurosci2001}}

@article{Farber:2006,
	Abstract = {In this review we summarize mechanisms of Ca(2+) signaling in microglial cells and the impact of Ca(2+) signaling and Ca(2+) levels on microglial function. So far, Ca(2+) signaling has been only characterized in cultured microglia and thus these data refer rather to activated microglia as observed in pathology when compared with the resting form found under physiological conditions. Purinergic receptors are the most prominently expressed ligand-gated Ca(2+)-permeable channels in microglia and control several microglial functions such as cytokine release in a Ca(2+)-dependent fashion. A large variety of metabotropic receptors are linked to Ca(2+) release from intracellular stores. Depletion of these intracellular stores triggers a capacitative Ca(2+) entry. While microglia are already in an activated state in culture, they can be further activated, for example, by exposure to bacterial endotoxin. This activation leads to a chronic increase of [Ca(2+)](i) and this Ca(2+) increase is a prerequisite for the release of nitric oxide and cytokines. Moreover, several factors (TNFalpha, IL-1beta, and IFN-gamma) regulate resting [Ca(2+)](i) levels. (c) 2006 Wiley-Liss, Inc.},
	Author = {F{\"a}rber, and Kettenmann,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {14 Immune;11 Glia;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {8806785},
	Number = {7},
	Organization = {Cellular Neuroscience, MaxDelbrueckCenter for Molecular Medicine, RobertR{\"o}ssleStra$\beta$e 10, 13092 Berlin, Germany.},
	Pages = {656-665},
	Pubmed = {17006894},
	Title = {Functional role of calcium signals for microglial function},
	Uuid = {235CC9B7-8023-4910-8E16-37722F559487},
	Volume = {54},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20412}}

@article{Fedoroff:1997,
	Abstract = {A marked effect of colony stimulating factor-1(CSF-1) on microglial response and neuron survival in cerebral cortex ischemic damage was observed. In osteopetrotic op/op mice, which lack systemically functional CSF-1 microglia do not respond to ischemic damage to the cerebral cortex, and the infarcts are considerably larger than in CSF-1 producing mice with similar vascular impairment. Delivery of extraneous CSF-1 to op/op mice alleviates the functional deficiency of the microglia and potentiates neuron survival in ischemic lesion. Delivery of extraneous recombinant CSF-1 to normal CSF-1 producing mice does not increase either the number or degree of activation of microglia, but does further potentiate neuronal survival. We found that neurons in the cerebral cortex have active CSF-1 receptors, and we therefore propose that neuronal rescue in cerebral cortex ischemic damage is linked to activation of the CSF-1 receptor on neurons.},
	Author = {Fedoroff, S. and Berezovskaya, O. and Maysinger, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0149-7634},
	Journal = {Neurosci Biobehav Rev},
	Keywords = {Brain Ischemia;11 Glia;Cell Death;Colony-Stimulating Factors;review, tutorial;Support, Non-U.S. Gov't;Animals;Mice;review},
	Medline = {97216773},
	Month = {3},
	Nlm_Id = {7806090},
	Number = {2},
	Organization = {Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.},
	Pages = {187-91},
	Pii = {S0149763496000097},
	Pubmed = {9062942},
	Title = {Role of colony stimulating factor-1 in brain damage caused by ischemia},
	Uuid = {F420C84F-208D-4CA7-8C99-5D16D0ABCBB1},
	Volume = {21},
	Year = {1997}}

@article{Feinberg:2008,
	Abstract = {The identification of synaptic partners is challenging in dense nerve bundles, where many processes occupy regions beneath the resolution of conventional light microscopy. To address this difficulty, we have developed GRASP, a system to label membrane contacts and synapses between two cells in living animals. Two complementary fragments of GFP are expressed on different cells, tethered to extracellular domains of transmembrane carrier proteins. When the complementary GFP fragments are fused to ubiquitous transmembrane proteins, GFP fluorescence appears uniformly along membrane contacts between the two cells. When one or both GFP fragments are fused to synaptic transmembrane proteins, GFP fluorescence is tightly localized to synapses. GRASP marks known synaptic contacts in C. elegans, correctly identifies changes in mutants with altered synaptic specificity, and can uncover new information about synaptic locations as confirmed by electron microscopy. GRASP may prove particularly useful for defining connectivity in complex nervous systems.},
	Author = {Feinberg, Evan H. and Vanhoven, Miri K. and Bendesky, Andres and Wang, George and Fetter, Richard D. and Shen, Kang and Bargmann, Cornelia I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;10 circuit formation;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.},
	Pages = {353-63},
	Pii = {S0896-6273(07)01020-3},
	Pubmed = {18255029},
	Title = {GFP Reconstitution Across Synaptic Partners (GRASP) Defines Cell Contacts and Synapses in Living Nervous Systems},
	Uuid = {9408D907-BB62-42D7-8EF1-165DA1E4DDFC},
	Volume = {57},
	Year = {2008},
	url = {papers/Feinberg_Neuron2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.11.030}}

@article{Feinstein:2004,
	Abstract = {No models fully account for how odorant receptors (ORs) function in the guidance of axons of olfactory sensory neurons (OSNs) to glomeruli in the olfactory bulb. Here, we use gene targeting in mice to demonstrate that the OR amino acid sequence imparts OSN axons with an identity that allows them to coalesce into glomeruli. Replacements between the coding regions of the M71 and M72 OR genes reroute axons to their respective glomeruli. A series of M71-M72 hybrid ORs uncover a spectrum of glomerular phenotypes, leading to the concept that the identity of OSN axons is revealed depending on what other axons are present. Naturally occurring amino acid polymorphisms in other ORs also produce distinct axonal identities. These critical amino acid residues are distributed throughout the protein and reside predominantly within transmembrane domains. We propose a contextual model for axon guidance in which ORs mediate homotypic interactions between like axons.},
	Author = {Feinstein, Paul and Mombaerts, Peter},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:46 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {13 Olfactory bulb anatomy;Cell Differentiation;Animals;Gene Targeting;Synapses;Gene Expression Regulation, Developmental;Olfactory Receptor Neurons;Phenotype;Models, Biological;Cell Membrane;Cell Communication;Mice, Transgenic;Open Reading Frames;Olfactory Bulb;Support, Non-U.S. Gov't;Protein Structure, Tertiary;Polymorphism (Genetics);Support, U.S. Gov't, P.H.S.;Receptors, Odorant;Mice;Growth Cones;Amino Acid Sequence},
	Month = {6},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. feinstp\@rockefeller.edu},
	Pages = {817-31},
	Pii = {S0092867404004957},
	Pubmed = {15186781},
	Title = {A contextual model for axonal sorting into glomeruli in the mouse olfactory system},
	Uuid = {53CE646C-22FA-49F4-8603-2D22759C7223},
	Volume = {117},
	Year = {2004},
	url = {papers/Feinstein_Cell2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2004.05.011}}

@article{Feinstein:2004a,
	Abstract = {Odorant receptors (ORs) provide the core determinant of identity for axons of olfactory sensory neurons (OSNs) to coalesce into glomeruli in the olfactory bulb. Here, using gene targeting in mice, we examine how the OR protein determines axonal identity. An OR::GFP fusion protein is present in axons, consistent with a direct function of ORs in axon guidance. When the OR coding region is deleted, we observe OSNs that coexpress other ORs that function in odorant reception and axonal identity. It remains unclear if such coexpression is normally prevented by negative feedback on OR gene choice. A drastic reduction in OR protein level produces axonal coalescence into novel, remote glomeruli. By contrast, chimeric ORs and ORs with minor mutations perturb axon outgrowth. Strikingly, the beta2 adrenergic receptor can substitute for an OR in glomerular formation when expressed from an OR locus. Thus, ORs have not evolved a unique function in axon guidance.},
	Author = {Feinstein, Paul and Bozza, Thomas and Rodriguez, Ivan and Vassalli, Anne and Mombaerts, Peter},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:46 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {13 Olfactory bulb anatomy;Cell Differentiation;Animals;Gene Targeting;Synapses;Gene Expression Regulation, Developmental;Olfactory Receptor Neurons;Mutation;Cell Communication;Mice, Transgenic;Open Reading Frames;Recombinant Fusion Proteins;Olfactory Bulb;Support, Non-U.S. Gov't;Receptors, Adrenergic, beta-2;Alleles;Chimeric Proteins;Support, U.S. Gov't, P.H.S.;Receptors, Odorant;Cilia;Mice;Luminescent Proteins;Growth Cones},
	Month = {6},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. feinstp\@rockefeller.edu},
	Pages = {833-46},
	Pii = {S0092867404005318},
	Pubmed = {15186782},
	Title = {Axon guidance of mouse olfactory sensory neurons by odorant receptors and the beta2 adrenergic receptor},
	Uuid = {4987D273-9AE3-4FDA-AD75-51A0E25E1087},
	Volume = {117},
	Year = {2004},
	url = {papers/Feinstein_Cell2004a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2004.05.013}}

@article{Feng:2000,
	Abstract = {We generated transgenic mice in which red, green, yellow, or cyan fluorescent proteins (together termed XFPs) were selectively expressed in neurons. All four XFPs labeled neurons in their entirety, including axons, nerve terminals, dendrites, and dendritic spines. Remarkably, each of 25 independently generated transgenic lines expressed XFP in a unique pattern, even though all incorporated identical regulatory elements (from the thyl gene). For example, all retinal ganglion cells or many cortical neurons were XFP positive in some lines, whereas only a few ganglion cells or only layer 5 cortical pyramids were labeled in others. In some lines, intense labeling of small neuronal subsets provided a Golgi-like vital stain. In double transgenic mice expressing two different XFPs, it was possible to differentially label 3 neuronal subsets in a single animal.},
	Author = {Feng, G. and Mellor, R. H. and Bernstein, M. and Keller-Peck, C. and Nguyen, Q. T. and Wallace, M. and Nerbonne, J. M. and Lichtman, J. W. and Sanes, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Transgenes;Presynaptic Terminals;Animals;Synapses;research support, u.s. gov't, p.h.s. ;Axons;Mice, Transgenic;Antigens, Thy-1;Green Fluorescent Proteins;Color;Microscopy, Fluorescence;Dendrites;research support, non-u.s. gov't ;Cell Lineage;Neuromuscular Junction;Cerebral Cortex;Neurons;21 Neurophysiology;Light;Regulatory Sequences, Nucleic Acid;Mice;24 Pubmed search results 2008;Luminescent Proteins;Retinal Ganglion Cells},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, Missouri 63110, USA.},
	Pages = {41-51},
	Pii = {S0896-6273(00)00084-2},
	Pubmed = {11086982},
	Title = {Imaging neuronal subsets in transgenic mice expressing multiple spectral variants of GFP},
	Uuid = {07CC9EFF-9170-42FC-B0BB-B172E7263262},
	Volume = {28},
	Year = {2000},
	url = {papers/Feng_Neuron2000.pdf}}

@article{Feng:2001,
	Abstract = {To examine the in vivo function of presenilin-1 (PS1), we selectively deleted the PS1 gene in excitatory neurons of the adult mouse forebrain. These conditional knockout mice were viable and grew normally, but they exhibited a pronounced deficiency in enrichment- induced neurogenesis in the dentate gyrus. This reduction in neurogenesis did not result in appreciable learning deficits, indicating that addition of new neurons is not required for memory formation. However, our postlearning enrichment experiments lead us to postulate that adult dentate neurogenesis may play a role in the periodic clearance of outdated hippocampal memory traces after cortical memory consolidation, thereby ensuring that the hippocampus is continuously available to process new memories. A chronic, abnormal clearance process in the hippocampus may conceivably lead to memory disorders in the mammalian brain.},
	Author = {Feng, R. and Rampon, C. and Tang, Y. P. and Shrom, D. and Jin, J. and Kyin, M. and Sopher, B. and Martin, G. M. and Kim, S. H. and Langdon, R. B. and Sisodia, S. S. and Tsien, J. Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Neuron},
	Keywords = {Membrane Proteins/*deficiency/*genetics;Alzheimer Disease/genetics;Electrophysiology;Neurons/pathology;Memory/*physiology;Animal;C abstr;Mice, Transgenic;Mice, Inbred C57BL;Prosencephalon/*growth &development/pathology;Mice, Inbred CBA;Support, Non-U.S. Gov't;Mice, Knockout;RNA, Messenger/genetics/metabolism;Hippocampus/*growth &development/pathology;04 Adult neurogenesis factors;Amyloid beta-Protein Precursor/*analogs &derivatives/metabolism;Support, U.S. Gov't, P.H.S.;Mice;Memory Disorders/genetics/pathology/physiopathology;Brain Chemistry/genetics},
	Number = {5},
	Organization = {Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.},
	Pages = {911-26.},
	Title = {Deficient neurogenesis in forebrain-specific presenilin-1 knockout mice is associated with reduced clearance of hippocampal memory traces},
	Uuid = {E4D9AA44-7777-4AE9-9DE8-7CC404832F16},
	Volume = {32},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11738035}}

@article{Feng:2006,
	Abstract = {Mutations in the human Filamin A (FLNA) gene disrupt neuronal migration to the cerebral cortex and cause cardiovascular defects. Complete loss of Flna in mice results in embryonic lethality with severe cardiac structural defects involving ventricles, atria, and outflow tracts, as well as widespread aberrant vascular patterning. Despite these widespread developmental defects, migration and motility of many cell types does not appear to be affected. Instead, Flna-null embryos display abnormal epithelial and endothelial organization and aberrant adherens junctions in developing blood vessels, heart, brain, and other tissues. Essential roles for FLNA in intercellular junctions provide a mechanism for the diverse developmental defects seen in patients with FLNA mutations.},
	Author = {Feng, Yuanyi and Chen, Ming Hui and Moskowitz, Ivan P. and Mendonza, Ashley M. and Vidali, Luis and Nakamura, Fumihiko and Kwiatkowski, David J. and Walsh, Christopher A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {52},
	Organization = {*Division of Genetics and Department of Cardiology, Children's Hospital Boston, Boston, MA 02215.},
	Pages = {19836-41},
	Pii = {0609628104},
	Pubmed = {17172441},
	Title = {Filamin A (FLNA) is required for cell-cell contact in vascular development and cardiac morphogenesis},
	Uuid = {AE2B8A9F-7FCC-40A2-9EDC-4EE55D453544},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0609628104}}

@article{Ferrer:1993,
	Abstract = {Different cortical malformations were produced in rats by a single dose of X-rays (200 cGy) given on different days during gestation. These include large cortical ectopic masses after irradiation on day 14; segmentation of the cerebral cortex following irradiation on days 15, 17, 19; and a four-layered "lissencephalic" cortex following irradiation on day 16. Other types of cortical malformation were produced in rats aged 0-2 days by one of the following procedures: focal cortical freezing, focal electrocoagulation, cortical aspiration, and focal brushing of the meninges with a blunt needle covered with cotton. These latter abnormalities include laminar necrosis of layer V, focal cortical dysplasia reminiscent of microgyria, status verrucosus deformis and porencephaly. Experimentally induced cortical malformations in rats can help to increase our understanding of normal and abnormal neurogenesis and organisation of the human cerebral cortex.},
	Author = {Ferrer, I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0256-7040},
	Journal = {Childs Nerv Syst},
	Keywords = {Disease Models, Animal;Gestational Age;21 Epilepsy;Research Support, Non-U.S. Gov't;21 Neurophysiology;Rats;Inhalation;Electrocoagulation;Female;Fetal Diseases;Rats, Wistar;Pregnancy;Animals;Radiation Injuries, Experimental;24 Pubmed search results 2008;Freezing;Cerebral Cortex},
	Medline = {94138960},
	Month = {11},
	Nlm_Id = {8503227},
	Number = {7},
	Organization = {Unidad Neuropatolog{\'\i}a, Servicio Anatom{\'\i}a Patol{\'o}gica, Hospital Pr{\'\i}ncipes de Espa\~{n}a, Universidad de Barcelona, Hospitalet de Llobregat, Spain.},
	Pages = {403-7},
	Pubmed = {8306356},
	Title = {Experimentally induced cortical malformations in rats},
	Uuid = {7D2ACF23-19E8-43D6-9F49-625172276D64},
	Volume = {9},
	Year = {1993}}

@article{Ferrer:1993a,
	Abstract = {Different types of cortical malformation were produced, following focal cortical freezing, electrocoagulation, focal cortical aspiration or gentle brushing of uncovered meninges, in newborn or 1- to 3-day-old rats. Malformations included laminar necrosis of the cerebral cortex, status verrucosus, focal cortical dysplasia reminiscent of microgyria, and porencephaly. Similar procedures from postnatal day 4 onwards, at a time when a reactive astrogliosis is possible, produced cavitating infarcts and tissue scars. Cytoarchitectonic studies revealed an abnormal distribution of different types of pyramidal and non-pyramidal neurons in these malformations. These indicated three subtypes of focal cortical dysplasia, which probably depend on different pathogenic mechanisms. Autoradiographic studies with [3H] methylthymidine showed normal positioning of late-generated neuroblasts in the cerebral cortex, thus suggesting preserved migration. The present experimentally induced cortical malformations are useful models of similar cortical abnormalities in humans.},
	Author = {Ferrer, I. and Alc{\'a}ntara, S. and Catal{\'a}, I. and Z{\'u}jar, M. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0014-4819},
	Journal = {Exp Brain Res},
	Keywords = {Animals;Meninges;Rats;Brain;21 Epilepsy;Thymidine;Rats, Wistar;Disease Models, Animal;Animals, Newborn;Cerebral Cortex;Freezing;Neurons;21 Neurophysiology;Parvalbumins;24 Pubmed search results 2008;Autoradiography;Tritium;Necrosis;Biological Markers;Research Support, Non-U.S. Gov't},
	Medline = {93365596},
	Nlm_Id = {0043312},
	Number = {2},
	Organization = {Unidad Neuropatolog{\'\i}a, Hospital Pr{\'\i}ncipes de Espa\~{n}a, Universidad de Barcelona, Hospitalet de Llobregat, Spain.},
	Pages = {261-9},
	Pubmed = {8359242},
	Title = {Experimentally induced laminar necrosis, status verrucosus, focal cortical dysplasia reminiscent of microgyria, and porencephaly in the rat},
	Uuid = {F9982979-C05A-4473-9631-AB37EF69555D},
	Volume = {94},
	Year = {1993}}

@article{Ferrer:1996,
	Abstract = {Transforming growth factor alpha (TGF-alpha) and epidermal growth factor-receptor (EGF-R) immunoreactivity is observed in the majority of neurons, and in maturing astrocytes, in the developing and adult brain of humans and different species of animals. TGF-alpha and EGF-R co-localize in most neurons and maturing astrocytes, suggesting that most TGF-alpha-producing cells are EGF-R-expressing cells. TGF-alpha and EGF-R immunoreactivity decrease in damaged areas following different insults. However, EGF-R appears in reactive glia, mostly reactive astrocytes, within and surrounding the damaged areas. TGF-alpha and EGF-R immunoreactivity is found in neurons of patients affected by Alzheimer's disease and other forms of dementia, and in neurons of patients suffering from epilepsy owing to different causes, thus pointing to the conclusion that TGF-alpha does not play a significant role in these pathologies. However, EGF-R immunoreactivity occurs in reactive astrocytes and microglia in subacute but not chronic lesions in human cases. Since TGF-alpha is a membrane-anchored growth factor, which may be cleaved leading to the formation of soluble forms, and both the membrane-anchored and soluble forms have the capacity to activate the EGF-R, it is feasible that TGF-alpha in the nervous system may act upon EGF-R-containing neurons through different mechanisms. In addition to distant effects resulting from the release of soluble TGF-alpha, local effects may be produced by establishing direct cell-to-cell contacts (juxtacrine stimulation), or in cells expressing both TGF-alpha and EGF-R (autocrine stimulation).},
	Author = {Ferrer, I. and Alc{\'a}ntara, S. and Ballabriga, J. and Oliv{\'e}, M. and Blanco, R. and Rivera, R. and Carmona, M. and Berruezo, M. and Pitarch, S. and Planas, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0301-0082},
	Journal = {Prog Neurobiol},
	Keywords = {Receptor, Epidermal Growth Factor;Research Support, Non-U.S. Gov't;Alpha;11 Glia;Antibody Specificity;Transforming Growth Factor alpha;review, tutorial;Humans;Brain;Animals;review;Brain Chemistry},
	Medline = {97001830},
	Month = {6},
	Nlm_Id = {0370121},
	Number = {2},
	Organization = {Unitat de Neuropatologia, Hospital Princeps d'Espanya, Universitat de Barcelona, Spain.},
	Pages = {99-123},
	Pii = {S0301008296000093},
	Pubmed = {8844822},
	Title = {Transforming growth factor-alpha (TGF-alpha) and epidermal growth factor-receptor (EGF-R) immunoreactivity in normal and pathologic brain},
	Uuid = {C7FC955C-CC13-42FF-8A3F-6566D5D7AF9B},
	Volume = {49},
	Year = {1996}}

@article{Ferri:2004,
	Abstract = {In many species, the Sox2 transcription factor is a marker of the nervous system from the beginning of its development, and we have previously shown that Sox2 is expressed in embryonic neural stem cells. It is also expressed in, and is essential for, totipotent inner cell mass stem cells and other multipotent cell lineages, and its ablation causes early embryonic lethality. To investigate the role of Sox2 in the nervous system, we generated different mouse mutant alleles: a null allele (Sox2(beta-geo) 'knock-in'), and a regulatory mutant allele (Sox2(DeltaENH)), in which a neural cell-specific enhancer is deleted. Sox2 is expressed in embryonic early neural precursors of the ventricular zone and, in the adult, in ependyma (a descendant of the ventricular zone). It is also expressed in the vast majority of dividing precursors in the neurogenic regions, and in a small proportion of differentiated neurones, particularly in the thalamus, striatum and septum. Compound Sox2(beta-geo/DeltaENH) heterozygotes show important cerebral malformations, with parenchymal loss and ventricle enlargement, and L-dopa-rescuable circling behaviour and epilepsy. We observed striking abnormalities in neurones; degeneration and cytoplasmic protein aggregates, a feature common to diverse human neurodegenerative diseases, are observed in thalamus, striatum and septum. Furthermore, ependymal cells show ciliary loss and pathological lipid inclusions. Finally, precursor cell proliferation and the generation of new neurones in adult neurogenic regions are greatly decreased, and GFAP/nestin-positive hippocampal cells, which include the earliest neurogenic precursors, are strikingly diminished. These findings highlight a crucial and unexpected role for Sox2 in the maintenance of neurones in selected brain areas, and suggest a contribution of neural cell proliferative defects to the pathological phenotype. 0950-1991 Journal article},
	Author = {Ferri, A. L. and Cavallaro, M. and Braida, D. and Di Cristofano, A. and Canta, A. and Vezzani, A. and Ottolenghi, S. and Pandolfi, P. P. and Sala, M. and DeBiasi, S. and Nicolis, S. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {Development},
	Keywords = {04 Adult neurogenesis factors;C pdf flathead mutant},
	Title = {Sox2 deficiency causes neurodegeneration and impaired neurogenesis in the adult mouse brain},
	Uuid = {7F0A3878-57A1-4BA0-820A-032F1EF97E47},
	Year = {2004},
	url = {papers/Ferri_Development2004.pdf}}

@article{Fetler:2005,
	Author = {Fetler, Luc and Amigorena, Sebastian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Receptors, Purinergic P2;Adenosine Triphosphate;Brain Injuries;Cells, Cultured;Movement;Capillaries;Astrocytes;11 Glia;Mice, Transgenic;Photons;Microglia;Cell Surface Extensions;Animals;Brain;Phagocytosis;Mice;Microscopy},
	Month = {7},
	Nlm_Id = {0404511},
	Number = {5733},
	Organization = {Laboratoire Physico-Chimie Curie, CNRS UMR 168, Institut Curie, Paris, France. luc.fetler\@curie.fr},
	Pages = {392-3},
	Pii = {309/5733/392},
	Pubmed = {16020721},
	Title = {Neuroscience. Brain under surveillance: the microglia patrol},
	Uuid = {43BC98C6-CD87-4154-9045-6ADA42956C08},
	Volume = {309},
	Year = {2005},
	url = {papers/Fetler_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1114852}}

@article{Figlewicz:1988,
	Abstract = {In the course of development, corticocortical axons seem to first appear in a labile state from which they either mature into a stable state or are eliminated. These state transitions may be related to cytoskeletal modifications. By immunohistochemistry and immunobiochemistry we found that, in the corpus callosum of the cat, the heavy (200 kDa) subunit of neurofilaments (NF) becomes progressively more visible during the first postnatal month. This aspect of cytoskeletal maturation parallels the developmental loss of callosal axons, i.e. probably the stabilization of the axons which are not eliminated. A similar maturation of the heavy subunit was observed in the visual cortical areas 17 and 18. The medium (150 kDa) and to a lesser extent the light (70 kDa) NF subunits are already present a few days after birth.},
	Author = {Figlewicz, D. A. and Gremo, F. and Innocenti, G. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Aging;Macromolecular Systems;Antibodies;Cytoskeleton;Cats;Neurofilament Proteins;Antibodies, Monoclonal;Not relevant;11 Glia;Intermediate Filaments;Fluorescent Antibody Technique;Support, Non-U.S. Gov't;Molecular Weight;Intermediate Filament Proteins;Animals;Corpus Callosum},
	Medline = {89118978},
	Month = {8},
	Nlm_Id = {0045503},
	Number = {2},
	Organization = {Service de Neurologie, CHUV, Lausanne, Switzerland.},
	Pages = {181-9},
	Pubmed = {3146406},
	Title = {Differential expression of neurofilament subunits in the developing corpus callosum},
	Uuid = {10C043D4-C1B6-4C45-A19B-5338A1873D61},
	Volume = {470},
	Year = {1988}}

@article{Filipkowski:2005,
	Abstract = {In the central nervous system (CNS) generation of new neurons continues throughout adulthood, when it is limited to the olfactory bulb and hippocampus. The knowledge regarding the function of newly-generated neurons remains limited and is vigorously investigated using diverse approaches. Among these are genetically modified mice, most of them of knock-out type (KO). Results from 23 diverse KO mouse models demonstrate the importance of particular proteins (growth factors, nitric oxide synthases, receptors, cyclins/cyclin-associated proteins, transcription factors, etc.) in adult neurogenesis (ANGE) as well as separate it from developmental neurogenesis. These results bring us closer to revealing the function of newly generated neurons in adult brains.},
	Author = {Filipkowski, Robert K. and Kiryk, Anna and Kowalczyk, Anna and Kaczmarek, Leszek},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0001-527X},
	Journal = {Acta Biochim Pol},
	Keywords = {24 Pubmed search results 2008},
	Nlm_Id = {14520300R},
	Number = {2},
	Organization = {Laboratory of Molecular Neurobiology, Department of Molecular and Cellular Neurobiology, Nencki Institute, Warszawa, Poland.},
	Pages = {359-72},
	Pii = {055202359},
	Pubmed = {15990921},
	Title = {Genetic models to study adult neurogenesis},
	Uuid = {6A17A3E1-5502-4ED0-A87D-9B1134D4DDD9},
	Volume = {52},
	Year = {2005}}

@article{Filippov:2003,
	Abstract = {Based on the expression of glial fibrillary acidic protein (GFAP), a recent hypothesis considered stem or progenitor cells in the adult hippocampus to be a type of astrocyte. In a complementary approach, we used transgenic mice expressing green fluorescent protein (GFP) under the promoter for nestin, an intermediate filament present in progenitor cells, to demonstrate astrocytic features in nestin-GFP-positive cells. Morphologically, two subpopulations of nestin-GFP-positive cells were distinguishable; one had an elaborate tree of processes in the granule cell layer and expression of GFAP (but not of S100beta, another astrocytic marker). Electron microscopy revealed vascular end feet of nestin-positive cells, further supporting astrocytic differentiation. Electrophysiological examination of nestin-GFP-positive cells on acutely isolated hippocampal slices showed passive current characteristics of astrocytes in one subset of cells. Among the nestin-GFP-expressing cells with lacking astrocytic features, two cell types could be identified electrophysiologically: cells with delayed-rectifying potassium currents and a very small number of cells with sodium currents, potentially representing signs of the earliest steps of neuronal differentiation.},
	Author = {Filippov, Vitali and Kronenberg, Golo and Pivneva, Tatjyana and Reuter, Katja and Steiner, Barbara and Wang, Li Ping and Yamaguchi, Masahiro and Kettenmann, Helmut and Kempermann, Gerd},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Fluorescent Dyes;10 Development;10 Hippocampus;Animals;Astrocytes;Microscopy, Immunoelectron;Mice, Transgenic;Green Fluorescent Proteins;Potassium Channels;Capillaries;Dentate Gyrus;Membrane Potentials;Age Factors;Intermediate Filament Proteins;Mice;Isoquinolines;Luminescent Proteins;Stem Cells;Nerve Tissue Proteins;24 Pubmed search results 2008;Promoter Regions (Genetics);Research Support, Non-U.S. Gov't},
	Medline = {22722094},
	Month = {7},
	Nlm_Id = {9100095},
	Number = {3},
	Organization = {Max Delbr{\"u}ck Center for Molecular Medicine (MDS) Berlin-Buch, Robert-R{\"o}ssle-Strasse 10, 13125 Berlin, Germany.},
	Pages = {373-82},
	Pii = {S1044743103000605},
	Pubmed = {12837622},
	Title = {Subpopulation of nestin-expressing progenitor cells in the adult murine hippocampus shows electrophysiological and morphological characteristics of astrocytes},
	Uuid = {65CE90B1-5941-4768-850B-D0F75D5AD631},
	Volume = {23},
	Year = {2003}}

@article{Fincher:1996,
	Abstract = {Excess sleep and fever are central nervous system (CNS) facets of the acute phase response; these responses are induced by microbial products, such as muramyl peptides, via their ability to enhance cytokine production. Although peripheral macrophages are known to digest bacteria, thereby releasing muramyl peptides that, in turn, stimulate cytokine production, it was unknown whether CNS phagocytes such as microglia also had this capacity. Primary cultures of microglia were allowed to phagocytize and digest Staphylococcus aureus radiolabeled with a cell wall-specific marker. Radiolabeled low molecular weight substances released into the culture medium were partially purified and tested for the ability to induce excess sleep, fever, and cytokine production. These substances increased non-rapid eye movement sleep, electroencephalographic slow-wave activity, and brain temperature after intracerebroventricular injection into rabbits. They also induced interleukin-1, tumor necrosis factor, and the interleukin-1 receptor antagonist production in human monocytes. Results suggest that microglia perform fundamental macrophage functions and further implicate microglia as resident immunocompetent cells.},
	Author = {Fincher, E. F. and Johannsen, L. and Kap{\'a}s, L. and Takahashi, S. and Krueger, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0002-9513},
	Journal = {Am J Physiol},
	Keywords = {Mice, Inbred BALB C;Rabbits;Phagocytosis;Animals;Latex;Monocytes;Cell Extracts;Humans;Cells, Cultured;Research Support, U.S. Gov't, Non-P.H.S.;Microglia;Fever;11 Glia;Microscopy, Fluorescence;Male;Sleep;Microspheres;Research Support, U.S. Gov't, P.H.S.;Staphylococcus aureus;Molecular Weight;Mice;Cytokines},
	Medline = {96331499},
	Month = {7},
	Nlm_Id = {0370511},
	Number = {1 Pt 2},
	Organization = {Department of Physiology and Biophysics, University of Tennessee, Memphis 38163, USA.},
	Pages = {R149-56},
	Pubmed = {8760216},
	Title = {Microglia digest Staphylococcus aureus into low molecular weight biologically active compounds},
	Uuid = {D8599E16-7DAC-4B32-B1BB-DEF35C726885},
	Volume = {271},
	Year = {1996}}

@article{Fischer:1972,
	Author = {Fischer, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0008-7335},
	Journal = {Cas Lek Cesk},
	Keywords = {Epilepsy;Cerebral Cortex;24 Pubmed search results 2008;21 Epilepsy;21 Neurophysiology;Rats;Gelatin;Electrophysiology;Ganglia;Animals;Disease Models, Animal;Neurons;Cobalt},
	Medline = {72258774},
	Month = {8},
	Nlm_Id = {0004743},
	Number = {33},
	Pages = {772-7},
	Pubmed = {5052540},
	Title = {[Experimental cobalt-gelatinous epileptogenic focus in the brain cortex of rat]},
	Uuid = {4E1D8EBB-08E0-442B-BDE4-D1E5FF89C7E6},
	Volume = {111},
	Year = {1972}}

@article{Fischer:2001a,
	Abstract = {Microglia subpopulations were studied in mouse experimental autoimmune encephalomyelitis and toxoplasmic encephalitis. CNS inflammation was associated with the proliferation of CD11b(+) brain cells that exhibited the dendritic cell (DC) marker CD11c. These cells constituted up to 30\%of the total CD11b(+) brain cell population. In both diseases CD11c(+) brain cells displayed the surface phenotype of myeloid DC and resided at perivascular and intraparenchymatic inflammatory sites. By lacking prominent phagocytic organelles, CD11c(+) cells from inflamed brain proved distinct from other microglia, but strikingly resembled bone marrow-derived DC and thus were identified as DC. This brain DC population comprised cells strongly secreting IL-12p70, whereas coisolated CD11c(-) microglia/brain macrophages predominantly produced TNF-alpha, GM-CSF, and NO. In comparison, the DC were more potent stimulators of naive or allogeneic T cell proliferation. Both DC and CD11c(-) microglia/macrophages from inflamed brain primed naive T cells from DO11.10 TCR transgenic mice for production of Th1 cytokines IFN-gamma and IL-2. Resting microglia that had been purified from normal adult brain generated immature DC upon exposure to GM-CSF, while CD40 ligation triggered terminal maturation. Consistently, a functional maturation of brain DC was observed to occur following the onset of encephalitis. In conclusion, these findings indicate that in addition to inflammatory macrophage-like brain cells, intraparenchymatical DC exist in autoimmune and infectious encephalitis. These DC functionally mature upon disease onset and can differentiate from resident microglia. Their emergence, maturation, and prolonged activity within the brain might contribute to the chronicity of intracerebral Th1 responses.},
	Author = {Fischer, H. G. and Reichmann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Cell Differentiation;Granulocyte-Macrophage Colony-Stimulating Factor;Th1 Cells;T-Lymphocyte Subsets;Immunophenotyping;Brain;Cells, Cultured;Interphase;Lymphocyte Activation;Animals;Macrophage-1 Antigen;Toxoplasmosis, Animal;Mice, Inbred BALB C;Cell Aging;Mice, Inbred C57BL;Integrin alphaXbeta2;Dendritic Cells;Macrophages;CD40 Ligand;11 Glia;Leukocytes, Mononuclear;Comparative Study;Nitric Oxide;Leukocyte Count;Coculture Techniques;Female;Microglia;Cytokines;Encephalomyelitis, Autoimmune, Experimental;Mice;Research Support, Non-U.S. Gov't;Mice, Transgenic},
	Medline = {21103309},
	Month = {2},
	Nlm_Id = {2985117R},
	Number = {4},
	Organization = {Institute for Medical Microbiology and Virology, Heinrich Heine University, Duesseldorf, Germany. hans-georg.fischer\@uni-duesseldorf.de},
	Pages = {2717-26},
	Pubmed = {11160337},
	Title = {Brain dendritic cells and macrophages/microglia in central nervous system inflammation},
	Uuid = {D4D34E3F-D8D0-470C-A684-B448B6653302},
	Volume = {166},
	Year = {2001}}

@article{Fischer:2001,
	Abstract = {The retina of warm-blooded vertebrates is believed to be incapable of neural regeneration. Here we provide evidence that the retina of postnatal chickens has the potential to generate new neurons. In response to acute damage, numerous Muller glia re-entered the cell cycle, and shortly thereafter, expressed CASH-1, Pax6 and Chx10, transcription factors expressed by embryonic retinal progenitors. These progenitor-like cells transiently expressed neurofilament. Newly formed cells became distributed throughout the inner and outer nuclear layers of the retina, and remained for at least three weeks after damage. Some of these newly formed cells differentiated into retinal neurons, a few formed Muller glia, and most remained undifferentiated, with continued expression of Pax6 and Chx10. These cells continued to proliferate when grown in culture, with some differentiating into retinal neurons or Muller glia. We propose that, in response to damage, Muller glia in the retina are a potential source of neural regeneration.},
	Author = {Fischer, A. J. and Reh, T. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Neuroglia/cytology/*metabolism;Nerve Regeneration/*physiology;N-Methylaspartate/pharmacology;Bromodeoxyuridine/pharmacology;Cells, Cultured/drug effects/metabolism;DNA-Binding Proteins/drug effects/metabolism;Neurons/cytology/*metabolism;Animal;Transcription Factors/drug effects/metabolism;Cell Division/drug effects/physiology;Receptors, Retinoic Acid/drug effects/metabolism;Retina/cytology/*metabolism;Support, Non-U.S. Gov't;Homeodomain Proteins/drug effects/metabolism;Neurotoxins/pharmacology;06 Adult neurogenesis injury induced;Neurofilament Proteins/drug effects/metabolism;D-13;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Glutamate-Ammonia Ligase/metabolism;Chickens},
	Number = {3},
	Organization = {Department of Biological Structure, University of Washington School of Medicine, Health Science Center, PO Box 357420, Seattle, Washington 98195, USA.},
	Pages = {247-52.},
	Title = {Muller glia are a potential source of neural regeneration in the postnatal chicken retina},
	Uuid = {2BABCDFF-41CF-4419-87B9-4B39597517CD},
	Volume = {4},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11224540}}

@article{Fischer:2005,
	Abstract = {While deregulation of cyclin-dependent kinase 5 (Cdk5) has been implicated in neurodegenerative diseases, its precise role in synaptic plasticity and memory remains elusive. Proteolytic cleavage of p35, a regulatory subunit of Cdk5, by calpain results in the generation of the truncated p25 protein, which causes hyperactivation of Cdk5. Using region-specific and inducible transgenic mice, we show that transiently increased p25 expression in the hippocampus enhanced long-term potentiation (LTP) and facilitated hippocampus-dependent memory. Moreover, p25 expression increased the number of dendritic spines and synapses. Importantly, enhanced memory achieved by a transient expression of p25 followed by its repression did not cause neurodegeneration. In contrast, prolonged p25 production caused severe cognitive deficits, which were accompanied by synaptic and neuronal loss and impaired LTP. Our data suggest a role for p25 in synaptic plasticity, synaptogenesis, learning, and memory and provide a model whereby deregulation of a plasticity factor can contribute to neurodegeneration.},
	Author = {Fischer, Andre and Sananbenesi, Farahnaz and Pang, Petti T. and Lu, Bai and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {research support, n.i.h., extramural ;Nerve Degeneration;Animals;Synapses;Fear;Memory;Conditioning (Psychology);Neuronal Plasticity;Space Perception;Mice, Transgenic;Hippocampus;research support, n.i.h., intramural ;Association Learning;Time Factors;Dendrites;Learning;21 Neurophysiology;Maze Learning;Mice;24 Pubmed search results 2008;Nerve Tissue Proteins;Anxiety;Cognition Disorders;Swimming},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Harvard Medical School, Department of Pathology, Boston, Massachusetts 02115, USA.},
	Pages = {825-38},
	Pii = {S0896-6273(05)00951-7},
	Pubmed = {16337919},
	Title = {Opposing roles of transient and prolonged expression of p25 in synaptic plasticity and hippocampus-dependent memory},
	Uuid = {7891483B-1EA8-4E32-B449-3094871B2734},
	Volume = {48},
	Year = {2005},
	url = {papers/Fischer_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.10.033}}

@article{Flanary:2004,
	Abstract = {Normal somatic cells have a finite replicative capacity. With each cell division, telomeres shorten progressively until they reach a critical length, at which point the cells enter replicative senescence. Some cells maintain their telomeres by the action of the telomerase enzyme. Glia, particularly microglia, are the only adult cell types in the central nervous system (CNS) that exhibit a significant mitotic potential, and are thus susceptible to telomere shortening. In this study, we show that telomere shortening accompanied by low to moderate telomerase activity, and ultimately senescence, occurs in rat microglia in vitro. When microglia are stimulated to divide with the mitogen granulocyte macrophage-colony stimulating factor (GM-CSF), longer telomeres are allowed to shorten, while shorter telomeres are lengthened. Telomerase activity is nearly 3-fold higher in GM-CSF-stimulated microglia initially, relative to unstimulated controls, and then declines to levels below those seen in controls before increasing again. Telomere attrition is also more rapid when microglia are grown in culture dishes of increasing size. Fluorescence in situ hybridization (FISH) analysis indicates that a nearly 3-fold variation in both inter- and intra-chromosomal telomere length exists in microglia. In contrast to microglia, cultured astrocytes exhibit a cyclical pattern of telomere lengthening and shortening over time, corresponding to a similar cycle of higher and lower telomerase activity. When astrocytes are passaged, mean telomere length increases initially from passage 1-2, remaining constant until passage 5, while the shortest telomeres are continually lengthened. In conclusion, the telomere shortening evident in microglia is accompanied by their progression to senescence by 32 days in vitro. In contrast, astrocytes, perhaps due to greater telomerase activity, have longer life spans and may be passaged repeatedly before entering senescence. Our findings provide an impetus to investigate the possibility that microglial telomere shortening may occur in vivo.},
	Author = {Flanary, Barry E. and Streit, Wolfgang J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Rats;Comparative Study;Astrocytes;Not relevant;Cell Division;Telomere;11 Glia;Microglia;Colony-Stimulating Factors;Telomerase;Support, Non-U.S. Gov't;Cells, Cultured;Animals},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida College of Medicine, McKnight Brain Institute, Gainesville, Florida 32610-0244, USA.},
	Pages = {75-88},
	Pubmed = {14648548},
	Title = {Progressive telomere shortening occurs in cultured rat microglia, but not astrocytes},
	Uuid = {1E30F4D9-C51A-4BC0-9410-99B608908626},
	Volume = {45},
	Year = {2004},
	url = {papers/Flanary_Glia2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10301}}

@article{Flanary:2003,
	Abstract = {Normal somatic cells have a finite replicative capacity. With each cell division, telomeres, the ends of linear chromosomes, progressively shorten until they reach a critical length, at which point the cells enter replicative senescence. Some cells maintain their telomeres by the action of the telomerase enzyme. Glia, particularly microglia, are the only adult cell type in the central nervous system (CNS) that exhibit a significant mitotic potential, and are thus susceptible to telomere shortening. Previous research in our laboratory has found that telomeres shorten in rat microglia with increasing time in vitro. Our current hypothesis is that telomeres shorten in rat brain in vivo with increasing age. Tissue samples of cerebellum and cortex were obtained from Sprague-Dawley rats of various ages. Genomic DNA and total protein was isolated from each sample for telomere length measurement via Southern blot analysis (up to 5 months) and telomerase activity measurement via TRAP analysis (up to 6 months), respectively. Telomere shortening occurs in vivo in both rat cerebellum and cortex from day 21 to approximately 5 months of age. Cortex samples possessed shorter telomeres than did cerebellum samples. The longest telomeres undergo the most dramatic shortening, while the shortest telomeres exhibit only slight attrition. Telomerase activity slowly increases from day 21 to approximately 6 months of age, with the cerebellum exhibiting higher activity than cortex in all instances. These results indicate that telomere shortening occurs in rat brain in vivo with increasing age, and that the low levels of telomerase activity present may be preferentially recruited to maintain the shortest telomeres while allowing the longer ones to shorten more rapidly. Since microglia are thought to be the only mature cells of the postnatal CNS undergoing appreciable cell division, we propose that the telomere shortening occurring in the adult rat brain with age can be largely attributed to microglial cell division. Our findings provide an impetus to further investigate the pattern of telomere length and telomerase activity that emerges with further aging in the rat brain.},
	Author = {Flanary, Barry E. and Streit, Wolfgang J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1094-5458},
	Journal = {J Anti Aging Med},
	Keywords = {Aging;Rats, Sprague-Dawley;Rats;Not relevant;Telomere;Cerebellum;11 Glia;Support, Non-U.S. Gov't;Animals;Cerebral Cortex},
	Nlm_Id = {9815684},
	Number = {4},
	Organization = {Department of Neuroscience, University of Florida College of Medicine, Gainesville, Florida 32610, USA.},
	Pages = {299-308},
	Pubmed = {15142431},
	Title = {Telomeres shorten with age in rat cerebellum and cortex in vivo},
	Uuid = {BC3D7885-6B86-43B0-A99E-2EA360D19B6E},
	Volume = {6},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/109454503323028894}}

@article{Flax:1998,
	Abstract = {Stable clones of neural stem cells (NSCs) have been isolated from the human fetal telencephalon. These self-renewing clones give rise to all fundamental neural lineages in vitro. Following transplantation into germinal zones of the newborn mouse brain they participate in aspects of normal development, including migration along established migratory pathways to disseminated central nervous system regions, differentiation into multiple developmentally and regionally appropriate cell types, and nondisruptive interspersion with host progenitors and their progeny. These human NSCs can be genetically engineered and are capable of expressing foreign transgenes in vivo. Supporting their gene therapy potential, secretory products from NSCs can correct a prototypical genetic metabolic defect in neurons and glia in vitro. The human NSCs can also replace specific deficient neuronal populations. Cryopreservable human NSCs may be propagated by both epigenetic and genetic means that are comparably safe and effective. By analogy to rodent NSCs, these observations may allow the development of NSC transplantation for a range of disorders. 1087-0156 Journal Article},
	Author = {Flax, J. D. and Aurora, S. and Yang, C. and Simonin, C. and Wills, A. M. and Billinghurst, L. L. and Jendoubi, M. and Sidman, R. L. and Wolfe, J. H. and Kim, S. U. and Snyder, E. Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Nat Biotechnol},
	Keywords = {Human;Stem Cells/cytology/physiology;Animals;Biotechnology;Cells, Cultured;10 Development;Transplantation, Heterologous;*Fetal Tissue Transplantation;*Stem Cell Transplantation;Cell Movement;Neurons/cytology/physiology/*transplantation;Genetic Engineering;Tay-Sachs Disease/enzymology/genetics/therapy;Animals, Newborn;Gene Therapy;Support, Non-U.S. Gov't;beta-N-Acetylhexosaminidase/deficiency/genetics;Support, U.S. Gov't, P.H.S.;Mice;*Brain Tissue Transplantation;Brain/cytology/growth &development/surgery;F},
	Number = {11},
	Organization = {Department of Neurology, Children's Hospital, Harvard Medical School, Boston, MA, USA.},
	Pages = {1033-9},
	Pubmed = {9831031},
	Title = {Engraftable human neural stem cells respond to developmental cues, replace neurons, and express foreign genes},
	Uuid = {238E4693-3F74-4738-AEBC-3636CCBF6D14},
	Volume = {16},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9831031}}

@article{Floden:2007,
	Abstract = {In vitro culture of rodent microglia is a common system used to model proinflammatory changes in the brain. However, typical postnatal brain isolation protocols are time consuming and cell numbers acquired are often a rate-limiting factor for experimental progress. Large studies that rely on the use of primary microglia can, therefore, require excessive numbers of animals at considerable expense, additional technical support and culture incubator space. Although the addition of mitogens such as macrophage colony-stimulating factor, granulocyte macrophage-colony stimulating factor, and epidermal growth factor to the cultures can facilitate a higher yield, this adds additional expense and likely alters the microglial phenotype. We have defined a simple, inexpensive modification of our standard culture protocol that allows us to repetitively isolate microglia. In order to define a method for improving microglia yield, we utilized our standard mixed glial culture preparation derived from postnatal day 1-3 mouse brains. After isolating microglia from mixed cultures at 14 days in vitro, we added fresh media to the cultures for an additional 7 and 14 days to monitor microglial proliferation. We acquired a constant number of cells at each successive time point although the numbers were reduced from the first isolation. More importantly, in order to determine if our successive microglia isolates differed phenotypically we characterized several parameters of function. We compared their ability to secrete the proinflammatory cytokines interleukin-6 and tumor necrosis factor alpha after LPS stimulation. We also contrasted the phagocytic ability, morphology, and specific immunoreactivity (CD11b, CD68, CD45 and MHC II) of the culture ages. Our data demonstrate that microglia can be obtained from extended-time cultures provided periodic isolation is performed. Moreover, the cells retain a comparable in vitro phenotype. This demonstrates that cells from all ages can be combined for any given study. These findings are a viable and inexpensive way to increase and extend the microglial yield without increasing the number of animals used or adding costly mitogens. This method will be particularly useful for the preparation of microglia cultures from limited transgenic colonies.},
	Author = {Floden, A. M. and Combs, C. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {Animals;Cell Separation;Gene Expression Regulation;Cells, Cultured;Tumor Necrosis Factor-alpha;Phenotype;Brain;Microglia;Lipopolysaccharides;Antigens, CD;Cell Count;Mice, Inbred C57BL;11 Glia;Time Factors;Animals, Newborn;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Interleukin-6},
	Month = {8},
	Nlm_Id = {7905558},
	Number = {2},
	Organization = {Department of Pharmacology, Physiology & Therapeutics, University of North Dakota School of Medicine and Health Sciences, Neuroscience Building, 504 Hamline Street, Grand Forks, ND 58202-9037, United States.},
	Pages = {218-24},
	Pii = {S0165-0270(07)00207-5},
	Pubmed = {17553568},
	Title = {Microglia repetitively isolated from in vitro mixed glial cultures retain their initial phenotype},
	Uuid = {86B54A08-BE99-4358-ADB1-A9D519D88A3F},
	Volume = {164},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jneumeth.2007.04.018}}

@article{Florkiewicz:1984,
	Abstract = {A stable cell line expressing a complementary DNA clone encoding the vesicular stomatitis virus glycoprotein fused and formed polykaryons at pH 5.5. The formation of polykaryons was dependent on the presence of glycoprotein anchored at the cell surface and could be prevented by incubation of cells with a monoclonal antibody to the glycoprotein. Fusion occurred at a pH 0.5 unit lower than that observed for cells infected with vesicular stomatitis virus.},
	Author = {Florkiewicz, R. Z. and Rose, J. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Cell Membrane;Membrane Glycoproteins;Cell Fusion;Antibodies, Monoclonal;Research Support, U.S. Gov't, P.H.S.;Cell Line;Viral Proteins;Vesicular stomatitis-Indiana virus;Glycoproteins;15 Retrovirus mechanism;Animals;Hydrogen-Ion Concentration;Mice;Viral Envelope Proteins;24 Pubmed search results 2008},
	Medline = {84274419},
	Month = {8},
	Nlm_Id = {0404511},
	Number = {4663},
	Pages = {721-3},
	Pubmed = {6087454},
	Title = {A cell line expressing vesicular stomatitis virus glycoprotein fuses at low pH},
	Uuid = {249DF706-EE2C-11DA-8605-000D9346EC2A},
	Volume = {225},
	Year = {1984}}

@article{Flugel:1999,
	Abstract = {Microglia and brain macrophages represent a substantial fraction of the cells present in astrocytic gliomas. Yet, the functional role of microglia in these tumors has remained enigmatic. We have compared rat microglial cells and thymocytes with regard to their ability to present purified CNS proteins, MBP and S100beta, as well as C6 glioma cells to specific T lymphocytes. In addition, a new cytotoxicity assay based on fluorescence activated cell sorting of tumor cells carrying the green fluorescent protein was established. This assay was used to determine the influence of microglial population density and activational state on C6 glioma cell survival in vitro. Microglia were consistently found to present MBP and S100beta less efficiently than thymocytes and appeared to be unable to present C6 glioma cells to cytotoxic T lymphocytes. In addition, high concentrations of microglial cells attenuated the cytotoxic effects of these T cells on C6 glioma cells whereas thymocytes significantly supported their specific killing. It is suggested that defense functions of microglial cells against C6 glioma are severely compromised and that the observed deficiency in antigen presentation may play an important role for astrocytoma growth in vivo.},
	Author = {Fl{\"u}gel, A. and Labeur, M. S. and Grasbon-Frodl, E. M. and Kreutzberg, G. W. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0736-5748},
	Journal = {Int J Dev Neurosci},
	Keywords = {Antigens, Neoplasm;Flow Cytometry;Tumor Cells, Cultured;Luminescent Proteins;Glioma;Rats;T-Lymphocytes, Cytotoxic;Animals, Genetically Modified;Thymus Gland;11 Glia;Microglia;Antigen-Presenting Cells;Brain Neoplasms;Green Fluorescent Proteins;Animals;Cells, Cultured;Cell Separation},
	Medline = {20036194},
	Nlm_Id = {8401784},
	Number = {5-6},
	Organization = {Department of Neuroimmunology, Max-Planck-Institute of Neurobiology, Martinsried, Germany.},
	Pages = {547-56},
	Pubmed = {10571416},
	Title = {Microglia only weakly present glioma antigen to cytotoxic T cells},
	Uuid = {E4D20645-9E41-4FD4-9094-8155D4F69AAF},
	Volume = {17},
	Year = {1999}}

@article{Flugel:2001,
	Abstract = {Direct injury of the brain is followed by inflammatory responses regulated by cytokines and chemoattractants secreted from resident glia and invading cells of the peripheral immune system. In contrast, after remote lesion of the central nervous system, exemplified here by peripheral transection or crush of the facial and hypoglossal nerve, the locally observed inflammatory activation is most likely triggered by the damaged cells themselves, that is, the injured neurons. The authors investigated the expression of the chemoattractants monocyte chemoattractant protein MCP-1, regulation on activation normal T-cell expressed and secreted (RANTES), and interferon-gamma inducible protein IP10 after peripheral nerve lesion of the facial and hypoglossal nuclei. In situ hybridization and immunohistochemistry revealed an induction of neuronal MCP-1 expression within 6 hours postoperation, reaching a peak at 3 days and remaining up-regulated for up to 6 weeks. MCP-1 expression was almost exclusively confined to neurons but was also present on a few scattered glial cells. The authors found no alterations in the level of expression and cellular distribution of RANTES or IP10, which were both confined to neurons. Protein expression of the MCP-1 receptor CCR2 did not change. MCP-1, expressed by astrocytes and activated microglia, has been shown to be crucial for monocytic, or T-cell chemoattraction, or both. Accordingly, expression of MCP-1 by neurons and its corresponding receptor in microglia suggests that this chemokine is involved in neuron and microglia interaction.},
	Author = {Fl{\"u}gel, A. and Hager, G. and Horvat, A. and Spitzer, C. and Singer, G. M. and Graeber, M. B. and Kreutzberg, G. W. and Schwaiger, F. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0271-678X},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {Receptors, Cytokine;Microtubule-Associated Proteins;Animals;Gene Expression Regulation;Rats;Brain;Rats, Wistar;11 Glia;RNA, Messenger;Male;In Situ Hybridization;Neurons;RANTES;Axotomy;Laterality;Immunohistochemistry;Monocyte Chemoattractant Protein-1;Facial Nerve;Hypoglossal Nerve;Research Support, Non-U.S. Gov't},
	Medline = {21024390},
	Month = {1},
	Nlm_Id = {8112566},
	Number = {1},
	Organization = {Department of Neuroimmunology, Max-Planck-Institute of Neurobiology, Martinsried, Germany.},
	Pages = {69-76},
	Pubmed = {11149670},
	Title = {Neuronal MCP-1 expression in response to remote nerve injury},
	Uuid = {239DA0B5-EA6B-4C76-BFB6-777DAEF163A5},
	Volume = {21},
	Year = {2001}}

@article{Flugel:2001a,
	Abstract = {Macrophages in the brain can have a triple source. They may originate from recently blood-derived precursors, from the largely resident perivascular cell population (perivascular macrophages and related cells), and from intrinsic parenchymal as well as perivascular microglia. Although continuous exchange of part of the perivascular cell population with bone marrow-derived precursors is now accepted, the turnover of adult parenchymal microglia has remained enigmatic. Using bone-marrow chimeras carrying an unexpressed marker gene and carbon labeling of peripheral monocyte/macrophages in a combined model of facial nerve axotomy and transfer experimental autoimmune encephalitis, we demonstrate for the first time that there is an easy to induce exchange between parenchymal central nervous system (CNS) microglia and the macrophage precursor cell pool of the bone marrow. Furthermore, very low level infiltration of the CNS parenchyma by recently bone marrow-derived microglia could be observed after simple peripheral nerve axotomy that is followed by neuronal regeneration. Thus, microglial cells can be considered wanderers between the peripheral immune system and the CNS where they may act as a "Trojan horse" in infections. The fact that recently bone marrow-derived parenchymal microglia fully integrate into a regenerating brain nucleus' architecture encourages entirely new approaches for delivering genes into the adult CNS.},
	Author = {Fl{\"u}gel, A. and Bradl, M. and Kreutzberg, G. W. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Transgenes;Cell Differentiation;Multiple Sclerosis;Rats, Inbred Lew;Monocytes;Macrophages;Chimera;Rats;Thymidine Kinase;Animals;Microglia;11 Glia;Immunophenotyping;Nerve Regeneration;In Situ Hybridization;Bone Marrow Cells;Cell Lineage;Gene Therapy;Encephalomyelitis, Autoimmune, Experimental;Axotomy;Simplexvirus;Biological Markers;Facial Nerve;Research Support, Non-U.S. Gov't},
	Medline = {21482213},
	Month = {10},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuroimmunology, Max-Planck-Institute of Neurobiology, Martinsried, Germany.},
	Pages = {74-82},
	Pii = {10.1002/jnr.1198},
	Pubmed = {11599003},
	Title = {Transformation of donor-derived bone marrow precursors into host microglia during autoimmune CNS inflammation and during the retrograde response to axotomy},
	Uuid = {EE80116F-5DC4-47A4-80CC-86BA7088D759},
	Volume = {66},
	Year = {2001}}

@article{Fordyce:2005,
	Abstract = {Many CNS disorders involve an inflammatory response that is orchestrated by cells of the innate immune system: macrophages, neutrophils, and microglia (the endogenous CNS immune cell). Hence, there is considerable interest in anti-inflammatory strategies that target these cells. Microglia express Kv1.3 (KCNA3) channels, which we showed previously are important for their proliferation and the NADPH-mediated respiratory burst. Here, we demonstrate the potential for targeting Kv1.3 channels to control CNS inflammation. Rat microglia express Kv1.2, Kv1.3, and Kv1.5 transcripts and protein, but only a Kv1.3 current was detected. When microglia were activated with lipopolysaccharide or a phorbol ester, only the Kv1.3 transcript (but not protein) expression changed. Using a Transwell cell-culture system that allows separate drug treatment of microglia or neurons, we found that activated microglia killed postnatal hippocampal neurons through a process that requires Kv1.3 channel activity in microglia but not in neurons. A major neurotoxic molecule in this model was peroxynitrite, which is formed from superoxide and nitric oxide; thus, it is significant that Kv1.3 channel blockers reduced the respiratory burst, but not nitric oxide production, by the activated microglia. In addressing the biochemical pathway affected by Kv1.3 channel activity, we found that Kv1.3 acts via a different cellular mechanism from the broad-spectrum drug minocycline, which is often used in animal models of neuroinflammation. That is, the dose-dependent reduction in neuron killing by minocycline corresponded with a reduction in p38 mitogen-activated protein kinase activation in microglia; however, none of the Kv1.3 blockers affected p38 activation.},
	Author = {Fordyce, Christopher B. and Jagasia, Ravi and Zhu, Xiaoping and Schlichter, Lyanne C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {07 Excitotoxicity Apoptosis;Alpha;11 Glia},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {31},
	Organization = {Division of Cellular and Molecular Biology, Toronto Western Research Institute, University Health Network, Toronto, Ontario, M5T 2S8, Canada.},
	Pages = {7139-49},
	Pii = {25/31/7139},
	Pubmed = {16079396},
	Title = {Microglia Kv1.3 channels contribute to their ability to kill neurons},
	Uuid = {2D7ACEB2-BBAB-4C96-9F19-5FF427A2E23C},
	Volume = {25},
	Year = {2005},
	url = {papers/Fordyce_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1251-05.2005}}

@article{Forni:2006,
	Abstract = {Hydrocephalus is a common and variegated pathology often emerging in newborn children after genotoxic insults during pregnancy (Hicks and D'Amato, 1980). Cre recombinase is known to have possible toxic effects that can compromise normal cell cycle and survival. Here we show, by using three independent nestin Cre transgenic lines, that high levels of Cre recombinase expression into the nucleus of neuronal progenitors can compromise normal brain development. The transgenics analyzed are the nestin Cre Balancer (Bal1) line, expressing the Cre recombinase with a nuclear localization signal, and two nestin CreER(T2) (Cre recombinase fused with a truncated estrogen receptor) mice lines with different levels of expression of a hybrid CreER(T2) recombinase that translocates into the nucleus after tamoxifen treatment. All homozygous Bal1 nestin Cre embryos displayed reduced neuronal proliferation, increased aneuploidy and cell death, as well as defects in ependymal lining and lamination of the cortex, leading to microencephaly and to a form of communicating hydrocephalus. An essentially overlapping phenotype was observed in the two nestin CreER(T2) transgenic lines after tamoxifen mediated-CreER(T2) translocation into the nucleus. Neither tamoxifen-treated wild-type nor nestin CreER(T2) oil-treated control mice displayed these defects. These results indicate that some forms of hydrocephalus may derive from a defect in neuronal precursors proliferation. Furthermore, they underscore the potential risks for developmental studies of high levels of nuclear Cre in neurogenic cells.},
	Author = {Forni, Paolo E. and Scuoppo, Claudio and Imayoshi, Itaru and Taulli, Riccardo and Dastr\`{u}, Walter and Sala, Valentina and Betz, Ulrich A. K. and Muzzi, Patrizia and Martinuzzi, Daniela and Vercelli, Alessandro E. and Kageyama, Ryoichiro and Ponzetto, Carola},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Gene Expression Regulation, Developmental;Selective Estrogen Receptor Modulators;Brain;Integrases;Hydrocephalus;Receptors, Estrogen;21 Dysplasia-heterotopia;Mice, Transgenic;Cell Proliferation;Microcephaly;23 Technique;Aneuploidy;Nuclear Localization Signals;Nervous System Malformations;21 Neurophysiology;Intermediate Filament Proteins;Neurons;Ependyma;Tamoxifen;Mice;24 Pubmed search results 2008;Biological Markers;Cell Death;Nerve Tissue Proteins;Stem Cells},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {37},
	Organization = {Department of Anatomy, Pharmacology, and Forensic Medicine, University of Turin, 10126 Turin, Italy. paolo.forni\@unito.it},
	Pages = {9593-602},
	Pii = {26/37/9593},
	Pubmed = {16971543},
	Title = {High levels of Cre expression in neuronal progenitors cause defects in brain development leading to microencephaly and hydrocephaly},
	Uuid = {59FB2871-68E4-468C-B492-A314FFE82130},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2815-06.2006}}

@article{Fouad:2005,
	Abstract = {Numerous obstacles to successful regeneration of injured axons in the adult mammalian spinal cord exist. Consequently, a treatment strategy inducing axonal regeneration and significant functional recovery after spinal cord injury has to overcome these obstacles. The current study attempted to address multiple impediments to regeneration by using a combinatory strategy after complete spinal cord transection in adult rats: (1) to reduce inhibitory cues in the glial scar (chondroitinase ABC), (2) to provide a growth-supportive substrate for axonal regeneration [Schwann cells (SCs)], and (3) to enable regenerated axons to exit the bridge to re-enter the spinal cord (olfactory ensheathing glia). The combination of SC bridge, olfactory ensheathing glia, and chondroitinase ABC provided significant benefit compared with grafts only or the untreated group. Significant improvements were observed in the Basso, Beattie, and Bresnahan score and in forelimb/hindlimb coupling. This recovery was accompanied by increased numbers of both myelinated axons in the SC bridge and serotonergic fibers that grew through the bridge and into the caudal spinal cord. Although prominent descending tracts such as the corticospinal and reticulospinal tracts did not successfully regenerate through the bridge, it appeared that other populations of regenerated fibers were the driving force for the observed recovery; there was a significant correlation between numbers of myelinated fibers in the bridge and improved coupling of forelimb and hindlimb as well as open-field locomotion. Our study tests how proven experimental treatments interact in a well-established animal model, thus providing needed direction for the development of future combinatory treatment regimens.},
	Author = {Fouad, Karim and Schnell, Lisa and Bunge, Mary B. and Schwab, Martin E. and Liebscher, Thomas and Pearse, Damien D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {5},
	Organization = {University of Alberta, Faculty of Rehabilitation Medicine, Edmonton, Canada T6G 2G4. karim.fouad\@ualberta.ca},
	Pages = {1169-78},
	Pii = {25/5/1169},
	Pubmed = {15689553},
	Title = {Combining Schwann cell bridges and olfactory-ensheathing glia grafts with chondroitinase promotes locomotor recovery after complete transection of the spinal cord},
	Uuid = {1F1A6936-8500-449E-8DB1-8D28F5562C95},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3562-04.2005}}

@article{Fowler:2002,
	Abstract = {In the mammalian brain, adult neurogenesis has been found to occur primarily in the subventricular zone (SVZ) and dentate gyrus of the hippocampus (DG) and to be influenced by both exogenous and endogenous factors. In the present study, we examined the effects of male exposure or social isolation on neurogenesis in adult female prairie voles (Microtus ochrogaster). Newly proliferated cells labeled by a cell proliferation marker, 5-bromo-2'-deoxyuridine (BrdU), were found in the SVZ and DG, as well as in other brain areas, such as the amygdala, hypothalamus, neocortex, and caudate/putamen. Two days of male exposure significantly increased the number of BrdU-labeled cells in the amygdala and hypothalamus in comparison to social isolation. Three weeks later, group differences in BrdU labeling generally persisted in the amygdala, whereas in the hypothalamus, the male-exposed animals had more BrdU-labeled cells than did the female-exposed animals. In the SVZ, 2 days of social isolation increased the number of BrdU-labeled cells compared to female exposure, but this difference was no longer present 3 weeks later. We have also found that the vast majority of the BrdU-labeled cells contained a neuronal marker, indicating neuronal phenotypes. Finally, group differences in the number of cells undergoing apoptosis were subtle and did not seem to account for the observed differences in BrdU labeling. Together, our data indicate that social environment affects neuron proliferation in a stimulus- and site- specific manner in adult female prairie voles.},
	Author = {Fowler, C. D. and Liu, Y. and Ouimet, C. and Wang, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:35:09 -0400},
	Journal = {J Neurobiol},
	Keywords = {B pdf;02 Adult neurogenesis migration},
	Number = {2},
	Organization = {Department of Psychology and Program of Neuroscience, Florida State University, Tallahassee, Florida 32306.},
	Pages = {115-28.},
	Title = {The effects of social environment on adult neurogenesis in the female prairie vole},
	Uuid = {151E41B7-11F9-4662-B800-070C658211C6},
	Volume = {51},
	Year = {2002},
	url = {papers/Fowler_JNeurobiol2002.pdf}}

@article{Fox:1998,
	Abstract = {Long-range, directed migration is particularly dramatic in the cerebral cortex, where postmitotic neurons generated deep in the brain migrate to form layers with distinct form and function. In the X-linked dominant human disorder periventricular heterotopia (PH), many neurons fail to migrate and persist as nodules lining the ventricular surface. Females with PH present with epilepsy and other signs, including patent ductus arteriosus and coagulopathy, while hemizygous males die embryonically. We have identified the PH gene as filamin 1 (FLN1), which encodes an actin-cross-linking phosphoprotein that transduces ligand-receptor binding into actin reorganization, and which is required for locomotion of many cell types. FLN1 shows previously unrecognized, high-level expression in the developing cortex, is required for neuronal migration to the cortex, and is essential for embryogenesis.},
	Author = {Fox, J. W. and Lamperti, E. D. and Ekiolu, Y. Z. and Hong, S. E. and Feng, Y. and Graham, D. A. and Scheffer, I. E. and Dobyns, W. B. and Hirsch, B. A. and Radtke, R. A. and Berkovic, S. F. and Huttenlocher, P. R. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:45:45 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Cerebral Ventricles;Epilepsy;Fetal Death;24 Pubmed search results 2008;Microfilament Proteins;Male;Contractile Proteins;Brain Diseases;Cerebral Cortex;Sex Characteristics;Animals;Brain;Research Support, U.S. Gov't, P.H.S.;Gene Expression Regulation, Developmental;Phenotype;X Chromosome;Magnetic Resonance Imaging;Chromosome Mapping;21 Epilepsy;Abnormalities, Multiple;Aging;Pedigree;Female;21 Neurophysiology;Mice;Research Support, Non-U.S. Gov't;Neurons;Humans;Choristoma;Embryonic and Fetal Development},
	Medline = {99098194},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA.},
	Pages = {1315-25},
	Pii = {S0896-6273(00)80651-0},
	Pubmed = {9883725},
	Title = {Mutations in filamin 1 prevent migration of cerebral cortical neurons in human periventricular heterotopia},
	Uuid = {0E99B0A5-1E09-450C-9E36-AFD3AF9FF4A3},
	Volume = {21},
	Year = {1998},
	url = {papers/Fox_Neuron1998.pdf}}

@article{Forster:2002,
	Abstract = {The mammary glands of prepubertal estrogen receptor (ER)beta-- mice are morphologically indistinguishable from those of WT littermates. It appears that, although ERbeta is expressed in the mouse mammary gland, it is not involved in ductal growth of the gland. In this study, we examined the possibility that ERbeta has a role in the differentiated function of the mammary gland. Pregnancy is rare in ERbeta-- mice, but an intensive breeding program produced seven pregnant ERbeta-- mice, of which five did not eat their offspring and continued to successful lactation. Histomorphological comparison of lactating glands revealed that alveoli were larger and there was less secretory epithelium in ERbeta-- than in WT mice. Ultrastructural analysis showed abundant milk droplets and normal apical villi in the luminal epithelial cells, but the extracellular matrix and lamina basalis were reduced, and very frequently the interepithelial cell space was increased. Levels of the adhesion molecules, E-cadherin, connexin 32, occludin, and integrin alpha2 were reduced, and no zona occludens was detectable. In addition, there was widespread expression of the proliferation marker, Ki-67, in luminal epithelial cells in ERbeta-- but not in WT mice. These findings suggest a role for ERbeta in organization and adhesion of epithelial cells and hence for differentiated tissue morphology. We speculate that, because a reduced risk for breast cancer is conferred on women who breast-feed at an early age, ERbeta could contribute to this risk reduction by facilitating terminal differentiation of the mammary gland.},
	Author = {F{\"o}rster, Carola and M{\"a}kela, Sari and W{\"a}rri, Anni and Kietz, Silke and Becker, David and Hultenby, Kjell and Warner, Margaret and Gustafsson, Jan-Ake A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {10 Development;Cell Differentiation;Animals;10 Hippocampus;Pregnancy;Mammary Glands, Animal;Tight Junctions;Epithelial Cells;Lactation;Female;Receptors, Estrogen;Cell Polarity;Fertility;Gap Junctions;Integrin alpha6;Integrin alpha2;Cadherins;Mice, Knockout;Estrogen Receptor beta;Mice;Research Support, Non-U.S. Gov't},
	Medline = {22342748},
	Month = {11},
	Nlm_Id = {7505876},
	Number = {24},
	Organization = {Department of Medical Nutrition, Karolinska Institute, Novum, S-141 86 Huddinge, Sweden.},
	Pages = {15578-83},
	Pii = {192561299},
	Pubmed = {12438700},
	Title = {Involvement of estrogen receptor beta in terminal differentiation of mammary gland epithelium},
	Uuid = {BF311DFC-72AB-4126-A3B7-03AA185587AB},
	Volume = {99},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.192561299}}

@article{Forster:2002a,
	Abstract = {The extracellular matrix molecule Reelin is required for the correct positioning of neurons during the development of the forebrain. However, the mechanism of Reelin action on neuronal migration is poorly understood. Reelin is assumed to act on neurons directly, but it may also affect the differentiation of glial cells necessary for neuronal migration. Here we show that a regular glial scaffold fails to form in vivo in the dentate gyrus of mice deficient of Reelin or Disabled 1, a neuronal adaptor protein in the Reelin signaling pathway. A subset of these defects is observed in mice that lack beta(1)-class integrins, known to bind Reelin. Moreover, recombinant Reelin induced branching of glial processes in vitro. Our data suggest that Reelin affects glial differentiation via Disabled 1 and beta(1)-class integrin-dependent signaling pathways.},
	Author = {F{\"o}rster, Eckart and Tielsch, Albrecht and Saum, Barbara and Weiss, Karl Heinz and Johanssen, Celine and Graus-Porta, Diana and M{\"u}ller, Ulrich and Frotscher, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Glial Fibrillary Acidic Protein;Golgi Apparatus;Signal Transduction;Animals;Humans;Mutation;Hippocampus;Serine Endopeptidases;Cell Adhesion Molecules, Neuronal;RNA, Messenger;Prosencephalon;In Situ Hybridization;Extracellular Matrix Proteins;Cell Line;Animals, Newborn;Antigens, CD29;Neuroglia;DNA, Complementary;Mice;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22247732},
	Month = {10},
	Nlm_Id = {7505876},
	Number = {20},
	Organization = {Anatomisches Institut, Universit{\"a}t Freiburg, P.O. Box 111, D-79001 Freiburg, Germany. foerster\@uni-feiburg.de},
	Pages = {13178-83},
	Pii = {202035899},
	Pubmed = {12244214},
	Title = {Reelin, Disabled 1, and beta 1 integrins are required for the formation of the radial glial scaffold in the hippocampus},
	Uuid = {59B7EE44-C34B-11DA-969D-000D9346EC2A},
	Volume = {99},
	Year = {2002},
	url = {papers/Förster_ProcNatlAcadSciUSA2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.202035899}}

@article{Frade:2000,
	Abstract = {During their early postmitotic life, a proportion of the nascent retinal ganglion cells (RGCs) are induced to die as a result of the interaction of nerve growth factor (NGF) with the neurotrophin receptor p75. To analyse the mechanisms by which NGF promotes apoptosis, an in vitro culture system consisting of dissociated E5 retinal cells was established. In this system, NGF-induced apoptosis was only observed in the presence of insulin and neurotrophin-3, conditions that favour the birth of RGCs and other neurones expressing the glycoprotein G4. The pro-apoptotic effect of NGF on the G4-positive neurones was evident after 10 hours in vitro and was preceded by a significant upregulation of cyclin B2, but not cyclin D1, and the presence of mitotic nuclei in these cells. Brain-derived neurotrophic factor prevented both the increase of cyclin B2 expression in the G4-positive neurones and the NGF-induced cell death. Finally, pharmacologically blocking cell-cycle progression using the cyclin-dependent kinase inhibitor roscovitine prevented NGF-induced cell death in a dose-dependent manner. These results strongly suggest that the apoptotic signalling initiated by NGF requires a driving stimulus manifested by the neuronal birth and is preceded by the unscheduled re-entry of postmitotic neurones into the cell cycle. 0021-9533 Journal Article},
	Author = {Frade, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Journal = {J Cell Sci},
	Keywords = {Animals;Brain-Derived Neurotrophic Factor/physiology;Cells, Cultured;Purines/pharmacology;Neurons/cytology/*physiology;Insulin/physiology;EE pdf;Culture Media, Conditioned;08 Aberrant cell cycle;Retina/cytology/*embryology;Support, Non-U.S. Gov't;Chick Embryo;Cell Death/drug effects/physiology;Apoptosis/drug effects/physiology;Cell Cycle/*physiology;Growth Inhibitors/pharmacology;Neurotrophin 3/physiology;Cell Differentiation/physiology;Nerve Growth Factor/antagonists &inhibitors/*physiology},
	Organization = {Instituto Cajal de Neurobiologia, CSIC, Avenida Doctor Arce 37, Madrid E28002, Spain. isrf303\@fresno.csic.es.},
	Pages = {1139-48},
	Pubmed = {10704365},
	Title = {Unscheduled re-entry into the cell cycle induced by NGF precedes cell death in nascent retinal neurones},
	Uuid = {4813D1CA-F1B2-4F96-AB25-4D667BD935A8},
	Volume = {113 ( Pt 7)},
	Year = {2000},
	url = {papers/Frade_JCellSci2000.pdf}}

@article{Franceschini:2004,
	Abstract = {Polysialic acid (PSA) on NCAM is an important modulator of cell-cell interactions during development and regeneration. Here we investigated whether PSA overexpression influences neural cell migration and myelination. We stably expressed a GFP-tagged polysialytransferase, PSTGFP, in mouse neurospheres and induced prolonged PSA synthesis. Using a chick xenograft assay for migration, we show that PSA can instruct precursor migration along the ventral pathway. PSA persistence did not change neural precursor multipotentiality in vitro but induced a delay in oligodendrocyte differentiation. PSTGFP+ precursors showed widespread engraftment in shiverer brain, closely similar to that observed with control precursors expressing a fluorescent protein. Initially, myelination by oligodendrocytes was delayed but, eventually, down-regulation of PSTGFP occurred, allowing myelination to proceed. Thus down-regulation of polysialyltransferases takes place even in cells where its RNA is under the control of a heterologous promoter and engineering PSA overexpression in neural precursors does not cause irreversible unphysiological effects.},
	Author = {Franceschini, Isabelle and Vitry, Sandrine and Padilla, Fran\c{c}oise and Casanova, Philippe and Tham, To Nam and Fukuda, Minoru and Rougon, Genevi\`{e}ve and Durbec, Pascale and Dubois-Dalcq, Monique},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:21 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Animals;Gene Expression Regulation;Cells, Cultured;Humans;Comparative Study;Cell Movement;Mice, Transgenic;Nerve Fibers, Myelinated;Mice, Inbred C57BL;Research Support, U.S. Gov't, P.H.S.;Sialic Acids;Chick Embryo;3T3 Cells;Neurons;Mice;Protein Engineering;24 Pubmed search results 2008;Neural Cell Adhesion Molecule L1;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {10},
	Nlm_Id = {9100095},
	Number = {2},
	Organization = {Unit{\'e} de Neurovirologie et R{\'e}g{\'e}n{\'e}ration du Syst\`{e}me Nerveux, Institut Pasteur, 75724 Paris cedex 15, France.},
	Pages = {151-62},
	Pii = {S1044-7431(04)00127-7},
	Pubmed = {15485771},
	Title = {Migrating and myelinating potential of neural precursors engineered to overexpress PSA-NCAM},
	Uuid = {779B993B-A63D-4899-9CA5-C2C814245E14},
	Volume = {27},
	Year = {2004},
	url = {papers/Franceschini_MolCellNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2004.05.006}}

@article{Francis:1999,
	Abstract = {Recently, we and others reported that the doublecortin gene is responsible for X-linked lissencephaly and subcortical laminar heterotopia. Here, we show that Doublecortin is expressed in the brain throughout the period of corticogenesis in migrating and differentiating neurons. Immunohistochemical studies show its localization in the soma and leading processes of tangentially migrating neurons, and a strong axonal labeling is observed in differentiating neurons. In cultured neurons, Doublecortin expression is highest in the distal parts of developing processes. We demonstrate by sedimentation and microscopy studies that Doublecortin is associated with microtubules (MTs) and postulate that it is a novel MAP. Our data suggest that the cortical dysgeneses associated with the loss of Doublecortin function might result from abnormal cytoskeletal dynamics in neuronal cell development.},
	Author = {Francis, F. and Koulakoff, A. and Boucher, D. and Chafey, P. and Schaar, B. and Vinet, M. C. and Friocourt, G. and McDonnell, N. and Reiner, O. and Kahn, A. and McConnell, S. K. and Berwald-Netter, Y. and Denoulet, P. and Chelly, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Neuron},
	Keywords = {RNA, Messenger/biosynthesis;10 Development;Rats, Long-Evans;Cells, Cultured;Rats;Animal;Cytoskeleton/metabolism/ultrastructure;Microtubule-Associated Proteins/biosynthesis/*physiology;In Situ Hybridization;Support, Non-U.S. Gov't;Antibody Specificity;Neurons/metabolism/*physiology/ultrastructure;Brain/cytology/embryology/metabolism;Support, U.S. Gov't, P.H.S.;Tubulin/isolation &purification/metabolism;Mice;Cell Differentiation/physiology;Immunohistochemistry;Neuropeptides/biosynthesis/*physiology;Cell Movement/physiology;Phosphoproteins/biosynthesis/*physiology;F},
	Number = {2},
	Organization = {U129 de l'INSERM, Institut Cochin de Genetique Moleculaire, Paris. ffrancis\@infobiogen.fr},
	Pages = {247-56.},
	Title = {Doublecortin is a developmentally regulated, microtubule-associated protein expressed in migrating and differentiating neurons},
	Uuid = {9AD7D46C-6D0F-11DA-A4FE-000D9346EC2A},
	Volume = {23},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10399932}}

@article{Frank:1996,
	Abstract = {Rat optic nerves were subjected to crush injury to study the local tissue reactions leading to wound healing and tissue repair. We used antibodies against glial fibrillary acidic protein (GFAP), vimentin, the S1OO protein (S1OOP), lysozyme, and ED1 as markers for astroglial cells and microglia/macrophages at the light and electron microscopic level during the 3 weeks following the crush. The crush injury produced a vast area of tissue damage including the disruption of the blood-brain barrier (BBB). In the first days after crushing, astrocytes were absent from the lesion site. S1OOP-positive astrocytes reappeared in the lesion center as early as 6 days after crushing. These astrocytes reestablished former topological structures such as perivascular and subpial glia limitans. At the edges of the lesion site reactive astrocytes enclosed and embedded axonal and myelin debris. Preceding the astroglial repopulation, a massive infiltration of microglia/macrophages (phagocytes) into the lesion center took place. ED1-positive/lysozyme- positive cells of round shape were seen in the lesion center at 2 days after crushing, and their number peaked around 1 week after crushing. They efficiently cleared the debris from the lesion site and mostly disappeared after 3 weeks. With immuno-electron microscopy we found the ED1 antigen related to the membranes of phagosomes. The microglia/macrophages observed in the nerve segments distal of the lesion (Wallerian degeneration site) were different from those in the lesion center: 1) they appeared later, about 6 days after crushing; 2) they were ED1 positive, but lysozyme negative and showed a branched morphology; and 3) they persisted in the distal nerve segment but showed little phagocytosis. We suggest that these cells are mostly activated microglia.},
	Author = {Frank, M. and Wolburg, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Animals;Astrocytes;Macrophages;Rats;Microglia;Cell Count;Optic Nerve;Rats, Wistar;Not relevant;11 Glia;Time Factors;Male;Support, Non-U.S. Gov't;Nerve Crush;Immunohistochemistry;Microscopy, Electron;Biological Markers;Optic Nerve Injuries},
	Medline = {96430043},
	Month = {3},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Universitat Tubingen, Institut fur Pathologie, Germany.},
	Pages = {227-40},
	Pii = {10.1002/(SICI)1098-1136(199603)16:3<227::AID-GLIA5>3.0.CO;2-Z},
	Pubmed = {8833193},
	Title = {Cellular reactions at the lesion site after crushing of the rat optic nerve},
	Uuid = {2FFB7CB9-821C-4426-B9B7-9FCCB1821FA9},
	Volume = {16},
	Year = {1996}}

@article{Frankshten:1986,
	Abstract = {Influence of cerebral hypoxia and hyperventilatory hypocapnia on the ECoG and focal epileptiform activity of the cerebral cortex induced with local application of strychnine was studied in cats with transection of spinal cord at C1. Although both hypoxia and hypocapnia produced synchronization of the cerebral cortex electrical activity, i.e. exerted the same effects on the ECoG, their influence on cortical excitability was quite different: hypoxia suppressed the epileptiform activity whereas hypocapnia facilitated it.},
	Author = {Frankshten, S. I. and Smolin, L. N. and Sergeeva, L. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0015-329X},
	Journal = {Fiziol Zh SSSR Im I M Sechenova},
	Keywords = {Epilepsy;21 Epilepsy;Electroencephalography;24 Pubmed search results 2008;21 Neurophysiology;Cats;English Abstract;Strychnine;Animals;Hypoxia, Brain;Decerebrate State;Cerebral Cortex;Carbon Dioxide},
	Medline = {86248217},
	Month = {5},
	Nlm_Id = {0427673},
	Number = {5},
	Pages = {576-9},
	Pubmed = {3087794},
	Title = {[Effect of cerebral hypoxia and hyperventilation hypocapnia on the epileptiform activity of the cerebral cortex of the cat]},
	Uuid = {DE725F61-1204-44F2-963B-C8ACC3BFC952},
	Volume = {72},
	Year = {1986}}

@article{Frantseva:2002,
	Abstract = {Traumatic brain injury results in neuronal loss and associated neurological deficits. Although most research on the factors leading to trauma-induced damage focuses on synaptic or ionic mechanisms, the possible role of direct intercellular communication via gap junctions has remained unexplored. Gap junctions connect directly the cytoplasms of coupled cells; hence, they offer a way to propagate stress signals from cell to cell. We investigated the contribution of gap junctional communication (GJC) to cell death using an in vitro trauma model. The impact injury, induced by a weight dropped on the distal CA1 area of organotypic hippocampal slices, results in glutamate-dependent cell loss. The gap junctional blockers carbenoxolone and octanol decreased significantly post-traumatic cell death, measured by propidium iodide staining over a 72 hr period after the impact. Dye coupling in the pyramidal layers was enhanced immediately after the injury and decreased over the following 24 hr. To determine whether specific connexins were involved in the spread of trauma-induced cell death, we used organotypic slices from connexin43 (Cx43) knock-out mice, as well as acute knock-outs by incubation with antisense oligodeoxynucleotides. Simultaneous knockdown of two neuronal connexins resulted in significant neuroprotection. Slices from the null-mutant Cx43 mice, as well as the acute Cx43 knockdown, also showed decreased cell death after the impact. The gap junctional blockers alleviated the trauma- induced impairment of synaptic function as measured by electrophysiological field potential recordings. These results indicate that GJC enhances the cellular vulnerability to traumatic injury. Hence, specific gap junctions could be a novel target to reduce injury and secondary damage to the brain and maximize recovery from trauma.},
	Author = {Frantseva, M. V. and Kokarovtseva, L. and Naus, C. G. and Carlen, P. L. and MacFabe, D. and Perez Velazquez, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurosci},
	Keywords = {07 Excitotoxicity Apoptosis;E},
	Number = {3},
	Organization = {The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada.},
	Pages = {644-53.},
	Title = {Specific gap junctions enhance the neuronal vulnerability to brain traumatic injury},
	Uuid = {8A0A16F0-61D2-48D1-9256-A344B1426C32},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11826094%20http://www.jneurosci.org/cgi/content/full/22/3/644%20http://www.jneurosci.org/cgi/content/abstract/22/3/644}}

@article{Frantz:1996,
	Abstract = {Early in development, neural progenitors in cerebral cortex normally produce neurons of several layers during successive cell divisions. The laminar fate of their daughters depends on environmental cues encountered just before mitosis. At the close of neurogenesis, however, cortical progenitors normally produce neurons destined only for the upper layers. To assess the developmental potential of these cells, upper-layer progenitors were transplanted into the cerebral cortex of younger hosts, in which deep-layer neurons were being generated. These studies reveal that late cortical progenitors are not competent to generate deep-layer neurons and are instead restricted to producing the upper layers.},
	Author = {Frantz, G. D. and McConnell, S. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Research Support, Non-U.S. Gov't;Cell Line;Stem Cells;Research Support, U.S. Gov't, P.H.S.;Ferrets;Mitosis;Animals;Cell Movement;Cerebral Cortex;Neurons;Stem Cell Transplantation},
	Medline = {96310877},
	Month = {7},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Biological Sciences, Stanford University, California 94305, USA.},
	Pages = {55-61},
	Pubmed = {8755478},
	Title = {Restriction of late cerebral cortical progenitors to an upper-layer fate},
	Uuid = {5215BB39-AFA2-4689-A713-2535E5A584BE},
	Volume = {17},
	Year = {1996}}

@article{Fraser:1995,
	Abstract = {The ability to determine the functional capacity of putative human hematopoietic stem cell (HSC) populations requires in vivo assays in which long-term multilineage differentiation can be assessed. We hypothesized that if human fetal bone was transplanted adjacent to a fetal thymus fragment in severe combined immunodeficient (SCID) mice, a conjoint organ might form in which HSC in the human bone marrow (BM) would mimic human multilineage differentiation into progenitor cells, B cells, and myeloid cells; undergo self-renewal; and migrate to and differentiate into T cells within the thymic microenvironment. To test this possibility, SCID mice were transplanted subcutaneously with HLA class I mismatched fetal bone, thymus, and spleen fragments (SCID-hu BTS). We found that the BM of SCID-hu BTS grafts maintained B cells, myeloid cells, CD34+ cells for at least 36 weeks posttransplant. Assayable hematopoietic progenitors colony-forming units-granulocyte-macrophage were present in 100\%(66/66) of grafts over a period of 28 weeks. Cells with a HSC phenotype (CD34+Thy-1+Lin-) were maintained for 20 weeks in SCID-hu BTS grafts. These CD34+Thy-1+Lin- cells had potent secondary multilineage reconstituting potential when isolated and injected into a secondary HLA mismatched SCID-hu bone assay and analyzed 8 weeks later. In addition, early progenitors within the BM of SCID-hu BTS grafts were capable of migrating to the human thymus and undergoing differentiation through immature CD4+CD8+ double-positive T cells and produce mature T cells with a CD4+CD8- or CD8+CD4- phenotype that could be detected for at least 36 weeks. Phenotypically defined human fetal liver (FL) and umbilical cord blood (UCB) hematopoietic stem cell populations were injected into irradiated SCID-hu BTS grafts to assess their multilineage repopulating capacity and to assess the ability of the BTS system to provide an environment where multiple lineages might differentiate from a common stem cell pool. Injection of irradiated grafts with FL HSC or UCB HSC cells resulted in donor-derived B cells, myeloid cells, immature and mature T cells, and CD34+ cells in individual grafts when analyzed 8 weeks postreconstitution, further showing the multipotential nature of these stem cell populations. In addition, a strong correlation was observed between maintenance of host graft-derived CD8+ cells and failure of donor stem cell engraftment.(ABSTRACT TRUNCATED AT 400 WORDS)},
	Author = {Fraser, C. C. and Kaneshima, H. and Hansteen, G. and Kilpatrick, M. and Hoffman, R. and Chen, B. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Cell Differentiation;Animals;Humans;Transplantation, Heterologous;Lymphocytes;Bone Transplantation;Antigens, CD;Mice, SCID;Kinetics;11 Glia;Fetal Tissue Transplantation;Hematopoietic Stem Cell Transplantation;Bone Marrow Cells;Transplantation, Homologous;Flow Cytometry;Hematopoietic Stem Cells;Mice;HLA Antigens},
	Medline = {95383636},
	Month = {9},
	Nlm_Id = {7603509},
	Number = {5},
	Organization = {Experimental Cell Therapy Group, SyStemix Inc, Palo Alto, CA 94304, USA.},
	Pages = {1680-93},
	Pubmed = {7655000},
	Title = {Human allogeneic stem cell maintenance and differentiation in a long-term multilineage SCID-hu graft},
	Uuid = {F764731F-B01D-4A2A-AB8B-7236CD92238B},
	Volume = {86},
	Year = {1995}}

@article{Freed:1987,
	Abstract = {The murine leukemia virus envelope protein is synthesized as a precursor molecule, Pr85env, which is proteolytically cleaved at an arginine residue to produce two mature envelope proteins, gp70 and p15(E). The results presented here indicate that mutation to lysine of the arginine found at the envelope precursor cleavage site results in a precursor which is cleaved with an efficiency at least 10-fold lower than the efficiency with which the wild-type protein is cleaved. This mutation has been used to investigate the requirement for envelope protein processing in various aspects of retroviral infection. Viruses produced by cells transfected with mutant proviral clones are approximately 10-fold less infectious than wild-type viruses. Mutant viruses are incapable of inducing XC cell syncytium formation and are 100-fold less efficient than wild-type viruses at rendering cells resistant to superinfection. Envelope glycoproteins bearing the lysine mutation are found in reduced amounts on the surface of infected cells, and as a result mutant virions contain significantly less envelope protein than do wild-type virions. The phenotypic effects of the processing mutation described here are most likely the result of this paucity of envelope glycoproteins in virions carrying the mutation.},
	Author = {Freed, E. O. and Risser, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Mice, Inbred AKR;Transfection;Mutation;Cell Fusion;Cell Membrane;Mice, Inbred BALB C;24 Pubmed search results 2008;Glycosylation;Research Support, U.S. Gov't, P.H.S.;Glycoproteins;15 Retrovirus mechanism;Animals;Cells, Cultured;Leukemia Virus, Murine;Viral Envelope Proteins;Mice},
	Medline = {87284162},
	Month = {9},
	Nlm_Id = {0113724},
	Number = {9},
	Pages = {2852-6},
	Pubmed = {3039173},
	Title = {The role of envelope glycoprotein processing in murine leukemia virus infection},
	Uuid = {0206842C-4327-11DB-A5D2-000D9346EC2A},
	Volume = {61},
	Year = {1987}}

@article{Freeman:2006,
	Abstract = {Glial cells are not passive spectators during nervous system assembly, rather they are active participants that exert significant control over neuronal development. Well-established roles for glia in shaping the developing nervous system include providing trophic support to neurons, modulating axon pathfinding, and driving nerve fasciculation. Exciting recent studies have revealed additional ways in which glial cells also modulate neurodevelopment. Glial cells regulate the number of neurons at early developmental stages by dynamically influencing neural precursor divisions, and at later stages by promoting neuronal cell death through engulfment. Glia also participate in the fine sculpting of neuronal connections by pruning excess axonal projections, shaping dendritic spines, and secreting multiple factors that promote synapse formation and functional maturation. These recent insights provide further compelling evidence that glial cells, through their diverse cellular actions, are essential contributors to the construction of a functionally mature nervous system.},
	Author = {Freeman, Marc R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {review;Synapses;Neuroglia;Research Support, Non-U.S. Gov't;Dendrites;Stem Cells;Cell Death;Nervous System;Animals;24 Pubmed search results 2008;Neurons;Axons},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605-2324, USA. Marc.Freeman\@umassmed.edu},
	Pages = {119-25},
	Pii = {S0959-4388(05)00186-8},
	Pubmed = {16387489},
	Title = {Sculpting the nervous system: glial control of neuronal development},
	Uuid = {901FC932-DBE7-425A-8085-D1C7EBA7551F},
	Volume = {16},
	Year = {2006},
	url = {papers/Freeman_CurrOpinNeurobiol2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.12.004}}

@article{Freundlieb:2006,
	Abstract = {The subventricular zone of the adult primate brain contains neural stem cells that can produce new neurons. Endogenous neurogenesis might therefore be used to replace lost neurons in neurodegenerative diseases. This would require, however, a precise understanding of the molecular regulation of stem cell proliferation and differentiation in vivo. Several regulatory factors, including dopamine, have been identified in rodents, but none in primates. We have, therefore, studied the origin and function of the dopaminergic innervation of the subventricular zone in nonhuman primates. Tracing experiments in three macaques revealed a topographically organized projection from the substantia nigra pars compacta (SNpc), but not the adjacent retrorubral field, to the subventricular zone: the anteromedial SNpc projects to the anteroventral subventricular zone, the posterolateral SNpc to the posterodorsal subventricular zone. Double immunolabeling for tyrosine hydroxylase and BrdU (5-bromo-2'deoxyuridine) incorporated into the DNA of proliferating cells showed that dopaminergic fibers approach proliferating cells in the subventricular zone. We investigated the effect of this nigro-subventricular projection on cell proliferation in six aged macaques, because the rate of neurogenesis differs between young adult and aged primates and because neurodegenerative diseases mainly affect aged humans. Three macaques were treated with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to decrease dopaminergic innervation of the subventricular zone. A significant decrease in the number of PCNA+ (proliferating cell nuclear antigen-positive) proliferating cells (-44\%) and PSA-NCAM(+) (polysialylated neural cell adhesion molecule-positive) neuroblasts (-59\%) was found in the denervated regions of the subventricular zone, suggesting that an intact dopaminergic nigro-subventricular innervation is crucial for sustained neurogenesis in aged primates.},
	Author = {Freundlieb, Nils and Fran\c{c}ois, Chantal and Tand{\'e}, Dominique and Oertel, Wolfgang H. and Hirsch, Etienne C. and H{\"o}glinger, G{\"u}nter U.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Aging;Substantia Nigra;Tissue Distribution;Cell Differentiation;Research Support, Non-U.S. Gov't;24 Pubmed search results 2008;Macaca mulatta;Cell Proliferation;Neural Pathways;Stem Cells;Cercopithecus aethiops;Cerebral Ventricles;Cells, Cultured;Dopamine;Animals;Neurons},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {8},
	Organization = {Experimental Neurology, Philipps University, D-35033 Marburg, Germany.},
	Pages = {2321-5},
	Pii = {26/8/2321},
	Pubmed = {16495459},
	Title = {Dopaminergic substantia nigra neurons project topographically organized to the subventricular zone and stimulate precursor cell proliferation in aged primates},
	Uuid = {1129FCFA-C8AE-48D6-B133-D350DFCA78D7},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4859-05.2006}}

@article{Fricker:1999,
	Abstract = {Neural progenitor cells obtained from the embryonic human forebrain were expanded up to 10(7)-fold in culture in the presence of epidermal growth factor, basic fibroblast growth factor, and leukemia inhibitory growth factor. When transplanted into neurogenic regions in the adult rat brain, the subventricular zone, and hippocampus, the in vitro propagated cells migrated specifically along the routes normally taken by the endogenous neuronal precursors: along the rostral migratory stream to the olfactory bulb and within the subgranular zone in the dentate gyrus, and exhibited site-specific neuronal differentiation in the granular and periglomerular layers of the bulb and in the dentate granular cell layer. The cells exhibited substantial migration also within the non-neurogenic region, the striatum, in a seemingly nondirected manner up to approximately 1-1.5 mm from the graft core, and showed differentiation into both neuronal and glial phenotypes. Only cells with glial-like features migrated over longer distances within the mature striatum, whereas the cells expressing neuronal phenotypes remained close to the implantation site. The ability of the human neural progenitors to respond in vivo to guidance cues and signals that can direct their differentiation along multiple phenotypic pathways suggests that they can provide a powerful and virtually unlimited source of cells for experimental and clinical transplantation.},
	Author = {Fricker, R. A. and Carpenter, M. K. and Winkler, C. and Greco, C. and Gates, M. A. and Bjorklund, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Olfactory Bulb/physiology;Cell Differentiation;Human;Cells, Cultured;Rats;Female;Hippocampus/cytology/physiology;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Brain/cytology/*physiology;Animal;Cell Movement;Stem Cells/*cytology;Corpus Striatum/cytology/physiology;Cell Line;Support, Non-U.S. Gov't;B;Fetal Tissue Transplantation/*physiology;Brain Tissue Transplantation/*physiology;Transplantation, Heterologous/physiology;Neurons/*cytology/*physiology/transplantation},
	Number = {14},
	Organization = {Wallenberg Neuroscience Center, Division of Neurobiology, Lund University, S-223 Lund, Sweden.},
	Pages = {5990-6005.},
	Title = {Site-specific migration and neuronal differentiation of human neural progenitor cells after transplantation in the adult rat brain},
	Uuid = {015B7B59-ADC4-484C-B552-879EE9A2507A},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10407037%20http://www.jneurosci.org/cgi/content/full/19/14/5990%20http://www.jneurosci.org/cgi/content/abstract/19/14/5990}}

@article{Fricker-Gates:2004,
	Abstract = {Transplants of embryonic striatal tissue are characteristically heterogeneous, containing patches (P-zones) of striatal medium spiny projection neurons. It is not yet known how this morphology develops, and whether the striatal neurons in the grafts are derived from post-mitotic neuroblasts in the embryonic brain or from striatal progenitors that continue to divide after transplantation. To address this question we labelled dividing cells in the transplants with bromodeoxyuridine (BrdU), either prior to or after transplantation into the adult lesioned rat striatum. Cells for transplantation were either pre-labelled in utero by intraperitoneal (i.p.) injections of BrdU, or post-labelled after transplantation by i.p. injections to the hosts. Either two or six months after transplantation the brains were processed using double immunohistochemical techniques to detect BrdU and calbindin-positive neurons in the transplants. In the transplants pre-labelled with BrdU, approximately 30\%of calbindin-positive cells were heavily labelled with BrdU, suggesting these had undergone a final division prior to transplantation. In transplants where cells had been labelled post-transplantation, approximately 17\%of calbindin cells were heavily BrdU labelled. These results suggest that whereas a proportion of striatal medium spiny neurons in the striatal grafts were post-mitotic at the time of transplantation, other striatal progenitor cells can continue to divide after transplantation, and then complete an appropriate neuronal maturation programme in the adult host brain environment.},
	Author = {Fricker-Gates, Rosemary A. and White, Anna and Gates, Monte A. and Dunnett, Stephen B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Survival;Pregnancy;Animals;Corpus Striatum;Cells, Cultured;Aging;Brain Tissue Transplantation;Rats;Comparative Study;Mitosis;Phosphopyruvate Hydratase;Female;Cell Count;Calcium-Binding Protein, Vitamin D-Dependent;Ibotenic Acid;Embryo;Time Factors;Neurons;Transplants;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Stem Cells;Acetylcholinesterase;Bromodeoxyuridine;Research Support, Non-U.S. Gov't},
	Month = {2},
	Nlm_Id = {8918110},
	Number = {3},
	Organization = {School of Biosciences, Cardiff University, Cardiff, Wales.},
	Pages = {513-20},
	Pii = {3149},
	Pubmed = {14984402},
	Title = {Striatal neurons in striatal grafts are derived from both post-mitotic cells and dividing progenitors},
	Uuid = {451975DC-A9B6-4BF4-977B-CCEFE0DF8355},
	Volume = {19},
	Year = {2004}}

@article{Friedel:2007,
	Abstract = {Cerebellar granule cell progenitors proliferate postnatally in the upper part of the external granule cell layer (EGL) of the cerebellum. Postmitotic granule cells differentiate and migrate, tangentially in the EGL and then radially through the molecular and Purkinje cell layers. The molecular control of the transition between proliferation and differentiation in cerebellar granule cells is poorly understood. We show here that the transmembrane receptor Plexin-B2 is expressed by proliferating granule cell progenitors. To study Plexin-B2 function, we generated a targeted mutation of mouse Plexin-B2. Most Plexin-B2(-/-) mutants die at birth as a result of neural tube closure defects. Some mutants survive but their cerebellum cytoarchitecture is profoundly altered. This is correlated with a disorganization of the timing of granule cell proliferation and differentiation in the EGL. Many differentiated granule cells migrate inside the cerebellum and keep proliferating. These results reveal that Plexin-B2 controls the balance between proliferation and differentiation in granule cells.},
	Author = {Friedel, Roland H. and Kerjan, G{\'e}raldine and Rayburn, Helen and Sch{\"u}ller, Ulrich and Sotelo, Constantino and Tessier-Lavigne, Marc and Ch{\'e}dotal, Alain},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't;10 Development;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {Department of Biological Sciences, Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.},
	Pages = {3921-32},
	Pii = {27/14/3921},
	Pubmed = {17409257},
	Title = {Plexin-B2 controls the development of cerebellar granule cells},
	Uuid = {2D2A28EA-F315-4577-88DF-1B3626D22215},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4710-06.2007}}

@article{Friedman:2004,
	Abstract = {High-throughput genome-wide molecular assays, which probe cellular networks from different perspectives, have become central to molecular biology. Probabilistic graphical models are useful for extracting meaningful biological insights from the resulting data sets. These models provide a concise representation of complex cellular networks by composing simpler submodels. Procedures based on well-understood principles for inferring such models from data facilitate a model-based methodology for analysis and discovery. This methodology and its capabilities are illustrated by several recent applications to gene expression data.},
	Author = {Friedman, Nir},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:46 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Models, Biological;Mathematics;Computational Biology;Bayes Theorem;Gene Expression Regulation;Gene Expression Profiling;Gene Expression;Models, Statistical;review, tutorial;Models, Genetic;Support, Non-U.S. Gov't;Cell Physiology;review;23 Technique},
	Month = {2},
	Nlm_Id = {0404511},
	Number = {5659},
	Organization = {School of Computer Science and Engineering, Hebrew University, 91904 Jerusalem, Israel. nir\@cs.huji.ac.il},
	Pages = {799-805},
	Pii = {303/5659/799},
	Pubmed = {14764868},
	Title = {Inferring cellular networks using probabilistic graphical models},
	Uuid = {311F933C-D057-47BC-862A-2D7766353E90},
	Volume = {303},
	Year = {2004},
	url = {papers/Friedman_Science2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1094068}}

@article{Friocourt:2003,
	Abstract = {Type I lissencephaly is a cortical malformation disorder characterized by disorganized cortical layers and gyral abnormalities and associated with severe cognitive impairment and epilepsy. The exact pathophysiological mechanisms underlying the epilepsy and mental retardation in this and related disorders remain unknown. Two genes, LIS1 and doublecortin, have both been shown to be mutated in a large proportion of cases of type I lissencephaly and a milder allelic disorder, subcortical laminar heterotopia (SCLH). Studying the protein products of these genes and the biochemical pathways in which they belong is likely to yield important information concerning both normal and abnormal cortical development. The relationships between the LIS1 and Doublecortin proteins are not yet well defined, but both are believed to play a critical role in cortical neuronal migration. Lis1 is expressed from very early development in the mouse and in both proliferating cells and post-mitotic neurons of the cortex. This protein is likely to have multiple functions since it is a subunit of the enzyme platelet-activating factor acetylhydrolase, which degrades platelet activating factor, and has also been shown to be involved in microtubule dynamics, potentially influencing nuclear migration through its interaction with the dynein motor protein complex. Doublecortin on the other hand is exclusively expressed in post-mitotic neurons and is developmentally regulated. In young developing neurons Doublecortin has a specific subcellular localization at the ends of neuritic and leading processes. This localization, combined with our previous data showing that it is a microtubule-associated protein and that it interacts with adapter complexes involved in vesicle trafficking, suggests a role in the growth of neuronal processes, downstream of directional or guidance signals. The observations summarized here favor the suggestion that whereas LIS1 may play a role in nuclear migration, Doublecortin is instead restricted to functions at the leading edge of the cell. 1047-3211 Journal Article Review Review, Tutorial},
	Author = {Friocourt, G. and Koulakoff, A. and Chafey, P. and Boucher, D. and Fauchereau, F. and Chelly, J. and Francis, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Cereb Cortex},
	Keywords = {Neuropeptides/genetics/*physiology;Nerve Tissue Proteins/metabolism;Cerebral Cortex/cytology/embryology/*physiology;10 Development;Gene Expression Regulation, Developmental;Microtubules/physiology;Neurons/cytology/*physiology;Cell Division;Ca(2+)-Calmodulin Dependent Protein Kinase/metabolism;Astrocytes/metabolism;F;Microtubule-Associated Proteins/genetics/*physiology;Cell Movement/*physiology;Animals;Support, Non-U.S. Gov't;Mice},
	Number = {6},
	Organization = {Laboratoire de Genetique et Physiopathologie des Retards Mentaux, GDPM, Institut Cochin, 24 Rue du Faubourg Saint Jacques, F-75014 Paris, France.},
	Pages = {620-6},
	Pubmed = {12764037},
	Title = {Doublecortin functions at the extremities of growing neuronal processes},
	Uuid = {F768A71E-D0D3-4722-A13F-B02C852D9120},
	Volume = {13},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12764037}}

@article{Friocourt:2006,
	Abstract = {The ARX protein (encoded by the aristaless-related homeobox gene) is a member of the paired class of homeoproteins. More precisely, it is a member of the Aristaless subclass of proteins with a glutamine residue (Q) at the critical position 50 of the homeodomain (Q50). Through identification of diverse inherited or de novo mutations, genetic investigations of X-linked mental retardation conditions have demonstrated the implication of ARX in a wide spectrum of disorders extending from phenotypes with severe neuronal migration defects, such as lissencephaly, to mild forms of X-linked mental retardation without apparent brain abnormalities. These investigations have recently directed attention to the role of this gene in brain development. Analysis of its spatiotemporal localization profile have revealed expression mainly in telencephalic structures at all stages of development. Interestingly, in adult, ARX expression becomes restricted to a population of GABAergic neurons. Although the identification of the target genes regulated by ARX remains a crucial step to better understanding its role during brain development, studies of the role of ARX orthologs in different models have indicated that it is essential for important developmental processes such as proliferation, cell differentiation and neuronal migration.},
	Author = {Friocourt, Ga{\"e}lle and Poirier, Karine and Raki\'{c}, Sonja and Parnavelas, John G. and Chelly, Jamel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Homeodomain Proteins;Mutation;Gene Expression Regulation, Developmental;Research Support, Non-U.S. Gov't;24 Pubmed search results 2008;21 Neurophysiology;21 Epilepsy;Gene Expression;Animals;Humans;Cerebral Cortex;review;Transcription Factors},
	Month = {2},
	Nlm_Id = {8918110},
	Number = {4},
	Organization = {Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, UK.},
	Pages = {869-76},
	Pii = {EJN4629},
	Pubmed = {16519652},
	Title = {The role of ARX in cortical development},
	Uuid = {8EE0A372-926A-4929-9E1B-CB994F6C1C46},
	Volume = {23},
	Year = {2006},
	url = {papers/Friocourt_EurJNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2006.04629.x}}

@article{Friocourt:2007,
	Abstract = {Type I lissencephaly, a genetic disease characterized by disorganized cortical layers and gyral abnormalities, is associated with severe cognitive impairment and epilepsy. Two genes, LIS1 and doublecortin (DCX), have been shown to be responsible for a large proportion of cases of type I lissencephaly. Both genes encode microtubule-associated proteins that have been shown to be important for radial migration of cortical pyramidal neurons. To investigate whether DCX also plays a role in cortical interneuron migration, we inactivated DCX in the ganglionic eminence of rat embryonic day 17 brain slices using short hairpin RNA. We found that, when DCX expression was blocked, the migration of interneurons from the ganglionic eminence to the cerebral cortex was slowed but not absent, similar to what had previously been reported for radial neuronal migration. In addition, the processes of DCX-deficient migrating interneurons were more branched than their counterparts in control experiments. These effects were rescued by DCX overexpression, confirming the specificity to DCX inactivation. A similar delay in interneuron migration was observed when Doublecortin-like kinase (DCLK), a microtubule-associated protein related to DCX, was inactivated, although the morphology of the cells was not affected. The importance of these genes in interneuron migration was confirmed by our finding that the cortices of Dcx, Dclk, and Dcx/Dclk mutant mice contained a reduced number of such cells in the cortex and their distribution was different compared with wild-type controls. However, the defect was different for each group of mutant animals, suggesting that DCX and DCLK have distinct roles in cortical interneuron migration.},
	Author = {Friocourt, Ga{\"e}lle and Liu, Judy S. and Antypa, Mary and Rakic, Sonja and Walsh, Christopher A. and Parnavelas, John G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't;10 Development;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom.},
	Pages = {3875-83},
	Pii = {27/14/3875},
	Pubmed = {17409252},
	Title = {Both doublecortin and doublecortin-like kinase play a role in cortical interneuron migration},
	Uuid = {400F1113-7961-4560-8B0E-83AFC00DCA91},
	Volume = {27},
	Year = {2007},
	url = {papers/Friocourt_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4530-06.2007}}

@article{Frotscher:2003,
	Abstract = {Reelin, synthesized and secreted by Cajal-Retzius (CR) cells in the marginal zone of the cortex, is an extracellular matrix protein important for the development of cortical layers. In reeler mutant mice lacking Reelin, there are severe malformations of neocortical and hippocampal lamination. It has been assumed that Reelin acts as a stop signal for migrating neurons. Here we show, by using the dentate gyrus as a model in in vivo studies and in vitro assays, that Reelin exerts its effects, at least in part, by acting on the radial glial scaffold required for neuronal migration. Migration defects of dentate granule cells, reminiscent of those seen in reeler mutants, are observed in tissue from patients with temporal lobe epilepsy (TLE). The extent of granule cell dispersion in TLE was found to be inversely correlated with the number of reelin mRNA synthesizing CR cells and reelin mRNA expression as revealed in quantitative RT-PCR studies. These findings show that the Reelin signaling pathway is essential for the correct positioning of human hippocampal neurons and that a Reelin deficiency is involved in the pathological changes associated with epilepsy.},
	Author = {Frotscher, Michael and Haas, Carola A. and F{\"o}rster, Eckart},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {Signal Transduction;Animals;Gene Expression Regulation;Kidney;Humans;Comparative Study;Cell Movement;Hippocampus;Reference Values;Cell Adhesion Molecules, Neuronal;Cell Line;Extracellular Matrix Proteins;Mice, Knockout;Neuroglia;Epilepsy, Temporal Lobe;Dentate Gyrus;Neurons;Adult;Mice;Research Support, Non-U.S. Gov't},
	Medline = {22648203},
	Month = {6},
	Nlm_Id = {9110718},
	Number = {6},
	Organization = {Anatomisches Institut, Universit{\"a}t Freiburg, Albertstrasse 17, D-79104 Freiburg, Germany. michael.frotscher\@anat.uni-freiburg.de},
	Pages = {634-40},
	Pubmed = {12764039},
	Title = {Reelin controls granule cell migration in the dentate gyrus by acting on the radial glial scaffold},
	Uuid = {021B383A-716E-11DA-A383-000D9346EC2A},
	Volume = {13},
	Year = {2003},
	url = {papers/Frotscher_CerebCortex2003.pdf}}

@article{Frotscher:1998,
	Abstract = {Early-generated Cajal-Retzius cells in the marginal zone of the cortex synthesize and secrete the glycoprotein Reelin. The reelin gene is deleted in reeler mice, which show characteristic alterations in cortical lamination. Recent studies have shed some light on the role of Cajal-Retzius cells and Reelin in the formation of cell and fiber layers in the neocortex and hippocampus.},
	Author = {Frotscher, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {review;10 Development;Research Support, Non-U.S. Gov't;Extracellular Matrix Proteins;Hippocampus;10 Hippocampus;Nerve Tissue Proteins;Neocortex;review, tutorial;Mice;Animals;Cell Adhesion Molecules, Neuronal;Mice, Neurologic Mutants;Neurons},
	Medline = {99035600},
	Month = {10},
	Nlm_Id = {9111376},
	Number = {5},
	Organization = {Institute of Anatomy, University of Freiburg, Germany. frotsch\@uni-freiburg.de},
	Pages = {570-5},
	Pubmed = {9811621},
	Title = {Cajal-Retzius cells, Reelin, and the formation of layers},
	Uuid = {E6DE3558-E453-408B-91BF-4FE890EDAA1B},
	Volume = {8},
	Year = {1998}}

@article{Fuchs:2004,
	Abstract = {The potential of stem cells in regenerative medicine relies upon removing them from their natural habitat, propagating them in culture, and placing them into a foreign tissue environment. To do so, it is essential to understand how stem cells interact with their microenvironment, the so-called stem cell niche, to establish and maintain their properties. In this review, we examine adult stem cell niches and their impact on stem cell biology. 0092-8674 Journal Article},
	Author = {Fuchs, E. and Tumbar, T. and Guasch, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Cell},
	Keywords = {02 Adult neurogenesis migration;BB pdf;03 Adult neurogenesis progenitor source},
	Number = {6},
	Organization = {Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10021, USA. fuchslb\@rockefeller.edu},
	Pages = {769-78},
	Title = {Socializing with the neighbors: stem cells and their niche},
	Uuid = {D9EAE568-620A-4AEA-8E4D-0B5E36673000},
	Volume = {116},
	Year = {2004},
	url = {papers/Fuchs_Cell2004.pdf}}

@article{Fuchs:2007,
	Abstract = {With the growing recognition that rhythmic and oscillatory patterns are widespread in the brain and play important roles in all aspects of the function of our nervous system, there has been a resurgence of interest in neuronal synchronized bursting activity. Here, we were interested in understanding the development of synchronized bursts as information-bearing neuronal activity patterns. For that, we have monitored the morphological organization and spontaneous activity of neuronal networks cultured on multielectrode-arrays during their self-executed evolvement from a mixture of dissociated cells into an active network. Complex collective network electrical activity evolved from sporadic firing patterns of the single neurons. On the system (network) level, the activity was marked by bursting events with interneuronal synchronization and nonarbitrary temporal ordering. We quantified these individual-to-collective activity transitions using newly-developed system level quantitative measures of time series regularity and complexity. We found that individual neuronal activity before synchronization was characterized by high regularity and low complexity. During neuronal wiring, there was a transient period of reorganization marked by low regularity, which then leads to coemergence of elevated regularity and functional (nonstochastic) complexity. We further investigated the morphology-activity interplay by modeling artificial neuronal networks with different topological organizations and connectivity schemes. The simulations support our experimental results by showing increased levels of complexity of neuronal activity patterns when neurons are wired up and organized in clusters (similar to mature real networks), as well as network-level activity regulation once collective activity forms.},
	Author = {Fuchs, E. and Ayali, A. and Robinson, A. and Hulata, E. and Ben-Jacob, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1932-8451},
	Journal = {Dev Neurobiol},
	Keywords = {research support, non-u.s. gov't;21 Neurophysiology;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {101300215},
	Number = {13},
	Organization = {Department of Zoology, Tel-Aviv University, Tel-Aviv 69978, Israel.},
	Pages = {1802-14},
	Pubmed = {17701997},
	Title = {Coemergence of regularity and complexity during neural network development},
	Uuid = {073AF7DB-8882-4905-8ACB-B5ED8E47F8A1},
	Volume = {67},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/dneu.20557}}

@article{Fuchs:2000,
	Author = {Fuchs, E. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {01 Adult neurogenesis general;Mammals;Brain/*cytology/*physiology;Cell Differentiation/physiology;Neurons/*cytology;Animal;A-9b;Age Factors},
	Number = {7},
	Organization = {Division of Neurobiology, German Primate Center, Gottingen, Germany. efuchs\@gwdg.de},
	Pages = {2211-4.},
	Title = {Mini-review: in vivo neurogenesis in the adult brain: regulation and functional implications},
	Uuid = {58B572B0-CC41-4E13-80FF-91A23DED5DAA},
	Volume = {12},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10947799}}

@article{Fueyo:2003,
	Abstract = {BACKGROUND: Oncolytic adenoviruses are promising therapies for the treatment of gliomas. However, untargeted viral replication and the paucity of coxsackie-adenovirus receptors (CARs) on tumor cells are major stumbling blocks for adenovirus-based treatment. We studied the antiglioma activity of the tumor-selective Delta-24 adenovirus, which encompasses an early 1 A adenoviral (E1A) deletion in the retinoblastoma (Rb) protein-binding region, and of the Delta-24-RGD adenovirus. Delta-24-RGD has an RGD-4C peptide motif inserted into the adenoviral fiber, which allows the adenovirus to anchor directly to integrins. METHODS: CAR and integrin expression were examined by flow cytometry in six glioma cell lines and in normal human astrocytes (NHAs). Adenoviral vectors containing green fluorescent protein (GFP) (AdGFP and AdGFP-RGD) were used to infect glioma cell lines with high or low CAR expression. Viability of glioma cells infected with different adenoviruses was assessed by trypan blue staining. Adenovirus replication was quantified with the infection-dose replication assay. Athymic mice carrying glioma xenografts received intratumoral injections of Delta-24-RGD or Delta-24 and were followed for survival, which was analyzed by the Kaplan-Meier method and the log-rank test. All statistical tests were two-sided. RESULTS: Half the glioma cell lines expressed low levels of CAR (defined as <50\%of cells expressing detectable CAR); all lines expressed integrins in more than 50\%of cells. Infection of U-87 MG cells (a low-CAR-expressing line) with AdGFP-RGD resulted in approximately six times more GFP-positive cells than infection with AdGFP. Delta-24-RGD was more cytopathic to both low- and high-CAR-expressing glioma lines than Delta-24, and it replicated more efficiently in both cell lines. In the xenografted mice, intratumoral injection of Delta-24-RGD was associated with longer survival than intratumoral injection of Delta-24 (P<.001, log-rank test). Furthermore, 60\%of Delta-24-RGD-treated mice but only 15\%of Delta-24-treated mice survived more than 4 months (difference = 45\%, 95\%CI = 21\%to 68\%). CONCLUSIONS: The antitumor activity of Delta-24-RGD suggests that it has the potential to be an effective agent in the treatment of gliomas. 1460-2105 Journal Article},
	Author = {Fueyo, J. and Alemany, R. and Gomez-Manzano, C. and Fuller, G. N. and Khan, A. and Conrad, C. A. and Liu, T. J. and Jiang, H. and Lemoine, M. G. and Suzuki, K. and Sawaya, R. and Curiel, D. T. and Yung, W. K. and Lang, F. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Natl Cancer Inst},
	Keywords = {Fluorescent Dyes;Human;Gene Expression Regulation, Neoplastic;Animals;Tumor Markers, Biological/*analysis;Trypan Blue;Retinoblastoma;Injections, Intralesional;Integrins/analysis;Transplantation, Heterologous;Calcium-Binding Proteins/*analysis;15 Retrovirus mechanism;J pdf;Brain Neoplasms/drug therapy/immunology/pathology/radiotherapy/*therapy;Dyes;Mice, Nude;Support, Non-U.S. Gov't;Tumor Cells, Cultured;Flow Cytometry;*Adenoviridae;Mice;Immunohistochemistry;Antigens, Neoplasm/*analysis;Astrocytes/immunology;Glioma/drug therapy/immunology/pathology/radiotherapy/*therapy},
	Number = {9},
	Organization = {Department of Neuro-Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA. jfueyo\@mdanderson.org},
	Pages = {652-60},
	Pubmed = {12734316},
	Title = {Preclinical characterization of the antiglioma activity of a tropism-enhanced adenovirus targeted to the retinoblastoma pathway},
	Uuid = {8972B1EB-F38E-459C-A2D5-71ED9D19E95F},
	Volume = {95},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12734316}}

@article{Fujii:2002,
	Abstract = {BACKGROUND/AIMS: We examined whether bone marrow (BM) cells can commit to liver-consisting cells during liver regeneration after partial hepatectomy, using mice transplanted with green fluorescent protein (GFP) positive BM from GFP transgenic mice. METHODS: Partial hepatectomy or sham operation was performed. Lineage marker analysis of GFP positive liver cells was by immunostaining and flow cytometry. DiI-labeled acetylated low-density lipoprotein uptake or microsphere phagocytosis was examined in vitro. Lineage marker expression in BM and peripheral blood (PB) cells, and the vascular endothelial growth factor (VEGF) concentration in the liver were also examined. RESULTS: In hepatectomized mice, significantly more GFP positive cells participated in liver sinusoid than in sham-operated mice, expressing CD31 but not albumin. The percentage of cells that incorporated acetylated low-density lipoprotein but not microspheres was 69.5+/-3.4\%, while 28.3+/-2.6\%incorporated both, revealing sinusoidal endothelial and Kupffer cells, respectively. Increased expression of the CD31 and CD16/CD32 on GFP positive liver cells was also detected. The elevation of the VEGF concentration during liver regeneration and the increase in the CD34 and Flk-1 expression in the liver, BM, and PB cells suggested endothelial progenitor cell mobilization. CONCLUSIONS: GFP cell-marking provided direct evidence of the BM cells participation in liver regeneration after hepatectomy, where the majority was committed to sinusoidal endothelial cells probably through endothelial progenitor cell mobilization.},
	Author = {Fujii, Hideaki and Hirose, Tetsuro and Oe, Shoshiro and Yasuchika, Kentaro and Azuma, Hisaya and Fujikawa, Takahisa and Nagao, Masaya and Yamaoka, Yoshio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0168-8278},
	Journal = {J Hepatol},
	Keywords = {Cell Differentiation;Green Fluorescent Proteins;Immunohistochemistry;Luminescent Proteins;Vascular Endothelial Growth Factor A;Animals;Hepatectomy;Phagocytosis;Flow Cytometry;Genes, Reporter;In Vitro;Liver Regeneration;Liver;Vascular Endothelial Growth Factor Receptor-2;Bone Marrow Transplantation;Mice, Inbred C57BL;11 Glia;Endothelial Growth Factors;Antigens, CD34;Intercellular Signaling Peptides and Proteins;Lymphokines;Bone Marrow Cells;Stem Cells;Indicators and Reagents;Mice;Research Support, Non-U.S. Gov't;Mice, Transgenic;Lipoproteins, LDL;Vascular Endothelial Growth Factors;Microscopy, Fluorescence},
	Medline = {21979759},
	Month = {5},
	Nlm_Id = {8503886},
	Number = {5},
	Organization = {Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, 54, Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. hideaki\@kuhp.kyoto-u.ac.jp},
	Pages = {653-9},
	Pii = {S0168827802000430},
	Pubmed = {11983449},
	Title = {Contribution of bone marrow cells to liver regeneration after partial hepatectomy in mice},
	Uuid = {5659871C-3E9F-4082-B8FC-3DD7B7CB73B7},
	Volume = {36},
	Year = {2002},
	url = {papers/Fujii_JHepatol2002.pdf}}

@article{Fujioka:2004,
	Abstract = {Previous studies have demonstrated that activation of the cAMP cascade, including the cAMP response element-binding protein (CREB), increases the proliferation and survival of newborn neurons in adult mouse hippocampus. In the present study, we determined whether the cAMP-CREB cascade also influences the morphological maturation of newborn neurons in the subgranular zone of the hippocampus. Rolipram, a selective inhibitor of the cAMP-specific phosphodiesterase type 4, was administered to activate the cAMP cascade, and neuronal morphology was determined by analysis of Golgi-impregnated neurons in the subgranular zone of hippocampus. Rolipram administration significantly increased the number of branch points and length of dendrites relative to vehicle treatment. Increased branch number and length were accompanied by increased levels of phosphorylated CREB, the active form of this transcription factor, in immature neurons. In contrast, the morphology of Golgi-impregnated neurons was not significantly influenced by rolipram treatment in inducible transgenic mice expressing a dominant-negative mutant of CREB in hippocampus. We also tested the influence of cAMP analogs in primary hippocampal cultures and found that activation of the cAMP pathway increased and inhibition of the cAMP cascade decreased the number of branches and length of processes as observed in vivo. These findings indicate that the cAMP-CREB cascade plays an important role in the differentiation and maturation of newborn neurons in hippocampus. 1529-2401 Journal Article},
	Author = {Fujioka, T. and Fujioka, A. and Duman, R. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {J Neurosci},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {2},
	Organization = {Division of Molecular Psychiatry, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, Yale University School of Medicine, New Haven, Connecticut 06508, USA.},
	Pages = {319-28},
	Pubmed = {14724230},
	Title = {Activation of cAMP signaling facilitates the morphological maturation of newborn neurons in adult hippocampus},
	Uuid = {FDDFD87E-5A6C-4E49-A2D0-5D97BDD25EC0},
	Volume = {24},
	Year = {2004},
	url = {papers/Fujioka_JNeurosci2004.pdf}}

@article{Fujisawa:1998,
	Abstract = {The tempo and intensity of retroviral neuropathogenesis are dependent on the capacity of the virus to invade the central nervous system. For murine leukemia viruses, an important determinant of neuroinvasiveness is the virus-encoded protein glycosylated Gag, the function of which in the virus life cycle is not known. While this protein is dispensable for virus replication, mutations which prevent its expression slow the spread of virus in vivo and restrict virus dissemination to the brain. To further explore the function of this protein, we compared two viruses, CasFrKP (KP) and CasFrKP41 (KP41), which differ dramatically in neurovirulence. KP expresses high early viremia titers, is neuroinvasive, and induces clinical neurologic disease in 100\%of neonatally inoculated mice, with an incubation period of 18 to 23 days. In contrast, KP41 expresses early viremia titers 100- fold lower than those of KP, exhibits attenuated neuroinvasiveness, and induces clinical neurologic disease infrequently, with a relatively long incubation period. The genomes of these two viruses differ by only 10 nucleotides, resulting in differences at five residues, all located within the N-terminal cytoplasmic tail of glycosylated Gag. In this study, using KP as the parental virus, we systematically mutated each of the five amino acid residues to those of KP41 and found that substitution mutation of two membrane-proximal residues, E53 and L56, to K and P, respectively produced the greatest effect on early viremia kinetics and neurovirulence. These mutations disrupted the KP sequence E53FLL56, the leucine dipeptide of which suggests the possibility that it may represent a sorting signal for glycosylated Gag. Supporting this idea was the finding that alteration of this sequence motif increased the level of cell surface expression of the protein, which suggests that analysis of the intracellular trafficking of glycosylated Gag may provide further clues to its function.},
	Author = {Fujisawa, R. and McAtee, F. J. and Wehrly, K. and Portis, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Leukemia Virus, Murine;Viremia;Virulence;Gene Products, gag;Molecular Sequence Data;Cytoplasm;Glycosylation;Leucine;Not relevant;11 Glia;Amino Acid Sequence;Support, U.S. Gov't, P.H.S.;Mice;Animals;Brain;Spleen;Support, Non-U.S. Gov't},
	Medline = {98285718},
	Month = {7},
	Nlm_Id = {0113724},
	Number = {7},
	Organization = {Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840, USA.},
	Pages = {5619-25},
	Pubmed = {9621020},
	Title = {The neuroinvasiveness of a murine retrovirus is influenced by a dileucine-containing sequence in the cytoplasmic tail of glycosylated Gag},
	Uuid = {76420E59-D360-4B88-AC79-C78F2620EA46},
	Volume = {72},
	Year = {1998},
	url = {papers/Fujisawa_JVirol1998.pdf}}

@article{Fukuda:2003,
	Abstract = {Neurogenesis in the dentate gyrus of the adult mammalian hippocampus has been proven in a series of studies, but the differentiation process toward newborn neurons is still unclear. In addition to the immunohistochemical study, electrophysiological membrane recordings of precursor cells could provide an alternative view to address this differentiation process. In this study, we performed green fluorescent protein (GFP)-guided selective recordings of nestin-positive progenitor cells in adult dentate gyrus by means of nestin-promoter GFP transgenic mice, because nestin is a typical marker for precursor cells in the adult dentate gyrus. The patch-clamp recordings clearly demonstrated the presence of two distinct subpopulations (type I and type II) of nestin-positive cells. Type I cells had a lower input resistance value of 77.1 M(Omega) (geometric mean), and their radial processes were stained with anti-glial fibrillary acidic protein antibody. On the other hand, type II nestin-positive cells had a higher input resistance value of 2110 MOmega and expressed voltage-dependent sodium current. In most cases, type II cells were stained with anti-polysialylated neural cell adhesion molecule. Taken together with a bromodeoxyuridine pulse-chase analysis, our results may reflect a rapid and dynamic cell conversion of nestin-positive progenitor, from type I to type II, at an early stage of adult neurogenesis in the dentate gyrus.},
	Author = {Fukuda, Satoshi and Kato, Fusao and Tozuka, Yusuke and Yamaguchi, Masahiro and Miyamoto, Yusei and Hisatsune, Tatsuhiro},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Glial Fibrillary Acidic Protein;Research Support, Non-U.S. Gov't;Electrophysiology;Animals;In Vitro;Antigens, Differentiation;Patch-Clamp Techniques;Cell Count;Mice, Transgenic;Recombinant Fusion Proteins;Green Fluorescent Proteins;Sialic Acids;Intermediate Filament Proteins;Dentate Gyrus;Neurons;Mice;Neural Cell Adhesion Molecule L1;Immunohistochemistry;Bromodeoxyuridine;Luminescent Proteins;Nerve Tissue Proteins;Transgenes},
	Medline = {22923783},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {28},
	Organization = {Department of Integrated Biosciences, University of Tokyo, Kashiwa 277-8562, Japan.},
	Pages = {9357-66},
	Pii = {23/28/9357},
	Pubmed = {14561863},
	Title = {Two distinct subpopulations of nestin-positive cells in adult mouse dentate gyrus},
	Uuid = {AD8B35FE-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {23},
	Year = {2003}}

@article{Fukuhara:2002,
	Author = {Fukuhara, S. and Tomita, S. and Nakatani, T. and Kishida, A. and Morisaki, T. and Yutani, C. and Kitamura, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0041-1345},
	Journal = {Transplant Proc},
	Keywords = {Transfection;Luminescent Proteins;Rats, Inbred Lew;Cell Transplantation;Bone Marrow Cells;Rats;Fluorescent Dyes;Heart Failure, Congestive;11 Glia;Mice, Transgenic;Bone Marrow Transplantation;Green Fluorescent Proteins;Disease Models, Animal;Genes, Reporter;Animals;Mice},
	Medline = {22319876},
	Month = {11},
	Nlm_Id = {0243532},
	Number = {7},
	Organization = {Department of Pathology, National Cardiovascular Center, Osaka, Japan.},
	Pages = {2718-21},
	Pii = {S0041134502033869},
	Pubmed = {12431585},
	Title = {Comparison of cell labeling procedures for bone marrow cell transplantation to treat heart failure: long-term quantitative analysis},
	Uuid = {B6157254-60B5-4C80-A04B-60CB657B603B},
	Volume = {34},
	Year = {2002}}

@article{Fukumitsu:2002,
	Abstract = {In order to invent a screening system to check in vivo gene function and the efficiency of gene transfer mediated by a retroviral vector system, we established a novel packaging cell, PacC6/A8, that is transplantable to rat brains. The packaging cell is based on the gene of the neuropatogenic retrovirus, A8-V. For expression in the brain, a vector that expresses brain-derived neurotrophic factor (BDNF) tagged by c-Myc-His6 (LxA/bdmh) was constructed. After transfection of LxA/bdmh to PacC6/A8, a cloned cell line, PacC6/A8/bmh, was established. PacC6/A8/bmh cells stably produced pseudotyped retroviruses carrying LxA/bdmh. For a control, a retroviral vector that bears the gene that codes enhanced green fluorescent protein (EGFP) tagged by C-Mic-His6 was also created and used for the establishment of PacC6/A8/gfmh cells that produce pseudotyped retroviruses carrying LxA/gfmh. PacC6/A8/bmh and PacC6/A8/gfmh cells were injected to the brain of newborn rats. A tumor was formed in all the rats injected that did not exhibit any symptoms until 3-4 weeks after the injection. A histological study of the injected rats revealed that the transferred BDNF gene was expressed in the brain of rats injected with PacC6/A8/bmh cells, but not in rats with PacC6/A8/gfmh cells. Interestingly, many activated microglia had migrated into the tumor induced by PacC6/A8/bmh cells, and expressed a high amount of BDNF.},
	Author = {Fukumitsu, Hidefumi and Takase-Yoden, Sayaka and Furukawa, Shoei and Nemoto, Kiyomitsu and Ikeda, Tomio and Watanabe, Rihito},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0963-6897},
	Journal = {Cell Transplant},
	Keywords = {Tumor Cells, Cultured;Luminescent Proteins;Virus Assembly;Cell Transplantation;Transduction, Genetic;Immunohistochemistry;Rats;Research Support, Non-U.S. Gov't;Retroviridae;11 Glia;Brain-Derived Neurotrophic Factor;Green Fluorescent Proteins;COS Cells;Brain;Animals;Gene Therapy;Genetic Vectors},
	Medline = {22270116},
	Nlm_Id = {9208854},
	Number = {5},
	Organization = {Institute of Life Science, Soka University, Hachioji, Tokyo, Japan.},
	Pages = {459-64},
	Pubmed = {12382674},
	Title = {Implantation of BDNF-producing packaging cells into brain},
	Uuid = {B3E1234E-5ECF-4F8B-9571-520D0490CEA5},
	Volume = {11},
	Year = {2002}}

@article{Furukawa:2000,
	Abstract = {We are interested in the mechanisms of glial cell development in the vertebrate central nervous system. We have identified genes that can direct the formation of glia in the retina. rax, a homeobox gene, Hes1, a basic helix-loop-helix gene, and notch1, a transmembrane receptor gene, are expressed in retinal progenitor cells, downregulated in differentiated neurons, and expressed in Muller glia. Retroviral transduction of any of these genes resulted in expression of glial markers. In contrast, misexpression of a dominant-negative Hes1 gene reduced the number of glia. Cotransfection of rax with reporter constructs containing the Hes1 or notch1 regulatory regions led to the upregulation of reporter transcription. These data suggest a regulatory heirarchy that controls the formation of glia at the expense of neurons. 0896-6273 Journal Article},
	Author = {Furukawa, T. and Mukherjee, S. and Bao, Z. Z. and Morrow, E. M. and Cepko, C. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Neuron},
	Keywords = {G;Animals;Up-Regulation;Rats;Eye Proteins/*physiology;Retina/*cytology;Stem Cells/cytology;11 Glia;Genes, Dominant/physiology;Gene Expression/physiology;Support, Non-U.S. Gov't;3T3 Cells;Cell Division/physiology;Support, U.S. Gov't, P.H.S.;Homeodomain Proteins/genetics/*physiology;Mice;Animals, Newborn/physiology;Cell Differentiation/physiology;Biological Markers;Neuroglia/*cytology;Membrane Proteins/*physiology},
	Number = {2},
	Organization = {Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {383-94},
	Title = {rax, Hes1, and notch1 promote the formation of Muller glia by postnatal retinal progenitor cells},
	Uuid = {F13B7105-12CC-46DF-BE34-69B1826A985D},
	Volume = {26},
	Year = {2000},
	url = {papers/Furukawa_Neuron2000}}

@article{Furusho:2006,
	Abstract = {Cholinergic neurons, which express choline acetyltransferase (ChAT), are a major neuron subset generated in the basal forebrain. Areas presumed to be sites of origin of cholinergic neurons are roughly demarcated by expression of Olig2, a basic helix-loop-helix transcription factor, which includes the medial ganglionic eminence, septal area, and anterior entopeduncular/preoptic area. In the present study, we examined the involvement of Olig2 in cholinergic differentiation. When the Olig2-expressing cells at E12.5 were permanently modified to express the lacZ or EGFP gene by tamoxifen-induced Cre-mediated recombination, the cells marked by reporter gene expression were widely distributed in the basal forebrain by E18.5, some of which expressed neuronal markers. We showed that a small number of cells were double-positive for ChAT and X-gal or EGFP in almost all cases. In addition, the number of ChAT+ cells was reduced to 60\%in the Olig2 knockout mouse basal forebrain. No evidence of elevated apoptosis or reduced proliferation was observed in the knockout mouse forebrain. The present study provides the first direct evidence for involvement of the Olig2 gene in cholinergic differentiation in the basal forebrain.},
	Author = {Furusho, and Ono, and Takebayashi, and Masahira, and Kagawa, and Ikeda, and Ikenaka,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {0372762},
	Organization = {Department of Physiological Sciences, School of Life Science, The Graduate University for Advanced Studies (SOKENDAI), Okazaki, Aichi 444-8787, Japan; Division of Neurobiology and Bioinformatics, National Institute for Physiological Sciences, Okazaki, Aichi 444-8787, Japan.},
	Pii = {S0012-1606(06)00074-1},
	Pubmed = {16537079},
	Title = {Involvement of the Olig2 transcription factor in cholinergic neuron development of the basal forebrain},
	Uuid = {51909473-676C-4467-A989-5C435BA3BA3E},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2006.01.031}}

@article{Furuya:2003,
	Abstract = {Chimeric mice stably reconstituted with bone marrow cells represent a good model for analysis of the mechanism of bone marrow cell infiltration in the brain. However, in preparing chimeric mice, irradiation of the recipient mice is necessary to kill their own bone marrow before transplantation, which induces gliosis and inflammatory response by activation of astrocytes and microglia in the brain. Here, we determined the most suitable dose of irradiation associated with the least brain damage before transplantation for reconstitution of chimeric mice, using FACS analysis. Our mouse model of 10 Gy body/5 Gy head irradiation should be useful for investigating the mechanism(s) of microglial activation in various neurological disorders such as stroke, Alzheimer's disease and Parkinson's disease.},
	Author = {Furuya, Tsuyoshi and Tanaka, Ryota and Urabe, Takao and Hayakawa, Jun and Migita, Makoto and Shimada, Takashi and Mizuno, Yoshikuni and Mochizuki, Hideki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0959-4965},
	Journal = {Neuroreport},
	Keywords = {Animals;Head;Macrophages;Bone Marrow Transplantation;Comparative Study;Nervous System Diseases;Mice, Transgenic;Substantia Nigra;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Disease Models, Animal;Radiation Chimera;Olfactory Bulb;Bone Marrow;Bone Marrow Cells;Pia Mater;Choroid Plexus;Flow Cytometry;Mice;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22544995},
	Month = {3},
	Nlm_Id = {9100935},
	Number = {4},
	Organization = {Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.},
	Pages = {629-31},
	Pubmed = {12657900},
	Title = {Establishment of modified chimeric mice using GFP bone marrow as a model for neurological disorders},
	Uuid = {4564C259-78AF-4623-9CCE-2991A2BDEB23},
	Volume = {14},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1097/01.wnr.0000063507.18654.d8}}

@article{Gage:1995,
	Abstract = {The nervous system of adult mammals, unlike the rest of the organs in the body, has been considered unique in its apparent inability to replace neurons following injury. However, in certain regions of the brain, neurogenesis occurs postnatally and continues through adulthood. The nature, fate, and longevity of cells undergoing proliferation within the CNS are unknown. These cells are increasingly becoming the focus of intense scrutiny; this is a recent development that has led to considerable controversy over the appropriate terminology to describe neural cells as they pass through different stages of proliferation, migration, and differentiation. Continuing studies detailing the properties of mitotic populations in the adult CNS will provide a better understanding of the nature of these cells during their development and should lead to a more consistent nomenclature. Studies of neural precursors isolated from the embryonic brain have indicated that many subgroups of cells undergo mitosis and subsequent differentiation into neurons and glia in vitro. A number of substances, such as growth factors and substrate molecules, are essential for these processes and also for lineage restriction and fate determination of these cells. Recent studies have shown that cells with proliferative capabilities can also be isolated from the adult brain. The nature of these cells is unknown, but there is evidence that both multipotent cells (stem cells) and lineage-restricted cells (neuroblasts or glioblasts) are resident within the mature CNS and that they can be maintained and induced to divide and differentiate in response to many of the same factors that influence their embryonic counterparts. Presently, it is unclear how many potentially quiescent precursor cells exist in the adult brain or what combination of growth factors and substrate molecules is involved in the proliferation and differentiation of these cells. Some of these questions are currently being addressed by using immortalized neural precursors or growth factor-expanded populations of primary precursors to model precursor responsiveness to environmental manipulations. Because in vitro culture conditions are unlikely to provide all of the factors necessary for inducing the proliferation and differentiation of neural precursors, recent studies have explored the properties of well-characterized precursor populations after implantation back into specific regions of the developing or adult CNS. These studies have highlighted the importance of the microenvironment in precursor differentiation and further suggested that precursor plasticity is a characteristic that is probably common to neural precursors throughout the CNS.(ABSTRACT TRUNCATED AT 400 WORDS) Using Smart Source Parsing},
	Author = {Gage, F. H. and Ray, J. and Fisher, L. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Annu Rev Neurosci},
	Keywords = {BB abstr;02 Adult neurogenesis migration;Brain Tissue Transplantation;Adult;03 Adult neurogenesis progenitor source;Human;Stem Cells/*cytology/transplantation;Animal;Neuronal Plasticity/*physiology;Brain/*cytology/growth &development;Cell Separation;Fetal Tissue Transplantation},
	Organization = {Department of Neurosciences, School of Medicine, University of California, San Diego, La Jolla 92093-0627, USA.},
	Pages = {159-92},
	Title = {Isolation, characterization, and use of stem cells from the CNS},
	Uuid = {B2799C98-9006-4907-AE3F-8F003E16490D},
	Volume = {18},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7605059}}

@article{Gage:1998,
	Abstract = {Neurogenesis persists in the adult dentate gyrus of rodents throughout the life of the organism. The factors regulating proliferation, survival, migration, and differentiation of neuronal progenitors are now being elucidated. Cells from the adult hippocampus can be propagated, cloned in vitro, and induced to differentiate into neurons and glial cells. Cells cultured from the adult rodent hippocampus can be genetically marked and transplanted back to the adult brain, where they survive and differentiate into mature neurons and glial cells. Although multipotent stem cells exist in the adult rodent dentate gyrus, their biological significance remains elusive.},
	Author = {Gage, F. H. and Kempermann, G. and Palmer, T. D. and Peterson, D. A. and Ray, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurobiol},
	Keywords = {02 Adult neurogenesis migration;Hippocampus/cytology/embryology/growth &development;Stem Cells/*physiology/transplantation;Dentate Gyrus/*cytology;Human;Spinal Cord/cytology;03 Adult neurogenesis progenitor source;Animal;Support, U.S. Gov't, P.H.S.;BB;Neurons/*physiology/transplantation;Support, Non-U.S. Gov't;Brain/embryology/physiology;Fetal Development/physiology},
	Number = {2},
	Organization = {Laboratory of Genetics, The Salk Institute, La Jolla, CA 92037, USA.},
	Pages = {249-66.},
	Title = {Multipotent progenitor cells in the adult dentate gyrus},
	Uuid = {201358F4-F598-45E0-AC16-CE2C56AA880C},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9712308}}

@article{Gage:2002,
	Author = {Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {J Neurosci},
	Keywords = {Brain/*cytology/growth &development/physiology;01 Adult neurogenesis general;Cell Division/physiology;Neuronal Plasticity/physiology;Neurons/*cytology/physiology;Human;Models, Neurological;A both;Animal;Cell Differentiation/physiology;Stem Cells/cytology/physiology},
	Number = {3},
	Organization = {Laboratory of Genetics, The Salk Institute, La Jolla, California 92037, USA. gage\@salk.edu},
	Pages = {612-3.},
	Title = {Neurogenesis in the adult brain},
	Uuid = {42746EF9-0CA5-4997-A654-BD0E1CEC06D0},
	Volume = {22},
	Year = {2002},
	url = {papers/Gage_JNeurosci2002.pdf}}

@article{Gage:1995a,
	Abstract = {The dentate gyrus of the hippocampus is one of the few areas of the adult brain that undergoes neurogenesis. In the present study, cells capable of proliferation and neurogenesis were isolated and cultured from the adult rat hippocampus. In defined medium containing basic fibroblast growth factor (FGF-2), cells can survive, proliferate, and express neuronal and glial markers. Cells have been maintained in culture for 1 year through multiple passages. These cultured adult cells were labeled in vitro with bromodeoxyuridine and adenovirus expressing beta-galactosidase and were transplanted to the adult rat hippocampus. Surviving cells were evident through 3 months postimplantation with no evidence of tumor formation. Within 2 months postgrafting, labeled cells were found in the dentate gyrus, where they differentiated into neurons only in the intact region of the granule cell layer. Our results indicate that FGF-2 responsive progenitors can be isolated from the adult hippocampus and that these cells retain the capacity to generate mature neurons when grafted into the adult rat brain.},
	Author = {Gage, F. H. and Coates, P. W. and Palmer, T. D. and Kuhn, H. G. and Fisher, L. J. and Suhonen, J. O. and Peterson, D. A. and Suhr, S. T. and Ray, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Survival;10 Development;Cell Differentiation;Fibroblast Growth Factor, Basic/pharmacology;10 Hippocampus;Rats;Fluorescent Antibody Technique;Hippocampus/*cytology/*surgery;Female;Tissue Culture/*methods;02 Adult neurogenesis migration;Animal;BB abstr;03 Adult neurogenesis progenitor source;Rats, Inbred F344;Stem Cells/drug effects/*transplantation/ultrastructure;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;*Brain Tissue Transplantation;Biological Markers;Neurons/drug effects/*transplantation/ultrastructure},
	Number = {25},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.},
	Pages = {11879-83.},
	Title = {Survival and differentiation of adult neuronal progenitor cells transplanted to the adult brain},
	Uuid = {F21C7EC2-6875-11DA-A4B6-000D9346EC2A},
	Volume = {92},
	Year = {1995},
	url = {papers/Gage_ProcNatlAcadSciUSA1995.pdf}}

@article{Gage:2000,
	Abstract = {Neural stem cells exist not only in the developing mammalian nervous system but also in the adult nervous system of all mammalian organisms, including humans. Neural stem cells can also be derived from more primitive embryonic stem cells. The location of the adult stem cells and the brain regions to which their progeny migrate in order to differentiate remain unresolved, although the number of viable locations is limited in the adult. The mechanisms that regulate endogenous stem cells are poorly understood. Potential uses of stem cells in repair include transplantation to repair missing cells and the activation of endogenous cells to provide "self-repair. "Before the full potential of neural stem cells can be realized, we need to learn what controls their proliferation, as well as the various pathways of differentiation available to their daughter cells.},
	Author = {Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Science},
	Keywords = {02 Adult neurogenesis migration;Cell Differentiation;Embryo/cytology;Spinal Cord/cytology/embryology;Human;Neurons/*cytology/physiology;Brain/*cytology/embryology;Cell Division;Animal;Cell Death;Support, U.S. Gov't, P.H.S.;*Stem Cells/cytology/physiology/transplantation;Support, Non-U.S. Gov't;B-22;Cell Separation;Cell Movement},
	Number = {5457},
	Organization = {The Salk Institute, Laboratory of Genetics, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. gage\@salk.edu.},
	Pages = {1433-8.},
	Title = {Mammalian neural stem cells},
	Uuid = {68F252B8-D58B-4B84-AAD6-40DF4E8D3081},
	Volume = {287},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10688783}}

@article{Gaiano:2000,
	Abstract = {In vertebrates, Notch signaling is generally thought to inhibit neural differentiation. However, whether Notch can also promote specific early cell fates in this context is unknown. We introduced activated Notch1 (NIC) into the mouse forebrain, before the onset of neurogenesis, using a retroviral vector and ultrasound imaging. During embryogenesis, NIC-infected cells became radial glia, the first specialized cell type evident in the forebrain. Thus, rather than simply inhibiting differentiation, Notch1 signaling promoted the acquisition of an early cellular phenotype. Postnatally, many NIC-infected cells became periventricular astrocytes, cells previously shown to be neural stem cells in the adult. These results suggest that Notch1 promotes radial glial identity during embryogenesis, and that radial glia may be lineally related to stem cells in the adult nervous system. 0896-6273 Journal Article},
	Author = {Gaiano, N. and Nye, J. S. and Fishell, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Neuron},
	Keywords = {Neuroglia/*physiology;10 Development;Phenotype;Membrane Proteins/metabolism/*physiology;Retroviridae/metabolism;Animals, Newborn/physiology;F;Support, U.S. Gov't, P.H.S.;Signal Transduction/*physiology;Retroviridae Infections/pathology;Support, Non-U.S. Gov't;Animals;Mice;Prosencephalon/*cytology/*physiology},
	Number = {2},
	Organization = {Skirball Institute of Biomolecular Medicine, Department of Cell Biology, New York University School of Medicine, New York 10016, USA.},
	Pages = {395-404},
	Pubmed = {10839358},
	Title = {Radial glial identity is promoted by Notch1 signaling in the murine forebrain},
	Uuid = {88917F31-915C-423B-BC06-33CD6D9439F8},
	Volume = {26},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10839358}}

@article{Gal:2006,
	Abstract = {The proliferative ventricular zone (VZ) is the main source of projection neurons for the overlying cerebral neocortex. The number and diversity of neocortical neurons is determined, in part, by factors controlling the proliferation and specification of VZ cells during embryonic development. We used a variety of methods, including in utero electroporation with specific cellular markers, computer-assisted serial EM cell reconstruction, and time-lapse multiphoton imaging to characterize the molecular and morphological characteristics of the VZ constituents and to capture their behavior during cell division. Our analyses reveal at least two types of dividing cells in the VZ: (1) radial glial cells (RGCs) that span the entire neocortical wall and maintain contact both at the ventricular and pial surfaces throughout mitotic division, and (2) short neural precursors (SNPs) that possess a ventricular endfoot and a basal process of variable length that is retracted during mitotic division. These two precursor cell classes are present concomitantly in the VZ, but their relative number changes over the course of cortical neurogenesis. Moreover, the SNPs are morphologically, ultrastructurally and molecularly distinct from dividing RGCs. For example, SNPs are marked by their preferential expression of the tubulin alpha-1 promoter whereas RGCs instead express the glutamate-aspartate transporter and brain lipid binding protein promoters. In contrast to recent studies that suggest that RGCs are the sole type of VZ precursor, the present study indicates that the VZ in murine dorsal telencephalon is similar to that in human and nonhuman primates, because it contains multiple types of neuronal precursors.},
	Author = {Gal, Jonathan S. and Morozov, Yury M. and Ayoub, Albert E. and Chatterjee, Mitali and Rakic, Pasko and Haydar, Tarik F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Embryo;10 Development;Research Support, Non-U.S. Gov't;Comparative Study;Cell Proliferation;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Neocortex;Female;Research Support, N.I.H., Extramural;Pregnancy;Animals;Mice;24 Pubmed search results 2008;Humans;Neurons},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {3},
	Organization = {Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC 20010, USA.},
	Pages = {1045-56},
	Pii = {26/3/1045},
	Pubmed = {16421324},
	Title = {Molecular and morphological heterogeneity of neural precursors in the mouse neocortical proliferative zones},
	Uuid = {BCADD2EC-7480-4326-A2F5-1CB88B4B9F60},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4499-05.2006}}

@article{Galceran:2000,
	Abstract = {Lef1 and other genes of the LEF1/TCF family of transcription factors are nuclear mediators of Wnt signaling. Here we examine the expression pattern and functional importance of Lef1 in the developing forebrain of the mouse. Lef1 is expressed in the developing hippocampus, and LEF1-deficient embryos lack dentate gyrus granule cells but contain glial cells and interneurons in the region of the dentate gyrus. In mouse embryos homozygous for a Lef1-lacZ fusion gene, which encodes a protein that is not only deficient in DNA binding but also interferes with (beta)-catenin-mediated transcriptional activation by other LEF1/TCF proteins, the entire hippocampus including the CA fields is missing. Thus, LEF1 regulates the generation of dentate gyrus granule cells, and together with other LEF1/TCF proteins, the development of the hippocampus.},
	Author = {Galceran, J. and Miyashita-Lin, E. M. and Devaney, E. and Rubenstein, J. L. and Grosschedl, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Trans-Activation (Genetics);Transcription Factors;beta-Galactosidase;Animals;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Transfection;Recombinant Proteins;Apoptosis;Mice, Transgenic;Hippocampus;Embryonic and Fetal Development;Prosencephalon;Research Support, U.S. Gov't, P.H.S.;Mice, Knockout;Tumor Cells, Cultured;Dentate Gyrus;Homozygote;Neuroglia;Mice;Interneurons;Research Support, Non-U.S. Gov't},
	Medline = {20098486},
	Month = {2},
	Nlm_Id = {8701744},
	Number = {3},
	Organization = {Howard Hughes Medical Institute, Department of Microbiology, University of California, San Francisco, CA 94143, USA.},
	Pages = {469-82},
	Pubmed = {10631168},
	Title = {Hippocampus development and generation of dentate gyrus granule cells is regulated by LEF1},
	Uuid = {E08412AA-7113-11DA-9A4D-000D9346EC2A},
	Volume = {127},
	Year = {2000},
	url = {papers/Galceran_Development2000.pdf}}

@article{Galea:2005,
	Abstract = {Perivascular macrophages are believed to have a significant role in inflammation in the central nervous system (CNS). They express a number of different receptors that point toward functions in both innate immunity, through pathogen-associated molecular pattern recognition, phagocytosis, and cytokine responsiveness, and acquired immunity, through antigen presentation and co-stimulation. We are interested in the receptors that are differentially expressed by perivascular macrophages and microglia in both the normal CNS as well as in neuroinflammation and neurodegeneration. In this article we report the use of a well-characterized monoclonal antibody, 5D3, to localize the expression of the mannose receptor to perivascular macrophages in the normal CNS and in various models of brain pathology. Mannose receptor expression was limited to perivascular, meningeal, and choroid plexus macrophages in normal, inflamed, injured, and diseased CNS. In particular, activated microglia and invading hematogenous leukocytes were mannose receptor negative while expressing the F4/80 antigen, macrosialin (CD68), FcRII (CD32), scavenger receptor (CD204), and CR3 (CD11b/CD18). Since the perivascular macrophages expressing the mannose receptor are known to be the only constitutively phagocytic cells in the normal CNS, we injected clodronate-loaded liposomes intracerebroventricularly in control mice to deplete these cells. In these mice, there was no detectable mannose receptor expression in perivascular spaces after immunocytochemistry with the 5D3 monoclonal antibody. This finding underlines the value of the monoclonal antibody 5D3 as a tool to study murine perivascular macrophages selectively. Mannose receptor expression by macrophages located at blood-brain (perivascular), brain-cerebrospinal fluid (CSF) (meningeal), and CSF-blood (choroid plexus) interfaces supports a functional role of these cells in responding to external stimuli such as infection.},
	Author = {Galea, Ian and Palin, Karine and Newman, Tracey A. and Van Rooijen, Nico and Perry, V. Hugh and Boche, Delphine},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Research Support, Non-U.S. Gov't;Receptors, Cell Surface;Blood-Brain Barrier;Neurodegenerative Diseases;Female;Gene Expression Regulation;Lectins, C-Type;Mice, Inbred C57BL;11 Glia;Mannose-Binding Lectins;Macrophages;Mice;Brain;Animals},
	Month = {2},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {CNS Inflammation Group, School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. i.galea\@soton.ac.uk},
	Pages = {375-84},
	Pubmed = {15538754},
	Title = {Mannose receptor expression specifically reveals perivascular macrophages in normal, injured, and diseased mouse brain},
	Uuid = {109E3A92-8A02-4CA3-A9DB-F3DF2EDADA8E},
	Volume = {49},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20124}}

@article{Galiano:2001,
	Abstract = {Nerve injury triggers numerous changes in the injured neurons and surrounding non-neuronal cells. Of particular interest are molecular signals that play a role in the overall orchestration of this multifaceted cellular response. Here we investigated the function of interleukin-6 (IL6), a multifunctional neurotrophin and cytokine rapidly expressed in the injured nervous system, using the facial axotomy model in IL6-deficient mice and wild-type controls. Transgenic deletion of IL6 caused a massive decrease in the recruitment of CD3-positive T-lymphocytes and early microglial activation during the first 4 days after injury in the axotomized facial nucleus. This was accompanied by a more moderate reduction in peripheral regeneration at day 4, lymphocyte recruitment (day 14) and enhanced perikaryal sprouting (day 14). Motoneuron cell death, phagocytosis by microglial cells and recruitment of granulocytes and macrophages into injured peripheral nerve were not affected. In summary, IL6 lead to a variety of effects on the cellular response to neural trauma. However, the particularly strong actions on lymphocytes and microglia suggest that this cytokine plays a central role in the initiation of immune surveillance in the injured central nervous system.},
	Author = {Galiano, M. and Liu, Z. Q. and Kalla, R. and Bohatschek, M. and Koppius, A. and Gschwendtner, A. and Xu, S. and Werner, A. and Kloss, C. U. and Jones, L. L. and Bluethmann, H. and Raivich, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Survival;Animals;Fluorescent Antibody Technique;Microglia;Lymphocyte Activation;Not relevant;11 Glia;Time Factors;Disease Models, Animal;Nerve Regeneration;Facial Nerve Injuries;Support, Non-U.S. Gov't;Mice, Knockout;Motor Neurons;Gliosis;Mice;Interleukin-6;Retrograde Degeneration;Nerve Tissue Proteins;Growth Cones;Facial Nerve},
	Medline = {21437552},
	Month = {7},
	Nlm_Id = {8918110},
	Number = {2},
	Organization = {Department of Neuromorphology, Max-Planck Institute for Neurobiology, Am Klopferspitz 18A, D-82152 Martinsried, Germany.},
	Pages = {327-41},
	Pii = {ejn1647},
	Pubmed = {11553283},
	Title = {Interleukin-6 (IL6) and cellular response to facial nerve injury: effects on lymphocyte recruitment, early microglial activation and axonal outgrowth in IL6-deficient mice},
	Uuid = {03B51EF1-360A-40DE-94DC-FAC4F961597A},
	Volume = {14},
	Year = {2001}}

@article{Gallay:1997,
	Abstract = {The karyophilic properties of the HIV-1 nucleoprotein complex facilitate infection of nondividing cells such as macrophages and quiescent T lymphocytes, and allow the in vivo delivery of transgenes by HIV-derived retroviral vectors into terminally differentiated cells such as neurons. Although the viral matrix (MA) and Vpr proteins have previously been shown to play important roles in this process, we demonstrate here that integrase, the enzyme responsible for mediating the integration of the viral genome in the host cell chromosome, can suffice to connect the HIV-1 preintegration complex with the cell nuclear import machinery. This novel function of integrase reflects the recognition of an atypical bipartite nuclear localization signal by the importin/karyopherin pathway.},
	Author = {Gallay, P. and Hope, T. and Chin, D. and Trono, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;HIV Infections;HIV-1;Integrases;Virus Replication;Research Support, U.S. Gov't, P.H.S.;Signal Transduction;Cell Line;Cell Division;Karyopherins;Nuclear Proteins;15 Retrovirus mechanism;Humans;24 Pubmed search results 2008;Neurons},
	Medline = {97420768},
	Month = {9},
	Nlm_Id = {7505876},
	Number = {18},
	Organization = {The Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037-1099, USA.},
	Pages = {9825-30},
	Pubmed = {9275210},
	Title = {HIV-1 infection of nondividing cells through the recognition of integrase by the importin/karyopherin pathway},
	Uuid = {197877FC-68FF-472E-B6BD-149FC9B38081},
	Volume = {94},
	Year = {1997}}

@article{Galle:1994,
	Abstract = {BACKGROUND/AIMS: Studies on the interaction of hepatitis B virus (HBV) with its host cell require a suitable tissue culture system. This study used primary adult hepatocytes from healthy human liver tissue to establish productive infection in vitro. METHODS: Hepatocytes were inoculated overnight with HBV. Production of viral proteins was assessed by radioimmunoassay and by [35S]methionine labeling, and production of viral DNA was assessed by Southern blotting and endogenous polymerase assay. RESULTS: Secretion of high levels of hepatitis B surface antigen (HBsAg) and low levels of hepatitis B virus e antigen (HBeAg) into the medium was detectable 6 days after infection and reached maximum values after 12 days. Metabolic labeling showed production of viral proteins to be a result of de novo synthesis. The appearance of single-stranded HBV DNA in the cytoplasm of infected cells, typically present in immature cores, indicated viral replication. HBV DNA containing particles possessing an active viral DNA polymerase could be immunoprecipitated from the medium 12 days after infection. An antiserum specific for the preS1 region of the viral envelope was capable to block infection. Presence of dimethyl sulfoxide in the medium greatly improved the yield of viral proteins. CONCLUSIONS: Primary adult human liver cells are competent for infection with HBV. 0016-5085 Journal Article},
	Author = {Galle, P. R. and Hagelstein, J. and Kommerell, B. and Volkmann, M. and Schranz, P. and Zentgraf, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Gastroenterology},
	Keywords = {Human;Animals;Cells, Cultured;Fluorescent Antibody Technique;Virion/metabolism;DNA, Viral/metabolism;Disease Susceptibility;08 Aberrant cell cycle;EE, DMSO, abstr;Dimethyl Sulfoxide/pharmacology;Viral Proteins/biosynthesis;Support, Non-U.S. Gov't;Immune Sera/pharmacology;Methionine/metabolism;Fetal Blood;Cattle/embryology;Hepatitis B/*metabolism/pathology/prevention &control;Radioimmunoassay;Culture Media;Liver/*metabolism/pathology},
	Number = {3},
	Organization = {Department of Internal Medicine, University of Heidelberg, Germany.},
	Pages = {664-73},
	Pubmed = {8119538},
	Title = {In vitro experimental infection of primary human hepatocytes with hepatitis B virus},
	Uuid = {8F3D3E38-6561-4832-8E37-24CD7E7A33AE},
	Volume = {106},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8119538}}

@article{Gallo:1971,
	Author = {Gallo, R. C. and Sarin, P. S. and Allen, P. T. and Newton, W. A. and Priori, E. S. and Bowen, J. M. and Dmochowski, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0090-0028},
	Journal = {Nat New Biol},
	Keywords = {Oncogenic Viruses;RNA Viruses;Humans;Mycoplasma;Guanine Nucleotides;Centrifugation, Density Gradient;15 Retrovirus mechanism;Neoplasms;Male;Adenosine Triphosphate;Magnesium;DNA Nucleotidyltransferases;Cytosine Nucleotides;24 Pubmed search results 2008;Burkitt Lymphoma;Autoradiography;15 ERVs retroelements;Tritium;Microscopy, Electron},
	Medline = {71291919},
	Month = {8},
	Nlm_Id = {0410463},
	Number = {31},
	Pages = {140-2},
	Pubmed = {5285568},
	Title = {Reverse transcriptase in type C virus particles of human origin},
	Uuid = {8DFFAA0C-4328-11DB-A5D2-000D9346EC2A},
	Volume = {232},
	Year = {1971}}

@article{Galvez:2005,
	Abstract = {The Fragile-X mental retardation syndrome is the leading form of inherited mental retardation. Dendritic analysis in a mouse model (FraX) found abnormal pruning in somatosensory cortex. To further characterize dendritic abnormalities and assess their occurrence in other brain regions, we examined mitral cells in FraX mice olfactory bulbs. FraX mice exhibited dendritic abnormalities consistent with somatosensory cortex, suggesting that deficient pruning is found in multiple brain regions.},
	Author = {Galvez, and Smith, and Greenough,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0165-3806},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {10 Development;10 Structural plasticity},
	Month = {5},
	Nlm_Id = {8908639},
	Organization = {Neuroscience Program, University of Illinois, Urbana, IL 61801, USA; Beckman Institute, University of Illinois, 405 N Mathews, Urbana, IL 61801, USA.},
	Pii = {S0165-3806(05)00107-0},
	Pubmed = {15878626},
	Title = {Olfactory bulb mitral cell dendritic pruning abnormalities in a mouse model of the Fragile-X mental retardation syndrome: Further support for FMRP's involvement in dendritic development},
	Uuid = {0F1C4B6E-2BF1-46C0-9180-74E3B79D9E6B},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.devbrainres.2005.03.010}}

@article{Ganat:2006,
	Abstract = {To identify the fates that astroglial cells can attain in the postnatal brain, we generated mice carrying an inducible Cre recombinase (Cre-ER(T2)) controlled by the human GFAP promoter (hGFAP). In mice carrying the GCE (hGFAP-Cre-ER(T2)) transgene, OHT (4-hydroxy-tamoxifen) injections induced Cre recombination in astroglial cells at postnatal day 5 and allowed us to permanently tag these cells with reporter genes. Three days after recombination, reporter-tagged cells were quiescent astroglial cells that expressed the stem cell marker LeX in the subventricular zone (SVZ) and dentate gyrus (DG). After 2-4 weeks, the tagged GFAP lineage included proliferating progenitors expressing the neuronal marker Dcx (Doublecortin) in the SVZ and the DG. After 4 weeks, the GFAP lineage generated mature neurons in the olfactory bulb (OB), DG, and, strikingly, also in the cerebral cortex. A major portion of all neurons in the DG and OB born at the end of the first postnatal week were generated from GFAP+ cells. In addition to neurons, mature oligodendrocytes and astrocytes populating the cerebral cortex and white matter were also the progeny of GFAP+ astroglial ancestors. Thus, genetic fate mapping of postnatal GFAP+ cells reveals that they seed the postnatal brain with neural progenitors/stem cells that in turn give rise to neural precursors and their mature neuronal and oligodendrocytic progeny in many CNS regions, including the cerebral cortex.},
	Author = {Ganat, Yosif M. and Silbereis, John and Cave, Clinton and Ngu, Hai and Anderson, George M. and Ohkubo, Yasushi and Ment, Laura R. and Vaccarino, Flora M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Transgenes;Cell Differentiation;research support, n.i.h., extramural ;Astrocytes;Animals;Humans;Brain;Oligodendroglia;Female;Integrases;Mice, Transgenic;Male;research support, non-u.s. gov't ;Cerebral Ventricles;Olfactory Bulb;Cell Lineage;Animals, Newborn;Neurons;Recombination, Genetic;Mice;Promoter Regions (Genetics);24 Pubmed search results 2008;Stem Cells;Glial Fibrillary Acidic Protein},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {33},
	Organization = {Child Study Center, Yale University Medical School, New Haven, Connecticut 06520, USA.},
	Pages = {8609-21},
	Pii = {26/33/8609},
	Pubmed = {16914687},
	Title = {Early postnatal astroglial cells produce multilineage precursors and neural stem cells in vivo},
	Uuid = {A8D22CFF-9EDA-485E-B7AF-3BFC9E93F1EF},
	Volume = {26},
	Year = {2006},
	url = {papers/Ganat_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2532-06.2006}}

@article{Ganat:2002,
	Abstract = {A number of signaling molecules have been implicated in the acute response to hypoxia/ischemia in the adult brain. In contrast, the reaction to chronic hypoxemia is largely unexplored. We used a protocol of chronic hypoxia in rat pups during the first three postnatal weeks, encompassing the period of cellular plasticity in the cerebral cortex. We find that the levels of fibroblast growth factor 1 (FGF1) and FGF2, two members of the FGF family, increase after 2 weeks of chronic hypoxia. In contrast, members of the neurotrophin family are unaffected. FGF2 is normally expressed in the nucleus of mature, glial fibrillary acidic protein (GFAP)-containing astrocytes. Under hypoxia, most FGF2-containing cells do not express detectable levels of GFAP, suggesting that chronic low O(2) induces their transformation into more immature glial phenotypes. Remarkably, hypoxia promotes the appearance of radial glia throughout the sub-ventricular and ependymal zones. Most of these cells express vimentin and brain lipid binding protein. A subset of these radial glial cells expresses FGF receptor 1, and are in close contact with FGF2-positive cells in the sub-ventricular zone. Thus, FGF receptor signaling in radial glia may foster cell genesis after chronic hypoxic damage.From the results of this study we suggest that after the chronic exposure to low levels of oxygen during development, the expression of radial glia increases in the forebrain periventricular region. We envision that astroglia, which are the direct descendants of radial glia, are reverting back to immature glial cells. Alternatively, hypoxia hinders the normal maturation of radial glia into GFAP-expressing astrocytes. Interestingly, hypoxia increases the levels of expression of FGF2, a factor that is essential for neuronal development. Furthermore, chronic hypoxia up-regulated FGF2's major receptor in the periventricular region. Because radial glia have been suggested to play a key role in neurogenesis and cell migration, our data suggests that hypoxia-induced FGF signaling in radial glia may represent part of a conserved program capable of regenerating neurons in the brain after injury. 0306-4522 Journal Article},
	Author = {Ganat, Y. and Soni, S. and Chacon, M. and Schwartz, M. L. and Vaccarino, F. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:47 -0400},
	Journal = {Neuroscience},
	Keywords = {Animals;Neuroglia/*metabolism;Up-Regulation;Rats;D pdf;Cerebral Cortex/metabolism;Receptor Protein-Tyrosine Kinases/*metabolism;Fibroblast Growth Factor 1/*metabolism;Anoxia/*metabolism;Receptors, Fibroblast Growth Factor/*metabolism;Cerebral Ventricles/embryology/*metabolism;Ependyma/embryology/*metabolism;Blotting, Western;06 Adult neurogenesis injury induced;Fibroblast Growth Factor 2/*metabolism;Support, U.S. Gov't, P.H.S.;Enzyme-Linked Immunosorbent Assay;Immunohistochemistry;Regeneration},
	Number = {4},
	Organization = {Child Study Center, Yale University, 230 South Frontage Road, New Haven, CT 06520, USA.},
	Pages = {977-91},
	Title = {Chronic hypoxia up-regulates fibroblast growth factor ligands in the perinatal brain and induces fibroblast growth factor-responsive radial glial cells in the sub-ependymal zone},
	Uuid = {604CD542-952D-4565-9E2F-59A9575FC663},
	Volume = {112},
	Year = {2002},
	url = {papers/Ganat_Neuroscience2002.pdf}}

@article{Garcia:2004,
	Abstract = {Establishing the cellular identity in vivo of adult multipotent neural progenitors is fundamental to understanding their biology. We used two transgenic strategies to determine the relative contribution of glial fibrillary acidic protein (GFAP)-expressing progenitors to constitutive neurogenesis in the adult forebrain. Transgenically targeted ablation of dividing GFAP-expressing cells in the adult mouse subependymal and subgranular zones stopped the generation of immunohistochemically identified neuroblasts and new neurons in the olfactory bulb and the hippocampal dentate gyrus. Transgenically targeted cell fate mapping showed that essentially all neuroblasts and neurons newly generated in the adult mouse forebrain in vivo, and in adult multipotent neurospheres in vitro, derived from progenitors that expressed GFAP. Constitutively dividing GFAP-expressing progenitors showed predominantly bipolar or unipolar morphologies with significantly fewer processes than non-neurogenic multipolar astrocytes. These findings identify morphologically distinctive GFAP-expressing progenitor cells as the predominant sources of constitutive adult neurogenesis, and provide new methods for manipulating and investigating these cells.},
	Author = {Garcia, A. Denise R. and Doan, Ngan B. and Imura, Tetsuya and Bush, Toby G. and Sofroniew, Michael V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Cell Differentiation;Phosphopyruvate Hydratase;Green Fluorescent Proteins;Immunohistochemistry;Sialic Acids;Thymidine Kinase;Neural Cell Adhesion Molecule L1;Animals;Ganciclovir;Hippocampus;Integrases;Research Support, U.S. Gov't, P.H.S.;Cell Count;Bromodeoxyuridine;Analysis of Variance;Olfactory Bulb;Microtubule-Associated Proteins;Tubulin;Gene Expression Regulation;Neuropeptides;Comparative Study;Glial Fibrillary Acidic Protein;beta-Galactosidase;Neuroglia;Prosencephalon;Cell Size;Stem Cells;Mice;Research Support, Non-U.S. Gov't;Neurons;Mice, Transgenic},
	Month = {11},
	Nlm_Id = {9809671},
	Number = {11},
	Organization = {Department of Neurobiology and Brain Research Institute, University of California, Los Angeles, California 90095-1763, USA.},
	Pages = {1233-41},
	Pii = {nn1340},
	Pubmed = {15494728},
	Title = {GFAP-expressing progenitors are the principal source of constitutive neurogenesis in adult mouse forebrain},
	Uuid = {D6F585BF-C9B5-11DA-8A64-000D9346EC2A},
	Volume = {7},
	Year = {2004},
	url = {papers/Garcia_NatNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1340}}

@article{Garcia-Valenzuela:1999,
	Abstract = {Following optic nerve transection, most of the retinal ganglion cells die. Their debris is promptly cleared by phagocytic cells. It is currently not known to what extent peripherally derived macrophages contribute to this activity. Using antibodies OX42 and ED-1, phagocytic cells were labeled in the retinas of optic nerve lesioned adult rats. To distinguish whether the cells were reactive microglial or macrophagic in origin, blood-borne monocytes were labeled with fluorescent microspheres while in the systemic circulation. Macrophages invaded the retina, but only in the nerve fiber layer, sparing the ganglion cell and other layers. These macrophages engulfed only the axonal debris from dying ganglion cells, not their degenerating cell bodies. These results indicate that although peripherally derived monocytic cells are recruited into the retrogradely degenerating retina, their role in clearing debris is limited to the optic fiber layer.},
	Author = {Garcia-Valenzuela, E. and Sharma, S. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Retina;Glial Fibrillary Acidic Protein;Phagocytosis;Animals;Macrophages;Rats;Microscopy, Confocal;Microglia;Optic Nerve;Antigens, Surface;Rats, Wistar;Not relevant;11 Glia;Time Factors;Membrane Glycoproteins;Axotomy;Support, U.S. Gov't, P.H.S.;Retinal Ganglion Cells},
	Medline = {99326793},
	Month = {7},
	Nlm_Id = {0213640},
	Number = {1},
	Organization = {Departments of Cell Biology and Anatomy and Ophthalmology, New York Medical College, Valhalla, New York 10595, USA.},
	Pages = {55-66},
	Pii = {10.1002/(SICI)1097-4695(199907)40:1<55::AID-NEU5>3.0.CO;2-E},
	Pubmed = {10398071},
	Title = {Laminar restriction of retinal macrophagic response to optic nerve axotomy in the rat},
	Uuid = {D82C3775-E8DF-41CD-9E0C-5444CA4ACFE1},
	Volume = {40},
	Year = {1999},
	url = {papers/Garcia-Valenzuela_JNeurobiol1999.pdf}}

@article{Garcia-Verdugo:1998,
	Abstract = {Neural stem cells are maintained in the subventricular zone (SVZ) of the adult mammalian brain. Here, we review the cellular organization of this germinal layer and propose lineage relationships of the three main cell types found in this area. The majority of cells in the adult SVZ are migrating neuroblasts (type A cells) that continue to proliferate. These cells form an extensive network of tangentially oriented pathways throughout the lateral wall of the lateral ventricle. Type A cells move long distances through this network at high speeds by means of chain migration. Cells in the SVZ network enter the rostral migratory stream (RMS) and migrate anteriorly into the olfactory bulb, where they differentiate into interneurons. The chains of type A cells are ensheathed by slowly proliferating astrocytes (type B cells), the second most common cell type in this germinal layer. The most actively proliferating cells in the SVZ, type C, form small clusters dispersed throughout the network. These foci of proliferating type C cells are in close proximity to chains of type A cells. We discuss possible lineage relationships among these cells and hypothesize which are the neural stem cells in the adult SVZ. In addition, we suggest that interactions between type A, B, and C cells may regulate proliferation and initial differentiation within this germinal layer.},
	Author = {Garcia-Verdugo, J. M. and Doetsch, F. and Wichterle, H. and Lim, D. A. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurobiol},
	Keywords = {02 Adult neurogenesis migration;Cell Division/physiology;Cerebral Ventricles/*cytology/embryology/growth &development;Interneurons/cytology;Olfactory Bulb/cytology;Neurons/*cytology/physiology;Stem Cells/*cytology/physiology;03 Adult neurogenesis progenitor source;Animal;Support, U.S. Gov't, P.H.S.;BB;Cell Movement/physiology},
	Number = {2},
	Organization = {University of Valencia, Spain.},
	Pages = {234-48.},
	Title = {Architecture and cell types of the adult subventricular zone: in search of the stem cells},
	Uuid = {771B0138-B931-4335-838A-83A8C4E2D946},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9712307}}

@article{Garland:2007,
	Abstract = {CASE:: Tony is an 11-year old boy in the fifth grade whose mother describes him as "really a good kid who is bright and tries to be friendly. But he's always doing things that get him in trouble at school and sometimes at home." Tony was diagnosed with ADHD (combined type) 2 years ago. Stimulant therapy improved his attention and concentration during school, decreased hyperactivity in the classroom and improved educational achievements. However, Tony is oppositional and disruptive on the playground, during team sports and at home. His teacher observed that he wants to fit in, but he quickly gets in arguments with other children. He has difficulty sustaining friendships because he typically annoys others with unreasonable demands. He often has temper tantrums when things do not go his way; the tantrums are not prolonged but frequent. At home, on several occasions Tony hit his younger sister, and he once threw a dinner plate against the wall during a family meal. Although his mother describes these behaviors as present for many years, they seem to be escalating. Tony lives with both parents and his younger sister. There is no history of marital discord or major life event change in the past year. Standardized achievement tests demonstrate average to above average achievement scores. He continues to get mostly B grades and an occasional C. Tony's parents have tried to limit television time as a punishment for disruptive behaviors without any apparent effect. His mother reports that she yelled at him on several occasions when he refused to carry out household chores. "He gets angry at the simplest request for help." After meeting with Tony and his mother and completing a normal physical examination, the pediatrician referred Tony to a child psychologist for behavioral therapy.},
	Author = {Garland, Ann and Augustyn, Marilyn and Stein, Martin T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0196-206X},
	Journal = {J Dev Behav Pediatr},
	Keywords = {24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8006933},
	Number = {5},
	Pages = {406-8},
	Pii = {00004703-200710000-00012},
	Pubmed = {18049326},
	Title = {Disruptive and oppositional behavior in an 11-year old boy},
	Uuid = {E8B87309-9595-4384-9C99-398E6E736F45},
	Volume = {28},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1097/DBP.0b013e3181570cf1}}

@article{Garnier:1996,
	Abstract = {Several recent experiments using neocortical transplantation paradigms indicated that embryonic neurons grafted in a heterotopic locus retain development characteristics corresponding to their site of origin. In the present study, limited portions of lateral (lateral-to-lateral) or medial (medial-to-lateral) sectors of embryonic (E16) frontal cortex were grafted into the lateral frontal cortex of newborn rats. A retrograde tracer was injected 3-4 months later into the dorsomedial or ventrolateral sectors of the host caudate-putamen (CPU). The results indicate that the mediolateral arrangement of striatal projection developed by lateral-to-lateral transplants is virtually identical to that found in intact rats. A very weak proportion of the transplanted cells distribute fibers to the dorsomedial sector of the CPU. In marked contrast, the proportion of efferents from medial-to-lateral transplants projecting to the dorsomedial CPU is by far larger than the one directed to the ventrolateral CPU. Our findings provide evidence that even within one single neocortical area (the frontal neocortex) some degree of prespecification (medial versus lateral patterns of efferent projections) is already present at E16.},
	Author = {Garnier, C. and Arnault, P. and L{\'e}tang, J. and Roger, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Neostriatum;Frontal Lobe;Cell Differentiation;Brain Tissue Transplantation;Rats;Neural Pathways;Rats, Wistar;Silver Staining;Cholera Toxin;Animals, Newborn;Age Factors;Animals;24 Pubmed search results 2008;Fetal Tissue Transplantation;Microinjections},
	Medline = {97001714},
	Month = {7},
	Nlm_Id = {7600130},
	Number = {1},
	Organization = {CNRS, URA 1869, D{\'e}partement des Neurosciences, Facult{\'e} des Sciences, Universit{\'e} de Poitiers, France.},
	Pages = {33-6},
	Pii = {0304394096128330},
	Pubmed = {8844706},
	Title = {Development of projections from transplants of embryonic medial or lateral frontal cortex placed in the lateral frontal cortex of newborn hosts},
	Uuid = {5D090C26-63E1-4037-9587-5571FC419E46},
	Volume = {213},
	Year = {1996}}

@article{Gates:1995,
	Abstract = {The subventricular zone (SVZ) of the lateral ventricle remains mitotically active in the adult mammalian central nervous system (CNS). Recent studies have suggested that this region may contain neuronal precursors (neural stem cells) in adult rodents. A variety of neuronal and glial markers as well as three extracellular matrix (ECM) markers were examined with the hope of understanding factors that may affect the growth and migration of neurons from this region throughout development and in the adult. This study has characterized the subventricular zone of late embryonic, postnatal, and adult mice using several neuronal markers [TuJ1, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), neuron-specific enolase (NSE)], glial markers [RC-2, vimentin, glial fibrillary acidic protein (GFAP), galactocerebroside (Gal-C)], ECM markers [tenascin-C (TN-C), chondroitin sulfate, a chondroitin sulfate proteoglycan termed dermatan sulfate-dependent proteoglycan-1 (DSD-1-PG)], stem-cell marker (nestin), and proliferation-specific marker [bromodeoxyuridine (BrdU)]. TuJ1+ and nestin+ cells (neurons and stem cells, respectively) persist in the region into adulthood, although the numbers of these cells become more sparse as the animal develops, and they appear to be immature compared to the cells in surrounding forebrain structures (e.g., not expressing NSE and having few, if any, processes). Likewise, NADPH-d+ cells are found in and around the SVZ during early postnatal development but become more sparse in the proliferative zone through maturity, and, by adulthood, only a few labeled cells can be found at the border between the SVZ and surrounding forebrain structures (e.g., the striatum), and even smaller numbers of positive cells can be found within the adult SVZ proper. BrdU labeling also seems to decrease significantly after the first postnatal week, but it still persists in the SVZ of adult animals. The disappearance of RC-2+ (radial) glia during postnatal development and the persistence of glial-derived ECM molecules such as tenascin and chondroitin sulfate proteoglycans (as well as other "boundary"molecules) in the adult SVZ may be associated with a persistence of immaturity, cell death, and a lack of cell emigration from the SVZ in the adult. 0021-9967 Journal Article},
	Author = {Gates, M. A. and Thomas, L. B. and Howard, E. M. and Laywell, E. D. and Sajin, B. and Faissner, A. and Gotz, B. and Silver, J. and Steindler, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Comp Neurol},
	Keywords = {In Situ Hybridization;Embryo/cytology/*metabolism;Neurons/cytology/metabolism;02 Adult neurogenesis migration;Aging/metabolism;Immunohistochemistry;B, G abstr;Extracellular Matrix/metabolism;Biological Markers;Brain/cytology/*embryology/*growth &development;Cell Division;Animals, Newborn;Support, U.S. Gov't, P.H.S.;Animals;Cerebral Ventricles;Support, Non-U.S. Gov't;Mice},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, University of Tennessee, Memphis 38163, USA.},
	Pages = {249-66},
	Pubmed = {8543661},
	Title = {Cell and molecular analysis of the developing and adult mouse subventricular zone of the cerebral hemispheres},
	Uuid = {BE1CEA9B-6144-4C81-B543-E6013567D349},
	Volume = {361},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8543661}}

@article{Ge:2006,
	Abstract = {Adult neurogenesis, the birth and integration of new neurons from adult neural stem cells, is a striking form of structural plasticity and highlights the regenerative capacity of the adult mammalian brain. Accumulating evidence suggests that neuronal activity regulates adult neurogenesis and that new neurons contribute to specific brain functions. The mechanism that regulates the integration of newly generated neurons into the pre-existing functional circuitry in the adult brain is unknown. Here we show that newborn granule cells in the dentate gyrus of the adult hippocampus are tonically activated by ambient GABA (gamma-aminobutyric acid) before being sequentially innervated by GABA- and glutamate-mediated synaptic inputs. GABA, the major inhibitory neurotransmitter in the adult brain, initially exerts an excitatory action on newborn neurons owing to their high cytoplasmic chloride ion content. Conversion of GABA-induced depolarization (excitation) into hyperpolarization (inhibition) in newborn neurons leads to marked defects in their synapse formation and dendritic development in vivo. Our study identifies an essential role for GABA in the synaptic integration of newly generated neurons in the adult brain, and suggests an unexpected mechanism for activity-dependent regulation of adult neurogenesis, in which newborn neurons may sense neuronal network activity through tonic and phasic GABA activation.},
	Author = {Ge, Shaoyu and Goh, Eyleen L. K. and Sailor, Kurt A. and Kitabatake, Yasuji and Ming, Guo-li L. and Song, Hongjun},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {01 Adult neurogenesis general;04 Adult neurogenesis factors},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {7076},
	Organization = {Institute for Cell Engineering, Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.},
	Pages = {589-93},
	Pii = {nature04404},
	Pubmed = {16341203},
	Title = {GABA regulates synaptic integration of newly generated neurons in the adult brain},
	Uuid = {85E9564C-A32E-4FA1-AADE-1D7463C8EF8D},
	Volume = {439},
	Year = {2006},
	url = {papers/Ge_Nature2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature04404}}

@article{Gehrmann:1995,
	Abstract = {Microglia form a regularly spaced network of resident glial cells throughout the central nervous system (CNS). They are morphologically, immunophenotypically and functionally related to cells of the monocyte/macrophage lineage. In the ultimate vicinity of the blood-brain barrier two specialized subsets of macrophages/microglia can be distinguished: firstly, perivascular cells which are enclosed within the basal lamina and secondly juxtavascular microglia which make direct contact with the parenchymal side of the CNS vascular basal lamina but represent true intraparenchymal resident microglia. Bone marrow chimera experiments indicates that a high percentage of the perivascular cells undergoes replacement with bone marrow-derived cells. In contrast, juxtavascular microglia like other resident microglia form a highly stable pool of CNS cells with extremely little turnover with the bone marrow compartment. Both the perivascular cells and the juxtavascular microglia play an important role in initiating and maintaining CNS autoimmune injury due to their strategic localization at a site close to the blood-brain barrier, their rapid inducibility for MHC class II antigens and their potential scavenger role as phagocytic cells. The constantly replaced pool of perivascular cells probably represents an entry route by which HIV gets access to the brain. Microglia are the first cell type to respond to several types of CNS injury. Microglial activation involves a stereotypic pattern of cellular responses, such as proliferation, increased or de-novo expression of immunomolecules, recruitment to the site of injury and functional changes, e.g., the release of cytotoxic and/or inflammatory mediators. In addition, microglia have a strong antigen presenting function and a pronounced cytotoxic function. Microglial activation is a graded response, i.e., microglia only transform into intrinsic brain phagocytes under conditions of neuronal and or synaptic/terminal degeneration. In T-cell-mediated autoimmune injury of the nervous system, microglial activation follows these lines and occurs at an early stage of disease development. In experimental autoimmune encephalomyelitis (EAE), microglia proliferate vigorously, show a strong expression of MHC class I and II antigens, cell adhesion molecules, release of reactive oxygen intermediates and inflammatory cytokines and transform into phagocytic cells. Due to their pronounced antigen presenting function in vitro, activated microglia rather than astrocytes or endothelial cells are the candidates as intrinsic antigen presenting cel of the brain. In contrast to microglia, astrocytes react with a delay, appear to encase morphologically the inflammatory lesion and may be instrumental in downregulating the T-cell-mediated immune injury by inducing T-cell apoptosis.(ABSTRACT TRUNCATED AT 400 WORDS)},
	Author = {Gehrmann, J. and Matsumoto, Y. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0165-0173},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {Research Support, Non-U.S. Gov't;11 Glia;Microglia;review, tutorial;Brain;review},
	Medline = {96031752},
	Month = {3},
	Nlm_Id = {8908638},
	Number = {3},
	Organization = {Department of Pathology, University Hospital, Z{\"u}rich, Switzerland.},
	Pages = {269-87},
	Pii = {016501739400015H},
	Pubmed = {7550361},
	Title = {Microglia: intrinsic immuneffector cell of the brain},
	Uuid = {420EE321-E693-4444-8CB0-6F73D2EC7E2E},
	Volume = {20},
	Year = {1995}}

@article{Georges:2001,
	Abstract = {Genetically modified donor T cells with an inducible "suicide" gene have the potential to improve the safety and availability of allogeneic hematopoietic stem cell transplantation by enhancing engraftment and permitting control of graft-versus-host disease (GVHD). However, several clinical studies of gene-modified T cells have shown limited to no in vivo function of the ex vivo expanded T cells. Using the well-established dog model of allogeneic marrow transplantation, the question was asked if retrovirally transduced, donor derived, ex vivo expanded cytotoxic T lymphocytes (CTLs) that are recipient specific could enhance engraftment of dog leukocyte antigen (DLA)-haploidentical marrow following a single dose of 9.2 Gy total body irradiation and no postgrafting immunosuppression. In this setting, only 4 of 11 control recipients of DLA-haploidentical marrow without added CTLs engrafted. CTLs did not enhance engraftment of CD34(+) selected peripheral blood stem cells. However, recipient-specific CTLs enhanced engraftment of DLA-haploidentical marrow in 9 of 11 evaluable recipients (P =.049). All dogs that engrafted developed multiorgan GVHD. To facilitate in vivo tracking, 8 dogs received CTLs transduced with a retroviral vector encoding green fluorescent protein (GFP) and neomycin phosphotransferase (neo). Recipients that engrafted had sharp increases in the numbers of circulating GFP(+) CTLs on days +5 to +6 after transplantation. GFP(+) CTLs isolated from blood were capable of recipient-specific lysis. At necropsy, up to 7.1\%of CD3(+) cells in tissues were GFP(+) and polymerase chain reaction in situ hybridization for neo showed infiltration of transduced CTLs in GVHD-affected organs. These results show that ex vivo expanded, transduced T cells maintained in vivo function and enhanced marrow engraftment.},
	Author = {Georges, G. E. and Storb, R. and Bruno, B. and Brodie, S. J. and Thompson, J. D. and Taranova, A. G. and Zaucha, J. M. and Little, M. T. and Zellmer, E. and Moore, P. F. and Gooley, T. and Sale, G. and Kiem, H. P. and Sandmaier, B. M. and Lyons, R. M. and Nash, R. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Histocompatibility;Research Support, Non-U.S. Gov't;Animals;Cell Separation;Whole-Body Irradiation;Transfection;Bone Marrow Transplantation;Kanamycin Kinase;Retroviridae;Antigens, CD34;11 Glia;Green Fluorescent Proteins;Genetic Vectors;In Situ Hybridization;Haplotypes;Research Support, U.S. Gov't, P.H.S.;T-Lymphocytes, Cytotoxic;Transplantation, Homologous;Graft Rejection;Polymerase Chain Reaction;Graft vs Host Disease;Luminescent Proteins;Graft Survival;Gene Expression;Dogs;HLA Antigens},
	Medline = {21575734},
	Month = {12},
	Nlm_Id = {7603509},
	Number = {12},
	Organization = {Clinical Research Division, Fred Hutchinson Cancer Research Center, University of Washington, Seattle 98109, USA. ggeorges\@fhcrc.org},
	Pages = {3447-55},
	Pubmed = {11719387},
	Title = {Engraftment of DLA-haploidentical marrow with ex vivo expanded, retrovirally transduced cytotoxic T lymphocytes},
	Uuid = {895C165A-D9F9-47E7-BB3B-AF130D193B77},
	Volume = {98},
	Year = {2001}}

@article{German:2002,
	Abstract = {A mouse model of Niemann-Pick type C disease has been found that exhibits neuropathology similar to the human condition. There is an age-related neurodegeneration in several brain regions and a lack of myelin in the corpus callosum in these mice. The purpose of the present study was to examine the Niemann-Pick mouse and determine whether: (1) microglia and astrocytes exhibit ultrastructural pathology similar to that found in neurons; (2) nerve fiber number is reduced when the myelin sheath is absent; and (3) the lysosomal hydrolase, cathepsin-D, is involved in the neurodegenerative process. Using light and electron microscopic methods, and immunocytochemistry, Niemann-Pick and control animals were examined at several ages. Cathepsin-D content was semi-quantitatively measured in neurons and glial cells in brain regions known to exhibit neurodegeneration, as was the density of glial fibrillary acidic protein-labeled astrocytes. The Niemann-Pick mouse exhibited: (1) an age-related increase in inclusion bodies in microglia and astrocytes, similar to that observed within neurons; (2) an almost complete absence of myelin in the corpus callosum by 7-8 weeks of age, along with a 30\%reduction in the number of corpus callosum axons; (3) a mild age-related increase in cathepsin-D content within nerve cells in many brain regions. However, the cathepsin-D elevation was greatest in microglial cells; (4) an age-related increase in the number of microglial cells containing intense cathepsin-D immunoreactivity in both the thalamus and cerebellum. Both of these brain regions have been shown previously to exhibit an age-related loss of neurons; and (5) an increase in the number of reactive astrocytes immunostained for glial fibrillary acidic protein, especially in the thalamus and cerebellum.These data indicate that glial cells are a major target for pathology in the Niemann-Pick mouse. The lack of myelin within the corpus callosum may be related to the loss of nerve fibers in this structure. The increase in cathepsin-D-laden microglial cells, in brain regions previously shown to undergo neurodegeneration, is consistent with a role for microglia in the phagocytosis of dead neurons and in actively contributing to the neurodegenerative process. The activation of astrocytes in regions that undergo neurodegeneration is also consistent with a role for these glial cells in the neurodegenerative process.},
	Author = {German, D. C. and Liang, C-L L. and Song, T. and Yazdani, U. and Xie, C. and Dietschy, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Animals;Proteins;Brain;Microglia;Female;Cell Count;Cathepsin D;Nerve Fibers, Myelinated;Not relevant;Disease Models, Animal;Male;11 Glia;Mice, Neurologic Mutants;Support, Non-U.S. Gov't;Wallerian Degeneration;Cell Size;Neuroglia;Support, U.S. Gov't, P.H.S.;Inclusion Bodies;Mice;Niemann-Pick Diseases;Microscopy, Electron;Corpus Callosum;Immunohistochemistry},
	Medline = {21681898},
	Nlm_Id = {7605074},
	Number = {3},
	Organization = {Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390-9070, USA. dwight.german\@utsouthwestern.edu},
	Pages = {437-50},
	Pii = {S0306452201005176},
	Pubmed = {11823057},
	Title = {Neurodegeneration in the Niemann-Pick C mouse: glial involvement},
	Uuid = {8713B419-812C-40DF-B669-3EB2AAA65D9D},
	Volume = {109},
	Year = {2002}}

@article{Ghashghaei:2006,
	Abstract = {Coordinated regulation of neuronal progenitor differentiation in the subventricular zone (SVZ) is a fundamental feature of adult neurogenesis. However, the molecular control of this process remains mostly undeciphered. Here, we investigate the role of neuregulins (NRGs) in this process and show that a NRG receptor, ErbB4, is primarily expressed by polysialylated neural cell adhesion molecule immature neuroblasts but is also detected in a subset of GFAP(+) astroglial cells, ependymal cells, and Dlx2(+) precursors in the SVZ. Of the NRG ligands, both NRG1 and -2 are expressed by immature polysialylated neural cell adhesion molecule neuroblasts in the SVZ. NRG2 is also expressed by some of the GFAP(+) putative stem cells lining the ventricles. Infusion of exogenous NRG1 leads to rapid aggregation of Dlx2(+) cells in the SVZ and affects the initiation and maintenance of organized neuroblast migration from the SVZ toward the olfactory bulb. In contrast, the infusion of NRG2 increased the number of Sox2 and GFAP(+) precursors in the SVZ. An outcome of this NRG2 effect is an increase in the number of newly generated migrating neuroblasts in the rostral migratory stream and GABAergic interneurons in the olfactory bulb. The analysis of conditional null mice that lack NRG receptor, ErbB4, in the nervous system revealed that the observed activities of NRG2 require ErbB4 activation. These results indicate that different NRG ligands affect distinct populations of differentiating neural precursors in the neurogenic regions of the mature forebrain. Furthermore, these studies identify NRG2 as a factor capable of promoting SVZ proliferation, leading to the formation of new neurons in vivo.},
	Author = {Ghashghaei, H. T. and Weber, Janet and Pevny, Larysa and Schmid, Ralf and Schwab, Markus H. and Lloyd, K. C. Kent and Eisenstat, David D. and Lai, Cary and Anton, E. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {03 Adult neurogenesis progenitor source;04 Adult neurogenesis factors},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {6},
	Organization = {*University of North Carolina Neuroscience Center and the Department of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, NC 27599.},
	Pages = {1930-5},
	Pii = {0510410103},
	Pubmed = {16446434},
	Title = {The role of neuregulin-ErbB4 interactions on the proliferation and organization of cells in the subventricular zone},
	Uuid = {EC9D63C1-2ACB-4454-8500-E51901DD85D6},
	Volume = {103},
	Year = {2006},
	url = {papers/Ghashghaei_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0510410103}}

@article{Gheusi:2007,
	Abstract = {The mature brain needs to have flexible control over behavior in the face of ever-changing needs. It achieves this control through morphological and physiological changes at the level of molecules, spines, dendrites, and axons and through processes of adult neurogenesis, entire cells. The functional maturation of newly generated cells in the adult forebrain involves the expression of neurotransmitter receptors before synaptic activity and excitatory gamma-aminobutyric acid (GABAergic) influences prior to glutamatergic input. The production of new cells for incorporation into neural circuits that are already up and running gives rise to a unique situation that may require epigenetic regulation. However, once mature, new neurons must carve out a niche among more established cells to be useful. How do they survive and what are they used for? Recent studies have revealed that adult neurogenesis alters the olfactory bulb at all levels, from single cells to the network and system levels. It has also been suggested that cell turnover may be particularly beneficial for the processing of new information in dynamic networks. However, elucidating the functional meaning of adult neurogenesis must wait for the development of new paradigms to eliminate the pool of newly generated neurons but sparing the preexisting ones. Nevertheless, there is already considerable correlative evidence to indicate that adult neurogenesis is a plastic mechanism by which the performance of the brain can be optimized in a given environment.},
	Author = {Gheusi, and Lledo,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0379-864X},
	Journal = {Chem Senses},
	Keywords = {01 Adult neurogenesis general;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8217190},
	Organization = {Laboratory of Perception and Memory, Pasteur Institute, CNRS URA 2182, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France.},
	Pii = {bjm012},
	Pubmed = {17404148},
	Title = {Control of Early Events in Olfactory Processing by Adult Neurogenesis},
	Uuid = {59AE2ADC-C072-49E9-BCFD-1AB276302DF7},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/chemse/bjm012}}

@article{Gheusi:2000,
	Abstract = {In adult rodents, neurons are continually generated in the subventricular zone of the forebrain, from where they migrate tangentially toward the olfactory bulb, the only known target for these neuronal precursors. Within the main olfactory bulb, they ascend radially into the granule and periglomerular cell layers, where they differentiate mainly into local interneurons. The functional consequences of this permanent generation and integration of new neurons into existing circuits are unknown. To address this question, we used neural cell adhesion molecule-deficient mice that have documented deficits in the migration of olfactory-bulb neuron precursors, leading to about 40\%size reduction of this structure. Our anatomical study reveals that this reduction is restricted to the granule cell layer, a structure that contains exclusively gamma- aminobutyric acid (GABA)ergic interneurons. Furthermore, mutant mice were subjected to experiments designed to examine the behavioral consequences of such anatomical alteration. We found that the specific reduction in the newly generated interneuron population resulted in an impairment of discrimination between odors. In contrast, both the detection thresholds for odors and short-term olfactory memory were unaltered, demonstrating that a critical number of bulbar granule cells is crucial only for odor discrimination but not for general olfactory functions.},
	Author = {Gheusi, G. and Cremer, H. and McLean, H. and Chazal, G. and Vincent, J. D. and Lledo, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Olfactory Bulb/*cytology;Prosencephalon/metabolism;Memory, Short-Term;Neurons, Afferent/*metabolism;Animal;Mutation;02 Adult neurogenesis migration;Mice, Transgenic;Neural Cell Adhesion Molecules/*genetics;Smell/*genetics;Male;Support, Non-U.S. Gov't;Cell Division/genetics;B;Psychomotor Performance;Mice;Immunohistochemistry;Bromodeoxyuridine},
	Number = {4},
	Organization = {Centre National de la Recherche Scientifique, Institut Alfred Fessard, Avenue de la Terrasse, 91198 Gif-sur-Yvette Cedex, France.},
	Pages = {1823-8.},
	Title = {Importance of newly generated neurons in the adult olfactory bulb for odor discrimination},
	Uuid = {E9590325-910B-44B8-B651-3A700F64B38C},
	Volume = {97},
	Year = {2000},
	url = {../Data/Papers/text/dissertation/dissertation.pdf}}

@article{Ghoumari:2005,
	Abstract = {We have previously demonstrated that progesterone significantly increases the rate of myelination in organotypic slice cultures of 7-day-old rat and mouse cerebellum. Here, we show that progesterone (20muM) stimulates the proliferation of oligodendrocyte precursors in cultured cerebellar slices of 7-day-old rats. The steroid increased the number of pre-oligodendrocytes (NG2(+), O4(+)) and to some extent of oligodendrocyte precursors, corresponding to an earlier developmental stage (nestin(+), PDGFalphaR(+), NG2(+), O4(-)). Progesterone stimulated the proliferation of both NG2(+) and O4(+) cells as shown by increased double-immunolabeling with the cell proliferation marker Ki67. The mitogenic effect of progesterone was inhibited by the progesterone receptor antagonist mifepristone (10muM) and could not be mimicked by its GABA-active metabolite 3alpha,5alpha-tetrahydroprogesterone (allopregnanolone), even at the high concentration of 50muM. Results indicate that progesterone first strongly and transiently stimulates the proliferation of oligodendrocyte precursors, and that it may thereafter accelerate their maturation into myelinating oligodendrocytes. Although oligodendrocyte precursors may be a direct target for the actions of progesterone, their number may also be indirectly influenced by the effects of the steroid on neurons and microglial cells, since treatment of the cerebellar slices with progesterone enhanced staining of the neuronal cytoskeleton marker microtubule-associated protein-2 and increased the number of OX-42(+) microglia. A small percentage (about 0.1\%) of the NG2(+) cells transiently became OX-42(+) in response to progesterone. These results point to novel mechanisms by which progesterone may promote myelination in the CNS, specifically by stimulating the proliferation and maturation of oligodendrocyte precursors into myelinating oligodendrocytes.},
	Author = {Ghoumari, and Baulieu, and Schumacher,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {11 Glia},
	Month = {7},
	Nlm_Id = {7605074},
	Organization = {INSERM U488, Batiment Gregory Pincus, 80 rue du G{\'e}n{\'e}ral Leclerc, 94276 Bic\^{e}tre, France.},
	Pii = {S0306-4522(05)00551-8},
	Pubmed = {16054770},
	Title = {Progesterone increases oligodendroglial cell proliferation in rat cerebellar slice cultures},
	Uuid = {48A93EED-B2A2-4AC8-943F-57C001BD76FE},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2005.05.023}}

@article{Giannetti:2000,
	Abstract = {Microgyria was experimentally induced by focal freezing lesions of the frontal cortex in newborn rats. Adult microgyric animals received cortical injections of biotinylated dextran amine combined with NMDA, in order to obtain a Golgi-like retrograde labeling of cortico-cortical association neurons. Injections were performed either rostrally or caudally to the microgyric lesion. Results demonstrate that long-range association projections traveling across the zone of the microgyric lesion arise mainly from infragranular layers. In normal animals the same projections originate both from supragranular and infragranular layers. The analysis of single basal dendrites of layer 2/3 in microgyric animals demonstrates a simplified branching pattern, with a number of end points lower than in control animals. Potential implications for microgyria-associated epilepsy are discussed.},
	Author = {Giannetti, S. and Gaglini, P. and Di Rocco, F. and Di Rocco, C. and Granato, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0959-4965},
	Journal = {Neuroreport},
	Keywords = {Frontal Lobe;N-Methylaspartate;Disease Models, Animal;Research Support, Non-U.S. Gov't;Axonal Transport;Rats;Neural Pathways;Dextrans;Fluorescent Dyes;Rats, Wistar;Animals, Newborn;Biotin;Animals;Brain;24 Pubmed search results 2008;Cerebral Cortex;Neurons},
	Medline = {20378179},
	Month = {7},
	Nlm_Id = {9100935},
	Number = {10},
	Organization = {Institute of Anatomy, Catholic University Medical School, Rome, Italy.},
	Pages = {2185-9},
	Pubmed = {10923667},
	Title = {Organization of cortico-cortical associative projections in a rat model of microgyria},
	Uuid = {B7B58DA5-D81A-4E2E-AFAC-EC54B987F887},
	Volume = {11},
	Year = {2000}}

@article{Gianola:2002,
	Abstract = {Long-distance axon regeneration requires the activation of a specific set of neuronal growth-associated genes. Adult Purkinje cells fail to upregulate these molecules in response to axotomy and show extremely weak regenerative properties. Nevertheless, starting from several months after injury, transected Purkinje axons undergo spontaneous sprouting. Here, we asked whether long-term injured Purkinje cells acquire novel intrinsic growth properties that enable them to upregulate growth-associated genes and sustain axon regeneration. To test this hypothesis, we examined axon growth and cell body changes in adult rat Purkinje neurons following axotomy and implantation of embryonic neocortical tissue or Schwann cells into the injury track. Purkinje cells that survived over 6 months after injury/transplantation displayed profuse sprouting in the injured cerebellum and developed extensive networks of terminal branches into embryonic neocortical grafts. In addition, severed Purkinje axons exposed to these transplants 6 months after injury grew faster than their counterparts confronted with the same environment immediately after axotomy. Nevertheless, long-term injured Purkinje cells failed to regenerate stem neurites into Schwann cell grafts, and, under all experimental conditions, they did not upregulate growth-associated molecules, including c-Jun, GAP-43, SNAP-25, and NADPH-diaphorase. These results indicate that the long-term injured Purkinje cells remain unable to activate the gene program required to sustain axon regeneration and their plasticity is restricted to terminal arbor remodeling. We propose that the delayed growth of injured Purkinje cells reflects an adaptive phenomenon by which the severed axon stump develops a new terminal arbor searching for alternative connections with local partners.},
	Author = {Gianola, Sara and Rossi, Ferdinando},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {GAP-43 Protein;Purkinje Cells;Animals;Brain Tissue Transplantation;Rats;Neuronal Plasticity;Neocortex;Axons;Neurites;Rats, Wistar;RNA, Messenger;Fetal Tissue Transplantation;Nerve Regeneration;In Situ Hybridization;Schwann Cells;Time;Animals, Newborn;Axotomy;Cerebellum;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Biological Markers;Research Support, Non-U.S. Gov't},
	Medline = {22088426},
	Month = {7},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Neuroscience and Rita Levi Montalcini Center for Brain Repair, University of Turin, Turin, Italy.},
	Pages = {25-40},
	Pii = {S0014488602979240},
	Pubmed = {12093080},
	Title = {Long-term injured purkinje cells are competent for terminal arbor growth, but remain unable to sustain stem axon regeneration},
	Uuid = {2ED98C73-4B9A-415D-807F-FB9D783CD214},
	Volume = {176},
	Year = {2002}}

@article{Gibson:2003,
	Abstract = {Periventricular leukomalacia (PVL) is either a diffuse or cystic lesion of the periventricular white matter that leaves the overlying cortical grey matter largely intact. It is believed to result from hypoxia occurring pre- or perinatally and is a major cause of cerebral palsy. We have modelled PVL in rats comparing the effects of discrete injections of 3-nitropropionic acid (3-NP), a mitochondrial toxin, ibotenic acid (IBA), a glutamate analogue, or saline into the sub-cortical white matter on postnatal day 7 (P7). Following recovery times ranging from 3 days to 4 weeks, forebrain sections were Nissl stained or immunostained for Bax, cJun, calbindin (CB), parvalbumin (PV) or non-phosphorylated neurofilaments (NPNF). Compared to saline injections, ibotenic acid caused large lesions of both grey and white matter not characteristic of periventricular leukomalacia. 3-Nitropropionic acid injections caused small focal lesions restricted to the sub-cortical white matter. 3-Nitropropionic acid treatment initially increased expression of the apoptosis promoting proteins Bax and cJun, as well as non-phosphorylated neurofilaments in cortical layer V overlying the injection site. Non-phosphorylated neurofilament expression distal to the lesion was decreased representing a loss of cortical axons, but persisted and even increased with time within the cortex, demonstrating persistence of the parent cell bodies and local sprouting of neurites. There were significantly fewer calbindin and parvalbumin positive neurones in the motor cortex (MC) side ipsilateral to the 3-nitropropionic acid injection compared to the contralateral side. These persistent differences in expression of activity sensitive calcium binding proteins suggest alterations in local cortical circuitry without substantial loss of grey matter as is characteristic of periventricular leukomalacia. Changes in expression of Bax, cJun and non-phosphorylated neurofilaments during normal development are also described.},
	Author = {Gibson, Claire L. and Clowry, Gavin J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0736-5748},
	Journal = {Int J Dev Neurosci},
	Keywords = {Propionic Acids;Animals;Humans;Rats;Comparative Study;21 Epilepsy;Apoptosis;Nitro Compounds;Axons;Leukomalacia, Periventricular;Reference Values;Rats, Wistar;Disease Models, Animal;Ibotenic Acid;Motor Cortex;Animals, Newborn;21 Neurophysiology;Neurons;Infant, Newborn;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {22666659},
	Month = {6},
	Nlm_Id = {8401784},
	Number = {4},
	Organization = {Brain Development, Plasticity and Repair Group, School of Clinical Medical Sciences (Child Health), University of Newcastle upon Tyne, UK.},
	Pages = {171-82},
	Pii = {S0736574803000418},
	Pubmed = {12781784},
	Title = {The effect on motor cortical neuronal development of focal lesions to the sub-cortical white matter in the neonatal rat: a model for periventricular leukomalacia},
	Uuid = {5C551320-73C7-4670-92EA-057D1E575CD2},
	Volume = {21},
	Year = {2003}}

@article{Gifford:2003,
	Abstract = {The retroviral capacity for integration into the host genome can give rise to endogenous retroviruses (ERVs): retroviral sequences that are transmitted vertically as part of the host germ line, within which they may continue to replicate and evolve. ERVs represent both a unique archive of ancient viral sequence information and a dynamic component of host genomes. As such they hold great potential as informative markers for studies of both virus evolution and host genome evolution. Numerous novel ERVs have been described in recent years, particularly as genome sequencing projects have advanced. This review discusses the evolution of ERV lineages, considering the processes by which ERV distribution and diversity is generated. The diversity of ERVs isolated so far is summarised in terms of both their distribution across host taxa, and their relationships to recognised retroviral genera. Finally the relevance of ERVs to studies of genome evolution, host disease and viral ecology is considered, and recent findings discussed.},
	Author = {Gifford, Robert and Tristem, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0920-8569},
	Journal = {Virus Genes},
	Keywords = {15 ERVs retroelements;Endogenous Retroviruses;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Evolution, Molecular;15 Retrovirus mechanism;Variation (Genetics);Humans;Animals;Vertebrates;review},
	Medline = {22759165},
	Month = {5},
	Nlm_Id = {8803967},
	Number = {3},
	Organization = {Department of Biological Sciences, Imperial College, Silwood Park, Buckhurst Road, Ascot Berkshire, SL5 7PY, UK.},
	Pages = {291-315},
	Pii = {5127076},
	Pubmed = {12876457},
	Title = {The evolution, distribution and diversity of endogenous retroviruses},
	Uuid = {28AD1074-EF57-4816-8C33-AD09D5CD10BB},
	Volume = {26},
	Year = {2003}}

@article{Gilmore:2001,
	Abstract = {The adult mammalian cerebral cortex arises from a complex series of neuronal migrations. The primitive layer known as the preplate is split into an outer marginal zone and an inner subplate by invading cortical plate neurons in an "inside-out"pattern of layering with respect to time of neuronal origin. In cyclin-dependent kinase 5 (Cdk5)-deficient mice (cdk5(-/-)), the earliest born cortical neurons split the preplate, but later born neurons arrest below the subplate, resulting in an ectopic "outside-in"layer of neurons normally destined for layers II-V. We have pursued this analysis in cdk5(-/-) <-->wild-type chimeric mice coupled with experiments in cell culture. In vitro migration assays show no difference in migrational ability between embryonic cdk5(-/-) and wild-type neurons. In cdk5(-/-) chimeras, layers I and VI are made up of both mutant and wild-type genotype neurons, whereas layers II-V contain predominantly wild-type cells. In addition, a thin layer of neurons is found below layer VI, made up of cdk5(-/-) cells; bromodeoxyuridine labeling suggests that these neurons were destined for layers II-V. Scattered cdk5(-/-) cells are found throughout layers II-V, but these neurons are always found to be GABAergic. The findings suggest that Cdk5 is not required for migration of either the deepest cortical plate neurons or the GABAergic neurons from the ganglionic eminences. The migration of layer II-V pyramidal neurons, however, is intrinsically blocked by Cdk5 deficiency, thus suggesting that different neuronal cell types use distinct mechanisms of migration. 1529-2401 Journal Article},
	Author = {Gilmore, E. C. and Herrup, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurosci},
	Keywords = {Neocortex/cytology/*embryology/metabolism;Animals;Cyclin-Dependent Kinases/deficiency/genetics/*metabolism;Neurons/cytology/*metabolism;Cells, Cultured;Chimera;Cell Movement/*physiology;Female;Stem Cells/cytology;Cell Count;gamma-Aminobutyric Acid/*metabolism;Interneurons/cytology/metabolism;Mice, Inbred C57BL;Male;H abstr;Support, U.S. Gov't, P.H.S.;Purkinje Cells/cytology;Mice;Immunohistochemistry;Bromodeoxyuridine;12 Interneuron development},
	Number = {24},
	Organization = {Department of Neurosciences, School of Medicine, Case Western Reserve University, and Alzheimer Research Laboratory, University Hospitals of Cleveland, Cleveland, Ohio 44106.},
	Pages = {9690-700},
	Pubmed = {11739578},
	Title = {Neocortical cell migration: GABAergic neurons and cells in layers I and VI move in a cyclin-dependent kinase 5-independent manner},
	Uuid = {299F7385-C835-4C65-B6AF-6D6A72E372D4},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11739578}}

@article{Gimsa:2000,
	Abstract = {Neuroinflammation in the course of multiple sclerosis and experimental autoimmune encephalomyelitis results in demyelination and, recently demonstrated, axonal loss. Invading neuroantigen specific T cells are the crucial cellular elements in these processes. Here we demonstrate that invasion of activated T cells induces a massive microglial attack on myelinated axons in entorhinal-hippocampal slice cultures. Flow cytometry analysis of activation markers revealed that the activation state of invading MBP-specific T cells was significantly lower in comparison to PMA-activated T cells. Moreover, MBP-specific T cells showed a significantly lower secretion of IFN-gamma. Conversely, MBP-specific T cells displayed a significantly higher potential to trigger activation of microglial cells, i.e. upregulation of MHC class II and ICAM-1 expression, and, most importantly, microglial phagocytosis of pre-traced axons. Our data suggest that this was mediated via specific cellular interactions of T cells and microglial cells since IFN-gamma alone was not sufficient to induce axonal damage while such damage was apparent in response to TNF-alpha which is released by activated microglial cells. TNF-alpha secretion by both T cell populations was negligible. Thus, MBP-specific T cells which invade nervous tissue in the course of neuroinflammation are more effective in axon-damaging recruiting microglial cells than activated T cells of other specificities.},
	Author = {Gimsa, U. and Peter, S. V. and Lehmann, K. and Bechmann, I. and Nitsch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {1015-6305},
	Journal = {Brain Pathol},
	Keywords = {Cell Survival;T-Lymphocytes;Tumor Necrosis Factor;Animals;Phagocytosis;Research Support, Non-U.S. Gov't;Intercellular Adhesion Molecule-1;Tumor Necrosis Factor-alpha;Microglia;Interferon Type II;Entorhinal Cortex;Lymphocyte Activation;Hippocampus;Axons;Not relevant;11 Glia;Organ Culture Techniques;Support, Non-U.S. Gov't;Mice, Inbred Strains;Neurons;Mice;Organ Culture;Histocompatibility Antigens Class II;Cytokines},
	Medline = {20340164},
	Month = {7},
	Nlm_Id = {9216781},
	Number = {3},
	Organization = {Department of Cell and Neurobiology, Institute of Anatomy, Humboldt-University Clinic Charit{\'e}, Berlin, Germany. ulrike.gimsa\@charite.de},
	Pages = {365-77},
	Pubmed = {10885655},
	Title = {Axonal damage induced by invading T cells in organotypic central nervous system tissue in vitro: involvement of microglial cells},
	Uuid = {8DFF539F-01EC-4EA8-BDA8-BAA20ADFBB21},
	Volume = {10},
	Year = {2000}}

@article{Giordana:1994,
	Abstract = {The non-astrocytic cells which proliferate in the rat brain after the induction of an area of necrosis have been characterized and counted by means of combined in vivo bromodeoxyuridine (BrdU) administration and immunohistochemical demonstration of glial fibrillary acid protein (GFAP), vimentin, Ricinus communis agglutinin 120 (RCA-1), Griffonia simplicifolia B4 isolectin (GSI-B4), keratan sulphate (KS), carbonic anhydrase C (CA.C), transferrin (TF) and ferritin. Two days after the injury, 7.5\%of the proliferating cells were GFAP-positive reactive astrocytes, 5.7\%were RCA-1-positive cells and 17.4\%were GSI-B4-positive cells. Lectin-binding cells had the microscopic and ultrastructural aspects of microglia; they proliferated around the needle track and in the corpus callosum. Microglia represented a large fraction of the proliferating cells. Evidence is presented for the origin of at least a proportion of perilesional astrocytes and microglia from the periventricular matrix, and of microglia from blood precursors. Other non-proliferating microglia cells transiently appeared in the normal brain around the wound, in agreement with the existence of two different microglia cell populations reacting with different modalities to an area of necrosis.},
	Author = {Giordana, M. T. and Attanasio, A. and Cavalla, P. and Migheli, A. and Vigliani, M. C. and Schiffer, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Rats, Inbred F344;Rats;Antibodies, Monoclonal;Astrocytes;Immunohistochemistry;Cell Division;Not relevant;11 Glia;Microglia;Microscopy, Immunoelectron;Animals;Bromodeoxyuridine;Brain Injuries},
	Medline = {94352525},
	Month = {4},
	Nlm_Id = {7609829},
	Number = {2},
	Organization = {Second Department of Neurology, University of Turin, Italy.},
	Pages = {163-74},
	Pubmed = {8072646},
	Title = {Reactive cell proliferation and microglia following injury to the rat brain},
	Uuid = {973E4AA5-F58E-47EE-8804-FA2DE30FAAB2},
	Volume = {20},
	Year = {1994}}

@article{Giulian:1986,
	Abstract = {Ameboid microglia are isolated from the cerebral tissue of neonatal rat by selective cell adhesion to plastic. Histochemical markers show that the microglial preparations are homogeneous (95 +/- 3\%) and represent a 10\%yield from starting cultures. Isolated ameboid microglia contain nonspecific esterase activity, the macrophage surface antigens MAC-1 and MAC-3, and acetylated low-density lipoprotein receptors. Ameboid cells have functional properties similar to those of macrophages, including the ability to engulf 5 micron latex beads, to secrete Interleukin-1 (IL-1) and to release superoxide anion. Unlike monocytes and adherent spleen cells, ameboid microglia do not show peroxidase activity by histochemical stain. Unlike resident peritoneal macrophages, ameboid microglia proliferate in vitro. Scanning electron microscopy shows that ameboid cells have short, spinous processes that can be distinguished from the ruffled surfaces of body macrophages. Our observations suggest that ameboid microglia are a distinct class of mononuclear phagocytic cells. Retinoic acid and dimethyl sulfoxide, agents known to accelerate differentiation in vitro, stimulate ameboid cells to develop thin processes several hundred microns in length. These "process-bearing" microglia eventually lose the capacity to engulf latex beads and to proliferate. They also show reductions in nonspecific esterase activity and in the binding of acetylated low-density lipoprotein. We suggest that in vitro ameboid microglia differentiate into nonphagocytic cells similar to ramified microglia found in normal adult brain. The isolation techniques described here provide the opportunity to study the composition and function of different microglial subpopulations during the development of the CNS.},
	Author = {Giulian, D. and Baker, T. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Microscopy, Phase-Contrast;Microscopy, Electron, Scanning;Animals;Cell Separation;Macrophages;Rats;Brain;Oligodendroglia;Esterases;Superoxides;Not relevant;11 Glia;Animals, Newborn;Histocytochemistry;Support, Non-U.S. Gov't;Neuroglia;Interleukin-1;Support, U.S. Gov't, P.H.S.;Spleen},
	Medline = {86307003},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {8},
	Pages = {2163-78},
	Pubmed = {3018187},
	Title = {Characterization of ameboid microglia isolated from developing mammalian brain},
	Uuid = {3B91C779-CB93-4B92-93FE-9FDE8AF1B7F1},
	Volume = {6},
	Year = {1986},
	url = {papers/Giulian_JNeurosci1986.pdf}}

@article{Giulian:1989,
	Abstract = {We monitor cellular responses to a penetrating wound in the cerebral cortex of adult rat during the first weeks after injury. Two classes of activated mononuclear phagocytes containing acetylated low-density lipoprotein (ac-LDL) receptors appear within hours at the wound site. One type of cell surrounding the lesion edge had thin, delicate processes and is identical in appearance to ramified microglia found in developing brain. Within the lesion, round cells are recognized as blood-borne macrophages when labeled by intravenous injection of carbon particles. Thus, both process-bearing reactive microglia and invading macrophages respond to brain trauma. The greatest number of ac-LDL(+) or nonspecific esterase(+) mononuclear phagocytes appears 2 days after injury within the wound site and are associated with a peak production of the cytokine interleukin-1 (IL-1). Because intracerebral infusion of IL-1 is known to stimulate astrogliosis and neovascularization (Giulian et al., 1988), we examine the time course of injury-induced reactive astrogliosis and angiogenesis. A 5-fold increase in the number of reactive astroglia is found at 3 d and a marked neovascularization at 5 d after injury. During the first week, mononuclear phagocytes engulf particles and clear them from the wound site either by migrating to the brain surface or by entering newly formed brain vasculature. To investigate further the role of reactive brain mononuclear phagocytes in CNS injury, we use drugs to inhibit trauma-induced inflammation. When applied in vivo, chloroquine or colchicine reduce the number of mononuclear phagocytes in damaged brain, help to block reactive astrogliosis and neovascularization, and slow the rate of debris clearance from sites of traumatic injury. In contrast, the glucocorticoid dexamethasone neither reduces the number of brain inflammatory cells nor hampers such responses as phagocytosis, astrogliosis, neovascularization, or debris clearance in vivo. Our observations show that mononuclear phagocytes play a major role in wound healing after CNS trauma with some events controlled by secretion of cytokines. Moreover, certain classes of immunosuppressive drugs may be useful in the treatment of acute brain injury.},
	Author = {Giulian, D. and Chen, J. and Ingeman, J. E. and George, J. K. and Noponen, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Wound Healing;Astrocytes;Animals;Encephalitis;Rats;Colchicine;Rats, Inbred Strains;Wounds, Penetrating;11 Glia;Phagocytes;Chloroquine;Microspheres;Research Support, U.S. Gov't, P.H.S.;Neovascularization, Pathologic;Brain Injuries;Cerebral Cortex;Gliosis;Dexamethasone},
	Medline = {90079552},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Department of Neurology, Baylor College of Medicine, Houston, Texas 77031.},
	Pages = {4416-29},
	Pubmed = {2480402},
	Title = {The role of mononuclear phagocytes in wound healing after traumatic injury to adult mammalian brain},
	Uuid = {614F2A40-6849-4A86-8987-A7E1F726A4C7},
	Volume = {9},
	Year = {1989}}

@article{Givogri:2006,
	Abstract = {The postnatal subventricular zone (SVZ) is a niche for continuous neurogenesis in the adult brain and likely plays a fundamental role in self-repair responses in neurodegenerative conditions. Maintenance of the pool of neural stem cells within this area depends on cell-cell communication such as that provided by the Notch signaling pathway. Notch1 receptor mRNA has been found distributed in different areas of the postnatal brain including the SVZ. Although the identity of Notch1-expressing cells has been established in the majority of these areas, it is still unclear what cell types within the SVZ are expressing components of this pathway. Here we demonstrate that most of expression of Notch1 in the adult SVZ occurs in polysialylated neural cell adhesion molecule (PSA-NCAM)-positive neural precursors and in glial fibrillary acidic protein-positive SVZ astrocytes. Notch1 was also found in PSA-NCAM-positive neuroblasts located within the rostral migratory stream (RMS) but much less in those that have reached the olfactory bulb. We show that two of the naturally occurring Notch1 activators, Jagged1 and Delta1, are also expressed in the SVZ and within the RMS in the adult mouse brain. Finally, using a model of cortical stab wound, we show that the astrogliogenic response of the SVZ to injury is accompanied by activation of the Notch pathway.},
	Author = {Givogri, Maria I. and de Planell, Maria and Galbiati, Francesca and Superchi, Daniela and Gritti, Angela and Vescovi, Angelo and de Vellis, Jean and Bongarzone, Ernesto R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Nlm_Id = {7809375},
	Number = {1-2},
	Organization = {Laboratory for Gene Therapy of Neurodegenerative Disorders, San Raffaele Telethon Institute for Gene Therapy, Milan, Italy. givogri.maria\@hsr.it},
	Pages = {81-91},
	Pii = {DNE20060281_2081},
	Pubmed = {16508306},
	Title = {Notch signaling in astrocytes and neuroblasts of the adult subventricular zone in health and after cortical injury},
	Uuid = {73022267-5C23-4F7E-A3E8-1932ADAEE50A},
	Volume = {28},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000090755}}

@article{Gleeson:1998,
	Abstract = {X-linked lissencephaly and "double cortex" are allelic human disorders mapping to Xq22.3-Xq23 associated with arrest of migrating cerebral cortical neurons. We identified a novel 10 kb brain-specific cDNA interrupted by a balanced translocation in an XLIS patient that encodes a novel 40 kDa predicted protein named Doublecortin. Four double cortex/X-linked lissencephaly families and three sporadic double cortex patients show independent doublecortin mutations, at least one of them a de novo mutation. Doublecortin contains a consensus Abl phosphorylation site and other sites of potential phosphorylation. Although Doublecortin does not contain a kinase domain, it is homologous to the amino terminus of a predicted kinase protein, indicating a likely role in signal transduction. Doublecortin, along with the newly characterized mDab1, may define an Abl-dependent pathway regulating neuronal migration.},
	Author = {Gleeson, J. G. and Allen, K. M. and Fox, J. W. and Lamperti, E. D. and Berkovic, S. and Scheffer, I. and Cooper, E. C. and Dobyns, W. B. and Minnerath, S. R. and Ross, M. E. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Microtubule-Associated Proteins;Signal Transduction;10 Development;Chromosome Fragility;Syndrome;Base Sequence;Sequence Homology, Amino Acid;Humans;Proteins;Brain;Epilepsy;Mutation;Protein-Serine-Threonine Kinases;Genes;Translocation, Genetic;Neuropeptides;Research Support, U.S. Gov't, P.H.S.;X Chromosome;Cerebral Cortex;Sex Chromosome Aberrations;Family Health;DNA, Complementary;Chromosome Mapping;Molecular Sequence Data;Amino Acid Sequence;Research Support, Non-U.S. Gov't},
	Medline = {98149344},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA.},
	Pages = {63-72},
	Pubmed = {9489700},
	Title = {Doublecortin, a brain-specific gene mutated in human X-linked lissencephaly and double cortex syndrome, encodes a putative signaling protein},
	Uuid = {CB455028-6D11-11DA-A4FE-000D9346EC2A},
	Volume = {92},
	Year = {1998},
	url = {papers/Gleeson_Cell1998.pdf}}

@article{Gleeson:1999,
	Abstract = {Doublecortin (DCX) is required for normal migration of neurons into the cerebral cortex, since mutations in the human gene cause a disruption of cortical neuronal migration. To date, little is known about the distribution of DCX protein or its function. Here, we demonstrate that DCX is expressed in migrating neurons throughout the central and peripheral nervous system during embryonic and postnatal development. DCX protein localization overlaps with microtubules in cultured primary cortical neurons, and this overlapping expression is disrupted by microtubule depolymerization. DCX coassembles with brain microtubules, and recombinant DCX stimulates the polymerization of purified tubulin. Finally, overexpression of DCX in heterologous cells leads to a dramatic microtubule phenotype that is resistant to depolymerization. Therefore, DCX likely directs neuronal migration by regulating the organization and stability of microtubules.},
	Author = {Gleeson, J. G. and Lin, P. T. and Flanagan, L. A. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Microtubule-Associated Proteins;Purkinje Cells;Rats, Long-Evans;Animals;Cells, Cultured;Rats;Humans;Phosphoproteins;Tubulin;Mitosis;Colchicine;Cell Movement;RNA, Messenger;Neuropeptides;Microtubules;In Situ Hybridization;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Cerebral Cortex;Neurons;Blotting, Western;Mice;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {99325520},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA.},
	Pages = {257-71},
	Pii = {S0896-6273(00)80778-3},
	Pubmed = {10399933},
	Title = {Doublecortin is a microtubule-associated protein and is expressed widely by migrating neurons},
	Uuid = {AD8AFBA3-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {23},
	Year = {1999},
	url = {papers/Gleeson_Neuron1999.pdf}}

@article{Gleeson:2007,
	Abstract = {Conductance-based neuronal network models can help us understand how synaptic and cellular mechanisms underlie brain function. However, these complex models are difficult to develop and are inaccessible to most neuroscientists. Moreover, even the most biologically realistic network models disregard many 3D anatomical features of the brain. Here, we describe a new software application, neuroConstruct, that facilitates the creation, visualization, and analysis of networks of multicompartmental neurons in 3D space. A graphical user interface allows model generation and modification without programming. Models within neuroConstruct are based on new simulator-independent NeuroML standards, allowing automatic generation of code for NEURON or GENESIS simulators. neuroConstruct was tested by reproducing published models and its simulator independence verified by comparing the same model on two simulators. We show how more anatomically realistic network models can be created and their properties compared with experimental measurements by extending a published 1D cerebellar granule cell layer model to 3D.},
	Author = {Gleeson, Padraig and Steuber, Volker and Silver, R. Angus},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {24 Pubmed search results 2008;23 Technique},
	Month = {4},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Department of Physiology, University College London, Gower Street, London WC1E 6BT, United Kingdom.},
	Pages = {219-35},
	Pii = {S0896-6273(07)00248-6},
	Pubmed = {17442244},
	Title = {neuroConstruct: A Tool for Modeling Networks of Neurons in 3D Space},
	Uuid = {B7854664-01C2-45F7-8A4E-B4B465AFA5DA},
	Volume = {54},
	Year = {2007},
	url = {papers/Gleeson_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.03.025}}

@article{Glezer:2006,
	Abstract = {Regarded as a damaging reaction, innate immune response can either improve or worsen brain outcome after injury. Hence, inflammatory molecules might modulate cell susceptibility or healing events. The remyelination that follows brain lesions is dependent on the recruitment of oligodendrocyte progenitor cells (OPCs) and expression of genes controlling differentiation and myelin production, such as Olig1 and Olig2 bHLH transcription factors. We aimed to determine how innate immunity affects these processes. Here we report that lipopolysaccharide (LPS) infusion triggered OPC reactivity. Acute inflammation changed the distribution of Olig1- and Olig2-expressing cells following chemical demyelination, enhanced reappearance of transcription signals linked to remyelination and rapidly cleared myelin debris. Although cells expressing Olig1, Olig2, and proteolipid protein were attracted to demyelinated sites in the course of chronic inflammation, myelin loss was not associated with the effects of inflammation on OPC reactivity. In addition, the beneficial properties of brain immunity are broadened to an aggressive model of injury, wherein LPS through Toll-like receptor 4 (TLR4) reduced surfactant-mediated damage while anti-inflammatory treatment enlarged the lesion. In conclusion, TLR4 activation in microglia is a powerful mechanism for improving repair at the remyelination level and protecting the cerebral tissue in presence of agents with strong cytolytic properties.},
	Author = {Glezer, and Lapointe, and Rivest,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {8804484},
	Pii = {05-5234fje},
	Pubmed = {16464958},
	Title = {Innate immunity triggers oligodendrocyte progenitor reactivity and confines damages to brain injuries},
	Uuid = {856C4583-1B47-449C-AA17-DA97384D0B73},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.05-5234fje}}

@article{Goergen:2002,
	Abstract = {The life-long addition of new neurons has been documented in many regions of the vertebrate and invertebrate brain, including the hippocampus of mammals (Altman and Das, 1965; Eriksson et al., 1998; Jacobs et al., 2000), song control nuclei of birds (Alvarez-Buylla et al., 1990), and olfactory pathway of rodents (Lois and Alvarez-Buylla, 1994), insects (Cayre et al., 1996) and crustaceans (Harzsch and Dawirs, 1996; Sandeman et al., 1998; Harzsch et al., 1999; Schmidt, 2001). The possibility of persistent neurogenesis in the neocortex of primates is also being widely discussed (Gould et al., 1999; Kornack and Rakic, 2001). In these systems, an effort is underway to understand the regulatory mechanisms that control the timing and rate of neurogenesis. Hormonal cycles (Rasika et al., 1994; Harrison et al., 2001), serotonin (Gould, 1999; Brezun and Daszuta, 2000; Beltz et al., 2001), physical activity (Van Praag et al., 1999) and living conditions (Kemperman and Gage, 1999; Sandeman and Sandeman, 2000) influence the rate of neuronal proliferation and survival in a variety of organisms, suggesting that mechanisms controlling life-long neurogenesis are conserved across a range of vertebrate and invertebrate species. The present article extends these findings by demonstrating circadian control of neurogenesis. Data show a diurnal rhythm of neurogenesis among the olfactory projection neurons in the crustacean brain, with peak proliferation during the hours surrounding dusk, the most active period for lobsters. These data raise the possibility that light-controlled rhythms are a primary regulator of neuronal proliferation, and that previously-demonstrated hormonal and activity-driven influences over neurogenesis may be secondary events in a complex circadian control pathway. 0022-3034 Journal Article},
	Author = {Goergen, E. M. and Bagay, L. A. and Rehm, K. and Benton, J. L. and Beltz, B. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurobiol},
	Keywords = {F abstr;10 Development;Brain/*physiology;Neuronal Plasticity;Cell Division;Cell Count;Circadian Rhythm/*physiology;Support, U.S. Gov't, Non-P.H.S.;Nephropidae/*physiology;Neurons/physiology;Support, Non-U.S. Gov't;Animals;Feeding Behavior/physiology;Morphogenesis/physiology},
	Number = {1},
	Organization = {Department of Biological Sciences, Wellesley College, Wellesley, Massacusetts 02481, USA.},
	Pages = {90-5},
	Pubmed = {12360586},
	Title = {Circadian control of neurogenesis},
	Uuid = {6DFCC4CE-CCDC-11D9-8C77-000D9346EC2A},
	Volume = {53},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12360586}}

@article{Goerner:2001,
	Abstract = {Previous studies have shown that the choice of envelope protein (pseudotype) can have a significant effect on the efficiency of retroviral gene transfer into hematopoietic stem cells. This study used a competitive repopulation assay in the dog model to evaluate oncoretroviral vectors carrying the envelope protein of the endogenous feline virus, RD114. CD34-enriched marrow cells were divided into equal aliquots and transduced with vectors produced by the RD114-pseudotype packaging cells FLYRD (LgGLSN and LNX) or by the gibbon ape leukemia virus (GALV)-pseudotype packaging cells PG13 (LNY). A total of 5 dogs were studied. One dog died because of infection before sustained engraftment could be achieved, and monitoring was discontinued after 9 months in another animal that had very low overall gene-marking levels. The 3 remaining animals are alive with follow-ups at 11, 22, and 23 months. Analyses of gene marking frequencies in peripheral blood and marrow by polymerase chain reaction revealed no significant differences between the RD114 and GALV-pseudotype vectors. The LgGLSN vector also contained the enhanced green fluorescent protein (GFP), enabling us to monitor proviral expression by flow cytometry. Up to 10\%of peripheral blood cells expressed GFP shortly after transplantation and approximately 6\%after the longest follow-up of 23 months. Flow cytometric analysis of hematopoietic subpopulations showed that most of the GFP-expressing cells were granulocytes, although GFP-positive lymphocytes and monocytes were also detected. In summary, these results show that RD114-pseudotype oncoretroviral vectors are able to transduce hematopoietic long-term repopulating cells and, thus, may be useful for human stem cell gene therapy.},
	Author = {Goerner, M. and Horn, P. A. and Peterson, L. and Kurre, P. and Storb, R. and Rasko, J. E. and Kiem, H. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Transduction, Genetic;Follow-Up Studies;Animals;Blood Cells;Bone Marrow Transplantation;Comparative Study;Endogenous Retroviruses;Antigens, CD34;Retroviridae Proteins;11 Glia;Green Fluorescent Proteins;Genetic Vectors;Bone Marrow Cells;Hematopoiesis;Leukemia Virus, Gibbon Ape;Survival Rate;Cell Lineage;Amino Acid Transport System ASC;Research Support, U.S. Gov't, P.H.S.;Receptors, Virus;Luminescent Proteins;Graft Survival;Cats;Dogs;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {21452787},
	Month = {10},
	Nlm_Id = {7603509},
	Number = {7},
	Organization = {Divisions of Clinical Research and Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA.},
	Pages = {2065-70},
	Pubmed = {11567991},
	Title = {Sustained multilineage gene persistence and expression in dogs transplanted with CD34(+) marrow cells transduced by RD114-pseudotype oncoretrovirus vectors},
	Uuid = {6A2C0978-748A-4762-99BA-FA62503D8398},
	Volume = {98},
	Year = {2001}}

@article{Gofflot:2007,
	Abstract = {Nuclear receptors (NRs) compose a large family of transcription factors that operate at the interface between genes and environment, acting as sensors and effectors that translate endocrine and metabolic cues into well-defined gene expression programs. We report here on a systematic quantitative and anatomical expression atlas of the 49 NR genes in 104 regions of the adult mouse brain, organized in the interactive MousePat database. MousePat defines NR expression patterns to cellular resolution, a requirement for functional genomic strategies to understand the function of a highly heterogeneous and complex organ such as the brain. Using MousePat data, NR expression patterns can be clustered into anatomical and regulatory networks that delineate the role of NRs in brain functions, like the control of feeding and learning/memory. Mining the MousePat resource will improve the understanding of NR function in the brain and elucidate hierarchical networks that control behavior and whole body homeostasis.},
	Author = {Gofflot, Fran\c{c}oise and Chartoire, Nathalie and Vasseur, Laurent and Heikkinen, Sami and Dembele, Doulaye and Le Merrer, Julie and Auwerx, Johan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {In Situ Hybridization;24 Pubmed search results 2008;10 Development;Databases, Nucleic Acid;Hypothalamus;Hippocampus;Receptors, Cytoplasmic and Nuclear;Reverse Transcriptase Polymerase Chain Reaction;Mice, Inbred C57BL;Gene Expression Profiling;Learning;Animals;Male;Mice;Feeding Behavior;Transcription Factors},
	Month = {10},
	Nlm_Id = {0413066},
	Number = {2},
	Organization = {Institut Clinique de la Souris, 67404 Illkirch, France.},
	Pages = {405-18},
	Pii = {S0092-8674(07)01196-8},
	Pubmed = {17956739},
	Title = {Systematic gene expression mapping clusters nuclear receptors according to their function in the brain},
	Uuid = {DA8601FE-031D-4023-9A95-E407D997D428},
	Volume = {131},
	Year = {2007},
	url = {papers/Gofflot_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2007.09.012}}

@article{Gohlke:2004,
	Abstract = {We are quantitatively evaluating the acquisition of neocortical neurons through key stages of development including neurogenesis, migration, and synaptogenesis. Here we expand upon a previous computational model describing neocortical neurogenesis in the rat and mouse [Dev. Neurosci. 24 (2002) 467], to include the period of synaptogenesis (P0-P14) when programmed cell death (PCD) is known to play a major role in shaping the neocortex. We also quantitatively evaluate differing hypotheses on the role of cell death during neurogenesis. This new model construct allows prediction of acquisition of adult neuronal number in the rat and mouse neocortex from the beginning of neurogenesis through synaptogenesis. The mathematical model output is validated by independently derived stereologically determined neuron number estimates in the adult rat and mouse. Simulations suggest cell death during synaptogenesis reduces the neocortical neuronal population by 20-30\%, while cell death of progenitor cells and newly formed neurons during neurogenesis may reduce output by as much as 24\%. However, higher death rates during neurogenesis as suggested by some research would deplete the progenitor population, not allowing for the vast expansion that is the hallmark of the mammalian neocortex. Furthermore, our simulations suggest the clearance time of dying neurons labeled by TUNEL or pyknosis is relatively short, between 1 and 4 h, corroborating experimental research. This novel mathematical model for adult neocortical neuronal acquisition allows for in silico analysis of normal and perturbed states of neocortical development as well as interspecies and evolutionary analyses of neocortical development. 0165-3806 Journal Article},
	Author = {Gohlke, J. M. and Griffith, W. C. and Faustman, E. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {F, EE pdf;08 Aberrant cell cycle},
	Number = {1-2},
	Organization = {Center for Child Environmental Health Risks Research, Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98105-6099, USA.},
	Pages = {43-54},
	Title = {The role of cell death during neocortical neurogenesis and synaptogenesis: implications from a computational model for the rat and mouse},
	Uuid = {EA1D2407-C723-44FF-9845-50AA6D4BEB49},
	Volume = {151},
	Year = {2004},
	url = {papers/Gohlke_BrainResDevBrainRes2004.pdf}}

@article{Goings:2004,
	Abstract = {The subventricular zone (SVZ) generates the largest number of migratory cells in the adult brain. SVZ neuroblasts migrate to the olfactory bulbs (OB) in the adult, whereas during development, SVZ cells migrate into many adjacent nuclei. Previously, we showed that cerebral cortex injury in the adult causes molecular and cellular changes which may recapitulate the developmental migratory directions. Consistent with this, growth factors, as well as models of illness or injury can cause adult SVZ cells to migrate into non-olfactory bulb nuclei. Here, we tested the hypothesis that cerebral cortex injury in the adult mouse induces changes in migration, by labeling adult SVZ cells with a retroviral vector and examining the distribution of cells 4 days and 3 weeks later. Four days after cortical lesions, disproportionately fewer retrovirally-labeled cells had migrated to the olfactory bulb in lesioned mice than in controls. Conversely, the number of cells found in non-olfactory bulb regions (primarily the area of the lesion and the corpus callosum) was increased in lesioned mice. The morphology of these emigrated cells suggested that they were differentiating into glial cells. Three weeks after cortical injury, the majority of retrovirally-labeled cells in both groups of mice had migrated into the granule and periglomerular layers of the olfactory bulb. At 3 weeks, we still observed retrovirally-labeled glial cells in the corpus callosum and in the area of the injury in lesioned mice. These results suggest that cortical lesions cause a transient change in migration patterns of SVZ progeny, which is characterized by decreases in migration to the olfactory bulb but increased migration towards the injury. Our studies also suggest that cortical lesions induce the production of new glial cells which survive for at least 3 weeks after injury. The data support the concept that in the adult, SVZ cells can generate progeny that migrate towards injured areas and thus potentially be harnessed for neural repair. 0006-8993 Journal Article},
	Author = {Goings, G. E. and Sahni, V. and Szele, F. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Brain Res},
	Keywords = {06 Adult neurogenesis injury induced;D pdf},
	Number = {2},
	Organization = {CMIER Neurobiology Program, Department of Pediatrics, 2300 Children's Plaza, No. 209, Children's Memorial Hospital, Feinberg School of Medicine, Northwestern University, 60614-3394, Chicago, IL, USA},
	Pages = {213-26},
	Title = {Migration patterns of subventricular zone cells in adult mice change after cerebral cortex injury},
	Uuid = {187A79A0-DCD9-41B5-91D9-41F2E3E64208},
	Volume = {996},
	Year = {2004},
	url = {papers/Goings_BrainRes2004.pdf}}

@article{Goldman:1997,
	Author = {Goldman, S. A. and Nedergaard, M. and Crystal, R. G. and Fraser, R. A. and Goodman, R. and Harrison-Restelli, C. and Jiang, J. and Keyoung, H. M. and Leventhal, C. and Pincus, D. W. and Shahar, A. and Wang, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {02 Adult neurogenesis migration;Cell Division/physiology;Adult;03 Adult neurogenesis progenitor source;Human;Mammals;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Age Factors;Brain/*cytology;BB abstr;Stem Cells/*cytology},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA.},
	Pages = {30-55.},
	Title = {Neural precursors and neuronal production in the adult mammalian forebrain},
	Uuid = {861ED51D-D6FE-468D-93CC-28256DE22A03},
	Volume = {835},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9616760}}

@article{Goldman:1996,
	Abstract = {The songbird forebrain continues to generate neurons in adulthood, from precursor cells located in the ependymal /subependymal zone (SZ) over the mediocaudal neostriatum. Precursor mitosis is followed by migration of neuronal daughter cells into the underlying forebrain, along radial fibers derived from the SZ. To define the ontogeny of both the new neurons and their radial guide cells, we employed retroviral insertion of the lacZ gene into neostriatal SZ precursor cells derived from postnatal and adult songbirds. We found that single SZ cells generate both neurons and substrate glia in vitro, and in an analogous fashion, both neurons and radial cells in vivo. This suggests that newly generated neurons and radial cells of the adult avian brain derive from a common pluripotential progenitor.},
	Author = {Goldman, S. A. and Zukhar, A. and Barami, K. and Mikawa, T. and Niedzwiecki, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurobiol},
	Keywords = {Cells, Cultured;Neurons/*cytology/physiology;Brain/*cytology;Animal;Cell Movement;02 Adult neurogenesis migration;Birds/*physiology;Stem Cells/cytology;Ependyma/*cytology;Retroviridae;Genetic Vectors;BB abstr;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;Gene Transfer Techniques;Animals, Newborn/*physiology;Lac Operon;Support, U.S. Gov't, P.H.S.;Canaries/*physiology;Cell Division},
	Number = {4},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York 10021, USA.},
	Pages = {505-20.},
	Title = {Ependymal/subependymal zone cells of postnatal and adult songbird brain generate both neurons and nonneuronal siblings in vitro and in vivo},
	Uuid = {1D86CC3C-F01A-4066-8A6C-C85E78F7BD34},
	Volume = {30},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8844514}}

@article{Goldman:1997a,
	Abstract = {The adult mammalian brain continues to harbor ependymal/subependymal zone (SZ) precursor cells, which can give rise to neurons in vitro. In adult rats, explants of the rostral 6-7 mm of the SZ give rise to neurons in vitro, and over this entire expanse, neuronal survival is supported specifically by brain-derived neurotrophic factor (BDNF). We asked whether either the (a) spatial distribution, (b) abundance, or (c) BDNF responsiveness of the neuronal precursor population was affected by age. Explants of three rostrocaudally defined regions were taken from both young and old rats (3 and 20 months old, respectively), and cultured in 2\%fetal bovine serum-containing media with or without added BDNF (20 ng/ml). The extent of neuronal production by these explants varied only minimally with their level of derivation, such that substantial outgrowth was observed at each level tested. Neuronal outgrowth was marginally higher and more rapid in achieving its maximal extent in the 3-month-old rats compared with their aged counterparts, but neuronal outgrowth was robust at each age tested. The duration of survival of SZ-derived neurons did not differ between the young and old rats. At both ages, BDNF supported the survival of these new adult neurons. The extent of BDNF's influence was independent of both the age of the donor rat and the rostrocaudal level at which the parent SZ explant was taken. Thus, the neuronal precursors of the rat brain persist into senescence; the size of the precursor pool attenuates minimally with age, and its spatial extent remains constant. The neurons generated from these precursors can respond to BDNF throughout life. 0022-3034 Journal Article},
	Author = {Goldman, S. A. and Kirschenbaum, B. and Harrison-Restelli, C. and Thaler, H. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurobiol},
	Keywords = {Neurons/*cytology/drug effects/physiology;Animals;Cell Survival/drug effects;Rats;Rats, Sprague-Dawley;Mammals;Brain-Derived Neurotrophic Factor/*pharmacology;Aging/*physiology;C abstr;Male;Brain/*cytology/growth &development;Cattle;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Culture Media;Recombinant Proteins/pharmacology;Organ Culture},
	Number = {6},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA.},
	Pages = {554-66},
	Pubmed = {9183737},
	Title = {Neuronal precursors of the adult rat subependymal zone persist into senescence, with no decline in spatial extent or response to BDNF},
	Uuid = {06BB6542-5673-4260-B89F-409BA40FA723},
	Volume = {32},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9183737}}

@article{Goldman:1998,
	Abstract = {Neuronal precursor cells persist in the adult vertebrate forebrain, residing primarily in the ventricular/subventricular zone (SZ). In vivo, SZ precursors yield progeny which may die or give rise to glia. Yet they may also generate neurons, which are recruited to restricted regions such as the avian telencephalon and mammalian olfactory bulb. The survival of neurons arising from adult progenitors is dictated by both the availability of a permissive pathway for migration and the environment into which migration occurs. In the songbird higher vocal center (HVC), both humoral and contact-mediated signals modulate the migration and survival of new neurons, through an orchestrated set of hormonally regulated paracrine interactions. New neurons of the songbird brain depart the SZ to enter the brain parenchyma by migrating upon radial guide fibers, which emanate from cell bodies in the ventricular epithelium. The radial guide cells coderive with new neurons from a common progenitor, which is widespread throughout the songbird SZ. Neural precursors are also widely distributed in the adult mammalian SZ, although it is unclear whether avian and mammalian progenitor cells are homologous: Whereas neuronal recruitment persists throughout much of the songbird forebrain, in mammals it is limited to the olfactory bulb. In humans, the adult SZ appears to largely cease neurogenesis in vivo, although it, too, can produce neurons in vitro. In both rats and humans, the differentiation and survival of neurons arising from the postnatal SZ may be regulated by access to postmitotic trophic factors. Indeed, serial application of fibroblast growth factor- 2 (FGF-2) and brain-derived neurotrophic factor (BDNF) has allowed the generation and maintenance of neurons from the adult human SZ. This suggests the feasibility of inducing neurogenesis in the human brain, both in situ and through implanted progenitors. In this regard, using cell-specific neural promoters coupled to fluorescent reporters, defined progenitor phenotypes may now be isolated by fluorescence- activated cell sorting. Together, these findings give hope that structural brain repair through induced neurogenesis and neurogenic implants will soon be a clinical reality.},
	Author = {Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Neurobiol},
	Keywords = {Brain/cytology/*growth &development;01 Adult neurogenesis general;Human;A-8c;Rodentia/growth &development;Aging/physiology;Animal;Support, U.S. Gov't, P.H.S.;Neurons/physiology;Stem Cells/physiology;Support, Non-U.S. Gov't;Canaries/growth &development;Cell Movement/physiology},
	Number = {2},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA.},
	Pages = {267-86.},
	Title = {Adult neurogenesis: from canaries to the clinic},
	Uuid = {AFE0F4C6-64C4-4CB5-9550-D089FDEC1DB6},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9712309}}

@article{Goldman:1995,
	Abstract = {We have been examining the developmental fates and migrational patterns of the immature cells in the subventricular zone (SVZ) of the mammalian forebrain by labeling postnatal rat SVZ cells by stereotactic injection of replication-deficient murine retroviruses bearing reporter genes. SVZ cells migrate into adjacent white matter, cortex, and striatum, and differentiate into astrocytes and oligodendrocytes. In white matter, they largely differentiate into oligodendrocytes, whereas in gray matter, they differentiate into both oligodendrocytes and astrocytes. In vitro, SVZ cells are multipotential, able to generate both types of glia, as well as neurons. We infer that developmental fates are in part controlled by important environmental cues that the cells encounter during their migration. Using Smart Source Parsing},
	Author = {Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {J Neurooncol},
	Keywords = {Prosencephalon/*cytology;02 Adult neurogenesis migration;Cell Division/physiology;Neurons/immunology;Rats;Stereotaxic Techniques;Neuroglia/immunology;Animal;Support, U.S. Gov't, P.H.S.;Stem Cells/physiology;B abstr;Cell Movement/*physiology;Cell Aging/*physiology},
	Number = {1},
	Organization = {Department of Pathology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.},
	Pages = {61-4},
	Title = {Lineage, migration, and fate determination of postnatal subventricular zone cells in the mammalian CNS},
	Uuid = {63B8C239-2DA7-4357-AE72-27F057F246A2},
	Volume = {24},
	Year = {1995},
	url = {papers/Goldman_JNeurooncol1995.pdf}}

@article{Goldman:1983,
	Abstract = {The vocal control nucleus designated HVc (hyperstriatum ventrale, pars caudalis) of adult female canaries expands in response to systemic testosterone administration, which also induces the females to sing in a male-like manner. We became interested in the possibility of neurogenesis as a potential basis for this phenomenon. Intact adult female canaries were injected with [3H]thymidine over a 2-day period. Some birds were given testosterone implants at various times before thymidine. The birds were sacrificed 5 wk after hormone implantation, and their brains were processed for autoradiography. In parallel control experiments, some birds were given implants of cholesterol instead of testosterone. All birds showed considerable numbers of labeled neurons, glia, endothelia, and ventricular zone cells in and around HVc. Ultrastructural analysis confirmed the identity of these labeled neurons. Cholesterol- and testosterone-treated birds had similar neuronal labeling indices, which ranged from 1.8\%to 4.0\%in HVc. Thus, neurogenesis occurred in these adults independently of exogenous hormone treatment. Conversely, both glial and endothelial proliferation rates were markedly stimulated by exogenous testosterone treatment. We determined the origin of the thymidine-incorporating neurons by sacrificing two thymidine-treated females soon after their thymidine injections, precluding any significant migration of newly labeled cells. Analysis of these brains revealed no cells of neuronal morphology present in HVc but a very heavily labeled ventricular zone overlying HVc. We conclude that neuronal precursors exist in the HVc ventricular zone that incorporate tritiated thymidine during the S phase preceding their mitosis; after division these cells migrate into, and to some extent beyond, HVc. This ventricular zone neurogenesis seems to be a normally occurring phenomenon in intact adult female canaries.},
	Author = {Goldman, S. A. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Division/drug effects;02 Adult neurogenesis migration;B;Neurons/cytology;Female;Thymidine/metabolism;Animal;Testosterone/pharmacology;Brain/physiology;Canaries/*physiology;Neuroglia/cytology;Endothelium/cytology;Support, U.S. Gov't, P.H.S.;Vocalization, Animal/drug effects/*physiology},
	Number = {8},
	Pages = {2390-4.},
	Title = {Neuronal production, migration, and differentiation in a vocal control nucleus of the adult female canary brain},
	Uuid = {1C2C47F9-0048-4145-94BA-24181CA18484},
	Volume = {80},
	Year = {1983},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=6572982}}

@article{Goldman:1998a,
	Abstract = {Structural brain repair has become a possibility with the identification and characterization of persistent neuronal progenitor cells in both the neonatal and adult brain. However, despite recent advances in the identification, propagation and expansion of these cells, they will not be useful therapeutically until methods are available for directing or delivering them to sites of need. As a result, the natural history and induction of neuronal migration into adult brain tissue has assumed new importance in clinical neurobiology. In this review we consider the cellular and molecular bases of neuronal migration into the postnatal forebrain. In particular, we discuss two natural paradigms of postnatal neuronal recruitment: radial-cell- directed neuronal migration to the songbird neostriatum, and neurophilic migration to the rodent olfactory bulb. In each, we will focus on the dynamic interactions between the migrants, their cellular guides and the local environment, and the effect of those interactions on migrational success.},
	Author = {Goldman, S. A. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Trends Neurosci},
	Keywords = {Prosencephalon/*cytology;Vertebrates/growth &development/*physiology;02 Adult neurogenesis migration;Neurons/*physiology;Aging/physiology;Animals, Newborn/*physiology;Animal;Support, U.S. Gov't, P.H.S.;B abstr;Support, Non-U.S. Gov't;Cell Movement/physiology},
	Number = {3},
	Organization = {Dept of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021, USA.},
	Pages = {107-14.},
	Title = {Strategies utilized by migrating neurons of the postnatal vertebrate forebrain},
	Uuid = {1C7BDB93-B13D-4020-A1D0-CEAAAF76327B},
	Volume = {21},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9530917%20http://www.biomednet.com/library/fulltext/pii.S0166223697011910}}

@article{Goldman:2003,
	Abstract = {Recent studies have substantially expanded our conception of the roles for glia in function and maintenance of the adult nervous system. Of these reports, several have re-examined the lineage relationships among neural stem cells, their early radial glial derivatives and their mitotically competent neurogenic daughters. These studies have highlighted the role of radial cells in development, and of their glial progeny postnatally, as both progenitors and regulators of neuronal production and phenotype. In the adult mammalian brain, radial cell populations are scant, but their glial derivatives participate in a gliovascular network that organizes not only the structural and functional architecture of the brain but also its generative niches for resident progenitors - glial as well as neuronal. As in other organs, these progenitors can reside as transit-amplifying pools, by which lineage-biased progenitors expand to replenish discrete mature phenotypes. This review will consider the types of transit-amplifying progenitor cells persistent in the adult mammalian CNS, and the extent to which these derive from glial phenotypes. It will also discuss the interactions of progenitor cells with their brethren that could specify their phenotype and fate, while defining the permissive niches for cell genesis in the adult CNS.},
	Author = {Goldman, Steve},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Cell Lineage;Ependyma;Glial Fibrillary Acidic Protein;Neuroglia;Cell Differentiation;03 Adult neurogenesis progenitor source;Mammals;Epithelial Cells;Stem Cells;11 Glia;Adaptation, Physiological;review, tutorial;Animals;Cell Movement;Cerebral Cortex;review;Neurons},
	Medline = {22949172},
	Month = {11},
	Nlm_Id = {7808616},
	Number = {11},
	Organization = {Department of Neurology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA. sgoldm\@med.cornell.edu},
	Pages = {590-6},
	Pii = {S0166223603002947},
	Pubmed = {14585598},
	Title = {Glia as neural progenitor cells},
	Uuid = {B0A8CADF-7213-4D5C-832D-2B29D25A6B1E},
	Volume = {26},
	Year = {2003}}

@article{Gong:2002,
	Abstract = {p21(WAF1/CIP1) is a universal cyclin-dependent kinase inhibitor. To investigate the role of p21(WAF1/CIP1) in proliferation of human liver cancer cells, we examined the expression of p53, p21(WAF1/CIP1), cdk2 and cdk4 expression in two human liver cancer cell lines (HepG2 and PLC/PRF/5 cells). The effects of p21(WAF1/CIP1) on [(3)H]thymidine incorporation and cdks were also examined in these cells. HepG2 cells expressed all these proteins with lower level of cdk4. PLC/PRF/5 cells expressed the other proteins except p21(WAF1/CIP1). Transfection of p21(WAF1/CIP1) gene inhibited [(3)H]thymidine incorporation of both cells with different extent. Although the transfection of p21(WAF1/CIP1) did not affect cdk2 and cdk4 expression, it did reduce cdk2 kinase activity by 20\%. These results suggest that: (a) p21(WAF1/CIP1) involved in DNA synthesis of human liver cancer cells; (b) p21(WAF1/CIP1) could be a target gene for the treatment of human hepatocellular carcinoma. 0007-0920 Journal Article},
	Author = {Gong, Y. and Deng, S. and Zhang, M. and Wang, G. and Minuk, G. Y. and Burczynski, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Br J Cancer},
	Keywords = {Human;EE both;Cyclin-Dependent Kinases/metabolism;Carcinoma, Hepatocellular/*metabolism;Liver Neoplasms/*metabolism;Transfection;Adenosine Triphosphate/metabolism;Protein-Serine-Threonine Kinases/metabolism;08 Aberrant cell cycle;DNA/biosynthesis;Thymidine/*metabolism;Blotting, Northern;Cyclins/*physiology;Blotting, Western;Tumor Cells, Cultured;*CDC2-CDC28 Kinases;Support, Non-U.S. Gov't;Protein p53/metabolism;DNA, Neoplasm/*metabolism},
	Number = {4},
	Organization = {Department of Internal Medicine, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. ygong\@ms.umanitoba.ca},
	Pages = {625-9},
	Title = {A cyclin-dependent kinase inhibitor (p21(WAF1/CIP1)) affects thymidine incorporation in human liver cancer cells},
	Uuid = {4CC88BDC-2BE4-4C20-AE32-957E4BA19249},
	Volume = {86},
	Year = {2002},
	url = {papers/Gong_BrJCancer2002.pdf}}

@article{Gongidi:2004,
	Abstract = {Differential adhesion between migrating neurons and transient radial glial fibers enables the deployment of neurons into appropriate layers in the developing cerebral cortex. The identity of radial glial signals that regulate the termination of migration remains unclear. Here, we identified a radial glial surface antigen, SPARC (secreted protein acidic and rich in cysteine)-like 1, distributed predominantly in radial glial fibers passing through the upper strata of the cortical plate (CP) where neurons end their migration. Neuronal migration and adhesion assays indicate that SPARC-like 1 functions to terminate neuronal migration by reducing the adhesivity of neurons at the top of the CP. Cortical neurons fail to achieve appropriate positions in the absence of SPARC-like 1 function in vivo. Together, these data suggest that antiadhesive signaling via SPARC-like 1 on radial glial cell surfaces may enable neurons to recognize the end of migration in the developing cerebral cortex. 0896-6273 Journal Article},
	Author = {Gongidi, V. and Ring, C. and Moody, M. and Brekken, R. and Sage, E. H. and Rakic, P. and Anton, E. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Neuron},
	Keywords = {F abstr;10 Development},
	Number = {1},
	Organization = {UNC Neuroscience Center, Department of Cell and Molecular Physiology, The University of North Carolina School of Medicine, 27599, Chapel Hill, NC, USA},
	Pages = {57-69},
	Pubmed = {14715135},
	Title = {SPARC-like 1 Regulates the Terminal Phase of Radial Glia-Guided Migration in the Cerebral Cortex},
	Uuid = {6C97D6B0-E94C-48A2-B8F2-7E3E62A48027},
	Volume = {41},
	Year = {2004},
	url = {papers/Gongidi_Neuron2004.pdf}}

@article{Gonzalez:2003,
	Abstract = {Neonatal posterior cingulate cortex lesions spare the spatial deficits that characterize adult lesions. The present experiments examined the possibility that the anterior cingulate cortex mediates the spared spatial behavior. Rats were given bilateral lesions of the posterior cingulate cortex or anterior plus posterior cingulate cortex on postnatal days 4 (P4), 10 (P10), or in adulthood (P120). All groups were tested for spatial learning on the Morris place task in adulthood. Adult animals were impaired on place learning relative to controls whereas place learning was spared in all the neonatal groups and sparing was complete in the group receiving day 10 lesions. The results are discussed in relation to neural mechanisms, including fiber rerouting, synaptic changes and generation of new neurons, that may mediate spared spatial following neonatal posterior cingulate cortex lesions. Also discussed is evidence indicating that the neonatal brain, especially the day 10, has a special ability to compensate for injury.},
	Author = {Gonzalez, C. L. R. and Whishaw, I. Q. and Kolb, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Gyrus Cinguli;Research Support, Non-U.S. Gov't;Rats, Long-Evans;Female;Comparative Study;Rats;Spatial Behavior;Animals, Newborn;Learning;Reaction Time;Male;Animals;Cerebral Cortex;24 Pubmed search results 2008},
	Medline = {22980524},
	Nlm_Id = {7605074},
	Number = {2},
	Organization = {Canadian Centre for Behavioural Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge T1K 3M4, AB, Canada.},
	Pages = {563-71},
	Pii = {S0306452203002951},
	Pubmed = {14614920},
	Title = {Complete sparing of spatial learning following posterior and posterior plus anterior cingulate cortex lesions at 10 days of age in the rat},
	Uuid = {5F7C14C0-FD2B-4994-8703-C7B4A32854CE},
	Volume = {122},
	Year = {2003}}

@article{Gonzalez:2002,
	Abstract = {Rats received lesions of the posterior cingulate cortex or both the anterior and posterior cingulate cortex (total cingulate), or sham procedures, on postnatal Day 10. As adults, animals were trained in the Morris water task. Both the cingulate lesion groups showed substantial functional recovery relative to our previous studies of adult operates or animals with perinatal cingulate lesions. A Golgi analyis of layer III pyramidal cells in parietal cortex showed an increase in dendritic length in the lesion animals relative to sham controls, which is similar to previous findings for rats with anterior cingulate but not motor or parietal lesions. In addition, there was a partial regeneration of the anterior tissue in the total cingulates, which in some cases extended into the posterior region. This is consistent with earlier findings that anterior cingulate lesions around Day 10 stimulate neurogenesis. It appears that there is something special about the reparative processes and subsequent functional recovery that follow midline neocortical lesions. 21845910 0012-1630 Journal Article},
	Author = {Gonzalez, C. L. and Gibb, R. and Kolb, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0012-1630},
	Journal = {Dev Psychobiol},
	Keywords = {06 Adult neurogenesis injury induced;Dendrites/*physiology/ultrasonography;Nerve Regeneration;24 Pubmed search results 2008;Gyrus Cinguli;Male;Escape Reaction;Cerebral Cortex;Animals;Recall/physiology;Mental Recall;Rats, Long-Evans;Brain Mapping;Dendrites;Nerve Regeneration/*physiology;D;Neuronal Plasticity;Maze Learning;Pyramidal Cells/physiology/ultrasonography;Escape Reaction/physiology;Gyrus Cinguli/anatomy &histology/*physiology;Animal;Reference Values;Pyramidal Cells;Maze Learning/physiology;Rats;Female;Cerebral Cortex/anatomy &histology/physiology;Support, Non-U.S. Gov't;Research Support, Non-U.S. Gov't;Neuronal Plasticity/*physiology},
	Medline = {21845910},
	Month = {3},
	Nlm_Id = {0164074},
	Number = {2},
	Organization = {Department of Psychology and Neuroscience, University of Lethbridge, Lethbridge, Canada T1K 3M4.},
	Pages = {138-46},
	Pii = {10.1002/dev.10024},
	Pubmed = {11857328},
	Title = {Functional recovery and dendritic hypertrophy after posterior and complete cingulate lesions on postnatal day 10},
	Uuid = {8FE5D68B-9D2C-47D3-A97A-8457BD1E5F4C},
	Volume = {40},
	Year = {2002},
	url = {papers/Gonzalez_DevPsychobiol2002.pdf}}

@article{Gonzalez:1997,
	Abstract = {The reeler mutation in mice produces an especially well characterized disorder, with systematically abnormal migration of cerebral cortical neurons. The reeler gene encodes a large protein, termed Reelin, that in the cortex is synthesized and secreted exclusively in the Cajal-Retzius neurons of the cortical marginal zone (D'Arcangelo et al., 1995). In reeler mutant mice, loss of Reelin protein is associated with a systematic loss of the normal, "inside-out" sequence of neurogenesis in the cortex: neurons are formed in the normal sequence but become localized in the cortex in a somewhat inverted, although relatively disorganized "outside-in" pattern. Here we show that the scrambler mutant mouse exhibits a loss of lamination in the cortex and hippocampus that is indistinguishable from that seen in the reeler mouse. We use BrdU birthdating studies to show that scrambler cortex shows a somewhat inverted "outside-in" sequence of birthdates for cortical neurons that is similar to that previously described in reeler cortex. Finally, we perform staining with the CR-50 monoclonal antibody (Ogawa et al., 1995), which recognizes the Reelin protein (D'Arcangelo et al., 1997). We show that Reelin immunoreactivity is present in the scrambler cortex in a normal pattern, suggesting that Reelin is synthesized and released normally. Our data suggest that scrambler is a mutation in the same gene pathway as the reeler gene (Relnrl) and is most likely downstream of Relnrl.},
	Author = {Gonz{\'a}lez, J. L. and Russo, C. J. and Goldowitz, D. and Sweet, H. O. and Davisson, M. T. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:45:46 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {10 Development;Animals;Gene Expression Regulation, Developmental;comparative study;Phenotype;Cell Movement;Hippocampus;Serine Endopeptidases;Cell Adhesion Molecules, Neuronal;research support, non-u.s. gov't;Mice, Neurologic Mutants;Cerebellar Cortex;Extracellular Matrix Proteins;Cell Lineage;Morphogenesis;research support, u.s. gov't, p.h.s.;Cerebral Cortex;10 genetics malformation;Neurons;Genetic Heterogeneity;Mice;24 Pubmed search results 2008;Biological Markers;Gestational Age;research support, u.s. gov't, non-p.h.s.;Nerve Tissue Proteins},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {23},
	Organization = {Division of Neurogenetics, Department of Neurology, Beth Israel Deaconess Medical Center, and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {9204-11},
	Pubmed = {9364067},
	Title = {Birthdate and cell marker analysis of scrambler: a novel mutation affecting cortical development with a reeler-like phenotype},
	Uuid = {EE57A0FC-9E1E-4098-AD8D-59B261531242},
	Volume = {17},
	Year = {1997},
	url = {papers/González_JNeurosci1997.pdf}}

@article{Gonzalez-Scarano:1999,
	Abstract = {Microglia are the principal immune cells in the central nervous system (CNS) and have a critical role in host defense against invading microorganisms and neoplastic cells. However, as with immune cells in other organs, microglia may play a dual role, amplifying the effects of inflammation and mediating cellular degeneration as well as protecting the CNS. In entities like human immunodeficiency virus (HIV) infection of the nervous system, microglia are also critical to viral persistence. In this review we discuss the role of microglia in three diseases in which their activity is at least partially deleterious: HIV, multiple sclerosis, and Alzheimer's disease.},
	Author = {Gonz{\'a}lez-Scarano, F. and Baltuch, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0147-006X},
	Journal = {Annu Rev Neurosci},
	Keywords = {HIV Infections;Multiple Sclerosis;Nerve Degeneration;Inflammation;Research Support, U.S. Gov't, P.H.S.;Alzheimer Disease;Microglia;review, tutorial;11 Glia;Animals;Humans;Central Nervous System Diseases;review},
	Medline = {99218863},
	Nlm_Id = {7804039},
	Organization = {Department of Neurology, University of Pennsylvania Medical Center, Philadelphia 19104-6146, USA. Scarano\@mail.med.upenn.edu},
	Pages = {219-40},
	Pubmed = {10202538},
	Title = {Microglia as mediators of inflammatory and degenerative diseases},
	Uuid = {EDECA05C-A0DE-4DE5-ADF8-3B20E06AAE0D},
	Volume = {22},
	Year = {1999},
	url = {papers/González-Scarano_AnnuRevNeurosci1999.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1146/annurev.neuro.22.1.219}}

@article{Goodier:2008,
	Abstract = {Retrotransposons, mainly LINEs, SINEs, and endogenous retroviruses, make up roughly 40\%of the mammalian genome and have played an important role in genome evolution. Their prevalence in genomes reflects a delicate balance between their further expansion and the restraint imposed by the host. In any human genome only a small number of LINE1s (L1s) are active, moving their own and SINE sequences into new genomic locations and occasionally causing disease. Recent insights and new technologies promise answers to fundamental questions about the biology of transposable elements.},
	Author = {Goodier, John L. and Kazazian, Haig H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {research support, u.s. gov't, non-p.h.s.;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Department of Genetics, University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA. jgoodier\@mail.med.upenn.edu},
	Pages = {23-35},
	Pii = {S0092-8674(08)01179-3},
	Pubmed = {18854152},
	Title = {Retrotransposons revisited: the restraint and rehabilitation of parasites},
	Uuid = {6DAD9E9C-47EE-4388-977F-7EA386EB0339},
	Volume = {135},
	Year = {2008},
	url = {papers/Goodier_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.09.022}}

@article{Gopal:2007,
	Abstract = {The mammalian neocortex comprises two major neuronal subtypes; interneurons derived from the ganglionic eminence (GE) and projection neurons from the cortical ventricular zone (VZ). These separate origins necessitate distinct pathways of migration. Using mouse genetics and embryonic forebrain slice culture assays, we sought to identify substrates and/or guidance molecules for nonradial cell migration (NRCM). Mice carrying a mutation in Pax6 (Sey(-/-)), a paired domain transcription factor, are reported to have increased numbers of cortical inhibitory interneurons, suggesting that Pax6 could induce inhibitors of interneuron development or alternatively play a repressive role in guiding NRCM and/or specifying interneurons. Unexpectedly, we found a cell nonautonomous reduction in the distance Sey(-/-) neurons migrated, reflecting a disorganized migration, with frequent changes in direction. In contrast, no difference in the number of nonradially migrating GE cells was observed in Sey(-/-) mice. Our data indicate that the increased numbers of interneurons observed in Sey(-/-) do not result from an increased rate or number of nonradially migrating cells; instead, loss of Pax6 results in the ectopic specification of interneurons in the cortical VZ. Further, our data indicate that the known axonal disorganization in Sey(-/-) mice contributes to the observed reduced distance of NRCM.},
	Author = {Gopal, and Golden,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {9110718},
	Organization = {Neuroscience Program, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.},
	Pii = {bhm114},
	Pubmed = {17634386},
	Title = {Pax6 / Mice Have a Cell Nonautonomous Defect in Nonradial Interneuron Migration},
	Uuid = {3CF564F6-1FFC-4E7D-846C-71E1094DAF44},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhm114}}

@article{Gotts:2005,
	Abstract = {Neural cell migration and differentiation may participate in neural repair after adult brain injury; however, the survival and differentiation of newly born cells after different brain lesions are poorly understood. We have examined the migration and fate of bromodeoxyuridine (BrdU)-labeled cells after a highly reproducible focal ischemic lesion restricted to the frontoparietal cortex in adult rats. Thermocoagulation of pial blood vessels induces a circumscribed degeneration of all cortical layers while sparing the corpus callosum and striatum and increases cell proliferation in the subventricular zone (SVZ) and rostral migratory stream (RMS) within 7 days. We now show that, although the rostral migration of the newly born SVZ cells and their differentiation into neurons in the olfactory bulb were not affected by the lesion, numerous cells expressing the neuroblast marker doublecortin migrated laterally in the striatum and corpus callosum 5 days postinjury. In addition to the SVZ, BrdU-labeled cells were seen in the striatum, in the corpus callosum, and around the lesion. One month later, BrdU-labeled cells in the corpus callosum expressed transferrin and the pi isoform of glutathione-S-transferase (GST-pi), markers of oligodendrocytes. Other BrdU(+) cells expressed a marker of astrocytes, but none expressed neuronal markers, suggesting that new neurons do not form or survive under these conditions. Numerous BrdU-labeled cells were still observed in the SVZ and RMS. The data show that focal cortical ischemia does not lead to the long-term survival of new neurons in the striatum or cortex but induces long-term alterations in the SVZ and the production of new oligodendrocytes that may contribute to neural repair. (c) 2005 Wiley-Liss, Inc.},
	Author = {Gotts, Jeffrey E. and Chesselet, Marie-Franc\c{c}oise F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {06 Adult neurogenesis injury induced},
	Month = {4},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Departments of Neurology and Neurobiology, Geffen School of Medicine at UCLA, Los Angeles, California.},
	Pages = {160-71},
	Pubmed = {15751027},
	Title = {Migration and fate of newly born cells after focal cortical ischemia in adult rats},
	Uuid = {2797906E-D6C4-4165-8084-960A6857795C},
	Volume = {80},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20434}}

@article{Gotz:1998,
	Abstract = {Radial glia cells perform a dual function in the developing nervous system as precursor cells and guides for migrating neurons. We show here that during forebrain neurogenesis, the transcription factor Pax6 is specifically localized in radial glia cells of the cortex but not of the basal telencephalon. In Pax6-deficient mice, cortical radial glia cells were altered in their morphology, number, tenascin-C (TN-C) expression, and cell cycle. We show that some of these alterations are cell-autonomous, whereas others were rescued by coculturing with wild-type cortical cells. Our results suggest that Pax6 plays an essential role in the differentiation of cortical radial glia. Thus, despite their widespread distribution, radial glia cells are regionally specified in the developing CNS. 0896-6273 Journal Article},
	Author = {Gotz, M. and Stoykova, A. and Gruss, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Neuron},
	Keywords = {10 Development;Growth Substances/*physiology;DNA-Binding Proteins/genetics/*physiology;Cell Differentiation/genetics;Cells, Cultured;Animals;Cerebral Cortex/*cytology/growth &development/pathology;Neuroglia/*cytology/metabolism/pathology;Stem Cells/metabolism;Mice, Mutant Strains;Mutation;Mice, Inbred C57BL;Embryo;F both;Support, Non-U.S. Gov't;Mice, Knockout;Mice;*Homeodomain Proteins},
	Number = {5},
	Organization = {Department of Molecular Cell Biology, Max-Planck Institute of Biophysical Chemistry, Gottingen, Federal Republic of Germany.},
	Pages = {1031-44},
	Title = {Pax6 controls radial glia differentiation in the cerebral cortex},
	Uuid = {7B1C5503-424A-4A4B-90A1-6B0B8FAD5569},
	Volume = {21},
	Year = {1998},
	url = {papers/Gotz_Neuron1998}}

@article{Gould:1994,
	Abstract = {The dentate gyrus of the rat forms in three developmental phases, each of which is characterized by neuronal birth, migration and death. Recent evidence indicates that adrenal steroids regulate neuronal birth, death, and possibly migration throughout the life of the animal. However, the observation that very few neuroblasts in the developing or adult dentate gyrus express adrenal steroid receptors suggests that the effects of adrenal steroid manipulations on neurogenesis are indirect. Additional evidence indicates that NMDA receptor activation regulates neuronal birth and death in this brain region presenting the possibility that adrenal steroids influence these processes through direct actions on excitatory afferents. Future studies will address this possibility.},
	Author = {Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {Aging;Neurons/*cytology/*physiology;Amino Acids/*physiology;Cell Division;Cell Survival;Adrenal Cortex Hormones/*physiology;Hippocampus/embryology/growth &development;Fetal Development;Animal;04 Adult neurogenesis factors;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;C- abst only},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021.},
	Pages = {73-92; discussion 92-3.},
	Title = {The effects of adrenal steroids and excitatory input on neuronal birth and survival},
	Uuid = {7317F0BA-AE69-43AC-989F-92E12679505C},
	Volume = {743},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7802420}}

@article{Gould:1991,
	Abstract = {The rat dentate gyrus undergoes a period of naturally occurring cell death during the first postnatal week. In the adult rat, removal of circulating adrenal steroids by adrenalectomy is followed by massive death in the granule cell layer, thus raising the possibility that developmental cell death results from low levels of these hormones. Interestingly, the first two postnatal weeks of life in the rat, termed the stress hyporesponsive period, are characterized by very low levels of adrenal steroids. In order to determine whether low levels of adrenal steroids enable developmental cell death to occur in the dentate gyrus, we examined the density of pyknotic and healthy cells in the dentate gyrus of rat pups which received one of the following treatments: (1) injections of the endogenous rat glucocorticoid corticosterone during the first postnatal week, or (2) adrenalectomy at the time when glucocorticoid levels normally rise. Quantitative analysis of the density of pyknotic cells in the granule cell layers revealed significant decreases with corticosterone treatment by the end of the first postnatal week. In these same brains, treatment with corticosterone resulted in a substantial increase in the density of pyknotic cells in the hilus. Adrenalectomy resulted in a significant increase in the density of pyknotic cells in the granule cell layer as well as in the hilus. Despite the dramatic alterations in the density of pyknotic cells with both increases and decreases in glucocorticoid levels, the density of healthy cells remained the same. These observations suggest that glucocorticoids regulate several processes, possibly including neurogenesis and migration, in addition to cell death.},
	Author = {Gould, E. and Woolley, C. S. and McEwen, B. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:53 -0400},
	Journal = {J Comp Neurol},
	Keywords = {C abst only;Rats;Corticosterone/*pharmacology;Adrenal Cortex Hormones/*physiology;Animal;Neurons/*drug effects/physiology;04 Adult neurogenesis factors;Hippocampus/cytology/drug effects/*growth &development;Animals, Newborn;Support, Non-U.S. Gov't;Cell Survival/drug effects;Adrenalectomy;Rats, Inbred Strains;Support, U.S. Gov't, P.H.S.},
	Number = {3},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021.},
	Pages = {479-85.},
	Title = {Adrenal steroids regulate postnatal development of the rat dentate gyrus: I. Effects of glucocorticoids on cell death},
	Uuid = {6746B068-A216-4610-A627-18447C845B24},
	Volume = {313},
	Year = {1991},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1770171}}

@article{Gould:2002,
	Author = {Gould, E. and Gross, C. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;Brain/*cytology/growth &development/metabolism;Cell Division/physiology;Bromodeoxyuridine/pharmacokinetics;Cell Survival/physiology;Human;Antigens, Differentiation/biosynthesis;A both;Cell Count;Cell Differentiation/physiology;Animal;Neuroglia/cytology;Neurons/*cytology/metabolism;Staining and Labeling/methods;Dentate Gyrus/cytology},
	Number = {3},
	Organization = {Department of Psychology, Princeton University, Princeton, New Jersey 08544, USA. goulde\@princeton.edu},
	Pages = {619-23.},
	Title = {Neurogenesis in adult mammals: some progress and problems},
	Uuid = {9C09BCDE-D20C-11D9-B244-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	url = {papers/Gould_JNeurosci2002.pdf}}

@article{Gould:1999,
	Abstract = {Thousands of hippocampal neurons are born in adulthood, suggesting that new cells could be important for hippocampal function. To determine whether hippocampus-dependent learning affects adult-generated neurons, we examined the fate of new cells labeled with the thymidine analog bromodeoxyuridine following specific behavioral tasks. Here we report that the number of adult-generated neurons doubles in the rat dentate gyrus in response to training on associative learning tasks that require the hippocampus. In contrast, training on associative learning tasks that do not require the hippocampus did not alter the number of new cells. These findings indicate that adult-generated hippocampal neurons are specifically affected by, and potentially involved in, associative memory formation.},
	Author = {Gould, E. and Beylin, A. and Tanapat, P. and Reeves, A. and Shors, T. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Physical Conditioning, Animal/physiology;Rats;Association Learning/physiology;Animal;Rats, Sprague-Dawley;Male;01 Adult neurogenesis general;A-8b;Cell Division/physiology;Dentate Gyrus/*cytology/*physiology;Blinking/physiology;Maze Learning/physiology;Neurons/cytology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Learning/*physiology;Cues;Conditioning, Classical/physiology},
	Number = {3},
	Organization = {Department of Psychology, Princeton University, Princeton, New Jersey 08544, USA.},
	Pages = {260-5.},
	Title = {Learning enhances adult neurogenesis in the hippocampal formation},
	Uuid = {A888F3BE-8662-4ED1-90CE-A7608C12B9CD},
	Volume = {2},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10195219}}

@article{Gould:2007,
	Abstract = {It is now widely accepted that neurogenesis occurs in two regions of the adult mammalian brain - the hippocampus and the olfactory bulb. There is evidence for adult neurogenesis in several additional areas, including the neocortex, striatum, amygdala and substantia nigra, but this has been difficult to replicate consistently other than in the damaged brain. The discrepancies may be due to variations in the sensitivity of the methods used to detect new neurons.},
	Author = {Gould, Elizabeth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {1471-003X},
	Journal = {Nat Rev Neurosci},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {100962781},
	Number = {6},
	Organization = {Elizabeth Gould is at the Department of Psychology, Princeton University, Princeton, New Jersey 08544, USA. goulde\@princeton.edu.},
	Pages = {481-8},
	Pii = {nrn2147},
	Pubmed = {17514200},
	Title = {How widespread is adult neurogenesis in mammals?},
	Uuid = {73BDD42A-0BDA-4D14-AFA9-CFA577D0E620},
	Volume = {8},
	Year = {2007},
	url = {papers/Gould_NatRevNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrn2147}}

@article{Gould:1999a,
	Abstract = {The production of new hippocampal neurons in adulthood has been well documented in rodents. Recent studies have extended these findings to other mammalian species, such as tree shrews and marmoset monkeys. However, hippocampal neurogenesis has not been demonstrated in adult Old World primates. To investigate this possibility, we injected 11 adult Old World monkeys of different ages (5-23 years) with the thymidine analog bromodeoxyuridine and examined the fate of the labeled cells at different survival times by using neuronal and glial markers. In the young-adult and middle-aged monkeys, we found a substantial number of cells that incorporated bromodeoxyuridine and exhibited morphological and biochemical characteristics of immature and mature neurons. New cells located in the dentate gyrus expressed a marker of immature granule neurons, Turned On After Division 64 kDa protein, as well as markers of mature granule neurons including neuron specific enolase, neuronal nuclei, and the calcium-binding protein calbindin. Fewer new cells expressed the astroglial marker glial fibrillary acidic protein. Evidence of neurogenesis was observed in the oldest monkeys (23 years) as well, but it appeared to be less robust. These results indicate that the adult brains of Old World monkeys produce new hippocampal neurons. Adult macaque monkeys may provide a useful primate model for studying the functional significance of adult neurogenesis.},
	Author = {Gould, E. and Reeves, A. J. and Fallah, M. and Tanapat, P. and Gross, C. G. and Fuchs, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Microscopy, Confocal;Aging;Cell Division/physiology;Female;Neurons/*cytology/physiology;A abstr;Hippocampus/*cytology/physiology;Cell Count;Cercopithecidae;Cell Differentiation/physiology;Animal;Support, U.S. Gov't, P.H.S.;Male},
	Number = {9},
	Organization = {Department of Psychology, Princeton University, Princeton NJ 08544, USA. goulde\@princeton.edu},
	Pages = {5263-7.},
	Title = {Hippocampal neurogenesis in adult Old World primates},
	Uuid = {9FB6E308-67A7-11DA-A4B6-000D9346EC2A},
	Volume = {96},
	Year = {1999},
	url = {papers/Gould_ProcNatlAcadSciUSA1999.pdf}}

@article{Gould:2001,
	Abstract = {Previously we reported that new neurons are added to the hippocampus and neocortex of adult macaque monkeys. Here we compare the production and survival of adult-generated neurons and glia in the dentate gyrus, prefrontal cortex, and inferior temporal cortex. Twelve adult macaques were injected with the thymidine analogue BrdUrd, and the phenotypes of labeled cells were examined after 2 h, 24 h, 2 wk, 5 wk, 9 wk, and 12 wk by using the following immunocytochemical markers: for immature and mature neurons, class III beta-tubulin (TuJ1); for mature neurons, neuronal nuclei; for astrocytes, glial fibrillary acidic protein; and for oligodendrocytes, 2',3'-cyclic nucleotide 3'phosphodiesterase. We found that the dentate gyrus had many more BrdUrd-labeled cells than either neocortical area. Furthermore, a greater percentage of BrdUrd- labeled cells expressed a neuronal marker in the dentate gyrus than in either neocortical area. The number of new cells in all three areas declined by 9 wk after BrdUrd labeling, suggesting that some of the new cells have a transient existence. BrdUrd-labeled cells also were found in the subventricular zone and in the white matter between the lateral ventricle and neocortex; some of the latter cells were double-labeled for BrdUrd and TuJ1. Adult neocortical neurogenesis is not restricted to primates. Five adult rats were injected with BrdUrd, and after a 3- wk survival time, there were cells double-labeled for BrdUrd and either TuJ1 or neuronal nuclei in the anterior neocortex as well as the dentate gyrus. Using Smart Source Parsing Aug},
	Author = {Gould, E. and Vail, N. and Wagers, M. and Gross, C. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {A;01 Adult neurogenesis general},
	Organization = {Department of Psychology, Princeton University, Princeton, NJ 08544.},
	Pages = {28},
	Title = {Adult-generated hippocampal and neocortical neurons in macaques have a transient existence},
	Uuid = {66B2AFC8-D247-11D9-A0E9-000D9346EC2A},
	Volume = {28},
	Year = {2001},
	url = {papers/Gould_ProcNatlAcadSciUSA2001.pdf}}

@article{Gould:1999b,
	Abstract = {In primates, prefrontal, inferior temporal, and posterior parietal cortex are important for cognitive function. It is shown that in adult macaques, new neurons are added to these three neocortical association areas, but not to a primary sensory area (striate cortex). The new neurons appeared to originate in the subventricular zone and to migrate through the white matter to the neocortex, where they extended axons. These new neurons, which are continually added in adulthood, may play a role in the functions of association neocortex.},
	Author = {Gould, E. and Reeves, A. J. and Graziano, M. S. and Gross, C. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Journal = {Science},
	Keywords = {Cell Survival;Cell Differentiation;Temporal Lobe/*cytology/physiology;Aging;Neurons/*cytology/physiology;Microscopy, Confocal;Axons/ultrastructure;Prefrontal Cortex/*cytology/physiology;Female;Cell Movement;Animal;Parietal Lobe/*cytology/physiology;Macaca fascicularis;Male;Support, Non-U.S. Gov't;Lateral Ventricles/cytology;Support, U.S. Gov't, P.H.S.;Visual Cortex/cytology/physiology;A-9 both;Neocortex/*cytology/physiology;Cell Division;Bromodeoxyuridine;Astrocytes/cytology},
	Number = {5439},
	Organization = {Department of Psychology, Princeton University, Princeton, NJ 08544, USA. goulde\@princeton.edu},
	Pages = {548-52.},
	Title = {Neurogenesis in the neocortex of adult primates},
	Uuid = {F334DD1F-CDEF-11D9-B244-000D9346EC2A},
	Volume = {286},
	Year = {1999},
	url = {papers/Gould_Science1999.pdf}}

@article{Gotz:2005a,
	Abstract = {Radial glial cells have been identified as a major source of neurons during development. Here, we review the evidence for the distinct "glial" nature of radial glial cells and contrast these cells with their progenitors, the neuroepithelial cells. Recent results also suggest that not only during neurogenesis in vivo, but also during the differentiation of cultured embryonic stem cells toward neurons, progenitors with clear glial antigenic characteristics act as cellular intermediates.},
	Author = {G{\"o}tz, Magdalena and Barde, Yves-Alain A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Cell Differentiation;Neuroglia;Stem Cells;Humans;Animals;Brain;Neurons;review},
	Month = {5},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Institute of Stem Cell Research, GSF-National Research Center for Environment and Health, Ingolst{\"a}dter Landstr. 1, D-85764 Neuherberg/Munich, Germany. magdalena.goetz\@gsf.de},
	Pages = {369-72},
	Pii = {S0896-6273(05)00348-X},
	Pubmed = {15882633},
	Title = {Radial glial cells defined and major intermediates between embryonic stem cells and CNS neurons},
	Uuid = {AD8B2FA9-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {46},
	Year = {2005},
	url = {papers/Götz_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.04.012}}

@article{Graber:2004,
	Abstract = {Penetrating cortical trauma frequently results in delayed development of epilepsy. In the rat undercut model of neocortical posttraumatic hyperexcitability, suppression of neuronal activity by exposing the injured cortex to tetrodotoxin (TTX) in vivo for approximately 2 weeks prevents the expression of abnormal hypersynchronous discharges in neocortical slices. We examined the relationship between neuronal activity during the latent period after trauma and subsequent expression of hyperexcitability by varying the timing of TTX treatment. Partially isolated islands of rat sensorimotor cortex were treated with Elvax polymer containing TTX to suppress cortical activity and slices obtained for in vitro experiments 10 to 15 days later. TTX treatment was either started immediately after injury and discontinued after a variable number of days or delayed for a variable time after the lesion was placed. Immediate treatment lasting only 2 to 3 days and treatment delayed up to 3 days prevented hyperexcitability. Thus, there is a critical period for development of hyperexcitability in this model that depends on cortical activity. We propose that the hyperexcitability caused by partial cortical isolation may represent an early stage of posttraumatic epileptogenesis. A hypothetical cascade of events leading to subsequent pathophysiological activity is likely initiated at the time of injury but remains plastic during this critical period.},
	Author = {Graber, Kevin D. and Prince, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0364-5134},
	Journal = {Ann Neurol},
	Keywords = {Drug Administration Schedule;Electrophysiology;Animals;In Vitro;Rats;Comparative Study;Polyvinyls;21 Epilepsy;Neocortex;Epilepsy;Rats, Sprague-Dawley;Tetrodotoxin;Disease Models, Animal;Behavior, Animal;Critical Period (Psychology);Time Factors;Male;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Evoked Potentials, Somatosensory;21 Neurophysiology;Anesthetics, Local;24 Pubmed search results 2008;Immunohistochemistry;Electroencephalography;Research Support, Non-U.S. Gov't},
	Month = {6},
	Nlm_Id = {7707449},
	Number = {6},
	Organization = {Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305-5300, USA. graberk\@stanford.edu},
	Pages = {860-70},
	Pubmed = {15174021},
	Title = {A critical period for prevention of posttraumatic neocortical hyperexcitability in rats},
	Uuid = {E3B67B95-FEDA-4E7D-8D93-24F5FFCD7730},
	Volume = {55},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/ana.20124}}

@article{Grabowski:1995,
	Abstract = {The purpose of this work was to study if enriched housing conditions and fetal neocortical transplantation could enhance the functional outcome after focal brain ischemia in adult rats. The right middle cerebral artery (MCA) was ligated in 34 inbred, spontaneously hypertensive male rats, which were then randomly divided into three groups. Groups A and B were transferred to an enriched environment, i.e., a large cage with opportunities for various activities but not forcing the rats to do any particular tasks; group C was kept in standard laboratory cages. Three weeks after the MCA occlusion blocks of fetal neocortical tissue (Embryonic Day 17) were transplanted to the infarct cavity in groups B and C. Rats in group A (n = 11) and group B (n = 11) performed equally well and significantly better than rats in group C (n = 10) when placed on an inclined plane and when traversing a rotating pole 6 and 9 weeks after the MCA occlusion and in a leg placement test at 9, but not 6 and 12 weeks. Skilled forelimb function did not differ between the groups. Infarct size and thalamic atrophy did not differ between the groups and graft size was similar in group B and C. There was no correlation between infarct size and motor function in any of the tests in rats housed in an enriched environment. Since the environment can significantly alter functional outcome without reducing infarct size we suggest that more attention should be given to the role of the laboratory environment and to long term behavioral outcome in experimental stroke. 0014-4886 Journal Article},
	Author = {Grabowski, M. and Sorensen, J. C. and Mattsson, B. and Zimmer, J. and Johansson, B. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Exp Neurol},
	Keywords = {Cerebral Cortex/physiology/*transplantation;17 Transplant Regeneration;Thalamus/pathology;Rats;L abstr;*Social Environment;*Motor Activity;Brain Tissue Transplantation/*physiology;Cerebral Arteries;Cerebral Infarction/pathology/*physiopathology/therapy;Rats, Inbred SHR;Support, Non-U.S. Gov't;Animals;Male;Fetal Tissue Transplantation;*Psychomotor Performance},
	Number = {1},
	Organization = {Department of Neurology, Lund University Hospital, Sweden.},
	Pages = {96-102},
	Pubmed = {7601267},
	Title = {Influence of an enriched environment and cortical grafting on functional outcome in brain infarcts of adult rats},
	Uuid = {9336428B-EC80-11DA-8605-000D9346EC2A},
	Volume = {133},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7601267}}

@article{Gracia-Llanes:2003,
	Abstract = {This study investigates the targets of the population of vasoactive intestinal polypeptide (VIP)-containing deep short-axon cells of the rat olfactory bulb (OB), combining single- and double-immunocytochemical approaches under light and electron microscopy. It has been assumed that deep short-axon cells innervate granule cells in the mammalian OB, but their synaptic connectivity has not been demonstrated to date. Our results indicate that, instead of the accepted scheme of the bulbar circuitry, VIP-containing deep short-axon cells are gamma-aminobutyric acid (GABA)ergic interneurons specialized in the selective innervation of other GABAergic deep short-axon cells. Their axons contact with the perisomatic region and the dendritic portions of subsets of deep short-axon cells that contain VIP, calbindin D-28k and neuropeptide Y. Electron microscopy reveals axo-somatic and axo-dendritic symmetrical synapses from VIP-containing boutons. Taken altogether, our data show that the VIP-containing deep short-axon cells of the rat OB form an interneuronal network that modulates the function of other interneurons different from granule cells. They might be involved indirectly in the inhibition or disinhibition of principal cells or might participate in the generation of oscillatory activity and in the synchronization of populations of interneurons and, then, of principal cells. Present data demonstrate that modulation of the OB by local circuits is more complex than the simple inhibition from periglomerular cells and granule cells, and remark the importance of considering the contribution of other classes of GABAergic interneurons different from periglomerular cells and granule cells to the bulbar circuitry. 0953-816x Journal Article},
	Author = {Gracia-Llanes, F. J. and Crespo, C. and Blasco-Ibanez, J. M. and Marques-Mari, A. I. and Martinez-Guijarro, F. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Vasoactive Intestinal Peptide/*metabolism;13 Olfactory bulb anatomy;Animals;Olfactory Bulb/*cytology;Rats;Axons/classification/*metabolism/ultrastructure;Comparative Study;Female;Rats, Wistar;Support, Non-U.S. Gov't;Neurons/classification/*metabolism/ultrastructure;Calcium-Binding Protein, Vitamin D-Dependent/metabolism;Neuropeptide Y/metabolism;I pdf;Parvalbumins/metabolism;Immunohistochemistry;Microscopy, Electron;gamma-Aminobutyric Acid/metabolism},
	Number = {7},
	Organization = {Departamento de Biologia Celular, Facultad de Ciencias Biologicas, Universidad de Valencia, E-46100, Burjasot, Spain.},
	Pages = {1751-63},
	Pubmed = {14622210},
	Title = {VIP-containing deep short-axon cells of the olfactory bulb innervate interneurons different from granule cells},
	Uuid = {934A8DE9-ACEE-4FF8-BA96-53E29811A249},
	Volume = {18},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14622210}}

@article{Graeber:1990,
	Author = {Graeber, M. B. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0567-7556},
	Journal = {Acta Histochem Suppl},
	Keywords = {Neuroglia;Phagocytes;Nerve Tissue Proteins;Human;Not relevant;Biological Markers;11 Glia;Mesoderm;review, tutorial;Humans;Brain;Nervous System Diseases;review;Animals},
	Medline = {91180327},
	Nlm_Id = {0061372},
	Organization = {Department of Neuromorphology, Max Planck Institute for Psychiatry, Martinsried, FRG.},
	Pages = {157-60},
	Pubmed = {2080239},
	Title = {The third glial cell type, the microglia: cellular markers of activation in situ},
	Uuid = {A55312EE-29EB-40D3-ACC2-77E7DE034494},
	Volume = {38},
	Year = {1990}}

@article{Graeber:1989,
	Abstract = {Injection of ricin, the toxic lectin from Ricinus communis, into the rat facial nerve leads to rapid degeneration of motor neurons and concomitant proliferation and transformation of endogenous microglia into brain macrophages. Using [3H]-thymidine autoradiography, immunocytochemistry for microglial markers and electron microscopy, we could show that when ricin was administered together with the cytostatic drug adriamycin, the retrogradely transported adriamycin inhibits the macrophage response induced by toxic ricin. It is concluded that under conditions of neuronal degeneration, e.g., following ricin intoxication, brain macrophages are predominantly, if not exclusively, derived from endogenous microglia.},
	Author = {Graeber, M. B. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Thymidine;Ricin;Glial Fibrillary Acidic Protein;Neuroglia;Nerve Degeneration;Rats;Microscopy, Electron;Doxorubicin;Not relevant;Cell Division;11 Glia;Macrophages;Male;Animals;Rats, Inbred Strains;Brain;Vimentin},
	Medline = {89389837},
	Nlm_Id = {0412041},
	Number = {4},
	Organization = {Abteilung f{\"u}r Neuromorphologie, Max-Planck-Institut f{\"u}r Psychiatrie, Martinsried, Federal Republic of Germany.},
	Pages = {348-58},
	Pubmed = {2782046},
	Title = {Formation of microglia-derived brain macrophages is blocked by adriamycin},
	Uuid = {0246CCE4-CFC4-4662-987C-B29882280F3C},
	Volume = {78},
	Year = {1989}}

@article{Graeber:1993,
	Abstract = {An autopsy case of severe peripheral facial nerve paresis with disconnection of synapses from facial motor neurons is reported. A 77-year-old man presented with left-sided otitis media and subsequent development of facial nerve paresis. Three months later, the patient died of an acute gastrointestinal bleeding from a chronic duodenal ulcer. Gross inspection of the brain revealed non-stenosing arteriosclerotic vascular changes and a single small cystic lesion in the right putamen. Microscopically, marked chromatolytic changes were observed in the left facial nucleus. Immunocytochemistry for synaptophysin revealed a marked loss of afferent synaptic contacts from somatic and stem dendritic surface membranes of all chromatolytic motor neurons. Wrapping of a number of neurons by newly formed glial fibrillary acidic protein-positive astrocytic cell processes could be detected in the regenerating facial motor nucleus. In addition, expression of HLA-DR was increased on a small number of microglia and perivascular cells. These changes were absent from the contralateral, normal-appearing facial nucleus. To our knowledge, this case provides the first evidence for disconnection of synapses following peripheral nerve lesioning in humans. Occurrence of synaptic stripping is likely to explain nuclear hyperexcitability and failure of recovery of complex fine motor movements that are commonly observed following peripheral injury to the facial nerve.},
	Author = {Graeber, M. B. and Bise, K. and Mehraein, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Synapses;Facial Paralysis;Glial Fibrillary Acidic Protein;Aged;Facial Nerve;Motor Neurons;Immunohistochemistry;HLA-DR Antigens;11 Glia;Synaptophysin;Male;Humans;case reports},
	Medline = {94026193},
	Nlm_Id = {0412041},
	Number = {2},
	Organization = {Institute of Neuropathology, Ludwig Maximilians University, Munich, Germany.},
	Pages = {179-81},
	Pubmed = {8213072},
	Title = {Synaptic stripping in the human facial nucleus},
	Uuid = {500C19CC-1037-4A06-92A5-53A9B95EA658},
	Volume = {86},
	Year = {1993},
	url = {papers/Graeber_ActaNeuropathol(Berl)1993.PDF}}

@article{Graeber:1990a,
	Abstract = {In recent years much progress has been made toward a better understanding of the nature and function of microglial cells. This review summarizes new developments and attempts to provide a perspective for future avenues to take in microglial research. Microglia are considered to play an active role in a variety of neurological diseases. Their function in forming a network of immune competent cells within the CNS is discussed.},
	Author = {Graeber, M. B. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {1015-6305},
	Journal = {Brain Pathol},
	Keywords = {Research Support, Non-U.S. Gov't;Central Nervous System;Human;Mammals;Not relevant;11 Glia;Antigen-Presenting Cells;review, tutorial;Microglia;Humans;Support, Non-U.S. Gov't;Central Nervous System Diseases;Animals;review},
	Medline = {94122928},
	Month = {9},
	Nlm_Id = {9216781},
	Number = {1},
	Organization = {Center for Neurologic Diseases, Harvard Medical School, Boston, MA.},
	Pages = {2-5},
	Pubmed = {1669689},
	Title = {Microglia: immune network in the CNS},
	Uuid = {66BC1F86-D771-4054-9C67-A34FE0B12EF3},
	Volume = {1},
	Year = {1990}}

@article{Graeber:1998,
	Abstract = {Microglia represent a population of brain macrophage precursor cells which are intrinsic to the CNS parenchyma. Transection of the facial nerve in the newborn rat causes death of the affected motor neurons which is accompanied by massive activation of local microglia. Many of these cells develop into macrophages as can be shown by immunocytochemistry for OX-42 and ED1. Using the new polyclonal microglial marker ionized calcium binding adapter molecule 1, iba1, in combination with immunocytochemical double-labeling for the proliferating cell nuclear antigen (PCNA), or [3H]thymidine autoradiography, and confocal microscopy, qualitative as well as quantitative differences can be demonstrated between the newborn and the adult axotomized rat facial nucleus. While microglial cells are the only cell population which responds to axotomy by cell division in the adult facial nucleus, GFAP positive reactive astrocytes can be shown to undergo mitosis following axotomy in the newborn rat. Furthermore, ED1 immunoreactivity, early expression of MHC class II molecules and morphological transformation of microglia into macrophages can only be observed under conditions of neuronal degeneration, i.e., in the neonatal rat facial nucleus. Thus, the combination of cellular markers described here should be useful for studies employing the neonatal rat facial nucleus as an in vivo assay system to test the efficacy of neurotrophic factors.},
	Author = {Graeber, M. B. and L{\'o}pez-Redondo, F. and Ikoma, E. and Ishikawa, M. and Imai, Y. and Nakajima, K. and Kreutzberg, G. W. and Kohsaka, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Nerve Degeneration;Animals;Macrophages;Rats;Major Histocompatibility Complex;Microglia;Proliferating Cell Nuclear Antigen;Rats, Wistar;11 Glia;Male;Animals, Newborn;Calcium-Binding Proteins;Axotomy;Age Factors;Motor Neurons;Cell Division;Facial Nerve;Research Support, Non-U.S. Gov't},
	Medline = {99057683},
	Month = {12},
	Nlm_Id = {0045503},
	Number = {2},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried 82152, Germany.},
	Pages = {241-53},
	Pii = {S0006899398008592},
	Pubmed = {9838143},
	Title = {The microglia/macrophage response in the neonatal rat facial nucleus following axotomy},
	Uuid = {738E60DA-A48C-4B9C-96C1-2DB2208AAD2F},
	Volume = {813},
	Year = {1998}}

@article{Graeber:1993a,
	Author = {Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0722-5091},
	Journal = {Clin Neuropathol},
	Keywords = {Multiple Sclerosis;Central Nervous System;Blood-Brain Barrier;Encephalomyelitis, Autoimmune, Experimental;11 Glia;Microglia;Macrophages;Antigen-Presenting Cells;Humans;Animals},
	Medline = {94037718},
	Nlm_Id = {8214420},
	Number = {5},
	Organization = {Institute of Neuropathology, Ludwig Maximilians University, M{\"u}nchen, Germany.},
	Pages = {296-7},
	Pubmed = {8222403},
	Title = {Microglia, macrophages and the blood-brain barrier},
	Uuid = {8194C4B2-3B49-493C-ADE0-E1167601C7B1},
	Volume = {12},
	Year = {1993}}

@article{Graeber:2002,
	Abstract = {Microglia have long been ignored by neurooncologists. This has changed with the realization that microglial cells not only occur within and around brain tumors but also contribute significantly to the actual tumor mass, notably in astrocytic gliomas. In addition, it has been speculated that microglia could play a role in the defense against neoplasms of the nervous system. However, the biological success of these tumors, i.e., their highly malignant behavior, indicates that natural microglial defense mechanisms do not function properly in astrocytomas. In fact, there is evidence that microglial behavior is controlled by tumor cells, supporting their growth and infiltration. This unexpected "Achilles heel" of microglial immune defense illustrates the risk of generalizing on the basis of a single aspect of microglial biology. Microglia are highly plastic cells, capable of exerting cytotoxic functions under conditions of CNS infections, but not necessarily during glioma progression. Thus, the suggestion that microglial activation through stimulation by cytokines (e.g., interferon-gamma) will benefit patients with brain tumors could prove fatally wrong. Therapeutic recruitment of microglia to treat such diffusely infiltrative brain tumors as astrocytic gliomas must be considered premature.},
	Author = {Graeber, Manuel B. and Scheithauer, Bernd W. and Kreutzberg, Georg W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Cell Lineage;Immunotherapy;Antigen Presentation;Glioma;Cell Division;Cell Count;11 Glia;Microglia;Macrophages;Brain Neoplasms;review, tutorial;Neoplasm Invasiveness;Humans;Oligodendroglioma;review;Astrocytoma},
	Medline = {22267070},
	Month = {11},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Neuropathology, Faculty of Medicine, Imperial College, London, United Kingdom. m.graeber\@ic.ac.uk},
	Pages = {252-9},
	Pubmed = {12379912},
	Title = {Microglia in brain tumors},
	Uuid = {5368CC39-8682-42FF-BDAF-D0B22FCD262E},
	Volume = {40},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10147}}

@article{Graeber:1988,
	Abstract = {Unlike astrocytes and oligodendrocytes, microglia are extremely plastic making them the chameleon among the glial cells in the CNS. This great mutability of the microglial cell shape suggests the presence of an elaborate cytoskeleton which is demonstrated here by applying a new ultrastructural method. Electron microscopic immunocytochemistry shows the presence of vimentin at intermediate filament sites in reactive microglia stimulated by rat facial nerve axotomy. It is suggested that vimentin-expression may serve as a marker for activated states of microglia, including brain macrophages.},
	Author = {Graeber, M. B. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Cytoskeleton;Facial Nerve;Immunohistochemistry;Microscopy, Electron;Rats;Not relevant;11 Glia;Microscopy, Fluorescence;Animals;Male;Rats, Inbred Strains;Vimentin},
	Medline = {89055215},
	Month = {8},
	Nlm_Id = {0364620},
	Number = {4},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, FRG.},
	Pages = {573-80},
	Pubmed = {3193132},
	Title = {The microglial cytoskeleton: vimentin is localized within activated cells in situ},
	Uuid = {BE85D32B-F765-4F3A-96A2-FEF88797AAD4},
	Volume = {17},
	Year = {1988}}

@article{Graeber:1990b,
	Abstract = {The results of the present study demonstrate that following lethal motor neuron injury microglia and perivascular cells, as well as brain macrophages derived from the latter two cell types, newly express antigens of the myelomonocytic lineage as recognized by the monoclonal antibodies ED1 and ED3. It is suggested that differences in the immunophenotype of resident brain macrophage precursor cells, i.e. microglia and perivascular cells, and macrophages occurring outside the central nervous system (CNS) may be explained by differences in local macrophage antigen expression rather than by a different embryological lineage. The new appearance of antigens common to peripheral macrophages on neural phagocytes in CNS lesions may therefore not necessarily imply that most or all of these cells are of recent blood origin.},
	Author = {Graeber, M. B. and Streit, W. J. and Kiefer, R. and Schoen, S. W. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {T-Lymphocytes;Animals;Ricin;Macrophages;Rats;Brain;Rats, Inbred Strains;Doxorubicin;Not relevant;11 Glia;Male;Blood-Brain Barrier;Antigens;Antibodies, Monoclonal;Neuroglia;Motor Neurons;Microscopy, Electron;Stem Cells},
	Medline = {90237177},
	Month = {5},
	Nlm_Id = {8109498},
	Number = {2-3},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, F.R.G.},
	Pages = {121-32},
	Pubmed = {2332482},
	Title = {New expression of myelomonocytic antigens by microglia and perivascular cells following lethal motor neuron injury},
	Uuid = {F636D1D7-2C50-4460-9353-140C75A975EC},
	Volume = {27},
	Year = {1990}}

@article{Graeber:1992,
	Abstract = {The expression of major histocompatibility complex (MHC) class I and II antigens was studied in surgical and postmortem brain biopsy tissue using light and electron microscopic immunocytochemistry. In addition, monoclonal antibodies directed against human macrophages (EBM11) and alpha-smooth muscle actin were applied. It is shown that blood vessel-associated MHC class II immunoreactivity in histologically normal human brain can be localized to a distinct class of cells, termed perivascular cells, which share macrophage but not smooth muscle cell antigen. This immunophenotype, the location in the perivascular space as well as the morphology, frequency and tissue distribution distinguish perivascular cells from pericytes and intraparenchymal microglia. It is suggested that MHC class II positive perivascular cells are a normal constituent of the human cerebral microvasculature. The potential role of these cells in immunological reactions occurring at the blood-brain interface is discussed.},
	Author = {Graeber, M. B. and Streit, W. J. and B{\"u}ringer, D. and Sparks, D. L. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Reference Values;Neuroglia;Research Support, Non-U.S. Gov't;Human;Immunohistochemistry;Histocompatibility Antigens Class II;Microscopy, Electron;Meninges;Antibodies, Monoclonal;11 Glia;Cerebrovascular Circulation;Not relevant;Humans;Support, Non-U.S. Gov't;Brain},
	Medline = {92260276},
	Month = {5},
	Nlm_Id = {2985192R},
	Number = {3},
	Organization = {Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts.},
	Pages = {303-11},
	Pubmed = {1583535},
	Title = {Ultrastructural location of major histocompatibility complex (MHC) class II positive perivascular cells in histologically normal human brain},
	Uuid = {3F0C3357-D672-41CF-92DE-93267C2B0E36},
	Volume = {51},
	Year = {1992}}

@article{Graeber:1988a,
	Abstract = {Axotomy of the rat facial nerve leads to mitotic divisions of microglial cells without developing into phagocytes. In order to study the functional characteristics of those activated, i.e., proliferating but nonphagocytic, microglia we investigated the expression of monocyte/macrophage antigens by these cells. Our results show that activated microglia lack monocyte/macrophage antigens recognized by the monoclonal antibodies Ox-41, ED1, ED2, and Ki-M2R but express high levels of CR3 complement receptors in situ.},
	Author = {Graeber, M. B. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Complement Activation;Receptors, Complement;Neuroglia;Facial Nerve;Rats;Antibodies, Monoclonal;Not relevant;11 Glia;Macrophages;Animals;Male;Rats, Inbred Strains},
	Medline = {89111061},
	Month = {9},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, Federal Republic of Germany.},
	Pages = {18-24},
	Pubmed = {3216409},
	Title = {Axotomy of the rat facial nerve leads to increased CR3 complement receptor expression by activated microglial cells},
	Uuid = {B19EB1D1-CC18-46F7-95F9-10C7F5183659},
	Volume = {21},
	Year = {1988}}

@article{Graeber:1989a,
	Abstract = {A controversial, though fundamental, issue in neurobiology concerns the nature, origin, and function of brain macrophages. By immunocytochemical analysis using monoclonal antibodies directed against rat macrophage antigens, i.e., ED1-3, Ox-41, Ox-42, and Ki-M2R, we show that a group of perivascular cells located within the basal membrane of CNS blood vessels are immunoreactive. These cells, which resemble pericytes in terms of their anatomical distribution, are distinct from resting parenchymal microglia immunologically as well as morphologically. Our results demonstrate considerable heterogeneity in the immunophenotype of resident brain macrophages, which may be part of the immune-nervous system interface.},
	Author = {Graeber, M. B. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Immunohistochemistry;Rats;Antibodies, Monoclonal;Get paper from library;Not relevant;11 Glia;Cerebrovascular Circulation;Macrophages;Blood Vessels;Animals;Brain;Rats, Inbred Strains;Male},
	Medline = {89178769},
	Month = {1},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuromorphology, Max Planck Institute for Psychiatry, Martinsried, Federal Republic of Germany.},
	Pages = {103-6},
	Pubmed = {2926837},
	Title = {Identity of ED2-positive perivascular cells in rat brain},
	Uuid = {2968D13D-5D96-4297-BBC2-46E050E54C05},
	Volume = {22},
	Year = {1989}}

@article{Graeber:1994,
	Author = {Graeber, M. B. and Bise, K. and Mehraein, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {letter;Research Support, Non-U.S. Gov't;Genes, MHC Class II;Immunohistochemistry;Antibodies, Monoclonal;Biological Markers;11 Glia;Microglia;Humans;Nervous System Diseases},
	Medline = {95107467},
	Month = {8},
	Nlm_Id = {7609829},
	Number = {4},
	Pages = {406-8},
	Pubmed = {7808591},
	Title = {CR3/43, a marker for activated human microglia: application to diagnostic neuropathology},
	Uuid = {300AF937-DD52-4AEB-A08D-386544A47FE5},
	Volume = {20},
	Year = {1994}}

@article{Graeber:1994a,
	Author = {Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Bibliography;11 Glia;Microglia;MEDLINE;Publishing},
	Medline = {94352553},
	Month = {4},
	Nlm_Id = {7609829},
	Number = {2},
	Organization = {Molecular Neuropathology Laboratory, Ludwig-Maximilians-University, Munich.},
	Pages = {215-6},
	Pubmed = {8072671},
	Title = {Development of the microglia literature},
	Uuid = {C823B66A-486A-4225-84CE-14A4FA1C12A8},
	Volume = {20},
	Year = {1994}}

@article{Graeber:1994b,
	Author = {Graeber, M. B. and Mehraein, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Pyramidal Cells;11 Glia;Microglia;Animals;Humans;Cerebral Cortex;Nervous System Diseases},
	Medline = {94352529},
	Month = {4},
	Nlm_Id = {7609829},
	Number = {2},
	Organization = {Institute of Neuropathology, Ludwig-Maximilians-University, Munich.},
	Pages = {178-80},
	Pubmed = {8072649},
	Title = {Microglial rod cells},
	Uuid = {35B5680B-0D78-44A8-A7DA-7B6D83B78FE5},
	Volume = {20},
	Year = {1994}}

@article{Graeber:1989b,
	Abstract = {Five monoclonal antibodies specific for rat monocytes/macrophages were used to characterize macrophages/microglia bulk isolated from neonatal and adult rat brain. The majority of brain macrophages was positive for all antibodies tested with minor differences between cultures derived from developing and mature central nervous tissue. These results contrast in vivo findings indicating that most antigens of peripheral macrophages are absent from resting, activated and phagocytic microglia in situ. We conclude that brain macrophages/microglia newly express antigens of the myelomonocytic lineage when in culture and that cultured brain macrophages may be derived from different types of precursor cells normally present within the CNS.},
	Author = {Graeber, M. B. and Banati, R. B. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Monocytes;Rats;Phenotype;Antibodies, Monoclonal;Comparative Study;Not relevant;Antigens, Surface;11 Glia;Macrophages;Immunoenzyme Techniques;Animals;Cells, Cultured;Brain;Age Factors},
	Medline = {90045041},
	Month = {9},
	Nlm_Id = {7600130},
	Number = {3},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, F.R.G.},
	Pages = {241-6},
	Pubmed = {2682390},
	Title = {Immunophenotypic characterization of rat brain macrophages in culture},
	Uuid = {D6B5752D-FD0B-4FE7-B25B-ED53E5648261},
	Volume = {103},
	Year = {1989}}

@article{Graeber:1990c,
	Author = {Graeber, M. B. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Neuroglia;letter;Terminology;Blood-Brain Barrier;Human;Not relevant;11 Glia;comment;Humans;Brain},
	Medline = {91020405},
	Month = {9},
	Nlm_Id = {7808616},
	Number = {9},
	Pages = {366},
	Pubmed = {1699325},
	Title = {Perivascular microglia defined},
	Uuid = {9A5C5331-B860-4F0E-9407-D40EC2C66CB7},
	Volume = {13},
	Year = {1990}}

@article{Grandbarbe:2007,
	Abstract = {The Notch signaling pathway plays a crucial role in specifying cellular fate in metazoan development by regulating communication between adjacent cells. Correlative studies suggested an involvement of Notch in hematopoietic cell development. Here, we report that the Notch pathway is expressed and active in microglial cells. During inflammatory activation, the transcription of the Notch down-stream effector Hes1 is downregulated. When Notch1 transcription in microglia is inhibited, an upregulation of the expression of pro-inflammatory cytokines is observed. Notch stimulation in activated microglia, using a soluble form of its ligand Jagged1, induces a decrease in pro-inflammatory cytokines secretion and nitric oxide production as well as an increase in phagocytic activity. Notch-stimulation is accompanied by an increase in the rate of STAT3 phosphorylation and nuclear translocation. Our results show that the Notch pathway plays an important role in the control of inflammatory reactions in the CNS.},
	Author = {Grandbarbe, Luc and Michelucci, Alessandro and Heurtaux, Tony and Hemmer, Karin and Morga, Eleonora and Heuschling, Paul},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:22 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {research support, non-u.s. gov't;11 Glia;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {8806785},
	Number = {15},
	Organization = {Department of Life Sciences, University of Luxembourg, Luxembourg.},
	Pages = {1519-30},
	Pubmed = {17705199},
	Title = {Notch signaling modulates the activation of microglial cells},
	Uuid = {D083863B-CD51-4EE2-8AF7-D7A18CCFC68B},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20553}}

@article{Gravel:1993,
	Abstract = {The Cas-Br-E murine leukemia virus (MuLV) induces a progressive hindlimb paralysis accompanied by a spongiform myeloencephalopathy in susceptible mice. In order to better understand the pathological process leading to these neurodegenerative lesions, we have investigated the nature of the cell type(s) infected by the virus during the course of the disease in CFW/D and SWR/J mice. For this purpose, we used in situ hybridization with virus-specific probes in combination with cell-type-specific histochemical (lectin) and immunological markers as well as morphological assessment. In the early stage of infection, endothelial cells represented the main cell type expressing viral RNA in the central nervous system (CNS). With disease progression and the appearance of lesions, microglial cells became the major cell type infected, accounting for up to 65\%of the total infected cell population in diseased areas. Morphologically, these cells appeared activated and were frequently found in clusters. Infection and activation of microglial cells were almost exclusively restricted to diseased regions of the CNS. Neurons in diseased regions were not discernibly infected with virus at either early or late times of disease progression. Similarly, the proportion of infected astrocytes was typically <1\%. Although some endothelial cells and oligodendrocytes were infected by the virus, their infection was not limited to diseased CNS regions. These results are consistent with a model of indirect motor neuron degeneration, subsequent to the infection of nonneuronal CNS cells and especially of microglial cells. Infected microglial cells may play a role in the disease process by releasing not only virions or viral env-gene-encoded gp70 proteins but also other factors which may be directly or indirectly toxic to neurons. Parallels between microglial cell infection by MuLV and by lentiviruses, and specifically by human immunodeficiency virus, are discussed.},
	Author = {Gravel, C. and Kay, D. G. and Jolicoeur, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {In Situ Hybridization;Neurons;Mice, Inbred Strains;Oligodendroglia;Central Nervous System;Nerve Degeneration;Astrocytes;Endothelium;Not relevant;11 Glia;Microglia;Paralysis;Animals;Mice;Leukemia Virus, Murine;Prion Diseases;Support, Non-U.S. Gov't},
	Medline = {94016849},
	Month = {11},
	Nlm_Id = {0113724},
	Number = {11},
	Organization = {Laboratory of Molecular Biology, Institut de Recherches Cliniques de Montr{\'e}al, Quebec, Canada.},
	Pages = {6648-58},
	Pubmed = {8411367},
	Title = {Identification of the infected target cell type in spongiform myeloencephalopathy induced by the neurotropic Cas-Br-E murine leukemia virus},
	Uuid = {175F8E91-1868-421A-8480-DCC349AA0A15},
	Volume = {67},
	Year = {1993}}

@article{Gray:1998,
	Abstract = {Granule cell progenitors in the dentate gyrus of the hippocampal formation have the unusual capacity to be able to divide in the brains of adult rats and primates. The basal proliferation rate of granule cell progenitors in the adult rat is low compared with development, however, it is possible that this rate may become significantly altered under pathological conditions such as epilepsy. We have investigated whether the proliferation of granule cell progenitors is increased in adult rats in a model of temporal lobe epilepsy, by using systemic bromodeoxyuridine injections to label dividing cells. We report here for the first time that granule cell neurogenesis is increased bilaterally 1 week after a single unilateral intracerebroventricular injection of kainic acid. Bromodeoxyuridine labeled neurons increased at least 6-fold on the side ipsilateral to the kainic acid injection compared to controls, but significantly, were also increased, by at least 3-fold on the side contralateral to the injection. The dividing cells in the subgranular zone were identified as neurons since they expressed Class III beta tubulin but not glial fibrillary acidic protein.},
	Author = {Gray, W. P. and Sundstrom, L. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Brain Res},
	Keywords = {Kainic Acid/*pharmacology;Rats;Neurons/*cytology;Fluorescent Antibody Technique;Excitatory Amino Acid Agonists/*pharmacology;Animal;Neuroglia/chemistry;Glial Fibrillary Acidic Protein/analysis;Dentate Gyrus/*cytology/drug effects;Cell Count;Rats, Wistar;Stem Cells/*cytology;Antimetabolites;Male;Injections, Intraventricular;Support, Non-U.S. Gov't;D-8;06 Adult neurogenesis injury induced;Epilepsy/chemically induced/physiopathology;Bromodeoxyuridine;Cell Division/drug effects},
	Number = {1-2},
	Organization = {Department of Clinical Neurosciences, University of Southampton, Tremona Rd., Southampton SO16 6YD, UK.},
	Pages = {52-9.},
	Title = {Kainic acid increases the proliferation of granule cell progenitors in the dentate gyrus of the adult rat},
	Uuid = {A1B511F1-1FFE-485A-B5EC-7D8A50459DB1},
	Volume = {790},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9593820%20http://www.elsevier.com:80/cgi-bin/cas/tree/store/bres/cas_sub/browse/browse.cgi?year=1998&volume=790&issue=1-2&aid=14397}}

@article{Green:2000,
	Author = {Green, D. R. and Beere, H. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Nature},
	Keywords = {07 Excitotoxicity Apoptosis;Human;Dendritic Cells/physiology;*Apoptosis;Phosphatidylserines/physiology;Histocompatibility Antigens Class I/physiology;Macrophages/*physiology;Receptors, Cell Surface/*physiology;Necrosis;E-12;T-Lymphocytes/physiology;Phagocytosis;Major Histocompatibility Complex;Self Tolerance},
	Number = {6782},
	Pages = {28-9.},
	Title = {Apoptosis. Gone but not forgotten},
	Uuid = {3018653F-A538-4EA1-8BDC-A2091B4F65D2},
	Volume = {405},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10811203}}

@article{Green:2006,
	Abstract = {To prevent duplication or loss of genomic regions during DNA replication, it is essential that the entire genome is copied precisely once every S phase. Cells achieve this by mutually exclusive regulation of origin firing and licensing. A crucial protein that is involved in origin licensing is chromatin licensing and DNA replication factor 1 (CDT1) and, therefore, activity of this protein must be strictly controlled. Four recent articles have demonstrated that proliferating cell nuclear antigen (PCNA), an essential sliding clamp used in replication and DNA repair, has a crucial role in this process by mediating the proteasomal degradation of CDT1.},
	Author = {Green, Catherine M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1471-4914},
	Journal = {Trends Mol Med},
	Keywords = {Models, Biological;DNA-Binding Proteins;Cell Cycle Proteins;DNA Damage;Xenopus Proteins;Proteasome Endopeptidase Complex;Proliferating Cell Nuclear Antigen;Cell Cycle;Animals;Humans;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {100966035},
	Number = {10},
	Organization = {Genome Damage and Stability Centre, University of Sussex, Brighton, BN19RQ, UK. c.m.green\@sussex.ac.uk},
	Pages = {455-8},
	Pii = {S1471-4914(06)00173-0},
	Pubmed = {16931160},
	Title = {One ring to rule them all? Another cellular responsibility for PCNA},
	Uuid = {A1C10A2F-941E-4D81-9EB7-164317B0DF2E},
	Volume = {12},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.molmed.2006.08.004}}

@article{Greenberger:1980,
	Abstract = {Infection in vitro of freshly explanted N:NIH(S) mouse bone marrow with ectopic murine leukemia viruses produced an increase over control uninfected cultures in the 50 or more cell granulocyte-macrophage (GM) colonies and 10-49 cell clusters detected after 7 days of incubation in 0.3\%agar at 37 degrees C and 7\%CO2. This effect was observed only at plating densities above 5.0 X 10(4) cells/ml and was not observed with macrophage-depleted populations of colony-forming units of GM progenitor cells (GM-CFUc) purified by isopyknic density gradient centrifugation of nonadherent cells harvested from long-term bone marrow cultures. Fewer virus-infected, compared to uninfected, peritoneal exudate macrophages were required to stimulate the same number of GM colonies and clusters in a given number of purified GM-CFUc. In contrast, murine leukemia virus infection of T-lymphocytes or NIH/3T3 embryo fibroblasts did not stimulate release of GM-CFUc coloney-stimulating factor (CSF). Single Cell suspensions of virus-infected freshly explanted whole bone marrow grown in CSF concentrated from L929 or WEHI-3 cell-conditioned medium produced more GM-CFUc colonies and GM clusters/1 X 10(5) cells compared to single cell suspensions of uninfected marrow. This phenomenon suggests that the colonoy-forming cells responding to CSF from virus-infected marrow may have been different from those responding to L929 or WEHI-3 cell CSF. The data indicate that increased granulopoiesis observed following retrovirus infection in vivo or in long-term marrow cultures was attributable in part to virus stimulation of production of CSF by adherent marrow stromal cells including macrophages.},
	Author = {Greenberger, J. S. and Wroble, L. M. and Sakakeeny, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0027-8874},
	Journal = {J Natl Cancer Inst},
	Keywords = {15 Retrovirus mechanism;24 Pubmed search results 2008;Mice, Inbred BALB C;Bone Marrow;L Cells (Cell Line);Research Support, U.S. Gov't, P.H.S.;Granulocytes;Mice, Inbred C57BL;Colony-Forming Units Assay;Macrophages;Colony-Stimulating Factors;Tumor Virus Infections;Cells, Cultured;Animals;Leukemia Virus, Murine;Mice, Nude;Mice},
	Medline = {81028739},
	Month = {10},
	Nlm_Id = {7503089},
	Number = {4},
	Pages = {841-51},
	Pubmed = {6252364},
	Title = {Murine leukemia viruses: induction of macrophage production of granulocyte-macrophage colony-stimulating factor in vitro},
	Uuid = {6694A74B-4328-11DB-A5D2-000D9346EC2A},
	Volume = {65},
	Year = {1980}}

@article{Gregg:2003,
	Abstract = {Radial glial cells (RGCs), a transient cell population present only in the developing CNS, function both as precursor cells and as scaffolds to support neuron migration. Their cellular origin, however, is not understood. In the present study, we tested the hypothesis that functional RGCs can be generated by multipotent neural stem cells. Embryonic forebrain neural stem cells were studied in vitro to identify putative signals that promote the generation and differentiation of functional RGCs, determined by their ability to support neuronal migration. Epidermal growth factor receptor signaling was sufficient to regulate both the generation and differentiation of morphologically, antigenically, and functionally defined RGCs. In contrast, fibroblast growth factor-2 promoted the generation of RGCs but was unable to support their differentiation. Although RGCs are not normally present in the adult brain, epidermal growth factor stimulated adult forebrain neural stem cells to generate RGCs in vitro and functional RGCs within the adult forebrain subependyma in vivo. Surprisingly, epidermal growth factor receptor signaling also promoted adult forebrain ependymal cells to dedifferentiate and adopt a radial morphology in vivo. These results suggest that neural stem cells can give rise to RGCs and that RGC-guided neuronal migration can be recapitulated in the adult CNS. 1529-2401 Journal Article},
	Author = {Gregg, C. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Neurosci},
	Keywords = {Ependyma/cytology;Cell Differentiation;Animals;Cells, Cultured;Neuroglia/*cytology/physiology;Central Nervous System/cytology;Cell Movement;Receptor, Epidermal Growth Factor/metabolism;Male;Microscopy, Fluorescence;Stem Cells/cytology/drug effects/*physiology;Epidermal Growth Factor/pharmacology;Prosencephalon/*cytology/*embryology;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Fibroblast Growth Factor 2/pharmacology;Mice;C pdf},
	Number = {37},
	Organization = {Genes &Development Research Group, University of Calgary, Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1.},
	Pages = {11587-601},
	Pubmed = {14684861},
	Title = {Generation of functional radial glial cells by embryonic and adult forebrain neural stem cells},
	Uuid = {296B85F4-CE6D-4DC7-923D-73812A90B495},
	Volume = {23},
	Year = {2003},
	url = {papers/Gregg_JNeurosci2003.pdf}}

@article{Gressens:1992,
	Abstract = {The origin of astrocytes of the mouse neocortex during the fetal and early postnatal periods as determined by immunocytological, autoradiographic, electron microscopic and antimitotic methods is described. Most astrocytes destined for the white matter and the infragranular cortical layers are derived from the transformation of radial glial cells between P0 and P10 with an inside-out pattern. This cell metamorphosis is not directly preceded by mitosis and involves the activation of the radial glial lysosomal apparatus. In opposition to recent hypotheses, our findings suggest that most astrocytes destined for the supragranular cortical layers are produced in the germinative zone after the migration of the infragranular neurons and themselves migrate afterwards to the upper cortex between E16 and the first postnatal days. These astrocytes do not display an intermediate stage of the radial glial cell and do not participate in the pattern of appearance of the deeper astrocytes. This second step of astrocytogenesis is a condition for normal cytoarchitectonic development and the maintenance of the supragranular layers, since the deprivation of the astrocytic equipment of the supragranular layers by an antimitotic drug drastically reduces the number of supragranular neurons. Using Smart Source Parsing},
	Author = {Gressens, P. and Richelme, C. and Kadhim, H. J. and Gadisseux, J. F. and Evrard, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Biol Neonate},
	Keywords = {G;Pregnancy;Thymidine/metabolism;Cell Movement/*physiology;Female;Animal;Glial Fibrillary Acidic Protein/analysis;Astrocytes/chemistry/*physiology/ultrastructure;Staining and Labeling;11 Glia;Support, Non-U.S. Gov't;Methylazoxymethanol Acetate;Mice;Cell Differentiation/physiology;Neurons/chemistry/*physiology/ultrastructure;Immunohistochemistry;Autoradiography;Cerebral Cortex/chemistry/*embryology/metabolism},
	Number = {1},
	Organization = {Laboratory of Developmental Neurology, University of Louvain Medical School, Brussels, Belgium.},
	Pages = {4-24},
	Title = {The germinative zone produces the most cortical astrocytes after neuronal migration in the developing mammalian brain},
	Uuid = {004D588C-F899-4A42-8E29-A5090BF12A4A},
	Volume = {61},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1373658}}

@article{Griffiths:2001,
	Abstract = {The human genome contains many endogenous retroviral sequences, and these have been suggested to play important roles in a number of physiological and pathological processes. Can the draft human genome sequences help us to define the role of these elements more closely?},
	Author = {Griffiths, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1465-6914},
	Journal = {Genome Biol},
	Keywords = {15 ERVs retroelements;Endogenous Retroviruses;Cell Fusion;Autoimmune Diseases;Gene Expression Regulation;Genome, Human;Trophoblasts;Neoplasms;15 Retrovirus mechanism;Humans;24 Pubmed search results 2008;review},
	Medline = {21316070},
	Nlm_Id = {100960660},
	Number = {6},
	Organization = {Wohl Virion Centre, Department of Immunology and Molecular Pathology, Windeyer Institute of Medical Sciences, University College London, Cleveland Street, London W1T 4JF, UK. d.j.griffiths\@ucl.ac.uk},
	Pages = {REVIEWS1017},
	Pubmed = {11423012},
	Title = {Endogenous retroviruses in the human genome sequence},
	Uuid = {833A2342-4326-11DB-A5D2-000D9346EC2A},
	Volume = {2},
	Year = {2001},
	url = {papers/Griffiths_GenomeBiol2001.pdf}}

@article{Grimpe:2004,
	Abstract = {CNS lesions induce production of ECM molecules that inhibit axon regeneration. One major inhibitory family is the chondroitin sulfate proteoglycans (CSPGs). Reduction of their glycosaminoglycan (GAG) chains with chondroitinase ABC leads to increased axon regeneration that does not extend well past the lesion. Chondroitinase ABC, however, is unable to completely digest the GAG chains from the protein core, leaving an inhibitory "stub"carbohydrate behind. We used a newly designed DNA enzyme, which targets the mRNA of a critical enzyme that initiates glycosylation of the protein backbone of PGs, xylosyltransferase-1. DNA enzyme administration to TGF-beta-stimulated astrocytes in culture reduced specific GAG chains. The same DNA enzyme applied to the injured spinal cord led to a strong reduction of the GAG chains in the lesion penumbra and allowed axons to regenerate around the core of the lesion. Our experiments demonstrate the critical role of PGs, and particularly those in the penumbra, in causing regeneration failure in the adult spinal cord. 1529-2401 Journal Article},
	Author = {Grimpe, B. and Silver, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Neurosci},
	Keywords = {G, L pdf;11 Glia},
	Number = {6},
	Organization = {Case Western Reserve University, School of Medicine, Department of Neurosciences, Cleveland, Ohio 44106, USA. bxg15\@po.cwru.edu},
	Pages = {1393-7},
	Title = {A novel DNA enzyme reduces glycosaminoglycan chains in the glial scar and allows microtransplanted dorsal root ganglia axons to regenerate beyond lesions in the spinal cord},
	Uuid = {BE5C7373-FDE5-4FF4-A7A1-BCF3A2FA0878},
	Volume = {24},
	Year = {2004},
	url = {papers/Grimpe_JNeurosci2004.pdf}}

@article{Gripon:1988,
	Abstract = {We investigated the possibility of infecting normal adult human hepatocytes maintained in pure cultures or in cocultures with hepatitis B virus (HBV). Several assays with different infectious sera and hepatocyte populations from various donors identified only limited HBV replication, with significant variations from one cell preparation to another. The addition of 1.5\%dimethyl sulfoxide to the culture medium markedly enhanced the infection process. Indeed, hepatitis B e antigen secretion, the appearance of both HBV DNA replicative forms and major HBV transcripts, and the release of complete HBV particles into the medium were demonstrated. It is possible that the significant increase in intracellular HBV DNA in dimethyl sulfoxide-treated cells was related to enhanced adsorption of the virus. When viral particles produced by a transfected HepG2 cell line were used to infect normal hepatocytes, the same results were obtained. In addition, comparative assays with hepatocytes from three different donors showed that although high amounts of intracellular viral DNA were found in all cases, viral replicative intermediates were visualized in only one case. These findings suggest that this HBV-producing cell line could serve as a reproducible source of infectious virus and that primary culturing of human hepatocytes represents a unique tool for analyzing intracellular regulating factors which, in addition to the penetration step, modulate HBV replication. 0022-538x Journal Article},
	Author = {Gripon, P. and Diot, C. and Theze, N. and Fourel, I. and Loreal, O. and Brechot, C. and Guguen-Guillouzo, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {J Virol},
	Keywords = {RNA, Viral/analysis/biosynthesis;Human;Cell Survival/drug effects;Liver/cytology/*microbiology;Hepatitis B Virus/drug effects/*growth &development;Cells, Cultured;Transfection;Virion/isolation &purification/pathogenicity;Centrifugation, Density Gradient;Kinetics;EE, DMSO, abstr;08 Aberrant cell cycle;Immunoblotting;Support, Non-U.S. Gov't;Culture Media/analysis/pharmacology;Virus Cultivation/*methods;Dimethyl Sulfoxide/*pharmacology;DNA, Viral/analysis/biosynthesis;Hepatitis B Surface Antigens/biosynthesis;Hepatitis B e Antigens/biosynthesis},
	Number = {11},
	Organization = {INSERM Unite 49, Hopital de Pontchaillou, Rennes, France.},
	Pages = {4136-43},
	Pubmed = {3172341},
	Title = {Hepatitis B virus infection of adult human hepatocytes cultured in the presence of dimethyl sulfoxide},
	Uuid = {AB479F47-4284-452F-A2AF-2B423292A201},
	Volume = {62},
	Year = {1988},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3172341}}

@article{Gritti:1996,
	Abstract = {It has been established that the adult mouse forebrain contains multipotential (neuronal/glial) progenitor cells that can be induced to proliferate in vitro when epidermal growth factor is provided. These cells are found within the subventricular zone of the lateral ventricles, together with other progenitor cell populations, whose requirements for proliferation remain undefined. Using basic fibroblast growth factor (bFGF), we have isolated multipotential progenitors from adult mouse striatum. These progenitors proliferate and can differentiate into cells displaying the antigenic properties of astrocytes, oligodendrocytes, and neurons. The neuron-like cells possess neuronal features, exhibit neuronal electrophysiological properties, and are immunoreactive for GABA, substance P, choline acetyl-transferase, and glutamate. Clonal analysis confirmed the multipotency of these bFGF-dependent cells. Most significantly, subcloning experiments demonstrated that they were capable of self-renewal, which led to a progressive increase in population size over serial passaging. These results demonstrate that bFGF is mitogenic for multipotential cells from adult mammalian forebrain that possess stem cell properties. 0270-6474 Journal Article},
	Author = {Gritti, A. and Parati, E. A. and Cova, L. and Frolichsthal, P. and Galli, R. and Wanke, E. and Faravelli, L. and Morassutti, D. J. and Roisen, F. and Nickel, D. D. and Vescovi, A. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation/drug effects;Animals;Cells, Cultured;Stem Cells/cytology/*drug effects;Phenotype;Corpus Striatum/*cytology;C abstr;Support, Non-U.S. Gov't;Action Potentials;Cell Lineage;Neurotransmitters/metabolism;04 Adult neurogenesis factors;Neurons/cytology;Mice;Fibroblast Growth Factor 2/*pharmacology;Clone Cells;Biological Markers;Cell Division/drug effects;Neuroglia/cytology},
	Number = {3},
	Organization = {Laboratory of Cellular Neuropharmacology, National Neurological Institute C, Milan, Italy.},
	Pages = {1091-100},
	Pubmed = {8558238},
	Title = {Multipotential stem cells from the adult mouse brain proliferate and self-renew in response to basic fibroblast growth factor},
	Uuid = {D7078ABD-51BF-415B-B562-91C1FE08F6B8},
	Volume = {16},
	Year = {1996},
	url = {papers/Gritti_JNeurosci1996}}

@article{Gritti:1999,
	Abstract = {The subventricular zone (SVZ) of the adult mammalian forebrain contains kinetically distinct precursor populations that contribute new neurons to the olfactory bulb. Because among forebrain precursors there are stem-like cells that can be cultured in the presence of mitogens such as epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF2), we asked whether distinct subsets of stem-like cells coexist within the SVZ or whether the proliferation of a single type of SVZ stem-like cell is controlled by several GFs. We show that the latter is the case. Thus cells isolated from the SVZ coexpress the EGF and FGF receptors; by quantitative analysis, the number of stem-like cells isolated from the SVZ by either FGF2 or EGF is the same, whereas no additive effect occurs when these factors are used together. Furthermore, short-term administration of high-dose [3H]thymidine in vivo depletes both the EGF- and FGF2-responsive stem-like cell populations equally, showing they possess closely similar proliferation kinetics and likely belong to the constitutively proliferating SVZ compartment. By subcloning and population analysis, we demonstrate that responsiveness to more than one GF endows SVZ cells with an essential stem cell feature, the ability to vary self-renewal, that was until now undocumented in CNS stem-like cells. The multipotent stem cell-like population that expands slowly in the presence of FGF2 in culture switches to a faster growth mode when exposed to EGF alone and expands even faster when exposed to both GFs together. Analogous responses are observed when the GFs are used in the reverse order, and furthermore, these growth rate modifications are fully reversible. 0270-6474 Journal Article},
	Author = {Gritti, A. and Frolichsthal-Schoeller, P. and Galli, R. and Parati, E. A. and Cova, L. and Pagano, S. F. and Bjornson, C. R. and Vescovi, A. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Neurons/*cytology/drug effects/*physiology;Animals;Cells, Cultured;Stem Cells/*cytology/drug effects/physiology;C abstr;Kinetics;Fibroblast Growth Factor 2/*pharmacology/physiology;Receptor, Epidermal Growth Factor/*genetics/physiology;Receptor Protein-Tyrosine Kinases/*genetics/physiology;Corpus Striatum/cytology/physiology;Reverse Transcriptase Polymerase Chain Reaction;Support, Non-U.S. Gov't;Receptors, Fibroblast Growth Factor/*genetics/physiology;04 Adult neurogenesis factors;Mice;Epidermal Growth Factor/*pharmacology/physiology;Prosencephalon/*cytology/physiology;Cell Division/drug effects},
	Number = {9},
	Organization = {Laboratory of Neuropharmacology, National Neurological Institute C. Besta, Milan, Italy I-20133.},
	Pages = {3287-97},
	Pubmed = {10212288},
	Title = {Epidermal and fibroblast growth factors behave as mitogenic regulators for a single multipotent stem cell-like population from the subventricular region of the adult mouse forebrain},
	Uuid = {2F6D025D-5D42-46DF-A16E-0FD899702507},
	Volume = {19},
	Year = {1999},
	url = {papers/Gritti_JNeurosci1999.pdf}}

@article{Gritti:2002,
	Abstract = {The lateral walls of the forebrain lateral ventricles are the richest source of stem cells in the adult mammalian brain. These stem cells give rise to new olfactory neurons that are renewed throughout life. The neurons originate in the subventricular zone (SVZ), migrate within the rostral extension (RE) of the SVZ along the rostral migratory stream (RMS) within tube-like structures formed of glial cells, to eventually reach the olfactory bulb (OB). We demonstrate that, contrary to the current view, multipotential (neuronal-astroglial-oligodendroglial) precursors with stem cell features can be isolated not only from the SVZ but also from the entire RE, including the distal portion within the OB. Specifically, these stem cells do not derive from the migratory neuroblasts coming from the SVZ. Interestingly, stem cells isolated from the proximal RE generate significantly more oligodendrocytes, and those from the distal RE proliferate significantly more slowly than stem cells derived from the SVZ and other RE regions. These findings demonstrate that stem cells are not confined to the forebrain periventricular region and indicate that stem cells endowed with different functional characteristics occur at different levels of the SVZ-RE pathway. 1529-2401 Journal Article},
	Author = {Gritti, A. and Bonfanti, L. and Doetsch, F. and Caille, I. and Alvarez-Buylla, A. and Lim, D. A. and Galli, R. and Verdugo, J. M. and Herrera, D. G. and Vescovi, A. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Neurosci},
	Keywords = {Oligodendroglia/cytology;Animals;Cell Separation;Cells, Cultured;Olfactory Bulb/*cytology;Phenotype;Spheroids, Cellular/cytology;02 Adult neurogenesis migration;Neurons/classification/*cytology/metabolism;Time Factors;Cell Line/cytology;03 Adult neurogenesis progenitor source;BB pdf;Stem Cells/classification/*cytology/drug effects;Support, Non-U.S. Gov't;Clone Cells/classification/cytology/drug effects;Growth Substances/pharmacology;Lateral Ventricles/cytology;Neurotransmitters/metabolism;Cell Movement/physiology;Mice;Cell Culture/methods;Cell Differentiation/physiology;Cell Division/drug effects;Astrocytes/cytology},
	Number = {2},
	Organization = {Institute for Stem Cell Research, Department of Biotechnology, San Raffaele Hospital, 20132 Milan, Italy. gritti.angela\@hsr.it.},
	Pages = {437-45},
	Title = {Multipotent neural stem cells reside into the rostral extension and olfactory bulb of adult rodents},
	Uuid = {16268DDD-46C4-4257-AF20-F95217DD02BF},
	Volume = {22},
	Year = {2002},
	url = {papers/Gritti_JNeurosci2002.pdf}}

@article{Gritti:1995,
	Abstract = {Stem cells isolated from the CNS of both embryonic and adult mice undergo extensive proliferation in the presence of epidermal growth factor (EGF). Removal of EGF determines the differentiation of these cells into neurons and glia. We have recently demonstrated that basic fibroblast growth factor (bFGF) regulates the proliferation of EGF-generated progenitors of the embryonic mouse striatum. We report here that bFGF induces proliferation of some EGF-generated precursors of the adult mouse striatum which, in turn, differentiate in vitro into cells possessing neuron-like morphology and neuronal antigenic properties. These results demonstrate that EGF and bFGF can act sequentially to regulate the de novo generation of neurons from the adult mouse CNS in vitro and suggest the existence of a lineage relationship between EGF- and bFGF-responsive progenitor cells of the adult murine brain. 0304-3940 Journal Article},
	Author = {Gritti, A. and Cova, L. and Parati, E. A. and Galli, R. and Vescovi, A. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {Neurosci Lett},
	Keywords = {Stem Cells/*physiology;Fibroblast Growth Factor 2/*pharmacology;Epidermal Growth Factor/*physiology;Corpus Striatum;Cell Division;04 Adult neurogenesis factors;Support, Non-U.S. Gov't;Animals;Mice;C abstr;Central Nervous System/physiology},
	Number = {3},
	Organization = {Laboratory of Cellular Neuropharmacology, National Neurological Institute C. Besta, Milan, Italy.},
	Pages = {151-4},
	Pubmed = {7753479},
	Title = {Basic fibroblast growth factor supports the proliferation of epidermal growth factor-generated neuronal precursor cells of the adult mouse CNS},
	Uuid = {F6FDEAC7-42AC-4FE9-B6BE-807A6517D0A5},
	Volume = {185},
	Year = {1995},
	url = {papers/Gritti_NeurosciLett1995.pdf}}

@article{Gross:1996,
	Abstract = {The epigenetic signals that regulate lineage development in the embryonic mammalian brain are poorly understood. Here we demonstrate that a specific subclass of the transforming growth factor beta superfamily, the bone morphogenetic proteins (BMPs), cause the selective, dose-dependent elaboration of the astroglial lineage from murine embryonic subventricular zone (SVZ) multipotent progenitor cells. The astroglial inductive effect is characterized by enhanced morphological complexity and expression of glial fibrillary acidic protein, with concurrent suppression of neuronal and oligodendroglial cell fates. SVZ progenitor cells express transcripts for the appropriate BMP-specific type I and II receptor subunits and selective BMP ligands, suggesting the presence of paracrine or autocrine developmental signaling pathways (or both). These observations suggest that the BMPs have a selective role in determining the cell fate of SVZ multipotent progenitor cells or their more developmentally restricted progeny. 0896-6273 Journal Article},
	Author = {Gross, R. E. and Mehler, M. F. and Mabie, P. C. and Zang, Z. and Santschi, L. and Kessler, J. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neuron},
	Keywords = {Cell Differentiation/drug effects;Signal Transduction;Corpus Striatum/*cytology/embryology;Animals;Cells, Cultured;*Receptors, Growth Factor;Neurons/*cytology;Receptors, Cell Surface/*physiology;Astrocytes/*cytology/drug effects/physiology;Oligodendroglia/drug effects;Kinetics;Mammals;Bone Morphogenetic Proteins/*pharmacology;C abstr;Stem Cells/*cytology/drug effects;Glial Fibrillary Acidic Protein/analysis;Embryo;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice;Biological Markers},
	Number = {4},
	Organization = {Department of Neurology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.},
	Pages = {595-606},
	Pubmed = {8893018},
	Title = {Bone morphogenetic proteins promote astroglial lineage commitment by mammalian subventricular zone progenitor cells},
	Uuid = {F67C532E-66B1-49B3-890D-7D5704345015},
	Volume = {17},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8893018}}

@article{Grossmann:2002,
	Abstract = {Some parenchymal microglia in mammalian brain tissues, termed "juxtavascular microglia," directly contact the basal lamina of blood vessels; however, the functional consequences of this unique structural relationship are unknown. Here we used a rat brain slice model of traumatic brain injury to investigate the dynamic behavior of juxtavascular microglia following activation. Juxtavascular microglia were identified by confocal 3D reconstruction in tissue slices stained with a fluorescent lectin (FITC-IB4) that labels both microglia and blood vessel endothelial cells. Immunolabeling confirmed that juxtavascular cells were true parenchymal microglia (OX42+, ED2-) and not perivascular cells or pericytes. Time-lapse imaging in live tissue slices revealed that activating juxtavascular microglia withdraw most extant branches but often maintain contact with blood vessels, usually moving to the surface of a vessel within 1-4 h. Subsequently, some microglia migrate along the parenchymal surface of vessels, moving at rates up to 40 microm/h. Activated juxtavascular microglia sometimes repeatedly extend veil-like protrusions into the surrounding tissue, consistent with a role in tissue surveillance. Juxtavascular cells were twice as likely as nonjuxtavascular cells to be locomotory by 10 h in vitro, suggesting an enhanced activation response. Moreover, 38\%of all juxtavascular cells migrated along a vessel, whereas this was never observed for a nonjuxtavascular cell. These observations identify a mobile subpopulation (10\%-30\%) of parenchymal microglia that activate rapidly and are preferentially recruited to the surfaces of blood vessels following brain tissue injury. The dynamic and sustained interaction of microglia with brain microvessels may facilitate signaling between injured brain parenchyma and components of the blood-brain barrier or circulating immune cells of the blood in vivo.},
	Author = {Grossmann, Ruth and Stence, Nick and Carr, Jenny and Fuller, Leah and Waite, Marc and Dailey, Michael E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Fluorescent Dyes;Microscopy, Video;Research Support, Non-U.S. Gov't;Animals;Aging;Rats;Microscopy, Confocal;Fluorescent Antibody Technique;Brain;Microglia;Immunologic Surveillance;Rats, Sprague-Dawley;Hippocampus;Cell Movement;Not relevant;11 Glia;Time Factors;Organ Culture Techniques;Brain Injuries;Support, Non-U.S. Gov't;Gliosis;Organ Culture;Blood Vessels},
	Medline = {21846133},
	Month = {3},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA.},
	Pages = {229-40},
	Pii = {10.1002/glia.10031},
	Pubmed = {11857681},
	Title = {Juxtavascular microglia migrate along brain microvessels following activation during early postnatal development},
	Uuid = {9AE3B6B7-AD70-428B-BDE6-55C4611891AC},
	Volume = {37},
	Year = {2002},
	url = {papers/Grossmann_Glia2002.pdf}}

@article{Grove:2002,
	Abstract = {Gene therapy application to pulmonary airways and alveolar spaces holds tremendous promise for the treatment of lung diseases. However, safe and effective long-term gene expression using viral and nonviral vectors has not yet been achieved. Adenoviral vectors, with a natural affinity for airway epithelia, have been partially effective, but are inflammatory and induce only transient gene expression. We investigate the novel approach of using retrovirally transduced multipotent bone marrow-derived stem cells (BMSC) to deliver gene therapy to lung epithelium. We have shown previously that up to 20\%of lung epithelial cells can be derived from marrow following BMSC transplantation. Here, irradiated female mice were transplanted with male marrow that had been transduced with retrovirus encoding eGFP. Transgene expressing lung epithelial cells were present in all recipients analyzed at 2, 5, or 11 mo after transplant (n = 10), demonstrating that highly plastic BMSC can be stably transduced in vitro and retain their ability to differentiate into lung epithelium while maintaining long-term transgene expression.},
	Author = {Grove, Joanna E. and Lutzko, Carolyn and Priller, Josef and Henegariu, Octavian and Theise, Neil D. and Kohn, Donald B. and Krause, Diane S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {1044-1549},
	Journal = {Am J Respir Cell Mol Biol},
	Keywords = {Respiratory Mucosa;Animals;Protein Precursors;Bone Marrow Transplantation;Lung Diseases;Indicators and Reagents;Proteolipids;Female;Mice, Inbred C57BL;Retroviridae;11 Glia;Green Fluorescent Proteins;Hematopoietic Stem Cell Transplantation;RNA, Messenger;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Mice;Luminescent Proteins;Gene Expression},
	Medline = {22330667},
	Month = {12},
	Nlm_Id = {8917225},
	Number = {6},
	Organization = {Department of Laboratory Medicine, Yale University, New Haven, Connecticut, USA.},
	Pages = {645-51},
	Pubmed = {12444022},
	Title = {Marrow-derived cells as vehicles for delivery of gene therapy to pulmonary epithelium},
	Uuid = {251C0ACD-8FBF-498D-A0E8-246D2D0C1927},
	Volume = {27},
	Year = {2002}}

@article{Groves:2003,
	Abstract = {Following permanent transection of the adult rat sciatic nerve, sensory neuron apoptosis in the contributing L4 and L5 dorsal root ganglia can be observed for at least 6 months afterwards. To establish the profile of any sensory neuron apoptosis and loss over time when axonal regeneration is allowed, serial sections of L4 and L5 ganglia were examined and the neurons counted using a stereological technique 1, 2 and 3 months after crushing the right sciatic nerve at mid-thigh level. Our results show that an identical degree of sensory neuron loss and apoptosis occurs 1 month after crush as at 1 month after permanent transection. However, at 3 months no neurons undergoing apoptosis could be observed and no significant loss could be detected in the ipsilateral ganglia when compared to unoperated controls. One explanation was a neuronal replacement mechanism, which was investigated by administering bromodeoxyuridine to rats for 1 month after sciatic nerve transection or crush, prior to detection using immunohistochemistry on sections of their ganglia after 2 months. The presence of bromodeoxyuridine in the nuclei of occasional cells that would be counted as neurons on the basis of size and morphology indicates that a process of apparent neurogenesis may underlie the profile of sensory neuron loss after axotomy. 0300-4864 Journal Article},
	Author = {Groves, M. J. and Schanzer, A. and Simpson, A. J. and An, S. F. and Kuo, L. T. and Scaravilli, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {J Neurocytol},
	Keywords = {06 Adult neurogenesis injury induced;D pdf},
	Number = {2},
	Organization = {Department of Molecular Pathogenesis, Institute of Neurology, University College London, Queen Square, London, WC1N 3BG. m.groves\@ion.ucl.ac.uk},
	Pages = {113-22},
	Pubmed = {14707546},
	Title = {Profile of adult rat sensory neuron loss, apoptosis and replacement after sciatic nerve crush},
	Uuid = {D8FDED1D-636C-4B89-B53A-197F01EF7015},
	Volume = {32},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14707546}}

@article{Gu:2000,
	Abstract = {Neurogenesis occurs throughout life in the dentate gyrus of hippocampus and subventricular zone, but this phenomenon has rarely been observed in other brain regions of adult mammals. The aim of the current study was to investigate the cell proliferation process in the ischemically challenged region-at-risk after focal cerebral ischemia in the adult rat brain. A reversible photothrombotic ring stroke model was used, which features sustained hypoperfusion followed by late spontaneous reperfusion and a remarkable morphologic tissue recovery in the anatomically well defined somatosensory cortical region-at-risk. Twelve-week-old male Wistar rats received repeated intraperitoneal injections of the cell proliferation specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Immunocytochemistry of coronal brain sections revealed that the majority of BrdU-positive cells were of glial, macrophage, and endothelial origin, whereas 3\%to 6\%of the BrdU-positive cells were double-labeled by BrdU and the neuronspecific marker Map-2 at 7 and 100 days after stroke onset in the region-at-risk. They were distributed randomly in cortical layers II-VI. Three-dimensional confocal analyses of BrdU and the neuronal-specific marker Neu N by double immunofluorescence confirmed their colocalization within the same cells at 72 hours and 30 days after stroke induction. This study suggests that, as a potential pathway for brain repair, new neurons can be generated in the cerebral cortex of adult rats after sublethal focal cerebral ischemia. 0271-678x Journal Article},
	Author = {Gu, W. and Brannstrom, T. and Wester, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {Bromodeoxyuridine/pharmacokinetics;Intracranial Thrombosis/*complications/etiology;Rats;Cerebral Cortex/metabolism/pathology/*physiopathology;Cerebrovascular Accident/*etiology/metabolism/pathology/*physiopathology;Rats, Wistar;Radiation Injuries, Experimental/*complications;D pdf;Animals;Support, Non-U.S. Gov't;Male;*Nerve Regeneration},
	Number = {8},
	Organization = {Department of Medicine, Umea Stroke Center, University of Umea, Sweden.},
	Pages = {1166-73},
	Title = {Cortical neurogenesis in adult rats after reversible photothrombotic stroke},
	Uuid = {BAA17290-C26D-11DA-969D-000D9346EC2A},
	Volume = {20},
	Year = {2000},
	url = {papers/Gu_JCerebBloodFlowMetab2000.pdf}}

@article{Guegan:1998,
	Abstract = {After an ischemic episode induced by the electrocoagulation of the left middle cerebral artery (MCA) in mouse, neurons within the damaged territory die either by an apoptotic or by a necrotic process. Most of the cortical neurons within the ischemic area display both morphological and biochemical signs of programmed cell death: nuclear condensation, DNA degradation, formation of apoptotic bodies, and glutathione depletion. In fact, apoptosis essentially contributes to the expansion of the ischemic lesion and the maximum of damaged territory is reached 24 h postocclusion. Several potentially neuroprotective pathways have been evidenced in different experimental models of ischemia including the activation of antioxidant enzyme activities and/or the recruitment of neurotrophic as well as antiapoptotic factors. In our model of permanent focal ischemia induced by MCA occlusion, we measured the temporal synthesis of nerve growth factor (NGF) and examined the status of antioxidant enzymes as well as Bcl-2 antiapoptotic product. We detected in both cortices a transient increase of NGF which peaks at 6 h. Moreover, we reported that glutathione peroxidase is recruited with a time course which parallels NGF synthesis. Finally, we observed the induction of Bcl-2 in safe neurons; this may represent a self-protective response against ischemia- induced apoptosis. We provide evidence that in a model of permanent focal ischemia, several neuroprotective pathways could be coactivated.},
	Author = {Guegan, C. and Ceballos-Picot, I. and Nicole, A. and Kato, H. and Onteniente, B. and Sola, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Exp Neurol},
	Keywords = {Neurons/*cytology/*enzymology;Enzyme Activation/physiology;Neuroprotective Agents/*metabolism;Apoptosis/*physiology;Cerebral Cortex/cytology/pathology;Animal;Neuroglia/chemistry;Glial Fibrillary Acidic Protein/analysis;Cerebral Infarction/metabolism;Mice, Inbred C57BL;Brain Chemistry/physiology;Cell Survival/physiology;Male;Antioxidants/metabolism;Support, Non-U.S. Gov't;Superoxide Dismutase/analysis/metabolism;Mice, Inbred DBA;06 Adult neurogenesis injury induced;Proto-Oncogene Proteins c-bcl-2/analysis/metabolism;D;Mice;Brain Ischemia/*metabolism;Nerve Growth Factors/biosynthesis/metabolism;Immunohistochemistry;Necrosis;Glutathione/metabolism},
	Number = {2},
	Organization = {Laboratoire de Neurosciences, Universite de Caen, CNRS UMR 6551, Caen, 14074, France.},
	Pages = {371-80.},
	Title = {Recruitment of several neuroprotective pathways after permanent focal ischemia in mice},
	Uuid = {5FE21A2A-22D2-47CF-8354-C2EFED961004},
	Volume = {154},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9878175}}

@article{Guerrier:2007,
	Abstract = {The nuclei of dividing neural progenitors undergo a cell-cycle-dependent change in position along the apico-basal axis known as interkinetic nuclear migration (INM). The functional relationship between INM and the mode of division of neural progenitors remains elusive, in part because its regulation at the molecular level is poorly understood. In this issue of Neuron, Xie et al. identify two centrosomal proteins (Cep120 and TACCs) regulating the INM of cortical neural progenitors.},
	Author = {Guerrier, Sabrice and Polleux, Franck},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {comment;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Neuroscience Center, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7250, USA.},
	Pages = {1-3},
	Pii = {S0896-6273(07)00717-9},
	Pubmed = {17920006},
	Title = {The ups and downs of neural progenitors: Cep120 and TACCs control interkinetic nuclear migration},
	Uuid = {6555BD0E-F9A5-47A6-AA78-8D6C80325D2B},
	Volume = {56},
	Year = {2007},
	url = {papers/Guerrier_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.09.019}}

@article{Gueneau:1982,
	Abstract = {Cell genesis in the subgranular zone of the dentate gyrus of 2-month-old rabbits has been investigated. After incorporation of tritiated thymidine, electron microscopic autoradiography allowed description of the ultrastructure of the cells labelled and the progressive transformation of these cells into granular neurons to be followed. Quantitative evaluation of the time course of this transformation has been performed by light microscope autoradiography using 1-micrometer sections. Precursor cells, labelled initially with 3H-thymidine, were transformed after 5 days into early neuroblasts, these cells in turn giving rise to neurons some 8 days later. At the latest time period examined (42 days), 80\%of the labelled cells were neurons; more than 10\%remained as precursor cells. It is suspected that the latter may behave as reserve cells. Small numbers of glial cells, astrocytes, and microglia, scattered throughout the hilus of the dentate gyrus and the molecular layer, were found labelled, and it is possible that they arise from a different precusor pool. It is concluded that the subgranular zone functions as a secondary matrix for granule neurons of the dentate gyrus in young rabbits. These late-forming and apparently synaptically uncommitted neurons may be recruited during the development and refinement of postnatal behavioral substrates, by one or other of the dominant afferent systems.},
	Author = {Gu{\'e}neau, G. and Privat, A. and Drouet, J. and Court, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Thymidine;Cell Differentiation;10 Development;Research Support, Non-U.S. Gov't;Hippocampus;10 Hippocampus;Autoradiography;Microscopy, Electron;Cell Count;Rabbits;Mitosis;Animals;Cytoplasmic Granules;Neurons},
	Medline = {83052931},
	Nlm_Id = {7809375},
	Number = {4},
	Pages = {345-58},
	Pubmed = {7140583},
	Title = {Subgranular zone of the dentate gyrus of young rabbits as a secondary matrix. A high-resolution autoradiographic study},
	Uuid = {5E8639BC-698C-11DA-A4B6-000D9346EC2A},
	Volume = {5},
	Year = {1982}}

@article{Guillemin:2004,
	Abstract = {The phenotypic differentiation of systemic macrophages that have infiltrated the central nervous system, pericytes, perivascular macrophages, and the "real" resident microglial cells is a major immunocytochemical and immunohistochemical concern for all users of cultures of brain cells and brain sections. It is not only important in assessing the purity of cell cultures; it is also of fundamental importance in the assessment of the pathogenetic significance of perivascular inflammatory phenomena within the brain. The lack of a single membranous and/or biochemical marker allowing conclusive identification of these cells is still a major problem in neurobiology. This review briefly discusses the functions of these cells and catalogs a large number of membranous and biochemical markers, which can assist in the identification of these cells.},
	Author = {Guillemin, Gilles J. and Brew, Bruce J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0741-5400},
	Journal = {J Leukoc Biol},
	Keywords = {Pericytes;Research Support, Non-U.S. Gov't;Immunophenotyping;Biological Markers;11 Glia;Microglia;review, tutorial;Macrophages;Humans;Brain;review},
	Month = {3},
	Nlm_Id = {8405628},
	Number = {3},
	Organization = {Centre for Immunology, Neuroimmunology Department, St. Vincent's Hospital, Sydney, NSW, Australia. G.Guillemin\@cfi.unsw.edu.au},
	Pages = {388-97},
	Pii = {jlb.0303114},
	Pubmed = {14612429},
	Title = {Microglia, macrophages, perivascular macrophages, and pericytes: a review of function and identification},
	Uuid = {ACCD6844-43CB-4C65-8F7B-0D74FA12467F},
	Volume = {75},
	Year = {2004},
	url = {papers/Guillemin_JLeukocBiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1189/jlb.0303114}}

@article{Guo:2001,
	Abstract = {In the present study expression of estrogen receptor subtype -alpha (ERalpha) and -beta (ERbeta) in the cerebral cortex, cerebellum, and olfactory bulb was investigated and compared between neonatal (1 to approximately 3-days-old) and adult (250 to approximately 350 g) rats, using reverse transcription-polymerase chain reaction (RT-PCR). No ERalpha transcripts were detectable in the adult cerebellum and olfactory bulb, whereas very weak expression of ERalpha was present in the adult cerebral cortex. No significant difference in ERbeta transcripts was detectable between the neonatal and adult rats. While transcripts for both ER subtypes were co-expressed in these brain areas of neonatal rats, although ERalpha expression was significantly weaker than ERbeta. Even in the cerebral cortex known to contain both ER subtypes in adult rats, ERalpha transcripts in neonatal rats were much higher than in adult. These observations provide evidence for the existence of different expression patterns of ERalpha/ERbeta transcripts in these three brain areas between the neonatal and adult rats, suggesting that each ER subtype may play a distinct role in the regulation of differentiation, development, and functions of the brain by estrogen.},
	Author = {Guo, X. Z. and Su, J. D. and Sun, Q. W. and Jiao, B. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Cell Res},
	Keywords = {I abstr;13 Olfactory bulb anatomy},
	Number = {4},
	Organization = {Department of Biochemistry and Molecular Biology, Second Military Medical University, Shanghai, China. gxzhb\@online.sh.cn},
	Pages = {321-4.},
	Title = {Expression of estrogen receptor (ER) -alpha and -beta transcripts in the neonatal and adult rat cerebral cortex, cerebellum, and olfactory bulb},
	Uuid = {4E5203B2-A9FA-4F44-92C8-4287E6E5F1F2},
	Volume = {11},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11787778}}

@article{Guo:1996,
	Abstract = {During development of the Drosophila peripheral nervous system, a sensory organ precursor (SOP) cell undergoes rounds of asymmetric divisions to generate four distinct cells of a sensory organ. Numb, a membrane-associated protein, is asymmetrically segregated into one daughter cell during SOP division and acts as an inherited determinant of cell fate. Here, we show that Notch, a transmembrane receptor mediated cell-cell communication, functions as a binary switch in cell fate specification during asymmetric divisions of the SOP and its daughter cells in embryogenesis. Moreover, numb negatively regulates Notch, probably through direct protein-protein interaction that requires the phosphotyrosine-binding (PTB) domain of Numb and either the RAM23 region or the very C-terminal end of Notch. Notch then positively regulates a transcription factor encoded by tramtrack (ttk). This leads to Ttk expression in the daughter cell that does not inherit Numb. Thus, the inherited determinant Numb bestows a bias in the machinery for cell-cell communication to allow the specification of distinct daughter cell fates. 0896-6273 Journal Article},
	Author = {Guo, M. and Jan, L. Y. and Jan, Y. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neuron},
	Keywords = {Stem Cells/*cytology;Embryo and Fetal Development;Cell Differentiation;10 Development;Membrane Proteins/*physiology;Female;Cell Line;Sense Organs/*cytology;Juvenile Hormones/*physiology;Transcription Factors/physiology;F;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Animals;Male;Drosophila/embryology},
	Number = {1},
	Organization = {Howard Hughes Medical Institute, University of California, San Francisco 94143-0724, USA.},
	Pages = {27-41},
	Pubmed = {8755476},
	Title = {Control of daughter cell fates during asymmetric division: interaction of Numb and Notch},
	Uuid = {1EC00A62-0F3A-4931-9E95-CCAFBA9B7C19},
	Volume = {17},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8755476}}

@article{Gupta:2003,
	Abstract = {Several genes essential for neocortical layering have been identified in recent years, but their precise roles in this process remain to be elucidated. Mice deficient in p35--an activator of cyclin-dependent kinase 5 (Cdk5)--are characterized by a neocortex that has inverted layering. To decipher the physiological mechanisms that underlie this defect, we compared time-lapse recordings between p35(-/-) and wild-type cortical slices. In the p35(-/-) neocortex, the classic modes of radial migration--somal translocation and locomotion--were largely replaced by a distinct mode of migration: branched migration. Branched migration is cell-autonomous, associated with impaired neuronal-glial interaction and rare in neurons of scrambler mice, which are deficient in Dab1. Hence, our findings suggest that inside-out layering requires distinct functions of Reelin and p35/Cdk5 signaling, with the latter being important for proper glia-guided migration.},
	Author = {Gupta, Amitabh and Sanada, Kamon and Miyamoto, David T. and Rovelstad, Susan and Nadarajah, Bagirathy and Pearlman, Alan L. and Brunstrom, Jan and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {10 Development;research support, non-u.s. gov't;Mice, Knockout;Neuroglia;Female;Nerve Tissue Proteins;in vitro;10 genetics malformation;comparative study;Pregnancy;research support, u.s. gov't, p.h.s.;Animals;Cell Movement;Mice;Neurons;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {9809671},
	Number = {12},
	Organization = {Department of Pathology, Harvard Medical School and Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA.},
	Pages = {1284-91},
	Pii = {nn1151},
	Pubmed = {14608361},
	Title = {Layering defect in p35 deficiency is linked to improper neuronal-glial interaction in radial migration},
	Uuid = {A24FB364-379F-482D-BEE0-C069DC3D5708},
	Volume = {6},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1151}}

@article{Gupta:2002,
	Abstract = {Although the basic principles of neocortical development have been known for quite some time, it is only recently that our understanding of the molecular mechanisms that are involved has improved. Such understanding has been facilitated by genetic approaches that have identified key proteins involved in neocortical development, which have been placed into signalling pathways by molecular and cell-biological studies. The challenge of current research is to understand the manner in which these various signalling pathways are interconnected to gain a more comprehensive picture of the molecular intricacies that govern neocortical development. 1471-0056 Journal Article Review Review, Tutorial},
	Author = {Gupta, A. and Tsai, L. H. and Wynshaw-Boris, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:48 -0400},
	Journal = {Nat Rev Genet},
	Keywords = {Signal Transduction/*genetics/physiology;Extracellular Matrix Proteins/physiology;10 Development;Mice, Mutant Strains/physiology;Dynein ATPase/physiology;F both;Microtubule-Associated Proteins/genetics/physiology;Neocortex/*embryology/*physiology;Neuropeptides/genetics/physiology;Neurons/physiology;Animals;Mice;Cell Adhesion Molecules, Neuronal/physiology;Cyclin-Dependent Kinases/physiology;Cell Movement/*genetics/physiology},
	Number = {5},
	Organization = {Department of Pathology, Harvard Medical School, Howard Hughes Medical Institute, 200 Longwood Avenue, Boston, Massachusetts 02115, USA. amitabh-gupta\@student.hms.harvard.edu},
	Pages = {342-55},
	Title = {Life is a journey: a genetic look at neocortical development},
	Uuid = {EF1B178D-36A9-4B30-B031-F9E3BFF501A6},
	Volume = {3},
	Year = {2002},
	url = {papers/Gupta_NatRevGenet2002.pdf}}

@article{Gurevich:2002,
	Abstract = {Arrestins are adaptor proteins involved in homologous desensitization and trafficking of G protein-coupled receptors. Arrestins bind to activated phosphorylated receptors thus precluding further signal transduction. Two subtypes of non-visual arrestins, arrestin2 and arrestin3, have been cloned. Recently, specificity of various receptors to arrestins and differences in kinetics of receptor desensitization mediated by arrestins have been demonstrated. Both arrestins are expressed in the rat brain. However, quantitative assessment of their expression and detailed distribution are lacking. Here, we used quantitative ribonuclease protection assay and western blot to measure arrestin2 and arrestin3 mRNA and protein in the rat brain during postnatal development. In situ hybridization histochemistry was employed to study the detailed distribution of arrestin mRNAs in the adult and developing brain. Both arrestins were expressed from birth in all regions studied. Arrestin2 mRNA levels increased with development until the 14th postnatal day and then decreased, whereas arrestin2 protein levels continued to rise. Arrestin3 mRNA was maximal in neonates and then decreased, while arrestin3 protein changed little. In newborns and adults, the concentration of arrestin2 mRNA was two- to three-fold higher than that of arrestin3. In neonates, the excess of the arrestin2 protein over arrestin3 was commensurate with the excess of the arrestin2 mRNA (three-fold) but in the adult, the ratio was much higher (10-20-fold). Each arrestin demonstrated a unique distribution, although in many areas there was overlap suggesting co-localization. Both arrestins were highly expressed in the cortex and hippocampus. Arrestin2 was abundant in the thalamus, particularly in the anterior, intralaminar, and midline nuclei, while arrestin3 was abundant in the medial habenular. Arrestin3 was relatively abundant in most hypothalamic nuclei and extended amygdala. In the developing brain, arrestin3 was highly expressed in the subventricular zone, whereas arrestin2 was more abundant in differentiated areas.Our data demonstrate that arrestin2 is the major arrestin subtype in the rat brain, although arrestin3 is expressed in specific cell populations including postnatal proliferative zones. Because each arrestin appears to mediate receptor desensitization in a specific way, different kinetics of trafficking of the same receptor should be expected in different cells due to varying arrestin2/arrestin3 ratios. Thus, the response of receptors to specific drugs stimulating or blocking these receptors may depend on complement of arrestins in their target cells. 0306-4522 Journal Article},
	Author = {Gurevich, E. V. and Benovic, J. L. and Gurevich, V. V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neuroscience},
	Keywords = {Pregnancy;Animals;Brain/cytology/*growth &development/*metabolism;Neurons/cytology/*metabolism;Cell Differentiation/genetics;Rats;Receptors, Cell Surface/*metabolism;Comparative Study;Female;C abstr;Rats, Sprague-Dawley;In Situ Hybridization;Animals, Newborn;Blotting, Western;Phosphoproteins/genetics/*metabolism;Protein Transport/physiology;Support, U.S. Gov't, P.H.S.;GTP-Binding Proteins/*metabolism;Gene Expression Regulation, Developmental/*physiology;04 Adult neurogenesis factors;RNA, Messenger/metabolism;Arrestins/genetics/*metabolism;Signal Transduction/physiology;Aging/genetics/metabolism},
	Number = {3},
	Organization = {Sun Health Research Institute, Sun City, AZ 85351, USA. eugenia.gurevich\@mcmail.vanderbilt.edu},
	Pages = {421-36},
	Pubmed = {11823056},
	Title = {Arrestin2 and arrestin3 are differentially expressed in the rat brain during postnatal development},
	Uuid = {F0B5CE1E-6788-45E9-B433-CE2A438F36B1},
	Volume = {109},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11823056}}

@article{Gutierrez-Mecinas:2005,
	Abstract = {Periglomerular cells (PG) are interneurons of the olfactory bulb (OB) that modulate the first synaptic relay of the olfactory information from the olfactory nerve to the dendrites of the bulbar principal cells. Previous investigations have pointed to the heterogeneity of these interneurons and have demonstrated the presence of two different types of PG. In the rat OB, type 1 PG receive synaptic contacts from the olfactory axons and are gamma-aminobutyric acid (GABA)-ergic, whereas type 2 PG do not receive synaptic contacts from the olfactory axons and are GABA immunonegative. In this study, we analyze and characterize neurochemically a group of PG that has not been previously classified either as type 1 or type 2. These PG are immunoreactive for the neuropeptides somatostatin (SOM) or cholecystokinin (CCK). By using double immunocytochemistry, we demonstrate that neither the SOM- nor the CCK-immunoreactive PG contain GABA immunoreactivity, which is a neurochemical feature of type 1 PG. Moreover, they do not contain the calcium-binding proteins calbindin D-28k and calretinin, which are neurochemical markers of the type 2 PG. Electron microscopy demonstrates that the dendrites of the SOM- and CCK-containing PG are distributed in the synaptic and sensory subcompartments of the glomerular neuropil and receive synaptic contacts from the olfactory axons. Therefore, they should be included in the type 1 group rather than in the type 2. Altogether, these data indicate that the SOM- and the CCK-containing PG may constitute a group of GABA-immunonegative type 1 PG that has not been previously described. These results further extend the high degree of complexity of the glomerular circuitry. J. Comp. Neurol. 489:467-479, 2005. (c) 2005 Wiley-Liss, Inc.},
	Author = {Guti\`{e}rrez-Mecinas, Mar{\'\i}a and Crespo, Carlos and Blasco-Ib{\'a}\~{n}ez, Jose{\'e} Miguel and Gracia-Llanes, Francisco Javier and Marqu{\'e}s-Mar{\'\i}, Ana Isabel and Mart{\'\i}nez-Guijarro, Francisco Jos{\'e}},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {Departamento de Biolog{\'\i}a Celular, Facultad de Ciencias Biol{\'o}gicas, Universidad de Valencia, E-46100 Burjasot, Spain.},
	Pages = {467-79},
	Pubmed = {16025459},
	Title = {Characterization of somatostatin- and cholecystokinin-immunoreactive periglomerular cells in the rat olfactory bulb},
	Uuid = {1797B3C3-A243-438A-B0CF-8F43F195ED0D},
	Volume = {489},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20649}}

@article{Hack:2005,
	Abstract = {Adult neurogenesis in mammals is restricted to two small regions, including the olfactory bulb, where GABAergic and dopaminergic interneurons are newly generated throughout the entire lifespan. However, the mechanisms directing them towards a specific neuronal phenotype are not yet understood. Here, we demonstrate the dual role of the transcription factor Pax6 in generating neuronal progenitors and also in directing them towards a dopaminergic periglomerular phenotype in adult mice. We present further evidence that dopaminergic periglomerular neurons originate in a distinct niche, the rostral migratory stream, and are fewer derived from precursors in the zone lining the ventricle. This regionalization of the adult precursor cells is further supported by the restricted expression of the transcription factor Olig2, which specifies transit-amplifying precursor fate and opposes the neurogenic role of Pax6. Together, these data explain both extrinsic and intrinsic mechanisms controlling neuronal identity in adult neurogenesis.},
	Author = {Hack, and Saghatelyan, and de Chevigny, and Pfeifer, and Ashery-Padan, and Lledo, and G{\"o}tz,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration},
	Month = {6},
	Nlm_Id = {9809671},
	Organization = {[1] GSF-National Research Center for Environment and Health, Institute for Stem Cell Research, Ingolst{\"a}dter Landstr. 1, D-85764 Neuherberg, Germany. [2] These authors contributed equally to this work.},
	Pii = {nn1479},
	Pubmed = {15951811},
	Title = {Neuronal fate determinants of adult olfactory bulb neurogenesis},
	Uuid = {D42A890C-9208-46A3-B185-E84038D28E23},
	Year = {2005},
	url = {papers/Hack_NatNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1479}}

@article{Hadj-Sahraoui:2000,
	Abstract = {Circulating T(4) and T(3) were measured during the first three post-natal weeks in the mouse and found to increase in a triphasic manner. The first increase occurred at post-natal day 6 and was simultaneous with a decrease in bromodeoxyuridine incorporation in areas showing post-natal mitosis. We investigated whether there was a causal relationship between increased thyroid hormone levels and decreased proliferation by inducing hypothyroidism in dams and progeny. Hypothyroidism prolonged mitotic activity in the olfactory bulb, hippocampus, subventricular zone and the cerebellar cortex. This suggests that the increase in T(3) at the end of the first postnatal week is implicated in terminating progenitor proliferation in many parts of the mouse brain. 0304-3940 Journal Article},
	Author = {Hadj-Sahraoui, N. and Seugnet, I. and Ghorbel, M. T. and Demeneix, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neurosci Lett},
	Keywords = {Hippocampus/metabolism/physiopathology;Pregnancy;Animals;Hypothyroidism/chemically induced/*physiopathology;Triiodothyronine/blood;Olfactory Bulb/metabolism/physiopathology;Cerebellum/metabolism/physiopathology;Female;D pdf;Time Factors;Male;Brain/metabolism/*physiopathology;Support, Non-U.S. Gov't;Bromodeoxyuridine/metabolism;Animals, Newborn;06 Adult neurogenesis injury induced;Mitosis/*physiology;Propylthiouracil/adverse effects;Thyroxine/blood;Mice},
	Number = {2},
	Organization = {Laboratoire de Physiologie Generale et Comparee, UMR 8572 CNRS, Museum National d'Histoire Naturelle, F-75231, Paris, Cedex, France.},
	Pages = {79-82},
	Pubmed = {10686382},
	Title = {Hypothyroidism prolongs mitotic activity in the post-natal mouse brain},
	Uuid = {33FCB3E9-F887-4668-90E6-1F527A1E2194},
	Volume = {280},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10686382}}

@article{Hagino-Yamagishi:1999,
	Abstract = {The expression of Brain-2, a POU domain transcription factor, was examined in the developing olfactory bulb. Brain-2 was expressed mainly in the output neurons, mitral cell and tufted cells in the main olfactory bulb (MOB), and mitral/tufted cells (MT cells) in the accessory olfactory bulb (AOB). It was not expressed in granular cells in either the MOB or the AOB. Our results suggest that Brain-2 was specifically expressed in output neurons but not in interneurons in the developing olfactory bulb. Brain-2 may play a role in the development of these output neurons.},
	Author = {Hagino-Yamagishi, K. and Minamikawa-Tachino, R. and Ichikawa, M. and Yazaki, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Antimetabolites;13 Olfactory bulb anatomy;Brain Chemistry/physiology;Fluorescent Antibody Technique;Olfactory Receptor Neurons/chemistry/*physiology;Female;DNA-Binding Proteins/*analysis/*biosynthesis/immunology;Olfactory Bulb/*chemistry/*cytology/embryology;Animal;Pregnancy;I abstr;Transcription Factors/analysis/biosynthesis/immunology;Support, Non-U.S. Gov't;Bromodeoxyuridine;Antibodies;Nerve Tissue Proteins/*analysis/*biosynthesis/immunology;Mice},
	Number = {1-2},
	Organization = {Department of Ultrastructural Research, Tokyo Metropolitan Institute of Medical Science, Honkomagome 3-18-22, Bunkyo-ku, Tokyo 113, Japan. yamagishi\@rinshoken.or.jp},
	Pages = {133-7.},
	Title = {Expression of brain-2 in the developing olfactory bulb},
	Uuid = {14A9990D-010F-4D0D-8BED-C811FAF3BBD8},
	Volume = {113},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10064882%20http://www.elsevier.com:80/cgi-bin/cas/tree/store/bresd/cas_sub/browse/browse.cgi?year=1999&volume=113&issue=1-2&aid=60733}}

@article{Hains:2006,
	Abstract = {Traumatic spinal cord injury (SCI) results not only in motor impairment but also in chronic central pain, which can be refractory to conventional treatment approaches. It has been shown recently that in models of peripheral nerve injury, spinal cord microglia can become activated and contribute to development of pain. Considering their role in pain after peripheral injury, and because microglia are known to become activated after SCI, we tested the hypothesis that activated microglia contribute to chronic pain after SCI. In this study, adult male Sprague Dawley rats underwent T9 spinal cord contusion injury. Four weeks after injury, when lumbar dorsal horn multireceptive neurons became hyperresponsive and when behavioral nociceptive thresholds were decreased to both mechanical and thermal stimuli, intrathecal infusions of the microglial inhibitor minocycline were initiated. Electrophysiological experiments showed that minocycline rapidly attenuated hyperresponsiveness of lumbar dorsal horn neurons. Behavioral data showed that minocycline restored nociceptive thresholds, at which time spinal microglial cells assumed a quiescent morphological phenotype. Levels of phosphorylated-p38 were decreased in SCI animals receiving minocycline. Cessation of delivery of minocycline resulted in an immediate return of pain-related phenomena. These results suggest an important role for activated microglia in the maintenance of chronic central below-level pain after SCI and support the newly emerging role of non-neuronal immune cells as a contributing factor in post-SCI pain.},
	Author = {Hains, Bryan C. and Waxman, Stephen G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {16},
	Organization = {Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA.},
	Pages = {4308-17},
	Pii = {26/16/4308},
	Pubmed = {16624951},
	Title = {Activated microglia contribute to the maintenance of chronic pain after spinal cord injury},
	Uuid = {1840699A-DAAC-4A53-A14D-9E91FD840516},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0003-06.2006}}

@article{Halene:1999,
	Abstract = {Retroviral vectors based on the Moloney murine leukemia virus (MoMuLV) are currently the most commonly used vehicles for stable gene transfer into mammalian hematopoietic cells. But, even with reasonable transduction efficiency, expression only occurs in a low percentage of transduced cells and decreases to undetectable levels over time. We have previously reported the modified MND LTR (myeloproliferative sarcoma virus enhancer, negative control region deleted, dl587rev primer-binding site substituted) to show increased expression frequency and decreased methylation in transduced murine embryonic stem cells and hematopoietic stem cells. We have now compared expression of the enhanced green fluorescent protein (eGFP) from a vector using the MoMuLV LTR (LeGFPSN) with that from the modified vector (MNDeGFPSN) in mature hematopoietic and lymphoid cells in the mouse bone marrow transplant (BMT) model. In primary BMT recipients, we observed a higher frequency of expression from the MND LTR (20\%to 80\%) in hematopoietic cells of all lineages in spleen, bone marrow, thymus, and blood compared with expression from the MoMuLV LTR (5\%to 10\%). Expression from the MND LTR reached 88\%in thymic T lymphocytes and 54\%in splenic B lymphocytes for up to 8 months after BMT. The mean fluorescence intensity of the individual cells, indicating the amount of protein synthesized, was 6- to 10-fold higher in cells expressing MNDeGFPSN compared with cells expressing LeGFPSN. Transduction efficiencies determined by DNA polymerase chain reaction of vector copy number were comparable for the 2 vectors. Therefore, the MND vector offers an improved vehicle for reliable gene expression in hematopoietic cells.},
	Author = {Halene, S. and Wang, L. and Cooper, R. M. and Bockstoce, D. C. and Robbins, P. B. and Kohn, D. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Transduction, Genetic;Gene Dosage;Animals;Bone Marrow Transplantation;Lymphocytes;Female;Mice, Inbred C57BL;11 Glia;Retroviridae;Time Factors;Green Fluorescent Proteins;Male;Leukemia Virus, Murine;Research Support, U.S. Gov't, P.H.S.;Genetic Vectors;Gene Therapy;3T3 Cells;Gene Transfer Techniques;Polymerase Chain Reaction;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {20021682},
	Month = {11},
	Nlm_Id = {7603509},
	Number = {10},
	Organization = {Division of Research Immunology/Bone Marrow Transplantation, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA.},
	Pages = {3349-57},
	Pubmed = {10552944},
	Title = {Improved expression in hematopoietic and lymphoid cells in mice after transplantation of bone marrow transduced with a modified retroviral vector},
	Uuid = {8AC33AC9-260F-48F1-B6EC-168A17DDE914},
	Volume = {94},
	Year = {1999}}

@article{Hallbergson:2003,
	Abstract = {The brain shows limited ability to repair itself, but neurogenesis in certain areas of the adult brain suggests that neural stem cells may be used for structural brain repair. It will be necessary to understand how neurogenesis in the adult brain is regulated to develop strategies that harness neural stem cells for therapeutic use. 0021-9738 Journal Article Review Review, Tutorial},
	Author = {Hallbergson, A. F. and Gnatenco, C. and Peterson, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {J Clin Invest},
	Keywords = {B pdf;*Stem Cell Transplantation;02 Adult neurogenesis migration;Neurons/*physiology;Brain/*physiology;Human;Brain Injuries/physiopathology/*therapy;Brain Diseases/physiopathology/*therapy;Animals;Stem Cells/*physiology},
	Number = {8},
	Organization = {Neural Repair and Neurogenesis Laboratory, Department of Neuroscience, The Chicago Medical School, 3333 Green Bay Road, North Chicago, Illinois 60064, USA.},
	Pages = {1128-33},
	Title = {Neurogenesis and brain injury: managing a renewable resource for repair},
	Uuid = {CD111597-8CC7-4669-B9CD-6800F3426D9B},
	Volume = {112},
	Year = {2003},
	url = {papers/Hallbergson_JClinInvest2003.pdf}}

@article{Halliday:1992,
	Abstract = {The development of the rat striatum was investigated using a combination of two histochemically distinguishable retrovirus vectors. Using this method, it was possible to identify clonal boundaries within the embryonic striatum and thus determine patterns of proliferation, migration, and some lineal relationships. Several novel aspects of striatal histogenesis were discovered. Striatal progenitor cells do not exhibit a stem cell pattern of division between embryonic day 15 (E15) and E19; a progenitor-progeny relationship appears to exist for ventricular zone and subventricular zone (SVZ) cells; striatal progenitors produce a variety of clone types; some SVZ cells migrate radially, and some migrate tangentially within the SVZ; and radial glia and presumptive neurons can occur in the same clone. eng Journal Article},
	Author = {Halliday, A. L. and Cepko, C. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Journal = {Neuron},
	Keywords = {Pregnancy;B abstr;Escherichia coli/enzymology;Rats;Cells, Cultured;beta-Galactosidase/analysis/genetics;Female;Animal;02 Adult neurogenesis migration;Time Factors;Genetic Vectors;DNA, Bacterial/genetics;Support, Non-U.S. Gov't;Retroviridae/genetics;Neuroglia/cytology/physiology;DNA, Viral/genetics;Support, U.S. Gov't, P.H.S.;Cell Movement/physiology;Stem Cells/*cytology/physiology;Corpus Striatum/*cytology/*embryology/enzymology;Immunohistochemistry;Cell Differentiation/physiology;Neurons/cytology/physiology;Alkaline Phosphatase/analysis/genetics},
	Number = {1},
	Organization = {Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115.},
	Pages = {15-26.},
	Title = {Generation and migration of cells in the developing striatum},
	Uuid = {87B07A86-F3CA-4D06-95FD-0AD1F544E396},
	Volume = {9},
	Year = {1992}}

@article{Halloran:2006,
	Abstract = {Repulsive signaling plays a prominent role in regulating cell-cell interactions and is fundamental to multiple developmental processes. A proper balance between repulsion from and adhesion to other cells or the extracellular matrix is also important. Semaphorin-Plexin and ephrin-Eph ligand-receptor pairs compose two major repulsive signaling systems. Recent advances have elucidated mechanisms by which Semaphorin-Plexin and ephrin-Eph signaling control repulsion versus adhesion. Semaphorins act through a complex signaling pathway to inhibit integrin-mediated adhesion, allowing cell repulsion. Ephrin-Eph interactions can directly mediate cell adhesion and several mechanisms control whether ephrin-Eph binding and signaling induces repulsion or adhesion.},
	Author = {Halloran, Mary C. and Wolman, Marc A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0955-0674},
	Journal = {Curr Opin Cell Biol},
	Keywords = {Models, Biological;10 Development;Cell Adhesion;Cell Adhesion Molecules;Semaphorins;Nerve Tissue Proteins;Signal Transduction;10 circuit formation;research support, n.i.h., extramural;Ephrins;24 Pubmed search results 2008;review},
	Month = {10},
	Nlm_Id = {8913428},
	Number = {5},
	Organization = {Department of Zoology, Madison, WI 53706, USA. mchalloran\@wisc.edu},
	Pages = {533-40},
	Pii = {S0955-0674(06)00121-9},
	Pubmed = {16930978},
	Title = {Repulsion or adhesion: receptors make the call},
	Uuid = {693C6865-741A-4B40-96E1-D34648726817},
	Volume = {18},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ceb.2006.08.010}}

@article{Hamada:2003,
	Abstract = {The b-Zip transcription factor MafB is an essential determinant of neural development and an inducer of monocytic differentiation. The MafB protein is expressed in a variety of tissues including the developing spinal cord, retina, myelomonocytic lineages of hematopoietic cells, and peritoneal macrophages. However, the tissue-specific regulatory mechanism of mafB gene expression and its biological relevance have not been examined in detail. Here, we report, for the first time, analysis of the regulatory mechanism and tissue-specific expression of the mafB gene in vivo using transgenic mice. A transgene, containing the 8.2-kb sequence flanking the 5' end of the mafB exon, directed the expression of a GFP reporter gene specifically in the retina, myelomonocytic lineages of hematopoietic cells, peritoneal macrophages and the ventral spinal cord. In situ hybridization analysis showed that the reporter gene expression specifically recapitulates the endogenous expression profile of mafB in the retina and spinal cord. FACS analysis revealed that the Gr-1, Mac-1 and F4/80 antigens were present on most of the GFP-positive hematopoietic cells from transgenic adult bone marrow and spleen. On the other hand, B220 CD4, 8, and Ter119 cells were almost absent from among the GFP-positive cells examined. These observations suggest that gene regulatory regions located in the 8.2-kb upstream region of mafB are responsible for directing mafB expression in the retina, myelomonocytic lineages, peritoneal macrophages and the ventral spinal cord.},
	Author = {Hamada, Michito and Moriguchi, Takashi and Yokomizo, Tomomasa and Morito, Naoki and Zhang, Chuan and Takahashi, Satoru},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0021-924X},
	Journal = {J Biochem (Tokyo)},
	Keywords = {Retina;Cell Differentiation;5' Untranslated Regions;Gene Dosage;Monocytes;DNA-Binding Proteins;Gene Expression Regulation;Macrophages;Animals;Transcription Factors;Brain;Avian Proteins;Mice, Transgenic;RNA, Messenger;Peritoneum;11 Glia;Green Fluorescent Proteins;Spinal Cord;Bone Marrow;Cell Lineage;Oncogene Proteins;Organ Specificity;Mice;Luminescent Proteins;Genes, Reporter;Research Support, Non-U.S. Gov't},
	Medline = {22846658},
	Month = {8},
	Nlm_Id = {0376600},
	Number = {2},
	Organization = {Department of Anatomy, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575.},
	Pages = {203-10},
	Pubmed = {12966068},
	Title = {The mouse mafB 5'-upstream fragment directs gene expression in myelomonocytic cells, differentiated macrophages and the ventral spinal cord in transgenic mice},
	Uuid = {41AF6DF3-A7D4-41B3-9FB3-A0DB93796B59},
	Volume = {134},
	Year = {2003}}

@article{Hamel:2005,
	Abstract = {Brevican, a proteoglycan of the lectican family, inhibits neurite outgrowth and may also stabilize synapses. Little is known about its expression or function in vitro. This study seeks to determine whether a brevican-containing matrix is present in neural cultures, and if so, how the production of brevican may be modulated. To accomplish this, the content of brevican and its proteolytic fragments were measured in primary cultures of neurons, astrocytes and microglia after treatment with cytokines. These experiments revealed that astrocytes and neurons express several isoforms of brevican, whereas microglia do not produce this proteoglycan. Cleavage fragments of brevican were found primarily in neuronal and astrocyte culture medium. ADAMTS4 (a disintegrin and metalloproteinase with thrombospondin motifs), a protease that selectively cleaves lecticans, was detected in cultures of neurons, astrocytes and microglia. When astrocytes were challenged with various cytokines, it was found that treatment with transforming growth factor beta (TGFbeta) resulted in a marked increase in intact brevican in the culture medium that was accompanied by a trend for a decrease in ADAMTS-generated fragments of brevican and apparent ADAMTS activity. Thus, TGFbeta may play a role in neuronal plasticity through its regulation of brevican and the activity of the ADAMTSs.},
	Author = {Hamel, Michelle G. and Mayer, Joanne and Gottschall, Paul E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Cell Differentiation;Animals;Astrocytes;Cells, Cultured;Carrier Proteins;Rats;Neuronal Plasticity;Coculture Techniques;Up-Regulation;Transforming Growth Factor beta;Microglia;Peptide Hydrolases;Cell Communication;Rats, Sprague-Dawley;Neurites;Brain;Extracellular Matrix;Procollagen N-Endopeptidase;11 Glia;Animals, Newborn;Peptide Fragments;Protein Isoforms;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Month = {6},
	Nlm_Id = {2985190R},
	Number = {6},
	Organization = {University of South Florida College of Medicine, Department of Pharmacology and Therapeutics, Tampa, Florida, USA.},
	Pages = {1533-41},
	Pii = {JNC3144},
	Pubmed = {15935069},
	Title = {Altered production and proteolytic processing of brevican by transforming growth factor beta in cultured astrocytes},
	Uuid = {02B8774C-6033-457A-AAFD-C3F0AE1094D0},
	Volume = {93},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1471-4159.2005.03144.x}}

@article{Hammond:2004,
	Abstract = {The migration, arrest, and ultimately positioning of cortical neurons require signaling activity from Reelin as well as from cyclin-dependent kinase 5 (Cdk5). Although both molecules control neuronal positioning, they achieve their effects by quite separate molecular pathways. Cdk5 is a serine-threonine kinase, the activity of which is dependent on its activating subunits p35 and p39. Mice deficient in Cdk5, p35, or both p35 and p39 display the hallmarks of disturbed cortical development, including cortical layer inversion, neuronal disorientation, and abnormal fiber infiltration. To distinguish between the cell- and non cell-autonomous functions of p35, we constructed p35+/+ <--> p35-/- chimeras using the lacZ gene as an independent marker for p35+/+ cells. In this shared developmental space, wild-type and mutant neurons behaved cell-autonomously with respect to layering. Wild-type cells formed a properly layered supercortex that is mirrored by an inverted mutant cortex lying underneath. However, this genotype-specific behavior was confined to the pyramidal population, and interneurons belonging to either genotype were indiscriminately distributed. However, there was also non cell-autonomous rescue of mutant neurons, and this rescue was specific only to early-born pyramidal neurons belonging to layer V. Rescued neurons reached the correct layer address and possessed appropriate neuronal morphology, orientation, and projections. Later-born neurons belonging to layers II and III were not rescued. These results demonstrate that p35 signaling can have both cell- and non cell-autonomous consequences, and their effects are not uniformly shared by cortical neurons born at different times or born at different places (projection neurons vs interneurons).},
	Author = {Hammond, Vicki and Tsai, Li-Huei H. and Tan, Seong-Seng S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008;Nerve Fibers;10 Development;research support, non-u.s. gov't;Mice, Knockout;Chimera;Nerve Tissue Proteins;Pyramidal Cells;Interneurons;Animals;Cell Movement;Cerebral Cortex;Mice;Neurons},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {2},
	Organization = {Howard Florey Institute, The University of Melbourne, Victoria 3010, Australia.},
	Pages = {576-87},
	Pii = {24/2/576},
	Pubmed = {14724258},
	Title = {Control of cortical neuron migration and layering: cell and non cell-autonomous effects of p35},
	Uuid = {D3E1F685-40E7-47BF-A381-0339E7EBB854},
	Volume = {24},
	Year = {2004},
	url = {papers/Hammond_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4529-03.2004}}

@article{Hamo:2007,
	Abstract = {The potential interplay of glial cells with T cells during viral induced inflammation was assessed by comparing major histocompatibility complex molecule upregulation and retention on astrocytes and microglia. Transgenic mice expressing green fluorescent protein under control of the astrocyte-specific glial fibrillary acidic protein promoter were infected with a neurotropic coronavirus to facilitate phenotypic characterization of astrocytes and microglia using flow cytometry. Astrocytes in the adult central nervous system up-regulated class I surface expression, albeit delayed compared with microglia. Class II was barely detectable on astrocytes, in contrast to potent up-regulation on microglia. Maximal MHC expression in both glial cell types correlated with IFN-gamma levels and lymphocyte accumulation. Despite a decline of IFN-gamma concomitant to virus clearance, MHC molecule expression on glia was sustained. These data demonstrate distinct regulation of both class I and class II expression by microglia and astrocytes in vivo following viral induced inflammation. Furthermore, prolonged MHC expression subsequent to viral clearance implies a potential for ongoing presentation.},
	Author = {Hamo, Ludwig and Stohlman, Stephen A. and Otto-Duessel, Maya and Bergmann, Cornelia C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Animals;Astrocytes;Encephalomyelitis;Gene Expression Regulation;Cells, Cultured;Interferon Type II;Female;Microglia;Mice, Transgenic;Genes, MHC Class I;11 Glia;Green Fluorescent Proteins;Male;Genes, MHC Class II;Flow Cytometry;research support, n.i.h., extramural;Mice;Enzyme-Linked Immunosorbent Assay;24 Pubmed search results 2008;Inflammation;Maus Elberfeld virus;Glial Fibrillary Acidic Protein},
	Month = {8},
	Nlm_Id = {8806785},
	Number = {11},
	Organization = {Department of Neuroscience, University of Southern California Keck School of Medicine, Los Angeles, California, USA.},
	Pages = {1169-77},
	Pubmed = {17600339},
	Title = {Distinct regulation of MHC molecule expression on astrocytes and microglia during viral encephalomyelitis},
	Uuid = {673F9897-E43E-4D66-9BC4-9E0C911ED42D},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20538}}

@article{Hampton:2004,
	Abstract = {The cortical stab injury has been widely used for biochemical analysis of molecular changes following CNS injury. However, the cellular responses to this injury have not been accurately quantified. In order to provide a baseline for biochemical studies and future experiments on the manipulation of the CNS injury response we have undertaken a quantitative analysis of this injury. The proliferative and reactive responses of oligodendrocyte precursor cells, astrocytes and microglia were measured, using antibodies to NG2, glial fibrillary acidic protein (GFAP) and the cd11-b clone OX-42 to characterise these cell types at 2, 4, 7 and 14 days post-injury. Oligodendrocyte precursors and microglia proliferated rapidly during the first week, mostly within 0.3 mm of the lesion. Of the dividing cells over 60\%were oligodendrocyte precursor cells with microglia making up the balance of the dividing cells. Minimal numbers of astrocytes divided in response to the lesion. Large cells with one or two short processes that were both NG2 and OX-42 positive were identified very close to the lesion at 2 and 4 days post-lesion but not thereafter. They are likely to be blood-derived cells that express NG2 or have ingested it. NG2 immunohistochemistry and platelet-derived growth factor alpha receptor (PDGFalpha-R) in situ hybridisation on neighbouring sections was performed. In the lesioned area only 12\%of NG2 positive (+ive) cells were PDGFalpha-R +ive (a ratio of 1:8 for PDGFalpha-R +ive cells: NG2 +ive cells) compared with 33\%in the unlesioned cortex and an almost 100\%overlap in the spinal cord.},
	Author = {Hampton, D. W. and Rhodes, K. E. and Zhao, C. and Franklin, R. J. M. and Fawcett, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Cell Differentiation;Glial Fibrillary Acidic Protein;Wounds, Penetrating;Comparative Study;Rats;Astrocytes;Stem Cells;Not relevant;11 Glia;Microglia;Support, Non-U.S. Gov't;Animals;Cerebral Cortex;Oligodendroglia},
	Nlm_Id = {7605074},
	Number = {4},
	Organization = {Cambridge Centre for Brain Repair, E. D. Adrian Building, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK. dhampton\@icord.org},
	Pages = {813-20},
	Pii = {S0306452204003719},
	Pubmed = {15312894},
	Title = {The responses of oligodendrocyte precursor cells, astrocytes and microglia to a cortical stab injury, in the brain},
	Uuid = {5910240C-DDEE-4D0E-A055-4F084D2AD50F},
	Volume = {127},
	Year = {2004},
	url = {papers/Hampton_Neuroscience2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2004.05.028}}

@article{Hanazono:2002,
	Abstract = {BACKGROUND: The green fluorescent protein (GFP) has proven a useful marker in retroviral gene transfer studies targeting hematopoietic stem cells (HSCs) in mice. However, several investigators have reported very low in vivo peripheral blood marking levels in nonhuman primates after transplantation of HSCs transduced with the GFP gene. We retrovirally marked cynomolgus monkey HSCs with the GFP gene, and tracked in vivo marking levels within both bone marrow progenitor cells and mature peripheral blood cells following autologous transplantation after myeloablative conditioning. METHODS: Bone marrow cells were harvested from three cynomolgus macaques and enriched for the primitive fraction by CD34 selection. CD34(+) cells were transduced with one of three retroviral vectors all expressing the GFP gene and were infused after myeloablative total body irradiation (500 cGy x 2). Following transplantation, proviral levels and fluorescence were monitored among clonogenic bone marrow progenitors and mature peripheral blood cells. RESULTS: Although 13-37\%of transduced cells contained the GFP provirus and 11-13\%fluoresced ex vivo, both provirus and fluorescence became almost undetectable in the peripheral blood within several months after transplantation regardless of the vectors used. However, on sampling of bone marrow at multiple time points, significant fractions (5-10\%) of clonogenic progenitors contained the provirus and fluoresced ex vivo reflecting a significant discrepancy between GFP gene marking levels within bone marrow cells and their mature peripheral blood progeny. The discrepancy (at least one log) persisted for more than 1 year after transplantation. Since no cytotoxic T lymphocytes against GFP were detected in the animals, an immune response against GFP is an unlikely explanation for the low levels of transduced peripheral blood cells. Administration of granulocyte colony stimulating factor and stem cell factor resulted in mobilization of transduced bone marrow cells detectable as mature granulocyte progeny which expressed the GFP gene, suggesting that transduced progenitor cells in bone marrow could be mobilized into the peripheral blood and differentiated into granulocytes. CONCLUSIONS: Low levels of GFP-transduced mature cells in the peripheral blood of nonhuman primates may reflect a block to differentiation associated with GFP; this block can be overcome in part by nonphysiological cytokine treatment ex vivo and in vivo.},
	Author = {Hanazono, Yutaka and Terao, Keiji and Shibata, Hiroaki and Nagashima, Takeyuki and Ageyama, Naohide and Asano, Takayuki and Ueda, Yasuji and Kato, Ikunoshin and Kume, Akihiro and Hasegawa, Mamoru and Ozawa, Keiya},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1099-498X},
	Journal = {J Gene Med},
	Keywords = {Gene Transfer Techniques;Research Support, Non-U.S. Gov't;Luminescent Proteins;Hematopoietic Stem Cells;Transduction, Genetic;Macaca fascicularis;11 Glia;Green Fluorescent Proteins;Male;Animals;Leukocytes, Mononuclear},
	Medline = {22209487},
	Nlm_Id = {9815764},
	Number = {5},
	Organization = {Division of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical School, Tochigi, Japan. hanazono\@jichi.ac.jp},
	Pages = {470-7},
	Pubmed = {12221639},
	Title = {Introduction of the green fluorescent protein gene into hematopoietic stem cells results in prolonged discrepancy of in vivo transduction levels between bone marrow progenitors and peripheral blood cells in nonhuman primates},
	Uuid = {5EB26562-BC92-4A2D-8D46-4F2CAA4FEFD5},
	Volume = {4},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jgm.307}}

@article{Hand:2005,
	Abstract = {The molecular mechanisms specifying the dendritic morphology of different neuronal subtypes are poorly understood. Here we demonstrate that the bHLH transcription factor Neurogenin2 (Ngn2) is both necessary and sufficient for specifying the dendritic morphology of pyramidal neurons in vivo by specifying the polarity of its leading process during the initiation of radial migration. The ability of Ngn2 to promote a polarized leading process outgrowth requires the phosphorylation of a single tyrosine residue at position 241, an event that is neither involved in Ngn2 direct transactivation properties nor its proneural function. Interestingly, the migration defect observed in the Ngn2 knockout mouse and in progenitors expressing the Ngn2(Y241F) mutation can be rescued by inhibiting the activity of the small-GTPase RhoA in cortical progenitors. Our results demonstrate that Ngn2 coordinates the acquisition of the radial migration properties and the unipolar dendritic morphology characterizing pyramidal neurons through molecular mechanisms distinct from those mediating its proneural activity.},
	Author = {Hand, Randal and Bortone, Dante and Mattar, Pierre and Nguyen, Laurent and Heng, Julian Ik-Tsen and Guerrier, Sabrice and Boutt, Elizabeth and Peters, Eldon and Barnes, Anthony P. and Parras, Carlos and Schuurmans, Carol and Guillemot, Fran\c{c}ois and Polleux, Franck},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Research Support, N.I.H., Extramural;24 Pubmed search results 2008;Green Fluorescent Proteins;Male;Animals;Cells, Cultured;Age Factors;Sequence Alignment;rhoA GTP-Binding Protein;Research Support, U.S. Gov't, P.H.S.;Cell Movement;In Vitro;Gene Expression Regulation, Developmental;Cell Count;Pregnancy;Electrophoresis, Gel, Pulsed-Field;Basic Helix-Loop-Helix Transcription Factors;Microtubule-Associated Proteins;Tubulin;Neocortex;Dendrites;Pyramidal Cells;Comparative Study;Blotting, Western;Electroporation;Fluorescent Antibody Technique;Time Factors;Cloning, Molecular;Female;Embryo;Chickens;Stem Cells;Microscopy, Confocal;Mice;Models, Biological;Phosphorylation;Humans;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't;Tyrosine},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Phamacology, Neuroscience Center, University of North Carolina, Chapel Hill, North Carolina 27599, USA.},
	Pages = {45-62},
	Pii = {S0896-6273(05)00736-1},
	Pubmed = {16202708},
	Title = {Phosphorylation of Neurogenin2 specifies the migration properties and the dendritic morphology of pyramidal neurons in the neocortex},
	Uuid = {700AF376-B093-44DB-9CE1-F4E52B860725},
	Volume = {48},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.08.032}}

@article{Hanisch:2007,
	Abstract = {Microglial cells constitute the resident macrophage population of the CNS. Recent in vivo studies have shown that microglia carry out active tissue scanning, which challenges the traditional notion of 'resting' microglia in the normal brain. Transformation of microglia to reactive states in response to pathology has been known for decades as microglial activation, but seems to be more diverse and dynamic than ever anticipated--in both transcriptional and nontranscriptional features and functional consequences. This may help to explain why engagement of microglia can be either neuroprotective or neurotoxic, resulting in containment or aggravation of disease progression. Moreover, little is known about the heterogeneity of microglial responses in different pathologic contexts that results from regional adaptations or from the progression of a disease. In this review, we focus on several key observations that illustrate the multi-faceted activities of microglia in the normal and pathologic brain.},
	Author = {Hanisch, Uwe-Karsten K. and Kettenmann, Helmut},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {9809671},
	Number = {11},
	Organization = {Institute of Neuropathology, University of G{\"o}ttingen, D-37075 G{\"o}ttingen, Germany.},
	Pages = {1387-94},
	Pii = {nn1997},
	Pubmed = {17965659},
	Title = {Microglia: active sensor and versatile effector cells in the normal and pathologic brain},
	Uuid = {E6494B99-8A79-40FE-B215-0B4BA46890BE},
	Volume = {10},
	Year = {2007},
	url = {papers/Hanisch_NatNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1997}}

@article{Hanna:1973,
	Author = {Hanna, G. R. and Stalmaster, R. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0028-3878},
	Journal = {Neurology},
	Keywords = {Epilepsy;24 Pubmed search results 2008;Electroencephalography;21 Epilepsy;21 Neurophysiology;Nerve Degeneration;Cats;Motor Cortex;Animals;Disease Models, Animal;Cerebral Cortex;Freezing;Electrodes, Implanted},
	Medline = {73238377},
	Month = {9},
	Nlm_Id = {0401060},
	Number = {9},
	Pages = {918-25},
	Pubmed = {4737684},
	Title = {Cortical epileptic lesions produced by freezing},
	Uuid = {0988714F-434B-42EE-AE2E-AD50A0B45824},
	Volume = {23},
	Year = {1973}}

@article{Hannan:1999,
	Abstract = {Neuronal heterotopia are seen in various pathologies and are associated with intractable epilepsy. We examined brain tissue from four children with subcortical or periventricular nodular heterotopia of different aetiologies: one with severe epilepsy following focal brain trauma at 17 weeks gestation, one with hemimegalencephaly and intractable epilepsy, one with focal cortical dysplasia and intractable epilepsy, and one dysmorphic term infant with associated hydrocephalus and polymicrogyria. The connectivity of nodules was investigated using histological and carbocyanine dye (DiI) tracing techniques. DiI crystal placement adjacent to heterotopic nodules revealed numerous DiI-labelled fibres within a 2-3 mm radius of the crystals. Although we observed labelled fibres closely surrounding nodules, the majority did not penetrate them. Placement of DiI crystals within nodules also identified a limited number of projections out of the nodules and in one case there was evidence for connectivity between adjacent nodules. The cellular and neurochemical composition of nodules was also examined using immunohistochemistry for calretinin and neuropeptide Y (NPY), which are normally expressed in GABAergic cortical interneurons. Within heterotopic nodules from all cases, numerous calretinin-positive neurons were identified, along with a few cell bodies and many processes positive for NPY. Calretinin-positive neurons within nodules were less morphologically complex than those in the cortex, which may reflect incomplete differentiation into an inhibitory neuronal phenotype. There were also abnormal clusters of calretinin-positive cells in the overlying cortical plate, indicating that the migratory defect which produces heterotopic nodules also affects development of the cortex itself. Thus, heterotopic nodules consisting of multiple neuronal cell types are associated with malformation in the overlying cortical plate, and have limited connectivity with other brain regions. This abnormal development of connectivity may affect neuronal maturation and consequently the balance of excitation and inhibition in neuronal circuits, leading to their epileptogenic potential.},
	Author = {Hannan, A. J. and Servotte, S. and Katsnelson, A. and Sisodiya, S. and Blakemore, C. and Squier, M. and Moln{\'a}r, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0006-8950},
	Journal = {Brain},
	Keywords = {Fatal Outcome;10 Development;case reports;Magnetic Resonance Imaging;Fluorescent Dyes;Humans;gamma-Aminobutyric Acid;Fluorescent Antibody Technique;Female;Epilepsy;Child;research support, non-u.s. gov't;Calcium-Binding Protein, Vitamin D-Dependent;Male;Neuropeptide Y;Brain Chemistry;Cerebral Cortex;Cell Size;10 genetics malformation;Carbocyanines;Infant, Newborn;24 Pubmed search results 2008;Interneurons;Choristoma},
	Month = {2},
	Nlm_Id = {0372537},
	Organization = {University Laboratory of Physiology, University of Oxford, UK.},
	Pages = {219-38},
	Pubmed = {10071051},
	Title = {Characterization of nodular neuronal heterotopia in children},
	Uuid = {5E805D44-FFAB-493A-A39C-95B2279D7D07},
	Volume = {122 ( Pt 2)},
	Year = {1999}}

@article{Hannon:2002,
	Abstract = {A conserved biological response to double-stranded RNA, known variously as RNA interference (RNAi) or post-transcriptional gene silencing, mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes. RNAi has been cultivated as a means to manipulate gene expression experimentally and to probe gene function on a whole-genome scale. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Hannon, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:48 -0400},
	Journal = {Nature},
	Keywords = {RNA, Double-Stranded/chemistry/genetics/*metabolism;T pdf;*Gene Silencing;Genetic Techniques;Genome;Support, U.S. Gov't, Non-P.H.S.;RNA Processing, Post-Transcriptional;Models, Genetic;Support, U.S. Gov't, P.H.S.;Animals;Support, Non-U.S. Gov't;23 Technique},
	Number = {6894},
	Organization = {Cold Spring Harbour Laboratory, New York 11724, USA. hannon\@cshl.org},
	Pages = {244-51},
	Title = {RNA interference},
	Uuid = {C001D54E-371B-44E4-BB82-FE4A2A93F214},
	Volume = {418},
	Year = {2002},
	url = {papers/Hannon_Nature2002.pdf}}

@article{Hansen:2000,
	Abstract = {A pathogenetic hallmark of retroviral neurodegeneration is the affinity of neurovirulent retroviruses for microglia cells, while degenerating neurons are excluded from retroviral infections. Microglia isolated ex vivo from rats peripherally infected with a neurovirulent retrovirus released abundant mature type C virions; however, infectivity associated with microglia was very low. In microglia, viral transcription was unaffected but envelope proteins were insufficiently cleaved into mature viral proteins and were not detected on the microglia cell surface. These microglia-specific defects in envelope protein translocation and processing not only may have prevented formation of infectious virus particles but also may have caused further cellular defects in microglia with the consequence of indirect neuronal damage. It is conceivable that similar events play a role in neuro-AIDS.},
	Author = {Hansen, R. and Czub, S. and Werder, E. and Herold, J. and Gosztonyi, G. and Gelderblom, H. and Schimmer, S. and Mazgareanu, S. and ter Meulen, V. and Czub, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Macrophages, Peritoneal;Animals;Cells, Cultured;Rats;Microglia;Cell Membrane;Virion;Not relevant;11 Glia;Leukemia Virus, Murine;Intracellular Fluid;Defective Viruses;Viral Envelope Proteins;Support, Non-U.S. Gov't;Rats, Inbred F344;Protein Processing, Post-Translational;Mice;Retroviridae Proteins, Oncogenic;Transcription, Genetic},
	Medline = {20111297},
	Month = {2},
	Nlm_Id = {0113724},
	Number = {4},
	Organization = {Institut f]ur Virologie und Immunbiologie, Universit]at W]urzburg, D-97078 W]urzburg, Germany.},
	Pages = {1775-80},
	Pubmed = {10644349},
	Title = {Abundant defective viral particles budding from microglia in the course of retroviral spongiform encephalopathy},
	Uuid = {864ACFA8-C8FF-43DB-B4D3-ABDDE5924265},
	Volume = {74},
	Year = {2000},
	url = {papers/Hansen_JVirol2000.pdf}}

@article{Hao:1995,
	Abstract = {Gene therapy is a potential treatment for hemophilia, wherein cells transduced with a normal factor IX gene could provide a continuous in vivo source of circulating factor IX. In this study, we examined the potential use of hematopoietic cells as a target for factor IX gene therapy. Human myeloid leukemia cells (HL-60) were transduced by retroviral vectors carrying a normal human factor IX cDNA under control of either the Moloney murine leukemia virus long terminal repeat (MoMuLV LTR) (LIXSN), the SV40 promoter (LNSVIX), or a cytomegalovirus (CMV) promoter (LNCIX). Factor IX production was measured in the transduced cells both in the uninduced state and after induction of granulocytic differentiation [with dimethylsulfoxide (DMSO)] or monocytoid differentiation [with phorbol myristic acetate (PMA)]. Transcription of factor IX from the MoMuLV LTR was seen in all cells, with a two-fold increase upon differentiation. Induction with PMA led to an 8- to 15-fold increase in factor IX transcripts from an internal CMV promoter. No factor IX transcripts from the internal SV40 promoter were detected. Immunoreactive factor IX protein was identified by Western blot from induced HL-60 cells transduced by either LIXSN or LNCIX. Factor IX production by HL-60 cells transduced by LNCIX ranged from 38-93 ng/10(6) cells/24 hr following induction of monocytic differentiation. The factor IX antigen titer was directly related to factor IX coagulant titer (r = 0.98; p <0.001). These data indicate that human myelomonocytic cells are capable of performing the necessary post-translational modifications to produce functional factor IX.(ABSTRACT TRUNCATED AT 250 WORDS) 1043-0342 Journal Article},
	Author = {Hao, Q. L. and Malik, P. and Salazar, R. and Tang, H. and Gordon, E. M. and Kohn, D. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Hum Gene Ther},
	Keywords = {Retroviridae/*genetics;*Genetic Vectors;Coagulants/metabolism;Tetradecanoylphorbol Acetate/pharmacology;EE, DMSO, abstr;Human;08 Aberrant cell cycle;Hematopoietic System/metabolism;Blotting, Northern;HL-60 Cells;Factor IX/biosynthesis/*genetics/immunology;Support, Non-U.S. Gov't;*Gene Transfer Techniques},
	Number = {7},
	Organization = {Division of Research Immunology/Bone Marrow Transplantation, Childrens Hospital Los Angeles, CA, USA.},
	Pages = {873-80},
	Pubmed = {7578406},
	Title = {Expression of biologically active human factor IX in human hematopoietic cells after retroviral vector-mediated gene transduction},
	Uuid = {D0803E1F-5451-4AB3-813A-D65DDE720CC5},
	Volume = {6},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7578406}}

@article{Hardiman:1988,
	Abstract = {Fifty patients underwent superficial temporal lobectomy for intractable temporal lobe epilepsy. Total cure rate was 52\%, and significant improvement was achieved in 88\%. Cytoarchitectural changes in gray and white tissue were analyzed under light microscopy. Neuronal dysgenesis was correlated with the duration of seizure disorder, age of onset, and other etiologic factors, and with clinical outcome. Temporal lobes from 33 neurologically normal autopsy brains which were age- and sex-matched with patients were examined as controls. Severe neuronal ectopia (greater than 8 neurons/2 mm2 white matter) was present in 42\%of patients with epilepsy and in none of controls. There was neuronal clustering in 28\%of those with epilepsy, and Chaslin's (subpial) gliosis in 38\%. Controls did not have these changes. The presence of severe neuronal ectopia and clustering was predictive of a favorable clinical outcome following surgery (p less than 0.05). No correlation was found between microdysgenesis and other factors. These findings suggest that the presence of neuronal dysgenesis may be of significance in the clinical outcome following surgery, and that the abnormal tissue may be important as a morphologic substrate for seizures in some patients.},
	Author = {Hardiman, O. and Burke, T. and Phillips, J. and Murphy, S. and O'Moore, B. and Staunton, H. and Farrell, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0028-3878},
	Journal = {Neurology},
	Keywords = {Reference Values;10 Development;21 Dysplasia-heterotopia;21 Neurophysiology;Adolescent;Adult;Epilepsy, Temporal Lobe;Female;Middle Aged;10 genetics malformation;Child;Humans;Male;Temporal Lobe;Neurons;24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {0401060},
	Number = {7},
	Organization = {Richmond Institute of Neurology and Neurosurgery, Beaumont Hospital, Dublin, Ireland.},
	Pages = {1041-7},
	Pubmed = {3386820},
	Title = {Microdysgenesis in resected temporal neocortex: incidence and clinical significance in focal epilepsy},
	Uuid = {D4D5B7B9-4E8D-4600-80EC-6AF2216017D8},
	Volume = {38},
	Year = {1988}}

@article{Harkany:2004,
	Abstract = {Embryonic stem (ES) cells are multipotent progenitors with unlimited developmental potential, and in vitro differentiated ES cell-derived neuronal progenitors can develop into functional neurons when transplanted in the central nervous system. As the capacity of naive primary ES cells to integrate in the adult brain and the role of host neural tissue therein are yet largely unknown, we grafted low densities of undifferentiated mouse ES (mES) cells in adult mouse brain regions associated with neurodegenerative disorders; and we demonstrate that ES cell-derived neurons undergo gradual integration in recipient tissue and acquire morphological and electrophysiological properties indistinguishable from those of host neurons. Only some brain areas permitted survival of mES-derived neural progenitors and formed instructive environments for neuronal differentiation and functional integration of naive mES cells. Hence, region-specific presence of microenvironmental cues and their pivotal involvement in controlling ES cell integration in adult brain stress the importance of recipient tissue characteristics in formulating cell replacement strategies for neurodegenerative disorders.},
	Author = {Harkany, Tibor and And{\"a}ng, Michael and Kingma, Hylke Jan and G{\"o}rcs, Tam{\'a}s J. and Holmgren, Carl D. and Zilberter, Yuri and Ernfors, Patrik},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Cell Survival;Cell Differentiation;Electrophysiology;Animals;Cells, Cultured;Stem Cell Transplantation;Brain;Patch-Clamp Techniques;Mice, Transgenic;Mice, Inbred C57BL;Green Fluorescent Proteins;Male;17 Transplant Regeneration;Neurons;Mice;Luminescent Proteins;Stem Cells;22 Stem cells;Graft Survival;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {2985190R},
	Number = {5},
	Organization = {Department of Medical Biochemistry and Biophysics/Center of Excellence in Developmental Biology,Karolinska Institutet, Stockholm, Sweden.},
	Pages = {1229-39},
	Pii = {2243},
	Pubmed = {15009679},
	Title = {Region-specific generation of functional neurons from naive embryonic stem cells in adult brain},
	Uuid = {D2E0FE39-13B5-4E08-BA99-A78701AF481C},
	Volume = {88},
	Year = {2004},
	url = {papers/Harkany_JNeurochem2004.pdf}}

@article{Harris:1991,
	Abstract = {Based on morphological, virological, biochemical and molecular biological data, it is proposed that the presence of endogenous retrovirus particles in the placental cytotrophoblasts of many mammals is indicative of some beneficial action provided by the virus in relation to cell fusion, syncytiotrophoblast formation and the creation of the placenta. Further, it is hypothesised that the germ line retroviral infection of some primitive mammal-like species resulted in the evolution of the placental mammals.},
	Author = {Harris, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0014-5793},
	Journal = {FEBS Lett},
	Keywords = {15 ERVs retroelements;Female;Mammals;Placenta;Pregnancy;Evolution;15 Retrovirus mechanism;Animals;24 Pubmed search results 2008;review},
	Medline = {92111751},
	Month = {12},
	Nlm_Id = {0155157},
	Number = {1-3},
	Organization = {Institute of Cell and Tumour Biology, German Cancer Research Center, Heidelberg.},
	Pages = {3-4},
	Pii = {0014-5793(91)81370-N},
	Pubmed = {1765162},
	Title = {The evolution of placental mammals},
	Uuid = {6FE3A5AB-D6A0-41B1-B1DC-FAD397248927},
	Volume = {295},
	Year = {1991},
	url = {papers/Harris_FEBSLett1991.pdf}}

@article{Harris:2004,
	Abstract = {Analysis of developmental plasticity of bone marrow-derived cells (BMDCs) is complicated by the possibility of cell-cell fusion. Here we demonstrate that epithelial cells can develop from BMDCs without cell-cell fusion. We use the Cre/lox system together with beta-galactosidase and enhanced green fluorescent protein expression in transgenic mice to identify epithelial cells in the lung, liver, and skin that develop from BMDCs without cell fusion.},
	Author = {Harris, Robert G. and Herzog, Erica L. and Bruscia, Emanuela M. and Grove, Joanna E. and Van Arnam, John S. and Krause, Diane S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Cell Differentiation;22 Stem cells;Elapid Venoms;Recombinases;Epithelial Cells;Green Fluorescent Proteins;24 Pubmed search results 2008;Radiation, Ionizing;Luminescent Proteins;Male;Animals;Direct Lytic Factors;Research Support, U.S. Gov't, P.H.S.;X Chromosome;Y Chromosome;Keratin;Bone Marrow Transplantation;08 Aberrant cell cycle;Hepatocytes;beta-Galactosidase;Muscle Cells;Female;Bone Marrow Cells;Stem Cells;Recombination, Genetic;Mice;Cell Fusion;Research Support, Non-U.S. Gov't;Mice, Transgenic;Reverse Transcriptase Polymerase Chain Reaction;Keratinocytes},
	Month = {7},
	Nlm_Id = {0404511},
	Number = {5680},
	Organization = {Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.},
	Pages = {90-3},
	Pii = {305/5680/90},
	Pubmed = {15232107},
	Title = {Lack of a fusion requirement for development of bone marrow-derived epithelia},
	Uuid = {5CC0E045-CDD5-4813-B0E8-1F60CA48FCD5},
	Volume = {305},
	Year = {2004},
	url = {papers/Harris_Science2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1098925}}

@article{Harrison:2007,
	Abstract = {Sex is determined in Drosophila by the activity of the Sex-lethal master regulator. Activity of Sex-lethal is initiated early in females by chromosome-counting transcription factors, then reinforced by signaling through the Janus kinase pathway.},
	Author = {Harrison, Douglas A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {Janus Kinases;Sex Determination (Genetics);Female;Alternative Splicing;Drosophila Proteins;Gene Expression Regulation;Signal Transduction;Drosophila;comment;Animals;24 Pubmed search results 2008;review;Transcription Factors},
	Month = {5},
	Nlm_Id = {9107782},
	Number = {9},
	Organization = {Biology Department, University of Kentucky, Lexington, Kentucky 40506, USA. DougH\@email.uky.edu},
	Pages = {R328-30},
	Pii = {S0960-9822(07)01113-X},
	Pubmed = {17470347},
	Title = {Sex determination: controlling the master},
	Uuid = {A4DA062B-BB79-4093-895A-5FC6CB711E07},
	Volume = {17},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2007.03.012}}

@article{Harrison:2003,
	Abstract = {The expression of a number of chemokines and chemokine receptors by cells resident in normal and pathological central nervous system (CNS) tissue has been characterized by in situ hybridization techniques. As a result, our understanding of the role of this cytokine family in neurobiology has been enhanced greatly. Specific methods for detecting chemokine and chemokine receptor mRNAs in situ vary with the number of these genes that have been characterized and encompass approaches widely utilized by other investigators characterizing cell-specific gene expression patterns. We describe methods that our laboratory has used successfully in characterizing chemokine and chemokine receptor expression in the CNS, focusing on protocols that utilize radiolabeled in vitro-transcribed riboprobes for detecting these transcripts. Because general dye-based histological staining methods do not readily differentiate astrocytes and microglia, specific immunohistochemical protocols are required for definitive localization of gene expression to these glial cell types. As such, methods that are compatible with the in situ hybridization procedure are included for staining astrocytes and microglia.},
	Author = {Harrison, Jeffrey K. and Luo, Defang and Streit, Wolfgang J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {1046-2023},
	Journal = {Methods},
	Keywords = {In Situ Hybridization;Dyes;Neuroglia;Central Nervous System;Immunohistochemistry;Rats;Astrocytes;Not relevant;Plasmids;Chemokines;Transcription, Genetic;11 Glia;Blotting, Northern;Animals;RNA, Messenger;Receptors, Chemokine;Oxazines},
	Medline = {22613545},
	Month = {4},
	Nlm_Id = {9426302},
	Number = {4},
	Organization = {Department of Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, FL 32610-0267, USA. harrison\@pharmacology.ufl.edu},
	Pages = {312-8},
	Pii = {S1046202302003547},
	Pubmed = {12725797},
	Title = {In situ hybridization analysis of chemokines and chemokine receptors in the central nervous system},
	Uuid = {0F1225E4-DB47-4E80-9054-399F9D1F725E},
	Volume = {29},
	Year = {2003}}

@article{Harrison:1998,
	Abstract = {A recently identified chemokine, fractalkine, is a member of the chemokine gene family, which consists principally of secreted, proinflammatory molecules. Fractalkine is distinguished structurally by the presence of a CX3C motif as well as transmembrane spanning and mucin-like domains and shows atypical constitutive expression in a number of nonhematopoietic tissues, including brain. We undertook an extensive characterization of this chemokine and its receptor CX3CR1 in the brain to gain insights into use of chemokine-dependent systems in the central nervous system. Expression of fractalkine in rat brain was found to be widespread and localized principally to neurons. Recombinant rat CX3CR1, as expressed in Chinese hamster ovary cells, specifically bound fractalkine and signaled in the presence of either membrane-anchored or soluble forms of fractalkine protein. Fractalkine stimulated chemotaxis and elevated intracellular calcium levels of microglia; these responses were blocked by anti-CX3CR1 antibodies. After facial motor nerve axotomy, dramatic changes in the levels of CX3CR1 and fractalkine in the facial nucleus were evident. These included increases in the number and perineuronal location of CX3CR1-expressing microglia, decreased levels of motor neuron-expressed fractalkine mRNA, and an alteration in the forms of fractalkine protein expressed. These data describe mechanisms of cellular communication between neurons and microglia, involving fractalkine and CX3CR1, which occur in both normal and pathological states of the central nervous system.},
	Author = {Harrison, J. K. and Jiang, Y. and Chen, S. and Xia, Y. and Maciejewski, D. and McNamara, R. K. and Streit, W. J. and Salafranca, M. N. and Adhikari, S. and Thompson, D. A. and Botti, P. and Bacon, K. B. and Feng, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Hamsters;Animals;Cloning, Molecular;Rats;Brain;Microglia;CHO Cells;Rats, Sprague-Dawley;Recombinant Fusion Proteins;11 Glia;Male;Chemokines, CX3C;Chemokines, CXC;Support, U.S. Gov't, P.H.S.;Motor Neurons;Amino Acid Sequence;Molecular Sequence Data;Membrane Proteins},
	Medline = {98393742},
	Month = {9},
	Nlm_Id = {7505876},
	Number = {18},
	Organization = {Department of Pharmacology and Therapeutics, University of Florida, Gainesville, FL 32610, USA.},
	Pages = {10896-901},
	Pubmed = {9724801},
	Title = {Role for neuronally derived fractalkine in mediating interactions between neurons and CX3CR1-expressing microglia},
	Uuid = {1F5F030A-69AC-49DD-8ABF-F2D13794A159},
	Volume = {95},
	Year = {1998},
	url = {papers/Harrison_ProcNatlAcadSciUSA1998.pdf}}

@article{Hart:2006,
	Abstract = {The X-linked gene filamin A (Flna) encodes a widely expressed actin-binding protein that crosslinks actin into orthogonal networks and interacts with a variety of other proteins including membrane proteins, integrins, transmembrane receptor complexes and second messengers, thus forming an important intracellular signalling scaffold. Heterozygous loss of function of human FLNA causes periventricular nodular heterotopia in females and is generally lethal (cause unknown) in hemizygous males. Missense FLNA mutations underlie a spectrum of disorders affecting both sexes that feature skeletal dysplasia accompanied by a variety of other abnormalities. Dilp2 is an X-linked male-lethal mouse mutation that was induced by N-ethyl-N-nitrosourea. We report here that Dilp2 is caused by a T-to-A transversion that converts a tyrosine codon to a stop codon in the Flna gene (Y2388X), leading to absence of the Flna protein and male lethality because of incomplete septation of the outflow tract of the heart, which produces common arterial trunk. A proportion of both male and female mutant mice have other cardiac defects including ventricular septal defect. In addition, mutant males have midline fusion defects manifesting as sternum and palate abnormalities. Carrier females exhibit milder sternum and palate defects and misshapen pupils. These results define crucial roles for Flna in development, demonstrate that X-linked male lethal mutations can be recovered from ENU mutagenesis screens and suggest possible explanations for lethality of human males hemizygous for null alleles of FLNA.},
	Author = {Hart, Alan W. and Morgan, Joanne E. and Schneider, J{\"u}rgen and West, Katrine and McKie, Lisa and Bhattacharya, Shoumo and Jackson, Ian J. and Cross, Sally H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:45:47 -0400},
	Issn = {0964-6906},
	Journal = {Hum Mol Genet},
	Keywords = {Mice, Inbred BALB C;10 Development;Heterozygote;Embryo Loss;Genes, Lethal;Animals;Pupil Disorders;Mice, Mutant Strains;Microfilament Proteins;Pregnancy;Phenotype;Osteogenesis;Genes, X-Linked;Female;Heart Defects, Congenital;research support, non-u.s. gov't;Point Mutation;Male;Bone and Bones;10 genetics malformation;Sex Characteristics;Loss of Heterozygosity;Mice;24 Pubmed search results 2008;Contractile Proteins;Palate;Gene Expression;Mutant Proteins},
	Month = {8},
	Nlm_Id = {9208958},
	Number = {16},
	Organization = {Comparative and Developmental Genetics Section, MRC Human Genetics Unit, Edinburgh EH4 2XU, UK.},
	Pages = {2457-67},
	Pii = {ddl168},
	Pubmed = {16825286},
	Title = {Cardiac malformations and midline skeletal defects in mice lacking filamin A},
	Uuid = {54AE64C9-D05A-43D4-948F-5E7259B58154},
	Volume = {15},
	Year = {2006},
	url = {papers/Hart_HumMolGenet2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/hmg/ddl168}}

@article{Hartfuss:2003,
	Abstract = {Radial glial cells are characterized, besides their astroglial properties, by long radial processes extending from the ventricular zone to the pial surface, a crucial feature for the radial migration of neurons. The molecular signals that regulate this characteristic morphology, however, are largely unknown. We show an important role of the secreted molecule reelin for the establishment of radial glia processes. We describe a significant reduction in ventricular zone cells with long radial processes in the absence of reelin in the cortex of reeler mutant mice. These defects were correlated to a decrease in the content of brain lipid-binding protein (Blbp) and were detected exclusively in the cerebral cortex, but not in the basal ganglia of reeler mice. Conversely, reelin addition in vitro increased the Blbp content and process extension of radial glia from the cortex, but not the basal ganglia. Isolation of radial glia by fluorescent-activated cell sorting showed that these effects are due to direct signaling of reelin to radial glial cells. We could further demonstrate that this signaling requires Dab1, as the increase in Blbp upon reelin addition failed to occur in Dab1-/- mice. Taken together, these results unravel a novel role of reelin signaling to radial glial cells that is crucial for the regulation of their Blbp content and characteristic morphology in a region-specific manner.},
	Author = {Hartfuss, Eva and F{\"o}rster, Eckart and Bock, Hans H. and Hack, Michael A. and Leprince, Pierre and Luque, Juan M. and Herz, Joachim and Frotscher, Michael and G{\"o}tz, Magdalena},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {10 Development;Cell Differentiation;Signal Transduction;Animals;10 Hippocampus;Carrier Proteins;Cell Surface Extensions;Cell Adhesion Molecules, Neuronal;Mice, Inbred C57BL;Recombinant Fusion Proteins;Serine Endopeptidases;Mice, Neurologic Mutants;Extracellular Matrix Proteins;Research Support, U.S. Gov't, P.H.S.;Cell Size;Neurons;Neuroglia;Cerebral Cortex;Mice;Fatty Acid-Binding Proteins;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22806427},
	Month = {10},
	Nlm_Id = {8701744},
	Number = {19},
	Organization = {Max-Planck-Institute of Neurobiology, Neuronal Specification, Am Klopferspitz 18a, D-82152 Martinsried, Germany.},
	Pages = {4597-609},
	Pii = {130/19/4597},
	Pubmed = {12925587},
	Title = {Reelin signaling directly affects radial glia morphology and biochemical maturation},
	Uuid = {EEEA839C-8C1B-43ED-9391-BFD703C66BD5},
	Volume = {130},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.00654}}

@article{Hase:2002,
	Abstract = {The present study aimed to analyse how anatomical regeneration contributes to functional recovery after experimental spinal cord repair. Thoracic spinal cord of neonatal rats was completely transected to make a gap and repaired by grafting a section of embryonic spinal cord. Six weeks after surgery, outcome of locomotor performance was assessed using an open field locomotor scale (BBB scale). Axonal regeneration across the repaired site was quantitatively assessed in the raphe, vestibular, and red nuclei and the sensorimotor cortex by a retrograde tracing method. The rats that had no labelled neurons in any of the supraspinal nuclei showed no hind-forelimb coordination. The rats that had labelled neurons in the brainstem nuclei but not in the sensorimotor cortex showed hind-forelimb coordination of varying grades depending on the amount of regeneration. The rats that had labelled neurons in all of the examined nuclei showed almost normal locomotion. In addition to a relationship between distribution of the labelled neurons and functional recovery, a positive correlation was observed between number of the labelled neurons in each of the supraspinal nuclei and locomotor performance of the rat. Thus the grade of restored function appeared to be regulated by distribution and number of fibres regenerated across the repaired site and into the target region. These results suggest that accurate reconstruction of neural connections is essential for significant functional recovery after spinal cord repair.},
	Author = {Hase, Takao and Kawaguchi, Saburo and Hayashi, Hideki and Nishio, Takeshi and Mizoguchi, Akira and Nakamura, Takashi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Fetus;Pregnancy;Animals;Efferent Pathways;Brain Tissue Transplantation;Rats;Recovery of Function;Brain;Female;Axons;Rats, Wistar;Spinal Cord;Nerve Regeneration;Spinal Cord Injuries;Animals, Newborn;24 Pubmed search results 2008;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {21916982},
	Month = {3},
	Nlm_Id = {8918110},
	Number = {6},
	Organization = {Department of Integrative Brain Science, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan.},
	Pages = {969-74},
	Pii = {1932},
	Pubmed = {11918656},
	Title = {Spinal cord repair in neonatal rats: a correlation between axonal regeneration and functional recovery},
	Uuid = {4B23BFD2-24FC-43A5-A731-0AF2204ED832},
	Volume = {15},
	Year = {2002}}

@article{Hashizume:2004,
	Abstract = {The results of clinical and experimental studies on epilepsy associated with focal cortical dysplasia (FCD) are presented. We have been interested in the findings of abnormal increases in the numbers of small vessels in specimens of FCD resected from epilepsy patients. In the clinical study of 13 patients with epilepsy, specimens of FCD or dysembryoplastic neuroepithelial tumor (DNT) were examined using immunohistochemistry. The number of vessels in both lesions were greater than those in cortical specimens of autopsy cases without epilepsy. Because the vessels showed negative staining of VEGF, it was thought that the phenomenon of increase in the number of vessels was simply a hypervascularity, not a neovascularity. The local hypervascularity was expected to show local hyperperfusion in CBF-SPECT study, but interictal SPECT demonstrated local hypoperfusion and ictal SPECT showed hyperperfusion. This may have been caused by a functional change in those vessels. In the experimental study, we tried to make a new animal model of FCD to study epileptogenicity of FCD. When kainic acid had been infused into the neocortex in the neonatal rats, FCD was induced in adult Wistar rats. Histopathological examination revealed cortical dyslamination and abnormal neurons. On EEG, local spike bursts were elicited from the lesions, however, clinical seizures were not detected. Although the data are preliminary and observation over a longer period is required to determine whether spontaneous seizures will occur in this model, it is expected that this new model will be useful for studying epilepsy associated with FCD.},
	Author = {Hashizume, Kiyotaka and Tsuda, Hiroshige and Hodozuka, Akira and Tanaka, Tatsuya},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1323-1316},
	Journal = {Psychiatry Clin Neurosci},
	Keywords = {Animals;Neoplasms, Neuroepithelial;Rats;Brain;21 Epilepsy;Excitatory Amino Acid Agonists;Epilepsy;Rats, Wistar;Cerebrovascular Circulation;Motor Cortex;Male;Kainic Acid;Brain Neoplasms;Disease Models, Animal;Animals, Newborn;21 Neurophysiology;Somatosensory Cortex;24 Pubmed search results 2008;Immunohistochemistry;Electroencephalography;Blood Vessels},
	Month = {6},
	Nlm_Id = {9513551},
	Number = {3},
	Organization = {Department of Neurosurgery, Asahikawa Medical College, Asahikawa, Japan. kmark113\@asahikawa-med.ac.jp},
	Pages = {S26-9},
	Pii = {PCN1244_7},
	Pubmed = {15149312},
	Title = {Clinical and experimental studies of epilepsy associated with focal cortical dysplasia},
	Uuid = {0F343945-FDAC-4CC7-A141-8597E91BD0A8},
	Volume = {58},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1440-1819.2004.01244_7.x}}

@article{Hastings:1999,
	Abstract = {The dentate gyrus continues to produce granule neurons throughout adulthood. The present study examined the extension of axons by adult- generated granule neurons into hippocampal area CA3. We injected the fluorescent retrograde tracers Fast blue (FB) and FluoroRuby (FR) into area CA3 of adult male rats at various times after the administration of 5'-bromo-2'-deoxyuridine (BrdU), a marker of proliferating cells and their progeny. We report that immature granule cells extend axons into CA3 as rapidly as 4-10 days after mitosis. A significant increase in the percentage of BrdU-labeled cells that were labeled with FB or FR was observed by 2 weeks after BrdU administration. This proportion remained roughly constant up to 3 weeks after BrdU-labeling, a time at which markers of a mature neuronal phenotype are expressed. BrdU- labeled cells that contained either FB or FR often were located far from the tracer injection site, indicating that these cells had extended relatively long axons. Collectively these results suggest that adult-generated granule neurons may influence normal hippocampal function, even at a very early stage after their production.},
	Author = {Hastings, N. B. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Fluorescent Dyes;Neural Pathways/physiology/ultrastructure;Animals;Axons/*physiology;Aging;Rats;Neural Pathways;Hippocampus/*physiology/ultrastructure;Animal;Cell Count;02 Adult neurogenesis migration;Dentate Gyrus/physiology/ultrastructure;Rats, Sprague-Dawley;Axons;Hippocampus;Time Factors;Male;Aging/pathology/*physiology;Research Support, U.S. Gov't, P.H.S.;B;Neurons;Dentate Gyrus;Support, U.S. Gov't, P.H.S.;24 Pubmed search results 2008;Bromodeoxyuridine;Immunohistochemistry;Neurons/*physiology/ultrastructure},
	Medline = {99395198},
	Month = {10},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Psychology, Princeton University, Princeton, New Jersey 08544, USA. hastings\@princeton.edu},
	Pages = {146-54.},
	Pii = {10.1002/(SICI)1096-9861(19991011)413:1<146::AID-CNE10>3.0.CO;2-B},
	Pubmed = {10464376},
	Title = {Rapid extension of axons into the CA3 region by adult-generated granule cells},
	Uuid = {3992BB66-9C25-475A-9D68-33D10ABF2B9E},
	Volume = {413},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10464376}}

@article{Hatanaka:2002,
	Abstract = {During development neurons migrate from their site of origin to their final destinations under a variety of mechanisms. Although evidence has been accumulating that the cells from cortical ventricular zone (VZ) migrate radially and produce pyramidal cells, evidence that directly links the origin and the terminal phenotype of radially migrating cells has been limited. Further, the relation between the migratory behavior of these cells and their mature morphology remains obscure. To address these issues, we developed an in vitro preparation that enables visualization of cells derived from the cortical VZ. VZ cells of a rat cortex at embryonic days 18 to 19 were labeled by injecting green fluorescent protein (GFP)-encoding plasmid into the lateral ventricle, followed by electroporation. The cortex was then sliced and cultured organotypically. After 1 day, GFP(+) cells exhibited neural progenitor and radial glial cell natures. Over the next few days, many GFP(+) cells migrated toward the pial surface, extending leading processes toward the pial surface and leaving a thin trailing process that almost reached the VZ. The leading processes of these neurons were positive for microtubule-associated protein 2, and some transformed into dendritic arbor-like structures by day 5 or 6, and their trailing processes exhibited morphologic features indicative of prospective axons. Time-lapse analysis confirmed extension of the trailing processes. Expression of molecular markers and morphologic analysis demonstrated that the vast majority of the migrated GFP(+) cells differentiated into excitatory neurons with pyramidal cell-like morphology. These results strongly suggested that cells derived from the cortical VZ generate neurons that migrate radially. These neurons appeared to extend prospective dendrites in front and leave prospective axons behind, subsequently differentiating into pyramidal cells.},
	Author = {Hatanaka, Yumiko and Murakami, Fujio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Fluorescent Dyes;Microtubule-Associated Proteins;Cell Differentiation;Animals;In Vitro;Rats;Cell Movement;Axons;Pyramidal Cells;Rats, Wistar;11 Glia;Green Fluorescent Proteins;Injections, Intraventricular;Dendrites;Mice, Inbred ICR;Cerebral Ventricles;Plasmids;Cell Lineage;Cerebral Cortex;Neuroglia;Mice;Luminescent Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {22297222},
	Month = {12},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Division of Behavior and Neurobiology, National Institute for Basic Biology, Okazaki, Aichi 444-8585, Japan. yumiko\@nibb.ac.jp},
	Pages = {1-14},
	Pubmed = {12410614},
	Title = {In vitro analysis of the origin, migratory behavior, and maturation of cortical pyramidal cells},
	Uuid = {C3362B1A-A354-470B-98C6-BABD96FC287B},
	Volume = {454},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10421}}

@article{Hatch:1994,
	Abstract = {Some children infected by HIV-1 demonstrate nervous system disease. Because a significant percentage of these children are believed to be infected during gestation and it is thought that HIV-1 may infect distinct glial populations, this work tested the hypothesis that different HIV-1 isolates can infect cells of the developing human fetal central nervous system (CNS). Central nervous system organotypic tissue cultures derived from human fetal brain enable the study of complex interactions between CNS cell types. Central nervous system organotypic cultures were exposed to lymphocytotropic (L-tropic) or monocytotropic (M-tropic) HIV-1 isolates and monitored for viral infection. HIV-1 gp41 and p24 antigens were detected by immunocytochemistry (ICC), HIV-1 RNA was localized in the cytoplasm of CNS cells by in situ hybridization (ISH), and viral DNA was detected by polymerase chain reaction (PCR) in HIV-1-exposed cultures. Double-label ICC identified HIV-1 antigens in both microglia and astrocytes. These results demonstrate that both L- and M-tropic isolates infect microglia and astrocytes in human fetal organotypic cultures. In addition, HIV-1 infection was detected in culture supernatants up to day 57 postinfection and at 90 days by coculture with susceptible CEM cells. HIV-1 infection of neural cells appears to be productive. This model may permit further examination of the interaction of HIV-1 with the developing human CNS and the mechanisms of AIDS-associated neuropathology.},
	Author = {Hatch, W. C. and Pousada, E. and Losev, L. and Rashbaum, W. K. and Lyman, W. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0889-2229},
	Journal = {AIDS Res Hum Retroviruses},
	Keywords = {Fetus;Human;Tissue Culture;HIV-1;Astrocytes;Base Sequence;Humans;Microglia;Female;Culture Techniques;11 Glia;Giant Cells;DNA Primers;Research Support, U.S. Gov't, P.H.S.;Neurons;Support, U.S. Gov't, P.H.S.;Virus Replication;Molecular Sequence Data;Central Nervous System},
	Medline = {95194725},
	Month = {12},
	Nlm_Id = {8709376},
	Number = {12},
	Organization = {Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461.},
	Pages = {1597-607},
	Pubmed = {7888218},
	Title = {Neural cell targets of human immunodeficiency virus type 1 in human fetal organotypic cultures},
	Uuid = {BCFCEB98-EA03-4BAB-A599-A10CFE15A3A0},
	Volume = {10},
	Year = {1994}}

@article{Hatfield:2005,
	Abstract = {One of the key characteristics of stem cells is their capacity to divide for long periods of time in an environment where most of the cells are quiescent. Therefore, a critical question in stem cell biology is how stem cells escape cell division stop signals. Here, we report the necessity of the microRNA (miRNA) pathway for proper control of germline stem cell (GSC) division in Drosophila melanogaster. Analysis of GSCs mutant for dicer-1 (dcr-1), the double-stranded RNaseIII essential for miRNA biogenesis, revealed a marked reduction in the rate of germline cyst production. These dcr-1 mutant GSCs exhibit normal identity but are defective in cell cycle control. On the basis of cell cycle markers and genetic interactions, we conclude that dcr-1 mutant GSCs are delayed in the G1 to S transition, which is dependent on the cyclin-dependent kinase inhibitor Dacapo, suggesting that miRNAs are required for stem cells to bypass the normal G1/S checkpoint. Hence, the miRNA pathway might be part of a mechanism that makes stem cells insensitive to environmental signals that normally stop the cell cycle at the G1/S transition.},
	Author = {Hatfield, S. D. and Shcherbata, H. R. and Fischer, K. A. and Nakahara, K. and Carthew, R. W. and Ruohola-Baker, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-13 09:45:17 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Research Support, Non-U.S. Gov't;G1 Phase;S Phase;Gene Deletion;Research Support, U.S. Gov't, P.H.S.;Drosophila Proteins;Cell Division;Drosophila melanogaster;Genome;Nuclear Proteins;Research Support, N.I.H., Extramural;MicroRNAs;Stem Cells;Animals;Ribonuclease III;24 Pubmed search results 2008; microRNAs; development},
	Month = {6},
	Nlm_Id = {0410462},
	Number = {7044},
	Organization = {Department of Biochemistry, University of Washington, J591, HSB, Seattle, Washington 98195-7350, USA.},
	Pages = {974-8},
	Pii = {nature03816},
	Pubmed = {15944714},
	Title = {Stem cell division is regulated by the microRNA pathway},
	Uuid = {E9BF0371-4995-441E-9A68-31ABFFBFFAB4},
	Volume = {435},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03816}}

@article{Hatten:2002,
	Abstract = {Over the past decade, genetic analyses have yielded a more molecular view of neuronal migration and its role in central nervous system development. We now realize that many of the molecular mechanisms that guide migrations in invertebrates are recapitulated in the vertebrate nervous system. These mechanisms guide dorsoventral and anterior-posterior migrations and merge with radial migratory pathways that are prominent in the development of the mammalian cortex. This review discusses the choreography of these different migratory mechanisms within the context of genetic approaches that have defined their molecular mechanisms. 1095-9203 Journal Article Review Review, Tutorial},
	Author = {Hatten, M. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:48 -0400},
	Journal = {Science},
	Keywords = {10 Development;F both;*Caenorhabditis elegans Proteins;Telencephalon/cytology;Nerve Growth Factors/physiology;Neurons/*cytology;Cell Movement/*physiology;Animals;Vertebrates;*Nerve Tissue Proteins;Helminth Proteins/physiology;Neuroglia/physiology},
	Number = {5587},
	Organization = {Laboratory of Developmental Neurobiology, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6399, USA. hatten\@rockefeller.edu},
	Pages = {1660-3},
	Title = {New directions in neuronal migration},
	Uuid = {4071EC2D-FF38-4275-AC6E-D1F5CD50A1F4},
	Volume = {297},
	Year = {2002},
	url = {papers/Hatten_Science2002.pdf}}

@article{Hayakawa:2003,
	Abstract = {Studies have indicated that bone marrow contains both hematopoietic stem cells and mesenchymal stem cells that can differentiate into a variety of mesenchymal tissues, such as bone, cartilage, muscle, and adipose tissue. Therefore, bone marrow cells are thought to be very useful for cell and gene therapy for various diseases. However, the multipotentiality of these cells remains unclear. To address this issue, we established a chimeric model mouse stably reconstituted with green fluorescent protein (GFP)-marked bone marrow cells. We injected bone marrow cells from GFP-transgenic C57BL/6 mice into the tail veins of recipient wild-type C57BL/6 mice that had been irradiated with a lethal dose of 10 Gy from a cesium source. Microscopic examination and fluorescence-assisted cell sorter (FACS) analysis showed that bone marrow cells, including mesenchymal cells, were almost completely reconstituted with GFP+ cells 5 weeks after transplantation. FACS analysis with lineage-specific antibodies confirmed that the GFP+ cells could differentiate into all types of blood cells. To confirm the usefulness of this mouse model, we studied the role of circulating bone marrow-derived cells in healing of damaged intestine. We performed amputation and anastomosis of the jejunum 10 cm from the pyloric region of the stomach. On the third day after operation, a large number of GFP+ cells were infiltrated in the area of anastomosis, and these cells were positive for CD45 and F4/80 antigens. In 7 days, several cells became negative for CD45 and F4/80 and positive for alpha smooth muscle actin antigen, which is specific for smooth muscle. This finding suggested that bone marrow-derived cells had differentiated into smooth muscle. Because reconstituted bone marrow cells as opposed to injected bone marrow cells, behave naturally, this model is ideal for studying the multipotentiality of bone marrow cells in vivo.},
	Author = {Hayakawa, Jun and Migita, Makoto and Ueda, Takahiro and Shimada, Takashi and Fukunaga, Yoshitaka},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0925-5710},
	Journal = {Int J Hematol},
	Keywords = {Myocytes, Smooth Muscle;Flow Cytometry;Cell Differentiation;Luminescent Proteins;Models, Animal;Bone Marrow Cells;Regeneration;Mice, Inbred C57BL;Bone Marrow Transplantation;11 Glia;Mice, Transgenic;Green Fluorescent Proteins;Jejunum;Mice;Cell Movement;Animals;Transplantation Chimera},
	Medline = {22724912},
	Month = {6},
	Nlm_Id = {9111627},
	Number = {5},
	Organization = {Department of Pediatrics, Center for Advanced Medical Technology, Nippon Medical School, Tokyo, Japan.},
	Pages = {456-62},
	Pubmed = {12841383},
	Title = {Generation of a chimeric mouse reconstituted with green fluorescent protein-positive bone marrow cells: a useful model for studying the behavior of bone marrow cells in regeneration in vivo},
	Uuid = {AE8FD54A-504A-4FB2-B025-B47A7360BBC7},
	Volume = {77},
	Year = {2003}}

@article{Hayakawa:2005,
	Abstract = {Recent studies have shown multiple differences between humans and apes in sialic acid (Sia) biology, including Siglecs (Sia-recognizing-Ig-superfamily lectins). Comparisons with the chimpanzee genome indicate that human SIGLEC11 emerged through human-specific gene conversion by an adjacent pseudogene. Conversion involved 5 cent untranslated sequences and the Sia-recognition domain. This human protein shows reduced binding relative to the ancestral form but recognizes oligosialic acids, which are enriched in the brain. SIGLEC11 is expressed in human but not in chimpanzee brain microglia. Further studies will determine if this event was related to the evolution of Homo.},
	Author = {Hayakawa, Toshiyuki and Angata, Takashi and Lewis, Amanda L. and Mikkelsen, Tarjei S. and Varki, Nissi M. and Varki, Ajit},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Animals;Humans;Brain;Exons;Pan troglodytes;Phylogeny;Microglia;Pseudogenes;11 Glia;Gene Conversion;Pongo pygmaeus;Evolution;Research Support, U.S. Gov't, P.H.S.;Sialic Acids;19 Neocortical evolution;Regulatory Sequences, Nucleic Acid;Membrane Proteins;Research Support, N.I.H., Extramural;Lectins;Research Support, Non-U.S. Gov't},
	Month = {9},
	Nlm_Id = {0404511},
	Number = {5741},
	Organization = {Glycobiology Research and Training Center, University of California at San Diego, La Jolla, CA 92093, USA.},
	Pages = {1693},
	Pii = {309/5741/1693},
	Pubmed = {16151003},
	Title = {A human-specific gene in microglia},
	Uuid = {869DE839-F0EB-4AA3-80E6-FFF8094C90A1},
	Volume = {309},
	Year = {2005},
	url = {papers/Hayakawa_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1114321}}

@article{Haydar:2000,
	Abstract = {Recent studies have implicated the classical neurotransmitters GABA and glutamate in the regulation of neural progenitor proliferation. We now show that GABA and glutamate have opposite effects on the two neural progenitor populations in the ventricular zones (VZs) and subventricular zones (SVZs) of the embryonic cerebrum. Application of either molecule to organotypic slice cultures dramatically increases proliferation in the VZ by shortening the cell cycle, whereas proliferation in the SVZ is decreased. These disparate effects, measured both by bromodeoxyuridine uptake and the expansion of retrovirally labeled progenitor clones, are mimicked by the application of specific GABA and glutamate agonists and are blocked by antagonists. Thus, the relative contributions of the VZ and SVZ to neocortical growth may be regulated by differential responsiveness to GABA and glutamate. 0270-6474 Journal Article},
	Author = {Haydar, T. F. and Wang, F. and Schwartz, M. L. and Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {J Neurosci},
	Keywords = {10 Development;Animals;Bromodeoxyuridine/pharmacology;Kainic Acid/pharmacology;Neurons/*cytology;F abstr;Excitatory Amino Acid Antagonists/pharmacology;Cerebral Ventricles/chemistry/*cytology/embryology;Muscimol/pharmacology;Stem Cells/*cytology/drug effects;Cell Division/drug effects/physiology;Clone Cells/drug effects/physiology;Neocortex/chemistry/*cytology/embryology;Glutamic Acid/analysis/*pharmacology;Mice, Inbred ICR;Excitatory Amino Acid Agonists/pharmacology;Cell Movement/drug effects/physiology;Antimetabolites/pharmacology;GABA Agonists/pharmacology;Cell Differentiation/drug effects/physiology;Support, U.S. Gov't, P.H.S.;Mice;GABA Antagonists/pharmacology;6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology;Organ Culture;gamma-Aminobutyric Acid/analysis/*pharmacology;Fetus/cytology},
	Number = {15},
	Organization = {Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.},
	Pages = {5764-74},
	Pubmed = {10908617},
	Title = {Differential modulation of proliferation in the neocortical ventricular and subventricular zones},
	Uuid = {BB2FAF94-87DD-4C4A-87D8-9E6FF4E91144},
	Volume = {20},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10908617}}

@article{Haydar:2005,
	Abstract = {Studies on human patients and animal models of disease have shown that disruptions in prenatal and early postnatal brain development are a root cause of mental retardation. Since proper brain development is achieved by a strict spatiotemporal control of neurogenesis, cell migration, and patterning of synapses, abnormalities in one or more of these events during prenatal development can lead to cognitive dysfunction after birth. Many of underlying causes of mental retardation must therefore be studied in developing brains. To aid in this research, live imaging using laser scanning microscopy (LSM) has recently allowed neuroscientists to delve deeply into the complex three-dimensional environment of the living brain to record dynamic cellular events over time. This review will highlight recent examples of how LSM is being applied to elucidate both normal and abnormal cortical development.},
	Author = {Haydar, Tarik F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1080-4013},
	Journal = {Ment Retard Dev Disabil Res Rev},
	Keywords = {Pregnancy;Cell Differentiation;Down Syndrome;Absorptiometry, Photon;Humans;Microscopy, Confocal;Brain;Apoptosis;Female;Cell Movement;21 Epilepsy;review;Mental Retardation;Neurons;21 Neurophysiology;Prenatal Exposure Delayed Effects;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Fragile X Syndrome},
	Nlm_Id = {9517974},
	Number = {4},
	Organization = {Center for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC 20010, USA. thaydar\@cnmcresearch.org},
	Pages = {303-16},
	Pubmed = {16240412},
	Title = {Advanced microscopic imaging methods to investigate cortical development and the etiology of mental retardation},
	Uuid = {51D05EF6-F039-47F7-A44E-DDC3EF0F7015},
	Volume = {11},
	Year = {2005},
	url = {papers/Haydar_MentRetardDevDisabilResRev2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/mrdd.20088}}

@article{Haydar:2003,
	Abstract = {The mode of neural stem cell division in the forebrain proliferative zones profoundly influences neocortical growth by regulating the number and diversity of neurons and glia. Long-term time-lapse multiphoton microscopy of embryonic mouse cortex reveals new details of the complex three-dimensional rotation and oscillation of the mitotic spindle before stem cell division. Importantly, the duration and amplitude of spindle movement predicts and specifies the eventual mode of mitotic division. These technological advances have provided dramatic data and insights into the kinetics of neural stem cell division by elucidating the involvement of spindle rotation in selection of the cleavage plane and the mode of neural stem cell division that together determine the size of the mammalian neocortex. 22506285 0027-8424 Journal Article},
	Author = {Haydar, T. F. and Ang, E. and Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Nervous System/cytology;Telencephalon/*embryology/*metabolism;10 Development;Image Processing, Computer-Assisted;Time Factors;Cell Division;Animal;Mice, Inbred ICR;Brain/pathology;Support, U.S. Gov't, P.H.S.;F;Neurons/*cytology;Support, Non-U.S. Gov't;Mice;Photons;Mitotic Spindle Apparatus/chemistry/*physiology},
	Number = {5},
	Organization = {Department of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.},
	Pages = {2890-5},
	Pubmed = {12589023},
	Title = {Mitotic spindle rotation and mode of cell division in the developing telencephalon},
	Uuid = {0D76DEAD-EAF6-4831-AC44-171244E56F35},
	Volume = {100},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12589023}}

@article{Hayes:2000,
	Abstract = {Two S-phase markers for in vivo studies of cell proliferation in the developing central nervous system, tritiated thymidine ((3)H-TdR) and bromodeoxyuridine (BUdR), were compared using double-labeling techniques in the developing mouse cortex at embryonic day 14 (E14). The labeling efficiencies and detectability of the two tracers were approximately equivalent, and there was no evidence of significant tracer interactions that depend on order of administration. For both tracers, the loading time needed to label an S-phase cell to detectability is estimated at <0.2 h shortly after the injection of the label, but, as the concentration of the label falls, it increases to approximately 0.65 h after about 30 min. Thereafter, cells that enter the S-phase continue to become detectably labeled for approximately 5-6 h. The approximate equivalence of these two tracers was exploited to observe directly the numbers and positions of nuclei entering (labeled with the second tracer only) and leaving (labeled with the first tracer only) the S-phase. As expected, the numbers of nuclei entering and leaving the S-phase both increased as the interval between the two injections lengthened. Also, nuclei leaving the S-phase rapidly move towards the ventricular surface during G2, but, unexpectedly, the distribution of the entering nuclei does not differ significantly from the distribution of the nuclei in the S-phase. This indicates that: (1) the extent and rate of abventricular nuclear movement during G1 is variable, such that not all nuclei traverse the entire width of the ventricular zone, and (2) interkinetic nuclear movements are minimal during S-phase.},
	Author = {Hayes, N. L. and Nowakowski, R. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Embryo;Thymidine;Mice;24 Pubmed search results 2008;S Phase;Immunohistochemistry;Research Support, U.S. Gov't, P.H.S.;Research Support, U.S. Gov't, Non-P.H.S.;Animals;Bromodeoxyuridine;Cerebral Cortex;Cell Nucleus;Mice, Inbred Strains},
	Medline = {20125899},
	Nlm_Id = {7809375},
	Number = {1-2},
	Organization = {Department of Neuroscience, UMDNJ - Robert Wood Johnson Medical School, Piscataway, N.J., USA. hayes\@umdnj.edu},
	Pages = {44-55},
	Pii = {dne22044},
	Pubmed = {10657697},
	Title = {Exploiting the dynamics of S-phase tracers in developing brain: interkinetic nuclear migration for cells entering versus leaving the S-phase},
	Uuid = {4B306C29-E44B-4BE1-A9DA-D2D1386DA412},
	Volume = {22},
	Year = {2000}}

@article{Haynes:2006,
	Abstract = {Microglia are primary immune sentinels of the CNS. Following injury, these cells migrate or extend processes toward sites of tissue damage. CNS injury is accompanied by release of nucleotides, serving as signals for microglial activation or chemotaxis. Microglia express several purinoceptors, including a G(i)-coupled subtype that has been implicated in ATP- and ADP-mediated migration in vitro. Here we show that microglia from mice lacking G(i)-coupled P2Y(12) receptors exhibit normal baseline motility but are unable to polarize, migrate or extend processes toward nucleotides in vitro or in vivo. Microglia in P2ry(12)(-/-) mice show significantly diminished directional branch extension toward sites of cortical damage in the living mouse. Moreover, P2Y(12) expression is robust in the 'resting' state, but dramatically reduced after microglial activation. These results imply that P2Y(12) is a primary site at which nucleotides act to induce microglial chemotaxis at early stages of the response to local CNS injury.},
	Author = {Haynes, Sharon E. and Hollopeter, Gunther and Yang, Guang and Kurpius, Dana and Dailey, Michael E. and Gan, Wen-Biao B. and Julius, David},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {9809671},
	Number = {12},
	Organization = {Departments of Physiology & Cellular and Molecular Pharmacology, University of California, San Francisco (UCSF), 600 16th Street, San Francisco, California 94158-2517, USA.},
	Pages = {1512-9},
	Pii = {nn1805},
	Pubmed = {17115040},
	Title = {The P2Y(12) receptor regulates microglial activation by extracellular nucleotides},
	Uuid = {DA1AF3BF-16A3-4397-9B27-57EC6B0DDDCD},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1805}}

@article{Heck:2007,
	Abstract = {A massive neuronal loss during early postnatal development has been well documented in the murine cerebral cortex, but the factors that drive cells into apoptosis are largely unknown. The role of neuronal activity in developmental apoptosis was studied in organotypic neocortical slice cultures of newborn mice. Multielectrode array and whole-cell patch-clamp recordings revealed spontaneous network activity characterized by synchronized burst discharges, which could be blocked by tetrodotoxin and ionotropic glutamate receptor antagonists. The identical neuropharmacological manipulations also caused a significant increase in the number of apoptotic neurons as early as 6 h after the start of drug treatment. Moreover, inhibition of the NMDA receptor subunit NR2A or NR2B induced a differential short-term versus delayed increase in the apoptosis rate, respectively. Activation of L-type, voltage-dependent calcium channels was neuroprotective and could prevent activity-dependent apoptosis during NMDA receptor blockade. Furthermore, this effect involved phosphorylation of cAMP response element-binding protein and activation of the tropomyosin-related kinase (Trk) receptors. Inhibition of electrical synapses and blockade of ionotropic gamma-aminobutyric acid receptors induced specific changes in spontaneous electrical activity patterns, which caused an increase in caspase-3-dependent cell death. Our results demonstrate that synchronized spontaneous network bursts activating ionotropic glutamate receptors promote neuronal survival in the neonatal mouse cerebral cortex.},
	Author = {Heck, and Golbs, and Riedemann, and Sun, and Lessmann, and Luhmann,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {21 Neurophysiology;21 Activity-development;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {9110718},
	Organization = {Institute of Physiology and Pathophysiology, University of Mainz, Duesbergweg 6, D-55128 Mainz, Germany.},
	Pii = {bhm165},
	Pubmed = {17965127},
	Title = {Activity-Dependent Regulation of Neuronal Apoptosis in Neonatal Mouse Cerebral Cortex},
	Uuid = {EB33FE26-440E-4770-AF89-611D9E859833},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhm165}}

@article{Hegg:1999,
	Abstract = {Microglia- and macrophage-induced neuronal death may underlie a number of neurodegenerative diseases. The effects of factors secreted by monocytic cells were studied on glutamatergic synaptic transmission between cultured rat hippocampal neurons. Conditioned media from differentiated human U937 cells was collected after 24 h and applied to neurons (0.5\%-30\%dilution). Unactivated U937 cells spontaneously released factors that when applied to neuronal cultures evoked bursts of action potentials and elicited neuronal death (29+/-4\%). Conditioned media collected from U937 cells evoked intracellular calcium ([Ca(2+)](i)) spiking (0.5\%-2\%dilution) and at higher concentrations evoked sustained increases in intracellular calcium (3\%-30\%dilution), as measured by indo-1-based photometry in single neurons. Activation of the U937 cells with zymosin A (500 microg/ml) enhanced the potency of the conditioned media to increase intraneuronal [Ca(2+)](i) as indicated by a leftward shift in the concentration-response curve. Selective antagonists to voltage-gated Na(+) and Ca(2+) channels and NMDA-gated channels (tetrodotoxin, nimodipine, and (+/-)-2-amino-5-phosphonopentanoic acid, respectively) blocked the calcium transients elicited by unactivated and zymosin -A-treated conditioned media. This pharmacologic profile is consistent with U937-released factors that excite the synaptic network that forms between cultured hippocampal neurons.},
	Author = {Hegg, C. C. and Thayer, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0014-2999},
	Journal = {Eur J Pharmacol},
	Keywords = {U937 Cells;Neurotoxins;Excitatory Amino Acid Antagonists;Zymosan;6-Cyano-7-nitroquinoxaline-2,3-dione;Animals;Cells, Cultured;Hippocampus;Synapses;Receptors, N-Methyl-D-Aspartate;Nimodipine;Membrane Potentials;11 Glia;Culture Media, Conditioned;Support, U.S. Gov't, P.H.S.;Action Potentials;Support, U.S. Gov't, Non-P.H.S.;Tetrodotoxin;Pipecolic Acids;Rats;Glutamic Acid;Dose-Response Relationship, Drug;Fetus;Patch-Clamp Techniques;Monocytes;Calcium;Cell Death;Excitatory Amino Acids;Neurons;Human;Calcium Channel Blockers},
	Medline = {20076374},
	Month = {12},
	Nlm_Id = {1254354},
	Number = {2-3},
	Organization = {Department of Pharmacology, University of Minnesota Medical School, 6-120 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455-0217, USA.},
	Pages = {231-7},
	Pii = {S0014299999007128},
	Pubmed = {10607881},
	Title = {Monocytic cells secrete factors that evoke excitatory synaptic activity in rat hippocampal cultures},
	Uuid = {6BFA1FC8-1EB3-4A80-A8DE-663B7C383E9A},
	Volume = {385},
	Year = {1999}}

	Abstract = {During metamorphosis in the moth, Manduca sexta, the abdominal body-wall muscle DEO1 is remodeled to form the adult muscle DE5. As the larval muscle degenerates, its motoneuron loses its end plates and retracts axon branches from the degenerating muscle. Muscle degeneration is under the control of the insect hormones, the ecdysteroids. Topical application of an ecdysteroid mimic resulted in animals that produced a localized patch of pupal cuticle. Muscle fibers underlying the patch showed a gradient of degeneration. The motoneuron showed end-plate loss and axon retraction from degenerating regions of a given fiber but maintained its fine terminal branches and end plates on intact regions. The results suggest that local steroid treatments that result in local muscle degeneration bring about a loss of synaptic contacts from regions of muscle degeneration.},

@article{Heim:2007,
	Abstract = {Fluorescent Ca(2+) indicator proteins (FCIPs) are attractive tools for studying Ca(2+) dynamics in live cells. Here we describe transgenic mouse lines expressing a troponin C (TnC)-based biosensor. The biosensor is widely expressed in neurons and has improved Ca(2+) sensitivity both in vitro and in vivo. This allows FCIP-based two-photon Ca(2+) imaging of distinct neurons and their dendrites in vivo, and opens a new avenue for structure-function analysis of intact neuronal circuits.},
	Author = {Heim, Nicola and Garaschuk, Olga and Friedrich, Michael W. and Mank, Marco and Milos, Ruxandra I. and Kovalchuk, Yury and Konnerth, Arthur and Griesbeck, Oliver},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1548-7091},
	Journal = {Nat Methods},
	Keywords = {Calcium Signaling;Animals;Spectrometry, Fluorescence;Brain;Female;Mice, Transgenic;23 Technique;Mice, Inbred C57BL;Calcium;research support, non-u.s. gov't;Troponin C;Green Fluorescent Proteins;Dendrites;Male;Mice, Inbred Strains;Biosensing Techniques;Neurons;Mice;optical physiology;optical imaging;calcium imaging;frontiers review},
	Month = {2},
	Nlm_Id = {101215604},
	Number = {2},
	Organization = {Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany.},
	Pages = {127-9},
	Pii = {nmeth1009},
	Pubmed = {17259991},
	Title = {Improved calcium imaging in transgenic mice expressing a troponin C-based biosensor},
	Uuid = {FE9D0565-55D5-4CE8-8439-5477E2293DA1},
	Volume = {4},
	Year = {2007},
	url = {papers/Heim_NatMethods2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nmeth1009}}

@article{Heinrich:2006,
	Abstract = {Mesio-temporal lobe epilepsy (MTLE) is often accompanied by granule cell dispersion (GCD), a widening of the granule cell layer. The molecular determinants of GCD are poorly understood. Here, we used an animal model to study whether GCD results from an increased dentate neurogenesis associated with an abnormal migration of the newly generated granule cells. Adult mice were given intrahippocampal injections of kainate (KA) known to induce focal epileptic seizures and GCD, comparable to the changes observed in human MTLE. Ipsilateral GCD progressively developed after KA injection and was paralleled by a gradual decrease in the expression of doublecortin, a marker of newly generated granule cells, in the dentate subgranular layer. Staining with Fluoro-Jade B revealed little cell degeneration in the subgranular layer on the KA-injected side. Labeling with bromodeoxyuridine showed an early, transient increase in mitotic activity in the dentate gyrus of the KA-injected hippocampus that gave rise to microglial cells and astrocytes but not to new neurons. Moreover, at later time points, there was a virtually complete cessation of mitotic activity in the injected hippocampus (where GCD continued to develop), but not on the contralateral side (where no GCD was observed). Finally, a significant decrease in reelin mRNA synthesis in the injected hippocampus paralleled the development of GCD, and neutralization of reelin by application of the CR-50 antibody induced GCD. These results show that GCD does not result from increased neurogenesis but reflects a displacement of mature granule cells, most likely caused by a local reelin deficiency.},
	Author = {Heinrich, Christophe and Nitta, Naoki and Flubacher, Armin and M{\"u}ller, Martin and Fahrner, Alexander and Kirsch, Matthias and Freiman, Thomas and Suzuki, Fumio and Depaulis, Antoine and Frotscher, Michael and Haas, Carola A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Experimental Epilepsy Group, University of Freiburg, D-79106 Freiburg, Germany.},
	Pages = {4701-13},
	Pii = {26/17/4701},
	Pubmed = {16641251},
	Title = {Reelin deficiency and displacement of mature neurons, but not neurogenesis, underlie the formation of granule cell dispersion in the epileptic hippocampus},
	Uuid = {888A02A1-450F-4491-B7B0-234F4F557C71},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5516-05.2006}}

@article{Heins:2002,
	Abstract = {Radial glial cells, ubiquitous throughout the developing CNS, guide radially migrating neurons and are the precursors of astrocytes. Recent evidence indicates that radial glial cells also generate neurons in the developing cerebral cortex. Here we investigated the role of the transcription factor Pax6 expressed in cortical radial glia. We showed that radial glial cells isolated from the cortex of Pax6 mutant mice have a reduced neurogenic potential, whereas the neurogenic potential of non-radial glial precursors is not affected. Consistent with defects in only one neurogenic lineage, the number of neurons in the Pax6 mutant cortex in vivo is reduced by half. Conversely, retrovirally mediated Pax6 expression instructs neurogenesis even in astrocytes from postnatal cortex in vitro. These results demonstrated an important role of Pax6 as intrinsic fate determinant of the neurogenic potential of glial cells. 21912404 1097-6256 Journal Article},
	Author = {Heins, N. and Malatesta, P. and Cecconi, F. and Nakafuku, M. and Tucker, K. L. and Hack, M. A. and Chapouton, P. and Barde, Y. A. and Gotz, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Neurons/*physiology;Human;Cell Separation;10 Development;Cells, Cultured;Rats;Cell Movement/*physiology;Neuroglia/*physiology;Homeodomain Proteins/genetics/*metabolism;Animal;Mice, Transgenic;Mice, Inbred C57BL;Cerebral Cortex/cytology/embryology/*growth &development/physiology;Support, Non-U.S. Gov't;Cell Lineage;Flow Cytometry;Transcription Factors/genetics/metabolism;Mice;Luminescent Proteins/metabolism;F;Indicators and Reagents/metabolism;Transgenes/genetics},
	Number = {4},
	Organization = {Max-Planck Institute of Neurobiology, Am Klopferspitz 18a, 82152, Planegg-Martinsreid, Munich, Germany.},
	Pages = {308-15},
	Pubmed = {11896398},
	Title = {Glial cells generate neurons: the role of the transcription factor Pax6},
	Uuid = {82E2CF78-925E-47EB-B076-1ECE762D9814},
	Volume = {5},
	Year = {2002},
	url = {papers/Heins_NatNeurosci2002}}

@article{Helenius:1980,
	Author = {Helenius, A. and Kartenbeck, J. and Simons, K. and Fries, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {24 Pubmed search results 2008;Cell Membrane;Semliki forest virus;Chloroquine;Adsorption;Virus Replication;Cell Line;Get paper from library;Receptors, Virus;Lysosomes;Endocytosis;Fluorescent Antibody Technique;Animals;Kidney;Hamsters;15 Retrovirus mechanism;Microvilli},
	Medline = {80204437},
	Month = {2},
	Nlm_Id = {0375356},
	Number = {2},
	Pages = {404-20},
	Pubmed = {6991511},
	Title = {On the entry of Semliki forest virus into BHK-21 cells},
	Uuid = {79972FAC-6CA0-4959-B698-AC2F0A6AAC92},
	Volume = {84},
	Year = {1980}}

@article{Hellstrom:1999,
	Abstract = {Development of a vascular system involves the assembly of two principal cell types - endothelial cells and vascular smooth muscle cells/pericytes (vSMC/PC) - into many different types of blood vessels. Most, if not all, vessels begin as endothelial tubes that subsequently acquire a vSMC/PC coating. We have previously shown that PDGF-B is critically involved in the recruitment of pericytes to brain capillaries and to the kidney glomerular capillary tuft. Here, we used desmin and alpha-smooth muscle actin (ASMA) as markers to analyze vSMC/PC development in PDGF-B-/- and PDGFR-beta-/- embryos. Both mutants showed a site-specific reduction of desmin-positive pericytes and ASMA-positive vSMC. We found that endothelial expression of PDGF-B was restricted to immature capillary endothelial cells and to the endothelium of growing arteries. BrdU labeling showed that PDGFR-beta-positive vSMC/PC progenitors normally proliferate at sites of endothelial PDGF-B expression. In PDGF-B-/- embryos, limb arterial vSMC showed a reduced BrdU-labeling index. This suggests a role of PDGF-B in vSMC/PC cell proliferation during vascular growth. Two modes of vSMC recruitment to newly formed vessels have previously been suggested: (1) de novo formation of vSMC by induction of undifferentiated perivascular mesenchymal cells, and (2) co-migration of vSMC from a preexisting pool of vSMC. Our data support both modes of vSMC/PC development and lead to a model in which PDGFR-beta-positive vSMC/PC progenitors initially form around certain vessels by PDGF-B-independent induction. Subsequent angiogenic sprouting and vessel enlargement involves PDGF-B-dependent vSMC/PC progenitor co-migration and proliferation, and/or PDGF-B-independent new induction of vSMC/PC, depending on tissue context.},
	Author = {Hellstr{\"o}m, M. and Kal{\'e}n, M. and Lindahl, P. and Abramsson, A. and Betsholtz, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Blood Vessels;Cell Division;Animals;Receptors, Platelet-Derived Growth Factor;Mice, Mutant Strains;Pericytes;Brain;Arteries;Cell Movement;11 Glia;Mice, Inbred Strains;Platelet-Derived Growth Factor;Mice;Muscle, Smooth, Vascular;Proto-Oncogene Proteins;Proto-Oncogene Proteins c-sis;Desmin;Receptor, Platelet-Derived Growth Factor beta;Actins;Research Support, Non-U.S. Gov't},
	Medline = {99307070},
	Month = {6},
	Nlm_Id = {8701744},
	Number = {14},
	Organization = {Department of Medical Biochemistry, G{\"o}teborg University, Box 440, SE 405 30 G{\"o}teborg, Sweden. christer.betsholtz\@medkem.gu.se},
	Pages = {3047-55},
	Pubmed = {10375497},
	Title = {Role of PDGF-B and PDGFR-beta in recruitment of vascular smooth muscle cells and pericytes during embryonic blood vessel formation in the mouse},
	Uuid = {87E9B23C-1E32-4FC6-9FE5-69167DAAAF1C},
	Volume = {126},
	Year = {1999}}

@article{Hematti:2004,
	Abstract = {Murine leukemia virus (MLV)-derived vectors are widely used for hematopoietic stem cell (HSC) gene transfer, but lentiviral vectors such as the simian immunodeficiency virus (SIV) may allow higher efficiency transfer and better expression. Recent studies in cell lines have challenged the notion that retroviruses and retroviral vectors integrate randomly into their host genome. Medical applications using these vectors are aimed at HSCs, and thus large-scale comprehensive analysis of MLV and SIV integration in long-term repopulating HSCs is crucial to help develop improved integrating vectors. We studied integration sites in HSCs of rhesus monkeys that had been transplanted 6 mo to 6 y prior with MLV- or SIV-transduced CD34(+)cells. Unique MLV (491) and SIV (501) insertions were compared to a set of in silico-generated random integration sites. While MLV integrants were located predominantly around transcription start sites, SIV integrants strongly favored transcription units and gene-dense regions of the genome. These integration patterns suggest different mechanisms for integration as well as distinct safety implications for MLV versus SIV vectors.},
	Author = {Hematti, Peiman and Hong, Bum-Kee K. and Ferguson, Cole and Adler, Rima and Hanawa, Hideki and Sellers, Stephanie and Holt, Ingeborg E. and Eckfeldt, Craig E. and Sharma, Yugal and Schmidt, Manfred and von Kalle, Christof and Persons, Derek A. and Billings, Eric M. and Verfaillie, Catherine M. and Nienhuis, Arthur W. and Wolfsberg, Tyra G. and Dunbar, Cynthia E. and Calmels, Boris},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1545-7885},
	Journal = {PLoS Biol},
	Keywords = {22 Stem cells;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {101183755},
	Number = {12},
	Organization = {Hematology Branch, National Institutes of Health Bethesda, Maryland, USA.},
	Pages = {e423},
	Pubmed = {15550989},
	Title = {Distinct genomic integration of MLV and SIV vectors in primate hematopoietic stem and progenitor cells},
	Uuid = {C0683DDD-2CD5-4D37-B0E6-28F6B8DCC085},
	Volume = {2},
	Year = {2004},
	url = {papers/Hematti_PLoSBiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0020423}}

@article{Hempel:2007,
	Abstract = {Sorting of fluorescent cells is a powerful technique for revealing the cellular processes that differ among the various cell types found in complex tissues. With the recent availability of transgenic mouse strains in which specific subpopulations of neurons are labeled, it has become desirable to purify these fluorescent neurons from their surrounding hetereogeneous brain tissue for electrophysiological, biochemical and molecular analyses. This has been accomplished using automated fluorescence-activated cell sorting (FACS) and laser capture microdissection (LCM). Although these procedures can be effective, they have some serious disadvantages, including high equipment costs and difficulty in obtaining samples completely free of contaminating tissue. Here we offer an alternative protocol for purifying fluorescent neurons, which relies on less-expensive equipment, readily produces perfectly pure samples and can be applied to neurons that are only dimly labeled and present in low numbers. The entire protocol can be completed in 3-5 h.},
	Author = {Hempel, Chris M. and Sugino, Ken and Nelson, Sacha B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1750-2799},
	Journal = {Nat Protoc},
	Keywords = {24 Pubmed search results 2008},
	Nlm_Id = {101284307},
	Number = {11},
	Organization = {Department of Biology and National Center for Behavioral Genomics, Brandeis University, MS 008, 415 South Street, Waltham, Massachusetts 02454-9110, USA.},
	Pages = {2924-9},
	Pii = {nprot.2007.416},
	Pubmed = {18007629},
	Title = {A manual method for the purification of fluorescently labeled neurons from the mammalian brain},
	Uuid = {DAF6E242-CAEE-4678-96A2-7DAD44291983},
	Volume = {2},
	Year = {2007},
	url = {papers/Hempel_NatProtoc2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nprot.2007.416}}

@article{Hengartner:2000,
	Abstract = {Apoptosis--the regulated destruction of a cell--is a complicated process. The decision to die cannot be taken lightly, and the activity of many genes influence a cell's likelihood of activating its self- destruction programme. Once the decision is taken, proper execution of the apoptotic programme requires the coordinated activation and execution of multiple subprogrammes. Here I review the basic components of the death machinery, describe how they interact to regulate apoptosis in a coordinated manner, and discuss the main pathways that are used to activate cell death.},
	Author = {Hengartner, M. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Nature},
	Keywords = {E-11;07 Excitotoxicity Apoptosis;Human;*Apoptosis;Mitochondria/physiology;Animal;Caspases/metabolism},
	Number = {6805},
	Organization = {Cold Spring Harbor Laboratory, New York 11724, USA. hengartn\@cshl.org},
	Pages = {770-6.},
	Title = {The biochemistry of apoptosis},
	Uuid = {7FFC9FEF-E4A4-4D8C-AB0E-1C876C471CD8},
	Volume = {407},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11048727}}

@article{Henion:2005,
	Abstract = {During embryonic development, axons from sensory neurons in the olfactory epithelium (OE) extend into the olfactory bulb (OB) where they synapse with projection neurons and form glomerular structures. To determine whether glycans play a role in these processes, we analyzed mice deficient for the glycosyltransferase beta1,3-N-acetylglucosaminyltransferase 1 (beta3GnT1), a key enzyme in lactosamine glycan synthesis. Terminal lactosamine expression, as shown by immunoreactivity with the monoclonal antibody 1B2, is dramatically reduced in the neonatal null OE. Postnatal beta3GnT1-/- mice exhibit severely disorganized OB innervation and defective glomerular formation. Beginning in embryonic development, specific subsets of odorant receptor-expressing neurons are progressively lost from the OE of null mice, which exhibit a postnatal smell perception deficit. Axon guidance errors and increased neuronal cell death result in an absence of P2, I7, and M72 glomeruli, indicating a reduction in the repertoire of odorant receptor-specific glomeruli. By approximately 2 weeks of age, lactosamine is unexpectedly reexpressed in sensory neurons of null mice through a secondary pathway, which is accompanied by the regrowth of axons into the OB glomerular layer and the return of smell perception. Thus, both neonatal OE degeneration and the postnatal regeneration are lactosamine dependent. Lactosamine expression in beta3GnT1-/- mice is also reduced in pheromone-receptive vomeronasal neurons and dorsal root ganglion cells, suggesting that beta3GnT1 may perform a conserved function in multiple sensory systems. These results reveal an essential role for lactosamine in sensory axon pathfinding and in the formation of OB synaptic connections.},
	Author = {Henion, Timothy R. and Raitcheva, Denitza and Grosholz, Robert and Biellmann, Franziska and Skarnes, William C. and Hennet, Thierry and Schwarting, Gerald A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {8},
	Organization = {Shriver Center, Waltham, Massachusetts 02452, USA.},
	Pages = {1894-903},
	Pii = {25/8/1894},
	Pubmed = {15728829},
	Title = {Beta1,3-N-acetylglucosaminyltransferase 1 glycosylation is required for axon pathfinding by olfactory sensory neurons},
	Uuid = {B0D745DB-3AB6-48F1-BF9C-769F912D0D31},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4654-04.2005}}

@article{Henschler:2004,
	Abstract = {To study the homing behaviour of an enriched multipotent primitive haemopoietic progenitor cell (HPC) population in mice, undifferentiated murine factor-dependent multipotent HPCs (FDCP-mix), stably transfected with the green fluorescence protein gene, were intravenously injected into congenic mice. After 2 or 24 h, cell suspensions were prepared from bone marrow, spleen, lung, liver, muscle, colon, kidney, brain or blood of the mice and analysed by flow cytometry. Using direct quantifiable determination of total HPC numbers homed per organ and a method to estimate the degree of organ contamination by HPC that were present in blood vessels within the organs before preparation, the highest absolute numbers of HPC were detected in the liver and lungs at 2 h but this was sharply decreased at 24 h, whereas HPC selectively accumulated in the bone marrow and spleen at 24 h after transplantation. Only a few HPC were detected in other organs. The seeding efficiency of homed FDCP-mix HPC to the bone marrow and spleen was approximately 1.5\%and ranged between that of primary whole bone marrow cells and lineage-depleted freshly isolated bone marrow cells. Pretreatment of HPC with inhibitors of signal transduction indicated that short-term homing of multipotent HPC into haemopoietic organs is an active process requiring co-ordinated intracellular signalling through Rho family small GTPases and protein kinases. Thus, short-term homing of FDCP-mix HPC into haemopoietic organs is of low efficiency but high selectivity, and provides a system to analyse the mechanisms and manipulation of primitive HPC which saves large numbers of donor animals.},
	Author = {Henschler, R. and Fehervizyova, Z. and Bistrian, R. and Seifried, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0007-1048},
	Journal = {Br J Haematol},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Transfection;Multipotent Stem Cells;Cell Count;Cell Movement;Liver;Mice, Inbred C57BL;11 Glia;Time Factors;Green Fluorescent Proteins;Bone Marrow Cells;Mice, Inbred DBA;Flow Cytometry;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Models, Animal;Spleen;Lung},
	Month = {7},
	Nlm_Id = {0372544},
	Number = {1},
	Organization = {Institute of Transfusion Medicine and Immune Haematology, German Red Cross Blood Centre, Frankfurt, Germany. rhenschler\@bsdhessen.de},
	Pages = {111-9},
	Pii = {BJH4995},
	Pubmed = {15198741},
	Title = {A mouse model to study organ homing behaviour of haemopoietic progenitor cells reveals high selectivity but low efficiency of multipotent progenitors to home into haemopoietic organs},
	Uuid = {9D0ABAE4-32CD-4606-B86C-E43871B925F8},
	Volume = {126},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1365-2141.2004.04995.x}}

@article{Henske:1996,
	Abstract = {Tuberous sclerosis (TSC) is an autosomal dominant disorder characterized by seizures, mental retardation, and hamartomatous lesions. Although hamartomas can occur in almost any organ, they are most common in the brain, kidney, heart, and skin. Allelic loss or loss of heterozygosity (LOH) in TSC lesions has previously been reported on chromosomes 16p13 and 9q34, the locations of the TSC2 and TSC1 genes, respectively, suggesting that the TSC genes act as tumor-suppressor genes. In our study, 87 lesions from 47 TSC patients were analyzed for LOH in the TSC1 and TSC2 chromosomal regions. Three findings resulted from this analysis. First, we confirmed that the TSC1 critical region is distal to D9S149. Second, we found LOH more frequently on chromosome 16p13 than on 9q34. Of the 28 patients with angiomyolipomas or rhabdomyomas, 16p13 LOH was detected in lesions from 12 (57\%) of 21 informative patients, while 9q34 LOH was detected in lesions from only 1 patient (4\%). This could indicate that TSC2 tumors are more likely than TSC1 tumors to require surgical resection or that TSC2 is more common than TSC1 in our patient population. It is also possible that small regions of 9q34 LOH were missed. Lastly, LOH was found in 56\%of renal angiomyolipomas and cardiac rhabdomyormas but in only 4\%of TSC brain lesions. This suggests that brain lesions can result from different pathogenic mechanisms than kidney and heart lesions.},
	Author = {Henske, E. P. and Scheithauer, B. W. and Short, M. P. and Wollmann, R. and Nahmias, J. and Hornigold, N. and van Slegtenhorst, M. and Welsh, C. T. and Kwiatkowski, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0002-9297},
	Journal = {Am J Hum Genet},
	Keywords = {10 Development;Heterozygote;Chromosomes, Human, Pair 16;Kidney;Base Sequence;comparative study;Humans;Tuberous Sclerosis;Brain;Chromosome Deletion;research support, non-u.s. gov't;Angiomyolipoma;Chromosomes, Human, Pair 9;Alleles;10 genetics malformation;research support, u.s. gov't, p.h.s.;Rhabdomyoma;24 Pubmed search results 2008;Molecular Sequence Data},
	Month = {8},
	Nlm_Id = {0370475},
	Number = {2},
	Organization = {Experimental Medicine Division, Brigham and Women's Hospital, Boston, MA 02115, USA.},
	Pages = {400-6},
	Pubmed = {8755927},
	Title = {Allelic loss is frequent in tuberous sclerosis kidney lesions but rare in brain lesions},
	Uuid = {B0AD6056-680F-4F8E-AA1D-58D0DDFA4CA8},
	Volume = {59},
	Year = {1996}}

@article{Heppner:2005a,
	Abstract = {Although microglial activation occurs in inflammatory, degenerative and neoplastic central nervous system (CNS) disorders, its role in pathogenesis is unclear. We studied this question by generating CD11b-HSVTK transgenic mice, which express herpes simplex thymidine kinase in macrophages and microglia. Ganciclovir treatment of organotypic brain slice cultures derived from CD11b-HSVTK mice abolished microglial release of nitrite, proinflammatory cytokines and chemokines. Systemic ganciclovir administration to CD11b-HSVTK mice elicited hematopoietic toxicity, which was prevented by transfer of wild-type bone marrow. In bone marrow chimeras, ganciclovir blocked microglial activation in the facial nucleus upon axotomy and repressed the development of experimental autoimmune encephalomyelitis. We conclude that microglial paralysis inhibits the development and maintenance of inflammatory CNS lesions. The microglial compartment thus provides a potential therapeutic target in inflammatory CNS disorders. These results validate CD11b-HSVTK mice as a tool to study the impact of microglial activation on CNS diseases in vivo.},
	Author = {Heppner, Frank L. and Greter, Melanie and Marino, Denis and Falsig, Jeppe and Raivich, Gennadij and H{\"o}velmeyer, Nadine and Waisman, Ari and R{\"u}licke, Thomas and Prinz, Marco and Priller, Josef and Becher, Burkhard and Aguzzi, Adriano},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1078-8956},
	Journal = {Nat Med},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {9502015},
	Number = {2},
	Organization = {Institute of Neuropathology, University Hospital Zurich, CH-8091 Zurich, Switzerland.},
	Pages = {146-52},
	Pii = {nm1177},
	Pubmed = {15665833},
	Title = {Experimental autoimmune encephalomyelitis repressed by microglial paralysis},
	Uuid = {27249648-1844-4841-AB32-C381AAA67E96},
	Volume = {11},
	Year = {2005},
	url = {papers/Heppner_NatMed2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nm1177}}

@article{Heppner:2005,
	Author = {Heppner, F. L. and Greter, M. and Marino, D. and Falsig, J. and Raivich, G. and H{\"o}velmeyer, N. and Waisman, A. and R{\"u}licke, T. and Prinz, M. and Priller, J. and Becher, B. and Aguzzi, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1078-8956},
	Journal = {Nat Med},
	Keywords = {11 Glia},
	Month = {4},
	Nlm_Id = {9502015},
	Number = {4},
	Pages = {455},
	Pii = {nm0405-455},
	Pubmed = {15812520},
	Title = {CORRIGENDUM: Experimental autoimmune encephalomyelitis repressed by microglial paralysis},
	Uuid = {EEF0B380-A984-439B-858C-F2221609F477},
	Volume = {11},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nm0405-455}}

@article{Hermanson:2002, Abstract = {Understanding the gene programmes that regulate maintenance and differentiation of neural stem cells is a central question in stem cell biology. Virtually all neural stem cells maintain an undifferentiated state and the capacity to self-renew in response to fibroblast growth factor-2 (FGF2). Here we report that a repressor of transcription, the nuclear receptor co-repressor (N-CoR), is a principal regulator in neural stem cells, as FGF2-treated embryonic cortical progenitors from N-CoR gene-disrupted mice display impaired self-renewal and spontaneous differentiation into astroglia-like cells. Stimulation of wild-type neural stem cells with ciliary neurotrophic factor (CNTF), a differentiation-inducing cytokine, results in phosphatidylinositol-3-OH kinase/Akt1 kinase-dependent phosphorylation of N-CoR, and causes a temporally correlated redistribution of N-CoR to the cytoplasm. We find that this is a critical strategy for cytokine-induced astroglia differentiation and lineage-characteristic gene expression. Recruitment of protein phosphatase-1 to a specific binding site on N-CoR exerts a reciprocal effect on the cellular localization of N-CoR. We propose that repression by N-CoR, modulated by opposing enzymatic activities, is a critical mechanism in neural stem cells that underlies the inhibition of glial differentiation. 0028-0836 Journal Article},
	Author = {Hermanson, O. and Jepsen, K. and Rosenfeld, M. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:48 -0400},
	Journal = {Nature},
	Keywords = {Human;Chromatin/metabolism;Animals;Enzyme Activation;1-Phosphatidylinositol 3-Kinase/metabolism;Protein-Serine-Threonine Kinases/metabolism;Stem Cells/*cytology/drug effects/enzymology/metabolism;Protein Transport;11 Glia;Phosphoprotein Phosphatase/antagonists &inhibitors/metabolism;Cell Line;Support, Non-U.S. Gov't;Ciliary Neurotrophic Factor/pharmacology;*Cell Differentiation/drug effects;Phosphorylation/drug effects;Astrocytes/*cytology/drug effects/enzymology/metabolism;Cytoplasm/metabolism;Repressor Proteins/*metabolism;Fibroblast Growth Factor 2/pharmacology;Support, U.S. Gov't, P.H.S.;Nuclear Proteins/*metabolism;Cell Nucleus/metabolism;Neurons/*cytology/drug effects/enzymology/metabolism;Mice;Cell Division/drug effects;G pdf},
	Number = {6910},
	Organization = {Howard Hughes Medical Institute, Department of Molecular Medicine, University of California, San Diego, School of Medicine, 9500 Gilman Drive, Room 345, La Jolla, California 92093-0648, USA.},
	Pages = {934-9},
	Title = {N-CoR controls differentiation of neural stem cells into astrocytes},
	Uuid = {014877D0-8701-43CA-9E16-2DBCA8F78DBC},
	Volume = {419},
	Year = {2002},
	url = {papers/Hermanson_Nature2002.pdf}}

@article{Hernandez:1996,
	Abstract = {Significant progress has been made in elucidating the mechanisms of viral membrane fusion proteins; both those that function at low, as well as those that function at neutral, pH. For many viral fusion proteins evidence now suggests that a triggered conformational change that exposes a previously cryptic fusion peptide, along with a rearrangement of the fusion protein oligomer, allows the fusion peptide to gain access to the target bilayer and thus initiate the fusion reaction. Although the topologically equivalent process of cell-cell fusion is less well understood, several cell surface proteins, including members of the newly described ADAM gene family, have emerged as candidate adhesion/fusion proteins.},
	Author = {Hernandez, L. D. and Hoffman, L. R. and Wolfsberg, T. G. and White, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1081-0706},
	Journal = {Annu Rev Cell Dev Biol},
	Keywords = {Cell Membrane;Viral Fusion Proteins;Recombinant Fusion Proteins;Membrane Fusion;08 Aberrant cell cycle;Viruses;review, tutorial;15 Retrovirus mechanism;24 Pubmed search results 2008;review},
	Medline = {97125667},
	Nlm_Id = {9600627},
	Organization = {Department of Cell Biology, University of Virginia, Charlottesville 22908, USA.},
	Pages = {627-61},
	Pubmed = {8970739},
	Title = {Virus-cell and cell-cell fusion},
	Uuid = {33DA7E2C-216C-11DB-96D3-000D9346EC2A},
	Volume = {12},
	Year = {1996},
	url = {papers/Hernandez_AnnuRevCellDevBiol1996.pdf}}

@article{Hernit-Grant:1996,
	Abstract = {In the neocortex, the effectiveness of potential transplantation therapy for diseases involving neuronal loss may depend upon whether donor neurons can reestablish the precise long-distance projections that form the basis of sensory, motor, and cognitive function. During corticogenesis, the formation of these connections is affected by tropic factors, extracellular matrix, structural pathways, and developmental cell death. Previous studies demonstrated that embryonic neurons and multipotent neural precursors transplanted into neocortex or mice undergoing photolytically induced, synchronous, apoptotic neuronal degeneration selectively migrate into these regions, where they differentiate into pyramidal neurons and accept afferent synaptic input. The experiments presented here assess whether embryonic neurons transplanted into regions of somatosensory cortex undergoing targeted cell death differentiate further and develop long-distance axons and whether this outgrowth is target specific. Neocortical neurons from Gestational Day 17 mouse embryos were dissociated, prelabeled with fluorescent nanospheres and a lipophilic dye (DiI or PKH), and transplanted into adult mouse primary somatosensory cortex (S1) undergoing apoptotic degeneration of callosal projection neurons. Donor neurons selectively migrated into and differentiated within regions of targeted neuronal death in lamina II/III over a 2-week period, in agreement with our prior studies. To detect possible projections made by donor neurons 2, 4, 6, 8, or 10 weeks following transplantation, the retrogradely transported dye fluorogold (FG) was stereotaxically injected into contralateral S1, ipsilateral secondary somatosensory cortex (S2), or ipsilateral thalamus. Ten weeks following transplantation, 21 +/- 5\%of the labeled donor neurons were labeled by FG injections into contralateral S1, demonstrating that donor neurons sent projections to the distant area, the original target of host neurons undergoing photolytically induced cell death. No donor neurons were labeled with FG injections into ipsilateral S2 or thalamus, nearby targets of other subpopulations of neurons in S1. These data indicate that in the adult neocortex: (1) transplanted immature neurons are capable of extending long-distance projections between hemispheres through the mature white matter of the corpus callosum and (2) these projections are formed with specificity to replace projections by neurons undergoing synchronous degeneration. These experiments provide an experimental system with which to test factors affecting such outgrowth and connectivity. Taken together, these results suggest that the reconstruction and repair of cortical circuitry responsible for sensory, motor, or cognitive function may be possible in the mature neocortex, if donor neurons or precursor cells are provided with the correct combination of local and distant signals within an appropriately permissive host environment. 0014-4886 Journal Article},
	Author = {Hernit-Grant, C. S. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Exp Neurol},
	Keywords = {Neurons/cytology/*transplantation;Mice;Fetal Tissue Transplantation;Cell Division/physiology;17 Transplant Regeneration;Photochemistry;L abstr;Neural Pathways;Mice, Inbred C57BL;Cell Death/physiology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Animals;Support, Non-U.S. Gov't;Somatosensory Cortex/*cytology;Age Factors;Corpus Callosum/*cytology},
	Number = {1},
	Organization = {Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {131-42},
	Pubmed = {8635560},
	Title = {Embryonic neurons transplanted to regions of targeted photolytic cell death in adult mouse somatosensory cortex re-form specific callosal projections},
	Uuid = {8756E0BE-EC7F-11DA-8605-000D9346EC2A},
	Volume = {139},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8635560}}

@article{Hattori:2007,
	Abstract = {Neurons are thought to use diverse families of cell-surface molecules for cell recognition during circuit assembly. In Drosophila, alternative splicing of the Down syndrome cell adhesion molecule (Dscam) gene potentially generates 38,016 closely related transmembrane proteins of the immunoglobulin superfamily, each comprising one of 19,008 alternative ectodomains linked to one of two alternative transmembrane segments. These ectodomains show isoform-specific homophilic binding, leading to speculation that Dscam proteins mediate cell recognition. Genetic studies have established that Dscam is required for neural circuit assembly, but the extent to which isoform diversity contributes to this process is not known. Here we provide conclusive evidence that Dscam diversity is essential for circuit assembly. Using homologous recombination, we reduced the entire repertoire of Dscam ectodomains to just a single isoform. Neural circuits in these mutants are severely disorganized. Furthermore, we show that it is crucial for neighbouring neurons to express distinct isoforms, but that the specific identity of the isoforms expressed in an individual neuron is unimportant. We conclude that Dscam diversity provides each neuron with a unique identity by which it can distinguish its own processes from those of other neurons, and that this self-recognition is essential for wiring the Drosophila brain.},
	Author = {Hattori, Daisuke and Demir, Ebru and Kim, Ho Won and Viragh, Erika and Zipursky, S. Lawrence and Dickson, Barry J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Mutation;10 Development;research support, non-u.s. gov't;Mushroom Bodies;Alleles;Alternative Splicing;Drosophila Proteins;10 circuit formation;Drosophila melanogaster;Protein Isoforms;research support, n.i.h., extramural;Animals;Brain;24 Pubmed search results 2008;Neurons},
	Month = {9},
	Nlm_Id = {0410462},
	Number = {7159},
	Organization = {Department of Biological Chemistry, Howard Hughes Medical Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90049, USA.},
	Pages = {223-7},
	Pii = {nature06099},
	Pubmed = {17851526},
	Title = {Dscam diversity is essential for neuronal wiring and self-recognition},
	Uuid = {8F5D54EB-70C7-4F5C-97E2-A763990A6D0E},
	Volume = {449},
	Year = {2007},
	url = {papers/Hattori_Nature2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06099}}

@article{Haubensak:2004,
	Abstract = {Neurons of the mammalian CNS are thought to originate from progenitors dividing at the apical surface of the neuroepithelium. Here we use mouse embryos expressing GFP from the Tis21 locus, a gene expressed throughout the neural tube in most, if not all, neuron-generating progenitors, to specifically reveal the cell divisions that produce CNS neurons. In addition to the apical, asymmetric divisions of neuroepithelial (NE) cells that generate another NE cell and a neuron, we find, from the onset of neurogenesis, a second population of progenitors that divide in the basal region of the neuroepithelium and generate two neurons. Basal progenitors are most frequent in the telencephalon, where they outnumber the apically dividing neuron-generating NE cells. Our observations reconcile previous data on the origin and lineage of CNS neurons and show that basal, rather than apical, progenitors are the major source of the neurons of the mammalian neocortex.},
	Author = {Haubensak, Wulf and Attardo, Alessio and Denk, Winfried and Huttner, Wieland B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {10 Development;Heterozygote;Cell Cycle Proteins;Animals;Microscopy, Video;Aging;Epithelial Cells;Rhombencephalon;Mitosis;Female;Telencephalon;Mice, Transgenic;Mice, Inbred C57BL;Recombinant Fusion Proteins;Green Fluorescent Proteins;Embryonic and Fetal Development;Crosses, Genetic;Male;Genes, Tumor Suppressor;Neurons;Immediate-Early Proteins;Mice;Luminescent Proteins;Genes, Reporter;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {7505876},
	Notes = {there is suppl pdf info in omega data as well},
	Number = {9},
	Organization = {Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, D-01307 Dresden, Germany.},
	Pages = {3196-201},
	Pii = {0308600100},
	Pubmed = {14963232},
	Title = {Neurons arise in the basal neuroepithelium of the early mammalian telencephalon: a major site of neurogenesis},
	Uuid = {53316EC6-8CBE-4D47-9A33-90C3446F85B4},
	Volume = {101},
	Year = {2004},
	url = {papers/Haubensak_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0308600100}}

@article{Haun:1993,
	Abstract = {Unilateral lesions extending across the boundary region of visual and parietal cortex in adult rats result in the death of 20-35\%of neurons in layers II-III of the caudal third of medial frontal cortex ipsilaterally, a neuron population labeled with 3H-thymidine on the 19th day of gestation (E19). Additionally, there is a consistent 15\%loss of these labeled neurons in an area between 50\%and 60\%of the distance along the caudal-rostral extent of medial frontal cortex, an area that may function analogously to the frontal eye field of primates. All of these neurons are rescued from axotomy-induced death by delivering into the posterior cortex lesion cavity for 2 weeks a macromolecular fraction of culture medium conditioned by embryonic primordia of the frontal-occipital pathway (CM). Moreover, the rescue is apparently permanent, with normal numbers of these neurons present in CM animals 6-7 weeks after the neurotrophic factor is no longer being supplied exogenously. Behaviorally, control operates receiving a similarly prepared fraction of unconditioned medium are significantly impaired in the number of trials needed to learn two visual discrimination tasks. This deficit is attributable in part to a bias in erroneous responses to the side contralateral to the lesion. The error bias reflects a failure to inhibit repeated incorrect responding contralaterally. In contrast, the CM animals learn both visual tasks in a normal number of trials and have no contralateral error bias. Rather, all CM animals have an contralateral error bias. Rather, all CM animals have an ipsilateral error bias (interpreted as an unmasking of the contralateral neglect expected after a parietal cortex lesion).(ABSTRACT TRUNCATED AT 250 WORDS)},
	Author = {Haun, F. and Cunningham, T. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Visual Cortex;Frontal Lobe;Neurons;Pattern Recognition, Visual;Discrimination Learning;Rats;Research Support, U.S. Gov't, P.H.S.;Cell Survival;Occipital Lobe;Vision;Parietal Lobe;Culture Techniques;Culture Media;Animals;24 Pubmed search results 2008;Nerve Growth Factors;Axons},
	Medline = {93147933},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129.},
	Pages = {614-22},
	Pubmed = {8426229},
	Title = {Recovery of frontal cortex-mediated visual behaviors following neurotrophic rescue of axotomized neurons in medial frontal cortex},
	Uuid = {6CEF1EF3-976B-4AB4-9943-AED60B470839},
	Volume = {13},
	Year = {1993}}

@article{Haydon:2001,
	Abstract = {Glial cells are emerging from the background to become more prominent in our thinking about integration in the nervous system. Given that glial cells associated with synapses integrate neuronal inputs and can release transmitters that modulate synaptic activity, it is time to rethink our understanding of the wiring diagram of the nervous system. It is no longer appropriate to consider solely neuron-neuron connections; we also need to develop a view of the intricate web of active connections among glial cells, and between glia and neurons. Without such a view, it might be impossible to decode the language of the brain. 1471-003x Journal Article Review Review, Tutorial},
	Author = {Haydon, P. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {G;Glutamic Acid/metabolism;Gap Junctions/physiology;Synapses/*physiology;Synaptic Transmission/*physiology;Signal Transduction/physiology;Schwann Cells/metabolism;11 Glia;Support, U.S. Gov't, P.H.S.;Neuroglia/*physiology/ultrastructure;Animals;Astrocytes/physiology;Calcium Signaling;Neurons/*physiology/ultrastructure;Calcium/metabolism},
	Number = {3},
	Organization = {Department of Zoology and Genetics, Iowa State University, Ames, Iowa 50011, USA. pghaydon\@iastate.edu},
	Pages = {185-93},
	Pubmed = {11256079},
	Title = {GLIA: listening and talking to the synapse},
	Uuid = {AD1698E7-784B-4923-837F-4B6E502CBE89},
	Volume = {2},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11256079}}

@article{Herman:1994,
	Abstract = {0301-0082 Journal Article Review Review, Academic},
	Author = {Herman, J. P. and Abrous, N. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Prog Neurobiol},
	Keywords = {Corpus Striatum/physiology;17 Transplant Regeneration;Homeostasis;Human;Neuronal Plasticity;L abstr;Dopamine/*physiology;Brain Tissue Transplantation/*physiology;Receptors, Dopamine/physiology;Motor Activity;Animals;Support, Non-U.S. Gov't;Neurons/physiology/*transplantation/ultrastructure;Mesencephalon/physiology},
	Number = {1},
	Organization = {CNRS UMR 9941, Laboratoire des Interactions Cellulaires Neuroendocriniennes, Faculte de Medecine Nord, Marseille, France.},
	Pages = {1-35},
	Pubmed = {7831470},
	Title = {Dopaminergic neural grafts after fifteen years: results and perspectives},
	Uuid = {83C31F35-4395-45F2-A9A9-2298A1D82374},
	Volume = {44},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7831470}}

@article{Herrera:1999,
	Abstract = {Neural stem cells persist in the adult brain subventricular zone (SVZ). These cells generate a large number of new neurons that migrate to the olfactory bulb, where they complete their differentiation. Here, we transplanted cells carrying beta-galactosidase under the control of neuron-specific enolase promoter (NSE::LacZ) from the SVZ of adult mice into the striatum cortex and olfactory bulb, with or without an excitotoxin lesion. Between 2 and 8 weeks after transplantation, grafted cells were present in the recipient regions, but extensive migration and differentiation into mature neurons of grafted cells were only observed in the olfactory bulb. Clusters of graft-derived neuroblasts forming chain-like structures were observed within or close to the grated sites in the cortex and striatum; electron microscopy confirmed that graft-derived cells in the olfactory bulb and a small number in the striatum were neurons. Surprisingly, most of the cells expressing NSE::LacZ outside the olfactory bulb were astrocytes. We conclude that primary precursors from the SVZ migrate and differentiate effectively only within the environment of the olfactory bulb. Only limited survival and differentiation were observed in other brain regions studied. 1st report showing that differentiation potential of postnatal svz precursors when transplanted into adult brain is largely limited to the astroglial fate.},
	Author = {Herrera, D. G. and Garcia-Verdugo, J. M. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {Ann Neurol},
	Keywords = {Lateral Ventricles/*cytology;Transfection;Kainic Acid/toxicity;Corpus Striatum/*cytology/drug effects;Animal;02 Adult neurogenesis migration;Transplantation, Heterotopic;beta-Galactosidase/genetics;Stem Cells/*cytology;Male;B-19;Cerebral Cortex/*cytology/drug effects;Recombinant Proteins/metabolism;Phosphopyruvate Hydratase/genetics;Transplantation, Isogeneic;Neurons/*cytology/*transplantation/ultrastructure;Support, U.S. Gov't, P.H.S.;Promoter Regions (Genetics);Brain Tissue Transplantation/*physiology;Mice;Olfactory Bulb/*cytology/drug effects},
	Number = {6},
	Organization = {Department of Psychiatry, The New York Hospital, Cornell Medical Center, NY, USA.},
	Pages = {867-77.},
	Title = {Adult-derived neural precursors transplanted into multiple regions in the adult brain},
	Uuid = {523387C0-C4AF-4CEC-B4A5-3B07A8CBDCB8},
	Volume = {46},
	Year = {1999},
	url = {papers/Herrera_AnnNeurol1999.pdf}}

@article{Herrup:1995,
	Abstract = {Unexpected nerve cell death has been reported in several experimental situations where neurons have been forced to re-enter the cell cycle after leaving the ventricular zone and entering the G0, non-mitotic stage. To determine whether an association between cell death and unscheduled cell cycling might be found in conjunction with any naturally occurring developmental events, we have examined target-related cell death in two neuronal populations, the granule cells of the cerebellar cortex and the neurons of the inferior olive. Both of these cell populations have a demonstrated developmental dependency on their synaptic target, the cerebellar Purkinje cell. Two mouse neurological mutants, staggerer (sg/sg) and lurcher (+/Lc), are characterized by intrinsic Purkinje cell deficiencies and, in both mutants, substantial numbers of cerebellar granule cells and inferior olive neurons die due to the absence of trophic support from their main postsynaptic target. We report here that the levels of three independent cell cycle markers--cyclin D, proliferating cell nuclear antigen and bromodeoxyuridine incorporation--are elevated in the granule cells before they die. Although lurcher Purkinje cells die during a similar developmental period, no compelling evidence for any cell cycle involvement in this instance of pre-programmed cell death could be found. While application of the TUNEL technique (in situ terminal transferase end-labeling of fragmented DNA) failed to label dying granule cells in either mutant, light and electron microscopic observations are consistent with the interpretation that the death of these cells is apoptotic in nature. Together, the data indicate that target-related cell death in the developing central nervous system is associated with a mechanism of cell death that involves an apparent loss of cell cycle control. 0950-1991 Journal Article},
	Author = {Herrup, K. and Busser, J. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {Development},
	Keywords = {EE pdf;*Cell Cycle;Olivary Nucleus/cytology/embryology;Biological Markers;Neurons/cytology/*physiology;Cerebellar Cortex/cytology/embryology;Mice, Mutant Strains;Support, U.S. Gov't, P.H.S.;Fluorescent Antibody Technique;Animals;Mice;Apoptosis/*physiology;Purkinje Cells/cytology/*physiology},
	Number = {8},
	Organization = {Department of Neurology, Case Western Reserve Medical School, Cleveland, OH 44106, USA.},
	Pages = {2385-95},
	Pubmed = {7671804},
	Title = {The induction of multiple cell cycle events precedes target-related neuronal death},
	Uuid = {32527EC2-D395-11D9-A0E9-000D9346EC2A},
	Volume = {121},
	Year = {1995},
	url = {papers/Herrup_Development1995.pdf}}

@article{Herzog:1999,
	Abstract = {Although it has been known for over 50 years that olfactory receptor neuron (ORN) neurogenesis and subsequent reinnervation of the olfactory bulb (OB) occurs following ORN injury, the precise intrinsic and extrinsic factors that regulate this dynamic process have not yet been fully identified. In the first of two experiments, we characterized the time course of anatomical recovery following zinc sulfate (ZnSO(4)) lesion of ORNs in adult male Sprague-Dawley rats. ZnSO(4) produced a near complete deafferentation of OB within 3 days following intranasal administration. A time-dependent increase in ORN reinnervation of OB was observed following 10, 20, and 30 day recovery intervals. Given the evidence that bFGF, EGF, and TGF-alpha have mitogenic effects on ORNs in vitro, a second experiment examined the extent to which these growth factors (GFs) might enhance ORN regeneration and subsequent reinnervation of OB in vivo. Rats received intranasal infusions of ZnSO(4) on day 0, followed by subcutaneous injections of either bFGF (5, 10, or 50 microgram/kg), EGF (5, 10, or 50 microgram/kg), or TGF- alpha (5 or 10 microgram/kg) on days 3-6. Horseradish peroxidase (HRP) histochemistry of OB following a 10-day recovery period revealed a dose- related enhancement in reinnervation of OB for each of the three growth factors examined, with the greatest enhancement produced by TGF-alpha. These data suggest that GFs may regulate ORN mitogenesis in vivo in a way similar to that which has been characterized in vitro.},
	Author = {Herzog, C. and Otto, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:23 -0400},
	Journal = {Brain Res},
	Keywords = {Nerve Regeneration/drug effects/*physiology;Olfactory Bulb/*physiology;Rats;Zinc Sulfate/administration &dosage/toxicity;Epidermal Growth Factor/*pharmacology;Animal;D pdf;Rats, Sprague-Dawley;Time Factors;Male;Transforming Growth Factor alpha/*pharmacology;Axonal Transport;Support, Non-U.S. Gov't;Nose;06 Adult neurogenesis injury induced;Horseradish Peroxidase;Infusions, Parenteral;Olfactory Receptor Neurons/cytology/drug effects/*physiology},
	Number = {1-2},
	Organization = {Program in Biopsychology and Behavioral Neuroscience, Department of Psychology, Rutgers University, New Brunswick, NJ, USA.},
	Pages = {155-61.},
	Title = {Regeneration of olfactory receptor neurons following chemical lesion: time course and enhancement with growth factor administration},
	Uuid = {DEFCD029-3919-4613-B3A5-A1F6F459642D},
	Volume = {849},
	Year = {1999},
	url = {papers/Herzog_BrainRes1999}}

@article{Hess:2004,
	Abstract = {BACKGROUND: Bone marrow (BM)-derived cells differentiate into a wide variety of cell types. BM contains a heterogeneous population of stem and progenitor cells including hematopoietic stem cells, marrow stromal cells, and perhaps other progenitor cells. To establish unequivocally the transdifferentiation capability of a hematopoietic cell to a nonhematopoietic cell (endothelial cells, neurons, and glial cells), it is imperative to demonstrate that a single cell or clone of that single cell (clonal analysis) differentiates into cells comprising vessels or other cells in the brain. METHODS: We generated mice that exhibited a high level of hematopoietic reconstitution from a single enhanced green fluorescent protein (EGFP) stem cell. To achieve this, we combined FACS sorting and cell culture to generate a population of cells derived from a single hematopoietic stem cell (Lin-, CD34-, c-kit+, and Sca-1+). Clonal populations of cells were then transplanted into lethally irradiated recipient mice. After 3-4 months of engraftment, some mice underwent middle cerebral artery (MCA) suture occlusion. EGFP immunocytochemistry and dual labeling was performed with cell-specific markers on tissue from various time points. RESULTS: In all transplanted mice, EGFP+ highly ramified cells were seen in the brain parenchyma. These cells stained with RCA120 lectin and had the characteristics of parenchymal microglial cells. In brains without infarction and in uninfarcted brain regions of mice that underwent MCA occlusion, there were many EGFP+ cells in a perivascular distribution, associated with both small and larger blood vessels. The cells were tightly apposed to the vessel wall and some had long processes that enveloped the endothelial cells. After MCA occlusion, there was an influx of EGFP expressing cells in the ischemic tissue that colocalized with the "neovascularization." These EGFP+ cells were wrapped around endothelial cells in an albuminal location and did not coexpress von Willebrand Factor or CD31. We detected rare dual-labeled EGFP and NeuN-expressing cells. We detected two staining patterns. The more frequent pattern was phagocytosis of NeuN cells by EGFP expressing cells. However, we also detected rarer cells where the EGFP and NeuN appeared to be colocalized by confocal microscopy. CONCLUSIONS: HSC differentiate into parenchymal microglial cells and perivascular cells in the brain. The numbers of these cells increase after cerebral ischemia. The HSC is therefore one source of parenchymal microglial cells and a source for perivascular cells. After a cerebral infarction, there are rare HSC-derived cells that stain with the neuronal marker, NeuN. However, the more common pattern appears to represent phagocytosis of damaged neurons by EGFP+ microglial cells.},
	Author = {Hess, David C. and Abe, Takanori and Hill, William D. and Studdard, Angeline Martin and Carothers, Jo and Masuya, Masahiro and Fleming, Paul A. and Drake, Christopher J. and Ogawa, Makio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cell Differentiation;Antigens, CD31;Phosphopyruvate Hydratase;Green Fluorescent Proteins;Alpha;Immunohistochemistry;Male;Antigens;Luminescent Proteins;Brain;Cells, Cultured;Carbocyanines;Plant Lectins;Animals;Flow Cytometry;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred C57BL;Hematopoietic Stem Cells;Research Support, U.S. Gov't, Non-P.H.S.;Endothelial Cells;11 Glia;Hematopoietic Stem Cell Transplantation;Laterality;Comparative Study;Radiation Chimera;Benzimidazoles;Time Factors;Female;Microglia;Endothelium, Vascular;Infarction, Middle Cerebral Artery;Microscopy, Confocal;Research Support, Non-U.S. Gov't;Hematopoiesis;Mice, Transgenic;Neurons;Mice},
	Month = {4},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Neurology, Medical College of Georgia, Augusta, GA 30912, USA. dhess\@mail.mcg.edu},
	Pages = {134-44},
	Pii = {S0014488603005740},
	Pubmed = {15026252},
	Title = {Hematopoietic origin of microglial and perivascular cells in brain},
	Uuid = {6E23815A-CEE1-11D9-B244-000D9346EC2A},
	Volume = {186},
	Year = {2004},
	url = {papers/Hess_ExpNeurol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2003.11.005}}

@article{Hess:2002,
	Abstract = {BACKGROUND AND PURPOSE: After an ischemic event, bone marrow-derived cells may be involved in reparative processes. There is increasing evidence that bone marrow-derived stem cells may be a source of endothelial cells and organ-specific cells. Our objectives were to determine whether bone marrow-derived cells were a source of endothelial cells and neurons after cerebral ischemia. METHODS: We transplanted bone marrow from male C57 BL/6-TgN (ACTbEGFP)1Osb mice, which express green fluorescent protein (GFP), into female C57 BL/6J mice. The recipient mice then underwent suture occlusion of the middle cerebral artery (MCA), and bone marrow- derived cells were tracked by GFP epifluorescence and Y chromosome probe. RESULTS: Within 3 days and at 7 and 14 days after MCA occlusion, bone marrow-derived cells incorporated into the vasculature in the ischemic zone and expressed an endothelial cell phenotype. Few bone marrow-derived cells incorporated into the vasculature 24 hours after MCA occlusion. Some bone marrow-derived cells also expressed the neuronal marker NeuN at 7 and 14 days after ischemia. CONCLUSIONS: Postnatal vasculogenesis occurs in the brain in the setting of a cerebral infarction. Bone marrow-derived cells are a source of endothelial cells and NeuN-expressing cells after cerebral infarction. This plasticity may be exploited in the future to enhance recovery after stroke.},
	Author = {Hess, David C. and Hill, William D. and Martin-Studdard, Angeline and Carroll, James and Brailer, Joanna and Carothers, Jo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {1524-4628},
	Journal = {Stroke},
	Keywords = {Endothelium, Vascular;Cell Differentiation;Animals;Stem Cell Transplantation;Infarction, Middle Cerebral Artery;Bone Marrow Transplantation;Research Support, U.S. Gov't, Non-P.H.S.;Antigens, Differentiation;Female;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Microscopy, Fluorescence;Male;Radiation Chimera;Green Fluorescent Proteins;Disease Models, Animal;Neovascularization, Physiologic;Bone Marrow Cells;Neurons;Cerebrovascular Accident;Mice;Immunohistochemistry;Stem Cells;Luminescent Proteins;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {21984760},
	Month = {5},
	Nlm_Id = {0235266},
	Number = {5},
	Organization = {Department of Neurology, Medical College of Georgia, Augusta, Ga 30912, USA. dhess\@neuro.mcg.edu},
	Pages = {1362-8},
	Pubmed = {11988616},
	Title = {Bone marrow as a source of endothelial cells and NeuN-expressing cells After stroke},
	Uuid = {80D65F16-BAED-4A65-B54A-3E979A46D347},
	Volume = {33},
	Year = {2002}}

@article{Hickey:1988,
	Abstract = {A crucial question in the study of immunological reactions in the central nervous system (CNS) concerns the identity of the parenchymal cells that function as the antigen-presenting cells in that organ. Rat bone marrow chimeras and encephalitogenic, major histocompatability--restricted T-helper lymphocytes were used to show that a subset of endogenous CNS cells, commonly termed "perivascular microglial cells," is bone marrow-derived. In addition, these perivascular cells are fully competent to present antigen to lymphocytes in an appropriately restricted manner. These findings are important for bone marrow transplantation and for neuroimmunological diseases such as multiple sclerosis.},
	Author = {Hickey, W. F. and Kimura, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {T-Lymphocytes;Endothelium;Rats, Inbred Lew;Multiple Sclerosis;Astrocytes;Antigen-Presenting Cells;Animals;Chimera;Rats;Bone Marrow Transplantation;Histocompatibility Antigens;Bone Marrow;Research Support, U.S. Gov't, P.H.S.;Encephalomyelitis, Autoimmune, Experimental;Neuroglia;Graft vs Host Disease;Immunohistochemistry;Central Nervous System;Research Support, Non-U.S. Gov't},
	Medline = {88099511},
	Month = {1},
	Nlm_Id = {0404511},
	Number = {4837},
	Organization = {Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104-6079.},
	Pages = {290-2},
	Pubmed = {3276004},
	Title = {Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo},
	Uuid = {8481DC25-D3B7-11D9-A0E9-000D9346EC2A},
	Volume = {239},
	Year = {1988}}

@article{Hienola:2006,
	Abstract = {N-syndecan (syndecan-3) is a transmembrane proteoglycan that is abundantly expressed in the major axonal pathways and in the migratory routes of the developing brain. When ligated by heparin-binding (HB) growth-associated molecule (GAM; pleiotrophin), N-syndecan mediates cortactin-Src kinase-dependent neurite outgrowth. However, the functional role of N-syndecan in brain development remains unexplored. In this study, we show that N-syndecan deficiency perturbs the laminar structure of the cerebral cortex as a result of impaired radial migration. In addition, neural migration in the rostral migratory stream is impaired in the N-syndecan-null mice. We suggest that the migration defect depends on impaired HB-GAM-induced Src kinase activation and haptotactic migration. Furthermore, we show that N-syndecan interacts with EGF receptor (EGFR) at the plasma membrane and is required in EGFR-induced neuronal migration.},
	Author = {Hienola, Anni and Tumova, Sarka and Kulesskiy, Evgeny and Rauvala, Heikki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {0375356},
	Number = {4},
	Organization = {Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland.},
	Pages = {569-80},
	Pii = {jcb.200602043},
	Pubmed = {16908672},
	Title = {N-syndecan deficiency impairs neural migration in brain},
	Uuid = {66F56733-9450-4F78-87DD-2877E231DA03},
	Volume = {174},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200602043}}

@article{Hienola:2004,
	Abstract = {Proliferation of neural stem cells in the embryonic cerebral cortex is regulated by many growth factors and their receptors. Among the key molecules stimulating stem cell proliferation are FGF-2 and the FGF receptor-1. This ligand-receptor system is highly dependent on the surrounding heparan sulfates. We have found that heparin-binding growth-associated molecule (HB-GAM, also designated as pleiotrophin) regulates neural stem cell proliferation in vivo and in vitro. Deficiency of HB-GAM results in a pronounced, up to 50\%increase in neuronal density in the adult mouse cerebral cortex. This phenotype arises during cortical neurogenesis, when HB-GAM knockout embryos display an enhanced proliferation rate as compared to wild-type embryos. Further, our in vitro studies show that exogenously added HB-GAM inhibits formation and growth of FGF-2, but not EGF, stimulated neurospheres, restricts the number of nestin-positive neural stem cells, and inhibits FGF receptor phosphorylation. We propose that HB-GAM functions as an endogenous inhibitor of FGF-2 in stem cell proliferation in the developing cortex. 1044-7431 Journal Article},
	Author = {Hienola, A. and Pekkanen, M. and Raulo, E. and Vanttola, P. and Rauvala, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {1},
	Organization = {Neuroscience Center, Department of Biosciences and Institute of Biotechnology, University of Helsinki, Helsinki 00014, Finland.},
	Pages = {75-88},
	Pubmed = {15121180},
	Title = {HB-GAM inhibits proliferation and enhances differentiation of neural stem cells},
	Uuid = {659798A1-FE87-460A-A228-1849EEE58C3A},
	Volume = {26},
	Year = {2004},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15121180}}

@article{Hill:2004,
	Abstract = {The chemokine stromal-derived factor-1 (SDF-1, also known as CXCL12) and its receptor CXCR4 have been implicated in homing of stem cells to the bone marrow and the homing of bone marrow-derived cells to sites of injury. Bone marrow cells infiltrate brain and give rise to long-term resident cells following injury. Therefore, SDF-1 and CXCR4 expression patterns in 40 mice were examined relative to the homing of bone marrow-derived cells to sites of ischemic injury using a stroke model. Mice received bone marrow transplants from green fluorescent protein (GFP) transgenic donors and later underwent a temporary middle cerebral artery suture occlusion (MCAo). SDF-1 was associated with blood vessels and cellular profiles by 24 hours through at least 30 days post-MCAo. SDF-1 expression was principally localized to the ischemic penumbra. The majority of SDF-1 expression was associated with reactive astrocytes; much of this was perivascular. GFP+ cells were associated with SDF-1-positive vessels and were also found in the neuropil of regions with increased SDF-1 immunoreactivity. Most vessel-associated GFP+ cells resemble pericytes or perivascular microglia and the majority of the GFP+ cells in the parenchyma displayed characteristics of activated microglial cells. These findings suggest SDF-1 is important in the homing of bone marrow-derived cells, especially monocytes, to areas of ischemic injury.},
	Author = {Hill, William D. and Hess, David C. and Martin-Studdard, Angeline and Carothers, Jo J. and Zheng, Jianqing and Hale, David and Maeda, Manabu and Fagan, Susan C. and Carroll, James E. and Conway, Simon J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Receptors, CXCR4;Animals;Astrocytes;Up-Regulation;Infarction, Middle Cerebral Artery;Bone Marrow Transplantation;Microscopy, Confocal;Research Support, U.S. Gov't, Non-P.H.S.;Microglia;Female;Brain;Mice, Transgenic;Cell Movement;Cerebrovascular Circulation;Green Fluorescent Proteins;Disease Models, Animal;Male;11 Glia;In Situ Hybridization;Research Support, U.S. Gov't, P.H.S.;Brain Ischemia;Chemokines, CXC;Mice;Immunohistochemistry;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {23109187},
	Month = {1},
	Nlm_Id = {2985192R},
	Number = {1},
	Organization = {Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912-2000, USA. whill\@mail.mcg.edu},
	Pages = {84-96},
	Pubmed = {14748564},
	Title = {SDF-1 (CXCL12) is upregulated in the ischemic penumbra following stroke: association with bone marrow cell homing to injury},
	Uuid = {48A02ED9-1852-4C21-832F-BD0326CA3CA0},
	Volume = {63},
	Year = {2004}}

@article{Hill:2005a,
	Abstract = {Rapidly advancing knowledge of genome structure and sequence enables new means for the analysis of specific DNA changes associated with the differences between the human brain and that of other mammals. Recent studies implicate evolutionary changes in messenger RNA and protein expression levels, as well as DNA changes that alter amino acid sequences. We can anticipate having a systematic catalogue of DNA changes in the lineage leading to humans, but an ongoing challenge will be relating these changes to the anatomical and functional differences between our brain and that of our ancient and more recent ancestors.},
	Author = {Hill, Robert Sean and Walsh, Christopher A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {10 Development;Research Support, Non-U.S. Gov't;Comparative Study;Phylogeny;Evolution, Molecular;Research Support, U.S. Gov't, P.H.S.;Gene Expression Regulation;Research Support, N.I.H., Extramural;Organ Size;Evolution;Animals;Humans;Cerebral Cortex;Brain;19 Neocortical evolution},
	Month = {9},
	Nlm_Id = {0410462},
	Number = {7055},
	Organization = {Division of Neurogenetics and Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, and Department of Neurology, Harvard Medical School, Room 266, New Research Building, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.},
	Pages = {64-7},
	Pii = {nature04103},
	Pubmed = {16136130},
	Title = {Molecular insights into human brain evolution},
	Uuid = {AAC914E8-31A2-411A-8655-39CC592B5B35},
	Volume = {437},
	Year = {2005},
	url = {papers/Hill_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature04103}}

@article{Himanen:2007,
	Abstract = {Eph receptors are the largest subfamily of receptor tyrosine kinases regulating cell shape, movements, and attachment. The interactions of the Ephs with their ephrin ligands are restricted to the sites of cell-cell contact since both molecules are membrane attached. This review summarizes recent advances in our understanding of the molecular mechanisms underlining the diverse functions of the molecules during development and in the adult organism. The unique properties of this signaling system that are of highest interest and have been the focus of intense investigations are as follows: (i) the signal is simultaneously transduced in both ligand-expressing cells and receptor-expressing cells, (ii) signaling via the same molecules can generate opposing cellular reactions depending on the context, and (iii) the Ephs and the ephrins are divided into two subclasses with promiscuous intrasubclass interactions, but rarely observed intersubclass interactions.},
	Author = {Himanen, Juha-Pekka P. and Saha, Nayanendu and Nikolov, Dimitar B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0955-0674},
	Journal = {Curr Opin Cell Biol},
	Keywords = {10 Development;Signal Transduction;Enzyme Activation;Humans;Ephrins;Enzyme Inhibitors;Nervous System;review;Cell Communication;research support, non-u.s. gov't;10 circuit formation;Cell Adhesion;Protein Structure, Tertiary;Endocytosis;research support, n.i.h., extramural;24 Pubmed search results 2008;Receptor, EphA1;Peptides},
	Month = {10},
	Nlm_Id = {8913428},
	Number = {5},
	Organization = {Structural Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.},
	Pages = {534-42},
	Pii = {S0955-0674(07)00121-4},
	Pubmed = {17928214},
	Title = {Cell-cell signaling via Eph receptors and ephrins},
	Uuid = {1AA9C550-4C59-408B-B3E5-9C14A638CCC7},
	Volume = {19},
	Year = {2007},
	url = {papers/Himanen_CurrOpinCellBiol2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ceb.2007.08.004}}

@article{Himanen:2003,
	Abstract = {Eph receptors, the largest subfamily of receptor tyrosine kinases, and their ephrin ligands are important mediators of cell-cell communication regulating cell attachment, shape and mobility. Both Ephs and ephrins are membrane-bound and their interactions at sites of cell-cell contact initiate unique bidirectional signaling cascades, with information transduced in both the receptor-expressing and the ligand-expressing cells. Recent structural and biophysical studies summarized in this review reveal unique molecular features not previously observed in any other receptor-ligand families and explain many of the biochemical and signaling properties of Ephs and ephrins. Of particular importance is the insight into how approximation of ligand-expressing and receptor-expressing cells could lead to the formation and activation of highly ordered signaling centers at cell-cell interfaces.},
	Author = {Himanen, Juha-Pekka P. and Nikolov, Dimitar B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Receptors, Eph Family;10 Development;research support, non-u.s. gov't;Ligands;Protein Conformation;Cell Communication;Signal Transduction;10 circuit formation;comparative study;Ephrins;research support, u.s. gov't, p.h.s.;Animals;Cells, Cultured;24 Pubmed search results 2008;review;Receptor Protein-Tyrosine Kinases},
	Month = {1},
	Nlm_Id = {7808616},
	Number = {1},
	Organization = {Cellular Biochemistry and Biophysics Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.},
	Pages = {46-51},
	Pii = {S016622360200005X},
	Pubmed = {12495863},
	Title = {Eph signaling: a structural view},
	Uuid = {5DC897E6-F938-4A45-8FBF-3F800AB03325},
	Volume = {26},
	Year = {2003}}

@article{Himes:2006,
	Abstract = {We report in this study that activation of the JNK by the growth factor, CSF-1 is critical for macrophage development, proliferation, and survival. Inhibition of JNK with two distinct classes of inhibitors, the pharmacological agent SP600125, or the peptide D-JNKI1 resulted in cell cycle inhibition with an arrest at the G(2)/M transition and subsequent apoptosis. JNK inhibition resulted in decreased expression of CSF-1R (c-fms) and Bcl-x(L) mRNA in mature macrophages and repressed CSF-1-dependent differentiation of bone marrow cells to macrophages. Macrophage sensitivity to JNK inhibitors may be linked to phosphorylation of the PU.1 transcription factor. Inhibition of JNK disrupted PU.1 binding to an element in the c-fms gene promoter and decreased promoter activity. Promoter activity could be restored by overexpression of PU.1. A comparison of expression profiles of macrophages with 22 other tissue types showed that genes that signal JNK activation downstream of tyrosine kinase receptors, such as focal adhesion kinase, Nck-interacting kinase, and Rac1 and scaffold proteins are highly expressed in macrophages relative to other tissues. This pattern of expression may underlie the novel role of JNK in macrophages.},
	Author = {Himes, S. Roy and Sester, David P. and Ravasi, Timothy and Cronau, Stephen L. and Sasmono, Tedjo and Hume, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {2985117R},
	Number = {4},
	Organization = {Cooperative Research Centre for Chronic Inflammatory Disease, Institute for Molecular Biosciences, University of Queensland, Brisbane, Australia.},
	Pages = {2219-28},
	Pii = {176/4/2219},
	Pubmed = {16455978},
	Title = {The JNK Are Important for Development and Survival of Macrophages},
	Uuid = {CF8CF5CA-FD34-45E0-8DFC-5B82BE2F2EF9},
	Volume = {176},
	Year = {2006}}

@article{Hirase:2004,
	Abstract = {Large and long-lasting cytosolic calcium surges in astrocytes have been described in cultured cells and acute slice preparations. The mechanisms that give rise to these calcium events have been extensively studied in vitro. However, their existence and functions in the intact brain are unknown. We have topically applied Fluo-4 AM on the cerebral cortex of anesthetized rats, and imaged cytosolic calcium fluctuation in astrocyte populations of superficial cortical layers in vivo, using two-photon laser scanning microscopy. Spontaneous [Ca(2+)](i) events in individual astrocytes were similar to those observed in vitro. Coordination of [Ca(2+)](i) events among astrocytes was indicated by the broad cross-correlograms. Increased neuronal discharge was associated with increased astrocytic [Ca(2+)](i) activity in individual cells and a robust coordination of [Ca(2+)](i) signals in neighboring astrocytes. These findings indicate potential neuron-glia communication in the intact brain.},
	Author = {Hirase, Hajime and Qian, Lifen and Barth{\'o}, Peter and Buzs{\'a}ki, Gy{\"o}rgy},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1545-7885},
	Journal = {PLoS Biol},
	Keywords = {Research Support, N.I.H., Extramural;24 Pubmed search results 2008;21 Calcium imaging;Immunohistochemistry;Xanthenes;Male;Cerebral Cortex;Animals;Cells, Cultured;Electrophysiology;Brain;Cytosol;Research Support, U.S. Gov't, P.H.S.;Signal Transduction;Calcium Signaling;Cell Communication;Aniline Compounds;Rats, Sprague-Dawley;Neuroglia;Calcium;Rats;Female;Microscopy, Video;Microscopy, Confocal;21 Neurophysiology;Models, Biological;Neurons;Research Support, Non-U.S. Gov't;Astrocytes;Fluorescent Dyes},
	Month = {4},
	Nlm_Id = {101183755},
	Number = {4},
	Organization = {Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey, USA. hirase\@axon.rutgers.edu},
	Pages = {E96},
	Pubmed = {15094801},
	Title = {Calcium dynamics of cortical astrocytic networks in vivo},
	Uuid = {D1F218D3-C597-4CC9-AEB6-82606B20E0F9},
	Volume = {2},
	Year = {2004},
	url = {papers/Hirase_PLoSBiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0020096}}

@article{Hirotsune:1998,
	Abstract = {Heterozygous mutation or deletion of the beta subunit of platelet-activating factor acetylhydrolase (PAFAH1B1, also known as LIS1) in humans is associated with type I lissencephaly, a severe developmental brain disorder thought to result from abnormal neuronal migration. To further understand the function of PAFAH1B1, we produced three different mutant alleles in mouse Pafah1b1. Homozygous null mice die early in embryogenesis soon after implantation. Mice with one inactive allele display cortical, hippocampal and olfactory bulb disorganization resulting from delayed neuronal migration by a cell-autonomous neuronal pathway. Mice with further reduction of Pafah1b1 activity display more severe brain disorganization as well as cerebellar defects. Our results demonstrate an essential, dosage-sensitive neuronal-specific role for Pafah1b1 in neuronal migration throughout the brain, and an essential role in early embryonic development. The phenotypes observed are distinct from those of other mouse mutants with neuronal migration defects, suggesting that Pafah1b1 participates in a novel pathway for neuronal migration.},
	Author = {Hirotsune, S. and Fleck, M. W. and Gambello, M. J. and Bix, G. J. and Chen, A. and Clark, G. D. and Ledbetter, D. H. and McBain, C. J. and Wynshaw-Boris, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {10 Development;Microtubule-Associated Proteins;Animals;Cells, Cultured;Proteins;1-Alkyl-2-acetylglycerophosphocholine Esterase;Cell Movement;Hippocampus;research support, non-u.s. gov't;Embryonic and Fetal Development;Olfactory Bulb;Abnormalities, Multiple;Cerebral Cortex;Neurons;Mice, Knockout;10 genetics malformation;Genotype;Cerebellum;research support, u.s. gov't, p.h.s.;Mice;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {9216904},
	Number = {4},
	Organization = {Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.},
	Pages = {333-9},
	Pubmed = {9697693},
	Title = {Graded reduction of Pafah1b1 (Lis1) activity results in neuronal migration defects and early embryonic lethality},
	Uuid = {C0F16862-BA39-4EE5-BDEB-CFBDA85B809B},
	Volume = {19},
	Year = {1998},
	url = {papers/Hirotsune_NatGenet1998.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/1221}}

@article{Hisatomi:2003,
	Abstract = {The effective phagocytotic clearance of apoptotic debris is fundamental to the maintenance of neural tissues during apoptosis. Retinal photoreceptors undergo apoptosis after retinal detachment. Although their induction phase of apoptosis has been well discussed, their phagocytotic process remains quite unclear. We herein demonstrate that apoptotic photoreceptors are selectively eliminated from their physiological localization, the outer nuclear layer, to the subretinal space, and then phagocytosed by monocyte-derived macrophages. This could be shown by an ultrastructural and immunophenotypic analysis. Moreover, in chimera mice expressing transgenic green fluorescent protein in bone marrow-derived cells, the local infiltration of macrophages could be detected after retinal detachment-induced photoreceptor apoptosis. The local injection of an antibody blocking the phosphatidylserine receptor (PSR) or a peptide (GRGDSP)-blocking integrin alphavbeta3 revealed that phagocytotic clearance involves the PSR as well as integrin alphavbeta3 in vivo. Importantly, the level of blockade obtained with these reagents was different. Although anti-PSR increased the frequency of apoptotic cells that fail to bind to macrophages, GRGDSP prevented the engulfment (but not the recognition) of apoptotic photoreceptor cells by macrophages. To our knowledge, this is the first report describing the mechanisms through which apoptotic photoreceptors are selectively eliminated via a directional process in the subretinal space.},
	Author = {Hisatomi, Toshio and Sakamoto, Taiji and Sonoda, Koh-Hei H. and Tsutsumi, Chikako and Qiao, Hong and Enaida, Hiroshi and Yamanaka, Ichiro and Kubota, Toshiaki and Ishibashi, Tatsuro and Kura, Shinobu and Susin, Santos A. and Kroemer, Guido},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Retina;Microscopy, Electron, Scanning;Phagocytosis;Animals;Rats, Inbred BN;Macrophages;Rats;Oligopeptides;Receptors, Cell Surface;Apoptosis;Retinal Degeneration;Mice, Transgenic;11 Glia;Immunophenotyping;Green Fluorescent Proteins;Microscopy, Fluorescence;Antibodies;Integrin alphaVbeta3;In Situ Nick-End Labeling;Photoreceptors;Mice;Luminescent Proteins;Membrane Proteins;Microscopy, Electron;Immunohistochemistry;Flavoproteins;Research Support, Non-U.S. Gov't},
	Medline = {22642309},
	Month = {6},
	Nlm_Id = {0370502},
	Number = {6},
	Organization = {Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hisatomi\@med.kyushu-u.ac.jp},
	Pages = {1869-79},
	Pubmed = {12759244},
	Title = {Clearance of apoptotic photoreceptors: elimination of apoptotic debris into the subretinal space and macrophage-mediated phagocytosis via phosphatidylserine receptor and integrin alphavbeta3},
	Uuid = {44A415D7-F573-40D2-871B-3F8516DEF038},
	Volume = {162},
	Year = {2003}}

@article{Hochedlinger:2005,
	Abstract = {The POU-domain transcription factor Oct-4 is normally expressed in pluripotent cells of the mammalian embryo. In addition, germ-cell tumors and a few somatic tumors show detectable expression of Oct-4. While Oct-4's role during preimplantation development is to maintain embryonic cells in a pluripotent state, little is known about its potential oncogenic properties. Here we investigate the effect of ectopic Oct-4 expression on somatic tissues of adult mice using a doxycycline-dependent expression system. Activation of Oct-4 results in dysplastic growths in epithelial tissues that are dependent on continuous Oct-4 expression. Dysplastic lesions show an expansion of progenitor cells and increased beta-catenin transcriptional activity. In the intestine, Oct-4 expression causes dysplasia by inhibiting cellular differentiation in a manner similar to that in embryonic cells. These data show that certain adult progenitors remain competent to interpret key embryonic signals and support the notion that progenitor cells are a driving force in tumorigenesis.},
	Author = {Hochedlinger, Konrad and Yamada, Yasuhiro and Beard, Caroline and Jaenisch, Rudolf},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {3},
	Organization = {Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.},
	Pages = {465-77},
	Pii = {S0092-8674(05)00163-7},
	Pubmed = {15882627},
	Title = {Ectopic expression of Oct-4 blocks progenitor-cell differentiation and causes dysplasia in epithelial tissues},
	Uuid = {9B6FD7A1-2DC4-493D-ACDA-6A8F7F18B155},
	Volume = {121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.02.018}}

@article{Hoek:2000,
	Abstract = {OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.},
	Author = {Hoek, R. M. and Ruuls, S. R. and Murphy, C. A. and Wright, G. J. and Goddard, R. and Zurawski, S. M. and Blom, B. and Homola, M. E. and Streit, W. J. and Brown, M. H. and Barclay, A. N. and Sedgwick, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Animals;Gene Targeting;Encephalomyelitis, Experimental Autoimmune;Macrophages;Rats;Microglia;Denervation;Antigens, Surface;Lymph Nodes;Macrophage Activation;Not relevant;11 Glia;Mice, Inbred C57BL;Joints;Arthritis, Experimental;Support, Non-U.S. Gov't;Receptors, Immunologic;Cell Lineage;Neurons;Down-Regulation;Mice;Central Nervous System;Facial Nerve;Spleen},
	Medline = {20553647},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5497},
	Organization = {DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA.},
	Pages = {1768-71},
	Pii = {9024},
	Pubmed = {11099416},
	Title = {Down-regulation of the macrophage lineage through interaction with OX2 (CD200)},
	Uuid = {96B560F1-4424-49F4-BBE0-C0533FCBD187},
	Volume = {290},
	Year = {2000}}

@article{Hoffman:1992,
	Abstract = {The pathogenesis of progressive spastic paraparesis [HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP)], a serious consequence of human T-cell leukemia virus type I (HTLV-I) infection, is unclear. T and B lymphocytes can be naturally infected by HTLV-I, but the susceptibility to HTLV-I infection of other cell types that could contribute to the pathogenesis of HAM/TSP has not been determined. We found that a human monocyte cell line (THP-1), primary human peripheral blood monocytes, and isolated microglial cells but not astrocytes or oligodendroglial cells derived from adult human brain were infected by HTLV-I in vitro. Infection with HTLV-I enhanced the secretion of interleukin 6 in human microglial cell-enriched cultures but did not stimulate the release of interleukin 1 from monocytes or microglial cells. Tumor necrosis factor alpha production was stimulated by HTLV-I infection of monocytes and microglial cells and could be enhanced by suboptimal amounts of lipopolysaccharide. Since both tumor necrosis factor alpha and interleukin 6 have been implicated in inflammatory demyelination and gliosis, our findings suggest that human microglial cells and monocytes infected with and activated by HTLV-I could play a role in the pathogenesis of HAM/TSP.},
	Author = {Hoffman, P. M. and Dhib-Jalbut, S. and Mikovits, J. A. and Robbins, D. S. and Wolf, A. L. and Bergey, G. K. and Lohrey, N. C. and Weislow, O. S. and Ruscetti, F. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Monocytes;Tumor Necrosis Factor;Neuroglia;Tumor Cells, Cultured;Human;Human T-lymphotropic virus 1;Not relevant;In Vitro;11 Glia;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;RNA, Viral;Interleukin-6;RNA, Messenger;Brain;Cells, Cultured;HTLV-I Infections},
	Medline = {93101611},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {24},
	Organization = {Retrovirus Research Center, Department of Veterans Affairs Medical Center, Baltimore, MD 21218.},
	Pages = {11784-8},
	Pubmed = {1465399},
	Title = {Human T-cell leukemia virus type I infection of monocytes and microglial cells in primary human cultures},
	Uuid = {D3E22DB7-9BFE-4429-9A56-B6886196E678},
	Volume = {89},
	Year = {1992},
	url = {papers/Hoffman_ProcNatlAcadSciUSA1992.pdf}}

@article{Holden:1977,
	Abstract = {Utilizing controlled cryopreservation techniques, we were able to standardize the 51Cr release cytotoxicity assay and thereby ensured reliable comparisons between results obtained on different days. Optimal conditions for freezing of both effector and target cells were quite similar. Dimethyl sulfoxide (DMSO) at a concentration of 7.5-10.0\%was employed as the cryoprotective agent and cells were frozen at the rate of -1 degrees C/minute. The handling procedures for the cells before and after freezing were important. Factors affecting recovery of functional reactivity were related to toxicity of DMSO for the cells, the osmotic stress placed upon the cells as the DMSO was being removed after thawing, the handling temperature of the freshly thawed cells, and the susceptibility of cells to mechanical damage immediately after thawing. The recovery of lymphocytes after freezing was about 70\%; the recovery of cytotoxicity was around 85\%. Syngeneic cytotoxic reactivity induced by inoculation with the Moloney strain of murine sarcoma virus was cryopreserved, as were allogeneic cytotoxicity and natural cytotoxic reactivity. Multiple tests employing effector cells from the same frozen pool gave reproducible results; the standard error of the mean percent cytotoxicity was less than 1.5\%. Cryopreserved target cells gave decreased day-to-day variability in susceptibility to lysis, since the same population of cells could be employed in each assay. These results demonstrated conclusively that we can now have a constant source of effector cells and target cells, which can be used from assay to assay as an internal standard. 0027-8874 Journal Article},
	Author = {Holden, H. T. and Oldham, R. K. and Ortaldo, J. R. and Herberman, R. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {J Natl Cancer Inst},
	Keywords = {Antigens, Viral;Animals;Cell Survival/drug effects;Chromium Radioisotopes;Cells, Cultured;Moloney murine leukemia virus/immunology;Comparative Study;Sarcoma, Experimental/immunology;Antigens, Neoplasm;EE, DMSO, abstr;08 Aberrant cell cycle;Antilymphocyte Serum;Male;Time Factors;Dimethyl Sulfoxide/pharmacology;Mice, Inbred Strains;Temperature;Cryoprotective Agents;Lymphocytes/immunology;Freezing;Cytotoxicity Tests, Immunologic/*methods;Support, U.S. Gov't, P.H.S.;Immunity, Cellular;Mice;Neoplasms, Experimental/immunology;Culture Media},
	Number = {3},
	Pages = {611-22},
	Pubmed = {839557},
	Title = {Standardization of the chromium-51 release, cell-mediated cytotoxicity assay: cryopreservation of mouse effector and target cells},
	Uuid = {F31C61FA-F566-4680-8832-3586A9DB5D08},
	Volume = {58},
	Year = {1977},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=839557}}

@article{Holevinsky:1995,
	Abstract = {Stimulation of macrophages induces the "respiratory burst" response which is associated with the generation of superoxide (O2-), a drop in cytoplasmic pH, and a pronounced depolarization of the membrane potential. The purpose of the present studies was to determine whether an increase in O2- was temporally related to changes in membrane potential and transmembrane current. Release of O2- at the single cell level was photometrically monitored during phagocytosis of immune complexes while simultaneously measuring whole-cell current. Membrane depolarization and the generation of a non-selective current followed an increase in O2- production with a variable lag time which was correlated with the state of cellular maturation in culture. In the absence of phagocytosis, the exposure of macrophages to O2- generated by a xanthine-xanthine oxidase reaction activated a non-selective current similar to that seen after phagocytosis. These results provide the first demonstration of the relationship between free radical release and the ensuing electrophysiological signaling events which are linked to particle engulfment in phagocytic cells.},
	Author = {Holevinsky, K. O. and Nelson, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {24 Pubmed search results 2008;Receptors, Fc;Respiratory Burst;Research Support, U.S. Gov't, P.H.S.;11 Glia;Macrophages;Superoxides;Cells, Cultured;Humans;Membrane Potentials;Phagocytosis;Free Radicals},
	Medline = {95229654},
	Month = {4},
	Nlm_Id = {2985121R},
	Number = {14},
	Organization = {Department of Neurology, University of Chicago, Illinois 60637, USA.},
	Pages = {8328-36},
	Pubmed = {7713941},
	Title = {Simultaneous detection of free radical release and membrane current during phagocytosis},
	Uuid = {4B8FA383-08EF-45F1-95E6-E4B088F526C0},
	Volume = {270},
	Year = {1995}}

@article{Holland:1996,
	Abstract = {Receptor tyrosine kinases of the EPH class have been implicated in the control of axon guidance and fasciculation, in regulating cell migration, and in defining compartments in the developing embryo. Efficient activation of EPH receptors generally requires that their ligands be anchored to the cell surface, either through a transmembrane (TM) region or a glycosyl phosphatidylinositol (GPI) group. These observations have suggested that EPH receptors can transduce signals initiated by direct cell-cell interaction. Genetic analysis of Nuk, a murine EPH receptor that binds TM ligands, has raised the possibility that these ligands might themselves have a signalling function. Consistent with this, the three known TM ligands have a highly conserved cytoplasmic region, with multiple potential sites for tyrosine phosphorylation. Here we show that challenging cells that express the TM ligands Elk-L or Htk-L with the clustered ectodomain of Nuk induces phosphorylation of the ligands on tyrosine, a process that can be mimicked both in vitro and in vivo by an activated Src tyrosine kinase. Co-culture of cells expressing a TM ligand with cells expressing Nuk leads to tyrosine phosphorylation of both the ligand and Nuk. These results suggest that the TM ligands are associated with a tyrosine kinase, and are inducibly phosphorylated upon binding Nuk, in a fashion reminiscent of cytokine receptors. Furthermore, we show that TM ligands, as well as Nuk, are phosphorylated on tyrosine in mouse embryos, indicating that this is a physiological process. EPH receptors and their TM ligands therefore mediate bidirectional cell signalling. 0028-0836 Journal Article},
	Author = {Holland, S. J. and Gale, N. W. and Mbamalu, G. and Yancopoulos, G. D. and Henkemeyer, M. and Pawson, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Nature},
	Keywords = {10 Development;Recombinant Fusion Proteins/metabolism;Animals;Rats;Phosphorylation;*Signal Transduction;Proto-Oncogene Proteins/*metabolism;COS Cells;Ephrin-B2;Membrane Proteins/*metabolism;Receptor Protein-Tyrosine Kinases/*metabolism;Support, Non-U.S. Gov't;Cell Membrane/metabolism;Tyrosine/metabolism;Coculture;Tumor Cells, Cultured;Mice;Amino Acid Sequence;Molecular Sequence Data;F;Ligands},
	Number = {6602},
	Organization = {Programme in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.},
	Pages = {722-5},
	Pubmed = {8878483},
	Title = {Bidirectional signalling through the EPH-family receptor Nuk and its transmembrane ligands},
	Uuid = {80E87EA1-5599-4F2F-81FA-1A5B7A878196},
	Volume = {383},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8878483}}

@article{Holland:1974,
	Author = {Holland, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0036-8733},
	Journal = {Sci Am},
	Keywords = {15 ERVs retroelements;24 Pubmed search results 2008;Cricetinae;Virus Replication;15 Retrovirus mechanism;Animals;Slow Virus Diseases;RNA Viruses;Humans;Mice},
	Medline = {74083540},
	Month = {2},
	Nlm_Id = {0404400},
	Number = {2},
	Pages = {32-40},
	Pubmed = {4810514},
	Title = {Slow, inapparent and recurrent viruses},
	Uuid = {8DFFA399-4328-11DB-A5D2-000D9346EC2A},
	Volume = {230},
	Year = {1974}}

@article{Holter:1991,
	Abstract = {Experimental gene transfer and viral infections can result in the accumulation of unintegrated DNA in target cells. The effects of such accumulation on target cell metabolism have not been directly studied. The experiments reported in this paper show that transfection of cloned retroviral long-terminal-repeat (LTR) DNA, or of a variety of eukaryotic promoters, into proliferating HeLa cells results in rapid, sequence-specific, and dose-dependent cell death. Plasmids containing the Rous sarcoma virus LTR or the human immunodeficiency virus LTR cloned in pUC-related plasmids are 5 to 10 times more toxic than pUC19. The demonstrated sensitivity of eukaryotic cells to exogenously introduced DNA has important implications for the interpretation of gene transfer experiments and may be relevant to the pathogenic mechanisms in the course of retroviral infections such as AIDS.},
	Author = {Holter, W. and Rabson, A. B. and Corsico, C. D. and Howard, B. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0014-4827},
	Journal = {Exp Cell Res},
	Keywords = {Cell Survival;Research Support, Non-U.S. Gov't;HIV;Cytopathogenic Effect, Viral;Humans;Repetitive Sequences, Nucleic Acid;Transfection;HIV Long Terminal Repeat;15 Retrovirus mechanism;23 Technique;Retroviridae;Hela Cells;Research Support, U.S. Gov't, P.H.S.;Sarcoma Viruses, Avian;DNA, Viral;Receptors, Interleukin-2;Promoter Regions (Genetics);24 Pubmed search results 2008;Transcription, Genetic},
	Medline = {91138647},
	Month = {3},
	Nlm_Id = {0373226},
	Number = {1},
	Organization = {Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.},
	Pages = {54-8},
	Pubmed = {1847335},
	Title = {Sequence-specific toxicity of transfected retroviral DNA},
	Uuid = {CE59C305-DC38-4F12-92EA-FC89DE1083E7},
	Volume = {193},
	Year = {1991}}

@article{Honda:1990,
	Abstract = {Employing immunohistochemical techniques and a panel of monoclonal antibodies that recognize rat cells of monocyte/macrophage lineage, we have demonstrated that cells labeled with these antibodies are widely distributed throughout the parenchyma of the rat brain. These cells have a remarkable microglial morphology and form phenotypically heterogenous populations. Double immunoperoxidase staining with the monoclonal antibody and anti-von Willebrand factor antiserum, which recognizes vascular endothelial cells, revealed that these cells are located exclusively at perivascular sites in the adult brain. These observations indicate that the microglial cells are perivascular cells of the monocyte/macrophage lineage, and may be intimately involved in various immunopathogenic conditions of the central nervous system.},
	Author = {Honda, H. and Kimura, H. and Silvers, W. K. and Rostami, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Monocytes;Research Support, Non-U.S. Gov't;Rats, Inbred Lew;Neuroglia;Rats;Immunohistochemistry;Research Support, U.S. Gov't, P.H.S.;Antibodies, Monoclonal;T-Lymphocytes;Phenotype;11 Glia;Antigens, CD4;Macrophages;Blood Vessels;Animals;Brain},
	Medline = {91009779},
	Nlm_Id = {8109498},
	Number = {1-3},
	Organization = {Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104.},
	Pages = {183-91},
	Pubmed = {2104520},
	Title = {Perivascular location and phenotypic heterogeneity of microglial cells in the rat brain},
	Uuid = {3B5146DE-CAA0-4705-8FC0-F32B036B21A3},
	Volume = {29},
	Year = {1990}}

@article{Honda:1999,
	Abstract = {The neurotrophic effect of glial cell line-derived neurotrophic factor (GDNF) has been well documented in both the central and peripheral nervous systems. From the histological findings, target cells of GDNF have been considered to be neurons. In the present study, the expression of GDNF receptors, ret and GFRalpha-1, was demonstrated in rat primary cultured microglia by reverse transcription-polymerase chain reaction and the protein-level expression of Ret was also confirmed by Western-blotting analyses. Moreover, GDNF stimulated the phosphorylation of MAP kinase (ERK1/2) in the cells. These results suggest that GDNF regulates not only neuronal survival and maturation but also certain functions of microglia in the brain.},
	Author = {Honda, S. and Nakajima, K. and Nakamura, Y. and Imai, Y. and Kohsaka, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {p42 MAP Kinase;Animals;Cells, Cultured;Rats;Microglia;Kinetics;RNA, Messenger;Not relevant;11 Glia;Nerve Growth Factors;Support, Non-U.S. Gov't;Animals, Newborn;Cerebral Cortex;Polymerase Chain Reaction;Receptor Protein-Tyrosine Kinases;Proto-Oncogene Proteins;Nerve Tissue Proteins;Drosophila Proteins;Mitogen-Activated Protein Kinases;Transcription, Genetic},
	Medline = {20046677},
	Month = {11},
	Nlm_Id = {7600130},
	Number = {3},
	Organization = {Department of Neurochemistry, National Institute of Neuroscience, Kodaira, Tokyo, Japan.},
	Pages = {203-6},
	Pii = {S0304394099007697},
	Pubmed = {10580710},
	Title = {Rat primary cultured microglia express glial cell line-derived neurotrophic factor receptors},
	Uuid = {09C55A16-0AD5-4080-BC31-2D8BEFE241B6},
	Volume = {275},
	Year = {1999},
	url = {papers/Honda_NeurosciLett1999.pdf}}

@article{Hong:2005,
	Abstract = {Cognitive development is determined by both genetics and environment. One point of convergence of these two influences is the neural activity-dependent regulation of programs of gene expression that specify neuronal fate and function. Human genetic studies have linked several transcriptional regulators to neurodevelopmental disorders including mental retardation and autism spectrum disorders. Recent reports on two such factors, CREB-binding protein and methyl-CpG-binding protein 2, have begun to reveal how epigenetics and neuronal activity act to modulate the program of gene expression required for synaptic development and function.},
	Author = {Hong, Elizabeth J. and West, Anne E. and Greenberg, Michael E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {Cognition Disorders;21 Neurophysiology;Transcription, Genetic;Cognition;Humans;Animals;24 Pubmed search results 2008;review;Transcription Factors},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Division of Neuroscience, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.},
	Pages = {21-8},
	Pii = {S0959-4388(05)00003-6},
	Pubmed = {15721740},
	Title = {Transcriptional control of cognitive development},
	Uuid = {5A4F74D5-899E-4B0C-88AE-B473DAE293A7},
	Volume = {15},
	Year = {2005},
	url = {papers/Hong_CurrOpinNeurobiol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.01.002}}

@article{Hong:2000,
	Abstract = {Normal development of the cerebral cortex requires long-range migration of cortical neurons from proliferative regions deep in the brain. Lissencephaly ("smooth brain," from "lissos," meaning smooth, and "encephalos," meaning brain) is a severe developmental disorder in which neuronal migration is impaired, leading to a thickened cerebral cortex whose normally folded contour is simplified and smooth. Two identified lissencephaly genes do not account for all known cases, and additional lissencephaly syndromes have been described. An autosomal recessive form of lissencephaly (LCH) associated with severe abnormalities of the cerebellum, hippocampus and brainstem maps to chromosome 7q22, and is associated with two independent mutations in the human gene encoding reelin (RELN). The mutations disrupt splicing of RELN cDNA, resulting in low or undetectable amounts of reelin protein. LCH parallels the reeler mouse mutant (Reln(rl)), in which Reln mutations cause cerebellar hypoplasia, abnormal cerebral cortical neuronal migration and abnormal axonal connectivity. RELN encodes a large (388 kD) secreted protein that acts on migrating cortical neurons by binding to the very low density lipoprotein receptor (VLDLR), the apolipoprotein E receptor 2 (ApoER2; refs 9-11 ), alpha3beta1 integrin and protocadherins. Although reelin was previously thought to function exclusively in brain, some humans with RELN mutations show abnormal neuromuscular connectivity and congenital lymphoedema, suggesting previously unsuspected functions for reelin in and outside of the brain.},
	Author = {Hong, S. E. and Shugart, Y. Y. and Huang, D. T. and Shahwan, S. A. and Grant, P. E. and Hourihane, J. O. and Martin, N. D. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {Brain Stem;24 Pubmed search results 2008;Male;Models, Genetic;Cerebral Cortex;10 Development;Animals;Linkage (Genetics);Hippocampus;Phenotype;Extracellular Matrix Proteins;Chromosomes, Human, Pair 7;Magnetic Resonance Imaging;research support, u.s. gov't, p.h.s.;Chromosome Mapping;Lod Score;Frameshift Mutation;Mutation;Serine Endopeptidases;Blotting, Western;Microsatellite Repeats;RNA Splicing;Cerebellum;Pedigree;Female;Cell Adhesion Molecules, Neuronal;Family Health;DNA, Complementary;research support, non-u.s. gov't;Mice;Genes, Recessive;Humans;Reverse Transcriptase Polymerase Chain Reaction;10 genetics malformation;Nerve Tissue Proteins},
	Month = {9},
	Nlm_Id = {9216904},
	Number = {1},
	Organization = {Division of Neurogenetics, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, Massachusetts, USA.},
	Pages = {93-6},
	Pubmed = {10973257},
	Title = {Autosomal recessive lissencephaly with cerebellar hypoplasia is associated with human RELN mutations},
	Uuid = {63D251FC-1EAE-48E3-BDD5-978BA32CFA29},
	Volume = {26},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/79246}}

@article{Hoopfer:2006,
	Abstract = {Axon pruning by degeneration remodels exuberant axonal connections and is widely required for the development of proper circuitry in the nervous system from insects to mammals. Developmental axon degeneration morphologically resembles injury-induced Wallerian degeneration, suggesting similar underlying mechanisms. As previously reported for mice, we show that Wlds protein substantially delays Wallerian degeneration in flies. Surprisingly, Wlds has no effect on naturally occurring developmental axon degeneration in flies or mice, although it protects against injury-induced degeneration of the same axons at the same developmental age. By contrast, the ubiquitin-proteasome system is intrinsically required for both developmental and injury-induced axon degeneration. We also show that the glial cell surface receptor Draper is required for efficient clearance of axon fragments during developmental axon degeneration, similar to its function in injury-induced degeneration. Thus, mechanistically, naturally occurring developmental axon pruning by degeneration and injury-induced axon degeneration differ significantly in early steps, but may converge onto a common execution pathway.},
	Author = {Hoopfer, Eric D. and McLaughlin, Todd and Watts, Ryan J. and Schuldiner, Oren and O'Leary, Dennis D. M. and Luo, Liqun},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Gene Expression Regulation, Developmental;10 Development;research support, n.i.h., extramural ;Wallerian Degeneration;Nerve Tissue Proteins;Animals, Genetically Modified;Drosophila Proteins;Mice, Inbred C57BL;Drosophila;10 Structural plasticity;Animals;comparative study ;Mice;24 Pubmed search results 2008;Axons},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Howard Hughes Medical Institute, Department of Biological Sciences and Neurosciences Program, Stanford University, 385 Serra Mall, Stanford, California 94305, USA.},
	Pages = {883-95},
	Pii = {S0896-6273(06)00380-1},
	Pubmed = {16772170},
	Title = {Wlds protection distinguishes axon degeneration following injury from naturally occurring developmental pruning},
	Uuid = {AEDC064D-5D0E-4823-8D0D-0637AEAF392F},
	Volume = {50},
	Year = {2006},
	url = {papers/Hoopfer_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.05.013}}

@article{Hori:2001,
	Abstract = {PURPOSE. To determine the extent to which donor cells persist and recipient cells repopulate each of the three cell layers of orthotopic corneal grafts in mice. METHODS. BALB/c, C57BL/6, and enhanced green fluorescence protein (EGFP) transgenic mice (B6 background) were used as donors and recipients for orthotopic syngeneic and allogeneic corneal grafts. Graft-bearing eyes were harvested at 5, 10, 15, 28, and 56 days, stained with propidium iodide, and observed (layer by layer) by confocal microscopy. Bone marrow-derived cells in the grafts were assessed immunohistochemically. RESULTS. Donor epithelium was totally replaced by recipient epithelial cells within 15 days in both syngeneic and allogeneic grafts, whereas donor stromal keratocytes and endothelial cells were retained virtually intact in syngeneic grafts and in accepted allografts. In rejected allografts, neither donor-derived keratocytes nor endothelial cells were detected, and, instead, recipient-derived stromal fibroblasts, neovessels, and infiltrating leukocytes were heavily represented. The posterior surface of rejected grafts was devoid of corneal endothelium and was covered incompletely with bone marrow-derived cells of recipient origin. CONCLUSIONS. Whereas in mice graft-derived epithelium is largely irrelevant to corneal allograft outcome, persistence of donor-derived endothelium and keratocytes correlates perfectly with graft acceptance. Recipient endothelium is incapable of covering the posterior surface of accepted or rejected corneal grafts, whereas bone marrow-derived cells of recipient origin come to occupy this site in rejected grafts.},
	Author = {Hori, J. and Streilein, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0146-0404},
	Journal = {Invest Ophthalmol Vis Sci},
	Keywords = {Cell Survival;Research Support, Non-U.S. Gov't;Keratoplasty, Penetrating;Animals;Mice, Inbred BALB C;Microscopy, Confocal;Fibroblasts;Cell Count;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Corneal Stroma;Microscopy, Fluorescence;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Transplantation, Homologous;Graft Rejection;Tissue Donors;Mice;Luminescent Proteins;Endothelium, Corneal;Epithelium, Corneal},
	Medline = {21324520},
	Month = {7},
	Nlm_Id = {7703701},
	Number = {8},
	Organization = {Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, MA 02114-2500, USA.},
	Pages = {1820-8},
	Pubmed = {11431448},
	Title = {Dynamics of donor cell persistence and recipient cell replacement in orthotopic corneal allografts in mice},
	Uuid = {4009C0FF-7634-4C33-B203-9C455A95B872},
	Volume = {42},
	Year = {2001}}

@article{Horn:2002,
	Abstract = {Efficient transduction of hematopoietic stem cells is a prerequisite for successful hematopoietic stem cell gene therapy. Oncoretroviral vectors are the most widely used vectors for hematopoietic gene therapy studies. However, these vectors require cell division, and thus efficient transduction of quiescent stem cells has been difficult to achieve. Lentiviral vectors can transduce non-dividing cells and therefore may be more efficient in transducing quiescent hematopoietic stem cells. We have used a competitive repopulation assay in the baboon to compare transduction of hematopoietic repopulating cells by lentiviral and oncoretroviral vectors. Baboon CD34-enriched marrow cells were transduced in the presence or absence of multiple hematopoietic growth factors using a short, 2-day, transduction protocol. Here, we show that efficient lentiviral transduction of hematopoietic repopulating cells was only achieved when cells were transduced in the presence of multiple growth factors. Using these conditions, up to 8.6\%of hematopoietic repopulating cells were genetically modified by the lentiviral vector more than 1 year after transplant. Interestingly, the number of lentivirally marked cells increased over time in three of four animals. In conclusion, these results suggest that lentiviral vectors are able to tranduce multilineage hematopoietic stem cells, and thus, may provide an alternative vector system for clinical stem cell gene therapy applications.},
	Author = {Horn, P. A. and Morris, J. C. and Bukovsky, A. A. and Andrews, R. G. and Naldini, L. and Kurre, P. and Kiem, H-P P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;Animals;Hematopoietic Cell Growth Factors;Cells, Cultured;Stem Cell Transplantation;Comparative Study;Recombinant Proteins;Lentivirus;Antigens, CD34;11 Glia;Retroviridae;Green Fluorescent Proteins;Papio;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Polymerase Chain Reaction;Transplantation, Autologous;Hematopoietic Stem Cells;Luminescent Proteins;Models, Animal;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {22265326},
	Month = {11},
	Nlm_Id = {9421525},
	Number = {21},
	Organization = {Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.},
	Pages = {1464-71},
	Pubmed = {12378409},
	Title = {Lentivirus-mediated gene transfer into hematopoietic repopulating cells in baboons},
	Uuid = {014DF188-FC7B-44C5-AA99-CD4685CCCB1E},
	Volume = {9},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3301820}}

@article{Horner:2002,
	Abstract = {The NG2 proteoglycan is believed to be an in vivo marker for oligodendrocyte progenitors found in the developing brain. The prevalence of NG2-expressing cells that remain in the adult CNS following the end of gliogenesis is significant. Current research is focused on how this cell participates in the normal function of the adult CNS and whether it may be activated by injury and/or contribute to repair. Despite substantial evidence for a sub-population of NG2-expressing cells playing a glial progenitor role in the adult CNS, there is much to be learned. Specifically, the heterogeneity of this population has not been adequately addressed for the adult CNS and while NG2 cells continue to divide in the adult CNS it is not clear what function they serve once myelination is complete. Future studies should elucidate the functional importance of NG2 in a variety of cell functions and shed light on the role NG2-expressing cells play in the intact and diseased CNS. 0300-4864 Journal Article},
	Author = {Horner, P. J. and Thallmair, M. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {J Neurocytol},
	Keywords = {11 Glia;G pdf},
	Number = {6-7},
	Organization = {Department of Neurological Surgery, University of Washington, 325 Ninth Ave Box 359655, Seattle, WA 98104, USA. phorner\@u.washington.edu},
	Pages = {469-80},
	Pubmed = {14501217},
	Title = {Defining the NG2-expressing cell of the adult CNS},
	Uuid = {A7903E18-3076-4402-9835-F686B182B0B1},
	Volume = {31},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14501217}}

@article{Horner:2000,
	Abstract = {The existence of multipotent progenitor populations in the adult forebrain has been widely studied. To extend this knowledge to the adult spinal cord we have examined the proliferation, distribution, and phenotypic fate of dividing cells in the adult rat spinal cord. Bromodeoxyuridine (BrdU) was used to label dividing cells in 13- to 14- week-old, intact Fischer rats. Single daily injections of BrdU were administered over a 12 d period. Animals were killed either 1 d or 4 weeks after the last injection of BrdU. We observed frequent cell division throughout the adult rodent spinal cord, particularly in white matter tracts (5-7\%of all nuclei). The majority of BrdU-labeled cells colocalized with markers of immature glial cells. At 4 weeks, 10\%of dividing cells expressed mature astrocyte and oligodendroglial markers. These data predict that 0.75\%of all astrocytes and 0.82\%of all oligodendrocytes are derived from a dividing population over a 4 week period. To determine the migratory nature of dividing cells, a single BrdU injection was given to animals that were killed 1 hr after the injection. In these tissues, the distribution and incidence of BrdU labeling matched those of the 4 week post injection (pi) groups, suggesting that proliferating cells divide in situ rather than migrate from the ependymal zone. These data suggest a higher level of cellular plasticity for the intact spinal cord than has previously been observed and that glial progenitors exist in the outer circumference of the spinal cord that can give rise to both astrocytes and oligodendrocytes.},
	Author = {Horner, P. J. and Power, A. E. and Kempermann, G. and Kuhn, H. G. and Palmer, T. D. and Winkler, J. and Thal, L. J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {J Neurosci},
	Keywords = {Salivary Proteins/analysis;Rats;Microscopy, Confocal;Stem Cells/chemistry/*cytology;Neurons/chemistry/*cytology;Animal;02 Adult neurogenesis migration;Astrocytes/chemistry/*cytology;Antimetabolites/analysis/pharmacokinetics;Spinal Cord/*cytology/growth &development;Male;BB abstr;03 Adult neurogenesis progenitor source;Oligodendroglia/chemistry/cytology;Rats, Inbred F344;Cell Division/physiology;Bromodeoxyuridine/analysis/pharmacokinetics;Support, Non-U.S. Gov't;Cell Nucleus;Support, U.S. Gov't, P.H.S.;Age Factors;Cell Movement/physiology;Cell Differentiation/physiology;Biological Markers},
	Number = {6},
	Organization = {The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California 92037, USA. fgage\@salk.edu},
	Pages = {2218-28.},
	Title = {Proliferation and differentiation of progenitor cells throughout the intact adult rat spinal cord},
	Uuid = {6C0060C8-1782-4721-9DEB-CA9909D02DCE},
	Volume = {20},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10704497%20http://www.jneurosci.org/cgi/content/full/20/6/2218%20http://www.jneurosci.org/cgi/content/abstract/20/6/2218}}

@article{Horner:2000a,
	Abstract = {It is self-evident that the adult mammalian brain and spinal cord do not regenerate after injury, but recent discoveries have forced a reconsideration of this accepted principle. Advances in our understanding of how the brain develops have provided a rough blueprint for how we may bring about regeneration in the damaged brain. Studies in developmental neurobiology, intracellular signalling and neuroimmunology are bringing the regeneration field closer to success. Notwithstanding these advances, clear and indisputable evidence for adult functional regeneration remains to be shown.},
	Author = {Horner, P. J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {Nature},
	Keywords = {01 Adult neurogenesis general;A, L both;Nervous System/immunology/*injuries;Nervous System Diseases/pathology;Signal Transduction;Animal;Nerve Growth Factors/physiology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;*Nerve Regeneration;Axons},
	Number = {6807},
	Organization = {The Laboratory of Genetics, The Salk Institute, La Jolla, California 92037, USA.},
	Pages = {963-70.},
	Title = {Regenerating the damaged central nervous system},
	Uuid = {E01EED99-D590-4C56-94FC-7C7966800116},
	Volume = {407},
	Year = {2000},
	url = {papers/Horner_Nature2000.pdf}}

@article{Horner:2003,
	Abstract = {Like a newly popular nightspot, the biology of adult stem cells has emerged from obscurity to become one of the most lively new disciplines of the decade. The neurosciences have not escaped this trendy pastime and, from amid the noise and excitement, the astrocyte emerges as a beguiling companion to the adult neural stem cell. A once receding partner to neurons and oligodendrocytes, the astrocyte even takes on an alter ego of the stem cell itself (S. Goldman, this issue of TINS). Putting ego aside, the 'astrocyte' is also (and perhaps more importantly) an integral component of neural progenitor hotspots, where the craziness or 'la vida loca' of the nightlife might not be so wild when compared with our traditional understanding of the astrocyte. Here, astrocytes contribute to the instructive confluence of location, atmosphere and cellular neighbors that define the daily 'vida local' or everyday local life of an adult stem cell. This review discusses astrocytes as influential components in the local stem cell niche.},
	Author = {Horner, Philip J. and Palmer, Theo D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {review;Neuroglia;Glial Fibrillary Acidic Protein;03 Adult neurogenesis progenitor source;Astrocytes;Stem Cells;Cell Division;11 Glia;review, tutorial;Animals;Cerebral Cortex;Cell Lineage;Neurons},
	Medline = {22949173},
	Month = {11},
	Nlm_Id = {7808616},
	Number = {11},
	Organization = {University of Washington, Department of Neurosurgery, Harborview R&T Building, 325 Ninth Ave - Box 359655, Seattle, WA 98104, USA. tpalmer\@stanford.edu},
	Pages = {597-603},
	Pii = {S0166223603002935},
	Pubmed = {14585599},
	Title = {New roles for astrocytes: the nightlife of an 'astrocyte'. La vida loca!},
	Uuid = {9353075F-1767-487C-AF7C-EB7B33616D4D},
	Volume = {26},
	Year = {2003},
	url = {papers/Horner_TrendsNeurosci2003.pdf}}

@article{Horowitz:1999,
	Abstract = {Mammalian nervous system function involves billions of neurons which are interconnected in a multitude of neural circuits. Here we describe a genetic approach to chart neural circuits. By using an olfactory- specific promoter, we selectively expressed barley lectin in sensory neurons in the olfactory epithelium and vomeronasal organ of transgenic mice. The lectin was transported through the axons of those neurons to the olfactory bulb, transferred to the bulb neurons with which they synapse, and transported through the axons of bulb neurons to the olfactory cortex. The lectin also was retrogradely transported from the bulb to neuromodulatory brain areas. No evidence could be obtained for adverse effects of the lectin on odorant receptor gene expression, sensory axon targeting in the bulb, or the generation or transmission of signals by olfactory sensory neurons. Transneuronal transfer was detected prenatally in the odor-sensing pathway, but only postnatally in the pheromone-sensing pathway, suggesting that odors, but not pheromones, may be sensed in utero. Our studies demonstrate that a plant lectin can serve as a transneuronal tracer when its expression is genetically targeted to a subset of neurons. This technology can potentially be applied to a variety of vertebrate and invertebrate neural systems and may be particularly valuable for mapping connections formed by small subsets of neurons and for studying the development of connectivity as it occurs in utero.},
	Author = {Horowitz, L. F. and Montmayeur, J. P. and Echelard, Y. and Buck, L. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Gene Transfer Techniques;Neurons/*physiology;23 Technique;Brain/*physiology;Human;Biological Markers;T;Axonal Transport/*physiology;Animal;Lectins/genetics;Mice, Transgenic;Support, Non-U.S. Gov't;Mice;Plant Proteins/genetics;Nerve Net/*physiology},
	Number = {6},
	Organization = {Department of Neurobiology, Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.},
	Pages = {3194-9.},
	Title = {A genetic approach to trace neural circuits},
	Uuid = {4F8C43AE-39AD-41BC-B307-EDAEB7283D37},
	Volume = {96},
	Year = {1999},
	url = {papers/Horowitz_ProcNatlAcadSciUSA1999}}

@article{Hossain:2004,
	Abstract = {Neonatal hypoxic-ischemic brain injury is a major cause of neurological disability and mortality. Its therapy will likely require a greater understanding of the discrete neurotoxic molecular mechanism(s) triggered by hypoxia-ischemia (HI). Here, we investigated the role of neuronal pentraxin 1 (NP1), a member of a newly recognized subfamily of "long pentraxins," in the HI injury cascade. Neonatal brains developed marked infarcts in the ipsilateral cerebral hemisphere at 24 hr and showed significant loss of ipsilateral striatal, cortical, and hippocampal volumes at 7 d after HI compared with the contralateral hemisphere and sham controls. Immunofluorescence analyses revealed elevated neuronal expression of NP1 in the ipsilateral cerebral cortex from 6 hr to 7 d and in the hippocampal CA1 and CA3 regions from 24 hr to 7 d after HI. These same brain areas developed infarcts and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling-positive cells within 24-48 hr of HI. In primary cortical neurons, NP1 protein was induced >2.5-fold (p < 0.001) after their exposure to hypoxia that caused approximately 30-40\%neuronal death. Transfecting cortical neurons with antisense oligodeoxyribonucleotides directed against NP1 mRNA (NP1AS) significantly inhibited (p < 0.01) hypoxia-induced NP1 protein induction and neuronal death (p < 0.001), demonstrating a specific requirement of NP1 in hypoxic neuronal injury. NP1 protein colocalized and coimmunoprecipitated with the fast excitatory AMPA glutamate receptor subunit (GluR1) in primary cortical neurons, and hypoxia induced a time-dependent increase in NP1-GluR1 interactions. NPIAS also protected against AMPA-induced neuronal death (p < 0.05), implicating a role for NP1 in the excitotoxic cascade. Our results show that NP1 induction mediates hypoxic-ischemic injury probably by interacting with and modulating GluR1 and potentially other excitatory glutamate receptors.},
	Author = {Hossain, Mir Ahamed and Russell, Juliet C. and O'Brien, Richard and Laterra, John},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {C-Reactive Protein;Dose-Response Relationship, Drug;Neurotoxins;Animals;Gene Expression Regulation;Cells, Cultured;Protein Binding;Rats;alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;21 Epilepsy;Apoptosis;Cell Hypoxia;Brain;RNA, Messenger;Receptors, AMPA;Disease Models, Animal;Hypoxia-Ischemia, Brain;Animals, Newborn;Rats, Inbred F344;In Situ Nick-End Labeling;Research Support, U.S. Gov't, P.H.S.;21 Neurophysiology;Neurons;24 Pubmed search results 2008;Nerve Tissue Proteins;Oligonucleotides, Antisense;Research Support, Non-U.S. Gov't},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. hossain\@kennedykrieger.org},
	Pages = {4187-96},
	Pii = {24/17/4187},
	Pubmed = {15115814},
	Title = {Neuronal pentraxin 1: a novel mediator of hypoxic-ischemic injury in neonatal brain},
	Uuid = {22F43975-E7F2-4C86-B8D6-95CE9A5E0F9D},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0347-04.2004}}

@article{Hossain-Ibrahim:2006,
	Abstract = {ABSTRACT: BACKGROUND: Inflammation around cell bodies of primary sensory neurons and retinal ganglion cells enhances expression of neuronal growth-associated genes and stimulates axonal regeneration. We have asked if inflammation would have similar effects on corticospinal neurons, which normally show little response to spinal cord injury. Lipopolysaccharide (LPS) was applied onto the pial surface of the motor cortex of adult rats with or without concomitant injury of the corticospinal tract at C4. Inflammation around corticospinal tract cell bodies in the motor cortex was assessed by immunohistochemistry for OX42 (a microglia and macrophage marker). Expression of growth-associated genes c-jun, ATF3, SCG10 and GAP-43 was investigated by immunohistochemistry or in situ hybridisation. RESULTS: Application of LPS-induced a gradient of inflammation through the entire depth of the motor cortex and promoted c-Jun and SCG10 expression for up to 2 weeks, and GAP-43 upregulation for 3 days by many corticospinal neurons, but had very limited effects on neuronal ATF3 expression. However, many glial cells in the subcortical white matter upregulated ATF3. LPS did not promote sprouting of anterogradely labelled corticospinal axons, which did not grow into or beyond a cervical lesion site. CONCLUSION: Inflammation produced by topical application of LPS promoted increased expression of some growth-associated genes in the cell bodies of corticospinal neurons, but was insufficient to promote regeneration of the corticospinal tract.},
	Author = {Hossain-Ibrahim, and Rezajooi, and Macnally, and Mason, and Lieberman, and Anderson,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1471-2202},
	Journal = {BMC Neurosci},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {100966986},
	Number = {1},
	Pages = {8},
	Pii = {1471-2202-7-8},
	Pubmed = {16433912},
	Title = {Effects of lipopolysaccharide-induced inflammation on expression of growth-associated genes by corticospinal neurons},
	Uuid = {41DA9E74-E89F-4076-8082-AAB65D70DEAB},
	Volume = {7},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2202-7-8}}

@article{Houalla:2003,
	Abstract = {We have developed a method for isolating goldfish microglia. Cells were identified as microglia immunohistochemically with NN-2, a monoclonal antibody (MAb) raised against teleost retinal microglial cells, and by their phagocytic abilities. Morphological characterization of the cells identified round, phase-bright cells as well as flattened macrophage-like cells. Ramified cells were also seen but they were rare. Fusion of macrophage-like cells occurred in high density cultures and resulted in the formation of giant cells that disintegrated a few days later. Immunohistochemical studies demonstrated that virtually all of the cells in our cultures were NN-2+ and did not label with either antiGFAP (an astrocyte marker) or MAb 6D2 (an oligodendrocyte marker). Cells identified as microglia were intensely phagocytic and ingested latex microspheres, DiIAcLDL and goldfish myelin in vitro. In addition, we labelled microglial cells in vivo with intracranial injections of fluorescent dextran and found that microglia isolated from these animals contained the dextran and phagocytosed microspheres. We also studied the effect of myelin on microsphere uptake and compared the effect of myelin and opsonized myelin on the phagocytic activity of the cells. Our results showed a clear increase in the phagocytic activity of microglia when incubated with myelin, with an enhanced effect of opsonized myelin.},
	Author = {Houalla, T. and Levine, R. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {Research Support, Non-U.S. Gov't;Glial Fibrillary Acidic Protein;Goldfish;Immunohistochemistry;Myelin Sheath;Comparative Study;Time Factors;Cell Count;11 Glia;Microglia;Cell Culture Techniques;Microspheres;Cells, Cultured;Brain;Animals;Phagocytosis;Cell Separation},
	Month = {12},
	Nlm_Id = {7905558},
	Number = {1-2},
	Organization = {Department of Biology, McGill University, Montr{\'e}al, Qu{\'e}, Canada H3A 1B1.},
	Pages = {121-31},
	Pii = {S0165027003002711},
	Pubmed = {14659832},
	Title = {The isolation and culture of microglia-like cells from the goldfish brain},
	Uuid = {014FFA6A-0663-46E1-8624-3CEBC24B8E22},
	Volume = {131},
	Year = {2003},
	url = {papers/Houalla_JNeurosciMethods2003.pdf}}

@article{Houser:1990,
	Abstract = {The distribution of granule cells in the dentate gyrus of the hippocampal formation was studied in control autopsy and temporal lobe epilepsy (TLE) specimens. In control tissue, the granule cell somata were closely approximated and formed a narrow lamina with a distinct, regular border with the molecular layer. In 11 of 15 TLE specimens, the granule cell somata were dispersed and formed a wider than normal granule cell layer. The granule cell somata extended into the molecular layer to varying extents, creating an irregular boundary between the lamina. The dispersed granule cells were frequently aligned in columns, and many of these neurons displayed elongated bipolar forms. The extent of granule cell dispersion appeared to be related to the amount of cell loss in the polymorph layer of the dentate gyrus. Granule cell dispersion was not consistently associated with granule cell loss although 5 of the 11 specimens with granule cell dispersion also showed moderate to marked granule cell loss. The most common features in the histories of the TLE cases with granule cell dispersion were severe febrile seizures or seizures associated with meningitis or encephalitis during the first 4 years of life. The dispersion of the granule cells suggests that there has been some alteration in the patterns of cell migration in a subpopulation of cases with severe TLE. The resultant ectopic positions of the granule cells could lead to changes in both the afferent and efferent connections of these neurons and, thus, contribute to the altered circuitry of the hippocampal formation in TLE.},
	Author = {Houser, C. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Staining and Labeling;Adolescent;Adult;Epilepsy, Temporal Lobe;Female;Hippocampus;Research Support, U.S. Gov't, P.H.S.;Risk Factors;Middle Aged;Research Support, U.S. Gov't, Non-P.H.S.;Male;Humans;Oxazines},
	Medline = {91159839},
	Month = {12},
	Nlm_Id = {0045503},
	Number = {2},
	Organization = {Neurology Service, Veterans Administration Medical Center, West Los Angeles, CA.},
	Pages = {195-204},
	Pubmed = {1705855},
	Title = {Granule cell dispersion in the dentate gyrus of humans with temporal lobe epilepsy},
	Uuid = {3379D824-810D-11DA-9009-000D9346EC2A},
	Volume = {535},
	Year = {1990}}

@article{Houser:1992,
	Abstract = {Multiple morphological and neurochemical changes are found in the dentate gyrus of humans with temporal lobe epilepsy (TLE). Three basically different types of changes will be discussed and some interrelationships considered. Neuronal loss in several regions of the hippocampal formation in human TLE has been recognized for many years, but only recently have the polymorph or hilar neurons been evaluated as a distinct group of neurons, and cell loss in this region is now being documented in many cases with severe TLE. Reorganization of afferents within the molecular layer of the dentate gyrus is also found in a high percentage of TLE specimens. The apparent reorganization of mossy fibers from the dentate granule cells is particularly striking, and aberrant innervation of the inner part of the molecular layer by zinc- and dynorphin-containing mossy fibers has been reported in human tissue by several groups of investigators. In a subpopulation of TLE specimens, there is also disorganization of the granule cell layer. Rather than being arranged in the compact, highly organized layer that is characteristic of control tissue, the granule cell bodies in some TLE cases are dispersed. In some additional cases, a bilaminar pattern of granule cells is observed. Each of these changes could contribute to altered circuitry within the dentate gyrus of humans with TLE, and such alterations could influence seizure susceptibility within the hippocampal formation.},
	Author = {Houser, C. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0922-9833},
	Journal = {Epilepsy Res Suppl},
	Keywords = {Axons;Nerve Fibers;Nerve Degeneration;Nerve Regeneration;Hippocampus;Neuronal Plasticity;Research Support, U.S. Gov't, P.H.S.;Epilepsy, Temporal Lobe;Research Support, U.S. Gov't, Non-P.H.S.;Afferent Pathways;Humans;review;Neurons},
	Medline = {93103514},
	Nlm_Id = {8913231},
	Organization = {Neurology Service, Veterans Administration Medical Center, West Los Angeles, Wadsworth Division, CA.},
	Pages = {223-34},
	Pubmed = {1466768},
	Title = {Morphological changes in the dentate gyrus in human temporal lobe epilepsy},
	Uuid = {3379DFA5-810D-11DA-9009-000D9346EC2A},
	Volume = {7},
	Year = {1992}}

@article{Hu:1996,
	Abstract = {During mammalian brain development, immature neurons often migrate considerable distances. A dramatic example is the rostral migration of olfactory interneuron precursors from near the septum to the olfactory bulb via a subventricular pathway. Heterotopic transplantations establish that this migration is unidirectional and that guidance cues operate over a considerable distance. The guidance cues for this translocation have not been identified, and the present studies provide evidence that a diffusible chemorepulsive factor, secreted by caudal septum but not by other tissue regions surrounding the pathway, may be involved. This activity is functionally distinct from that produced by factors that influence vertebrate axon outgrowth, such as netrin-1, netrin-2, and collapsin-1/semaphorin-III. The presence of this activity in the floor plate/ventral spinal cord as well as the septum suggests that it may influence other types of cell migration.},
	Author = {Hu, H. and Rutishauser, U.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neuron},
	Keywords = {Septal Nuclei/cytology;02 Adult neurogenesis migration;Olfactory Bulb/cytology/*growth &development;Cell Communication;Rats;Cerebral Ventricles/cytology;B-5;Animal;Support, U.S. Gov't, P.H.S.;Cells, Cultured;Cell Movement;Mice;Chemotaxis;Interneurons/*cytology},
	Number = {5},
	Organization = {Department of Genetics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4955, USA.},
	Pages = {933-40.},
	Title = {A septum-derived chemorepulsive factor for migrating olfactory interneuron precursors},
	Uuid = {E7501F31-B3D6-4E58-9E65-1C691485B60B},
	Volume = {16},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8630251}}

@article{Hu:1996a,
	Abstract = {Transplantation studies have been used to show that tangential migration of olfactory bulb interneuron precursors is retarded in NCAM- mutant mice, and that this defect reflects loss of NCAM polysialic acid (PSA). In contrast, radial migration of cells within the bulb did not require PSA. Reciprocal transplantations between wild-type and mutant mice have revealed that the mutation affects the in vivo migration environment in the subventricular zone, and not movement of individual cells. However, in vitro migration of the cells into a PSA-negative collagen matrix environment was also PSA dependent. The surprisingly similar results obtained in the in vivo and in vitro environments is consistent with the observation that migration of subventricular cells occurs as streams of closely apposed cells in which the PSA-positive cells appear to serve as their own migration substrate.},
	Author = {Hu, H. and Tomasiewicz, H. and Magnuson, T. and Rutishauser, U.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neuron},
	Keywords = {Tissue Culture;Fluorescent Antibody Technique, Indirect;B abstr;Mice, Mutant Strains;Cell Movement/*physiology;Sialic Acids/genetics/*physiology;Animal;Mutation;02 Adult neurogenesis migration;Neural Cell Adhesion Molecules/chemistry/genetics;Stem Cells/*cytology;Animals, Newborn;Support, Non-U.S. Gov't;Brain/cytology;Olfactory Bulb/*cytology/transplantation;Support, U.S. Gov't, P.H.S.;Interneurons/*cytology;Mice;Collagen;Culture Media},
	Number = {4},
	Organization = {Department of Genetics, Case Western Reserve University, Cleveland, Ohio 44106, USA.},
	Pages = {735-43.},
	Title = {The role of polysialic acid in migration of olfactory bulb interneuron precursors in the subventricular zone},
	Uuid = {042C2777-3C57-4CEA-AA88-88B2309B69CA},
	Volume = {16},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8607992}}

@article{Huang:2000,
	Abstract = {Our aims were to examine whether oxidative DNA damage was elevated in brain cells of male C57BL/6 mice after oxidative stress, and to determine whether neuronal nitric oxide synthase (nNOS) was involved in such damage. Oxidative stress was induced by occluding both common carotid arteries for 90 min, followed by reperfusion. Escherichia coli exonuclease III (Exo III) removes apyrimidinic or apurinic (AP) sites and 3'-phosphate termini in single-strand breaks, and converts these lesions to 3'OH termini. These ExoIII-sensitive sites (EXOSS) can then be postlabeled using digoxigenin-11-dUTP and Klenow DNA polymerase-I, and detected using fluorescein isothiocyanate-IgG against digoxigenin. Compared with the non-ischemia controls, the density of EXOSS-positive cells was elevated at least 20-fold (P <0.01) at 15 min of reperfusion, and remained elevated for another 30 min. EXOSS mainly occurred in the cell nuclei of the astrocytes and neurons. Signs of cell death were detected at 24 h of reperfusion and occurred mostly in the neurons. Both DNA damage and cell death in the cerebral cortical neurons were abolished by treatment with 3-bromo-7-nitroindazole (30 mg/kg, intraperitoneal), which specifically inhibited nNOS. Our results suggest that nNOS, its activator (calcium), and peroxynitrite exacerbate oxidative DNA damage after brain ischemia.-Huang, D., Shenoy, A., Cui, J., Huang, W., Liu, P. In situ detection of AP sites and DNA strand breaks bearing 3'-phosphate termini in ischemic mouse brain. 0892-6638 Journal Article},
	Author = {Huang, D. and Shenoy, A. and Cui, J. and Huang, W. and Liu, P. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Faseb J},
	Keywords = {Exodeoxyribonucleases/metabolism;Animals;Nitric-Oxide Synthase/metabolism;Reperfusion Injury/*metabolism;Arcuate Nucleus/chemistry;Cerebral Cortex/chemistry;Histocytochemistry/*methods;Astrocytes/chemistry;Mice, Inbred C57BL;08 Aberrant cell cycle;Male;EE;Support, Non-U.S. Gov't;DNA Polymerase I;In Situ Nick-End Labeling;NADP/isolation &purification;Oxidative Stress/*physiology;Support, U.S. Gov't, P.H.S.;*DNA Damage;Prosencephalon/chemistry;Brain Ischemia/*metabolism;Mice;Cell Death;Neurons/chemistry},
	Number = {2},
	Organization = {Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.},
	Pages = {407-17},
	Pubmed = {10657997},
	Title = {In situ detection of AP sites and DNA strand breaks bearing 3'-phosphate termini in ischemic mouse brain},
	Uuid = {DB2E6B2A-18DA-4888-8743-B1F16C7C0AE8},
	Volume = {14},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10657997}}

@article{Huang:2002,
	Abstract = {Two experiments were carried out to test whether cells which are born in adulthood and migrate to the olfactory bulb of adult male golden hamsters are activated during sexual behaviors, to determine the time course over which such responsiveness appears, and to ask whether activation is specific to sexual cues. In the first experiment, adult male hamsters were injected with 5'-bromodeoxyuridine (BrdU, 50mg/kg b.w.) 3 times over the course of one week in order to mark dividing cells. Ten days, three weeks, or seven weeks after the first BrdU injection, the animals were allowed to mate with an estrous female for half an hour before being sacrificed. Confocal analysis of fluorescent immunostaining of BrdU and c-Fos first revealed dual labeled cells in the olfactory bulb 3 weeks after injection of the thymidine analog. In order to determine whether the activation of these newly generated cells is specific to sexual cues, we next compared the incidence of c- Fos expression in newborn (BrdU positive) cells among male hamsters exposed to an estrous female, an aggressive male, a cotton swab containing vaginal secretion from an estrous female hamster (FHVS), a cotton swab containing peppermint, or a cotton swab containing distilled water. In the mitral and glomerular layers of the accessory olfactory bulb, animals exposed to an estrous female had significantly more double labeled cells than did those given other treatments (p <0.01). In the mitral layer of the main bulb, animals exposed to an estrous female had a significantly higher percentage of double labeled cells than those of other groups, except those exposed to an aggressive male (p <0.05). No double labeled cells were seen in medial preoptic area (MPOA), medial nucleus of the amygdala (Me), the bed nucleus of the stria terminalis (BNST), or the hypothalamus. Our results indicate that cells born in adulthood are more responsive to cues arising from estrous females than other stimuli, and thus may participate in sociosexual behaviors. (c) 2002 Elsevier Science (USA).},
	Author = {Huang, L. and Bittman, E. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:39:49 -0400},
	Journal = {Horm Behav},
	Keywords = {B both;02 Adult neurogenesis migration},
	Number = {3},
	Organization = {Department of Biology, The University of Massachusetts, Amherst, Massachusetts, 01003},
	Pages = {343-50.},
	Title = {Olfactory bulb cells generated in adult male golden hamsters are specifically activated by exposure to estrous females},
	Uuid = {16A33483-4D7A-4043-8422-11BF8BD31D9F},
	Volume = {41},
	Year = {2002},
	url = {papers/Huang_HormBehav2002.pdf}}

@article{Huang:1998,
	Abstract = {Seasonal changes in vertebrate brain function are pervasive, but annual cycles in the rates of neuronal incorporation are established only in songbirds. Although cell division continues in the subependymal and hippocampal subgranular zones of adult rodents, there exists no parallel evidence that seasonal plasticity in mammals extends to changes in neuronal or glial number. We examined the effect of photoperiod on incorporation of new neurons in the brain of the adult golden hamster, a long-day breeder. We administered the cell birth marker 5'-bromodeoxyuridine (BrdU) to males which had either been maintained in long days, transferred to short days for 10 weeks, or moved acutely from long to short or short to long days. The number of cells in specific brain regions immunoreactive (ir) for this thymidine analog was determined 7 weeks later. The number of BrdU-ir cells in the dentate gyrus and subependymal zone increased twofold in short days. Transfer between photoperiods 10 days before the BrdU injections produced intermediate numbers of BrdU-labeled cells in the dentate gyrus, but was as effective as long-term photoperiodic exposure in the subependymal zone. Photoperiod also had similar effects in the hypothalamus and cingulate/retrosplenial cortex, but not in the central gray or preoptic area. Double-label immunocytochemistry indicated that very few of the BrdU-ir cells were glia, but that a majority had neuronal phenotype. In the subependymal zone, short days significantly increased the number of BrdU-labeled neurons. We did not detect significant effects of photoperiod on the volume of either the granule cell layer of the hippocampus or the dentate gyrus as a whole. We conclude that short day lengths increase neuronal birth and/or survival in several brain regions of adult hamsters.},
	Author = {Huang, L. and DeVries, G. J. and Bittman, E. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:32 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Hamsters;Animals;Photoperiod;Research Support, U.S. Gov't, Non-P.H.S.;Brain;Male;Antimetabolites;Research Support, U.S. Gov't, P.H.S.;Testis;Body Weight;Mesocricetus;Neuroglia;Dentate Gyrus;Sex Behavior, Animal;Organ Size;Neurons;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine},
	Medline = {98401911},
	Month = {9},
	Nlm_Id = {0213640},
	Number = {3},
	Organization = {Department of Biology, University of Massachusetts, Amherst 01003, USA.},
	Pages = {410-20},
	Pii = {10.1002/(SICI)1097-4695(19980905)36:3<410::AID-NEU8>3.0.CO;2-Z},
	Pubmed = {9733075},
	Title = {Photoperiod regulates neuronal bromodeoxyuridine labeling in the brain of a seasonally breeding mammal},
	Uuid = {FD62AB0E-5C27-4F78-ACD9-349BBE6C6AD7},
	Volume = {36},
	Year = {1998}}

@article{Huang:2001,
	Abstract = {Papillary thyroid carcinoma (PTC) is clinically heterogeneous. Apart from an association with ionizing radiation, the etiology and molecular biology of PTC is poorly understood. We used oligo-based DNA arrays to study the expression profiles of eight matched pairs of normal thyroid and PTC tissues. Additional PTC tumors and other tissues were studied by reverse transcriptase-PCR and immunohistochemistry. The PTCs showed concordant expression of many genes and distinct clustered profiles. Genes with increased expression in PTC included many encoding adhesion and extracellular matrix proteins. Expression was increased in 8/8 tumors for 24 genes and in 7/8 tumors for 22 genes. Among these genes were several previously known to be overexpressed in PTC, such as MET, LGALS3, KRT19, DPP4, MDK, TIMP1, and FN1. The numerous additional genes include CITED1, CHI3L1, ODZ1, N33, SFTPB, and SCEL. Reverse transcriptase-PCR showed high expression of CITED1, CHI3L1, ODZ1, and SCEL in 6/6 additional PTCs. Immunohistochemical analysis detected CITED1 and SFTPB in 49/52 and 39/52 PTCs, respectively, but not in follicular thyroid carcinoma and normal thyroid tissue. Genes underexpressed in PTC included tumor suppressors, thyroid function-related proteins, and fatty acid binding proteins. Expression was decreased in 7/8 tumors for eight genes and decreased in 6/8 tumors for 19 genes. We conclude that, despite its clinical heterogeneity, PTC is characterized by consistent and specific molecular changes. These findings reveal clues to the molecular pathways involved in PTC and may provide biomarkers for clinical use. 0027-8424 Journal Article},
	Author = {Huang, Y. and Prasad, M. and Lemon, W. J. and Hampel, H. and Wright, F. A. and Kornacker, K. and LiVolsi, V. and Frankel, W. and Kloos, R. T. and Eng, C. and Pellegata, N. S. and de la Chapelle, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Tumor Markers, Biological;*Gene Expression Profiling;Cell Adhesion Molecules/genetics;Human;Oligonucleotide Array Sequence Analysis;Reverse Transcriptase Polymerase Chain Reaction;Cluster Analysis;Thyroid Neoplasms/*genetics;Support, U.S. Gov't, P.H.S.;N;19 Neocortical evolution},
	Number = {26},
	Organization = {Human Cancer Genetics Program, Comprehensive Cancer Center, Department of Pathology, Divisions of Sensory Biophysics and Endocrinology and Nuclear Medicine, Ohio State University, Columbus, OH 43210, USA.},
	Pages = {15044-9},
	Pubmed = {11752453},
	Title = {Gene expression in papillary thyroid carcinoma reveals highly consistent profiles},
	Uuid = {43A9DA02-3B33-431E-A9F9-9608D842DC51},
	Volume = {98},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11752453}}

@article{Huard:1998,
	Abstract = {We have infused replication-incompetent retroviral vectors into the nasal cavity of adult rats 1 day after exposure to the olfactotoxic gas methyl bromide (MeBr) to assess the lineage relationships of cells in the regenerating olfactory epithelium. The vast majority of the retrovirus-labeled clones fall into three broad categories: clones that invariably contain globose basal cells (GBCs) and/or neurons, clones that always include cells in the ducts of Bowman's glands, and clones that are composed of sustentacular cells only. Many of the GBC-related clones contain sustentacular cells and horizontal basal cells as well. Most of the duct-related clones contain gland cells, and some also include sustentacular cells. Thus, the destruction of both neurons and non-neuronal cells that is caused by MeBr activates two distinct types of multipotent cells. The multipotent progenitor that gives rise to neurons and non-neuronal cells is a basal cell, whereas the progenitor that gives rise to duct, gland, and sustentacular cells resides within the ducts, based on the pattern of sparing after lesion and the analysis of early regeneration by using cell type-specific markers. We conclude that the balance between multipotency and selective neuropotency, which is characteristic of globose basal cells in the normal olfactory epithelium, is determined by which cell types have been depleted and need to be replenished rapidly.},
	Author = {Huard, J. M. and Youngentob, S. L. and Goldstein, B. J. and Luskin, M. B. and Schwob, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {J Comp Neurol},
	Keywords = {I both;Retroviridae/genetics;Genetic Vectors;Rats, Sprague-Dawley;Cell Line;Rats/*anatomy &histology;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Olfactory Mucosa/*cytology;13 Olfactory bulb anatomy;Stem Cells/*cytology},
	Number = {4},
	Organization = {Department of Anatomy and Cell Biology, SUNY Health Science Center, Syracuse, New York 13210, USA.},
	Pages = {469-86.},
	Title = {Adult olfactory epithelium contains multipotent progenitors that give rise to neurons and non-neural cells},
	Uuid = {F732B3EC-67CC-4812-B3DC-82E826B3F8E6},
	Volume = {400},
	Year = {1998},
	url = {papers/Huard_JCompNeurol1998}}

@article{Huberman:2008,
	Abstract = {Our understanding of how mammalian sensory circuits are organized and develop has long been hindered by the lack of genetic markers of neurons with discrete functions. Here, we report a transgenic mouse selectively expressing GFP in a complete mosaic of transient OFF-alpha retinal ganglion cells (tOFF-alphaRGCs). This enabled us to relate the mosaic spacing, dendritic anatomy, and electrophysiology of these RGCs to their complete map of projections in the brain. We find that tOFF-alphaRGCs project exclusively to the superior colliculus (SC) and dorsal lateral geniculate nucleus and are restricted to a specific laminar depth within each of these targets. The axons of tOFF-alphaRGC are also organized into columns in the SC. Both laminar and columnar specificity develop through axon refinement. Disruption of cholinergic retinal waves prevents the emergence of columnar- but not laminar-specific tOFF-alphaRGC connections. Our findings reveal that in a genetically identified sensory map, spontaneous activity promotes synaptic specificity by segregating axons arising from RGCs of the same subtype.},
	Author = {Huberman, Andrew D. and Manu, Mihai and Koch, Selina M. and Susman, Michael W. and Lutz, Amanda Brosius and Ullian, Erik M. and Baccus, Stephen A. and Barres, Ben A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1097-4199},
	Journal = {Neuron},
	Keywords = {Retinal Ganglion Cells;Cholera Toxin;Retina;Animals;Gene Expression Regulation, Developmental;Superior Colliculi;Patch-Clamp Techniques;Visual Pathways;Axons;Mice, Transgenic;Mice, Inbred C57BL;Green Fluorescent Proteins;research support, non-u.s. gov't;Indoles;Vesicular Acetylcholine Transport Proteins;Dendrites;Animals, Newborn;Membrane Potentials;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Nerve Tissue Proteins;Geniculate Bodies;Receptors, Nicotinic;Brain Mapping},
	Month = {8},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Neurobiology, Fairchild Science Building D235, Stanford University School of Medicine, Palo Alto, CA 94305, USA. adh1\@stanford.edu},
	Pages = {425-38},
	Pii = {S0896-6273(08)00591-6},
	Pubmed = {18701068},
	Title = {Architecture and activity-mediated refinement of axonal projections from a mosaic of genetically identified retinal ganglion cells},
	Uuid = {959422B3-549E-47D7-BE16-25E33212B9E9},
	Volume = {59},
	Year = {2008},
	url = {papers/Huberman_Neuron2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2008.07.018}}

@article{Hudgins:1998,
	Abstract = {After insult or trauma, astrocytes become activated and endeavor to restore the brain's delicately balanced microenvironment. An index of their activated state is that they become enlarged or hypertrophic. Ciliary neurotrophic factor (CNTF), a member of the alpha helical family of cytokines, is synthesized by astrocytes and is generally regarded to be an autocrine and paracrine injury signal. To determine whether CNTF might be an endogenous signal that stimulates astrocyte hypertrophy in vivo, we intracerebrally injected 200 ng of recombinant human CNTF into the adult rat neocortex. To study the astrocytes their cytosol was stained with antibodies against S100beta and their nuclei were stained with propidium iodide (PI). Fluorescent images of astrocytic nuclei and somas were acquired using a confocal laser-scanning microscope and their areas were measured using the NIH image software. Within 24 h of treatment, CNTF induced a volume increase of the somas and nuclei of protoplasmic and fibrous astrocytes in vivo, and this effect persisted for at least 48 h. To determine whether CNTF activates astrocytes directly, glial cultures were treated with CNTF (10 ng/ml) and were evaluated by measuring the area of PI stained nuclei. CNTF stimulation increased the size of both polygonal and process-bearing astroglia. Since our studies in vivo have shown that CNTF induces other key aspects of gliosis (S. W. Levison et al., 1996; Exp. Neurol. 141, 256), we conclude that CNTF is a powerful activator of astrocytes and that it is likely responsible for the persistent glial hypertrophy observed following injuries and diseases of the CNS. 98197131 0014-4886 Journal Article},
	Author = {Hudgins, S. N. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Exp Neurol},
	Keywords = {Human;Glial Fibrillary Acidic Protein/biosynthesis;Ciliary Neurotrophic Factor;Nerve Growth Factors/*pharmacology;Cells, Cultured;Rats;Microscopy, Confocal;Female;Animal;Rats, Sprague-Dawley;11 Glia;G abstr;Support, Non-U.S. Gov't;Neocortex/cytology/*drug effects/pathology;Nerve Tissue Proteins/*pharmacology;Cell Nucleus/drug effects/ultrastructure;Hypertrophy;Nerve Tissue Protein S 100/biosynthesis;Astrocytes/cytology/*drug effects/pathology;Recombinant Proteins/pharmacology;Cytoplasm/drug effects/ultrastructure},
	Number = {2},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.},
	Pages = {171-82},
	Pubmed = {9527886},
	Title = {Ciliary neurotrophic factor stimulates astroglial hypertrophy in vivo and in vitro},
	Uuid = {CD3A96D3-A275-43A2-AF8F-72E3F22F7142},
	Volume = {150},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9527886}}

@article{Hudson:2004,
	Abstract = {Finding a reliable source of alternative neural stem cells for treatment of various diseases and injuries affecting the central nervous system is a challenge. Numerous studies have shown that hematopoietic and nonhematopoietic progenitors derived from bone marrow (BM) under specific conditions are able to differentiate into cells of all three germ layers. Recently, it was reported that cultured, unfractionated (whole) adult BM cells form nestin-positive spheres that can later initiate neural differentiation (Kabos et al., 2002). The identity of the subpopulation of BM cells that contributes to neural differentiation remains unknown. We therefore analyzed the hematopoietic and neural features of cultured, unfractionated BM cells derived from a transgenic mouse that expresses green fluorescent protein (GFP) in all tissues. We also transplanted the BM cells into the subventricular zone (SVZ), a region known to support postnatal neurogenesis. After injection of BM cells into the neurogenic SVZ in neonatal rats, we found surviving GFP+ BM cells close to the injection site and in various brain regions, including corpus callosum and subcortical white matter. Many of the grafted cells were detected within the rostral migratory stream (RMS), moving toward the olfactory bulb (OB), and some cells reached the subependymal zone of the OB. Our in vitro experiments revealed that murine GFP+ BM cells retained their proliferation and differentiation potential and predominantly preserved their hematopoietic identity (CD45, CD90, CD133), although a few expressed neural antigens (nestin, glial fibrillary acdiic protein, TuJ1).},
	Author = {Hudson, J. E. and Chen, N. and Song, S. and Walczak, P. and Jendelov{\'a}, P. and Sykova, E. and Willing, A. E. and Saporta, S. and Bickford, P. and Sanchez-Ramos, J. and Zigova, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Survival;Pregnancy;Animals;Stem Cell Transplantation;Cells, Cultured;Rats;Comparative Study;Brain;Female;Cell Count;Rats, Sprague-Dawley;Mice, Transgenic;11 Glia;Green Fluorescent Proteins;Time Factors;Male;Hematopoiesis;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Bone Marrow Cells;Neurons;Mice;Luminescent Proteins;Immunohistochemistry;Bromodeoxyuridine;Research Support, Non-U.S. Gov't},
	Month = {4},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Department of Neurosurgery, College of Medicine, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, Florida 33612, USA. jhudson\@hsc.usf.edu},
	Pages = {255-64},
	Pubmed = {15048923},
	Title = {Green fluorescent protein bone marrow cells express hematopoietic and neural antigens in culture and migrate within the neonatal rat brain},
	Uuid = {89B9DB35-4D71-44A0-8C6F-598FCA312A06},
	Volume = {76},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20043}}

@article{Huh:2000,
	Abstract = {Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).},
	Author = {Huh, G. S. and Boulanger, L. M. and Du, H. and Riquelme, P. A. and Brotz, T. M. and Shatz, C. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Retinal Ganglion Cells;24 Pubmed search results 2008;Retina;Animals;Brain;Histocompatibility Antigens Class I;Research Support, U.S. Gov't, P.H.S.;Visual Pathways;Hippocampus;Signal Transduction;Synaptic Transmission;Synapses;Mice, Inbred C57BL;Long-Term Potentiation;Mice, Mutant Strains;Antigens, CD3;In Situ Hybridization;Neural Pathways;Neuronal Plasticity;Receptors, N-Methyl-D-Aspartate;Gene Expression Profiling;21 Activity-development;Geniculate Bodies;Mice, Knockout;21 Neurophysiology;Genes, MHC Class I;Mice;Neurons;Research Support, Non-U.S. Gov't;Receptors, GABA-A;Excitatory Postsynaptic Potentials},
	Medline = {20568411},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5499},
	Organization = {Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh\@alum.mit.edu},
	Pages = {2155-9},
	Pii = {9062},
	Pubmed = {11118151},
	Title = {Functional requirement for class I MHC in CNS development and plasticity},
	Uuid = {1E586764-38E3-426B-A38E-9454C002292F},
	Volume = {290},
	Year = {2000}}

@article{Humphreys:1990,
	Abstract = {Brains from male cases with dyslexia show symmetry of the planum temporale and predominantly left-sided cerebrocortical microdysgenesis. We now report on three women with dyslexia. In all brains, the planum temporale was again symmetrical. Also, in two of the brains, multiple foci of cerebrocortical glial scarring were present. In both women, many of the scars were myelinated, suggesting origination during late intrauterine or early postnatal life. In one, scars were mainly left perisylvian and involved portions of the vascular border zone of the temporal cortex. In the other, scars were more numerous and occurred in the border zone of the anterior, middle, and posterior cerebral arteries symmetrically. All three cases showed to a variable extent brain warts, molecular layer ectopias, and focal architectonic dysplasia identical to those seen in the male cases. Two women had primary brain neoplasms, an oligodendroglioma and a low-grade astrocytoma, respectively, and two women showed small angiomas. Reexamination of previously reported male cases disclosed one with myelinated glial scars. Two control brains with asymmetrical plana temporale showed myelinated glial scars as well. The significance of the anatomical findings is discussed, and possible etiological factors are considered with known effects of autoimmune diseases on the nervous system.},
	Author = {Humphreys, P. and Kaufmann, W. E. and Galaburda, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0364-5134},
	Journal = {Ann Neurol},
	Keywords = {24 Pubmed search results 2008;10 Development;research support, non-u.s. gov't;Adult;Aged;Aged, 80 and over;Female;Dyslexia;10 genetics malformation;comparative study;research support, u.s. gov't, p.h.s.;Humans;Brain;Male;Temporal Lobe;case reports},
	Month = {12},
	Nlm_Id = {7707449},
	Number = {6},
	Organization = {Dyslexia Research Laboratory, Charles A. Dana Research Institute, Boston, MA.},
	Pages = {727-38},
	Pubmed = {2285260},
	Title = {Developmental dyslexia in women: neuropathological findings in three patients},
	Uuid = {E2EDD918-3CD7-4F08-A8B4-E27DDE953618},
	Volume = {28},
	Year = {1990},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/ana.410280602}}

@article{Hurley:1999,
	Abstract = {Because of morphological similarities between ameboid microglia in the developing central nervous system (CNS), brain macrophages in the injured CNS, and cultured microglia in vitro, it is thought that these cell types are functionally equivalent. To investigate the validity of this assumption, we have compared mRNA levels of interleukin-1alpha and -1beta (IL-1alpha and IL-1beta), tumor necrosis factor-alpha and -beta (TNF-alpha and TNF-beta), transforming growth factor-beta1 (TGF-beta1), and macrophage colony-stimulating factor (M-CSF) in the postnatal day 4 (P4) supraventricular corpus callosum (SVCC) with those in unstimulated cultured microglia. Control tissues included spleen, cortex, hippocampus, and cerebellum. Our analyses have shown that while IL-1alpha, IL-1beta, TNF-alpha, TNF-beta, and TGF-beta1 transcripts are abundantly expressed by cultured microglia, they are very low to virtually undetectable in the SVCC. These data strongly suggest that ameboid microglia, which are concentrated in the SVCC, are unlikely to be a significant source of these cytokines. Our study, which shows clear differences in the functional status of cultured microglia vs. ameboid microglia in vivo, stresses the importance of using caution when interpreting in vitro findings in terms of the in vivo functions of microglia.},
	Author = {Hurley, S. D. and Walter, S. A. and Semple-Rowland, S. L. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Macrophage Colony-Stimulating Factor;Tumor Necrosis Factor;Rats, Sprague-Dawley;Reverse Transcriptase Polymerase Chain Reaction;Hippocampus;Rats;Not relevant;Interleukin-1;Cerebellum;Gene Expression;Microglia;Support, U.S. Gov't, P.H.S.;11 Glia;Cells, Cultured;RNA, Messenger;Animals;Corpus Callosum},
	Medline = {99129656},
	Month = {2},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {University of Florida Brain Institute, University of Florida, Gainesville, USA.},
	Pages = {304-9},
	Pii = {10.1002/(SICI)1098-1136(19990201)25:3<304::AID-GLIA10>3.0.CO;2-W},
	Pubmed = {9932876},
	Title = {Cytokine transcripts expressed by microglia in vitro are not expressed by ameboid microglia of the developing rat central nervous system},
	Uuid = {3E52F359-8EA5-42AE-949E-38D7DD8DFEA8},
	Volume = {25},
	Year = {1999},
	url = {papers/Hurley_Glia1999.pdf}}

@article{Hurtado-Lorenzo:2006,
	Abstract = {The recruitment of the small GTPase Arf6 and ARNO from cytosol to endosomal membranes is driven by V-ATPase-dependent intra-endosomal acidification. The molecular mechanism that mediates this pH-sensitive recruitment and its role are unknown. Here, we demonstrate that Arf6 interacts with the c-subunit, and ARNO with the a2-isoform of V-ATPase. The a2-isoform is targeted to early endosomes, interacts with ARNO in an intra-endosomal acidification-dependent manner, and disruption of this interaction results in reversible inhibition of endocytosis. Inhibition of endosomal acidification abrogates protein trafficking between early and late endosomal compartments. These data demonstrate the crucial role of early endosomal acidification and V-ATPase/ARNO/Arf6 interactions in the regulation of the endocytic degradative pathway. They also indicate that V-ATPase could modulate membrane trafficking by recruiting and interacting with ARNO and Arf6; characteristics that are consistent with the role of V-ATPase as an essential component of the endosomal pH-sensing machinery.},
	Author = {Hurtado-Lorenzo, Andr{\'e}s and Skinner, Mhairi and El Annan, Jaafar and Futai, Masamitsu and Sun-Wada, Ge-Hong H. and Bourgoin, Sylvain and Casanova, James and Wildeman, Alan and Bechoua, Shaliha and Ausiello, Dennis A. and Brown, Dennis and Marshansky, Vladimir},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {Hydrogen-Ion Concentration;Research Support, N.I.H., Extramural;Cell Line;GTPase-Activating Proteins;Epithelial Cells;Green Fluorescent Proteins;24 Pubmed search results 2008;Kidney Tubules, Proximal;Endocytosis;Animals;Dynamins;Protein Interaction Mapping;Proteins;Isoenzymes;Transfection;Hela Cells;Vacuolar Proton-Translocating ATPases;Serum Albumin, Bovine;Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone;11 Glia;Mutation;Protein Binding;Protein Transport;ADP-Ribosylation Factors;Mice;Models, Biological;Macrolides;Humans;Endosomes;Research Support, Non-U.S. Gov't;Ammonium Chloride},
	Month = {2},
	Nlm_Id = {100890575},
	Number = {2},
	Organization = {Program in Membrane Biology & Nephrology Division, Richard Simches Research Center, Massachusetts General Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02114, USA.},
	Pages = {124-36},
	Pii = {ncb1348},
	Pubmed = {16415858},
	Title = {V-ATPase interacts with ARNO and Arf6 in early endosomes and regulates the protein degradative pathway},
	Uuid = {0F1B1181-3D9B-4C44-BF32-C890A10178F0},
	Volume = {8},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb1348}}

@article{Huttmann:2003,
	Abstract = {Kainate-induced seizures increase hippocampal neurogenesis. Glial fibrillary acidic protein-positive astrocytes with radial processes in the dentate gyrus share many of the characteristics of radial glia and appear to act as precursor cells for adult dentate neurogenesis. Using the chemoconvulsant kainate and transgenic mice with human glial-fibrillary acidic protein (hGFAP) promoter-controlled enhanced green fluorescent protein (EGFP) expression, we examined the proliferation, morphology and electrophysiological properties of astrocytes in the neurogenic subgranular zone of the dentate gyrus in control animals and upon the induction of seizure-induced cell proliferation, three days post-kainate. EGFP-positive cells with and without radial processes could easily be distinguished. Kainate treatment caused a significant increase in the total number of proliferating EGFP-positive cells, particularly a tenfold elevation in the number of proliferating radial glia-like astrocytes, and also caused a preferential shift in the dividing cell population towards cells expressing EGFP. Immunohistochemical analysis revealed a surprisingly low proportion of cells coexpressing the astroglial marker S100beta and EGFP. Kainate increased the number of EGFP-positive, S100beta-positive and S100beta-positive-EGFP-positive astrocytes in the subgranular zone. We also report a subset of faintly EGFP-positive cells expressing markers of early neuronal differentiation. Patch-clamp analysis revealed the presence of three functionally different populations of EGFP-positive cells in both kainate and control tissue. We conclude that there is an early increase in proliferating radial glia-like astrocytes in the dentate after kainate-induced seizures, consistent with a recruitment of precursors for seizure-induced neurogenesis. 0953-816x Journal Article},
	Author = {Huttmann, K. and Sadgrove, M. and Wallraff, A. and Hinterkeuser, S. and Kirchhoff, F. and Steinhauser, C. and Gray, W. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Human;Microscopy, Confocal/methods;Animals;Membrane Potentials/physiology;In Vitro;*Cell Differentiation;Comparative Study;Phenotype;Neural Cell Adhesion Molecule L1/metabolism;Immunohistochemistry/methods;Cell Count;D pdf;Mice, Transgenic;Kainic Acid;Bromodeoxyuridine/metabolism;Animals, Newborn;Support, Non-U.S. Gov't;Astrocytes/*physiology;Sialic Acids/metabolism;S100 Proteins/metabolism;06 Adult neurogenesis injury induced;Dentate Gyrus/*pathology;Nerve Tissue Proteins/metabolism;Mice;Luminescent Proteins/genetics/metabolism;Neurons/physiology;Seizures/chemically induced/*pathology;Patch-Clamp Techniques/methods;Glial Fibrillary Acidic Protein/genetics/*metabolism},
	Number = {10},
	Organization = {Experimental Neurobiology, Neurosurgery, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany.},
	Pages = {2769-78},
	Pubmed = {14656326},
	Title = {Seizures preferentially stimulate proliferation of radial glia-like astrocytes in the adult dentate gyrus: functional and immunocytochemical analysis},
	Uuid = {38BE8F9C-8731-453B-8F38-9E8E2A160AA5},
	Volume = {18},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14656326}}

@article{Hwang:1999,
	Abstract = {In human cells, efficient global genomic repair of DNA damage induced by ultraviolet radiation requires the p53 tumor suppressor, but the mechanism has been unclear. The p48 gene is required for expression of an ultraviolet radiation-damaged DNA binding activity and is disrupted by mutations in the subset of xeroderma pigmentosum group E cells that lack this activity. Here, we show that p48 mRNA levels strongly depend on basal p53 expression and increase further after DNA damage in a p53-dependent manner. Furthermore, like p53(-/-) cells, xeroderma pigmentosum group E cells are deficient in global genomic repair. These results identify p48 as the link between p53 and the nucleotide excision repair apparatus. 0027-8424 Journal Article},
	Author = {Hwang, B. J. and Ford, J. M. and Hanawalt, P. C. and Chu, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Protein p53/*genetics;Genes, Structural, Neoplasm/*genetics;Ultraviolet Rays;Gene Expression Regulation, Neoplastic/*genetics;DNA Repair/*genetics;Human;Xeroderma Pigmentosum/*genetics;08 Aberrant cell cycle;Support, U.S. Gov't, Non-P.H.S.;DNA Damage/genetics;Support, U.S. Gov't, P.H.S.;DNA-Binding Proteins/*genetics;Support, Non-U.S. Gov't;Fibroblasts;RNA, Messenger/genetics;Radiation, Ionizing;EE},
	Number = {2},
	Organization = {Departments of Medicine and Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5115, USA.},
	Pages = {424-8},
	Pubmed = {9892649},
	Title = {Expression of the p48 xeroderma pigmentosum gene is p53-dependent and is involved in global genomic repair},
	Uuid = {60D4D9DE-F438-4866-8F21-AB0A3F59BBE8},
	Volume = {96},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9892649}}

@article{Hynes:2000,
	Author = {Hynes, M. and Rosenthal, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Neuron},
	Keywords = {Neurons/cytology/metabolism;Parkinson Disease/*therapy;Dopamine/*metabolism;17 Transplant Regeneration;Cell Differentiation/*physiology;Human;Growth Substances/metabolism/pharmacology;L;Aging/physiology;Animal;Stem Cells/cytology/*metabolism/*transplantation;Bone Morphogenetic Proteins/metabolism;Cell Lineage},
	Number = {1},
	Organization = {Renovis, Inc, Oakland, California 94609, USA. mhynes\@concentric.net},
	Pages = {11-4.},
	Title = {Embryonic stem cells go dopaminergic},
	Uuid = {0C725360-55E8-4651-9B8D-6C544C0833D1},
	Volume = {28},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11086977}}

@article{Iannetti:2001,
	Abstract = {Band heterotopias are an example of genetic generalized neuronal migration disorders that may be present in patients with mild epilepsy and normal or slightly impaired intellect, as well as in patients with intractable epilepsy and mental retardation. The case of a 17-year-old left-handed female patient with epilepsy and normal cognitive development is reported in whom single-photon emission computed tomography (SPECT), proton magnetic resonance spectroscopy, and functional magnetic resonance imaging (fMRI) were performed. MRI revealed the presence of bilateral asymmetric band heterotopia. SPECT revealed a left frontoparietal and occipital hypoperfusion, demonstrating a good correlation with the electroencephalogram abnormalities. Because of the appearance of new types of seizures, the patient underwent a second MRI investigation together with a proton magnetic resonance spectroscopy (MRS) study. MRI confirmed bilateral band heterotopia characterized by greater thickness in the left hemisphere at the frontal and occipital level. MRI and SPECT findings were in agreement with left occipital electroencephalogram abnormalities and with occipital seizure type. Qualitative results of proton MRS revealed normal spectra profiles in the examined left frontal and occipital heterotopic area and in the normal overlying cortex. Later, fMRI was performed. The finger-tapping test of the right hand yielded the activation of both normal left sensory-motor cortex and the facing band heterotopia. In the right hemisphere, only the activation of the sensory-motor neocortex was observed; no involvement of the right misplaced brain tissue was present. This functional behavior could be considered the consequence of poor neuronal representation. On the contrary, the involvement of both band heterotopia and normal cortex observed in the left hemisphere could be the result of many synaptic interconnections. Functional investigations may have an important role in defining the activity of band heterotopia per se and in relation to the overlying neocortex.},
	Author = {Iannetti, P. and Spalice, A. and Raucci, U. and Perla, F. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0887-8994},
	Journal = {Pediatr Neurol},
	Keywords = {case reports;Magnetic Resonance Imaging;Radiopharmaceuticals;Humans;Dominance, Cerebral;Tomography, Emission-Computed, Single-Photon;Brain;21 Epilepsy;Female;Epilepsy;Cell Movement;Brain Diseases;Intelligence;Mutation, Missense;21 Neurophysiology;24 Pubmed search results 2008;Technetium Tc 99m Exametazime;Choristoma;Adolescent},
	Medline = {21172232},
	Month = {2},
	Nlm_Id = {8508183},
	Number = {2},
	Organization = {Division of Pediatric Neurology, Pediatrics Department, "La Sapienza" University, Roma, Italy.},
	Pages = {159-63},
	Pii = {S0887899400002472},
	Pubmed = {11275469},
	Title = {Functional neuroradiologic investigations in band heterotopia},
	Uuid = {C5655C1B-01E1-4F8E-8C68-52C5407F6D39},
	Volume = {24},
	Year = {2001}}

@article{Ikegami:2002,
	Abstract = {Transdifferentiation from retinal pigment epithelium (RPE) to neural retina (NR) was studied under a new culture system as an experimental model for newt retinal regeneration. Adult newt RPEs were organ cultured with surrounding connective tissues, such as the choroid and sclera, on a filter membrane. Around day 7 in vitro, lightly pigmented "neuron-like cells" with neuritic processes were found migrating out from the explant onto the filter membrane. Their number gradually increased day by day. BrdU-labeling study showed that RPE cells initiated to proliferate under the culture condition on day 4 in vitro, temporally correlating to the time course of retinal regeneration in vivo. Histological observations of cultured explants showed that proliferating RPE cells did not form the stratified structure typically observed in the NR but they rather migrated out from the explants. Neuronal differentiation was examined by immunohistochemical detection of various neuron-specific proteins; HPC-1 (syntaxin), GABA, serotonin, rhodopsin, and acetylated tubulin. Immunoreactive cells for these proteins always possessed fine and long neurite-like processes. Numerous lightly pigmented cells with neuron-like morphology showed HPC-1 immunoreactivity. Fibroblast growth factor-2 (FGF-2), known as a potent factor for the transdifferentiation of ocular tissues in various vertebrates, substantially increased the numbers of both neuron-like cells and HPC-1-like immunoreactive cells in a dose-dependent manner. These results indicate that our culture method ensures neural differentiation of newt RPE cells in vitro and provides, for the first time, a suitable in vitro experimental model system for studying tissue-intrinsic factors responsible for newt retinal regeneration.},
	Author = {Ikegami, Yoko and Mitsuda, Sanae and Araki, Masasuke},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;Pigment Epithelium of Eye;Nerve Regeneration;Immunohistochemistry;Salamandridae;Connective Tissue;Epithelial Cells;Female;Microscopy, Phase-Contrast;Cell Division;Organ Culture Techniques;Antimetabolites;Cells, Cultured;24 Pubmed search results 2008;Bromodeoxyuridine;Animals},
	Medline = {21668592},
	Month = {2},
	Nlm_Id = {0213640},
	Number = {3},
	Organization = {Developmental Neurobiology Laboratory, Department of Biological Sciences, Faculty of Science, Nara Women's University, Nara 630-8506, Japan.},
	Pages = {209-20},
	Pii = {10.1002/neu.10031},
	Pubmed = {11810636},
	Title = {Neural cell differentiation from retinal pigment epithelial cells of the newt: an organ culture model for the urodele retinal regeneration},
	Uuid = {04FD1661-131B-4164-BD98-A49F79C17B42},
	Volume = {50},
	Year = {2002}}

@article{Ikonomidou:1999,
	Abstract = {Programmed cell death (apoptosis) occurs during normal development of the central nervous system. However, the mechanisms that determine which neurons will succumb to apoptosis are poorly understood. Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors for only a few hours during late fetal or early neonatal life triggered widespread apoptotic neurodegeneration in the developing rat brain, suggesting that the excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal survival. These findings may have relevance to human neurodevelopmental disorders involving prenatal (drug-abusing mothers) or postnatal (pediatric anesthesia) exposure to drugs that block NMDA receptors.},
	Author = {Ikonomidou, C. and Bosch, F. and Miksa, M. and Bittigau, P. and Vockler, J. and Dikranian, K. and Tenkova, T. I. and Stefovska, V. and Turski, L. and Olney, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:54 -0400},
	Journal = {Science},
	Keywords = {Fetus;Quinoxalines/pharmacology;*Nerve Degeneration;Dopamine Antagonists/pharmacology;Dose-Response Relationship, Drug;Dizocilpine Maleate/pharmacology;Rats;Muscarinic Antagonists/pharmacology;Excitatory Amino Acid Antagonists/pharmacology;07 Excitotoxicity Apoptosis;Receptors, N-Methyl-D-Aspartate/*antagonists &inhibitors/metabolism;Animal;E-9;Calcium Channel Blockers/pharmacology;Haloperidol/pharmacology;Support, Non-U.S. Gov't;Neurons/*cytology/drug effects/metabolism;In Situ Nick-End Labeling;*Apoptosis;Scopolamine/pharmacology;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Microscopy, Electron;Brain/*cytology/drug effects/embryology/growth &development},
	Number = {5398},
	Organization = {Department of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. hrissanthi.ikonomidou\@charite.de},
	Pages = {70-4.},
	Title = {Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain},
	Uuid = {6AE9BA62-8306-4883-AF20-A7B98EF4ED9B},
	Volume = {283},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9872743}}

@article{Illes:2007,
	Abstract = {Embryonic stem cells can be differentiated into neurons of diverse neurotransmitter-specific phenotypes. While the time course of functional progression of ES cell-derived neural precursors towards mature neurons has been described in detail on single-cell level, the temporal development and pharmacological modulation of ES cell-derived neuronal network activity have not been explored yet. Neuronal network activity can be assessed by the microelectrode array (MEA) technology that allows simultaneous monitoring of the electrical activity exhibited by entire populations of neurons over several weeks or months in vitro. We demonstrate here that ES cell-derived neural precursors cultured on MEAs for 5 to 6 weeks develop neuronal networks with oscillating and synchronous spike patterns via distinct states of activity and change electrophysiological characteristics even after 5 to 6 weeks in culture pointing towards late maturational processes. These processes were accompanied by an increasing density of presynaptic vesicles. Furthermore, we demonstrated that ES cell-derived network activity was sensitive to synaptically acting drugs indicating that pharmacologically susceptible neuronal networks were generated. Thus, the MEA technology represents a powerful tool to describe the temporal progression of stem cell-derived neural populations towards mature, functioning neuronal networks that can be applied to investigate pharmacologically active compounds.},
	Author = {Illes, Sebastian and Fleischer, Wiebke and Siebler, Mario and Hartung, Hans-Peter P. and Dihn{\'e}, Marcel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {gamma-Aminobutyric Acid;Cell Differentiation;Electrophysiology;Animals;Synaptic Vesicles;Tetrodotoxin;research support, non-u.s. gov't;Time Factors;Cell Line;Embryonic Stem Cells;Action Potentials;Nerve Net;N-Methylaspartate;21 Neurophysiology;Neurons;GABA Antagonists;Microelectrodes;24 Pubmed search results 2008;Immunohistochemistry;Oscillometry},
	Month = {9},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Neurology, University Hospital D{\"u}sseldorf, Heinrich-Heine University, Germany.},
	Pages = {171-6},
	Pii = {S0014-4886(07)00218-X},
	Pubmed = {17644089},
	Title = {Development and pharmacological modulation of embryonic stem cell-derived neuronal network activity},
	Uuid = {05103017-A86E-4860-98E2-CF07433393D3},
	Volume = {207},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2007.05.020}}

@article{Imasawa:2001,
	Abstract = {Bone marrow stem cells (BMC) develop into hematopoietic and mesenchymal lineages but have not been known to differentiate into glomerular cells. To investigate whether such differentiation is possible, a search was made for donor glomerular cells in lethally irradiated C57BL/6j (B6) mice given transplants of BMC from syngeneic mice transgenic for green fluorescence protein (GFP) ([GFP-->B6] mice). After the recipients of donor BMC manifested GFP-positive cells in their glomeruli, the numbers of such cells increased markedly, in a time-dependent manner, from 2 wk to 24 wk after bone marrow transplantation. Immunohistochemical analyses revealed that most GFP-positive cells in the glomeruli were neither macrophages nor T cells. With the use of a laser-scanning confocal microscope, GFP-positive cells were observed within the mesangium of [GFP-->B6] mice. Furthermore, indirect immunofluorescence assays demonstrated that desmin-positive cells in the glomeruli of these chimeric mice were also positive for GFP. Among glomerular cells isolated from [GFP-->B6] mice 24 wk after bone marrow transplantation and then cultured, the majority of cells (approximately 84\%) stained for desmin and approximately 60\%of the desmin-positive cells expressed GFP. In addition, these GFP-positive cells in the cultures contracted in response to angiotensin II stimulation. These results suggest that bone marrow-derived cells may have the potential to differentiate into glomerular mesangial cells.},
	Author = {Imasawa, T. and Utsunomiya, Y. and Kawamura, T. and Zhong, Y. and Nagasawa, R. and Okabe, M. and Maruyama, N. and Hosoya, T. and Ohno, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {1046-6673},
	Journal = {J Am Soc Nephrol},
	Keywords = {Cell Differentiation;Glomerular Mesangium;Animals;Cells, Cultured;Bone Marrow Transplantation;Female;Indicators and Reagents;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Time Factors;Angiotensin II;Bone Marrow Cells;Tissue Donors;Desmin;Mice;Luminescent Proteins},
	Medline = {21316373},
	Month = {7},
	Nlm_Id = {9013836},
	Number = {7},
	Organization = {Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan. imasawa\@nifty.com},
	Pages = {1401-9},
	Pubmed = {11423569},
	Title = {The potential of bone marrow-derived cells to differentiate to glomerular mesangial cells},
	Uuid = {5EF0F651-7ABB-4CF8-A707-5012B0795D6A},
	Volume = {12},
	Year = {2001}}

@article{Imitola:2004,
	Abstract = {Migration toward pathology is the first critical step in stem cell engagement during regeneration. Neural stem cells (NSCs) migrate through the parenchyma along nonstereotypical routes in a precise directed manner across great distances to injury sites in the CNS, where they might engage niches harboring local transiently expressed reparative signals. The molecular mechanisms for NSC mobilization have not been identified. Because NSCs seem to home similarly to pathologic sites derived from disparate etiologies, we hypothesized that the inflammatory response itself, a characteristic common to all, guides the behavior of potentially reparative cells. As proof of concept, we show that human NSCs migrate in vivo (including from the contralateral hemisphere) toward an infarcted area (a representative CNS injury), where local astrocytes and endothelium up-regulate the inflammatory chemoattractant stromal cell-derived factor 1alpha (SDF-1alpha). NSCs express CXC chemokine receptor 4 (CXCR4), the cognate receptor for SDF-1alpha. Exposure of SDF-1alpha to quiescent NSCs enhances proliferation, promotes chain migration and transmigration, and activates intracellular molecular pathways mediating engagement. CXCR4 blockade abrogates their pathology-directed chain migration, a developmentally relevant mode of tangential migration that, if recapitulated, could explain homing along nonstereotypical paths. Our data implicate SDF-1alpha/CXCR4, representative of the inflammatory milieu characterizing many pathologies, as a pathway that activates NSC molecular programs during injury and suggest that inflammation may be viewed not simply as playing an adverse role but also as providing stimuli that recruit cells with a regenerative homeostasis-promoting capacity. CXCR4 expression within germinal zones suggests that NSC homing after injury and migration during development may invoke similar mechanisms.},
	Author = {Imitola, Jaime and Raddassi, Khadir and Park, Kook In and Mueller, Franz-Josef J. and Nieto, Marta and Teng, Yang D. and Frenkel, Dan and Li, Jianxue and Sidman, Richard L. and Walsh, Christopher A. and Snyder, Evan Y. and Khoury, Samia J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Receptors, CXCR4;Ischemia;Dose-Response Relationship, Drug;Animals;Stem Cell Transplantation;Humans;Up-Regulation;Neural Crest;Brain;Models, Statistical;Cell Movement;02 Adult neurogenesis migration;Anoxia;Cell Proliferation;Fibroblast Growth Factor 2;17 Transplant Regeneration;11 Glia;Cell Line;Microscopy, Fluorescence;Research Support, U.S. Gov't, P.H.S.;Mice;24 Pubmed search results 2008;Central Nervous System;Stem Cells;Inflammation;Research Support, Non-U.S. Gov't},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {52},
	Organization = {Center for Neurologic Diseases, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {18117-22},
	Pii = {0408258102},
	Pubmed = {15608062},
	Title = {Directed migration of neural stem cells to sites of CNS injury by the stromal cell-derived factor 1alpha/CXC chemokine receptor 4 pathway},
	Uuid = {23FB1259-216C-49B6-9D9F-85C499CACA85},
	Volume = {101},
	Year = {2004},
	url = {papers/Imitola_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0408258102}}

@article{Imura:2003,
	Abstract = {Periventricular germinal zones (GZs) of developing and adult brain contain neural stem cells (NSCs), the cellular identities and origins of which are not defined completely. We used tissue culture techniques and transgenic mice expressing herpes simplex virus thymidine kinase (HSV-TK) from the mouse glial fibrillary acid protein (GFAP) promoter to test the hypothesis that certain NSCs express GFAP. To do so, we determined the relative proportions of multipotent neurospheres that are formed by GFAP-expressing cells derived from GZs at different stages of development. In this transgenic model, dividing GFAP-expressing cells are ablated selectively by treatment with the antiviral agent ganciclovir (GCV). Single-cell analysis showed that transgene-derived HSV-TK was present only in GFAP-expressing cells. GCV applied in vitro eliminated growth of multipotent neurospheres from GZs of postnatal and adult transgenic mice but not early embryonic (embryonic day 12.5) transgenic mice. GCV prevented growth of secondary multipotent neurospheres prepared after passage of primary transgenic neurospheres derived from all three of these developmental stages. In addition, GCV prevented growth of multipotent neurospheres from transgenic astrocyte-enriched cell cultures derived from postnatal GZ, and elaidic acid GCV given for 4 d to adult transgenic mice in vivo abolished the ability to grow multipotent neurospheres from GZ. Extensive control experiments, including clonal analysis, demonstrated that failure of neurosphere growth was not merely secondary to loss of GFAP-expressing support cells or the result of a nonspecific toxic effect. Our findings demonstrate that the predominant multipotent NSCs isolated from postnatal and adult but not early embryonic GZs express GFAP, and that NSCs exhibit heterogeneous expression of intermediate filaments during developmental maturation. 1529-2401 Journal Article},
	Author = {Imura, T. and Kornblum, H. I. and Sofroniew, M. V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {J Neurosci},
	Keywords = {Stem Cells/cytology/*metabolism/physiology;Intermediate Filament Proteins/metabolism;02 Adult neurogenesis migration;Astrocytes/physiology;Support, Non-U.S. Gov't;BB pdf;03 Adult neurogenesis progenitor source;Prosencephalon/*cytology/embryology/*growth &development/metabolism;Neurons/*cytology;Mice, Transgenic;Support, U.S. Gov't, P.H.S.;Thymidine Kinase/genetics;Mice;Animals;Ganciclovir/pharmacology;Glial Fibrillary Acidic Protein/genetics/*metabolism;Cells, Cultured},
	Number = {7},
	Organization = {Department of Neurobiology, Brain Research Institute, University of California, Los Angeles, California 90095-1763, USA.},
	Pages = {2824-32},
	Pubmed = {12684469},
	Title = {The predominant neural stem cell isolated from postnatal and adult forebrain but not early embryonic forebrain expresses GFAP},
	Uuid = {7710F75A-68D7-11DA-A4B6-000D9346EC2A},
	Volume = {23},
	Year = {2003},
	url = {papers/Imura_JNeurosci2003.pdf}}

@article{Iosif:2006,
	Abstract = {Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine, acting through the TNF-R1 and TNF-R2 receptors. The two receptors have been proposed to mediate distinct TNF-alpha effects in the CNS, TNF-R1 contributing to neuronal damage and TNF-R2 being neuroprotective. Whether TNF-alpha and its receptors play any role for neurogenesis in the adult brain is unclear. Here we used mouse models with loss of TNF-R1 and TNF-R2 function to establish whether signaling through these receptors could influence hippocampal neurogenesis in vivo under basal conditions, as well as after status epilepticus (SE), which is associated with inflammation and elevated TNF-alpha levels. Notably, in the intact brain, the number of new, mature hippocampal neurons was elevated in TNF-R1(-/-) and TNF-R1/R2(-/-) mice, whereas no significant changes were detected in TNF-R2(-/-) mice. Also after SE, the TNF-R1(-/-) and TNF-R1/R2(-/-) mice produced more new neurons. In contrast, the TNF-R2(-/-) mice showed reduced SE-induced neurogenesis. Cell proliferation in the dentate subgranular zone was elevated in TNF-R1(-/-) and TNF-R1/R2(-/-) mice both under basal conditions and after SE. The TNF-R2(-/-) mice either showed no change or minor decrease of cell proliferation. TNF-R1 and TNF-R2 receptors were expressed by hippocampal progenitors, as assessed with reverse transcription-PCR on sorted or cultured cells and immunocytochemistry on cultures. Our data reveal differential actions of TNF-R1 and TNF-R2 signaling in adult hippocampal neurogenesis and identify for the first time TNF-R1 as a negative regulator of neural progenitor proliferation in both the intact and pathological brain.},
	Author = {Iosif, Robert E. and Ekdahl, Christine T. and Ahlenius, Henrik and Pronk, Cornelis J. H. and Bonde, Sara and Kokaia, Zaal and Jacobsen, Sten-Eirik W. E. and Lindvall, Olle},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {14 Immune;04 Adult neurogenesis factors;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {38},
	Organization = {Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, Wallenberg Neuroscience Center, University Hospital, SE 221 84 Lund, Sweden.},
	Pages = {9703-12},
	Pii = {26/38/9703},
	Pubmed = {16988041},
	Title = {Tumor necrosis factor receptor 1 is a negative regulator of progenitor proliferation in adult hippocampal neurogenesis},
	Uuid = {71C7A512-9E21-4CD2-893D-371D545EBD16},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2723-06.2006}}

@article{Iravani:2005,
	Abstract = {Sustained reactive microgliosis may contribute to the progressive degeneration of nigral dopaminergic neurons in Parkinson's disease (PD), in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposed human and in non-human primates. However, the temporal relationship between glial cell activation and nigral cell death is relatively unexplored. Consequently, the effects of acute (24 h) and chronic (30 days) glial cell activation induced by unilateral supranigral lipopolysaccharide (LPS) administration were studied in rats. At 24 h, LPS administration caused a marked reduction in the number of tyrosine hydroxylase-immunoreactive (TH-ir) neurons in the substantia nigra (SN) but striatal TH-ir was unaffected. By 30 days, the loss of TH-positive neurons in the LPS-treated nigra was no greater than at 24 h although a heterogeneous loss of striatal TH-ir was present. The loss of nigrostriatal neurons was of functional significance, as at 30 days, LPS-treated rats exhibited ipsiversive circling in response to (+)-amphetamine administration. At 24 h, there was a moderate increase in glial fibrillary acidic protein (GFAP)-ir astrocytes in the SN but a marked elevation of p47phox positive OX-42-ir microglia, and intense inducible nitric oxide synthase (iNOS)-ir and 3-nitrotyrosine (3-NT)-ir was present. However, by 30 days the morphology of OX-42-ir microglia returned to a resting state, the numbers were greatly reduced and no 3-NT-ir was present. At 30 days, GFAP-ir astrocytes were markedly increased in number and iNOS-ir was present in fibrillar astrocyte-like cells. This study shows that acute glial activation leading to dopaminergic neuron degeneration is an acute short-lasting response that does not itself perpetuate cell death or lead to prolonged microglial activation.},
	Author = {Iravani, and Leung, and Sadeghian, and Haddon, and Rose, and Jenner,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Alpha;11 Glia},
	Month = {7},
	Nlm_Id = {8918110},
	Number = {2},
	Organization = {Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College, London, SE11UL, UK.},
	Pages = {317-330},
	Pii = {EJN4220},
	Pubmed = {16045485},
	Title = {The acute and the long-term effects of nigral lipopolysaccharide administration on dopaminergic dysfunction and glial cell activation},
	Uuid = {AA1BA458-8B77-41B9-925C-49A31EF84F09},
	Volume = {22},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2005.04220.x}}

@article{Isgor:2005,
	Abstract = {Numerous factors modulate neurogenesis in the adult dentate gyrus and subventricular zone, but it is often not clear if the modulation is mediated by direct effects on the proliferating and differentiating cells or secondary to effects on other cells. Also, while some factors selectively affect neurogenesis in one of the neurogenetic zones, it is not clear how selectivity is achieved. Estrogen is a hormonal modulator of neurogenesis. To address the issues of direct versus indirect control and regional specificity we investigated the colocalization of immunoreactivity for a proliferating cell marker, Ki-67, and a marker for migrating and differentiating cells with a neuronal phenotype, doublecortin, with the expressions of mRNA for estrogen receptors alpha and beta. We found an extensive colocalization of estrogen receptor alpha with both markers in the dentate gyrus and only with Ki-67 in the subventricular zone. An extensive colocalization of estrogen receptor beta with both markers was found in the dentate gyrus, but only a few Ki-67-immunoreactive and no doublecortin-immunoreactive cells of the subventricular zone expressed estrogen receptor beta mRNA. Estrogen receptor alpha and beta mRNAs were not expressed in other telencephalic Ki-67-immunoreactive cells or in constitutively doublecortin-immunoreactive cells of the piriform cortex. The extensive colocalization of immunoreactive markers for cell proliferation and differentiation with mRNAs for estrogen receptor alpha and estrogen receptor beta points to the direct modulation of dentate cell proliferation, differentiation and survival by estrogen, while direct effects of estrogen in the subventricular zone appear restricted to estrogen receptor alpha-mediated effects operating at the time of cell proliferation.},
	Author = {Isgor, and Watson,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {7605074},
	Organization = {Department of Biomedical Science, Charles E. Schmidt Biomedical Center, Florida Atlantic University, Boca Raton, FL 33431-0991, USA.},
	Pii = {S0306-4522(05)00512-9},
	Pubmed = {15994024},
	Title = {Estrogen receptor alpha and beta mRNA expressions by proliferating and differentiating cells in the adult rat dentate gyrus and subventricular zone},
	Uuid = {211598C6-3E3D-4AE5-BE44-E1D86A55250E},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2005.05.008}}

@article{Ivanov:2006,
	Abstract = {The extracellular signal-regulated kinases (ERK) signalling cascade is a key pathway that mediates the NMDA receptor (NMDAR)-dependent neuronal plasticity and survival. However, it is not clear yet how NMDARs regulate ERK activity. Stimulation of the NMDARs induces a complex modification of ERK that includes both ERK activation and inactivation and depends on particular experimental conditions. Here we show that there exists a differential restriction in the regulation of ERK activity that depends on the pool of NMDAR that was activated. The synaptic pool of NMDARs activates ERK whereas the extrasynaptic pool does not; on the contrary, it triggers a signalling pathway that results in the inactivation of ERK. As a result, simultaneous activation of both extrasynaptic and synaptic NMDAR using bath application of NMDA or glutamate (a typical protocol explored in the majority of studies) produced ERK activation that depended on the concentration of agonists and was always significantly weaker than those mediated by synaptic NMDARs. Since the activation of the extrasynaptic NMDA is attributed mainly to global release of glutamate occurring at pathological conditions including hypoxic/ischaemic insults, traumas and epileptic brain damage, the reported differential regulation of ERK cascade by NMDARs provides a unique mechanism for an early identification of the physiological and/or pathophysiological consequences of NMDAR activation. The negative regulation of the ERK activity might be one of the first signalling events determining brain injury and constitutes a putative target of new pharmacological applications.},
	Author = {Ivanov, Anton and Pellegrino, Christophe and Rama, Sylvain and Dumalska, Iryna and Salyha, Yuriy and Ben-Ari, Yehezkel and Medina, Igor},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0022-3751},
	Journal = {J Physiol},
	Keywords = {Synapses;21 Epilepsy;Enzyme Activation;21 Neurophysiology;Action Potentials;Hippocampus;Rats;Extracellular Signal-Regulated MAP Kinases;Synaptic Transmission;Animals;Cells, Cultured;Receptors, N-Methyl-D-Aspartate;Neurons;24 Pubmed search results 2008},
	Medline = {103133006},
	Month = {5},
	Nlm_Id = {0266262},
	Number = {Pt 3},
	Organization = {INMED/INSERM Unite 29, 163 Route de Luminy, 13009 Marseille, France.},
	Pages = {789-98},
	Pii = {jphysiol.2006.105510},
	Pubmed = {16513670},
	Title = {Opposing role of synaptic and extrasynaptic NMDA receptors in regulation of the extracellular signal-regulated kinases (ERK) activity in cultured rat hippocampal neurons},
	Uuid = {656FC2AE-09A6-4E86-B34F-46BD04FAD168},
	Volume = {572},
	Year = {2006},
	url = {papers/Ivanov_JPhysiol2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1113/jphysiol.2006.105510}}

@article{Jackson:2002,
	Abstract = {Primary microcephaly (MIM 251200) is an autosomal recessive neurodevelopmental condition in which there is a global reduction in cerebral cortex volume, to a size comparable with that of early hominids. We previously mapped the MCPH1 locus, for primary microcephaly, to chromosome 8p23, and here we report that a gene within this interval, encoding a BRCA1 C-terminal domain-containing protein, is mutated in MCPH1 families sharing an ancestral 8p23 haplotype. This gene, microcephalin, is expressed in the developing cerebral cortex of the fetal brain. Further study of this and related genes may provide important new insights into neocortical development and evolution.},
	Author = {Jackson, Andrew P. and Eastwood, Helen and Bell, Sandra M. and Adu, Jimi and Toomes, Carmel and Carr, Ian M. and Roberts, Emma and Hampshire, Daniel J. and Crow, Yanick J. and Mighell, Alan J. and Karbani, Gulshan and Jafri, Hussain and Rashid, Yasmin and Mueller, Robert F. and Markham, Alexander F. and Woods, C. Geoffrey},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0002-9297},
	Journal = {Am J Hum Genet},
	Keywords = {10 Development;Chromosomes, Human, Pair 8;Animals;Cloning, Molecular;Humans;Base Sequence;Gene Expression Regulation, Developmental;Sequence Homology, Amino Acid;DNA;Brain;Female;Child;Microcephaly;RNA, Messenger;research support, non-u.s. gov't;Male;Embryonic and Fetal Development;In Situ Hybridization;10 genetics malformation;Adult;Organ Size;DNA Mutational Analysis;Mice;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;Nerve Tissue Proteins;Adolescent},
	Month = {7},
	Nlm_Id = {0370475},
	Number = {1},
	Organization = {Molecular Medicine Unit, University of Leeds, United Kingdom. medapj\@leeds.ac.uk},
	Pages = {136-42},
	Pii = {AJHG023908},
	Pubmed = {12046007},
	Title = {Identification of microcephalin, a protein implicated in determining the size of the human brain},
	Uuid = {0E7D5DA5-9A14-42AD-B963-277674308B69},
	Volume = {71},
	Year = {2002}}

@article{Jackson:2006,
	Abstract = {Neurons and oligodendrocytes are produced in the adult brain subventricular zone (SVZ) from neural stem cells (B cells), which express GFAP and have morphological properties of astrocytes. We report here on the identification B cells expressing the PDGFRalpha in the adult SVZ. Specifically labeled PDGFRalpha expressing B cells in vivo generate neurons and oligodendrocytes. Conditional ablation of PDGFRalpha in a subpopulation of postnatal stem cells showed that this receptor is required for oligodendrogenesis, but not neurogenesis. Infusion of PDGF alone was sufficient to arrest neuroblast production and induce SVZ B cell proliferation contributing to the generation of large hyperplasias with some features of gliomas. The work demonstrates that PDGFRalpha signaling occurs early in the adult stem cell lineage and may help regulate the balance between oligodendrocyte and neuron production. Excessive PDGF activation in the SVZ in stem cells is sufficient to induce hallmarks associated with early stages of tumor formation.},
	Author = {Jackson, Erica L. and Garcia-Verdugo, Jose Manuel and Gil-Perotin, Sara and Roy, Monica and Quinones-Hinojosa, Alfredo and VandenBerg, Scott and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Glioma;research support, n.i.h., extramural ;Signal Transduction;Animals;Humans;Middle Aged;Mice, Transgenic;comparative study ;Cell Proliferation;research support, non-u.s. gov't ;Platelet-Derived Growth Factor;Aged, 80 and over;Neurons;Mice;Receptor, Platelet-Derived Growth Factor alpha;24 Pubmed search results 2008;Stem Cells;Lateral Ventricles;Adolescent},
	Month = {7},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Department of Neurological Surgery and Program in Developmental and Stem Cell Biology, University of California, San Francisco, San Francisco, California 94143, USA.},
	Pages = {187-99},
	Pii = {S0896-6273(06)00466-1},
	Pubmed = {16846854},
	Title = {PDGFR alpha-positive B cells are neural stem cells in the adult SVZ that form glioma-like growths in response to increased PDGF signaling},
	Uuid = {2B7EF72C-EE6C-4F09-AFA8-90D6D860DD8E},
	Volume = {51},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.06.012}}

@article{Jacobs:2000,
	Abstract = {Neurogenesis (the birth of new neurons) continues postnatally and into adulthood in the brains of many animal species, including humans. This is particularly prominent in the dentate gyrus of the hippocampal formation. One of the factors that potently suppresses adult neurogenesis is stress, probably due to increased glucocorticoid release. Complementing this, we have recently found that increasing brain levels of serotonin enhance the basal rate of dentate gyrus neurogenesis. These and other data have led us to propose the following theory regarding clinical depression. Stress-induced decreases in dentate gyrus neurogenesis are an important causal factor in precipitating episodes of depression. Reciprocally, therapeutic interventions for depression that increase serotonergic neurotransmission act at least in part by augmenting dentate gyrus neurogenesis and thereby promoting recovery from depression. Thus, we hypothesize that the waning and waxing of neurogenesis in the hippocampal formation are important causal factors, respectively, in the precipitation of, and recovery from, episodes of clinical depression.},
	Author = {Jacobs, B. L. and Praag, H. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Mol Psychiatry},
	Keywords = {Stress, Psychological/pathology/physiopathology;01 Adult neurogenesis general;Adult;Brain/*pathology/*physiopathology;Human;Models, Neurological;A abstr;Models, Psychological;Depressive Disorder/pathology/*physiopathology;Depression/pathology/*physiopathology;Animal;Support, U.S. Gov't, P.H.S.;Neurons/*pathology/*physiology;Support, Non-U.S. Gov't},
	Number = {3},
	Organization = {Program in Neuroscience, Princeton University, Princeton, NJ 08544- 1010, USA. barryj\@princeton.edu},
	Pages = {262-9.},
	Title = {Adult brain neurogenesis and psychiatry: a novel theory of depression},
	Uuid = {40C8063E-5751-4D60-AB3F-09BD585E3DC7},
	Volume = {5},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10889528}}

@article{Jacobs:2006,
	Abstract = {Retinoic acid (RA) is commonly used in vitro to differentiate stem cell populations including adult neural stem cells into neurons; however, the in vivo function of RA during adult neurogenesis remains largely unexplored. We found that depletion of RA in adult mice leads to significantly decreased neuronal differentiation within the granular cell layer of the dentate gyrus. RA contribution to neurogenesis occurs early, for RA deficiency also results in a decrease in newborn cells expressing an immature neuronal marker. Furthermore, although proliferation is unaffected during RA absence, cell survival is significantly reduced. Finally, a screen for retinoid-induced genes identifies metabolic targets including the lipid transporters, CD-36 and ABCA-1, the lipogenic master regulator SREBP1c as well as components of the Wnt signaling pathway. Our results reveal RA as a crucial contributor to early stages of adult neurogenesis and survival in vivo.},
	Author = {Jacobs, Sharoni and Lie, D. Chichung and DeCicco, Kathleen L. and Shi, Yanhong and DeLuca, Luigi M. and Gage, Fred H. and Evans, Ronald M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7505876},
	Number = {10},
	Organization = {Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.},
	Pages = {3902-7},
	Pii = {0511294103},
	Pubmed = {16505366},
	Title = {Retinoic acid is required early during adult neurogenesis in the dentate gyrus},
	Uuid = {C6990B18-A61C-40F9-91A6-0BD3D40156A8},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0511294103}}

@article{Jadhav:2006,
	Abstract = {Signaling through the Notch pathway regulates multiple aspects of development. The vertebrate retina allows an investigation of the basis for these various effects, because the major cell types of the retina arise from a common progenitor that expresses Notch1. The Notch pathway was constitutively activated in distinct populations of retinal cells during development. Prolonged Notch activity in progenitor cells maintained cells in the progenitor state without perturbing temporal identity, promoting early progenitor characteristics early in development and late progenitor characteristics later in development. Eventually, constitutive Notch activation led these cells to acquire characteristics of glial and stem cells. In contrast, reactivating the Notch pathway in newly postmitotic retinal cells promoted mature glial cell formation in a subset of cells. These data suggest that prolonged Notch activity does not disrupt the normal progression of progenitor temporal states, and that down-regulating or overcoming Notch activity is required for proper formation of both neuronal and glial cell fates.},
	Author = {Jadhav, Ashutosh P. and Cho, Seo-Hee H. and Cepko, Constance L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {50},
	Organization = {Division of Health Sciences and Technology, Department of Genetics, Harvard-Massachusetts Institute of Technology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.},
	Pages = {18998-9003},
	Pii = {0608155103},
	Pubmed = {17148603},
	Title = {Notch activity permits retinal cells to progress through multiple progenitor states and acquire a stem cell property},
	Uuid = {19FCC327-AAED-4C04-B881-12FB89A8138D},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0608155103}}

@article{Jaenisch:1983,
	Author = {Jaenisch, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {15 ERVs retroelements;Genes, Viral;Gene Expression Regulation;Retroviridae;15 Retrovirus mechanism;DNA Transposable Elements;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {1},
	Pages = {5-6},
	Pii = {0092-8674(83)90491-9},
	Pubmed = {6297787},
	Title = {Endogenous retroviruses},
	Uuid = {AB21159F-769B-4DF5-BBD3-63ABC3923134},
	Volume = {32},
	Year = {1983},
	url = {papers/Jaenisch_Cell1983.pdf}}

@article{Jakubs:2006,
	Abstract = {Neural progenitors in the adult dentate gyrus continuously produce new functional granule cells. Here we used whole-cell patch-clamp recordings to explore whether a pathological environment influences synaptic properties of new granule cells labeled with a GFP-retroviral vector. Rats were exposed to a physiological stimulus, i.e., running, or a brain insult, i.e., status epilepticus, which gave rise to neuronal death, inflammation, and chronic seizures. Granule cells formed after these stimuli exhibited similar intrinsic membrane properties. However, the new neurons born into the pathological environment differed with respect to synaptic drive and short-term plasticity of both excitatory and inhibitory afferents. The new granule cells formed in the epileptic brain exhibited functional connectivity consistent with reduced excitability. We demonstrate a high degree of plasticity in synaptic inputs to adult-born new neurons, which could act to mitigate pathological brain function.},
	Author = {Jakubs, and Nanobashvili, and Bonde, and Ekdahl, and Kokaia, and Kokaia, and Lindvall,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008;21 Epilepsy},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, Wallenberg Neuroscience Center, University Hospital, SE-221 84 Lund, Sweden; Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Biomedical Center, SE-221 84 Lund, Sweden.},
	Pages = {1047-1059},
	Pii = {S0896-6273(06)00870-1},
	Pubmed = {17178407},
	Title = {Environment Matters: Synaptic Properties of Neurons Born in the Epileptic Adult Brain Develop to Reduce Excitability},
	Uuid = {745F4500-441F-4914-BEDB-87E73A41A60F},
	Volume = {52},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.11.004}}

@article{Jang:2004,
	Abstract = {Both plasticity and cell fusion have been suggested to have a role in germ-layer switching. To understand the mechanisms underlying cell fate changes, we have examined a highly enriched population of hematopoietic stem cells (HSCs) in vitro or in vivo in response to injury for liver-specific phenotypic and functional changes. Here we show that HSCs become liver cells when cocultured with injured liver separated by a barrier. Chromosomal analyses and tissue-specific gene and/or protein expression show that microenvironmental cues rather than fusion are responsible for conversion in vitro. We transplanted HSCs into liver-injured mice and observed that HSCs convert into viable hepatocytes with increasing injury. Notably, liver function was restored 2-7 d after transplantation. We conclude that HSCs contribute to the regeneration of injured liver by converting into functional hepatocytes without fusion. 1465-7392 Journal Article},
	Author = {Jang, Y. Y. and Collector, M. I. and Baylin, S. B. and Diehl, A. M. and Sharkis, S. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {Nat Cell Biol},
	Keywords = {EE pdf;08 Aberrant cell cycle},
	Number = {6},
	Organization = {Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.},
	Pages = {532-9},
	Title = {Hematopoietic stem cells convert into liver cells within days without fusion},
	Uuid = {F63C7309-6092-418C-95B3-16A4A6922502},
	Volume = {6},
	Year = {2004},
	url = {papers/Jang_NatCellBiol2004.pdf}}

@article{Jankovski:1998,
	Abstract = {The subventricular zone of the adult mammalian forebrain contains progenitor cells that, by migrating along a restricted pathway called the 'rostral migratory stream'(RMS), add new neurons to the olfactory bulb throughout life. To determine the influence of the olfactory bulb on the development of these progenitor cells, we performed lesions that interrupt this pathway and separate the olfactory bulb from the rest of the forebrain. By labelling cells born at several survival times after the lesions with the thymidine analogue bromodeoxyuridine (BrdU), we found that disconnection from the bulb influences the rate of BrdU incorporation by the progenitor cells. The number of labelled cells in lesioned mice was almost half that found in control mice. In the disconnected migratory pathway, the number of neurons expressing calretinin was increased indicating that neuronal differentiation was enhanced: newly born neurons occurred within and around the RMS, most of them expressed calretinin and left the pathway starting about 2 weeks after the lesion. Thereafter, these neurons preserving their phenotype, spread for long distances, and accumulated ectopically in dorsal regions of the anterior olfactory nucleus and the frontal cortex. Finally, transplantation of adult subventricular cells into the lesioned pathway showed that the lesion neither prevents neuronal migration nor alters its direction. Thus, although the olfactory bulb appears to regulate the pace of the developmental processes, its disconnection does not prevent the proliferation, migration and phenotypic acquisition of newly generated bulbar interneurons that, since they cannot reach their terminal domains, populate some precise regions of the lesioned adult forebrain.},
	Author = {Jankovski, A. and Garcia, C. and Soriano, E. and Sotelo, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Movement/*physiology;Stem Cells/chemistry/*cytology;Animal;Cell Count;02 Adult neurogenesis migration;Mice, Transgenic;Nerve Tissue Proteins/analysis;Bromodeoxyuridine/analysis;B-8;Cell Survival/physiology;Prosencephalon/cytology/growth &development/surgery;Calcium-Binding Protein, Vitamin D-Dependent/analysis;Support, Non-U.S. Gov't;Cell Division/physiology;Olfactory Bulb/*cytology/growth &development/*surgery;Age Factors;Mice;Cell Differentiation/physiology;Antimetabolites/analysis;Interneurons/chemistry/*cytology},
	Number = {12},
	Organization = {INSERM U-106, Paris, France.},
	Pages = {3853-68.},
	Title = {Proliferation, migration and differentiation of neuronal progenitor cells in the adult mouse subventricular zone surgically separated from its olfactory bulb},
	Uuid = {D736DC0B-48B1-4E33-AC7B-C71CA9465511},
	Volume = {10},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9875362}}

@article{Jankovski:1996,
	Abstract = {To gain insight into cellular and molecular mechanisms subserving neuronal cell migration in the adult mouse forebrain, we have first investigated the cellular composition of the subventricular zone- olfactory bulb pathway (SVZ-OB). The pathway was essentially composed of cells with neuronal and astrocytic identities, neuronal cells being four times more numerous than astrocytes. Neuronal cells (precursors and some young postmitotic neurons) formed continuous cellular strands of migratory cells from the anterior horn of the lateral ventricle to the olfactory bulb. These chains of migrating cells moved within channels formed by the processes of a special subpopulation of astrocytes. The neuronal cells expressed the embryonic form of polysialic acid neural cell adhesion molecule, and the astrocytes were tenascin-C positive, thus preserving an embryonic cellular environment. Through transplantation experiments, the second part of this study attempted to analyze the functional properties of the adult SVZ-OB pathway. Early postnatal (P2-13) cerebellar progenitor cells, taken from a transgenic mouse line in which cerebellar granule cells and molecular layer interneurons (basket/stellate cells) expressed the reporter gene lacZ, were implanted in the SVZ-OB pathway of adult wild- type mice. Unlike grafted SVZ cells that migrate all along the pathway, none of the cerebellar precursors reached the olfactory bulb, although some of them were able to migrate along the caudal one-third of the pathway. The majority (over 67\%) of the migrating cells were progenitors that acquired the phenotype of basket/stellate cells. Granule cell progenitors and most granule cells did not survive transplantation. These results show that the adult SVZ-OB pathway is not a "passive generic guidance"for all classes of premigratory neurons. From the two types of grafted cerebellar progenitors, only those with migratory capability and that do not follow radial glial axes are able to translocate along the SVZ-OB pathway. Furthermore, the basket/stellate cell progenitors are specified at the time of grafting: Neither their identity nor the pace of expression of their major distinctive features are influenced by local signals emanating from the adult forebrain.},
	Author = {Jankovski, A. and Sotelo, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Stem Cells/*transplantation;02 Adult neurogenesis migration;Cerebellum/cytology/*transplantation;B;Lac Operon;Microscopy, Electron;Neural Pathways/physiology;Animal;Neurons/*cytology;Mice, Transgenic;Olfactory Bulb/*physiology;Astrocytes/*cytology;Prosencephalon/*physiology;Mice;Neuroglia/cytology;*Transplantation, Heterotopic;Cell Movement/physiology},
	Number = {3},
	Organization = {INSERM U. 106, Hopital de la Salpetriere, Paris, France.},
	Pages = {376-96.},
	Title = {Subventricular zone-olfactory bulb migratory pathway in the adult mouse: cellular composition and specificity as determined by heterochronic and heterotopic transplantation},
	Uuid = {87D1F70B-B1AD-4361-BDD7-77AFF7DC5E10},
	Volume = {371},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8842894}}

@article{Jarrosson-Wuilleme:2006,
	Abstract = {It is commonly accepted that infection of nondividing cells by gammaretroviruses such as the murine leukemia viruses is inefficient due to their inability to cross the nuclear envelope barrier. Challenging this notion, we now show that human nondividing macrophages display a specific window of susceptibility to transduction with a Friend murine leukemia virus (F-MLV)-derived vector during their differentiation from monocytes. This finding suggests that factors other than the nuclear membrane govern permissiveness to gammaretroviral infection and raises the possibility of using the macrophage tropism of F-MLV in gene therapy.},
	Author = {Jarrosson-Wuilleme, Loraine and Goujon, Caroline and Bernaud, Jeanine and Rigal, Dominique and Darlix, Jean-Luc L. and Cimarelli, Andrea},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {11 Glia;15 Retrovirus mechanism},
	Month = {2},
	Nlm_Id = {0113724},
	Number = {3},
	Organization = {LaboRetro, INSERM U412, Ecole Normale Sup{\'e}rieure de Lyon, IFR 128 BioSciences Lyon-Gerland, 46 All{\'e}e d'Italie, 69364 Lyon, France. acimarel\@ens-lyon.fr.},
	Pages = {1152-9},
	Pii = {80/3/1152},
	Pubmed = {16414992},
	Title = {Transduction of nondividing human macrophages with gammaretrovirus-derived vectors},
	Uuid = {E2DA51BF-93D6-43B1-9797-CBE1972E3F3D},
	Volume = {80},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.80.3.1152-1159.2006}}

@article{Jiang:2004,
	Abstract = {Vectors suitable for delivery of therapeutic genes to the CNS for chronic neurodegenerative diseases will require regulatable transgene expression. In this study, three self-regulating rAAV vectors encoding humanized green fluorescent protein (hGFP) were made using the tetracycline (tet)-off system. Elements were cloned in different orientations relative to each other and to the AAV internal terminal repeat (ITRs). The advantage of this vector system is that all infected cells will carry both the 'therapeutic' gene and the tet-regulator. To compare the efficiency of the vectors, 293T cells infected by each vector were grown in the presence or absence of the tet-analog doxycycline (dox). Cells were analyzed by flow cytometry for hGFP protein expression, and quantitative RT-PCR (QRT-PCR) for levels of hGFP mRNA and the tet-activator (tTA) mRNA. In the presence of dox, cells infected with one of the vectors, rAAVS3, showed less than 2\%total fluorescent intensity and mRNA copy number than cells grown without dox. The other two vectors were significantly more leaky. Levels of tTA mRNA were not affected by dox. The S3 vector also displayed tight regulation in HeLa and HT1080 cells. To assess regulation in the brain, the S3 vector was injected into rat striatum and rats maintained on regular or dox-supplemented water. At 1 month after vector injection, numerous positive cells were observed in rats maintained on regular water whereas only rare positive cells with very low levels of fluorescence were observed in rats maintained on water containing dox. The QRT-PCR analysis showed that dox inhibited expression of hGFP mRNA in brain by greater than 99\%. These results demonstrate that exceedingly tight regulation of transgene expression is possible using the tet-off system in the context of a self-regulating rAAV vector and that the specific orientation of two promoters relative to each other and to the ITRs is important. Regulatable vectors based on this design are ideal for therapeutic gene delivery to the CNS.},
	Author = {Jiang, L. and Rampalli, S. and George, D. and Press, C. and Bremer, E. G. and O'Gorman, M. R. G. and Bohn, M. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Gene Expression Regulation;Humans;Rats;Tetracycline;Dependovirus;Recombinant Proteins;RNA, Messenger;11 Glia;Green Fluorescent Proteins;Hela Cells;Reverse Transcriptase Polymerase Chain Reaction;Genetic Vectors;Cell Line;Rats, Inbred F344;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Flow Cytometry;Neurodegenerative Diseases;Doxycycline;Luminescent Proteins;Central Nervous System;Gene Expression;Transgenes},
	Month = {7},
	Nlm_Id = {9421525},
	Number = {13},
	Organization = {1Department of Pediatrics, Children's Memorial Institute for Education &Research, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.},
	Pages = {1057-67},
	Pii = {3302245},
	Pubmed = {15152187},
	Title = {Tight regulation from a single tet-off rAAV vector as demonstrated by flow cytometry and quantitative, real-time PCR},
	Uuid = {BBB661F9-369A-473B-8FB8-0612CD24E4B7},
	Volume = {11},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3302245}}

@article{Jiang:1998,
	Abstract = {In the adult songbird forebrain, neurons continue to be produced from precursor cells in the forebrain ependymal/subependymal zone (SZ), from which they migrate upon radial guide fibers. The new neurons and their radial cell partners may coderive from a common SZ progenitor, which may be the radial cell itself. On this basis, we asked whether radial cells might provide trophic support for the migration or survival of newly generated neurons. We focused upon the insulin-like growth factors (IGFs) IGF-1 and IGF-2, which have previously been shown to support the survival and differentiation of neural progenitor cells. We found that IGF-1 immunoreactivity was expressed heavily by adult zebra finch radial cells and their fibers, with little expression otherwise. IGF-2, in contrast, was expressed by parenchymal astrocytes and exhibited little radial cell expression. Despite their distinct distributions, IGF-1 and IGF-2 exerted similar trophic effects on finch SZ cells in vitro; both greatly increased the number of neurons migrating from explants of the adult finch SZ, relative to explants raised in low-insulin, IGF-1-deficient media. However, neither factor extended neuronal survival. These results suggest that in neurogenic regions of the adult avian forebrain, IGF-1 acts as a radial cell- associated neuronal differentiation and/or departure factor, which may serve to regulate neuronal recruitment into the adult brain.},
	Author = {Jiang, J. and McMurtry, J. and Niedzwiecki, D. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurobiol},
	Keywords = {Nerve Growth Factors/*physiology;Ependyma/cytology/*physiology;Neurons/*physiology;C;Female;Corpus Striatum/cytology/metabolism/*physiology;Insulin-Like Growth Factor I/*physiology;Animal;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Astrocytes/metabolism;Vocalization, Animal/physiology;04 Adult neurogenesis factors;Insulin-Like Growth Factor II/metabolism;Birds/*physiology;Cell Movement/physiology},
	Number = {1},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA.},
	Pages = {1-15.},
	Title = {Insulin-like growth factor-1 is a radial cell-associated neurotrophin that promotes neuronal recruitment from the adult songbird edpendyma/subependyma},
	Uuid = {D422B255-D4C6-420E-A97C-76C25AC8EC22},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9658334}}

@article{Jiang:1998a,
	Abstract = {Chemokines are a group of pro-inflammatory peptides that mediate leukocyte migration and activation. Several members of the chemokine family have been shown to be synthesized by cells of the central nervous system (CNS). To begin to address the role of chemokine receptors in CNS physiology, we identified, by molecular cloning techniques, the rat orthologs of the chemokine receptors, CCR2, CCR3, CCR5, and CXCR4. CCR2 and CCR5 expression was detected in rat spleen, lung, kidney, thymus and macrophages; CCR5 mRNA was also detected in rat brain. Primary cultures of rat microglia expressed CCR5 mRNA that was regulated by IFN-gamma, while both cultured astrocytes and microglia were found to contain mRNA for CXCR4 and CX3CR1. Induction of experimental allergic encephalomyelitis (EAE) in the rat was accompanied by increased levels of CCR2, CCR5, CXCR4, and CX3CR1 mRNAs in the lumbar spinal cords of animals displaying clinical signs of the disease. These data identify the rat orthologs of chemokine receptors and demonstrate that brain, spinal cord, and cultured glial cells express chemokine receptors that can be regulated both in vitro and in vivo.},
	Author = {Jiang, Y. and Salafranca, M. N. and Adhikari, S. and Xia, Y. and Feng, L. and Sonntag, M. K. and deFiebre, C. M. and Pennell, N. A. and Streit, W. J. and Harrison, J. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Human;Rats, Inbred Lew;GTP-Binding Proteins;Astrocytes;Gene Expression Regulation;Kidney;Rats;Cells, Cultured;Animals;Cloning, Molecular;Encephalomyelitis, Experimental Autoimmune;Microglia;Rats, Sprague-Dawley;RNA, Messenger;Not relevant;11 Glia;Male;Spinal Cord;Xenopus laevis;Support, Non-U.S. Gov't;Brain Chemistry;Receptors, Chemokine;Support, U.S. Gov't, P.H.S.;Amino Acid Sequence;Molecular Sequence Data},
	Medline = {98318173},
	Month = {6},
	Nlm_Id = {8109498},
	Number = {1},
	Organization = {Department of Pharmacology and Therapeutics, College of Medicine, University of Florida, Gainesville 32610-0267, USA.},
	Pages = {1-12},
	Pii = {S0165572898000058},
	Pubmed = {9655467},
	Title = {Chemokine receptor expression in cultured glia and rat experimental allergic encephalomyelitis},
	Uuid = {3C442BDA-F2F7-4DCA-B025-D24B818306F7},
	Volume = {86},
	Year = {1998}}

@article{Jiang:2005,
	Abstract = {Apoptosis is an essential process during normal neuronal development. Approximately one-half of the neurons produced during neurogenesis die before completion of CNS maturation. To characterize the role of the inhibitor of apoptosis gene, survivin, during neurogenesis, we used the Cre-loxP-system to generate mice lacking survivin in neuronal precursor cells. Conditional deletion of survivin starting at embryonic day 10.5 leads to massive apoptosis of neuronal precursor cells in the CNS. Conditional mutants were born at the expected Mendelian ratios; however, these died shortly after birth from respiratory insufficiency, without primary cardiopulmonary pathology. Newborn conditional mutants showed a marked reduction in the size of the brain associated with severe, mutifocal apoptosis in the cerebrum, cerebellum, brainstem, spinal cord, and retina. Caspase-3 and caspase-9 activities in the mutant brains were significantly elevated, whereas bax expression was unchanged from controls. These results show that survivin is critically required for the survival of developing CNS neurons, and may impact on our understanding of neural repair, neural development, and neurodegenerative diseases. Our study is the first to solidify a role for survivin as an antiapoptotic protein during normal neuronal development in vivo.},
	Author = {Jiang, Yuying and de Bruin, Alain and Caldas, Hugo and Fangusaro, Jason and Hayes, John and Conway, Edward M. and Robinson, Michael L. and Altura, Rachel A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Retina;Microtubule-Associated Proteins;10 Development;Animals;Pregnancy;Mice, Mutant Strains;Phenotype;Brain;Apoptosis;Female;Integrases;Gene Deletion;08 Aberrant cell cycle;Male;Research Support, U.S. Gov't, P.H.S.;Neurons;Intermediate Filament Proteins;Mice;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {30},
	Organization = {Center for Childhood Cancer, Columbus Children's Research Institute, Columbus, Ohio 43205, USA.},
	Pages = {6962-70},
	Pii = {25/30/6962},
	Pubmed = {16049172},
	Title = {Essential role for survivin in early brain development},
	Uuid = {D46AB62D-22DF-44D9-8ECB-1390B9A67FB1},
	Volume = {25},
	Year = {2005},
	url = {papers/Jiang_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1446-05.2005}}

@article{Jiang:1999,
	Abstract = {Ciliary neurotrophic factor (CNTF) is produced and released in response to injury in the central nervous system (CNS). While CNTF initially was characterized as a trophic factor for neurons, more recent evidence supports roles for this factor in survival, proliferation, and maturation of oligodendrocyte lineage cells. Evidence is emerging to support the hypothesis that CNTF's actions may include enhancing other growth and trophic factors. Here we tested the hypothesis that CNTF can induce expression of receptors on oligodendrocytes for factors that are known to promote their generation, maturation, and survival. Specifically, we used an in vivo paradigm to test whether CNTF, when injected stereotactically into forebrain white matter of adult rats, could induce mRNA expression for the insulin-like growth factor (IGF) type I receptor (IGF-IR), fibroblast growth factor (FGF) receptor (FGFR)-1, FGFR3, and platelet-derived growth factor (PDGF) receptor- alpha (PDGFRalpha). We determined that CNTF injection increased expression of IGF-IR and FGFR1 mRNAs in adult white matter to 200-250\%of control levels. Cellular analysis indicated that these receptor mRNAs were induced in interfascicular oligodendrocytes. In contrast, CNTF had no effect on levels of FGFR3 and PDGFRalpha mRNAs. These results suggest that CNTF enhances the sensitivity of oligodendrocytes to other mitogens and trophic factors via induction of their receptors.},
	Author = {Jiang, F. and Levison, S. W. and Wood, T. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci Res},
	Keywords = {G;RNA, Messenger/*biosynthesis;Ciliary Neurotrophic Factor;Nerve Growth Factors/*pharmacology;Brain/*drug effects/metabolism;Cell Survival/drug effects;Receptors, Fibroblast Growth Factor/genetics;Rats;Oligodendroglia/*drug effects/metabolism;Receptor, IGF Type 1/*genetics;Female;Animal;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein/analysis;11 Glia;Support, Non-U.S. Gov't;Nerve Tissue Proteins/*pharmacology;Receptors, Platelet-Derived Growth Factor/genetics;Support, U.S. Gov't, P.H.S.},
	Number = {4},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey 17033, USA.},
	Pages = {447-57.},
	Title = {Ciliary neurotrophic factor induces expression of the IGF type I receptor and FGF receptor 1 mRNAs in adult rat brain oligodendrocytes},
	Uuid = {5054657A-B291-423C-BDB2-9B1DD1F7C8B1},
	Volume = {57},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10440894}}

@article{Jiang:2001,
	Abstract = {BACKGROUND AND PURPOSE: This study explored the possible occurrence of newly generated nerve cells in the ischemic cortex of adult rats after middle cerebral artery occlusion and reperfusion. METHODS: Nine- to 10-week-old male Wistar rats were subjected to 2 hours of middle cerebral artery occlusion by the monofilament method. Rats received repeated intraperitoneal injections of the cell proliferation-specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Brain sections were processed for immunohistochemistry with an avidin-biotin complex-alkaline phosphatase and/or -peroxidase method. Brain sections processed with double-immunofluorescent staining were further scanned by confocal microscopy. RESULTS: Interspersed among the predominantly newly formed glial cells, some cells were double labeled by BrdU and 1 of the neuron-specific markers, Map-2, beta-tubulin III, and Neu N, at 30 and 60 days after stroke onset. These cells were randomly distributed throughout cortical layers II through VI, occurring with highest density in the ischemic boundary zone. Three-dimensional confocal analyses of BrdU and the neuron-specific marker Neu N confirmed their colocalization within the same cortical cells. CONCLUSIONS: This study suggests that new neurons can be generated in the cerebral cortex of adult rats after transient focal cerebral ischemia. Cortical neurogenesis may be a potential pathway for brain repair after stroke. 1524-4628 Journal Article},
	Author = {Jiang, W. and Gu, W. and Brannstrom, T. and Rosqvist, R. and Wester, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {Stroke},
	Keywords = {Disease Models, Animal;Cerebral Cortex/*blood supply/pathology/*physiopathology;Neurons/*cytology/metabolism/pathology;Bromodeoxyuridine/pharmacokinetics;Immunohistochemistry;Rats;D;Cell Division;Cell Count;Rats, Wistar;Infarction, Middle Cerebral Artery/*pathology;Reperfusion;Animals;Support, Non-U.S. Gov't;Male;Neuroglia/cytology/metabolism;*Regeneration},
	Number = {5},
	Organization = {Departments of Public Health and Clinical Medicine, Medicine, Umea Stroke Center,Umea University (Sweden).},
	Pages = {1201-7},
	Pubmed = {11340234},
	Title = {Cortical neurogenesis in adult rats after transient middle cerebral artery occlusion},
	Uuid = {BAA170FE-C26D-11DA-969D-000D9346EC2A},
	Volume = {32},
	Year = {2001},
	url = {papers/Jiang_Stroke2001.pdf}}

@article{Jin:2003,
	Abstract = {Neurogenesis, which may contribute to the ability of the adult brain to function normally and adapt to disease, nevertheless declines with advancing age. Adult neurogenesis can be enhanced by administration of growth factors, but whether the aged brain remains responsive to these factors is unknown. We compared the effects of intracerebroventricular fibroblast growth factor (FGF)-2 and heparin-binding epidermal growth factor-like growth factor (HB-EGF) on neurogenesis in the hippocampal dentate subgranular zone (SGZ) and the subventricular zone (SVZ) of young adult (3-month) and aged (20-month) mice. Neurogenesis, measured by labelling with bromodeoxyuridine (BrdU) and by expression of doublecortin, was reduced by approximately 90\%in SGZ and by approximately 50\%in SVZ of aged mice. HB-EGF increased BrdU labelling in SGZ at 3 months by approximately 60\%and at 20 months by approximately 450\%, which increased the number of BrdU-labelled cells in SGZ of aged mice to approximately 25\%of that in young adults. FGF-2 also stimulated BrdU labelling in SGZ, by approximately 25\%at 3 months and by approximately 250\%at 20 months, increasing the number of newborn neurones in older mice to approximately 20\%of that in younger mice. In SVZ, HB-EGF and FGF-2 increased BrdU incorporation by approximately 140\%at 3 months and approximately 170\%at 20 months, so the number of BrdU-labelled cells was comparable in untreated 3-month-old and growth factor-treated 20-month-old mice. These results demonstrate that the aged brain retains the capacity to respond to exogenous growth factors with increased neurogenesis, which may have implications for the therapeutic potential of neurogenesis enhancement in age-associated neurological disorders. 1474-9718 Journal Article},
	Author = {Jin, K. and Sun, Y. and Xie, L. and Batteur, S. and Mao, X. O. and Smelick, C. and Logvinova, A. and Greenberg, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1474-9718},
	Journal = {Aging Cell},
	Keywords = {Hippocampus/cytology/drug effects/*metabolism;Animals;Dentate Gyrus/cytology/drug effects/metabolism;Aging;Comparative Study;Epidermal Growth Factor/*pharmacology;*Aging;Heparin/metabolism;Hippocampus;Male;Fibroblast Growth Factor 2;Cerebral Ventricles;Heparin;Mice, Inbred Strains;Research Support, U.S. Gov't, P.H.S.;Neurons;Cerebral Ventricles/cytology/drug effects/*metabolism;Dentate Gyrus;Support, U.S. Gov't, P.H.S.;04 Adult neurogenesis factors;Mice;Neurons/*drug effects/metabolism;Epidermal Growth Factor;Fibroblast Growth Factor 2/*pharmacology;C pdf},
	Medline = {22764190},
	Month = {6},
	Nlm_Id = {101130839},
	Number = {3},
	Organization = {Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA.},
	Pages = {175-83},
	Pubmed = {12882410},
	Title = {Neurogenesis and aging: FGF-2 and HB-EGF restore neurogenesis in hippocampus and subventricular zone of aged mice},
	Uuid = {3EF67BBC-8E5F-41FE-AA19-D45DD6F0F468},
	Volume = {2},
	Year = {2003},
	url = {papers/Jin_AgingCell2003.pdf}}

@article{Jin:2003a,
	Abstract = {Bone marrow cells (BMC) can be induced to express neuronal phenotypic features in vitro, but the extent to which they can transdifferentiate to mature, functional neurons is uncertain. We examined the effects of different growth factors and combinations thereof on the expression of neuronal marker proteins in cultures of BMC enriched in marrow stromal cells. Patterns of neuronal marker expression varied depending on the growth factor or factors to which BMC cultures were exposed. Cultures treated for up to 5 weeks with epidermal growth factor, fibroblast growth factor-2, retinoic acid, and nerve growth factor displayed neuron-like cellular processes and expressed neuronal markers, including the neuronal nuclear antigen NeuN, microtubule-associated protein 2, tau, synaptophysin, alpha(1A) and alpha(1B) calcium channel subunits, NR2A glutamate receptor subunits, and gamma-aminobutyric acid. However, the intracellular distribution of these markers was distinct from their usual distribution in mature neurons. We conclude that a variety of growth factors can drive BMC toward a neuronal phenotype or phenotypes, but that morphological neuronal features and the ectopic expression of neuronal proteins and neurotransmitters may not equate with the ability to execute normal neuronal functions.},
	Author = {Jin, Kunlin and Mao, Xiao Ou and Batteur, Sophie and Sun, Yunjuan and Greenberg, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cell Differentiation;Animals;Cells, Cultured;Nerve Growth Factors;08 Aberrant cell cycle;Fibroblast Growth Factor 2;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Neurons;Neuroglia;Epidermal Growth Factor;Mice;Cell Division;Immunohistochemistry;Biological Markers;Tretinoin;Growth Substances},
	Medline = {22999018},
	Month = {11},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA.},
	Pages = {78-89},
	Pii = {S001448860300133X},
	Pubmed = {14637082},
	Title = {Induction of neuronal markers in bone marrow cells: differential effects of growth factors and patterns of intracellular expression},
	Uuid = {65047487-57D3-4BCD-B055-A00CEDF47E06},
	Volume = {184},
	Year = {2003},
	url = {papers/Jin_ExpNeurol2003a.pdf}}

@article{Jin:2003b,
	Author = {Jin, Kunlin and Greenberg, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Stromal Cells;Cell Differentiation;Adipose Tissue;Research Support, Non-U.S. Gov't;Bone Marrow Cells;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Growth Substances;Culture Media;comment;Animals;Cells, Cultured;Humans;Neurons;Mice},
	Medline = {22916126},
	Month = {10},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA.},
	Pages = {255-7},
	Pii = {S0014488603002206},
	Pubmed = {14552865},
	Title = {Tales of transdifferentiation},
	Uuid = {04FE95CB-E28E-4F91-BFDB-77285DA34ABD},
	Volume = {183},
	Year = {2003},
	url = {papers/Jin_ExpNeurol2003.pdf}}

@article{Jin:2002,
	Abstract = {Heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) is found in cerebral neurons, and its expression is increased after hypoxic or ischemic injury, which also stimulates neurogenesis. To investigate the possible role of HB-EGF in hypoxic-ischemic induction of neurogenesis, we measured its expression, effects, and target receptors in embryonic murine cerebral cortical cultures and in adult rat brain. Hypoxia increased HB-EGF expression by approximately 50\%in cortical cultures, where expression was associated with mature and immature neurons. HB-EGF (5-100 ng/ml) stimulated by approximately 80\%the incorporation of bromodeoxyuridine (BrdU) into cultured cells that expressed the HB-EGF receptors epidermal growth factor receptor (EGFR)/avian erythroblastic leukemia viral oncogene homolog 1 (ErbB1) and N-arginine dibasic convertase (NRDc). Intracerebroventricular administration of HB-EGF in adult rats increased BrdU labeling in the subventricular zone and in the subgranular zone of dentate gyrus, where EGFR/ErbB1 and NRDc were also expressed and where ischemia-induced neurogenesis is observed. We conclude that HB-EGF stimulates neurogenesis in proliferative zones of the adult brain that are also affected in ischemia and that it does so by interacting with EGFR/ErbB1 and possibly NRDc. Therefore, HB-EGF may help to trigger proliferation of neuronal precursors in brain after hypoxic or ischemic injury. 1529-2401 Journal Article},
	Author = {Jin, K. and Mao, X. O. and Sun, Y. and Xie, L. and Jin, L. and Nishi, E. and Klagsbrun, M. and Greenberg, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Animals;Cell Survival/drug effects;Epidermal Growth Factor/*biosynthesis/*pharmacology;Cells, Cultured;Rats;Receptors, Growth Factor;Cerebral Cortex/cytology/*growth &development/metabolism;Cell Hypoxia;Receptors, Growth Factor/analysis;Rats, Sprague-Dawley;Neurons/drug effects/*metabolism;Stem Cells/drug effects/metabolism;C abstr;Male;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Neurons;Epidermal Growth Factor;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Stem Cells;Cell Division/drug effects},
	Medline = {22092348},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {13},
	Organization = {Buck Institute for Age Research, Novato, California 94945, USA.},
	Pages = {5365-73},
	Pii = {22/13/5365},
	Pubmed = {12097488},
	Title = {Heparin-binding epidermal growth factor-like growth factor: hypoxia-inducible expression in vitro and stimulation of neurogenesis in vitro and in vivo},
	Uuid = {88CAC002-4411-4BBC-B6AE-A4BDACAB79DA},
	Volume = {22},
	Year = {2002},
	url = {papers/Jin_JNeurosci2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/20026486}}

@article{Jin:2000,
	Abstract = {A major obstacle to stem-cell gene therapy rests in the inability to deliver a gene into a therapeutically relevant fraction of stem cells. One way to circumvent this obstacle is to use selection. Vectors containing two linked genes serve as the basis for selection, with one gene encoding a selectable product and the other, a therapeutic protein. Applying selection in vivo has the potential to bring a minor population of genetically corrected cells into the therapeutic range. But strategies for achieving in vivo selection have traditionally relied on genes that confer resistance to cytotoxic drugs and are encumbered by toxicity. Here we describe a new system for in vivo selection that uses a 'cell-growth switch', allowing a minor population of genetically corrected cells into the therapeutic range. But strategies for achieving in vivo selection have traditionally relied on genes that confer resistance to cytotoxic drugs and are encumbered by toxicity. Here we describe a new system for in vivo selection that uses a 'cell-growth switch', allowing a minor population of genetically modified cells to be inducibly amplified, thereby averting the risks associated with cytotoxic drugs. This system provides a general platform for conditionally expanding genetically modified cell populations in vivo, and may have widespread applications in gene and cell therapy.},
	Author = {Jin, L. and Zeng, H. and Chien, S. and Otto, K. G. and Richard, R. E. and Emery, D. W. and Blau, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {Protein Structure, Tertiary;Genetic Vectors;Green Fluorescent Proteins;Erythrocytes;Luminescent Proteins;Gene Therapy;Animals;Cell Separation;Flow Cytometry;Dimerization;Research Support, U.S. Gov't, P.H.S.;Transgenes;Kinetics;Phenotype;Proto-Oncogene Proteins;Bone Marrow Transplantation;Receptors, Cytokine;Blotting, Southern;Receptors, Erythropoietin;Granulocytes;11 Glia;Neoplasm Proteins;Blood Platelets;Retroviridae;Time Factors;Dose-Response Relationship, Drug;Recombinant Fusion Proteins;Mice;Research Support, Non-U.S. Gov't;Cell Culture Techniques;Oncogene Proteins},
	Medline = {20428183},
	Month = {9},
	Nlm_Id = {9216904},
	Number = {1},
	Organization = {Division of Hematology, Department of Medicine, University of Washington, Seattle, Washington, USA.},
	Pages = {64-6},
	Pubmed = {10973250},
	Title = {In vivo selection using a cell-growth switch},
	Uuid = {8339F942-B570-480C-8409-16F13336F199},
	Volume = {26},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/79194}}

@article{Jin:2001,
	Abstract = {Because neurogenesis persists in the adult mammalian brain and can be regulated by physiological and pathological events, we investigated its possible involvement in the brain's response to focal cerebral ischemia. Ischemia was induced by occlusion of the middle cerebral artery in the rat for 90 min, and proliferating cells were labeled with 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdUrd) over 2-day periods before sacrificing animals 1, 2 or 3 weeks after ischemia. Ischemia increased the incorporation of BrdUrd into cells in two neuroproliferative regions-the subgranular zone of the dentate gyrus and the rostral subventricular zone. Both effects were bilateral, but that in the subgranular zone was more prominent on the ischemic side. Cells labeled with BrdUrd coexpressed the immature neuronal markers doublecortin and proliferating cell nuclear antigen but did not express the more mature cell markers NeuN and Hu, suggesting that they were nascent neurons. These results support a role for ischemia-induced neurogenesis in what may be adaptive processes that contribute to recovery after stroke. 0027-8424 Journal Article},
	Author = {Jin, K. and Minami, M. and Lan, J. Q. and Mao, X. O. and Batteur, S. and Simon, R. P. and Greenberg, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Dentate Gyrus/metabolism/pathology/*physiopathology;Rats, Sprague-Dawley;Proliferating Cell Nuclear Antigen/metabolism;Immunohistochemistry;Rats;Bromodeoxyuridine/metabolism;06 Adult neurogenesis injury induced;Brain Ischemia/metabolism/pathology/*physiopathology;Neuropeptides/metabolism;Support, U.S. Gov't, P.H.S.;D pdf;Animals;Male},
	Number = {8},
	Organization = {Buck Institute for Age Research, Novato, CA 94945, USA.},
	Pages = {4710-5},
	Title = {Neurogenesis in dentate subgranular zone and rostral subventricular zone after focal cerebral ischemia in the rat},
	Uuid = {6D9248FE-EC81-11DA-8605-000D9346EC2A},
	Volume = {98},
	Year = {2001},
	url = {papers/Jin_ProcNatlAcadSciUSA2001.pdf}}

@article{Jin:2004,
	Abstract = {Neurogenesis, which persists in the adult mammalian brain, may provide a basis for neuronal replacement therapy in neurodegenerative diseases like Alzheimer's disease (AD). Neurogenesis is increased in certain acute neurological disorders, such as ischemia and epilepsy, but the effect of more chronic neurodegenerations is uncertain, and some animal models of AD show impaired neurogenesis. To determine how neurogenesis is affected in the brains of patients with AD, we investigated the expression of immature neuronal marker proteins that signal the birth of new neurons in the hippocampus of AD patients. Compared to controls, Alzheimer's brains showed increased expression of doublecortin, polysialylated nerve cell adhesion molecule, neurogenic differentiation factor and TUC-4. Expression of doublecortin and TUC-4 was associated with neurons in the neuroproliferative (subgranular) zone of the dentate gyrus, the physiological destination of these neurons (granule cell layer), and the CA1 region of Ammon's horn, which is the principal site of hippocampal pathology in AD. These findings suggest that neurogenesis is increased in AD hippocampus, where it may give rise to cells that replace neurons lost in the disease, and that stimulating hippocampal neurogenesis might provide a new treatment strategy.},
	Author = {Jin, Kunlin and Peel, Alyson L. and Mao, Xiao Ou and Xie, Lin and Cottrell, Barbara A. and Henshall, David C. and Greenberg, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Human;Nerve Degeneration;Animals;Middle Aged;Female;21 Neurodegenerative;Hippocampus;Male;Neuropeptides;Aged;Support, Non-U.S. Gov't;Case-Control Studies;Alzheimer Disease;Sialic Acids;21 Neurophysiology;Aged, 80 and over;Adult;Neurons;Support, U.S. Gov't, P.H.S.;Neural Cell Adhesion Molecule L1;Immunohistochemistry;Nerve Tissue Proteins;Adolescent},
	Month = {1},
	Nlm_Id = {7505876},
	Number = {1},
	Organization = {Buck Institute for Age Research, Novato, CA 94945, USA.},
	Pages = {343-7},
	Pii = {2634794100},
	Pubmed = {14660786},
	Title = {Increased hippocampal neurogenesis in Alzheimer's disease},
	Uuid = {54B36CC8-A2F6-4D51-BE18-BC66F92F6D1F},
	Volume = {101},
	Year = {2004},
	url = {papers/Jin_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.2634794100}}

@article{Jin:2004a,
	Abstract = {Neurogenesis continues in the adult brain and is increased in certain pathological states. We reported recently that neurogenesis is enhanced in hippocampus of patients with Alzheimer's disease (AD). We now report that the effect of AD on neurogenesis can be reproduced in a transgenic mouse model. PDGF-APP(Sw,Ind) mice, which express the Swedish and Indiana amyloid precursor protein mutations, show increased incorporation of BrdUrd and expression of immature neuronal markers in two neuroproliferative regions: the dentate gyrus and subventricular zone. These changes, consisting of approximately 2-fold increases in the number of BrdUrd-labeled cells, were observed at age 3 months, when neuronal loss and amyloid deposition are not detected. Because enhanced neurogenesis occurs in both AD and an animal model of AD, it seems to be caused by the disease itself and not by confounding clinical factors. As neurogenesis is increased in PDGF-APP(Sw,Ind) mice in the absence of neuronal loss, it must be triggered by more subtle disease manifestations, such as impaired neurotransmission. Enhanced neurogenesis in AD and animal models of AD suggests that neurogenesis may be a compensatory response and that measures to enhance neurogenesis further could have therapeutic potential.},
	Author = {Jin, Kunlin and Galvan, Veronica and Xie, Lin and Mao, Xiao Ou and Gorostiza, Olivia F. and Bredesen, Dale E. and Greenberg, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Platelet-Derived Growth Factor;Research Support, Non-U.S. Gov't;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred C57BL;06 Adult neurogenesis injury induced;Alzheimer Disease;Mice, Transgenic;Amyloid beta-Protein Precursor;Animals;Bromodeoxyuridine;Mice;Neurons},
	Month = {9},
	Nlm_Id = {7505876},
	Number = {36},
	Organization = {Buck Institute for Age Research, Novato, CA 94945, USA.},
	Pages = {13363-7},
	Pii = {0403678101},
	Pubmed = {15340159},
	Title = {Enhanced neurogenesis in Alzheimer's disease transgenic (PDGF-APPSw,Ind) mice},
	Uuid = {E5401220-E44E-4CD8-8DD5-0D7B1236A9EA},
	Volume = {101},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0403678101}}

@article{Jin:2006,
	Abstract = {Experimental stroke in rodents stimulates neurogenesis and migration of newborn neurons from their sites of origin into ischemic brain regions. We report that in patients with stroke, cells that express markers associated with newborn neurons are present in the ischemic penumbra surrounding cerebral cortical infarcts, where these cells are preferentially localized in the vicinity of blood vessels. These findings suggest that stroke-induced compensatory neurogenesis may occur in the human brain, where it could contribute to postischemic recovery and represent a target for stroke therapy.},
	Author = {Jin, Kunlin and Wang, Xiaomei and Xie, Lin and Mao, Xiao Ou and Zhu, Wei and Wang, Yin and Shen, Jianfeng and Mao, Ying and Banwait, Surita and Greenberg, David A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cerebrovascular Accident;Brain Ischemia;Cell Differentiation;research support, n.i.h., extramural ;Adult;Aged;Cell Proliferation;Female;Middle Aged;research support, u.s. gov't, non-p.h.s. ;Male;Humans;Cerebral Cortex;Neurons;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {35},
	Organization = {*Buck Institute for Age Research, Novato, CA 94945.},
	Pages = {13198-202},
	Pii = {0603512103},
	Pubmed = {16924107},
	Title = {Evidence for stroke-induced neurogenesis in the human brain},
	Uuid = {A9B027F8-A75F-44E1-BE3E-547680B65107},
	Volume = {103},
	Year = {2006},
	url = {papers/Jin_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0603512103}}

@article{Jinno:2007a,
	Abstract = {Microglia are classically considered to be immune cells in the brain, but have now been proven to be involved in neuronal activity as well. Here we stereologically analyzed the spatial arrangement of microglia in the mouse hippocampus. First, we estimated the numerical densities (NDs) of microglia identified by ionized calcium-binding adaptor molecule 1 (Iba1). Despite that microglia appeared to be evenly distributed throughout the hippocampal area, the NDs demonstrated significant dorsoventral, interregional, and interlaminar differences. Briefly, the NDs in the ventral hippocampus were significantly lower in the CA3 region than in the CA1 region and dentate gyrus, although no interregional differences were detectable in the dorsal hippocampus. Both in the CA1 and CA3 regions, the NDs were significantly higher in the stratum lacunosum-moleculare than in the remaining layers. Next, we investigated the spatial patterns of distribution of Iba1-labeled microglia and S100beta-labeled astrocytes. So far as we examined, the somato-somatic contacts were not seen among microglia or among astrocytes, whereas the close apposition between microglia and astrocytes were occasionally detected. The 3D point process analysis showed that the spatial distribution of microglia was significantly repulsive. Because the statistical territory of single microglia was larger than that estimated from process tracing, they are not likely to touch each other with their processes. Astrocytes were distributed slightly repulsively with overlapping areas. The 3D point process analysis also revealed a significant spatial attraction between microglia and astrocytes. The present findings provide a novel anatomical basis for glial research.},
	Author = {Jinno, Shozo and Fleischer, Frank and Eckel, Stefanie and Schmidt, Volker and Kosaka, Toshio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Animals;Astrocytes;Image Processing, Computer-Assisted;comparative study;Imaging, Three-Dimensional;Microglia;Cell Communication;Cell Count;Hippocampus;Staining and Labeling;Mice, Inbred C57BL;research support, non-u.s. gov't;11 Glia;Male;Nerve Growth Factors;Calcium-Binding Proteins;Dentate Gyrus;Poisson Distribution;Mice;24 Pubmed search results 2008;S100 Proteins;Immunologic Techniques},
	Month = {10},
	Nlm_Id = {8806785},
	Number = {13},
	Organization = {Department of Anatomy and Neurobiology, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan. sjnno\@med.kyushu-u.ac.jp},
	Pages = {1334-47},
	Pubmed = {17647290},
	Title = {Spatial arrangement of microglia in the mouse hippocampus: a stereological study in comparison with astrocytes},
	Uuid = {F972761F-0BBE-49D2-9521-103AB9AC3B8C},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20552}}

@article{Joannides:2004,
	Abstract = {Background Neural stem cells are a potential source of cells for drug screening or cell-based treatments for neurodegenerative diseases. However, ethical and practical considerations limit the availability of neural stem cells derived from human embryonic tissue. An alternative source of human neural stem cells is needed; a source that is readily accessible, easily expanded, and reliably induced to a neural fate. Methods Dermis isolated from biopsy samples of adult human skin was cultured and expanded in the presence of the mitogens epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF 2), and then by serum. We used immunocytochemical techniques, clonal analysis, and physiological characterisation to assess neural differentiation after the treatment of expanded cells with novel induction media. Findings Initial characterisation of skin samples confirmed the absence of nestin, a neural precursor marker. Sequential culture in EGF and FGF 2 followed by adherent expansion in serum, and re-exposure to mitogens in substrate-free conditions resulted in large numbers of nestin-positive/musashi-positive neural precursors. Subsequent exposure of these precursors to hippocampal-astrocyte-derived signals resulted in cells of neuronal morphology that had stable expression of markers of neuronal differentiation (neurofilament, beta tubulin). We also show the presence of voltage-dependent calcium transients, and demonstrate monoclonal neural potential. Interpretation We describe the isolation and characterisation of cells derived from adult human dermis that can be expanded for extended periods of time in vitro, while retaining inducible neural potential. The generation of almost limitless numbers of neural precursors from a readily accessible autologous adult human source provides a platform for further experimental studies and has potential therapeutic implications. 1474-547x Journal Article},
	Author = {Joannides, A. and Gaughwin, P. and Schwiening, C. and Majed, H. and Sterling, J. and Compston, P. A. and Chandran, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Lancet},
	Keywords = {S abstr;22 Stem cells},
	Number = {9429},
	Organization = {Department of Clinical Neurosciences, University of Cambridge and Addenbrooke's Hospital, Cambridge, UK.},
	Pages = {172-8},
	Pubmed = {15246730},
	Title = {Efficient generation of neural precursors from adult human skin: astrocytes promote neurogenesis from skin-derived stem cells},
	Uuid = {B400C25C-2D47-4C10-9082-55904A06C0E9},
	Volume = {364},
	Year = {2004},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15246730}}

@article{Jockusch:2003,
	Abstract = {We studied the migratory behaviour of adult muscle precursor cells in the mouse into and from skeletal muscle grafts using green fluorescent protein (GFP) and nuclear LacZ transgenes as complementary and double markers of the cell's origin. Owing to the small molecular mass and extreme solubility of GFP, this label provided a drastically increased sensitivity for detection compared with the markers that had been used previously. During the first six weeks after the operation, the graft/host border was well defined, with only occasional local intermingling and co-fusion of host and donor myogenic cells. Seven to eleven weeks after the operation we found that the host myogenic cells had migrated into the graft, and graft myogenic cells had migrated into the adjacent host muscle, with integration of donor nuclei into pre-existing myotubes or muscle fibres. There was no indication of an origin of, or target for, these myogenic cells besides neighbouring muscles. Our observations indicate migration of these cells through solid muscle tissue, over a distance of several millimetres. The migratory activity of adult myogenic precursor cells can be stimulated by traumatic events in either the target muscle or the muscle of origin.},
	Author = {Jockusch, Harald and Voigt, Sylvana},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0021-9533},
	Journal = {J Cell Sci},
	Keywords = {Animals;Female;Myoblasts;Cell Movement;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Time Factors;Mice, Nude;Male;Transplantation Chimera;Mice, Inbred Strains;Lac Operon;Mice;Muscle, Smooth, Vascular;Luminescent Proteins;Nuclear Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22526791},
	Month = {4},
	Nlm_Id = {0052457},
	Number = {Pt 8},
	Organization = {Developmental Biology and Molecular Pathology, W7, University of Bielefeld, D-33501 Bielefeld, Germany. h.jockusch\@uni-bielfeld.de},
	Pages = {1611-6},
	Pubmed = {12640044},
	Title = {Migration of adult myogenic precursor cells as revealed by GFP/nLacZ labelling of mouse transplantation chimeras},
	Uuid = {7ECC4343-24D5-464D-ADC1-0D67561C6026},
	Volume = {116},
	Year = {2003}}

@article{Joels:2004,
	Abstract = {It has become increasingly clear that the increase in corticosteroid levels, e.g. after a brief stressor induce molecular and cellular changes in brain, including the hippocampal formation. These effects eventually result in behavioral adaptation. Prolonged exposure to stress, though, may lead to mal-adaptation and even be a risk factor for diseases like major depression in genetically predisposed individuals. We conducted a series of experiments where changes in brain function were examined after 3 weeks of unpredictable stress. After unpredictable stress, inhibitory input to neurons involved in the hypothalamus-pituitary-adrenal (HPA) axis regulation was suppressed, which may dysregulate the axis and lead to overexposure of the brain to glucocorticoids. Furthermore, glutamate transmission in the dentate gyrus (DG) was enhanced, possibly through transcriptional regulation of receptor subunits. Combined with enhanced calcium channel expression this could increase vulnerability to cell death. Neurogenesis and apoptosis in the dentate were diminished. Synaptic plasticity was suppressed both in the dentate and CA1 area. Collectively, these effects may give rise to deficits in memory formation. Finally, we observed reduced responses to serotonin in the CA1 area, which could contribute to the onset of symptoms of depression in predisposed individuals. All of these endpoints provide potential targets for novel treatment strategies of stress-related brain disorders.},
	Author = {Jo{\"e}ls, Marian and Karst, Henk and Alfarez, Deborah and Heine, Vivi M. and Qin, Yongjun and van Riel, Els and Verkuyl, Martin and Lucassen, Paul J. and Krugers, Harm J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1025-3890},
	Journal = {Stress},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {9617529},
	Number = {4},
	Organization = {SILS-CNS, University of Amsterdam, The Netherlands. joels\@science.uva.nl},
	Pages = {221-31},
	Pii = {H7L632V754R125V0},
	Pubmed = {16019587},
	Title = {Effects of chronic stress on structure and cell function in rat hippocampus and hypothalamus},
	Uuid = {F42CD4B1-1DE9-49FA-A80C-B2F5792ECCA5},
	Volume = {7},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1080/10253890500070005}}

@article{Johansson:1999,
	Abstract = {New neurons are continuously added in specific regions of the adult mammalian central nervous system. These neurons are derived from multipotent stem cells whose identity has been enigmatic. In this work, we present evidence that ependymal cells are neural stem cells. Ependymal cells give rise to a rapidly proliferating cell type that generates neurons that migrate to the olfactory bulb. In response to spinal cord injury, ependymal cell proliferation increases dramatically to generate migratory cells that differentiate to astrocytes and participate in scar formation. These data demonstrate that ependymal cells are neural stem cells and identify a novel process in the response to central nervous system injury.},
	Author = {Johansson, C. B. and Momma, S. and Clarke, D. L. and Risling, M. and Lendahl, U. and Frisen, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Cell},
	Keywords = {Stem Cells/cytology/*physiology;Astrocytes/cytology/physiology;Rats;Spinal Cord Injuries/physiopathology;Neurons/cytology/*physiology;Animal;Central Nervous System/*cytology;02 Adult neurogenesis migration;Mammals;Membrane Proteins/analysis;Heart Ventricle/cytology;Support, Non-U.S. Gov't;Spinal Cord/cytology;Olfactory Bulb/cytology;Mice;Cell Division;B-15;Biological Markers},
	Number = {1},
	Organization = {Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.},
	Pages = {25-34.},
	Title = {Identification of a neural stem cell in the adult mammalian central nervous system},
	Uuid = {7D641BB2-71AE-4780-B5FE-EBC6DB7F0AF8},
	Volume = {96},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9989494}}

@article{John:2003,
	Abstract = {It is now clear that cytokines function as powerful regulators of glial cell function in the central nervous system (CNS), either inhibiting or promoting their contribution to CNS pathology. Although these interactions are complex, the availability of animals with targeted deletions of these genes and/or their receptors, as well as transgenic mice in which cytokine expression has been targeted to specific cell types, and the availability of purified populations of glia that can be studied in vitro, has provided a wealth of interesting and frequently surprising data relevant to this activity. A particular feature of many of these studies is that it is the nature of the receptor that is expressed, rather than the cytokine itself, that regulates the functional properties of these cytokines. Because cytokine receptors are themselves modulated by cytokines, it becomes evident that the effects of these cytokines may change dramatically depending upon the cytokine milieu present in the immediate environment. An additional exciting aspect of these studies is the previously underappreciated role of these factors in repair to the CNS. In this review, we focus on current information that has helped to define the role of cytokines in regulating glial cell function as it relates to the properties of microglia and astrocytes.},
	Author = {John, Gareth R. and Lee, Sunhee C. and Brosnan, Celia F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {1073-8584},
	Journal = {Neuroscientist},
	Keywords = {Human;Tumor Necrosis Factor;Animals;Astrocytes;Transforming Growth Factor beta;review, tutorial;review;Interferon Type II;Microglia;11 Glia;Nerve Growth Factors;Support, Non-U.S. Gov't;Neuroglia;Interleukin-1;Support, U.S. Gov't, P.H.S.;Interleukin-6;Central Nervous System;Cell Death;Cytokines},
	Medline = {22467748},
	Month = {2},
	Nlm_Id = {9504819},
	Number = {1},
	Organization = {Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.},
	Pages = {10-22},
	Pubmed = {12580336},
	Title = {Cytokines: powerful regulators of glial cell activation},
	Uuid = {7CBEC163-6F9A-4AFB-A4C5-C71C525F41C2},
	Volume = {9},
	Year = {2003},
	url = {papers/John_Neuroscientist2003.pdf}}

@article{Johnson:2005,
	Abstract = {It has been suggested that germline stem cells maintain oogenesis in postnatal mouse ovaries. Here we show that adult mouse ovaries rapidly generate hundreds of oocytes, despite a small premeiotic germ cell pool. In considering the possibility of an extragonadal source of germ cells, we show expression of germline markers in bone marrow (BM). Further, BM transplantation restores oocyte production in wild-type mice sterilized by chemotherapy, as well as in ataxia telangiectasia-mutated gene-deficient mice, which are otherwise incapable of making oocytes. Donor-derived oocytes are also observed in female mice following peripheral blood transplantation. Although the fertilizability and developmental competency of the BM and peripheral blood-derived oocytes remain to be established, their morphology, enclosure within follicles, and expression of germ-cell- and oocyte-specific markers collectively support that these cells are bona fide oocytes. These results identify BM as a potential source of germ cells that could sustain oocyte production in adulthood.},
	Author = {Johnson, Joshua and Bagley, Jessamyn and Skaznik-Wikiel, Malgorzata and Lee, Ho-Joon J. and Adams, Gregor B. and Niikura, Yuichi and Tschudy, Katherine S. and Tilly, Jacqueline Canning and Cortes, Maria L. and Forkert, Randolf and Spitzer, Thomas and Iacomini, John and Scadden, David T. and Tilly, Jonathan L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Cell Cycle Proteins;Oogenesis;DNA-Binding Proteins;Animals;Mice, Mutant Strains;Bone Marrow Transplantation;Humans;Female;Oocytes;Ovary;Mice, Transgenic;Protein-Serine-Threonine Kinases;Bone Marrow;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Adult;Peripheral Blood Stem Cell Transplantation;Mice;Tumor Suppressor Proteins;22 Stem cells;Sterilization, Reproductive;Biological Markers;Research Support, N.I.H., Extramural;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {0413066},
	Number = {2},
	Organization = {Vincent Center for Reproductive Biology, Vincent Obstetrics and Gynecology Service, Harvard Medical School, Boston, Massachusetts 02114, USA.},
	Pages = {303-15},
	Pii = {S0092-8674(05)00650-1},
	Pubmed = {16051153},
	Title = {Oocyte generation in adult mammalian ovaries by putative germ cells in bone marrow and peripheral blood},
	Uuid = {78DE01CF-7CDB-4F6A-A339-51B21FC6F9CD},
	Volume = {122},
	Year = {2005},
	url = {papers/Johnson_Cell2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.06.031}}

@article{Johnston:2001,
	Abstract = {Human endogenous retroviruses (HERVs) have been implicated as causative agents in diseases characterized by inflammation and macrophage activation, such as multiple sclerosis. Because monocyte activation and differentiation influence retroviral transcription and replication, we investigated the contribution of these processes to the expression of four HERV families (HERV-W, HERV-K, HERV-E, and HERV-H) in human monocytes, and autopsied brain tissue from patients with brain diseases associated with increased macrophage activity. Reverse transcriptase-polymerase chain reaction analysis of primary macrophages and U937 monocytoid cells stimulated with phorbol-12-myristate-13-acetate or lipopolysaccharide revealed three- to ninefold increases in HERV-W, HERV-K, and HERV-H RNA levels. In addition, elevated reverse transcriptase activity and HERV RNA were detectable in supernatants from PMA-stimulated U937 cultures, properties that could be attenuated with the inhibitor of monocyte differentiation threonine-lysine-proline. In contrast, stimulation of monocytes decreased or had no effect on HERV-E expression. Compared with controls, HERV-W and HERV-K expression was increased in brain tissue from patients with multiple sclerosis or human immunodeficiency virus infection or AIDS, with concomitant elevated tumor necrosis factor-alpha levels. Similarly, elevated HERV-W levels were detected in patients with Alzheimer's dementia only when tumor necrosis factor-alpha expression was also evident (2 of 6 cases). The detection of several HERVs in inflammatory brain diseases and the capacity to augment HERV expression in monocytes with compounds that influence cellular activity suggest that increased expression of these viruses is a consequence of increased immune activity rather than causative of distinct diseases.},
	Author = {Johnston, J. B. and Silva, C. and Holden, J. and Warren, K. G. and Clark, A. W. and Power, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0364-5134},
	Journal = {Ann Neurol},
	Keywords = {RNA, Viral;Cell Differentiation;Monocytes;Encephalitis;U937 Cells;Middle Aged;Tumor Necrosis Factor-alpha;Phenotype;Humans;Brain;Female;15 Retrovirus mechanism;Lipopolysaccharides;Endogenous Retroviruses;Male;Reverse Transcriptase Polymerase Chain Reaction;Aged;Carcinogens;Tetradecanoylphorbol Acetate;Adult;24 Pubmed search results 2008;Gene Expression;15 ERVs retroelements;Research Support, Non-U.S. Gov't},
	Medline = {21487102},
	Month = {10},
	Nlm_Id = {7707449},
	Number = {4},
	Organization = {Department of Clinical Neurosciences, University of Calgary, Alberta, Canada.},
	Pages = {434-42},
	Pubmed = {11601494},
	Title = {Monocyte activation and differentiation augment human endogenous retrovirus expression: implications for inflammatory brain diseases},
	Uuid = {833A2DFF-4326-11DB-A5D2-000D9346EC2A},
	Volume = {50},
	Year = {2001}}

@article{Jolicoeur:2003,
	Abstract = {Some murine leukemia viruses (MuLVs), among them Cas-Br-E and ts-1 MuLVs, are neurovirulent, inducing spongiform myeloencephalopathy and hind limb paralysis in susceptible mice. It has been shown that the env gene of these viruses harbors the determinant of neurovirulence. It appears that neuronal loss occurs by an indirect mechanism, since the target motor neurons have not been found to be infected. However, the pathogenesis of the disease remains unclear. Several lymphokines, cytokines, and other cellular effectors have been found to be aberrantly expressed in the brains of infected mice, but whether these are required for the development of the neurodegenerative lesions is not known. In an effort to identify the specific effectors which are indeed required for the initiation and/or development of spongiform myeloencephalopathy, we inoculated gene-deficient (knockout [KO]) mice with ts-1 MuLV. We show here that interleukin-6 (IL-6), inducible nitric oxide synthetase (iNOS), ICE, Fas, Fas ligand (FasL), and TNF-R1 KO mice still develop signs of disease. However, transgenic mice overexpressing Bcl-2 in neurons (NSE/Bcl-2) were largely protected from hind limb paralysis and had less-severe spongiform lesions. These results indicate that motor neuron death occurs in this disease at least in part by a Bcl-2-inhibitable pathway not requiring the ICE, iNOS, Fas/FasL, TNF-R1, and IL-6 gene products.},
	Author = {Jolicoeur, Paul and Hu, Chunyan and Mak, Tak W. and Martinou, Jean-Claude C. and Kay, Denis G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Caspase 1;Nerve Degeneration;Animals;Central Nervous System Viral Diseases;Mice, Inbred C3H;Antigens, CD;Mice, Transgenic;Nitric-Oxide Synthase;Not relevant;11 Glia;Receptors, Tumor Necrosis Factor;Leukemia Virus, Murine;Proto-Oncogene Proteins c-bcl-2;Retroviridae Infections;Support, Non-U.S. Gov't;Membrane Glycoproteins;Mice, Knockout;Neurons;Mice;Interleukin-6;Antigens, CD95},
	Month = {12},
	Nlm_Id = {0113724},
	Number = {24},
	Organization = {Laboratory of Molecular Biology, Clinical Research Institute of Montreal, Montreal, Quebec H2W 1R7, Canada. jolicop\@ircm.qc.ca},
	Pages = {13161-70},
	Pubmed = {14645573},
	Title = {Protection against murine leukemia virus-induced spongiform myeloencephalopathy in mice overexpressing Bcl-2 but not in mice deficient for interleukin-6, inducible nitric oxide synthetase, ICE, Fas, Fas ligand, or TNF-R1 genes},
	Uuid = {16309A3E-ACCF-4545-A5BF-BFBEA465FA7A},
	Volume = {77},
	Year = {2003},
	url = {papers/Jolicoeur_JVirol2003.pdf}}

@article{Jones:1997,
	Abstract = {Brain lesions, even of the most subtle type, are accompanied by the activation of microglia, the main immune cells of the brain. Microglial cells dramatically increase in number through proliferation and adhere to the injured neurons, where they displace the synaptic input. After proliferation, microglia gradually migrate into the nearby parenchyma and appear to decrease in number. Here we examined the possible involvement of apoptosis in the regulation of the microglial cell number using Terminal transferase mediated d-UTP Nick End-Labelling (TUNEL). In vitro, cell death is a common phenomenon in microglial cell cultures, and is enhanced by the withdrawal of the mitogen, granulocyte-macrophage colony stimulating factor. In vivo, application of the TUNEL-reaction revealed TUNEL-positive microglia beginning at day 4, with a peak 7 days after transection of the facial nerve. Surprisingly, TUNEL-labelling in vivo was localized on the outer side of the nuclear membrane and in the microglial cytoplasm, with very little staining within the nucleus itself. These TUNEL-labelled cells also lacked other classic morphological signs of apoptosis, like membrane blebbing, chromatin condensation and apoptotic bodies. These data suggest that the regulation of post-mitotic microglia is not mediated by the classic pathway of apoptosis.},
	Author = {Jones, L. L. and Banati, R. B. and Graeber, M. B. and Bonfanti, L. and Raivich, G. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Facial Nerve;Homeostasis;Rats;Microscopy, Electron;Apoptosis;Immunohistochemistry;Rats, Wistar;DNA Nucleotidylexotransferase;11 Glia;Microglia;Animals, Newborn;Male;Brain;Axotomy;Cells, Cultured;Animals},
	Medline = {98086141},
	Month = {11},
	Nlm_Id = {0364620},
	Number = {11},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, Germany.},
	Pages = {755-70},
	Pubmed = {9426172},
	Title = {Population control of microglia: does apoptosis play a role?},
	Uuid = {99AFF81C-CE04-447A-9AB7-33387F3B1BCE},
	Volume = {26},
	Year = {1997}}

@article{Jones:2007,
	Abstract = {Periodic bursts of activity in the disinhibited in vitro hippocampal CA3 network spread through the neural population by the glutamatergic recurrent collateral axons that link CA3 pyramidal cells. It was previously proposed that these bursts of activity are terminated by exhaustion of releasable glutamate at the recurrent collateral synapses so that the next periodic burst of network activity cannot occur until the supply of glutamate has been replenished. As a test of this hypothesis, the rate of glutamate release at CA3 axon terminals was reduced by substitution of extracellular Ca(2+) with Sr(2+). Reduction of the rate of glutamate release reduces the rate of depletion and should thereby prolong bursts. Here we demonstrate that Sr(2+) substitution prolongs spontaneous bursts in the disinhibited adult CA3 hippocampal slices to 37.2 +/- 7.6 (SE) times the duration in control conditions. Sr(2+) also decreased the probability of burst initiation and the rate of burst onset, consistent with reduced synchrony of glutamate release and a consequent reduced rate of spread of excitation through the slice. These findings support the supply of releasable glutamate as an important determinant of the probability and duration of synchronous CA3 network activity.},
	Author = {Jones, Jethro and Stubblefield, Elizabeth A. and Benke, Timothy A. and Staley, Kevin J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:24 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {in vitro;Dose-Response Relationship, Drug;Animals;Rats;Glutamic Acid;21 Epilepsy;Periodicity;Rats, Sprague-Dawley;Hippocampus;Pyramidal Cells;Calcium;Male;Strontium;Nerve Net;Action Potentials;21 Neurophysiology;Picrotoxin;GABA Antagonists;21 Cortical oscillations;24 Pubmed search results 2008;Excitatory Postsynaptic Potentials},
	Month = {5},
	Nlm_Id = {0375404},
	Number = {5},
	Organization = {VBK 910, Neurology Department, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114. kstaley\@partners.org).},
	Pages = {3812-8},
	Pii = {01310.2006},
	Pubmed = {17344368},
	Title = {Desynchronization of Glutamate Release Prolongs Synchronous CA3 Network Activity},
	Uuid = {6D113FD7-A8B1-46EB-A7A7-4288F2392572},
	Volume = {97},
	Year = {2007},
	url = {papers/Jones_JNeurophysiol2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1152/jn.01310.2006}}

@article{Jones:2003,
	Abstract = {Increased expression of certain extracellular matrix (ECM) molecules after CNS injury is believed to restrict axonal regeneration. The chondroitin sulfate proteoglycans (CSPGs) are one such class of ECM molecules that inhibit neurite outgrowth in vitro and are upregulated after CNS injury. We examined growth responses of several classes of axons to this inhibitory environment in the presence of a cellular fibroblast bridge in a spinal cord lesion site and after a growth factor stimulus at the lesion site (fibroblasts genetically modified to secrete NGF). Immunohistochemical analysis showed dense labeling of the CSPGs NG2, brevican, neurocan, versican, and phosphacan at the host-lesion interface after spinal cord injury (SCI). Furthermore, robust expression of NG2, and to a lesser extent versican, was also observed throughout grafts of control and NGF-secreting fibroblasts. Despite this inhibitory milieu, several axonal classes penetrated control fibroblast grafts, including dorsal column sensory, rubrospinal, and nociceptive axons. Axon growth was amplified more in the presence of NGF-secreting grafts. Confocal microscopy demonstrated that axon growth was, paradoxically, preferentially associated with NG2-rich substrates in both graft types. NG2 expression also increased after sciatic nerve injury, wherein axons successfully regenerate. Cellular sources of NG2 in SCI and peripheral nerve lesion sites included Schwann cells and endothelial cells. Notably, these same cellular sources in lesion sites produced the cell adhesion molecules L1 and laminin, and these molecules all colocalized. Thus, axons grow along substrates coexpressing both inhibitory and permissive molecules, suggesting that regeneration is successful when local permissive signals balance and exceed inhibitory signals. 1529-2401 Journal Article},
	Author = {Jones, L. L. and Sajed, D. and Tuszynski, M. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci},
	Keywords = {Axons/drug effects/*physiology;Extracellular Matrix/metabolism;Cell Adhesion Molecules/biosynthesis;Nerve Regeneration/*physiology;Animals;Antigens/biosynthesis;Cells, Cultured;Rats;Nerve Growth Factor/biosynthesis/genetics/pharmacology;Sciatic Neuropathy/pathology/physiopathology;Female;Fibroblasts/cytology/metabolism/transplantation;Proteochondroitin Sulfates/biosynthesis/*metabolism;11 Glia;Disease Models, Animal;Support, Non-U.S. Gov't;Endothelium, Vascular/cytology/metabolism;Rats, Inbred F344;Cell Division/physiology;Spinal Cord Injuries/pathology/*physiopathology;Laminin/metabolism;Proteoglycans/biosynthesis;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Spinal Cord/metabolism/pathology;Graft Survival;Schwann Cells/cytology/metabolism;G pdf},
	Number = {28},
	Organization = {Department of Neurosciences, University of California-San Diego, La Jolla, California 92093, USA.},
	Pages = {9276-88},
	Pubmed = {14561854},
	Title = {Axonal regeneration through regions of chondroitin sulfate proteoglycan deposition after spinal cord injury: a balance of permissiveness and inhibition},
	Uuid = {C17C4CB8-2102-4AF9-AC2B-638BD58BCBAF},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14561854}}

@article{Jones:1993,
	Abstract = {To determine whether ecotropic murine leukemia virus (MuLV) envelope glycoproteins are sufficient to cause cell-to-cell fusion when expressed in the absence of virus production, we used an ecotropic MuLV, AKV, to construct env expression vectors that lack the gag and pol genes. The rat cell line XC, which undergoes cell-to-cell fusion upon infection with ecotropic MuLV, was transfected with wild-type env expression vectors, and high levels of syncytium formation resulted. Transfection of the murine cell line NIH 3T3 with expression vectors containing the wild-type or mutated env region did not result in syncytium formation. Immunoprecipitation analysis of the envelope glycoproteins expressed in NIH 3T3 and XC cells showed that the mature surface glycoprotein expressed in XC cells was of a much lower apparent molecular weight than that expressed in NIH 3T3 cells. Further characterization showed that most if not all of this difference was the result of differences in glycosylation. Finally, site-directed mutagenesis was used to introduce several conservative and nonconservative changes into the amino-terminal region of the transmembrane protein. Analysis of the effect of these mutations confirmed that this region is a fusion domain.},
	Author = {Jones, J. S. and Risser, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Viral Fusion Proteins;Animals;Recombinant Proteins;15 Retrovirus mechanism;Cell Fusion;Glycosylation;Protein Structure, Secondary;Viral Envelope Proteins;Research Support, U.S. Gov't, P.H.S.;3T3 Cells;Protein Processing, Post-Translational;Mice;AKR murine leukemia virus;DNA Mutational Analysis;Amino Acid Sequence;Mutagenesis, Site-Directed;Viral Matrix Proteins;24 Pubmed search results 2008;Molecular Sequence Data},
	Medline = {93100857},
	Month = {1},
	Nlm_Id = {0113724},
	Number = {1},
	Organization = {McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706.},
	Pages = {67-74},
	Pubmed = {8416389},
	Title = {Cell fusion induced by the murine leukemia virus envelope glycoprotein},
	Uuid = {020678A8-4327-11DB-A5D2-000D9346EC2A},
	Volume = {67},
	Year = {1993},
	url = {papers/Jones_JVirol1993.pdf}}

@article{Jones:2004,
	Abstract = {Precise timing of mitosis is essential for high-fidelity cell duplication. However, temporal measurements of the mitotic clock have been challenging. Here we present a fluorescent mitosis biosensor that monitors the time between nuclear envelope breakdown (NEB) and re-formation using parallel total internal reflection fluorescence (TIRF) microscopy. By tracking tens to hundreds of mitotic events per experiment, we found that the mitotic clock of unsynchronized rat basophilic leukemia cells has a marked precision with 80\%of cells completing mitosis in 32 +/- 6 min. This assay further allowed us to observe delays in mitotic timing at Taxol concentrations 100 times lower than previous minimal effective doses, explaining why Taxol is clinically active at low concentrations. Inactivation of the spindle checkpoint by targeting the regulator Mad2 with RNAi consistently shortened mitosis, providing direct evidence that the internal mitotic timing mechanism is much faster in cells that lack the checkpoint.},
	Author = {Jones, Joshua T. and Myers, Jason W. and Ferrell, James E. and Meyer, Tobias},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {Image Interpretation, Computer-Assisted;Cell Culture;Rats;Comparative Study;Cell Line;Microscopy, Video;validation studies;evaluation studies;Biosensing Techniques;Microscopy, Fluorescence;Mitosis;Equipment Failure Analysis;Animals;Support, Non-U.S. Gov't;Cell Nucleus;23 Technique;Equipment Design},
	Month = {3},
	Nlm_Id = {9604648},
	Number = {3},
	Organization = {Department of Molecular Pharmacology, W200 Clark, 318 Campus Drive, Stanford University Medical School, Stanford, California 94305, USA.},
	Pages = {306-12},
	Pii = {nbt941},
	Pubmed = {14990952},
	Title = {Probing the precision of the mitotic clock with a live-cell fluorescent biosensor},
	Uuid = {BBCF2F8E-1301-45DD-93A8-1B0AD2662908},
	Volume = {22},
	Year = {2004},
	url = {papers/Jones_NatBiotechnol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt941}}

@article{Jongstra:1981,
	Abstract = {In contrast to those of many other mouse strains, spleen cell cultures of 129/J mice do not release reverse transcriptase activity into the supernatant upon stimulation with bacterial lipopolysaccharide. We report here that lipopolysaccharide induced the expression of intracellular viral proteins in 129/J spleen cells. Furthermore, we found that stimulated spleen cells released retroviral particles. We conclude that 129/J mice are inducible with lipopolysaccharide but that the virus produced is a defective particle deficient in reverse transcriptase activity.},
	Author = {Jongstra, J. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {15 ERVs retroelements;Lipopolysaccharides;Animals;RNA-Directed DNA Polymerase;Retroviridae;Lymphocytes;Defective Viruses;Viral Proteins;15 Retrovirus mechanism;Cells, Cultured;Mice;24 Pubmed search results 2008;Lymphocyte Activation;Antigens, Viral},
	Medline = {81194905},
	Month = {3},
	Nlm_Id = {0113724},
	Number = {3},
	Pages = {1044-50},
	Pubmed = {6164797},
	Title = {Lipopolysaccharide induces retroviral antigen expression in 129/J mouse lymphocytes: evidence for assembly of a defective viral particle},
	Uuid = {BE00E952-48FB-405D-B44A-1F6BA00D4B6D},
	Volume = {37},
	Year = {1981}}

@article{Juan:1996,
	Abstract = {It was observed before that DNA in situ in chromatin of mitotic cells is more sensitive to denaturation than DNA in chromatin of interphase cells. DNA sensitivity to denaturation, in these studies, was analyzed by exposing cells to heat or acid and using acridine orange (AO), the metachromatic fluorochrome which can differentially stain double-stranded (ds) vs single-stranded (ss) nucleic acids, as a marker of the degree of DNA denaturation. However, without prior cell treatment with heat or acid no presence of single-stranded DNA in either mitotic or interphase cells was detected by this assay. In the present experiments we demonstrate that DNA in situ in mitotic cells, without any prior treatment that can induce DNA denaturation, is sensitive to ss-specific S1 and mung bean nucleases. Incubation of permeabilized human T cell leukemic MOLT-4, promyelocytic HL-60, histiomonocytic lymphoma U937 cells, or normal PHA-stimulated lymphocytes with S1 or mung bean nucleases generated extensive DNA breakage in mitotic cells. DNA strand breaks were detected using fluorochrome-labeled triphosphonucleotides in the reaction catalyzed by exogenous terminal deoxynucleotidyl transferase. Under identical conditions of the cells' exposure to ss-specific nucleases, DNA breakage in interphase cells was of an order of magnitude less extensive compared to mitotic cells. The data indicate that segments of DNA in mitotic chromosomes, in contrast to interphase cells, may be in a conformation which is sensitive to ss nucleases. This may be a reflection of the differences in the torsional stress of DNA loops between interphase and mitotic chromatin. Namely, greater stress in mitotic loops may lead to formation of the hairpin-loop structures by inverted repeats; such structures are sensitive to ss nucleases. The present method of detection of such segments appears to be more sensitive than the use of AO. The identification of mitotic cells based on sensitivity of their DNA to ss nucleases provides an additional method for their quantification by flow cytometry.},
	Author = {Juan, G. and Pan, W. and Darzynkiewicz, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0014-4827},
	Journal = {Exp Cell Res},
	Keywords = {23 dNTPs-Brdu;Fluorescent Dyes;Interphase;Chromatin;Humans;Lymphocytes;Mitosis;Aspergillus Nuclease S1;23 Technique;DNA, Single-Stranded;Research Support, U.S. Gov't, P.H.S.;Tumor Cells, Cultured;Leukemia, Promyelocytic, Acute;Flow Cytometry;Nucleic Acid Denaturation;Uridine Triphosphate;24 Pubmed search results 2008;Bromodeoxyuridine;DNA Fragmentation;Research Support, Non-U.S. Gov't},
	Medline = {96428453},
	Month = {9},
	Nlm_Id = {0373226},
	Number = {2},
	Organization = {Cancer Research Institute, New York Medical College, Valhalla 10595, USA.},
	Pages = {197-202},
	Pii = {S0014482796902670},
	Pubmed = {8831556},
	Title = {DNA segments sensitive to single-strand-specific nucleases are present in chromatin of mitotic cells},
	Uuid = {6003D77A-B17A-465C-8990-004D63E3FE29},
	Volume = {227},
	Year = {1996},
	url = {papers/Juan_ExpCellRes1996.pdf}}

@article{Julien:1974,
	Author = {Julien, R. M. and Laxer, K. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0013-4694},
	Journal = {Electroencephalogr Clin Neurophysiol},
	Keywords = {Penicillins;Epilepsy;Purkinje Cells;Electroencephalography;Cerebellar Cortex;21 Neurophysiology;Cats;21 Epilepsy;Neural Pathways;Disease Models, Animal;Animals;Cerebral Cortex;Cerebellar Nuclei;24 Pubmed search results 2008},
	Medline = {74266348},
	Month = {8},
	Nlm_Id = {0375035},
	Number = {2},
	Pages = {123-32},
	Pubmed = {4135018},
	Title = {Cerebellar responses to penicillin-induced cerebral cortical epileptiform discharge},
	Uuid = {E5869FA4-882E-45BE-BDE7-185C56C61E5C},
	Volume = {37},
	Year = {1974}}

@article{Jung:2000,
	Abstract = {The seven-transmembrane receptor CX(3)CR1 is a specific receptor for the novel CX(3)C chemokine fractalkine (FKN) (neurotactin). In vitro data suggest that membrane anchoring of FKN, and the existence of a shed, soluble FKN isoform allow for both adhesive and chemoattractive properties. Expression on activated endothelium and neurons defines FKN as a potential target for therapeutic intervention in inflammatory conditions, particularly central nervous system diseases. To investigate the physiological function of CX(3)CR1-FKN interactions, we generated a mouse strain in which the CX(3)CR1 gene was replaced by a green fluorescent protein (GFP) reporter gene. In addition to the creation of a mutant CX(3)CR1 locus, this approach enabled us to assign murine CX(3)CR1 expression to monocytes, subsets of NK and dendritic cells, and the brain microglia. Analysis of CX(3)CR1-deficient mice indicates that CX(3)CR1 is the only murine FKN receptor. Yet, defying anticipated FKN functions, absence of CX(3)CR1 interferes neither with monocyte extravasation in a peritonitis model nor with DC migration and differentiation in response to microbial antigens or contact sensitizers. Furthermore, a prominent response of CX(3)CR1-deficient microglia to peripheral nerve injury indicates unimpaired neuronal-glial cross talk in the absence of CX(3)CR1.},
	Author = {Jung, S. and Aliberti, J. and Graemmel, P. and Sunshine, M. J. and Kreutzberg, G. W. and Sher, A. and Littman, D. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0270-7306},
	Journal = {Mol Cell Biol},
	Keywords = {Receptors, Cytokine;Luminescent Proteins;Receptors, HIV;Mutagenesis, Insertional;Research Support, Non-U.S. Gov't;Phenotype;Gene Expression;Mice, Mutant Strains;11 Glia;Gene Targeting;Green Fluorescent Proteins;Mice;Genes, Reporter;Animals},
	Medline = {20266298},
	Month = {6},
	Nlm_Id = {8109087},
	Number = {11},
	Organization = {Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute New York University Medical Center, New York, New York 10016, USA. jung\@saturn.med.nyu.edu},
	Pages = {4106-14},
	Pubmed = {10805752},
	Title = {Analysis of fractalkine receptor CX(3)CR1 function by targeted deletion and green fluorescent protein reporter gene insertion},
	Uuid = {03D24E18-43DD-4A75-A408-600AF9B50F9C},
	Volume = {20},
	Year = {2000},
	url = {papers/Jung_MolCellBiol2000.pdf}}

@article{Justice:2003,
	Abstract = {The tumor suppressor genes lethal giant larvae (lgl) and discs large (dlg) act together to maintain the apical basal polarity of epithelial cells in the Drosophila embryo. Neuroblasts that delaminate from the embryonic epithelium require lgl to promote formation of a basal Numb and Prospero crescent, which will be asymmetrically segregated to the basal daughter cell upon division to specify cell fate. Sensory organ precursors (SOPs) also segregate Numb asymmetrically at cell division. Numb functions to inhibit Notch signaling and to specify the fates of progenies of the SOP that constitute the cellular components of the adult sensory organ. We report here that, in contrast to the embryonic neuroblast, lgl is not required for asymmetric localization of Numb in the dividing SOP. Nevertheless, mosaic analysis reveals that lgl is required for cell fate specification within the SOP lineage; SOPs lacking Lgl fail to specify internal neurons and glia. Epistasis studies suggest that Lgl acts to inhibit Notch signaling by functioning downstream or in parallel with Numb. These findings uncover a previously unknown function of Lgl in the inhibition of Notch and reveal different modes of action by which Lgl can influence cell fate in the neuroblast and SOP lineages. 0960-9822 Journal Article},
	Author = {Justice, N. and Roegiers, F. and Jan, L. Y. and Jan, Y. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Curr Biol},
	Keywords = {10 Development;F},
	Number = {9},
	Organization = {Department of Physiology, Howard Hughes Medical Institute, University of California, San Francisco, 533 Parnassus Avenue, San Francisco, CA 94143-0725, USA.},
	Pages = {778-83},
	Pubmed = {12725738},
	Title = {Lethal giant larvae acts together with numb in notch inhibition and cell fate specification in the Drosophila adult sensory organ precursor lineage},
	Uuid = {13D321DA-99E3-46CB-B4F2-3BA2451ADB39},
	Volume = {13},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12725738}}

@article{Kacza:1997,
	Abstract = {OBJECTIVES AND METHODS: A fluorescence and electron microscopical approach, based on the transection of the rat optic nerve and the axotomy-induced transcellular labelling of activated retinal microglial cells, using the carbocyanine dye 4Di-10ASP, was employed to monitor phagocytosis in the injured central nervous system. After survival times ranging between two days up to three months, retinal flat-mounts were inspected and photoconverted. RESULTS: Fluorescence microscopy revealed that within a few days microglia became transcellularly stained due to the phagocytosed 4Di-10ASP-labelled neuronal debris. Ultrastructural analysis confirmed that marked ganglion cell-derived material was incorporated into phagosomes of various sizes. Though immediate phagocytic intake was not observed, the nature of the detected phagosomes suggests that small fractions of degenerated neurons are incorporated. CONCLUSIONS: The approach presented, utilizing function-dependent transcellular fluorescent labelling of phagocytic microglia, might enrich further experimental studies of glia-neuron interactions in the injured nervous system.},
	Author = {Kacza, J. and Seeger, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {1023-3830},
	Journal = {Inflamm Res},
	Keywords = {Retina;Cell Membrane;Neuroglia;Nerve Degeneration;Rats;Microscopy, Electron;Phagocytes;Not relevant;11 Glia;Microscopy, Fluorescence;Optic Nerve;Retinal Ganglion Cells;Support, Non-U.S. Gov't;Animals;Axotomy},
	Medline = {98039588},
	Month = {10},
	Nlm_Id = {9508160},
	Number = {10},
	Organization = {Institute of Veterinary Anatomy, University of Leipzig, Germany. kacza\@vetmed.uni-leipzig.de},
	Pages = {430-3},
	Pubmed = {9372319},
	Title = {Transcellular labelling of activated retinal microglia following transection of the optic nerve},
	Uuid = {29F1FFB2-31AE-45FA-A67C-F450A418284E},
	Volume = {46},
	Year = {1997}}

@article{Kageyama:2000,
	Abstract = {For embryos that have small pancreas and lack brain, eyes and thymus, the defects are caused by mutation of a single gene, Hes1. Hes1 encodes a basic helix-loop-helix (bHLH) transcriptional repressor and functionally antagonizes positive bHLH genes such as the neuronal determination gene, Mash1. Misexpression of Hes1 inhibits cell differentiation and keeps cells at the precursor stage or proliferative stage. Conversely, in the absence of Hes1, the expression of positive bHLH genes is upregulated and cells differentiate prematurely without sufficient cell growth. As a result, the development of many tissues such as the brain, eye and pancreas is severely affected. Thus, Hes1 regulates tissue morphogenesis by maintaining undifferentiated cells. In the case of T cell development, Hes1 mutation leads to defects of expansion of early T cell precursors and thereby suppresses T cell fate specification. Thus, Hes1 promotes differentiation of some cell types in addition to maintenance of the undifferentiated state. Interestingly, Hes1 expression is controlled by the transmembrane protein Notch, which is activated by the ligands expressed on the surface of neighboring cells. Taken together, these results indicate that the Notch-Hes1 pathway, which is controlled by cell-cell interaction, plays an essential role in differentiation of many cell types.},
	Author = {Kageyama, R. and Ohtsuka, T. and Tomita, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Mol Cells},
	Keywords = {Muscle Proteins/genetics/*physiology;Nervous System/cytology;T-Lymphocytes/cytology;Sequence Homology, Amino Acid;Molecular Sequence Data;Human;Transcription Factors/genetics/*physiology;Endocrine System/cytology;Animal;Amino Acid Sequence;04 Adult neurogenesis factors;Muscles/cytology;Exocrine Glands/cytology;Support, Non-U.S. Gov't;DNA-Binding Proteins/genetics/*physiology;Cell Differentiation/physiology;C abstr},
	Number = {1},
	Organization = {Institute for Virus Research, Kyoto University, Japan. rkageyam\@virus.kyoto-u.ac.jp},
	Pages = {1-7.},
	Title = {The bHLH gene Hes1 regulates differentiation of multiple cell types},
	Uuid = {F5F46DA0-8457-4B8A-8BCA-D5FC720E8618},
	Volume = {10},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10774739}}

@article{Kakita:2001,
	Abstract = {The postnatal subventricular zone (SVZ) gives rise to many of the glial cells in the forebrain. We investigated migration pathways and dynamics of motility of progenitors from the neonatal rat forebrain SVZ by labeling progenitors in vivo with a retrovirus encoding green fluorescent protein (GFP) and then visualizing the dynamics of their movements by time-lapse fluorescence microscopy in slice preparations. Cells within the dorso-lateral SVZ moved in an apparently undirected fashion, but migrated in a directed manner after emigration into white matter and cortex, displaying both radial and tangential migration. Cells in the striatal-SVZ, a region of SVZ along the lateral wall of the ventricle, migrated parallel to the ventricular surface, and entered the striatum, where they migrated both perpendicular and parallel to the ventricular surface. Sometimes, cells in all these regions reversed their migration back toward the SVZ. Migration involved either elongation of the leading process followed by a quick translocation of the nucleus or a synchronous advancement of the nucleus and the leading process. Two distinct patterns of cellular changes were observed at orthogonal turning: one involves the cessation of cell body movement and the formation of a new leading process, and the other involves continuous cell body movement and bending of the leading process. The dynamic behavior of progenitors may reflect local tissue architecture and contribute to the widespread distribution of glia.},
	Author = {Kakita, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Hum Cell},
	Keywords = {G abstr;11 Glia},
	Number = {1},
	Organization = {Department of Pathology, Brain Disease Research Center, Brain Research Institute, Niigata University. kakita\@bri.niigata-u.ac.jp},
	Pages = {59-75.},
	Title = {Migration pathways and behavior of glial progenitors in the postnatal forebrain},
	Uuid = {7F14D824-14ED-48F3-B9ED-95E85086F394},
	Volume = {14},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11436354}}

@article{Kakita:2003,
	Abstract = {Transplacental administration of methylmercury (MeHg) induces disruption of neuronal migration in the developing cerebral cortex. However, the effects of MeHg on glial progenitor migration remain unclear. To understand this, we performed double administration of MeHg and 5-bromo-2-deoxyuridine (BrdU) to neonatal rat pups on postnatal day 2 (P2), when glial cells are generated from progenitors in the subventricular zone (SVZ). Histopathological examination of a proportion of the MeHg-treated rats on P28 revealed no apparent abnormalities of cytoarchitecture or neuron count in either the primary motor or primary somatosensory cortex of the cerebrum. BrdU immunohistochemistry revealed abnormal accumulation of the labeled cells in the deeper layers of the cortices and underlying white matter of both areas, where an excessive number of astrocytes (glial fibrillary acidic protein- or S-100beta-immunolabeled cells) and oligodendrocytes (2',3'-cyclic-nucleotide 3'-phosphohydrolase-labeled cells) were located. Next, to investigate the migration of individual progenitors from the forebrain SVZ of P2 neonates, we labeled them in vivo with a retrovirus encoding green fluorescent protein (GFP), following administration of MeHg, and then examined the distribution pattern of the GFP-labeled cells in the P28 cerebrum. We found that the labeled cells developed into astrocytes and oligodendrocytes and were accumulated abnormally in the lateral white matter as well as in the adjacent deeper layer of the lateral cortex and lateral side of the striatum. Thus, exposure to MeHg in the gliogenic period induced irregular distribution of glia as a consequence of abnormal migration of the postnatal progenitors.},
	Author = {Kakita, Akiyoshi and Inenaga, Chikanori and Sakamoto, Mineshi and Takahashi, Hitoshi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Research Support, Non-U.S. Gov't;Tissue Distribution;Animals;Kidney;Aging;Rats;Comparative Study;Cell Count;Telencephalon;Cell Movement;Liver;Rats, Wistar;Nerve Growth Factors;Animals, Newborn;Methylmercury Compounds;Neuroglia;Neurons;Cerebellum;24 Pubmed search results 2008;Bromodeoxyuridine;Stem Cells;S100 Proteins;Brain Stem;Glial Fibrillary Acidic Protein},
	Medline = {22865166},
	Month = {8},
	Nlm_Id = {2985192R},
	Number = {8},
	Organization = {Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Asahimachi, Niigata, Japan. kakita\@bri.niigata-u.ac.jp},
	Pages = {835-47},
	Pubmed = {14503639},
	Title = {Disruption of postnatal progenitor migration and consequent abnormal pattern of glial distribution in the cerebrum following administration of methylmercury},
	Uuid = {5088C32F-81A2-4750-8253-EE9DD05F3F2C},
	Volume = {62},
	Year = {2003}}

@article{Kakita:1999,
	Abstract = {Glial progenitors colonize the CNS widely in the perinatal period, but the pathways and mechanisms of migration are not well understood. We investigated the migration of progenitors from the neonatal rat forebrain subventricular zone (SVZ) by labeling them in vivo with a retrovirus encoding green fluorescent protein and visualizing movements by time lapse microscopy in slices. Cells within the dorsolateral SVZ moved in an undirected fashion but migrated radially and tangentially after emigration into white matter, cortex, and striatum. Cells in the striatal SVZ migrated parallel to the ventricular surface. During migration, elongation of the leading process and nuclear translocation were independent or linked. Orthogonal turning involved either cessation of cell body movement and formation of a new leading process or continuous cell body movement and bending of the leading process.},
	Author = {Kakita, A. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Neuron},
	Keywords = {Rats;Transfection;Cell Movement/*physiology;Animal;Indicators and Reagents;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Cerebral Cortex/cytology/growth &development;Retroviridae;Stem Cells/*cytology;Animals, Newborn;Prosencephalon/*cytology/*growth &development;B-17;Support, U.S. Gov't, P.H.S.;Neuroglia/*cytology;Luminescent Proteins;Organ Culture;Corpus Striatum/cytology/growth &development},
	Number = {3},
	Organization = {Department of Pathology and The Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. ak463\@columbia.edu},
	Pages = {461-72.},
	Title = {Patterns and dynamics of SVZ cell migration in the postnatal forebrain: monitoring living progenitors in slice preparations},
	Uuid = {B59BBF33-8944-45AD-925B-95412E4FD0F7},
	Volume = {23},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10433259}}

@article{Kalberer:2000,
	Abstract = {Transcriptional silencing of genes transferred into hematopoietic stem cells poses one of the most significant challenges to the success of gene therapy. If the transferred gene is not completely silenced, a progressive decline in gene expression as the mice age often is encountered. These phenomena were observed to various degrees in mouse transplant experiments using retroviral vectors containing a human beta-globin gene, even when cis-linked to locus control region derivatives. Here, we have investigated whether ex vivo preselection of retrovirally transduced stem cells on the basis of expression of the green fluorescent protein driven by the CpG island phosphoglycerate kinase promoter can ensure subsequent long-term expression of a cis-linked beta-globin gene in the erythroid lineage of transplanted mice. We observed that 100\%of mice (n = 7) engrafted with preselected cells concurrently expressed human beta-globin and the green fluorescent protein in 20-95\%of their RBC for up to 9.5 mo posttransplantation, the longest time point assessed. This expression pattern was successfully transferred to secondary transplant recipients. In the presence of beta-locus control region hypersensitive site 2 alone, human beta-globin mRNA expression levels ranged from 0.15\%to 20\%with human beta-globin chains detected by HPLC. Neither the proportion of positive blood cells nor the average expression levels declined with time in transplanted recipients. Although suboptimal expression levels and heterocellular position effects persisted, in vivo stem cell gene silencing and age-dependent extinction of expression were avoided. These findings support the further investigation of this type of vector for the gene therapy of human hemoglobinopathies.},
	Author = {Kalberer, C. P. and Pawliuk, R. and Imren, S. and Bachelot, T. and Takekoshi, K. J. and Fabry, M. and Eaves, C. J. and London, I. M. and Humphries, R. K. and Leboulch, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Erythrocytes;Transcription, Genetic;Animals;Globins;comment;Humans;Transfection;Mice, Inbred C3H;Mice, Inbred C57BL;Recombinant Fusion Proteins;Retroviridae;Time Factors;11 Glia;Green Fluorescent Proteins;RNA, Messenger;Mice, Inbred Strains;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Genetic Vectors;Hematopoietic Stem Cell Transplantation;Locus Control Region;Gene Silencing;Mice;Hematopoietic Stem Cells;Luminescent Proteins;Phosphoglycerate Kinase;Promoter Regions (Genetics);Research Support, Non-U.S. Gov't},
	Medline = {20266379},
	Month = {5},
	Nlm_Id = {7505876},
	Number = {10},
	Organization = {The Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, BC, Canada Y5Z 1L3.},
	Pages = {5411-5},
	Pii = {100082597},
	Pubmed = {10792053},
	Title = {Preselection of retrovirally transduced bone marrow avoids subsequent stem cell gene silencing and age-dependent extinction of expression of human beta-globin in engrafted mice},
	Uuid = {01E9A09C-4F1A-473F-9DE4-A7A7D5C93C95},
	Volume = {97},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.100082597}}

@article{Kalman:1991,
	Abstract = {The majority of astroglia develop postnatally in rats. GFAP (glial fibrillary acidic protein)-immunoreactivity appears mainly during the 2nd and 3rd postnatal weeks throughout the brain. Hypothyroidism inhibits, among others, the cell proliferation, maturation, and migration of neurons. However, hardly any data on the effect of hypothyroidism on GFAP-immunoreactivity are available in the literature. In our experiments, thyroidectomy was performed between the 3rd and 5th postnatal days. Operated and control animals from the same litter were perfused transcardially and processed for immunohistochemistry in parallel after 2, 3, and 4 wk. On the basis of serial sections, the development of GFAP-immunoreactivity was not generally affected by hypothyroidism. We could observe only two phenomena that showed a tendency of retardation in the operated animals: (1) the decrease of the strong GFAP-immunopositivity of white matter tracts (for example, internal capsule and pyramidal tract) and (2) the gradual disappearance of the GFAP-immunoreactive radial fibers (for example, in the neocortex, in the olfactory bulb, and around the 3rd ventricle).},
	Author = {Kalman, M. and Moskovkin, G. N. and Martinez, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Mol Chem Neuropathol},
	Keywords = {Organ Specificity;Aging;*Thyroidectomy;Reference Values;Rats;Immunohistochemistry;Hypothyroidism/physiopathology;Animal;11 Glia;Glial Fibrillary Acidic Protein/*metabolism;Animals, Newborn;Immunoenzyme Techniques;G-need;Brain/cytology/*growth &development/metabolism;Astrocytes/cytology/metabolism/*physiology},
	Number = {2},
	Organization = {1st Dept of Anatomy, Semmelweis University of Medicine, Budapest, Hungary.},
	Pages = {103-16.},
	Title = {Development of glial fibrillary acidic protein immunoreactivity in thyroidectomized rats},
	Uuid = {761CA0F0-E3AC-46C2-B78C-89499C7204FB},
	Volume = {15},
	Year = {1991},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1776989}}

@article{Kaltschmidt:2000,
	Abstract = {The asymmetric segregation of cell-fate determinants and the generation of daughter cells of different sizes rely on the correct orientation and position of the mitotic spindle. In the Drosophila embryo, the determinant Prospero is localized basally and is segregated equally to daughters of similar cell size during epidermal cell division. In contrast, during neuroblast division Prospero is segregated asymmetrically to the smaller daughter cell. This simple switch between symmetric and asymmetric segregation is achieved by changing the orientation of cell division: neural cells divide in a plane perpendicular to that of epidermoblast division. Here, by labelling mitotic spindles in living Drosophila embryos, we show that neuroblast spindles are initially formed in the same axis as epidermal cells, but rotate before cell division. We find that daughter cells of different sizes arise because the spindle itself becomes asymmetric at anaphase: apical microtubules elongate, basal microtubules shorten, and the midbody moves basally until it is positioned asymmetrically between the two spindle poles. This observation contradicts the widely held hypothesis that the cleavage furrow is always placed midway between the two centrosomes. 20089045 1465-7392 Journal Article},
	Author = {Kaltschmidt, J. A. and Davidson, C. M. and Brown, N. H. and Brand, A. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Nat Cell Biol},
	Keywords = {10 Development;Stem Cells/cytology/physiology;Prophase/physiology;Nervous System/cytology/growth &development;Tubulin/analysis;Neurons/*cytology/physiology;Metaphase/physiology;Microscopy, Confocal;Phosphorylation;Rotation;Animal;Histones/analysis/metabolism;Mitotic Spindle Apparatus/chemistry/*physiology;Support, Non-U.S. Gov't;Anaphase/physiology;Drosophila/cytology/*growth &development;Epidermis/cytology/growth &development;F;Interphase/physiology},
	Number = {1},
	Organization = {Wellcome/CRC Institute and Department of Genetics, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK.},
	Pages = {7-12},
	Pubmed = {10620800},
	Title = {Rotation and asymmetry of the mitotic spindle direct asymmetric cell division in the developing central nervous system},
	Uuid = {0CC3007C-1A17-43F8-ABAE-E007136F1ACC},
	Volume = {2},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10620800}}

@article{Kamei:1998,
	Abstract = {Although accumulating data reveal patterns of proliferation, migration, and differentiation of neuronal lineage cells in the developing brain, gliogenesis in the brain has not been well elucidated. In the rat brain, vimentin is selectively expressed in radial glia and in their progeny, not in oligodendrocytes or neurons from embryonic day 15 (E15) until postnatal day 15 (P15). Here we examined mitotic radial glial lineage cells in the rat brain E17-P7, using the monoclonal antibody 4A4, which recognizes vimentin phosphorylated by a mitosis-specific kinase, cdc2 kinase. In the neocortex, mainly radial glia in the ventricular zone, but not their progeny, underwent cell division. In contrast, not only radial glia but also various types of radial glial progeny including Bergmann glia continued to proliferate in the cerebellum. Radial glia in the neocortex divided horizontally, obliquely, and vertically against the ventricular surface. The percentage of the vertical division increased with progress in the stage of development, concurrently with the decrease of the population of horizontal divisions. Thus, the monoclonal antibody 4A4 provides an useful tool to label mitotic glia in the developing brain and revealed different patterns of gliogenesis in the neocortex and cerebellum. A possibility is discussed that the dynamics of mitotic orientation observed here may be related to the change of the pattern of gliogenesis during development.},
	Author = {Kamei, Y. and Inagaki, N. and Nishizawa, M. and Tsutsumi, O. and Taketani, Y. and Inagaki, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Glia},
	Keywords = {G;Protein p34cdc2/metabolism;Neuroglia/chemistry/classification/*cytology;Rats;Phosphorylation;Mitosis;Animal;Neocortex/cytology/embryology/growth &development;Cell Polarity;11 Glia;Support, Non-U.S. Gov't;Cell Lineage;Astrocytes/cytology/metabolism;Vimentin/*analysis/immunology/metabolism;Phosphoproteins/*analysis/metabolism;Cerebellum/cytology/embryology/growth &development;Protein Processing, Post-Translational;Nerve Tissue Proteins/*analysis/metabolism;Brain/*cytology/embryology/growth &development;Biological Markers;Peptide Fragments/immunology;Enzyme-Linked Immunosorbent Assay;Antibodies, Monoclonal/immunology},
	Number = {3},
	Organization = {Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Japan.},
	Pages = {191-9.},
	Title = {Visualization of mitotic radial glial lineage cells in the developing rat brain by Cdc2 kinase-phosphorylated vimentin},
	Uuid = {1164A408-E5B1-47CA-A385-AB9FB21B45F2},
	Volume = {23},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9633804}}

@article{Kaneko:2000,
	Abstract = {In situ detection of neural progenitor cells including stem-like cells is essential for studying the basic mechanisms of the generation of cellular diversity in the CNS, upon which therapeutic treatments for CNS injuries, degenerative diseases, and brain tumors may be based. We have generated rat monoclonal antibodies (Mab 14H1 and 14B8) that recognize an RNA-binding protein Musashi1, but not a Musashi1-related protein, Musashi2. The amino acid sequences at the epitope sites of these anti-Musashi1 Mabs are remarkably conserved among the human, mouse, and Xenopus proteins. Spatiotemporal patterns of Musashi1 immunoreactivity in the developing and/or adult CNS tissues of frogs, birds, rodents, and humans indicated that our anti-Musashi1 Mabs reacted with undifferentiated, proliferative cells in the CNS of all the vertebrates tested. Double or triple immunostaining of embryonic mouse brain cells in monolayer cultures demonstrated strong Musashi1 expression in Nestin(+)/RC2(+) cells. The relative number of Musashi1(+)/Nestin(+)/RC2(+) cells increased fivefold when embryonic forebrain cells were cultured to form 'neurospheres'in which stem-like cells are known to be enriched through their self-renewing mode of growth. Nestin(+)/RC2(-) cells, which included Talpha1-GFP(+) neuronal progenitor cells and GLAST(+) astroglial precursor cells, were also Musashi1(+), as were GFAP(+) astrocytes. Young neurons showed a trace of Musashi1 expression. Cells committed to the oligodendroglial lineage were Musashi(-). Musashi1 was localized to the perikarya of CNS stem-like cells and non-oligodendroglial progenitor cells without shifting to cell processes or endfeet, and is therefore advantageous for identifying each cell and counting cells in situ. 20125908 0378-5866 Journal Article},
	Author = {Kaneko, Y. and Sakakibara, S. and Imai, T. and Suzuki, A. and Nakamura, Y. and Sawamoto, K. and Ogawa, Y. and Toyama, Y. and Miyata, T. and Okano, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Dev Neurosci},
	Keywords = {Central Nervous System/*cytology/*embryology/metabolism;Tissue Distribution;Animal;Cytological Techniques;02 Adult neurogenesis migration;RNA-Binding Proteins/genetics/*metabolism;Amino Acid Sequence/genetics;Nerve Tissue Proteins/genetics/*metabolism;BB abstr;03 Adult neurogenesis progenitor source;Evolution;Chick Embryo;Conserved Sequence/genetics;Xenopus/embryology;Antibodies, Monoclonal;Support, Non-U.S. Gov't;Mice/embryology;Epitopes;Neurons/metabolism;Molecular Sequence Data;Stem Cells/*metabolism;Genetic Markers},
	Number = {1-2},
	Organization = {Division of Neuroanatomy, Department of Neuroscience, Biomedical Research Center, Osaka University Graduate School of Medicine, Tokyo, Japan.},
	Pages = {139-53},
	Pubmed = {10657706},
	Title = {Musashi1: an evolutionally conserved marker for CNS progenitor cells including neural stem cells},
	Uuid = {CC6898D6-0650-4F57-A7A0-7512A1E92B35},
	Volume = {22},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10657706}}

@article{Kaneko:2006,
	Abstract = {Neurogenesis in the subgranular zone of the hippocampal dentate gyrus and olfactory bulbs continues into adulthood and has been implicated in the cognitive function of the adult brain. The basal forebrain cholinergic system has been suggested to play a role in regulating neurogenesis as well as learning and memory in these regions. Herein, we report that highly polysialylated neural cell adhesion molecule (PSA-NCAM)-positive immature cells as well as neuronal nuclei (NeuN)-positive mature neurons in the dentate gyrus and olfactory bulb express multiple acetylcholine receptor subunits and make contact with cholinergic fibers. To examine the function of acetylcholine in neurogenesis, we used donepezil (Aricept), a potent and selective acetylcholinesterase inhibitor that improves cognitive impairment in Alzheimer's disease. Intraperitoneal administrations of donepezil significantly enhanced the survival of newborn neurons, but not proliferation of neural progenitor cells in the subgranular zone or the subventricular zone of normal mice. Moreover, donepezil treatment reversed the chronic stress-induced decrease in neurogenesis. Taken together, these results suggest that activation of the cholinergic system promotes survival of newborn neurons in the adult dentate gyrus and olfactory bulb under both normal and stressed conditions.},
	Author = {Kaneko, Naoko and Okano, Hideyuki and Sawamoto, Kazunobu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1356-9597},
	Journal = {Genes Cells},
	Keywords = {24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {9607379},
	Number = {10},
	Organization = {Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.},
	Pages = {1145-59},
	Pii = {GTC1010},
	Pubmed = {16999735},
	Title = {Role of the cholinergic system in regulating survival of newborn neurons in the adult mouse dentate gyrus and olfactory bulb},
	Uuid = {BF122FB5-F258-4BBF-907B-98C4E2067C42},
	Volume = {11},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1365-2443.2006.01010.x}}

@article{Kanmogne:2002,
	Abstract = {Breakdown of the blood-brain barrier is commonly seen in patients with human immunodeficiency virus (HIV)-associated dementia, despite the lack of productive HIV-infection of the brain endothelium. Through this damaged blood-brain barrier, HIV and HIV-infected monocytes/macrophages infiltrate the brain and further infect microglia and brain macrophages. Neuronal cell death and dysfunction are the underlying cause of HIV-associated dementia, but no productive HIV-infection of neurons has been documented. It is likely that secreted viral products play a major role in blood-brain barrier damage and neuronal cell death. The aim of the present study was to examine the effect of HIV-1 gp160 peptides and gp120 proteins on brain microvascular endothelial cells and neurons from both human and rats. Four of the 7 gp160 peptides tested evoked significant neurotoxicity. Two different full-length recombinant HIV gp120 proteins (HIV-1CM235 gp120 and HIV-1MN gp120) also induced neuronal and brain endothelial cell death, and concentrations as little as 1 ng/ml evoked pronounced morphological changes in these cells and marked cytotoxicity. This study suggests that HIV proteins and peptides that are shed in vivo may be directly involved in blood-brain barrier damage and neuronal cell death in HIV-associated dementia.},
	Author = {Kanmogne, Georgette D. and Kennedy, R. C. and Grammas, Paula},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Fetus;Dose-Response Relationship, Drug;Endothelium, Vascular;Animals;HIV-1;Monocytes;Cells, Cultured;Rats;Humans;Research Support, Non-U.S. Gov't;HIV Envelope Protein gp160;Brain;Culture Media, Conditioned;Recombinant Fusion Proteins;11 Glia;Blood-Brain Barrier;Research Support, U.S. Gov't, P.H.S.;Peptide Fragments;Neurons;Cell Death;HIV Envelope Protein gp120;AIDS Dementia Complex},
	Medline = {22317806},
	Month = {11},
	Nlm_Id = {2985192R},
	Number = {11},
	Organization = {Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City 73104, USA.},
	Pages = {992-1000},
	Pubmed = {12430716},
	Title = {HIV-1 gp120 proteins and gp160 peptides are toxic to brain endothelial cells and neurons: possible pathway for HIV entry into the brain and HIV-associated dementia},
	Uuid = {56590B38-3B9D-4799-86A8-9657C4EC9B19},
	Volume = {61},
	Year = {2002}}

@article{Kaplan:1981,
	Abstract = {Newly formed neurons in the adult mammalian neocortex have been reported by several investigators using light microscopic radioautography, but these reports have not been confirmed by electron microscopy--probably because their rarity precludes any reasonable chance of observing these cells with electron microscopic radioautography. To overcome this problem I have used a recently developed method that allows serial thin sectioning and subsequent electron microscopic examination of plastic-embedded sections previously prepared for light microscopic radioautography. Ninety-day- old rats were injected with 4.3 microCi per gm body weight of [H3] thymidine and allowed to survive for 30 days. In the light radioautographs, labeled cells were found in layer IV of the visual cortex, and analysis of electron micrographs of selected examples of these labeled cells clearly demonstrated their neuronal nature wit synapses along their cell bodies and dendrites. In order to quantify the relative frequency of labeled neurons, the number of labeled cells seen in the light microscopic sections was expressed as a percentage of the total number of neurons found in sections through the entire thickness of the visual cortex; the percentage was 0.011\%, or about 1 in 10,000. The results of this study are in agreement with evidence of neurogenesis of granular neurons in the adult rat olfactory bulb and dentate gyrus (Kaplan and Hinds, '77). Thus, it has now been confirmed that relatively small labeled neurons and their synapses are found in at least 3 brain regions (olfactory bulb, dentate gyrus, and visual cortex) in a normal adult rodent.},
	Author = {Kaplan, M. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Comp Neurol},
	Keywords = {01 Adult neurogenesis general;Cell Differentiation;A-2;Neurons/cytology;Visual Cortex/cytology/*growth &development/metabolism;Microscopy, Electron;Rats;Thymidine/metabolism;Autoradiography;Animal;Support, U.S. Gov't, P.H.S.;Mitosis;Male},
	Number = {2},
	Pages = {323-38.},
	Title = {Neurogenesis in the 3-month-old rat visual cortex},
	Uuid = {5A160142-CD3D-11D9-8C77-000D9346EC2A},
	Volume = {195},
	Year = {1981},
	url = {papers/Kaplan_JCompNeurol1981.pdf},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7251929}}

@article{Kaplan:1984,
	Abstract = {Ultrastructural identification of mitotic neuronal precursors beneath the basal hippocampal granule cell layer was made using electron micrographs of [3H]thymidine-labeled cells. Ultrathin sections were obtained by a method that allows serial thin sectioning of reembedded sections previously prepared for light microscopic radioautography. The electron microscopic observations reported in this study reveal: (1) that a steady rate of granule cell neurogenesis occurs during the first year of a rodent's life; (2) that newly formed granule neurons in the dentate gyrus of the newborn mouse and adult rat are a result of neuroblast division; and (3) two distinct classes of mitotic cells can be identified during the peak period of postnatal neurogenesis--those with synapses on their cell bodies and processes and those with no synapses or processes.},
	Author = {Kaplan, M. S. and Bell, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {10 Development;Research Support, Non-U.S. Gov't;Hippocampus;10 Hippocampus;Microscopy, Electron;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Mitosis;Animals;Mice;Mice, Inbred Strains},
	Medline = {84215313},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {6},
	Pages = {1429-41},
	Pubmed = {6726341},
	Title = {Mitotic neuroblasts in the 9-day-old and 11-month-old rodent hippocampus},
	Uuid = {0317A407-AA4A-4235-A978-6324FEDB6198},
	Volume = {4},
	Year = {1984}}

@article{Kaplan:1977,
	Abstract = {Three-month-old rats were injected intraperitoneally with [3H]thymidine (4.3 microcuries per gram of body weight) and allowed to survive for 30 days. Radioautography of 1-micrometer sections revealed labeled cells in the granular layers of dentate gyrus and olfactory bulb; these were confirmed as neurons by electron microscopy of reembedded 1-micrometer sections.},
	Author = {Kaplan, M. S. and Hinds, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Science},
	Keywords = {A;01 Adult neurogenesis general;10 Development;Rats;10 Hippocampus;Hippocampus/cytology/*growth &development/metabolism;Thymidine/metabolism;Animal;Neurons/metabolism/*physiology;Support, U.S. Gov't, P.H.S.;Age Factors;Male;Olfactory Bulb/cytology/*growth &development/metabolism},
	Number = {4308},
	Pages = {1092-4.},
	Title = {Neurogenesis in the adult rat: electron microscopic analysis of light radioautographs},
	Uuid = {5A160966-CD3D-11D9-8C77-000D9346EC2A},
	Volume = {197},
	Year = {1977},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=887941}}

@article{Kaplan:2001,
	Abstract = {Introduction by the EditorOver the past few years, the classic idea that no new nerve cells are born in the adult mammalian brain has finally and conclusively been refuted by the scientific community. Yet, the first indications that neurogenesis occurs in the brain of adult mammals were obtained using light and electron microscopy over two decades ago. Why this went unrecognized is described in a personal account by the researcher who pioneered those studies: Michael Kaplan.},
	Author = {Kaplan, M. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {Trends Neurosci},
	Keywords = {01 Adult neurogenesis general;A pdf},
	Number = {10},
	Organization = {816 Frederick Road, 21228, Catonsville, MD, USA},
	Pages = {617-20.},
	Title = {Environment complexity stimulates visual cortex neurogenesis: death of a dogma and a research career},
	Uuid = {5A160546-CD3D-11D9-8C77-000D9346EC2A},
	Volume = {24},
	Year = {2001},
	url = {papers/Kaplan_TrendsNeurosci2001.pdf}}

@article{Kapsa:2002,
	Abstract = {In muscle, mutant genes can be targeted and corrected directly by intramuscular (i.m.) injection of corrective DNA, or by ex vivo delivery of DNA to myogenic cells, followed by cell transplantation. Short fragment homologous replacement (SFHR) has been used to repair the exon 23 nonsense transition at the Xp21.1 dys locus in cultured cells and also, directly in tibialis anterior from male mdx mice. Whilst mdx dys locus correction can be achieved in up to 20\%of cells in culture, much lower efficiency is evident by i.m. injection. The major consideration for application of targeted gene correction to muscle is delivery throughout relevant tissues. Systemically injected bone marrow (BM)-derived cells from wt C57BL/10 ScSn mice are known to remodel mdx muscle when injected into the systemic route. Provided that non muscle-derived cell types most capable of muscle remodeling activity can be more specifically identified, isolated and expanded, cell therapy seems presently the most favorable vehicle by which to deliver gene correction throughout muscle tissues. Using wt bone marrow as a model, this study investigates systemic application of bone marrow-derived cells as potential vehicles to deliver corrected (ie wt) dys locus to dystrophic muscle. Intravenous (i.v.) and intraperitoneal (i.p.) injections of wt BM were given to lethally and sub-lethally irradiated mdx mice. Despite both i.v. and surviving i.p. groups containing wt dys loci in 100\%and less than 1\%of peripheral blood nuclei, respectively, both groups displayed equivalent levels of wt dys transcript in muscle RNA. These results suggest that the muscle remodeling activity observed in systemically injected BM cells is not likely to be found in the hemopoietic fraction.},
	Author = {Kapsa, R. M. and Quigley, A. F. and Vadolas, J. and Steeper, K. and Ioannou, P. A. and Byrne, E. and Kornberg, A. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Animals;Gene Targeting;Bone Marrow Transplantation;Dystrophin;DNA;Mice, Inbred C57BL;11 Glia;Male;Bone Marrow Cells;Mice, Inbred mdx;Gene Therapy;Muscle, Skeletal;Muscular Dystrophies;Transplantation, Autologous;Mice;Injections, Intravenous;Injections, Intraperitoneal;Research Support, Non-U.S. Gov't},
	Medline = {22027842},
	Month = {6},
	Nlm_Id = {9421525},
	Number = {11},
	Organization = {Melbourne Neuromuscular Research Institute, Clinical Neurosciences, St Vincent's Hospital, Fitzroy Victoria, Australia.},
	Pages = {695-9},
	Pubmed = {12032690},
	Title = {Targeted gene correction in the mdx mouse using short DNA fragments: towards application with bone marrow-derived cells for autologous remodeling of dystrophic muscle},
	Uuid = {34789CF5-97EB-4B52-96F9-F111BBB807CC},
	Volume = {9},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301737}}

@article{Karishma:2002,
	Abstract = {Treating adult male rats with subcutaneous pellets of dehydroepiandrosterone (DHEA) increased the number of newly formed cells in the dentate gyrus of the hippocampus, and also antagonized the suppressive of corticosterone (40 mg/kg body weight daily for 5 days). Neither pregnenolone (40 mg/kg/day), a precursor of DHEA, nor androstenediol (40 mg/kg/day), a major metabolite, replicated the effect of DHEA (40 mg/kg/day). Corticosterone reduced the number of cells labelled with a marker for neurons (NeuN) following a 28-day survival period, and this was also prevented by DHEA. DHEA by itself increased the number of newly formed neurons, but only if treatment was continued throughout the period of survival. Subcutaneous DHEA pellets stimulated neurogenesis in a small number of older rats ( approximately 12 months old). These results show that DHEA, a steroid prominent in the blood and cerebral environment of humans, but which decreases markedly with age and during major depressive disorder, regulates neurogenesis in the hippocampus and modulates the inhibitory effect of increased corticoids on both the formation of new neurons and their survival. 0953-816x Journal Article},
	Author = {Karishma, K. K. and Herbert, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Dentate Gyrus/cytology/*drug effects/*growth &development;Drug Administration Schedule;Animals;Corticosterone/blood/*pharmacology;Drug Interactions/physiology;Rats;Neuroprotective Agents/metabolism/pharmacology;C abstr;Rats, Inbred Strains;Male;Neurons/cytology/*drug effects/metabolism;Support, Non-U.S. Gov't;Cell Division/drug effects/*physiology;Cell Death/drug effects/physiology;Cell Differentiation/drug effects/physiology;04 Adult neurogenesis factors;Age Factors;Stem Cells/cytology/drug effects/metabolism;Cell Survival/drug effects/*physiology;Dehydroepiandrosterone/metabolism/*pharmacology;Immunohistochemistry;Androstenediol/pharmacology;Depression, Involutional/metabolism/pathology/physiopathology;Pregnenolone/pharmacology},
	Number = {3},
	Organization = {Department of Anatomy, University of Cambridge, Cambridge, CB2 3DY, UK.},
	Pages = {445-53},
	Pubmed = {12193187},
	Title = {Dehydroepiandrosterone (DHEA) stimulates neurogenesis in the hippocampus of the rat, promotes survival of newly formed neurons and prevents corticosterone-induced suppression},
	Uuid = {29F93216-DF0C-463E-A85B-A85B114995ED},
	Volume = {16},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12193187}}

@article{Karl:2005,
	Abstract = {The doublecortin (DCX) gene encodes a 40-kDa microtubule-associated protein specifically expressed in neuronal precursors of the developing and adult CNS. Due to its specific expression pattern, attention was drawn to DCX as a marker for neuronal precursors and neurogenesis, thereby underscoring the importance of its promoter identification and promoter analysis. Here, we analysed the human DCX regulatory sequence and confined it to a 3.5-kb fragment upstream of the ATG start codon. We demonstrate by transient transfection experiments that this fragment is sufficient and specific to drive expression of reporter genes in embryonic and adult neuronal precursors. The activity of this regulatory fragment overlapped with the expression of endogenous DCX and with the young neuronal markers class III beta-tubulin isotype and microtubule-associated protein Map2ab but not with glial or oligodendroglial markers. Electrophysiological data further confirmed the immature neuronal nature of these cells. Deletions within the 3.5-kb region demonstrated the relevance of specific regions containing transcription factor-binding sites. Moreover, application of neurogenesis-related growth factors in the neuronal precursor cultures suggested the lack of direct signalling of these factors on the DCX promoter construct.},
	Author = {Karl, Claudia and Couillard-Despres, Sebastien and Prang, Peter and Munding, Matthias and Kilb, Werner and Brigadski, Tanja and Pl{\"o}tz, Sonja and Mages, Wolfgang and Luhmann, Heiko and Winkler, J{\"u}rgen and Bogdahn, Ulrich and Aigner, Ludwig},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {02 Adult neurogenesis migration},
	Month = {1},
	Nlm_Id = {2985190R},
	Number = {2},
	Organization = {Volkswagen-Foundation-Research Group, University of Regensburg, Regensburg, Germany.},
	Pages = {264-82},
	Pii = {JNC2879},
	Pubmed = {15663475},
	Title = {Neuronal precursor-specific activity of a human doublecortin regulatory sequence},
	Uuid = {52FAB77B-3251-4265-96E5-AA815626A9DF},
	Volume = {92},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1471-4159.2004.02879.x}}

@article{Karpova:2005,
	Abstract = {Inducible and reversible silencing of selected neurons in vivo is critical to understanding the structure and dynamics of brain circuits. We have developed Molecules for Inactivation of Synaptic Transmission (MISTs) that can be genetically targeted to allow the reversible inactivation of neurotransmitter release. MISTs consist of modified presynaptic proteins that interfere with the synaptic vesicle cycle when crosslinked by small molecule "dimerizers." MISTs based on the vesicle proteins VAMP2/Synaptobrevin and Synaptophysin induced rapid ( approximately 10 min) and reversible block of synaptic transmission in cultured neurons and brain slices. In transgenic mice expressing MISTs selectively in Purkinje neurons, administration of dimerizer reduced learning and performance of the rotarod behavior. MISTs allow for specific, inducible, and reversible lesions in neuronal circuits and may provide treatment of disorders associated with neuronal hyperactivity.},
	Author = {Karpova, Alla Y. and Tervo, Dougal G. R. and Gray, Noah W. and Svoboda, Karel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Vesicle-Associated Membrane Protein 2;research support, n.i.h., extramural ;Purkinje Cells;Gene Targeting;Animals;Cells, Cultured;Motor Activity;Synaptic Transmission;Synaptic Vesicles;Neurotransmitter Agents;in vitro ;Cross-Linking Reagents;Mice, Transgenic;Synaptophysin;Time Factors;research support, non-u.s. gov't ;Dimerization;Learning;21 Neurophysiology;Neurons;Mice;24 Pubmed search results 2008;Neural Inhibition},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Howard Hughes Medical Institute, USA.},
	Pages = {727-35},
	Pii = {S0896-6273(05)00963-3},
	Pubmed = {16337911},
	Title = {Rapid and reversible chemical inactivation of synaptic transmission in genetically targeted neurons},
	Uuid = {D46946D4-973F-4BC7-B20D-521F8F43044A},
	Volume = {48},
	Year = {2005},
	url = {papers/Karpova_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.11.015}}

@article{Kashiwakura:2003,
	Abstract = {BACKGROUND: Bone marrow stromal cells (BMSCs) have many characteristics of mesenchymal stem cells that can differentiate into smooth muscle cells (SMCs). However, there have been few studies closely following the cell development of smooth muscle lineage among BMSCs. METHODS AND RESULTS: To investigate the possible existence of a cell population committed to the SMC lineage among bone marrow adhesion cells, we tried to detect and follow the in vitro differentiation of such a cell type by using a promoter-sorting method with a human SM22alpha promoter (-480 bp)/green fluorescent protein (GFP) construct. The construct was transfected to adhesion cells that appeared 5 days after the seeding of mononuclear cells from bone marrow. GFP was first detectable 5 days after the transfection in a cell population [Ad(G) cells], which expressed PDGF-beta but neither mature (calponin) nor immature (SMemb) SMC-specific proteins at that time. However, the cells were eventually grown into individual clones that expressed SMC-specific proteins (alpha-smooth muscle actin, calponin, and SM-1), suggesting that Ad(G) cells have partly at least progenitor properties. Because early studies have reported that PDGF-beta signaling plays pivotal roles in the differentiation of mesenchymal smooth muscle progenitor cells, Ad(G) cells might be putative mesenchymal smooth muscle progenitors expressing PDGF-beta. CONCLUSIONS: We demonstrated the presence of a cell population fated to become SMCs and followed their differentiation into SMCs among BMSCs.},
	Author = {Kashiwakura, Yuji and Katoh, Youichi and Tamayose, Kenji and Konishi, Hakuoh and Takaya, Norihide and Yuhara, Senji and Yamada, Masanori and Sugimoto, Koichi and Daida, Hiroyuki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1524-4539},
	Journal = {Circulation},
	Keywords = {Stromal Cells;Cell Differentiation;Animals;Humans;Cells, Cultured;Muscle Proteins;Transfection;Microfilament Proteins;Mice, Inbred C57BL;Recombinant Fusion Proteins;11 Glia;Green Fluorescent Proteins;Antibodies;RNA, Messenger;Bone Marrow Cells;Cell Lineage;Calcium-Binding Proteins;Smooth Muscle Myosins;Promoter Regions (Genetics);Muscle, Smooth, Vascular;Mice;Stem Cells;Clone Cells;Receptor, Platelet-Derived Growth Factor beta;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22604924},
	Month = {4},
	Nlm_Id = {0147763},
	Number = {16},
	Organization = {Department of Cardiology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.},
	Pages = {2078-81},
	Pii = {01.CIR.0000070082.64414.B5},
	Pubmed = {12707231},
	Title = {Isolation of bone marrow stromal cell-derived smooth muscle cells by a human SM22alpha promoter: in vitro differentiation of putative smooth muscle progenitor cells of bone marrow},
	Uuid = {23D30BBE-0BC1-4C19-A5D1-0D234D1A26B8},
	Volume = {107},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.CIR.0000070082.64414.B5}}

@article{Kasowski:1999,
	Abstract = {Olfactory receptor cell (ORC) axons terminate in the olfactory bulb glomerular neuropil, where they synapse with dendrites of mitral, tufted, and periglomerular neurons. We investigated the organization of the glomerular neuropil by using antibodies to both single- and double- label constituents for analyses with confocal microscopy. Electron microscopy (EM) was employed to assess the distribution of synaptic appositions within the glomerulus. Adult Sprague-Dawley rats were processed for immunocytochemistry with olfactory marker protein (OMP), synaptophysin, synapsin 1, glial fibrillary acidic protein (GFAP), and/or microtubule-associated protein 2 (MAP2). Equivalent rats were processed for transmission EM. Double labeling for OMP and MAP2 revealed two distinctive subcompartments within glomeruli: an axonal compartment containing predominately primary afferent axons with individual dendritic inserts and a complementary dendritic compartment that excluded primary afferent axons. Areas not occupied by OMP or MAP2 immunoreactivity were either immunoreactive for GFAP, indicating a glial process, or were blood vessels. Synaptophysin and synapsin 1 also showed differential labeling within the glomerulus. Synaptophysin strongly colocalized with OMP, whereas synapsin 1 was associated most strongly with MAP2. Reconstructions of glomeruli from EM montages revealed interdigitating axonal and dendritic subcompartments. The axonal subcompartments were composed primarily of ORC processes with individual or small groups of dendrites interspersed. Dendritic subcompartments were composed predominately of dendritic processes. Primary afferent axodendritic and local-circuit dendrodendritic synapses segregated within the glomerulus into the axonal and dendritic subcompartments, respectively. The results support the hypothesis of subcompartmental organization within olfactory bulb glomeruli.},
	Author = {Kasowski, H. J. and Kim, H. and Greer, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Synapsins/analysis;13 Olfactory bulb anatomy;I;Rats;Neurons/*ultrastructure;Microscopy, Confocal;Microtubule-Associated Proteins/analysis;Axons/ultrastructure;Animal;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein/analysis;Nerve Tissue Proteins/analysis;Synaptophysin/analysis;Synapses/ultrastructure;Olfactory Bulb/*ultrastructure;Support, U.S. Gov't, P.H.S.;Olfactory Receptor Neurons/ultrastructure;Microscopy, Electron;Biological Markers;Models, Neurological;Dendrites/ultrastructure},
	Number = {2},
	Organization = {Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06520-8082, USA.},
	Pages = {261-74.},
	Title = {Compartmental organization of the olfactory bulb glomerulus},
	Uuid = {0A8A805C-BA19-4ACE-908E-A2A77A037E7B},
	Volume = {407},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10213094}}

@article{Kataoka:2003,
	Abstract = {Results of recent studies have indicated that bone marrow cells can differentiate into various cells of ectodermal, mesodermal, and endodermal origins when transplanted into the body. However, the problems associated with those experiments such as the long latent period, rareness of the event, and difficulty in controlling the processes have hampered detailed mechanistic studies. In the present study, we examined the potency of mouse bone marrow cells to differentiate into cells comprising skin tissues using a skin reconstitution assay. Bone marrow cells from adult green fluorescent protein (GFP)-transgenic mice were transplanted in a mixture of embryonic mouse skin cells (17.5 days post-coitus) onto skin defects made on the backs of nude mice. Within 3 weeks, fully differentiated skin with hair was reconstituted. GFP-positive cells were found in the epidermis, hair follicles, sebaceous glands, and dermis. The localization and morphology of the cells, results of immunohistochemistry, and results of specific staining confirmed that the bone marrow cells had differentiated into epidermal keratinocytes, sebaceous gland cells, follicular epithelial cells, dendritic cells, and endothelial cells under the present conditions. These results indicate that this system is suitable for molecular and cellular mechanistic studies on differentiation of stem cells to various epidermal and dermal cells.},
	Author = {Kataoka, Ken and Medina, Reinhold J. and Kageyama, Tomofumi and Miyazaki, Masahiro and Yoshino, Tadashi and Makino, Teruhiko and Huh, Nam-Ho H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Cell Differentiation;Wound Healing;Animals;Bone Marrow Transplantation;Indicators and Reagents;Hair Follicle;Mice, Transgenic;Wounds, Penetrating;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Embryo;Mice, Nude;Mice, Inbred ICR;Bone Marrow Cells;Skin;Mice;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22870326},
	Month = {10},
	Nlm_Id = {0370502},
	Number = {4},
	Organization = {Department of Cell Biology, Okayama University Graduate School of Medicine and Dentistry, Shikatachou, Okayama, Japan.},
	Pages = {1227-31},
	Pubmed = {14507632},
	Title = {Participation of adult mouse bone marrow cells in reconstitution of skin},
	Uuid = {D8DB25EE-40B6-4DB0-86E1-A2BB77A7D3FC},
	Volume = {163},
	Year = {2003}}

@article{Katayama:2006,
	Abstract = {Hematopoietic stem and progenitor cells (HSPC), attracted by the chemokine CXCL12, reside in specific niches in the bone marrow (BM). HSPC migration out of the BM is a critical process that underlies modern clinical stem cell transplantation. Here we demonstrate that enforced HSPC egress from BM niches depends critically on the nervous system. UDP-galactose ceramide galactosyltransferase-deficient (Cgt(-/-)) mice exhibit aberrant nerve conduction and display virtually no HSPC egress from BM following granulocyte colony-stimulating factor (G-CSF) or fucoidan administration. Adrenergic tone, osteoblast function, and bone CXCL12 are dysregulated in Cgt(-/-) mice. Pharmacological or genetic ablation of adrenergic neurotransmission indicates that norepinephrine (NE) signaling controls G-CSF-induced osteoblast suppression, bone CXCL12 downregulation, and HSPC mobilization. Further, administration of a beta(2) adrenergic agonist enhances mobilization in both control and NE-deficient mice. Thus, these results indicate that the sympathetic nervous system regulates the attraction of stem cells to their niche.},
	Author = {Katayama, Yoshio and Battista, Michela and Kao, Wei-Ming M. and Hidalgo, Andr{\'e}s and Peired, Anna J. and Thomas, Steven A. and Frenette, Paul S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {11 Glia;22 Stem cells;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {2},
	Organization = {Department of Medicine, Immunobiology Center and Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.},
	Pages = {407-21},
	Pii = {S0092-8674(05)01328-0},
	Pubmed = {16439213},
	Title = {Signals from the sympathetic nervous system regulate hematopoietic stem cell egress from bone marrow},
	Uuid = {C6B15F81-4AEE-49E1-930B-8B0967BCFBAF},
	Volume = {124},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.10.041}}

@article{Katchanov:2001,
	Abstract = {After mild ischemic insults, many neurons undergo delayed neuronal death. Aberrant activation of the cell cycle machinery is thought to contribute to apoptosis in various conditions including ischemia. We demonstrate that loss of endogenous cyclin-dependent kinase (Cdk) inhibitor p16(INK4a) is an early and reliable indicator of delayed neuronal death in striatal neurons after mild cerebral ischemia in vivo. Loss of p27(Kip1), another Cdk inhibitor, precedes cell death in neocortical neurons subjected to oxygen-glucose deprivation in vitro. The loss of Cdk inhibitors is followed by upregulation of cyclin D1, activation of Cdk2, and subsequent cytoskeletal disintegration. Most neurons undergo cell death before entering S-phase, albeit a small number ( approximately 1\%) do progress to the S-phase before their death. Treatment with Cdk inhibitors significantly reduces cell death in vitro. These results show that alteration of cell cycle regulatory mechanisms is a prelude to delayed neuronal death in focal cerebral ischemia and that pharmacological interventions aimed at neuroprotection may be usefully directed at cell cycle regulatory mechanisms. 1529-2401 Journal Article},
	Author = {Katchanov, J. and Harms, C. and Gertz, K. and Hauck, L. and Waeber, C. and Hirt, L. and Priller, J. and von Harsdorf, R. and Bruck, W. and Hortnagl, H. and Dirnagl, U. and Bhide, P. G. and Endres, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci},
	Keywords = {Cyclin-Dependent Kinases/*antagonists &inhibitors/metabolism;Cell Hypoxia;Brain Ischemia/*metabolism/pathology;EE pdf;Disease Models, Animal;*Tumor Suppressor Proteins;Cyclin D1/metabolism;Animals;Cells, Cultured;In Situ Nick-End Labeling;Cell Cycle/physiology;Protein p16/deficiency/*metabolism;Mice, Inbred Strains;*Cell Cycle Proteins;Protein-Serine-Threonine Kinases/metabolism;Bromodeoxyuridine;08 Aberrant cell cycle;Support, U.S. Gov't, P.H.S.;Enzyme Inhibitors/pharmacology;Cell Death;Rats;*CDC2-CDC28 Kinases;Microtubule-Associated Proteins/deficiency/*metabolism;Purines/pharmacology;Support, Non-U.S. Gov't;Mice;Rats, Wistar;Oxygen/metabolism;Neurons/*metabolism/pathology;Glucose/deficiency/metabolism},
	Number = {14},
	Organization = {Experimental Neurology, Department of Neurology, Institute of Pharmacology and Toxicology, Charite, Humboldt-University of Berlin, D-10098 Berlin, Germany.},
	Pages = {5045-53},
	Pubmed = {11438580},
	Title = {Mild cerebral ischemia induces loss of cyclin-dependent kinase inhibitors and activation of cell cycle machinery before delayed neuronal cell death},
	Uuid = {3252827C-D395-11D9-A0E9-000D9346EC2A},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11438580}}

@article{Kato:2000,
	Abstract = {It is well established that olfactory receptor cells are replaced during life. Periglomerular (PG) cells of the olfactory bulb have recently been demonstrated to be produced following proliferation and migration of periventricular neuronal precursor cells even in adulthood. The purpose of the present study was to examine the fate of newly formed PG cells in adult rodents. Using 5-bromodeoxyuridine (BrdU), we carried out a quantitative immunohistochemical analysis of BrdU-positive cells in the bulbar glomerular layer at different survival periods. Each number of BrdU-positive PG cells per 100 olfactory glomeruli was 34.1 +/- 3.3 (1 week), 57.2 +/- 2.7 (2 weeks), 28.0 +/- 4.7 (4 weeks) and 25.9 +/- 1.6 (8 weeks). These results indicate that bulbar PG cells, similar to olfactory receptor cells, are mostly replaced during life, and that the olfactory system is composed of disposable neuronal networks centrally as well as peripherally.},
	Author = {Kato, T. and Yokouchi, K. and Kawagishi, K. and Fukushima, N. and Miwa, T. and Moriizumi, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Acta Otolaryngol},
	Keywords = {I;13 Olfactory bulb anatomy},
	Number = {7},
	Organization = {Department of Anatomy, School of Medicine, Shinshu University, Matsumoto, Japan.},
	Pages = {876-9.},
	Title = {Fate of newly formed periglomerular cells in the olfactory bulb},
	Uuid = {D7D9EBB8-18E0-486B-89B5-C49FD62F966A},
	Volume = {120},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11132724}}

@article{Kato:2001,
	Abstract = {It has been known that stem cells do exist in the central nervous system, and adult neurogenesis is continually taking place in the olfactory bulb during life. We report here, with the combined method of autoradiography using (3)H-thymidine and immunohistochemistry for a neuronal marker, that 65.3-76.9\%of calretinin-immunoreactive bulbar neurons are replaced during the short period of 6 weeks in the adult rodent. The results indicate that neuronal replacement is a common phenomenon in the olfactory bulb during life.},
	Author = {Kato, T. and Yokouchi, K. and Fukushima, N. and Kawagishi, K. and Li, Z. and Moriizumi, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Neurosci Lett},
	Keywords = {I;13 Olfactory bulb anatomy},
	Number = {1},
	Organization = {Department of Anatomy, Shinshu University School of Medicine, 390-8621, Matsumoto, Japan},
	Pages = {17-20.},
	Title = {Continual replacement of newly-generated olfactory neurons in adult rats},
	Uuid = {EECDB633-E5B8-4C9E-B61F-1187913D0B0A},
	Volume = {307},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11516564}}

@article{Katou:2003,
	Abstract = {The checkpoint regulatory mechanism has an important role in maintaining the integrity of the genome. This is particularly important in S phase of the cell cycle, when genomic DNA is most susceptible to various environmental hazards. When chemical agents damage DNA, activation of checkpoint signalling pathways results in a temporary cessation of DNA replication. A replication-pausing complex is believed to be created at the arrested forks to activate further checkpoint cascades, leading to repair of the damaged DNA. Thus, checkpoint factors are thought to act not only to arrest replication but also to maintain a stable replication complex at replication forks. However, the molecular mechanism coupling checkpoint regulation and replication arrest is unknown. Here we demonstrate that the checkpoint regulatory proteins Tof1 and Mrc1 interact directly with the DNA replication machinery in Saccharomyces cerevisiae. When hydroxyurea blocks chromosomal replication, this assembly forms a stable pausing structure that serves to anchor subsequent DNA repair events. 1476-4687 Journal Article},
	Author = {Katou, Y. and Kanoh, Y. and Bando, M. and Noguchi, H. and Tanaka, H. and Ashikari, T. and Sugimoto, K. and Shirahige, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Nature},
	Keywords = {Mutation;Carrier Proteins/metabolism;*DNA Replication/drug effects/genetics;Saccharomyces cerevisiae/*cytology/drug effects/genetics/*metabolism;Hydroxyurea/pharmacology;*S Phase/drug effects;Chromosomes, Fungal/drug effects/*metabolism;Oligonucleotide Array Sequence Analysis;Bromodeoxyuridine/metabolism;08 Aberrant cell cycle;Protein Binding/drug effects;Nuclear Proteins/metabolism;Saccharomyces cerevisiae Proteins/genetics/*metabolism;Support, Non-U.S. Gov't;Macromolecular Systems;Cell Cycle Proteins/genetics/*metabolism;EE},
	Number = {6952},
	Organization = {Genome Structure and Function Team, Human Genome Research Group, RIKEN Genomic Science Center, 1-7-22 Suehiro-cho, Japan.},
	Pages = {1078-83},
	Pubmed = {12944972},
	Title = {S-phase checkpoint proteins Tof1 and Mrc1 form a stable replication-pausing complex},
	Uuid = {6C9875CF-9A4B-4ABF-A9BF-C0AA460DD90D},
	Volume = {424},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12944972}}

@article{Katz:2002,
	Abstract = {It has been generally believed that oncoretroviruses are dependent on mitosis for efficient nuclear entry of viral DNA. We previously identified a nuclear localization signal in the integrase protein of an oncoretrovirus, avian sarcoma virus (ASV), suggesting an active import mechanism for the integrase-DNA complex (G. Kukolj, R. A. Katz, and A. M. Skalka, Gene 223:157-163, 1998). Here, we have evaluated the requirement for mitosis in nuclear import and integration of ASV DNA. Using a modified ASV encoding a murine leukemia virus amphotropic env gene and a green fluorescent protein (GFP) reporter gene, DNA nuclear import was measured in cell cycle-arrested avian (DF-1) as well as human (HeLa) and mouse cells. The results showed efficient accumulation of nuclear forms of ASV DNA in gamma-irradiation-arrested cells. Efficient transduction of a GFP reporter gene was also observed after infection of cells that were arrested with gamma-irradiation, mitomycin C, nocodazole, or aphidicolin, confirming that nuclear import and integration of ASV DNA can occur in the absence of mitosis. By monitoring GFP expression in individual cells, we also obtained evidence for nuclear import of viral DNA during interphase in cycling cells. Lastly, we observed that ASV can transduce postmitotic mouse neurons. These results support an active nuclear import mechanism for the oncoretrovirus ASV and suggest that this mechanism can operate in both nondividing and dividing cells. 0022-538x Journal Article},
	Author = {Katz, R. A. and Greger, J. G. and Darby, K. and Boimel, P. and Rall, G. F. and Skalka, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Virol},
	Keywords = {Mitomycin/pharmacology;Human;Interphase;Animals;*Transduction, Genetic;Hydroxyurea/pharmacology;Nocodazole/pharmacology;Mitosis;Genetic Vectors/*genetics;15 Retrovirus mechanism;J pdf;Aphidicolin/pharmacology;DNA, Viral/metabolism;Mice, Inbred C57BL;G2 Phase;Hela Cells;Cell Line;Support, Non-U.S. Gov't;Chick Embryo;Sarcoma Viruses, Avian/*genetics;Research Design;Neurons;Active Transport, Cell Nucleus;Support, U.S. Gov't, P.H.S.;Mice;Genes, Reporter;Cell Nucleus/metabolism;Luminescent Proteins/genetics},
	Number = {11},
	Organization = {Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA. R\_Katz\@fccc.edu},
	Pages = {5422-34},
	Pubmed = {11991971},
	Title = {Transduction of interphase cells by avian sarcoma virus},
	Uuid = {AE49FE62-0E3E-4764-BBE4-7616314163CA},
	Volume = {76},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11991971}}

@article{Kaur:1997,
	Abstract = {The pineal gland of rats of various ages (1-21 days old) was examined by immunohistochemistry and electron microscopy. Numerous widely distributed cells identified as macrophages/microglia were immunoreactive with the monoclonal antibodies OX-42, OX-18, OX-6, and ED1, indicating that they expressed complement type 3 (CR3) receptors, major histocompatibility complex class I and II antigens, and antigens of monocyte/macrophage lineage as detected by the antibodies, respectively. Following an intraperitoneal injection of rhodamine isothiocyanate (RhIC) in all age groups, the cells emitted a bright fluorescence. They were also labeled by horseradish peroxidase (HRP), as demonstrated in both light and electron microscopy. An HRP reaction was observed in vesicles and lysosomes at the ultrastructural level. A remarkable feature was the uptake of these tracers by pinealocytes. In light microscopy, the pinealocytes showed a punctate reaction product 3-24 hours after HRP injection. By electron microscopy, the reaction product was observed in vesicles, lysosomes, and some rod-like structures in the cytoplasm. On the basis of their immunophenotypic features, it is suggested that the macrophages/microglia in the pineal gland are active phagocytes which are also probably involved in the immunoregulatory function in the gland. The avid uptake of RhIC and HRP from the circulation by these cells suggests that serum-derived substances that may gain access to the parenchyma of the gland are being constantly monitored. The labeling of pinealocytes with HRP suggests that the functional activities of these cells are being modulated by serum-derived substances.},
	Author = {Kaur, C. and Wu, C. H. and Ling, E. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0742-3098},
	Journal = {J Pineal Res},
	Keywords = {Fluorescent Dyes;Rhodamines;Pineal Gland;Animals;Macrophages;Rats;Antigens, Differentiation;Female;Microglia;Rats, Wistar;Not relevant;11 Glia;Male;Support, Non-U.S. Gov't;Macrophage-1 Antigen;Antibodies, Monoclonal;Horseradish Peroxidase;Immunohistochemistry;Microscopy, Electron;Histocompatibility Antigens Class I;Histocompatibility Antigens Class II},
	Medline = {97356831},
	Month = {4},
	Nlm_Id = {8504412},
	Number = {3},
	Organization = {Department of Anatomy, Faculty of Medicine, National University of Singapore, Kent Ridge, Singapore.},
	Pages = {137-44},
	Pubmed = {9213267},
	Title = {Immunohistochemical and tracer studies of macrophages/microglia in the pineal gland of postnatal rats},
	Uuid = {B79450A1-E7D9-49DD-978F-81CAB6CDC756},
	Volume = {22},
	Year = {1997},
	url = {papers/Kaur_JPinealRes1997.pdf}}

@article{Kaushal:2003,
	Abstract = {Frequent chromosomal aneuploidy has recently been discovered in normal neurons of the developing and mature murine CNS. Toward a more detailed understanding of aneuploidy and its effects on normal CNS cells, we examined the genomes of cells in the postnatal subventricular zone (SVZ), an area that harbors a large number of neural stem and progenitor cells (NPCs), which give rise to neurons and glia. Here we show that NPCs, neurons, and glia from the SVZ are frequently aneuploid. Karyotyping revealed that approximately 33\%of mitotic SVZ cells lost or gained chromosomes in vivo, whereas interphase fluorescence in situ hybridization demonstrated aneuploidy in postnatal-born cells in the olfactory bulb (OB) in vivo, along with neurons, glia, and NPCs in vitro. One possible consequence of aneuploidy is altered gene expression through loss of heterozygosity (LOH). This was examined in a model of LOH: loss of transgene expression in mice hemizygous for a ubiquitously expressed enhanced green fluorescent protein (eGFP) transgene on chromosome 15. Concurrent examination of eGFP expression, transgene abundance, and chromosome 15 copy number demonstrated that a preponderance of living SVZ and OB cells not expressing eGFP lost one copy of chromosome 15; the eGFP transgene was lost in these cells as well. Although gene expression profiling revealed changes in expression levels of several genes relative to GFP-expressing controls, cells with LOH at chromosome 15 were morphologically normal and proliferated or underwent apoptosis at rates similar to those of euploid cells in vitro. These findings support the view that NPCs and postnatal-born neurons and glia can be aneuploid in vivo and functional gene expression can be permanently altered in living neural cells by chromosomal aneuploidy. 1529-2401 Journal Article},
	Author = {Kaushal, D. and Contos, J. J. and Treuner, K. and Yang, A. H. and Kingsbury, M. A. and Rehen, S. K. and McConnell, M. J. and Okabe, M. and Barlow, C. and Chun, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {J Neurosci},
	Keywords = {Transgenes;In Situ Hybridization, Fluorescence;Animals;Brain/cytology/growth &development/*metabolism;*Gene Expression Regulation, Developmental;*Chromosomes;EE pdf;*Aneuploidy;Mice, Transgenic;08 Aberrant cell cycle;Cell Survival/genetics;Stem Cells/cytology/metabolism;Support, Non-U.S. Gov't;Cell Division/genetics;Karyotyping;Support, U.S. Gov't, P.H.S.;Loss of Heterozygosity;Mice;Neurons/cytology/metabolism;Lateral Ventricles/cytology/*metabolism;Luminescent Proteins/biosynthesis/genetics},
	Number = {13},
	Organization = {Neuroscience Program, Department of Pharmacology, University of California, San Diego, San Diego, California 92093, USA.},
	Pages = {5599-606},
	Title = {Alteration of gene expression by chromosome loss in the postnatal mouse brain},
	Uuid = {F7A64D80-10B9-4A3C-909D-D04D0CF976CB},
	Volume = {23},
	Year = {2003},
	url = {papers/Kaushal_JNeurosci2003.pdf}}

@article{Keays:2007,
	Abstract = {The development of the mammalian brain is dependent on extensive neuronal migration. Mutations in mice and humans that affect neuronal migration result in abnormal lamination of brain structures with associated behavioral deficits. Here, we report the identification of a hyperactive N-ethyl-N-nitrosourea (ENU)-induced mouse mutant with abnormalities in the laminar architecture of the hippocampus and cortex, accompanied by impaired neuronal migration. We show that the causative mutation lies in the guanosine triphosphate (GTP) binding pocket of alpha-1 tubulin (Tuba1) and affects tubulin heterodimer formation. Phenotypic similarity with existing mouse models of lissencephaly led us to screen a cohort of patients with developmental brain anomalies. We identified two patients with de novo mutations in TUBA3, the human homolog of Tuba1. This study demonstrates the utility of ENU mutagenesis in the mouse as a means to discover the basis of human neurodevelopmental disorders.},
	Author = {Keays, David A. and Tian, Guoling and Poirier, Karine and Huang, Guo-Jen J. and Siebold, Christian and Cleak, James and Oliver, Peter L. and Fray, Martin and Harvey, Robert J. and Moln{\'a}r, Zolt{\'a}n and Pi\~{n}on, Maria C. and Dear, Neil and Valdar, William and Brown, Steve D. M. and Davies, Kay E. and Rawlins, J. Nicholas P. and Cowan, Nicholas J. and Nolan, Patrick and Chelly, Jamel and Flint, Jonathan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008;Memory Disorders;Male;Cerebral Cortex;10 Development;Animals;Serine;Dimerization;Hippocampus;Cell Movement;Phenotype;research support, n.i.h., extramural;DNA Mutational Analysis;Anxiety;Molecular Sequence Data;Mice, Mutant Strains;Tubulin;Behavior, Animal;21 Epilepsy;Chromosome Mapping;Mutation;Amino Acid Sequence;Guanosine Triphosphate;Glutamic Acid;Female;research support, non-u.s. gov't;21 Neurophysiology;Mice;Neurons;Humans},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, OX3 7BN, UK.},
	Pages = {45-57},
	Pii = {S0092-8674(06)01611-4},
	Pubmed = {17218254},
	Title = {Mutations in alpha-tubulin cause abnormal neuronal migration in mice and lissencephaly in humans},
	Uuid = {A527F883-1A06-4BC0-8E22-212E34121B9E},
	Volume = {128},
	Year = {2007},
	url = {papers/Keays_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.12.017}}

@article{Kee:2001,
	Abstract = {The dentate gyrus is one of the few areas of the mammalian brain where new neurons are continuously produced in adulthood. Certain insults such as epileptic seizures and ischemia are known to enhance the rate of neuronal production. We analyzed this phenomenon using the temporary occlusion of the two carotid arteries combined with arterial hypotension as a method to induce ischemia in rats. We measured the rate of cell production and their state of differentiation with a mitotic indicator, bromodeoxyuridine (BrdU), in combination with the immunohistochemical detection of neuronal markers. One week after the ischemic episode, the cell production in dentate gyrus was increased two- to threefold more than the basal level seen in control animals. Two weeks after ischemia, over 60\%of these cells became young neurons as determined by colabeling with BrdU and a cytoplasmic protein (CRMP-4) involved in axonal guidance during development. Five weeks after the ischemia, over 60\%of new neurons expressed calbindin, a calcium-binding protein normally expressed in mature granule neurons. In addition to more cells being generated, a greater proportion of all new cells remained in the differentiated but not fully mature state during the 2- to 5-week period after ischemia. The maturation rate of neurons as determined by the calbindin labeling and by the rate of migration from a proliferative zone into the granule cell layer was not changed when examined 5 weeks after ischemia. The results support the hypothesis that survival of dentate gyrus after ischemia is linked with enhanced neurogenesis. Additional physiological stimulation after ischemia may be exploited to stimulate maturation of new neurons and to offer new therapeutic strategies for promoting recovery of neuronal circuitry in the injured brain. 0014-4819 Journal Article},
	Author = {Kee, N. J. and Preston, E. and Wojtowicz, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Exp Brain Res},
	Keywords = {Cerebrovascular Accident/pathology;Cytoplasm/chemistry;Ischemic Attack, Transient/*pathology;Rats, Sprague-Dawley;D abstr;Cell Division/physiology;Cell Survival/physiology;Rats;06 Adult neurogenesis injury induced;Neurons/chemistry/*cytology;Dentate Gyrus/*blood supply/*cytology;Cell Differentiation/physiology;Support, Non-U.S. Gov't;Animals;Bromodeoxyuridine;Antimetabolites;Calcium-Binding Protein, Vitamin D-Dependent/analysis},
	Number = {3},
	Organization = {Department of Physiology, University of Toronto, ON, Canada.},
	Pages = {313-20},
	Pubmed = {11243473},
	Title = {Enhanced neurogenesis after transient global ischemia in the dentate gyrus of the rat},
	Uuid = {2C5B9D0D-EC81-11DA-8605-000D9346EC2A},
	Volume = {136},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11243473}}

@article{Kee:2002,
	Abstract = {Adult animals continue to produce new neurons in the dentate gyrus of hippocampus. Until now, the principal method of studying neurogenesis has been to inject either tritiated thymidine or 5'-Bromo-2- deoxyuridine (BrdU) intraperitoneally followed by autoradiographic or immunohistochemical detection methods respectively. However, such exogenous markers may produce toxic effects. Our objective was to determine whether Ki-67, a nuclear protein expressed in all phases of the cell cycle except the resting phase, can be used as an alternative, endogenous marker. Using immunohistochemistry, we examined Ki-67 and BrdU expression pattern in rats. Ki-67 was expressed within the proliferative zone of the dentate gyrus and its expression pattern mimicked that of BrdU when examined soon after exogenous BrdU administration. Quantitative comparison of BrdU and Ki-67-positive cells showed 50\%higher numbers of the latter when examined 24 h after the BrdU injection. This was expected, since BrdU can be incorporated into DNA only during the S-phase of the mitotic process, whereas Ki-67 is expressed for its whole duration. Experimental increases (by ischemia) or reductions (by radiation) in the number of mitotic cells produced parallel changes in BrdU and Ki-67 signals. Thus, Ki-67 is an effective mitotic marker and has most of the benefits of BrdU and none of the costs. This study provides evidence for Ki-67 to be used as a marker of proliferation in the initial phase of adult neurogenesis.},
	Author = {Kee, N. and Sivalingam, S. and Boonstra, R. and Wojtowicz, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci Methods},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration;A, BB, T abstr},
	Number = {1},
	Organization = {Department of Physiology, Medical Sciences Building, University of Toronto, Ont., M5S 1A8, Toronto, Canada},
	Pages = {97-105.},
	Title = {The utility of Ki-67 and BrdU as proliferative markers of adult neurogenesis},
	Uuid = {0BD40556-A31E-4A73-BBEB-FC28380929C3},
	Volume = {115},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11897369}}

@article{Keirstead:1999,
	Abstract = {Transplantation offers a means of identifying the differentiation and myelination potential of early neural precursors, features relevant to myelin regeneration in demyelinating diseases. In the postnatal rat brain, precursor cells expressing the polysialylated (PSA) form of the neural cell adhesion molecule NCAM have been shown to generate mostly oligodendrocytes and astrocytes in vitro (Ben-Hur et al., 1998). Immunoselected PSA-NCAM+ newborn rat CNS precursors were expanded as clusters with FGF2 and grafted into a focal demyelinating lesion in adult rat spinal cord. We show that these neural precursors can completely remyelinate such CNS lesions. While PSA-NCAM+ precursor clusters contain rare P75+ putative neural crest precursors, they do not generate Schwann cells in vitro even in the presence of glial growth factor. Yet they generate oligodendrocytes, astrocytes, and Schwann cells in vivo when confronted with demyelinated axons in a glia-free area. We confirmed the transplant origin of these Schwann cells using Y chromosome in situ hybridization and immunostaining for the peripheral myelin protein P0 of tissue from female rats that had been grafted with male cell clusters. The number and distribution of Schwann cells within remyelinated tissue, and the absence of P0 mRNAs in donor cells, indicated that Schwann cells were generated by expansion and differentiation of transplanted PSA-NCAM+ neural precursors and were not derived from contaminating Schwann cells. Thus, transplantation into demyelinated CNS tissue reveals an unexpected differentiation potential of a neural precursor, resulting in remyelination of CNS axons by PNS and CNS myelin-forming cells.},
	Author = {Keirstead, H. S. and Ben-Hur, T. and Rogister, B. and O'Leary, M. T. and Dubois-Dalcq, M. and Blakemore, W. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Neural Cell Adhesion Molecules;Myelin P0 Protein;Cell Differentiation;Rats, Inbred Lew;Animals;Cells, Cultured;Coculture Techniques;Brain Tissue Transplantation;Rats;Nervous System;Brain;Oligodendroglia;Female;Axons;Nerve Fibers, Myelinated;Rats, Wistar;Male;Reverse Transcriptase Polymerase Chain Reaction;Nerve Regeneration;Schwann Cells;Animals, Newborn;Sialic Acids;Neural Cell Adhesion Molecule L1;24 Pubmed search results 2008;Y Chromosome;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {99389882},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Medical Research Council Cambridge Centre for Brain Repair and Department of Clinical Veterinary Medicine, Cambridge, United Kingdom CB3 0ES.},
	Pages = {7529-36},
	Pubmed = {10460259},
	Title = {Polysialylated neural cell adhesion molecule-positive CNS precursors generate both oligodendrocytes and Schwann cells to remyelinate the CNS after transplantation},
	Uuid = {32D0DC09-EB33-453A-B67A-B242BB5897DC},
	Volume = {19},
	Year = {1999}}

@article{Kempermann:2004,
	Abstract = {'Function' is the key criterion for determining whether adult neurogenesis - be it endogenous, induced, or after transplantation - is successful and has truly generated new nerve cells. Function, however, is an elusive and problematic term. A satisfying statement of function will require evaluation on the three conceptual levels of cells, networks, and systems - and potentially even beyond, on the level of psychology. Neuronal development is a lengthy process, a fact that must be considered when judging causes and consequences in experiments that address function and function-dependent regulation of adult neurogenesis. Nevertheless, the information that has been obtained and published so far provides ample evidence that neurons generated in the adult can function and even suggests how they might contribute to cognitive processes.},
	Author = {Kempermann, Gerd and Wiskott, Laurenz and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {Aging;01 Adult neurogenesis general;Cell Differentiation;Adult;Nerve Regeneration;Human;Neuronal Plasticity;Stem Cells;Cell Division;review, tutorial;Animals;Brain;review;Neurons},
	Month = {4},
	Nlm_Id = {9111376},
	Number = {2},
	Organization = {Max Delbr{\"u}ck Center for Molecular Medicine, Berlin-Buch and Volkswagenstiftung Research Group at the Department of Experimental Neurology, Charit{\'e} - University Medicine Berlin, Berlin, Germany.},
	Pages = {186-91},
	Pii = {S0959438804000339},
	Pubmed = {15082323},
	Title = {Functional significance of adult neurogenesis},
	Uuid = {F0AA4D53-BD0E-4090-8D66-893A3B7AF074},
	Volume = {14},
	Year = {2004},
	url = {papers/Kempermann_CurrOpinNeurobiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2004.03.001}}

@article{Kempermann:1998a,
	Abstract = {We demonstrate here that under physiological conditions neurogenesis continues to occur in the dentate gyrus of senescent mice and can be stimulated by living in an enriched environment. Neurogenesis was investigated by confocal microscopy of three-channel immunofluorescent staining for the proliferation marker bromodeoxyuridine (BrdU) and neuronal and glial markers. Quantification was performed with unbiased stereological counting techniques. Neurogenesis decreased with increasing age. Stimulation of adult and aged mice by switching from standard housing to an enriched environment with opportunities for social interaction, exploration, and physical activity for 68 d resulted in an increased survival of labeled cells. Phenotypic analysis revealed that, in enriched living animals, relatively more cells differentiated into neurons, resulting in a threefold net increase of BrdU-labeled neurons in 20-month-old mice (105 vs 32 cells) and a more than twofold increase in 8-month-old mice (684 vs 285 cells) compared with littermates living under standard laboratory conditions. Corresponding absolute numbers of BrdU-positive astrocytes and BrdU- positive cells that did not show colabeling for neuronal or glial markers were not influenced. The effect on the relative distribution of phenotypes can be interpreted as a survival-promoting effect that is selective for neurons. Proliferation of progenitor cells appeared unaffected by environmental stimulation.},
	Author = {Kempermann, G. and Kuhn, H. G. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci},
	Keywords = {Neurons/*cytology;Microscopy, Confocal;Phenotype;Female;Cell Count;C abstr;Animal;Mice, Inbred C57BL;Aging/*physiology;DNA/metabolism;Support, Non-U.S. Gov't;Dentate Gyrus/*physiology;Cell Division/physiology;Maze Learning/physiology;Support, U.S. Gov't, P.H.S.;Nerve Tissue/*growth &development;04 Adult neurogenesis factors;Mice;Immunohistochemistry;Bromodeoxyuridine},
	Number = {9},
	Organization = {The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California 92037, USA.},
	Pages = {3206-12.},
	Title = {Experience-induced neurogenesis in the senescent dentate gyrus},
	Uuid = {275CF215-A8A7-4495-AB0A-FAF51B763BBC},
	Volume = {18},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9547229}}

@article{Kempermann:2002,
	Author = {Kempermann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;Cell Division/physiology;Hippocampus/*cytology/growth &development/physiology;Adaptation, Physiological/physiology;Neurons/*cytology/physiology;Human;Nerve Net/cytology/physiology;A both;Animal;Memory/physiology},
	Number = {3},
	Organization = {Research Group VolkswagenStiftung at the Department of Experimental Neurology, Charite University Hospital, Humboldt University Berlin, 10117 Berlin, Germany. gerd.kempermann\@mdc-berlin.de},
	Pages = {635-8.},
	Title = {Why new neurons? Possible functions for adult hippocampal neurogenesis},
	Uuid = {03C2536B-8172-4F8F-A2DC-0AC6D4E571AC},
	Volume = {22},
	Year = {2002},
	url = {papers/Kempermann_JNeurosci2002.pdf}}

@article{Kempermann:1998b,
	Author = {Kempermann, G. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Nat Med},
	Keywords = {01 Adult neurogenesis general;Cell Differentiation;A abstr;Cell Division;Animal;Neurons/*cytology;Callithrix;Dentate Gyrus/*cytology/growth &development;Stem Cells/*cytology},
	Number = {5},
	Pages = {555-7.},
	Title = {Closer to neurogenesis in adult humans},
	Uuid = {6CDD6AE1-439C-4E14-8F23-D48FA4F12734},
	Volume = {4},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9585224}}

@article{Kempermann:1997,
	Abstract = {Neurogenesis occurs in the dentate gyrus of the hippocampus throughout the life of a rodent, but the function of these new neurons and the mechanisms that regulate their birth are unknown. Here we show that significantly more new neurons exist in the dentate gyrus of mice exposed to an enriched environment compared with littermates housed in standard cages. We also show, using unbiased stereology, that the enriched mice have a larger hippocampal granule cell layer and 15 per cent more granule cell neurons in the dentate gyrus.},
	Author = {Kempermann, G. and Kuhn, H. G. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Nature},
	Keywords = {Dentate Gyrus/*cytology;Female;Housing, Animal;Cell Division;Cell Count;*Environment;Animal;04 Adult neurogenesis factors;Neurons/*cytology;Maze Learning;Support, Non-U.S. Gov't;Bromodeoxyuridine;Mice;C abstr},
	Number = {6624},
	Organization = {The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California 92037, USA.},
	Pages = {493-5.},
	Title = {More hippocampal neurons in adult mice living in an enriched environment},
	Uuid = {4833BE8D-AF4F-4A87-A75A-24A777D63B80},
	Volume = {386},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9087407}}

@article{Kempermann:1997a,
	Abstract = {To address genetic influences on hippocampal neurogenesis in adult mice, we compared C57BL/6, BALB/c, CD1(ICR), and 129Sv/J mice to examine proliferation, survival, and differentiation of newborn cells in the dentate gyrus. Proliferation was highest in C57BL/6; the survival rate of newborn cells was highest in CD1. In all strains approximately 60\%of surviving newborn cells had a neuronal phenotype, but 129/SvJ produced more astrocytes. Over 6 days C57BL/6 produced 0.36\%of their total granule cell number of 239,000 as new neurons, BALB/c 0.30\%of 242,000, CD1 (ICR) 0.32\%of 351,000, and 129/SvJ 0.16\%of 280,000. These results show that different aspects of adult hippocampal neurogenesis are differentially influenced by the genetic background.},
	Author = {Kempermann, G. and Kuhn, H. G. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Mice, Inbred BALB C;Cell Survival;Cell Differentiation;Microscopy, Confocal;Comparative Study;Dentate Gyrus/cytology/*growth &development/metabolism;Animal;C abstr;Mice, Inbred C57BL;Species Specificity;Mice, Inbred ICR;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Neurons/cytology;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Immunohistochemistry},
	Number = {19},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.},
	Pages = {10409-14.},
	Title = {Genetic influence on neurogenesis in the dentate gyrus of adult mice},
	Uuid = {A5D2FF94-6417-4930-A432-11C53EACA67C},
	Volume = {94},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9294224}}

@article{Kempermann:2000,
	Abstract = {Plasticity is an essential characteristic of the brain: it is part of how the brain functions and is continuous while the brain interacts with the outer world. The state of activation and the level of activity of the entire organism affect the brain's plastic response. Brain plasticity has many substrates, ranging from synapses to neurites and entire cells. The production of new neurons is part of plasticity even in the adult and old brain, but under normal conditions neurogenesis only occurs in two privileged regions of the adult brain: hippocampus and olfactory system. At least in the hippocampus, physical activity stimulates neurogenesis by acting on the proliferation of neuronal stem cells. More specific functions such as learning may be able to recruit new neurons from the pool of cells with neurogenic potential. In a broader context neuronal stem cells can likely be found throughout the brain. Therefore, novel approaches to neuroregeneration will, when most effective, make use of the activity-related effects on neuronal stem cells in the adult brain to activate these stem cells in a targeted manner to enhance brain function. Using Smart Source Parsing},
	Author = {Kempermann, G. and van Praag, H. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Prog Brain Res},
	Keywords = {Support, U.S. Gov't, P.H.S.;Animal;Cell Division/physiology;Nerve Regeneration/*physiology;Human;Stem Cells/cytology/physiology/*transplantation;Exercise Therapy/trends;Neuronal Plasticity/*physiology;Brain Injuries/*therapy;Physical Conditioning, Animal/physiology;Central Nervous System/cytology/*embryology/physiology;04 Adult neurogenesis factors;Support, Non-U.S. Gov't;Hippocampus/cytology/growth &development/physiology;Cell Differentiation/physiology;C abstr;Tissue Transplantation/methods/*trends},
	Organization = {Salk Institute for Biological Studies, Laboratory of Genetics, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.},
	Pages = {35-48},
	Title = {Activity-dependent regulation of neuronal plasticity and self repair},
	Uuid = {8182F0DE-60A3-4BAA-9C52-1945425C61D0},
	Volume = {127},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11142036}}

@article{Kempermann:2003,
	Author = {Kempermann, Gerd and Neumann, Harald},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Cell Differentiation;Signal Transduction;Animals;comment;Anti-Inflammatory Agents, Non-Steroidal;Rats;Neuronal Plasticity;Brain-Derived Neurotrophic Factor;Microglia;Lipopolysaccharides;Hippocampus;11 Glia;Neurons;Inflammation Mediators;06 Adult neurogenesis injury induced;04 Adult neurogenesis factors;Minocycline;Mice;24 Pubmed search results 2008;Interleukin-6;Stem Cells;Inflammation;Immunity, Natural},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5651},
	Organization = {Neuronal Stem Cells Research Group, Max-Delbr{\"u}ck-Centrum f{\"u}r Molekulare Medizin Berlin-Buch, 13125 Berlin, Germany. gerd.kempermann\@mdc-berlin.de},
	Pages = {1689-90},
	Pii = {302/5651/1689},
	Pubmed = {14657479},
	Title = {Neuroscience. Microglia: the enemy within?},
	Uuid = {BC9ED3E2-C167-42E5-BD95-D5732CB79340},
	Volume = {302},
	Year = {2003},
	url = {papers/Kempermann_Science2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1092864}}

@article{Kennedy:1997,
	Abstract = {To determine the kinetics of tissue macrophage and microglial engraftment after bone marrow (BM) transplantation, we have developed a model using the ROSA 26 mouse. Transplanted ROSA 26 cells can be precisely identified in recipient animals because they constitutively express beta-galactosidase (beta-gal) and neomycin resistance. B6/129 F2 mice were irradiated and transplanted with BM from ROSA 26 donors and their tissues (spleen, marrow, brain, liver, and lung) examined at various time points to determine the kinetics of engraftment. Frozen sections from transplanted animals were stained histochemically for beta-gal to identify donor cells. At 1, 2, 6, and 12 months posttransplantation, 98\%to 100\%of granulocyte-macrophage colonies were of donor (ROSA 26) origin determined by beta-gal staining and by neomycin resistance. Splenic monocytes/macrophages were 89\%donor origin by 1 month confirming quick and complete engraftment of hematopoietic tissues. At this time, only rare ROSA 26 tissue macrophages or microglia were observed. Alveolar macrophage engraftment was evident by 2 months and had increased to 61\%of total tissue macrophages at 1 year posttransplantation. The kinetics of liver Kupffer cell engraftment were similar to those seen in the lung. However, donor microglial engraftment remained only 23\%of total microglia at 6 months and increased to only 30\%by 1 year. Also, donor microglia were predominantly seen at perivascular and leptomeningeal, and not parenchymal, sites. The data show that microglia derive from BM precursors but turn over at a significantly slower rate than other tissue macrophages. No clinical or histological graft-versus-host disease was observed in the recipients of ROSA 26 BM. These kinetics may impact strategies for the gene therapy of lysosomal storage diseases. Because individual donor cells can be identified in situ, the ROSA 26 model should have many applications in transplantation biology including studies of homing and differentiation.},
	Author = {Kennedy, D. W. and Abkowitz, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:33 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Genetic Markers;beta-Galactosidase;Macrophages, Alveolar;Colony-Forming Units Assay;Macrophages;Lysosomal Storage Diseases;Bone Marrow Transplantation;Humans;Animals;Microglia;Female;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Time Factors;Radiation Chimera;Male;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Gene Therapy;Mice;Central Nervous System;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {97385032},
	Month = {8},
	Nlm_Id = {7603509},
	Number = {3},
	Organization = {Division of Hematology, University of Washington, Seattle 98195, USA.},
	Pages = {986-93},
	Pubmed = {9242527},
	Title = {Kinetics of central nervous system microglial and macrophage engraftment: analysis using a transgenic bone marrow transplantation model},
	Uuid = {70684331-D5C8-4461-9266-81DF6D78A932},
	Volume = {90},
	Year = {1997}}

@article{Kennedy:2003,
	Abstract = {Genetic factors play a major role in the etiology of adult-onset neurodegenerative and neuropsychiatric disorders. Several highly penetrant genes have been cloned for rare, autosomal-dominant, early-onset forms of neurodegenerative diseases. These genes have provided important insights into the mechanisms of these diseases (often altering neuronal protein processing). However, the genes associated with inherited susceptibility to late-onset neurodegenerative diseases, schizophrenia, and bipolar disorder appear to have smaller effects and are likely to interact with each other (and with nongenetic factors) to modulate susceptibility and/or disease phenotype. Several strategies have recently been applied to address this complexity, leading to the identification of a number of candidate susceptibility loci/genes.},
	Author = {Kennedy, James L. and Farrer, Lindsay A. and Andreasen, Nancy C. and Mayeux, Richard and St George-Hyslop, Peter},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:50 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Human;Middle Aged;Bipolar Disorder;review, tutorial;Phenotype;review;Schizophrenia;21 Neurodegenerative;Genetic Predisposition to Disease;Neuregulin-1;Mental Disorders;Linkage (Genetics);Alzheimer Disease;Support, Non-U.S. Gov't;21 Neurophysiology;Adult;Genetic Heterogeneity;Support, U.S. Gov't, P.H.S.;Multifactorial Inheritance;Dementia;Chromosome Mapping;Neurodegenerative Diseases},
	Medline = {22954845},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5646},
	Organization = {Departments of Psychiatry and Medicine, Centre for Addiction and Mental Health, Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario M5S 3H9, Canada.},
	Pages = {822-6},
	Pii = {302/5646/822},
	Pubmed = {14593167},
	Title = {The genetics of adult-onset neuropsychiatric disease: complexities and conundra?},
	Uuid = {C034899D-793E-4248-9EDE-6C22556F796F},
	Volume = {302},
	Year = {2003},
	url = {papers/Kennedy_Science2003.pdf},
	Bdsk-File-2 = {papers/Kennedy_Science2003a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1092132}}

@article{Kerjan:2007,
	Abstract = {Classical lissencephaly is a human developmental brain disorder characterized by a paucity of cortical gyration and thickening of the cortical gray matter, leading to severe epilepsy and mental retardation. Loss-of-function mutations in the microtubule-associated protein encoding genes, PAFAH1B1 (encoding the protein LIS1), DCX and TUBA1A have been implicated in the pathogenesis of the condition. Animal models are required to understand the basis of this disease, which is a challenge, given that mice normally have a smooth cortex. Recent advances toward this goal have come from stepwise reduction in gene function, deletion of redundant genes and acute gene inactivation using short hairpin RNA (shRNA). These approaches have implicated genes that regulate the microtubule cytoskeleton during neuronal division, migration and maturation.},
	Author = {Kerjan, Geraldine and Gleeson, Joseph G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0168-9525},
	Journal = {Trends Genet},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {8507085},
	Number = {12},
	Organization = {Neurogenetics Laboratory, Department of Neurosciences, LBR3A16, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0691, USA.},
	Pages = {623-30},
	Pii = {S0168-9525(07)00328-9},
	Pubmed = {17997185},
	Title = {Genetic mechanisms underlying abnormal neuronal migration in classical lissencephaly},
	Uuid = {6C8EAF1F-EDFC-412C-B2FF-E8EE0E49B366},
	Volume = {23},
	Year = {2007},
	url = {papers/Kerjan_TrendsGenet2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tig.2007.09.003}}

@article{Kernie:2001,
	Abstract = {The persistence of neural stem cells into adulthood has been an area of intense investigation in recent years. There is limited knowledge about how an acquired brain injury might affect the ability of neural precursor cells to proliferate and repopulate injured areas. In the present study we utilize a controlled cortical impact model of traumatic brain injury in adult mice and subsequent BrdU labeling to demonstrate that there is significant proliferation of neural precursors in response to traumatic brain injury in areas both proximal and distal to the injury site. The fate of the proximal proliferation is almost exclusively astrocytic at 60-days post injury and demonstrates that newly generated cells make up much of the astrogliotic scar. Moreover, in areas more distal from the injury site, neurogenesis occurs within the granular layer of the dentate gyrus at a level more than five-fold greater than in controls. These data demonstrate that neural proliferation plays key roles in the remodeling that occurs after traumatic brain injury and suggests a mechanism as to how functional recovery after traumatic brain injuries continues to occur long after the injury itself.},
	Author = {Kernie, S. G. and Erwin, T. M. and Parada, L. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Intermediate Filament Proteins/metabolism;Support, Non-U.S. Gov't;Nerve Tissue Protein S 100/metabolism;06 Adult neurogenesis injury induced;Astrocytes;Dentate Gyrus;Up-Regulation/physiology;Disease Models, Animal;Recovery of Function;Brain Injuries/*physiopathology;Male;Up-Regulation;24 Pubmed search results 2008;Cerebral Cortex;Immunohistochemistry;Nerve Regeneration;Research Support, Non-U.S. Gov't;Recovery of Function/physiology;Animals;Mice, Inbred Strains;Astrocytes/cytology/*metabolism;Cell Division/*physiology;Intermediate Filament Proteins;Bromodeoxyuridine;Cell Division;Calcium-Binding Protein, Vitamin D-Dependent;Nerve Regeneration/*physiology;Gliosis;Neuronal Plasticity;Cerebral Cortex/cytology/injuries/metabolism;Animal;Glial Fibrillary Acidic Protein;D pdf;Dentate Gyrus/cytology/metabolism;Neurons/cytology/*metabolism;Calcium-Binding Protein, Vitamin D-Dependent/metabolism;Bromodeoxyuridine/diagnostic use/metabolism;Stem Cells/cytology/*metabolism;Stem Cells;S100 Proteins;Glial Fibrillary Acidic Protein/metabolism;Mice;Neuronal Plasticity/physiology;Brain Injuries;Nerve Tissue Proteins;Neurons;Gliosis/etiology/*physiopathology},
	Medline = {21611761},
	Month = {11},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Center for Developmental Biology and Kent Waldrep Foundation Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA. Steven.Kernie\@utsouthwestern.edu},
	Pages = {317-26.},
	Pii = {10.1002/jnr.10013},
	Pubmed = {11746349},
	Title = {Brain remodeling due to neuronal and astrocytic proliferation after controlled cortical injury in mice},
	Uuid = {702B0430-E8A9-46C1-8A06-9744D5668C95},
	Volume = {66},
	Year = {2001},
	url = {papers/Kernie_JNeurosciRes2001}}

@article{Kettenmann:1990,
	Abstract = {Microglia are the source of the resident macrophages of the brain and thus belong to one of the most reactive cell types in cerebral tissue. They are attributed to have an important role in a number of pathological conditions, such as multiple sclerosis, viral infections like AIDS, and in lethal or sublethal injuries of neurons where the blood-brain barrier is left intact (Streit et al., 1988; McGeer et al., 1988; Gendelman et al., 1989). Microglia share a number of macrophage characteristics but so far lack a distinguishing positive marker. In this study it is shown that microglia are distinguished from other macrophages by a unique pattern of ion channels. We compared membrane currents of microglial cells with those from peritoneal macrophages cultured under identical conditions. Although in macrophages a delayed outward K+ current was previously described (Randriamampita and Trautmann, 1987), microglial cells lacked any specific outward current. Instead, these cells were characterized by large inwardly rectifying currents, activated by hyperpolarizing voltage steps. The reversal potential in different K+ gradients and the sensitivity of the current to to Ba2+, TEA, and 4-AP indicates that this current is K+ selective. In single-channel recordings, a 30 pS K+ selective channel similar to the classical inward rectifier K+ channel was observed. Thus, the expression of membrane channels served not only to distinguish microglia from other cells inside and outside the brain, e.g., blood macrophages, but also suggests a unique functional state of this cell population.},
	Author = {Kettenmann, H. and Hoppe, D. and Gottmann, K. and Banati, R. and Kreutzberg, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Support, Non-U.S. Gov't;Potassium;Ion Channels;Peritoneal Cavity;Not relevant;11 Glia;Macrophages;Electrophysiology;Cells, Cultured;Potassium Channels;Brain;Membrane Potentials;Animals},
	Medline = {90376370},
	Month = {7},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Department of Neurobiology, University of Heidelberg, Federal Republic of Germany.},
	Pages = {278-87},
	Pubmed = {1697905},
	Title = {Cultured microglial cells have a distinct pattern of membrane channels different from peritoneal macrophages},
	Uuid = {DD16A7BA-6A0D-4274-AD98-AF4AFAB59673},
	Volume = {26},
	Year = {1990}}

@article{Kettenmann:2007,
	Author = {Kettenmann,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {0410462},
	Organization = {Helmut Kettenmann is at the Max Delbr{\"u}ck Center for Molecular Medicine, Robert-Roessle-Strasse 10, 13092 Berlin, Germany.kettenmann\@mdc-berlin.de.},
	Pii = {nature05713},
	Pubmed = {17410127},
	Title = {Neuroscience: The brain's garbage men},
	Uuid = {348AD2EC-2AC4-4078-B6E2-9F6A5E96D50D},
	Year = {2007},
	url = {papers/Kettenmann_Nature2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature05713}}

@article{Khapli:2003,
	Abstract = {Osteoclasts, the multinucleated cells that resorb bone, differentiate from hemopoietic precursors of the monocyte/macrophage lineage in the presence of M-CSF and receptor activator of NF-kappaB ligand (RANKL). In this study we investigated the role of IL-3 in osteoclast differentiation. We show here that IL-3, a cytokine secreted by activated T lymphocytes, inhibits RANKL-induced osteoclast differentiation by a direct action on early osteoclast precursors. Anti-IL-3 Ab neutralized the inhibitory effect of IL-3 on osteoclast differentiation. In addition, IL-3 inhibits TNF-alpha-induced osteoclast differentiation in bone marrow-derived macrophages. However, IL-3 has no inhibitory effect on mature osteoclasts. In osteoclast precursors, IL-3 prevents RANKL-induced nuclear translocation of NF-kappaB by inhibiting the phosphorylation and degradation of IkappaB. RT-PCR analysis revealed that IL-3 down-regulated c-Fos transcription. Interestingly, the osteoclast precursors in the presence of IL-3 showed strong expression of macrophage markers such as Mac-1, MOMA-2, and F4/80. Furthermore, the inhibitory effect of IL-3 on osteoclast differentiation was irreversible, and the osteoclast precursors preincubated in IL-3 were resistant to RANKL action. Thus, our results reveal for the first time that IL-3 acts directly on early osteoclast precursors and irreversibly blocks RANKL-induced osteoclast differentiation by diverting the cells to macrophage lineage.},
	Author = {Khapli, Shruti M. and Mangashetti, Latha S. and Yogesha, S. D. and Wani, Mohan R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Cell Differentiation;Interleukin-3;Ligands;Receptor, Macrophage Colony-Stimulating Factor;NF-kappa B;Animals;Cells, Cultured;Proto-Oncogene Proteins c-fos;Growth Inhibitors;Mice, Inbred BALB C;Proto-Oncogene Proteins;Osteoclasts;Receptors, Cytoplasmic and Nuclear;RNA, Messenger;Macrophages;11 Glia;Membrane Glycoproteins;Tumor Necrosis Factor-alpha;Carrier Proteins;Active Transport, Cell Nucleus;I-kappa B;Cell Lineage;Bone Marrow Cells;Cell Nucleus;Stem Cells;Glycoproteins;Mice;Research Support, Non-U.S. Gov't;Phosphorylation;Humans;Recombinant Proteins;Trans-Activators},
	Medline = {22701037},
	Month = {7},
	Nlm_Id = {2985117R},
	Number = {1},
	Organization = {National Center for Cell Science, Pune, India.},
	Pages = {142-51},
	Pubmed = {12816992},
	Title = {IL-3 acts directly on osteoclast precursors and irreversibly inhibits receptor activator of NF-kappa B ligand-induced osteoclast differentiation by diverting the cells to macrophage lineage},
	Uuid = {678AE7B2-553E-47B0-8FCE-E1418BC17388},
	Volume = {171},
	Year = {2003}}

@article{Kharlamov:1996,
	Abstract = {We have shown recently in rats that photothrombotic local brain injury that is induced by the intravenous injection of the photosensitive dye rose bengal and skull irradiation with a beam of focused light can trigger the expression of the protein p53 and initiate DNA damage in the area surrounding the thrombotic/necrotic core. We hypothesize that these changes are the signs of injury-induced apoptosis. We used pharmacological tools to characterize the injury-triggered DNA damage that we assayed by TUNEL-labeling, followed by a computer-assisted quantitative analysis. In addition, the morphology of apoptotic cells was visualized by fluorescent staining with propidium iodide. The pharmacological approach included: (a) the inhibition of endonucleases by intracerebroventricular injection of aurintricarboxylic acid (ATA, 20 micrograms/5 microliters); (b) the inhibition of protein synthesis by injecting cycloheximide subcutaneously (2.5 mg/kg); and (c) the blockade of glutamate receptors by injecting 2.5 mg/kg dizolcipine (MK- 801) intravenously. These treatments significantly reduced the number of apoptotic cells that we counted in the area surrounding the necrotic core. The results show that injury-induced DNA damage involved de novo synthesis of proteins and an activation of endonucleases, suggesting the occurrence of apoptosis. In this model, apoptosis was associated with an activation of glutamate receptors. Treatments targeted at halting the apoptotic process might provide protection after stroke or after trauma to the brain.},
	Author = {Kharlamov, A. and Uz, T. and Joo, J. Y. and Manev, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Brain Res},
	Keywords = {DNA/metabolism;Rats, Sprague-Dawley;Intracranial Embolism and Thrombosis/chemically;*Light;Rats;*Apoptosis;D;Genetic Techniques;Rose Bengal;Animal;06 Adult neurogenesis injury induced;Support, U.S. Gov't, P.H.S.;induced/etiology/*pathology;Support, Non-U.S. Gov't;Propidium;Male;Brain/metabolism/*pathology},
	Number = {1-2},
	Organization = {Psychiatric Institute, University of Illinois at Chicago 60612, USA.},
	Pages = {1-9.},
	Title = {Pharmacological characterization of apoptotic cell death in a model of photothrombotic brain injury in rats},
	Uuid = {7B3E9F29-D94D-46F9-9EDF-B60FC7D1B444},
	Volume = {734},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8896802}}

@article{Khoury:2007,
	Abstract = {Microglia are the principal immune cells of the brain. In Alzheimer disease, these brain mononuclear phagocytes are recruited from the blood and accumulate in senile plaques. However, the role of microglia in Alzheimer disease has not been resolved. Microglia may be neuroprotective by phagocytosing amyloid-beta (Abeta), but their activation and the secretion of neurotoxins may also cause neurodegeneration. Ccr2 is a chemokine receptor expressed on microglia, which mediates the accumulation of mononuclear phagocytes at sites of inflammation. Here we show that Ccr2 deficiency accelerates early disease progression and markedly impairs microglial accumulation in a transgenic mouse model of Alzheimer disease (Tg2576). Alzheimer disease mice deficient in Ccr2 accumulated Abeta earlier and died prematurely, in a manner that correlated with Ccr2 gene dosage, indicating that absence of early microglial accumulation leads to decreased Abeta clearance and increased mortality. Thus, Ccr2-dependent microglial accumulation plays a protective role in the early stages of Alzheimer disease by promoting Abeta clearance.},
	Author = {Khoury, and Toft, and Hickman, and Means, and Terada, and Geula, and Luster,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1078-8956},
	Journal = {Nat Med},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {9502015},
	Organization = {[1] Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology. 149 13th Street, Charlestown, Massachusetts 02129, USA. [2] Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA.},
	Pii = {nm1555},
	Pubmed = {17351623},
	Title = {Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease},
	Uuid = {9DA797ED-567C-4700-B52F-FA58172B53FB},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nm1555}}

@article{Kida:1993,
	Abstract = {Perivascular cells in the rat brain are an immunophenotypically defined group of cells which can be identified by their expression of the ED2 antigen. The present study investigates the role of perivascular cells as scavengers in the perivascular spaces of the rat brain and the relationship of these cells to microglia, macrophages, pericytes and smooth muscle cells. Particulate matter (Indian ink) was injected selectively into the perivascular spaces of the left caudoputamen of 59 rats. Animals were killed by cardiac perfusion of formalin or glutaraldehyde 2 h-2 years after ink injection. Cerebral hemispheres were examined histologically and immunocytochemically using the ED2 antibody for perivascular cells, ED1 for microglia and macrophages and OX-6 directed against Ia antigen [major histocompatibility complex (MHC) class II]. ED2+ perivascular cells ingested Indian ink in the perivascular spaces and expressed MHC class II antigen. Reactive microglia and macrophages in the perivascular parenchyma expressed ED1, but no ED2+ cells were seen outside the perivascular spaces. Transmission electron microscopy distinguished perivascular cells, which ingested carbon particles, from pericytes, which did not. The results of this study suggest that perivascular cells remain distinct from pericytes, microglia and macrophages and that they play a major role as scavengers in the perivascular spaces of the rat brain. This role reflects the importance of perivascular spaces as drainage pathways for soluble and insoluble material from the brain.},
	Author = {Kida, S. and Steart, P. V. and Zhang, E. T. and Weller, R. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Neuroglia;Research Support, Non-U.S. Gov't;Immunohistochemistry;Microscopy, Electron;Histocompatibility Antigens Class II;Subarachnoid Space;Rats, Wistar;Rats;11 Glia;Macrophages;Blood Vessels;Male;Animals;Brain},
	Medline = {93331866},
	Nlm_Id = {0412041},
	Number = {6},
	Organization = {Department of Neuropathology, Southampton University Medical School, UK.},
	Pages = {646-52},
	Pubmed = {8337943},
	Title = {Perivascular cells act as scavengers in the cerebral perivascular spaces and remain distinct from pericytes, microglia and macrophages},
	Uuid = {C91ADFE9-2E79-42ED-B856-AA615DEFBE13},
	Volume = {85},
	Year = {1993}}

@article{Kida:1995,
	Abstract = {Perivascular cells (PVCs) form an immunophenotypically defined population that plays an important scavenging role in the perivascular fluid drainage pathways in the rat brain; such cells may also act as antigen-presenting cells. The present study tests the hypotheses that (a) PVCs in human brain are distinct from microglia and haematogenous macrophages, and (b) PVCs within astrocytic tumours and peritumoral oedematous brain tissue react in a similar way to PVCs in the rat brain. Paraffin sections of formalin-fixed tissue from 10 astrocytomas, 10 anaplastic astrocytomas, 10 glioblastoma multiforme, peritumoral oedematous brain and from normal human brain were examined immunocytochemically using antibodies HLA-DR beta-chain for MHC class II antigen, PGM1 and MAC 387 directed against macrophage components, MT1 for T lymphocytes and GFAP for astrocytes. No PVCs, microglia or macrophages were labelled by these techniques in paraffin sections of normal brain. Microglia, macrophages recently derived from haematogenous monocytes and PVCs were labelled by immunocytochemistry in all tumours but were more numerous in glioblastomas than in astrocytomas or anaplastic astrocytomas. Perivascular cells were distinguished by their perivascular position, their expression of MHC class II antigen and were labelled by PGM1 antibody but not by MAC 387 antibody. Microglia and monocyte/macrophages, remote from blood vessels, on the other hand, were strongly labelled by MAC 387, moderately by PGM1 and showed weak expression of MHC class II antigen. A similar pattern of staining was seen in peritumoral oedematous tissue. These findings suggest that PVCs form a defined population of resident cells in the human brain and that they are distinct from microglia, monocytes and macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)},
	Author = {Kida, S. and Ellison, D. W. and Steart, P. V. and Weller, R. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Animals;Humans;Up-Regulation;Rats;Middle Aged;Macrophages;Lymphocytes;Brain Edema;Microglia;Major Histocompatibility Complex;11 Glia;Brain Neoplasms;Paraffin Embedding;HLA-DR Antigens;Glioblastoma;Astrocytoma;Adult;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {95334156},
	Month = {4},
	Nlm_Id = {7609829},
	Number = {2},
	Organization = {Department of Pathology (Neuropathology), Southampton General Hospital, UK.},
	Pages = {121-9},
	Pubmed = {7609842},
	Title = {Characterization of perivascular cells in astrocytic tumours and peritumoral oedematous brain},
	Uuid = {23143A5F-78E4-4ECA-8698-6A4E8F3012BC},
	Volume = {21},
	Year = {1995}}

@article{Kiefer:1995,
	Abstract = {Lesions to the nervous system are nearly universally accompanied by a glial response involving both microglia and astrocytes. The growth and immunoregulatory cytokine transforming growth factor-beta 1 (TGF-beta 1) has potent effects on glial cells in vitro and may play a role in regulating glial activation in vivo. Though present only at very low levels in the normal brain, TGF-beta 1 mRNA is strongly upregulated in a number of different experimental models suitable to study glial responses. Following axotomy of the facial nerve of the rat, about a three-fold increase of TGF-beta 1 mRNA in the regenerating nucleus was observed with a time-course closely matching that of glial activation. Putative activated microglial cells are the major cellular source as revealed by in-situ hybridization. TGF-beta 1 was also found to be upregulated around brain tumors, in the spinal cord in response to peripheral nerve inflammation and in the postischemic hippocampus. In all systems investigated, TGF-beta 1 mRNA could be localized predominantly to cells with the typical nuclear morphology of microglia. In the peripheral nervous system, nerve transection leads to a massive increase in TGF-beta mRNA expression both proximal and distal to the cut site. However, whereas TGF-beta 1 mRNA is restricted to the nerve stump in the proximal segment, expression is diffuse and widespread throughout the denervated distal segment where it was localized mainly to cells with macrophage morphology.(ABSTRACT TRUNCATED AT 250 WORDS)},
	Author = {Kiefer, R. and Streit, W. J. and Toyka, K. V. and Kreutzberg, G. W. and Hartung, H. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0736-5748},
	Journal = {Int J Dev Neurosci},
	Keywords = {Nervous System Physiology;Cytokines;Rats;Human;Not relevant;11 Glia;review, tutorial;Transforming Growth Factor beta;Animals;Trauma, Nervous System;review},
	Medline = {96035130},
	Nlm_Id = {8401784},
	Number = {3-4},
	Organization = {Department of Neurology, University of W{\"u}rzburg, Germany.},
	Pages = {331-9},
	Pubmed = {7572285},
	Title = {Transforming growth factor-beta 1: a lesion-associated cytokine of the nervous system},
	Uuid = {52ABA8C7-8B7D-4540-B267-0C4C7F98B1AB},
	Volume = {13},
	Year = {1995}}

@article{Kiefer:1994,
	Abstract = {Malignant gliomas are associated with a state of systemic immunosuppression which appears to be partially mediated by transforming growth factor beta (TGF-beta) secreted from glioma cells. In a recently described animal model of malignant glioma, massive activation of local microglial cells and formation of microglia-derived macrophages has been observed in the absence of detectable tumour regression. We have investigated the in situ expression of TGF-beta in rat glioma as a possible cause of ineffective tumour destruction. Two weeks following unilateral injection of glioma cells, large tumours were observed in the affected hemisphere. In situ hybridization for TGF-beta 1 mRNA revealed an intense signal over the entire tumour area. In the peritumoural area, at sites of glial activation, a lower signal was obtained over cellular profiles containing nuclei typical for microglia, as well as other unidentified cellular profiles. No signal was obtained over the contralateral unaffected hemisphere. Northern blot analysis revealed a strong expression of TGF-beta 1 mRNA in tumour tissue, a lesser signal in the peritumoural reactive brain tissue and virtually no signal in normal tissue. Our data indicate that the experimental rat glioma has the potential to secrete TGF-beta in vivo which might render the microglial infiltration ineffective. TGF-beta expressed by activated microglial cells themselves might further inhibit their tumoricidal potential, thus contributing further to unrestrained tumour growth.},
	Author = {Kiefer, R. and Supler, M. L. and Toyka, K. V. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Animals;Rats;Transforming Growth Factor beta;Neoplasm Transplantation;Female;RNA, Neoplasm;Rats, Wistar;Not relevant;11 Glia;RNA Probes;Brain Neoplasms;RNA, Messenger;In Situ Hybridization;Support, Non-U.S. Gov't;Blotting, Northern;Neuroglia;Cell Transplantation;Glioma},
	Medline = {94232536},
	Month = {1},
	Nlm_Id = {7600130},
	Number = {2},
	Organization = {Department of Neurology, University of W{\"u}rzburg, FRG.},
	Pages = {161-4},
	Pubmed = {8177493},
	Title = {In situ detection of transforming growth factor-beta mRNA in experimental rat glioma and reactive glial cells},
	Uuid = {0AC174DF-946A-48BF-81C9-E4237426B391},
	Volume = {166},
	Year = {1994}}

@article{Kiel:2005,
	Abstract = {To improve our ability to identify hematopoietic stem cells (HSCs) and their localization in vivo, we compared the gene expression profiles of highly purified HSCs and non-self-renewing multipotent hematopoietic progenitors (MPPs). Cell surface receptors of the SLAM family, including CD150, CD244, and CD48, were differentially expressed among functionally distinct progenitors. HSCs were highly purified as CD150(+)CD244(-)CD48(-) cells while MPPs were CD244(+)CD150(-)CD48(-) and most restricted progenitors were CD48(+)CD244(+)CD150(-). The primitiveness of hematopoietic progenitors could thus be predicted based on the combination of SLAM family members they expressed. This is the first family of receptors whose combinatorial expression precisely distinguishes stem and progenitor cells. The ability to purify HSCs based on a simple combination of SLAM receptors allowed us to identify HSCs in tissue sections. Many HSCs were associated with sinusoidal endothelium in spleen and bone marrow, though some HSCs were associated with endosteum. HSCs thus occupy multiple niches, including sinusoidal endothelium in diverse tissues.},
	Author = {Kiel, Mark J. and Yilmaz, Omer H. and Iwashita, Toshihide and Yilmaz, Osman H. and Terhorst, Cox and Morrison, Sean J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {0413066},
	Number = {7},
	Organization = {Howard Hughes Medical Institute andDepartments of Internal Medicine and Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, 48109.},
	Pages = {1109-21},
	Pii = {S0092-8674(05)00540-4},
	Pubmed = {15989959},
	Title = {SLAM Family Receptors Distinguish Hematopoietic Stem and Progenitor Cells and Reveal Endothelial Niches for Stem Cells},
	Uuid = {72AB4025-E7C8-4155-AE2B-D493724F7BC2},
	Volume = {121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.05.026}}

@article{Kiel:2007,
	Abstract = {Stem cells are proposed to segregate chromosomes asymmetrically during self-renewing divisions so that older ('immortal') DNA strands are retained in daughter stem cells whereas newly synthesized strands segregate to differentiating cells. Stem cells are also proposed to retain DNA labels, such as 5-bromo-2-deoxyuridine (BrdU), either because they segregate chromosomes asymmetrically or because they divide slowly. However, the purity of stem cells among BrdU-label-retaining cells has not been documented in any tissue, and the 'immortal strand hypothesis' has not been tested in a system with definitive stem cell markers. Here we tested these hypotheses in haematopoietic stem cells (HSCs), which can be highly purified using well characterized markers. We administered BrdU to newborn mice, mice treated with cyclophosphamide and granulocyte colony-stimulating factor, and normal adult mice for 4 to 10 days, followed by 70 days without BrdU. In each case, less than 6\%of HSCs retained BrdU and less than 0.5\%of all BrdU-retaining haematopoietic cells were HSCs, revealing that BrdU has poor specificity and poor sensitivity as an HSC marker. Sequential administration of 5-chloro-2-deoxyuridine and 5-iodo-2-deoxyuridine indicated that all HSCs segregate their chromosomes randomly. Division of individual HSCs in culture revealed no asymmetric segregation of the label. Thus, HSCs cannot be identified on the basis of BrdU-label retention and do not retain older DNA strands during division, indicating that these are not general properties of stem cells.},
	Author = {Kiel, Mark J. and He, Shenghui and Ashkenazi, Rina and Gentry, Sara N. and Teta, Monica and Kushner, Jake A. and Jackson, Trachette L. and Morrison, Sean J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Animals;Cells, Cultured;Aging;Cyclophosphamide;Chromosome Segregation;Granulocyte Colony-Stimulating Factor;research support, non-u.s. gov't;08 Aberrant cell cycle;Time Factors;Bone Marrow Cells;Animals, Newborn;research support, n.i.h., extramural;Hematopoietic Stem Cells;Mice;24 Pubmed search results 2008;Bromodeoxyuridine;research support, u.s. gov't, non-p.h.s.;Stochastic Processes},
	Month = {9},
	Nlm_Id = {0410462},
	Number = {7159},
	Organization = {Howard Hughes Medical Institute, Life Sciences Institute, Department of Internal Medicine, and Centre for Stem Cell Biology, University of Michigan, Ann Arbor, Michigan 48109-2216, USA.},
	Pages = {238-42},
	Pii = {nature06115},
	Pubmed = {17728714},
	Title = {Haematopoietic stem cells do not asymmetrically segregate chromosomes or retain BrdU},
	Uuid = {6B754168-7C58-4CA8-AC8D-5889E376307E},
	Volume = {449},
	Year = {2007},
	url = {papers/Kiel_Nature2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06115}}

@article{Kim:2000a,
	Abstract = {Inflammation in the brain has been increasingly associated with the development of a number of neurological diseases. The hallmark of neuroinflammation is the activation of microglia, the resident brain immune cells. Injection of bacterial endotoxin lipopolysaccharide (LPS) into the hippocampus, cortex, or substantia nigra of adult rats produced neurodegeneration only in the substantia nigra. Although LPS appeared to impact upon mesencephalic neurons in general, an extensive loss of dopaminergic neurons was observed. Analysis of the abundance of microglia revealed that the substantia nigra had the highest density of microglia. When mixed neuron-glia cultures derived from the rat hippocampus, cortex, or mesencephalon were treated with LPS, mesencephalic cultures became sensitive to LPS at a concentration as low as 10 ng/ml and responded in a dose-dependent manner with the production of inflammatory factors and a loss of dopaminergic and other neurons. In contrast, hippocampal or cortical cultures remained insensitive to LPS treatment at concentrations as high as 10 microg/ml. Consistent with in vivo observations, mesencephalic cultures had fourfold to eightfold more microglia than cultures from other regions. The positive correlation between abundance of microglia and sensitivity to LPS-induced neurotoxicity was further supported by the observation that supplementation with enriched microglia derived from mesencephalon or cortex rendered LPS-insensitive cortical neuron-glia cultures sensitive to LPS-induced neurotoxicity. These data indicate that the region-specific differential susceptibility of neurons to LPS is attributable to differences in the number of microglia present within the system and may reflect levels of inflammation-related factors produced by these cells.},
	Author = {Kim, W. G. and Mohney, R. P. and Wilson, B. and Jeohn, G. H. and Liu, B. and Hong, J. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Pregnancy;Tumor Necrosis Factor;Nerve Degeneration;Neurotoxins;Animals;Cells, Cultured;Rats;Brain;Microglia;Female;Cell Count;Lipopolysaccharides;Hippocampus;Substantia Nigra;11 Glia;Male;Alpha;Rats, Inbred F344;Cerebral Cortex;Neurons;Inflammation;Nitric Oxide},
	Medline = {20394118},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {16},
	Organization = {Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.},
	Pages = {6309-16},
	Pii = {20/16/6309},
	Pubmed = {10934283},
	Title = {Regional difference in susceptibility to lipopolysaccharide-induced neurotoxicity in the rat brain: role of microglia},
	Uuid = {9857E136-E13A-11DA-9DD9-000D9346EC2A},
	Volume = {20},
	Year = {2000},
	url = {papers/Kim_JNeurosci2000.pdf}}

@article{Kim:2005,
	Abstract = {RNA interference (RNAi) is the process of sequence-specific post-transcriptional gene silencing triggered by double-stranded RNAs. In attempts to identify RNAi triggers that effectively function at lower concentrations, we found that synthetic RNA duplexes 25-30 nucleotides in length can be up to 100-fold more potent than corresponding conventional 21-mer small interfering RNAs (siRNAs). Some sites that are refractory to silencing by 21-mer siRNAs can be effectively targeted by 27-mer duplexes, with silencing lasting up to 10 d. Notably, the 27-mers do not induce interferon or activate protein kinase R (PKR). The enhanced potency of the longer duplexes is attributed to the fact that they are substrates of the Dicer endonuclease, directly linking the production of siRNAs to incorporation in the RNA-induced silencing complex. These results provide an alternative strategy for eliciting RNAi-mediated target cleavage using low concentrations of synthetic RNA as substrates for cellular Dicer-mediated cleavage.},
	Author = {Kim, Dong-Ho H. and Behlke, Mark A. and Rose, Scott D. and Chang, Mi-Sook S. and Choi, Sangdun and Rossi, John J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {23 RNAi;23 Technique},
	Month = {2},
	Nlm_Id = {9604648},
	Number = {2},
	Organization = {Division of Molecular Biology, Beckman Research Institute of the City of Hope, 1450 East Duarte Rd., Duarte, California 91010, USA.},
	Pages = {222-6},
	Pii = {nbt1051},
	Pubmed = {15619617},
	Title = {Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy},
	Uuid = {A5A5822B-C605-4375-92D8-A67367AECD24},
	Volume = {23},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt1051}}

@article{Kim:1991,
	Abstract = {Susceptibility of rodent cells to infection by ecotropic murine leukaemia viruses (MuLV) is determined by binding of the virus envelope to a membrane receptor that has multiple membrane-spanning domains. Cells infected by ecotropic MuLV synthesize envelope protein, gp70, which binds to this receptor, thereby preventing additional infections. The consequences of envelope-MuLV receptor binding for the infected host cell have not been directly determined, partly because the cellular function of the MuLV receptor protein is unknown. Here we report a coincidence in the positions of the first eight putative membrane-spanning domains found in the virus receptor and in two related proteins, the arginine and histidine permeases of Saccharomyces cerevisiae (Fig. 1), but not in any other proteins identified by computer-based sequence comparison of the GenBank data base. Xenopus oocytes injected with receptor-encoding messenger RNA show increased uptake of L-arginine, L-lysine and L-ornithine. The transport properties and the expression pattern of the virus receptor behave in ways previously attributed to y+, the principal transporter of cationic L-amino acids in mammalian cells.},
	Author = {Kim, J. W. and Closs, E. I. and Albritton, L. M. and Cunningham, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Arginine;Histidine;Animals;In Vitro;Cations;Biological Transport;Recombinant Proteins;Oocytes;15 Retrovirus mechanism;Hydrogen-Ion Concentration;RNA, Messenger;Leukemia Virus, Murine;Xenopus laevis;Research Support, U.S. Gov't, P.H.S.;Blotting, Northern;Membrane Glycoproteins;Receptors, Virus;Mice;Membrane Transport Proteins;24 Pubmed search results 2008;Membrane Proteins;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {91343001},
	Month = {8},
	Nlm_Id = {0410462},
	Number = {6337},
	Organization = {Howard Hughes Medical Institute, Boston, Massachusetts.},
	Pages = {725-8},
	Pubmed = {1652100},
	Title = {Transport of cationic amino acids by the mouse ecotropic retrovirus receptor},
	Uuid = {068EAED3-EE2C-11DA-8605-000D9346EC2A},
	Volume = {352},
	Year = {1991},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/352725a0}}

@article{Kintner:2002,
	Author = {Kintner, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {J Neurosci},
	Keywords = {Neuroglia/cytology/physiology;Nerve Tissue Proteins/metabolism;01 Adult neurogenesis general;Body Patterning/physiology;Spinal Cord/cytology/embryology/metabolism;Helix-Loop-Helix Motifs;Neurons/*cytology/physiology;Stem Cells/*cytology/physiology;Human;Aging/physiology;A both;Cell Lineage/physiology;Animal;Central Nervous System/*cytology/*embryology/metabolism;Cell Differentiation/physiology;Vertebrates},
	Number = {3},
	Organization = {The Salk Institute for Biological Studies, San Diego, California 92186, USA. kintner\@salk.edu},
	Pages = {639-43.},
	Title = {Neurogenesis in embryos and in adult neural stem cells},
	Uuid = {9834F0AD-4004-4214-BBE9-8E7390087F92},
	Volume = {22},
	Year = {2002},
	url = {papers/Kintner_JNeurosci2002.pdf}}

@article{Kippin:2004,
	Abstract = {Many of the effects of prenatal stress on the endocrine function, brain morphology, and behavior in mammals can be reversed by brief sessions of postnatal separation and handling. We have tested the hypothesis that the effects of both the prenatal and postnatal experiences are mediated by negative and positive regulation of neural stem cell (NSC) number during critical stages in neurodevelopment. We used the in vitro clonal neurosphere assay to quantify NSCs in hamsters that had experienced prenatal stress (maternal restraint stress for 2 hr per day, for the last 7 d of gestation), postnatal handling (maternal-offspring separation for 15 min per day during postnatal days 1-21), orboth. Prenatal stress reduced the number of NSCs derived from the subependyma of the lateral ventricle. The effect was already present at postnatal day 1 and persisted into adulthood (at least 14 months of age). Similarly, prenatal stress reduced in vivo proliferation in the adult subependyma of the lateral ventricle. Conversely, postnatal handling increased NSC number and reversed the effect of prenatal stress. The effects of prenatal stress on NSCs and proliferation and the effect of postnatal handling on NSCs did not differ between male and females. The findings demonstrate that environmental factors can produce changes in NSC number that are present at birth and endure into late adulthood. These changes may underlie some of the behavioral effects produced by prenatal stress and postnatal handling. 1529-2401 Journal Article},
	Author = {Kippin, T. E. and Cain, S. W. and Masum, Z. and Ralph, M. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {J Neurosci},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {11},
	Organization = {Department of Medical Genetics and Microbiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada. tod.kippin\@utoronto.ca},
	Pages = {2832-6},
	Title = {Neural stem cells show bidirectional experience-dependent plasticity in the perinatal mammalian brain},
	Uuid = {64E39CC1-16F9-4642-ACEE-88FB9F0740CF},
	Volume = {24},
	Year = {2004},
	url = {papers/Kippin_JNeurosci2004.pdf}}

@article{Kirichok:2006,
	Abstract = {In mammals, sperm cells become motile during ejaculation and swim up the female reproductive tract. Before fertilization and to overcome various barriers, their motility must be hyperactivated, a motion that is characterized by vigorous asymmetric tail beating. Hyperactivation requires an increase in calcium in the flagella, a process that probably involves plasmalemmal ion channels. Numerous attempts in the past two decades to understand sperm cell channels have been frustrated by the difficulty of measuring spermatozoan transmembrane ion currents. Here, by using a simple approach to patch-clamp spermatozoa and to characterize whole-spermatozoan currents, we describe a constitutively active flagellar calcium channel that is strongly potentiated by intracellular alkalinization. This current is not present in spermatozoa lacking the sperm-specific putative ion channel protein, CatSper1. This plasma membrane protein of the six transmembrane-spanning ion channel superfamily is specifically localized to the principal piece of the sperm tail and is required for sperm cell hyperactivation and male fertility. Our results identify CatSper1 as a component of the key flagellar calcium channel, and suggest that intracellular alkalinization potentiates CatSper current to increase intraflagellar calcium and induce sperm hyperactivation.},
	Author = {Kirichok, Yuriy and Navarro, Betsy and Clapham, David E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Organ Specificity;Ion Channel Gating;Electric Conductivity;Male;Patch-Clamp Techniques;21 Neurophysiology;24 Pubmed search results 2008;Alkalies;Calcium Channels;Spermatozoa;Calcium;Substrate Specificity;Animals;Ion Transport;Sperm Tail;Mice;Hydrogen-Ion Concentration},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {7077},
	Organization = {Howard Hughes Medical Institute, Department of Cardiology, Children's Hospital and Harvard Medical School Enders 1309, Boston, Massachusetts 02115, USA.},
	Pages = {737-40},
	Pii = {nature04417},
	Pubmed = {16467839},
	Title = {Whole-cell patch-clamp measurements of spermatozoa reveal an alkaline-activated Ca2+ channel},
	Uuid = {0E16FF32-351B-4F6E-B06D-CB779D984702},
	Volume = {439},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature04417}}

@article{Kirn:1999,
	Abstract = {Projection neurons are added to the high vocal center (HVC) of adult songbirds. Here we report on events associated with their initial arrival in HVC. Neurons formed in adult canaries were labeled with [(3)H]-thymidine and examined 8, 15, 22, and 31 days later. By 8 days, some [(3)H]-labeled cells with the nuclear profile of postmigratory neurons were already present in HVC but could not be retrogradely labeled by Fluoro-Gold injections in the robust nucleus of the archistriatum (RA); 7 days later, a few such cells could be backfilled from RA. Thus, new neurons may arrive in HVC as much as 1 week prior to establishing connections with RA. By 31 days, 43\%of the [(3)H]-labeled neurons could be backfilled from RA. In no case were new neurons backfilled by tracer injections into Area X, suggesting that newly formed HVC cells do not establish a transient connection with this region. At all survival times, the somata of new neurons were often clustered tightly together with other HVC neurons that differed in age and projection. Between days 15 and 25 after their birth, half of the new HVC neurons disappeared. We conclude: (1) that neurons arrive in HVC earlier than previously thought, (2) that soon after their arrival they become part of cell clusters in HVC, and (3) that in addition to the previously described death of new neurons that occurs over a period of months, there is an early wave of death that occurs soon after new neurons adopt a postmigratory phenotype.},
	Author = {Kirn, J. R. and Fishman, Y. and Sasportas, K. and Alvarez-Buylla, A. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Comp Neurol},
	Keywords = {01 Adult neurogenesis general;Fluorescent Dyes/diagnostic use;Canaries/*anatomy &histology/growth &development;Cerebral Ventricles/cytology;A abstr;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Male;Cell Movement;Telencephalon/*cytology/growth &development;Cell Lineage},
	Number = {3},
	Organization = {Biology Department, Wesleyan University, Middletown, Connecticut 06459- 0170, USA. jrkirn\@wesleyan.edu},
	Pages = {487-94.},
	Title = {Fate of new neurons in adult canary high vocal center during the first 30 days after their formation},
	Uuid = {76F6D583-D85E-4F3D-8C5C-9C5D06DD8FC8},
	Volume = {411},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10413781}}

@article{Kirn:1991,
	Abstract = {Neurons are produced in the adult canary telencephalon. Many of these cells are incorporated into the high vocal center (nucleus HVC), which participates in the control of learned song. In the present work, 3H- thymidine and fluorogold were employed to follow the differentiation and survival of HVC neurons born in adulthood. We found that many HVC neurons born in September grow long axons to the robust nucleus of the archistriatum (nucleus RA) and thus become part of the efferent pathway for song control. Many of these new neurons have already established their connections with RA by 30 d after their birth. By 240 d, 75-80\%of the September-born HVC neurons project to RA. Most of these new projection neurons survive at least 8 months. The longevity of HVC neurons born in September suggests that these cells remain part of the vocal control circuit long enough to participate in the yearly renewal of the song repertoire.},
	Author = {Kirn, J. R. and Alvarez-Buylla, A. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Cell Differentiation;Axons/physiology;Thymidine/metabolism;Neurons/cytology/*physiology;Animal;Brain/cytology/*physiology;Telencephalon/cytology/*physiology;DNA Replication;Male;01 Adult neurogenesis general;Learning;Support, U.S. Gov't, P.H.S.;Canaries/*physiology;Tritium;*Vocalization, Animal;Autoradiography;A abstr},
	Number = {6},
	Organization = {Rockefeller University Field Research Center, Millbrook, New York 12545.},
	Pages = {1756-62.},
	Title = {Production and survival of projection neurons in a forebrain vocal center of adult male canaries},
	Uuid = {B7B2FBB3-655B-4AB3-BB47-055D74443A41},
	Volume = {11},
	Year = {1991},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=2045885}}

@article{Kirschenbaum:1994,
	Abstract = {It has traditionally been held that the adult brain is incapable of significant self-repair, due in part to its inability to generate new neurons. Nevertheless, rodents and birds have been found to harbor neural precursor cells in adulthood. We asked whether the adult human brain might retain such precursors, by culturing samples of temporal lobe under conditions permissive for neuronal differentiation, while exposed to 3H-thymidine. Adult human temporal lobe cultures, derived from cortex, subcortex, and periventricular subependymal zone (SZ), were incubated for 7-28 d, stained for neuronal and glial antigens, and autoradiographed. Neuron-like cells were found in explant outgrowths and monolayer dissociates of SZ and periventricular white matter, but not cortex; they expressed neuronal antigens including MAP-2, MAP-5, NF, and N-CAM, and were GFAP-. Neurons responded to K+ depolarization with rapid and reversible increases in intracellular Ca2+, with much greater increments than those noted in glia. Although most neurons were not 3H-thymidine labeled, a small number of MAP-2+ and MAP-5+/GFAP- cells did incorporate 3H-thymidine, suggesting neuronal production from precursor mitosis. Rare 3H-thymidine+ neurons were also found in cultures of subventricular white matter; in these, GFAP+ astrocytic mitogenesis was common, while O4+ oligodendrocytes, although the predominant cell type, were largely postmitotic. Thus, the adult human forebrain harbors precursor cells that retain the potential for neuronal production and differentiation in vitro. eng Journal Article},
	Author = {Kirschenbaum, B. and Nedergaard, M. and Preuss, A. and Barami, K. and Fraser, R. A. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Journal = {Cereb Cortex},
	Keywords = {Neurons/*physiology;Human;Cells, Cultured;Image Processing, Computer-Assisted;Thymidine/metabolism;Phenotype;Female;02 Adult neurogenesis migration;Calcium/metabolism;Male;BB abstr;03 Adult neurogenesis progenitor source;Middle Age;Support, Non-U.S. Gov't;Neuroglia/physiology;Adult;Support, U.S. Gov't, P.H.S.;Cell Differentiation/physiology;Immunohistochemistry;Autoradiography;Adolescence;Culture Media;Prosencephalon/cytology/*growth &development},
	Number = {6},
	Organization = {Department of Neurology, Cornell University Medical College, New York, New York 10021.},
	Pages = {576-89.},
	Title = {In vitro neuronal production and differentiation by precursor cells derived from the adult human forebrain},
	Uuid = {D78D30D6-98C3-450D-8FCC-D90921194C05},
	Volume = {4},
	Year = {1994}}

@article{Kirschenbaum:1999,
	Abstract = {Neurons continue to be born in the subventricular zone (SVZ) of the lateral ventricles of adult mice. These cells migrate as a network of chains through the SVZ and the rostral migratory stream (RMS) into the olfactory bulb (OB), where they differentiate into mature neurons. The OB is the only known target for these neuronal precursors. Here, we show that, after elimination of the OB, the SVZ and RMS persist and become dramatically larger. The proportion of dividing [bromodeoxyuridine (BrdU)-labeled] or dying (pyknotic or terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end- labeled) cells in the RMS was not significantly affected at 3 d or 3 weeks after bulbectomy (OBX). However, by 3 months after OBX, the percentage of BrdU-labeled cells in the RMS decreased by half and that of dying cells doubled. Surprisingly, the rostral migration of precursors continued along the RMS after OBX. This was demonstrated by focal microinjections of BrdU and grafts of SVZ cells carrying LacZ under the control of a neuron-specific promoter gene. Results indicate that the OB is not essential for proliferation and the directional migration of SVZ precursors.},
	Author = {Kirschenbaum, B. and Doetsch, F. and Lois, C. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Neurosci},
	Keywords = {Cerebral Ventricles/*cytology;Neurons/*cytology/enzymology/*physiology;Olfactory Bulb/*physiology;Animal;02 Adult neurogenesis migration;Time Factors;Mice, Transgenic/genetics;Male;Stem Cells/*cytology/*physiology;Mice, Inbred Strains;Phosphopyruvate Hydratase/genetics/metabolism;Cell Division/physiology;B-9;Nerve Net/physiology;Cell Transplantation;Support, U.S. Gov't, P.H.S.;Mice;Cell Movement/physiology},
	Number = {6},
	Organization = {The Rockefeller University, New York, New York 10021, USA.},
	Pages = {2171-80.},
	Title = {Adult subventricular zone neuronal precursors continue to proliferate and migrate in the absence of the olfactory bulb},
	Uuid = {0905D5EA-E218-4058-A12B-3A78647B6FF9},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10066270%20http://www.jneurosci.org/cgi/content/full/19/6/2171}}

@article{Kirschenbaum:1995,
	Abstract = {Neuronal precursor cells persist in the adult forebrain ependymal/subependymal zone (SZ) and have been found to produce neurons in cultures derived from birds, rodents, and humans. We postulated that the survival of neurons generated from these cells might be constrained in adulthood by the local absence of trophic support. To test this hypothesis, we established explant cultures of adult rat forebrain SZ and assessed the effect of defined neurotrophins on the survival of new neurons arising from these explants. We found that microtubule-associated protein 2+ neurons arose from explants derived from a wide area of the SZ, spanning the rostral 6 mm of the ventricular system. In cultures exposed to brain-derived neurotrophic factor (BDNF), >35\%of new neurons survived at 22 days in vitro (DIV), and >25\%survived at 42 DIV, concurrent with the virtually complete loss of neurons in unsupplemented controls. The surviving cells expressed trkB, the high-affinity receptor for BDNF. In contrast, neither nerve growth factor nor neurotrophic factor 3 enhanced neuronal survival. Thus, BDNF supports the survival of neurons produced by the adult rat forebrain and may act as a permissive factor for neuronal recruitment in adulthood. 0027-8424 Journal Article},
	Author = {Kirschenbaum, B. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Nerve Growth Factors/*pharmacology;Animals;Receptor, Ciliary Neurotrophic Factor;Rats;Thymidine/metabolism;Comparative Study;Brain-Derived Neurotrophic Factor;Neurotrophin 3;Rats, Sprague-Dawley;Kinetics;C abstr;Receptors, Nerve Growth Factor/analysis/biosynthesis;Analysis of Variance;Support, Non-U.S. Gov't;Nerve Tissue Proteins/*pharmacology;Prosencephalon/anatomy &histology/*cytology;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Tritium;Organ Culture;Neurons/*cytology/drug effects;Cell Division/drug effects},
	Number = {1},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.},
	Pages = {210-4},
	Pubmed = {7816819},
	Title = {Brain-derived neurotrophic factor promotes the survival of neurons arising from the adult rat forebrain subependymal zone},
	Uuid = {F8404A44-8522-4A3D-A530-4E67950EE7D9},
	Volume = {92},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7816819}}

@article{Kishi:1990,
	Abstract = {In order to examine the relationship between radial glial fibers and the migrating bipolar subependymal cells which are considered to be post-mitotic precursors of granule cells in the rat olfactory bulb, the arrangement of radial glial fibers along the anterior lateral and olfactory ventricles was analysed by Golgi techniques, immunohistochemical demonstration of glial fibrillary acidic protein, and electron microscopy. In rats during their first 3 weeks of life, the bipolar subependymal cells migrate along the anterior lateral and olfactory ventricles into the center of the olfactory bulb, whereas the radial glial fibers radiating from the ventricular surface are arranged rather perpendicularly to the direction of migration of bipolar cells. Hence radial glial fibers in this region are not considered to act as guides for the rostralwards migration of subependymal cells.},
	Author = {Kishi, K. and Peng, J. Y. and Kakuta, S. and Murakami, K. and Kuroda, M. and Yokota, S. and Hayakawa, S. and Kuge, T. and Asayama, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0914-9465},
	Journal = {Arch Histol Cytol},
	Keywords = {Ependyma;Glial Fibrillary Acidic Protein;Neuroglia;Immunohistochemistry;Microscopy, Electron;Rats;Stem Cells;Olfactory Bulb;Animals;Cell Movement;Rats, Inbred Strains;13 Olfactory bulb anatomy;Axons},
	Medline = {90321712},
	Month = {5},
	Nlm_Id = {8806082},
	Number = {2},
	Organization = {Department of Anatomy, Toho University School of Medicine, Tokyo, Japan.},
	Pages = {219-26},
	Pubmed = {2372444},
	Title = {Migration of bipolar subependymal cells, precursors of the granule cells of the rat olfactory bulb, with reference to the arrangement of the radial glial fibers},
	Uuid = {FBEC0A0A-D067-11DA-8A8C-000D9346EC2A},
	Volume = {53},
	Year = {1990}}

@article{Kishi:1987,
	Abstract = {The morphology and the development of the cells in the subependymal layer and of granule cells of the olfactory bulb were examined by Nissl and Golgi staining in postnatal rats. The subependymal layer around the anterior lateral ventricle extends into the center of the olfactory bulb. The mitotic indexes in the subependymal layer are high at the level of the anterior horn of the lateral ventricle and very low inside the olfactory bulb during the first 3 weeks after birth. Golgi-stained subependymal cells are classified into two main groups. One group consists of smoothly contoured bipolar cells with leading processes tipped by large growth cones and with trailing processes. They make up a majority of Golgi-stained subependymal cells during the first 3 weeks of age, and smaller numbers of them continue to exist at 37 and 60 days. They migrate with their growth cones oriented toward the olfactory bulb from the level of the anterior lateral ventricle into the granular layer of the olfactory bulb, where they differentiate into the definitive granule cells: their somata enlarge; the leading processes elongate, branch, sprout many gemmules, and become the peripheral processes; and the trailing processes become the basal dendrites. The other group contains relatively large cells with many cytoplasmic processes that are considered to belong to the glial cell line.},
	Author = {Kishi, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Cell Differentiation;Neuroglia;Rats;Olfactory Bulb;Animals;Cell Movement;13 Olfactory bulb anatomy;Neurons},
	Medline = {87195543},
	Month = {4},
	Nlm_Id = {0406041},
	Number = {1},
	Pages = {112-24},
	Pubmed = {3571532},
	Title = {Golgi studies on the development of granule cells of the rat olfactory bulb with reference to migration in the subependymal layer},
	Uuid = {FBEC1551-D067-11DA-8A8C-000D9346EC2A},
	Volume = {258},
	Year = {1987},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.902580109}}

@article{Kitai:2000,
	Abstract = {Microglia are the major target of HIV-1 infection in the brain. Microglial infection is CD4-dependent, but the role of chemokine receptors CCR5 and CCR3 and their natural ligands in modulating HIV-1 infection in microglia has been questioned. In primary human fetal microglial cultures, we demonstrate that HIV-1 infection of these cells is dependent on CCR5, since an antibody to CCR5 completely blocked productive infection. Anti-CCR3, in contrast, had a smaller inhibitory effect which was not statistically significant. The chemokine ligands for CCR5, RANTES and MIP-1beta, also potently inhibited HIV-1 infection in microglia, but the third ligand MIP-1alpha failed to show inhibition. Interestingly, when microglial cultures were treated with antibodies specific to each of these chemokines, HIV-1 infection was enhanced by anti-RANTES and anti-MIP-1beta, but not by anti-MIP-1alpha. These results demonstrate the presence of endogenous chemokines that act as endogenous inhibitors of HIV-1 infection in microglia. Additionally, IFNbeta, a known anti-viral cytokine, also provided potent inhibition of viral infection as well as induction of all three chemokines in microglia. These results suggest the possibility that type I interferon can down-modulate microglial HIV-1 infection in vivo by multiple mechanisms.},
	Author = {Kitai, R. and Zhao, M. L. and Zhang, N. and Hua, L. L. and Lee, S. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {AIDS Dementia Complex;Human;Antiviral Agents;HIV-1;Cells, Cultured;HIV Envelope Protein gp41;Humans;Brain;Microglia;Lipopolysaccharides;11 Glia;Giant Cells;Research Support, U.S. Gov't, P.H.S.;RANTES;Support, U.S. Gov't, P.H.S.;Receptors, CCR5;Macrophage Inflammatory Protein-1;Virus Replication;Interferon-beta;Neuroimmunomodulation},
	Medline = {20481316},
	Month = {10},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Pathology (Neuropathology), Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.},
	Pages = {230-9},
	Pii = {S0165572800003155},
	Pubmed = {11024554},
	Title = {Role of MIP-1beta and RANTES in HIV-1 infection of microglia: inhibition of infection and induction by IFNbeta},
	Uuid = {87A71E2F-EF88-4E69-BB21-4D5C3C1B5D04},
	Volume = {110},
	Year = {2000}}

@article{Kitamura:2003,
	Abstract = {Most of the human genome has now been sequenced and about 30,000 potential open reading frames have been identified, indicating that we use these 30,000 genes to functionally organize our biologic activities. However, functions of many genes are still unknown despite intensive efforts using bioinformatics as well as transgenic and knockout mice. Retrovirus-mediated gene transfer is a powerful tool that can be used to understand gene functions. We have developed a variety of retrovirus vectors and efficient packaging cell lines that have facilitated the development of efficient functional expression cloning methods. In this review, we describe retrovirus-mediated strategies used for investigation of gene functions and function-based screening strategies. 0301-472x Journal Article Review Review, Tutorial},
	Author = {Kitamura, T. and Koshino, Y. and Shibata, F. and Oki, T. and Nakajima, H. and Nosaka, T. and Kumagai, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {Exp Hematol},
	Keywords = {Retroviridae/*genetics;*Gene Transfer Techniques;Structure-Activity Relationship;Virus Assembly;*Genomics;Genetic Vectors/*genetics;Human;J, T, pdf;15 Retrovirus mechanism;Support, Non-U.S. Gov't;Animals;Cloning, Molecular;Protein Sorting Signals;Polymerase Chain Reaction},
	Number = {11},
	Organization = {Divisions of Cellular Therapy and Hematopoietic Factors, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. kitamura\@ims.u-tokyo.ac.jp},
	Pages = {1007-14},
	Title = {Retrovirus-mediated gene transfer and expression cloning: powerful tools in functional genomics},
	Uuid = {926A223C-1429-42DB-B3CA-F38163B75A74},
	Volume = {31},
	Year = {2003},
	url = {papers/Kitamura_ExpHematol2003.pdf}}

@article{Kitamura:2002,
	Abstract = {Male embryonic mice with mutations in the X-linked aristaless-related homeobox gene (Arx) developed with small brains due to suppressed proliferation and regional deficiencies in the forebrain. These mice also showed aberrant migration and differentiation of interneurons containing gamma-aminobutyric acid (GABAergic interneurons) in the ganglionic eminence and neocortex as well as abnormal testicular differentiation. These characteristics recapitulate some of the clinical features of X-linked lissencephaly with abnormal genitalia (XLAG) in humans. We found multiple loss-of-function mutations in ARX in individuals affected with XLAG and in some female relatives, and conclude that mutation of ARX causes XLAG. The present report is, to our knowledge, the first to use phenotypic analysis of a knockout mouse to identify a gene associated with an X-linked human brain malformation.},
	Author = {Kitamura, Kunio and Yanazawa, Masako and Sugiyama, Noriyuki and Miura, Hirohito and Iizuka-Kogo, Akiko and Kusaka, Masatomo and Omichi, Kayo and Suzuki, Rika and Kato-Fukui, Yuko and Kamiirisa, Kyoko and Matsuo, Mina and Kamijo, Shin-ichi and Kasahara, Megumi and Yoshioka, Hidefumi and Ogata, Tsutomu and Fukuda, Takayuki and Kondo, Ikuko and Kato, Mitsuhiro and Dobyns, William B. and Yokoyama, Minesuke and Morohashi, Ken-ichirou},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {Cell Differentiation;Apoptosis;Genetic Vectors;Alleles;24 Pubmed search results 2008;Epithelial Cells;Immunohistochemistry;Genitalia;Male;Models, Genetic;10 Development;Animals;Brain;Linkage (Genetics);Testis;Base Sequence;Cell Movement;Phenotype;Homeodomain Proteins;X Chromosome;Transcription Factors;Transfection;Cell Division;Molecular Sequence Data;Bromodeoxyuridine;research support, u.s. gov't, p.h.s.;Mutation;comparative study;Amino Acid Sequence;Prosencephalon;Syndrome;DNA, Complementary;research support, non-u.s. gov't;Mice, Knockout;Mice;Neurons;Humans;Microscopy, Fluorescence;10 genetics malformation},
	Month = {11},
	Nlm_Id = {9216904},
	Number = {3},
	Organization = {Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan. kunio\@libra.ls.m-kagaku.co.jp},
	Pages = {359-69},
	Pii = {ng1009},
	Pubmed = {12379852},
	Title = {Mutation of ARX causes abnormal development of forebrain and testes in mice and X-linked lissencephaly with abnormal genitalia in humans},
	Uuid = {4EA79F44-20F3-4D2D-99AE-DDC18EEF1381},
	Volume = {32},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ng1009}}

@article{Klein:2001,
	Abstract = {Ephrins are cell surface associated ligands for Eph receptor tyrosine kinases and are implicated in repulsive axon guidance, cell migration, topographic mapping and angiogenesis. During the past year, Eph receptors have been shown to associate with glutamate receptors in excitatory neurons, suggesting a role in synapse formation or function. Moreover, ephrin/Eph signaling appears to regulate neural stem cell proliferation and migration in adult mouse brains. The mode of action of ephrin/Ephs has been expanded from repulsion to adhesion and from cell surface attachment to regulated cleavage.},
	Author = {Klein, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0955-0674},
	Journal = {Curr Opin Cell Biol},
	Keywords = {Receptor Protein-Tyrosine Kinases;Synapses;Transcription Factors;10 Development;research support, non-u.s. gov't;Ephrin-A2;Signal Transduction;10 circuit formation;Receptor, EphA1;Animals;Humans;24 Pubmed search results 2008;review;Neurons},
	Month = {4},
	Nlm_Id = {8913428},
	Number = {2},
	Organization = {European Molecular Biology Laboratory, Meyerhofstrasse 1, D-69117 Heidelberg, Germany. klein\@embl-heidelberg.de},
	Pages = {196-203},
	Pii = {S0955-0674(00)00197-6},
	Pubmed = {11248553},
	Title = {Excitatory Eph receptors and adhesive ephrin ligands},
	Uuid = {A2F5110E-00E6-4675-9A8F-CA1B91EABB52},
	Volume = {13},
	Year = {2001}}

@article{Klein:2003,
	Abstract = {0021-9738 Journal Article Review Review, Tutorial},
	Author = {Klein, J. A. and Ackerman, S. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Clin Invest},
	Keywords = {*Cell Cycle;Human;Neurodegenerative Diseases/*etiology;Reactive Oxygen Species/metabolism;08 Aberrant cell cycle;EE pdf;Cell Death;Support, U.S. Gov't, P.H.S.;Superoxides/metabolism;Animals;Neurons/physiology;*Oxidative Stress},
	Number = {6},
	Organization = {The Jackson Laboratory, Bar Harbor, Maine 04609, USA.},
	Pages = {785-93},
	Pubmed = {12639981},
	Title = {Oxidative stress, cell cycle, and neurodegeneration},
	Uuid = {1A7BC487-7F66-4CC6-8002-D9272879163A},
	Volume = {111},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12639981}}

@article{Klein:2002,
	Abstract = {Harlequin (Hq) mutant mice have progressive degeneration of terminally differentiated cerebellar and retinal neurons. We have identified the Hq mutation as a proviral insertion in the apoptosis-inducing factor (Aif) gene, causing about an 80\%reduction in AIF expression. Mutant cerebellar granule cells are susceptible to exogenous and endogenous peroxide-mediated apoptosis, but can be rescued by AIF expression. Overexpression of AIF in wild-type granule cells further decreases peroxide-mediated cell death, suggesting that AIF serves as a free radical scavenger. In agreement, dying neurons in aged Hq mutant mice show oxidative stress. In addition, neurons damaged by oxidative stress in both the cerebellum and retina of Hq mutant mice re-enter the cell cycle before undergoing apoptosis. Our results provide a genetic model of oxidative stress-mediated neurodegeneration and demonstrate a direct connection between cell cycle re-entry and oxidative stress in the ageing central nervous system. 0028-0836 Journal Article},
	Author = {Klein, J. A. and Longo-Guess, C. M. and Rossmann, M. P. and Seburn, K. L. and Hurd, R. E. and Frankel, W. N. and Bronson, R. T. and Ackerman, S. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {Nature},
	Keywords = {Animals;Cell Survival/drug effects;Cells, Cultured;Apoptosis/drug effects;Mice, Mutant Strains;Aging;Hydrogen Peroxide/pharmacology;Phenotype;Membrane Proteins/*deficiency/*genetics/metabolism;Flavoproteins/*genetics/metabolism;Retina/metabolism/*pathology;EE pdf;Cell Cycle/drug effects;Neurons/drug effects/metabolism/*pathology;Mutation/*genetics;Lipid Peroxidation;08 Aberrant cell cycle;*Oxidative Stress/drug effects;Purkinje Cells/metabolism/pathology;Down-Regulation;Cerebellum/drug effects/metabolism/*pathology;Support, U.S. Gov't, P.H.S.;Mice;Microscopy, Electron;Free Radical Scavengers/metabolism;Polymerase Chain Reaction;Catalase/metabolism;Glutathione/metabolism},
	Number = {6905},
	Organization = {The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA.},
	Pages = {367-74},
	Title = {The harlequin mouse mutation downregulates apoptosis-inducing factor},
	Uuid = {24A4FF15-0393-4007-925A-5CFC42DA3471},
	Volume = {419},
	Year = {2002},
	url = {papers/Klein_Nature2002.pdf}}

@article{Klement:1972,
	Author = {Klement, V. and Nicolson, M. O. and Gilden, R. V. and Oroszlan, S. and Sarma, P. S. and Rongey, R. W. and Gardner, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0090-0028},
	Journal = {Nat New Biol},
	Keywords = {Microscopy, Electron;Oncogenic Viruses;Antigens, Viral;Animals;RNA Viruses;Rats;15 Retrovirus mechanism;Uridine;Retroviridae;Sarcoma, Experimental;Cell Line;Immunodiffusion;Sarcoma Viruses, Avian;DNA Nucleotidyltransferases;24 Pubmed search results 2008;Bromodeoxyuridine;Chickens;15 ERVs retroelements;Tritium;Cell Transformation, Neoplastic},
	Medline = {73020642},
	Month = {8},
	Nlm_Id = {0410463},
	Number = {86},
	Pages = {234-7},
	Pubmed = {4342693},
	Title = {Rat C-type virus induced in rat sarcoma cells by 5-bromodeoxyuridine},
	Uuid = {8DFFB767-4328-11DB-A5D2-000D9346EC2A},
	Volume = {238},
	Year = {1972}}

@article{Klesney-Tait:2006,
	Abstract = {TREM proteins are a family of cell surface receptors that participate in diverse cell processes, including inflammation, bone homeostasis, neurological development and coagulation. TREM-1, the first to be identified, acts to amplify inflammation. Other TREM proteins regulate the differentiation and function of macrophages, microglia, dendritic cells, osteoclasts and platelets. Here we discuss the state of the field, putative ligands of TREM proteins and the challenges that remain in understanding TREM biology.},
	Author = {Klesney-Tait, Julia and Turnbull, Isaiah R. and Colonna, Marco},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1529-2908},
	Journal = {Nat Immunol},
	Keywords = {14 Immune;11 Glia;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {100941354},
	Number = {12},
	Organization = {Washington University School of Medicine, Department of Pathology and Immunology, Saint Louis, Missouri 63110, USA.},
	Pages = {1266-73},
	Pii = {ni1411},
	Pubmed = {17110943},
	Title = {The TREM receptor family and signal integration},
	Uuid = {92CCE245-9D8E-441D-9EC6-540EF121B04F},
	Volume = {7},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ni1411}}

@article{Kloss:1999,
	Abstract = {Integrins are a large family of heterodimeric glycoproteins that play a crucial role in cell adhesion during development, inflammation, and tissue repair. In the current study, we investigated the localization of different integrin subunits in the mouse facial motor nucleus and their regulation after transection of the facial nerve. In the normal mouse brain, there was clear immunoreactivity for alpha5-, alpha6-, and beta1-integrin subunits on blood vessel endothelia and for alphaM- and beta2-subunits on resting parenchymal microglia. Facial nerve transection led to an up-regulation of the beta1-subunit on the axotomized neurons and an increase in the alpha4-, alpha5-, alpha6-, beta1-, alphaM-, alphaX-, and beta2-subunits on the adjacent, activated microglia. Quantification of the microglial integrins revealed two different expression patterns. The subunits alpha5 and alpha6 showed a monophasic increase with a maximum at day 4, the alphaM-subunit a biphasic regulation, with an early peak at day 1 and an elevated plateau between day 14 and 42. At day 14, there was also an influx of lymphocytes immunoreactive for the alpha4beta1- and alphaLbeta2-integrins, which aggregated at sites of neural debris and phagocytotic microglia. This finding was accompanied by a significant increase of the alpha5beta1-integrin on blood vessel endothelia. In summary, facial axotomy is followed by a strong and cell-type-specific expression of integrins on the affected neurons and on surrounding microglia, lymphocytes, and vascular endothelia. The presence of several, strikingly different temporal patterns suggests a selective involvement of these molecules in the different adhesive events during regeneration in the central nervous system.},
	Author = {Kloss, C. U. and Werner, A. and Klein, M. A. and Shen, J. and Menuz, K. and Probst, J. C. and Kreutzberg, G. W. and Raivich, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Nerve Regeneration;Organ Specificity;Facial Nerve Injuries;Antibodies, Monoclonal;Brain;Animals;Phagocytosis;Dimerization;Base Sequence;Molecular Sequence Data;Integrins;RNA, Messenger;Spleen;Retrograde Degeneration;11 Glia;Microscopy, Immunoelectron;Cell Adhesion;Gene Expression Regulation;Comparative Study;Facial Nerve;Time Factors;Female;Microglia;Endothelium, Vascular;Lymphocytes;Microscopy, Confocal;Support, Non-U.S. Gov't;Fluorescent Antibody Technique, Indirect;Image Processing, Computer-Assisted;Polymerase Chain Reaction;Nerve Tissue Proteins;Astrocytes;Mice},
	Medline = {99333552},
	Month = {8},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Neuromorphology, Max-Planck Institute for Neurobiology, D-82152 Martinsried, Germany.},
	Pages = {162-78},
	Pii = {10.1002/(SICI)1096-9861(19990816)411:1<162::AID-CNE12>3.0.CO;2-W},
	Pubmed = {10404114},
	Title = {Integrin family of cell adhesion molecules in the injured brain: regulation and cellular localization in the normal and regenerating mouse facial motor nucleus},
	Uuid = {B022642D-3E79-45C4-AEC4-783601F9509B},
	Volume = {411},
	Year = {1999}}

@article{Klump:2001,
	Abstract = {Retroviral vector-mediated expression of the homeoboxgene, HoxB4, in hematopoietic cells has been reported to mediate a benign expansion of gene-modified hematopoietic stem and precursor cells in vivo. In the present study, we used a novel coexpression strategy for coordinated expression of HoxB4 along with a cytoplasmic protein from a retroviral vector. The novel coexpression strategy, based on cotranslational protein separation mediated by the 2A sequence of foot-and-mouth disease virus (FMDV), allows an indirect quantification of HoxB4 expression levels when inserting a reporter such as the enhanced green fluorescent protein (GFP) in the retroviral vector. Presence of the 2A sequence did not interfere with the correct subcellular localization of HoxB4 (nuclear) and GFP (cytoplasmic), nor with the titer of bicistronic vectors, and mediated functional long-term coexpression (at least 1 year) of GFP and HoxB4 after transplantation of transduced mouse bone marrow cells in mice.},
	Author = {Klump, H. and Schiedlmeier, B. and Vogt, B. and Ryan, M. and Ostertag, W. and Baum, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;Animals;Fluorescent Antibody Technique;Cytoplasm;Female;Mice, Inbred C57BL;Retroviridae;11 Glia;Male;Time Factors;Aphthovirus;Green Fluorescent Proteins;Polioviruses;Genetic Vectors;Gene Therapy;Blotting, Western;Cell Nucleus;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {21313499},
	Month = {5},
	Nlm_Id = {9421525},
	Number = {10},
	Organization = {Heinrich-Pette-Institut for Experimental Virology and Immunology, Martinistrasse 52, D-20251 Hamburg, Germany.},
	Pages = {811-7},
	Pubmed = {11420646},
	Title = {Retroviral vector-mediated expression of HoxB4 in hematopoietic cells using a novel coexpression strategy},
	Uuid = {1E9F9CDB-7744-4712-88D5-E3C4838FCB72},
	Volume = {8},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301447}}

@article{Kobari:2000,
	Abstract = {The aim of the present report is to describe clinically relevant culture conditions that support the expansion of primitive hematopoietic progenitors/stem cells, with maintenance of their hematopoietic potential as assessed by in vitro assays and the NOD-SCID in vivo repopulating capacity.CD34(+) cord blood (CB) cells were cultured in serum-free medium containing stem cell factor, Flt3 ligand, megakaryocyte growth and development factor, and granulocyte colony-stimulating factor. After 14 days, the primitive functions of expanded and nonexpanded cells were determined in vitro using clonogenic cell (colony-forming cells, long-term culture initiating cell [LTC-IC], and extended [E]-LTC-IC) and lymphopoiesis assays (NK, B, and T) and in vivo by evaluating long-term engraftment of the bone marrow of NOD-SCID mice. The proliferative potential of these cells also was assessed by determining their telomere length and telomerase activity.Levels of expansion were up to 1,613-fold for total cells, 278-fold for colony-forming unit granulocyte-macrophage, 47-fold for LTC-IC, and 21-fold for E-LTC-IC. Lymphoid B-, NK, and T-progenitors could be detected. When the expanded populations were transplanted into NOD-SCID mice, they were able to generate myeloid progenitors and lymphoid cells for 5 months. These primitive progenitors engrafted the NOD-SCID bone marrow, which contained LTC-IC at the same frequency as that of control transplanted mice, with conservation of their clonogenic capacity. Moreover, human CD34(+)CDl9(-) cells sorted from the engrafted marrow were able to generate CD19(+) B-cells, CD56(+)CD3(-) NK cells, and CD4(+)CD8(+)alphabetaTCR(+) T-cells in specific cultures. Our expansion protocol also maintained the telomere length in CD34(+) cells, due to an 8.8-fold increase in telomerase activity over 2 weeks of culture.These experiments provide strong evidence that expanded CD34(+) CB cells retain their ability to support long-term hematopoiesis, as shown by their engraftment in the NOD-SCID model, and to undergo multilineage differentiation along all myeloid and the B-, NK, and T-lymphoid pathways. The expansion protocol described here appears to maintain the hematopoietic potential of CD34(+) CB cells, which suggests its relevance for clinical applications.},
	Author = {Kobari, L. and Pflumio, F. and Giarratana, M. and Li, X. and Titeux, M. and Izac, B. and Leteurtre, F. and Coulombel, L. and Douay, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0301-472X},
	Journal = {Exp Hematol},
	Keywords = {T-Lymphocytes;Cell Differentiation;Mice, Inbred NOD;Animals;Cells, Cultured;Humans;Granulocytes;Lymphocytes;Mice, SCID;Granulocyte Colony-Stimulating Factor;B-Lymphocytes;11 Glia;Antigens, CD34;Hematopoietic Stem Cell Transplantation;Killer Cells, Natural;Hematopoiesis;Thrombopoietin;Fetal Blood;Stem Cell Factor;Hematopoietic Stem Cells;Membrane Proteins;Graft Survival;Mice;Research Support, Non-U.S. Gov't},
	Medline = {20582384},
	Month = {12},
	Nlm_Id = {0402313},
	Number = {12},
	Organization = {INSERM U 417, H\^{o}pital Saint-Antoine, Paris, France.},
	Pages = {1470-80},
	Pii = {S0301472X00005579},
	Pubmed = {11146169},
	Title = {In vitro and in vivo evidence for the long-term multilineage (myeloid, B, NK, and T) reconstitution capacity of ex vivo expanded human CD34(+) cord blood cells},
	Uuid = {3BE3F751-1C76-4770-A2E6-63BEDBE1DD14},
	Volume = {28},
	Year = {2000}}

@article{Koenigsknecht-Talboo:2005,
	Abstract = {Microglia undergo a phenotypic activation in response to fibrillar beta-amyloid (fAbeta) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAbeta deposits. However, they can be induced to do so during Abeta vaccination therapy attributable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abeta plaques. We report that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fAbeta or complement receptor 3 and argue that this may, in part, underlie the accumulation of fAbeta-containing plaques within the AD brain. The proinflammatory suppression of fAbeta-elicited phagocytosis is dependent on nuclear factor kappaB activation. Significantly, the proinflammatory cytokines do not inhibit phagocytosis elicited by antibody-mediated activation of FcR, which may contribute to the efficiency of Abeta vaccination-based therapy. Importantly, the proinflammatory suppression of fAbeta phagocytosis can be relieved by the coincubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinflammatory cytokines induce the production of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis. These findings support anti-inflammatory therapies for the treatment of AD.},
	Author = {Koenigsknecht-Talboo, Jessica and Landreth, Gary E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {36},
	Organization = {Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.},
	Pages = {8240-9},
	Pii = {25/36/8240},
	Pubmed = {16148231},
	Title = {Microglial phagocytosis induced by fibrillar beta-amyloid and IgGs are differentially regulated by proinflammatory cytokines},
	Uuid = {99C72EAB-8DB4-4974-9E13-9E497D74CC87},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1808-05.2005}}

@article{Kohwi:2005,
	Abstract = {The subventricular zone (SVZ) produces different subclasses of olfactory bulb (OB) interneurons throughout life. Little is known about the molecular mechanisms controlling the production of different types of interneurons. Here we show that most proliferating adult SVZ progenitors express the transcription factor Pax6, but only a small subpopulation of migrating neuroblasts and new OB interneurons derived from these progenitors retains Pax6 expression. To elucidate the cell-autonomous role of Pax6 in OB neurogenesis, we transplanted green fluorescent protein-expressing embryonic forebrain progenitors of the dorsal lateral ganglionic eminence from Pax6 mutant Small Eye (Pax6(Sey/Sey)) mice into the SVZ of adult wild-type mice. Pax6(Sey/Sey) progenitors produce neuroblasts capable of migrating into the OB but fail to generate dopaminergic periglomerular and superficial granule cells. Interestingly, superficial granule neurons also express mRNA for tyrosine hydroxylase, the rate-limiting enzyme in dopamine synthesis. Our data show that SVZ neuroblasts are heterogeneous and that Pax6 is required in a cell-autonomous manner for the production of cells in the dopaminergic lineage.},
	Author = {Kohwi, Minoree and Osumi, Noriko and Rubenstein, John L. R. and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {30},
	Organization = {Department of Neurological Surgery, Program in Developmental and Stem Cell Biology, University of California, San Francisco, California 94143, USA.},
	Pages = {6997-7003},
	Pii = {25/30/6997},
	Pubmed = {16049175},
	Title = {Pax6 is required for making specific subpopulations of granule and periglomerular neurons in the olfactory bulb},
	Uuid = {AD8B0FB7-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {25},
	Year = {2005},
	url = {papers/Kohwi_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1435-05.2005}}

@article{Koizumi:2006,
	Abstract = {The ability of the mature mammalian nervous system to continually produce neuronal precursors is of considerable importance, as manipulation of this process might one day permit the replacement of cells lost as a result of injury or disease. In mammals, the anterior subventricular zone (SVZa) region is one of the primary sites of adult neurogenesis. Here we show that doublecortin (DCX), a widely used marker for newly generated neurons, when deleted in mice results in a severe morphological defect in the rostral migratory stream and delayed neuronal migration that is independent of direction or responsiveness to Slit chemorepulsion. DCX is required for nuclear translocation and maintenance of bipolar morphology during migration of these cells. Our data identifies a critical function for DCX in the movement of newly generated neurons in the adult brain.},
	Author = {Koizumi, Hiroyuki and Higginbotham, Holden and Poon, Tiffany and Tanaka, Teruyuki and Brinkman, Brendan C. and Gleeson, Joseph G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Mice, Inbred BALB C;Microtubule-Associated Proteins;Cell Differentiation;Animals;Gene Expression Regulation, Developmental;Phenotype;Chemotaxis;Protein Transport;Female;Mice, Transgenic;Neurites;Mice, Inbred C57BL;Cell Movement;Cell Proliferation;Male;Neuropeptides;Prosencephalon;Active Transport, Cell Nucleus;Cell Shape;Mice, Knockout;Neurons;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Stem Cells;Nerve Tissue Proteins},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Organization = {Neurogenetics Laboratory, Department of Neurosciences, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.},
	Pages = {779-86},
	Pii = {nn1704},
	Pubmed = {16699506},
	Title = {Doublecortin maintains bipolar shape and nuclear translocation during migration in the adult forebrain},
	Uuid = {CAFD7FBB-DA6F-47BF-ABBF-631E5BB4B1FC},
	Volume = {9},
	Year = {2006},
	url = {papers/Koizumi_NatNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1704}}

@article{Koizumi:2007,
	Abstract = {Microglia, brain immune cells, engage in the clearance of dead cells or dangerous debris, which is crucial to the maintenance of brain functions. When a neighbouring cell is injured, microglia move rapidly towards it or extend a process to engulf the injured cell. Because cells release or leak ATP when they are stimulated or injured, extracellular nucleotides are thought to be involved in these events. In fact, ATP triggers a dynamic change in the motility of microglia in vitro and in vivo, a previously unrecognized mechanism underlying microglial chemotaxis; in contrast, microglial phagocytosis has received only limited attention. Here we show that microglia express the metabotropic P2Y(6) receptor whose activation by endogenous agonist UDP triggers microglial phagocytosis. UDP facilitated the uptake of microspheres in a P2Y(6)-receptor-dependent manner, which was mimicked by the leakage of endogenous UDP when hippocampal neurons were damaged by kainic acid in vivo and in vitro. In addition, systemic administration of kainic acid in rats resulted in neuronal cell death in the hippocampal CA1 and CA3 regions, where increases in messenger RNA encoding P2Y(6) receptors that colocalized with activated microglia were observed. Thus, the P2Y(6) receptor is upregulated when neurons are damaged, and could function as a sensor for phagocytosis by sensing diffusible UDP signals, which is a previously unknown pathophysiological function of P2 receptors in microglia.},
	Author = {Koizumi, and Shigemoto-Mogami, and Nasu-Tada, and Shinozaki, and Ohsawa, and Tsuda, and Joshi, and Jacobson, and Kohsaka, and Inoue,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {0410462},
	Organization = {[1] Division of Pharmacology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya, Tokyo 158-8501, Japan [2] Department of Pharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409-3893, Japan [3] These authors contributed equally to this work.},
	Pii = {nature05704},
	Pubmed = {17410128},
	Title = {UDP acting at P2Y(6) receptors is a mediator of microglial phagocytosis},
	Uuid = {4A43664C-6A83-43B1-B669-2485BF0E03B5},
	Year = {2007},
	url = {papers/Koizumi_Nature2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature05704}}

@article{Koizumi:2006a,
	Abstract = {The potential role of doublecortin (Dcx), encoding a microtubule-associated protein, in brain development has remained controversial. Humans with mutations show profound alterations in cortical lamination, whereas in mouse, RNAi-mediated knockdown but not germline knockout shows abnormal positioning of cortical neurons. Here, we report that the doublecortin-like kinase (Dclk) gene functions in a partially redundant pathway with Dcx in the formation of axonal projections across the midline and migration of cortical neurons. Dosage-dependent genetic effects were observed in both interhemispheric connectivity and migration of cortically and subcortically derived neurons. Surprisingly, RNAi-mediated knockdown of either gene results in similar migration defects. These results indicate the Dcx microtubule-associated protein family is required for proper neuronal migration and axonal wiring.},
	Author = {Koizumi, Hiroyuki and Tanaka, Teruyuki and Gleeson, Joseph G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Microtubule-Associated Proteins;Animals;Gene Dosage;Gene Targeting;Aging;Congenital Abnormalities;Synaptic Transmission;Exons;Brain;Cell Movement;Embryo, Mammalian;Embryonic Development;Protein-Serine-Threonine Kinases;Axons;Embryo;Neuropeptides;Animals, Newborn;Mice, Inbred Strains;Mice, Knockout;Neurons;Cerebral Cortex;Protein Structure, Tertiary;Abnormalities;Mice;24 Pubmed search results 2008;Nerve Fibers;Corpus Callosum;Research Support, N.I.H., Extramural;Research Support, Non-U.S. Gov't},
	Month = {1},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Neurogenetics Laboratory, Department of Neurosciences, University of California, San Diego, La Jolla, California 93093, USA.},
	Pages = {55-66},
	Pii = {S0896-6273(05)01064-0},
	Pubmed = {16387639},
	Title = {Doublecortin-like kinase functions with doublecortin to mediate fiber tract decussation and neuronal migration},
	Uuid = {BE358A3B-7250-4B40-9F5C-EA1B1F1C61F3},
	Volume = {49},
	Year = {2006},
	url = {papers/Koizumi_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.10.040}}

@article{Kokaia:2003,
	Abstract = {Evidence for neuronal self-repair following insults to the adult brain has been scarce until very recently. Ischaemic insults have now been shown to trigger neurogenesis from neural stem cells or progenitor cells located in the dentate subgranular zone, the subventricular zone lining the lateral ventricle, and the posterior periventricle adjacent to the hippocampus. New neurons migrate to the granule cell layer or to the damaged CA1 region and striatum, where they express morphological markers characteristic of those neurons that have died. Some evidence indicates that these neurons can re-establish connections and contribute to functional recovery. 0959-4388 Journal Article Review Review, Tutorial},
	Author = {Kokaia, Z. and Lindvall, O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {Human;Cell Differentiation;Nerve Regeneration/*physiology;Signal Transduction;Animals;Humans;Recovery of Function;Neurons/*cytology/physiology;review, tutorial;Recovery of Function/*physiology;review;D pdf;Cell Movement;Telencephalon;Telencephalon/cytology/*growth &development/physiology;Nerve Regeneration;Support, Non-U.S. Gov't;Neurons;Brain Ischemia;06 Adult neurogenesis injury induced;Cell Movement/physiology;Stem Cells/*cytology/physiology;Cell Differentiation/physiology;Brain Ischemia/pathology/*physiopathology/therapy;24 Pubmed search results 2008;Stem Cells;Signal Transduction/physiology;Research Support, Non-U.S. Gov't},
	Medline = {22482251},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Section of Restorative Neurology, Wallenberg Neuroscience Centre, University Hospital, BMC A-11 SE- 221 84, Lund, Sweden. zaal.kokaia\@neurol.lu.se},
	Pages = {127-32},
	Pii = {S0959438803000175},
	Pubmed = {12593991},
	Title = {Neurogenesis after ischaemic brain insults},
	Uuid = {0B914C21-AA60-4BBA-A9D0-F3FDD711926F},
	Volume = {13},
	Year = {2003},
	url = {papers/Kokaia_CurrOpinNeurobiol2003.pdf}}

@article{Koketsu:2003,
	Abstract = {The concept that, after developmental periods, neocortical neurons become numerically stable and are normally nonrenewable has been challenged by a report of continuous neurogenesis in the association areas of the cerebral cortex in the adult Macaque monkey. Therefore, we have reexamined this issue in two different Macaque species using the thymidine analog bromodeoxyuridine (BrdU) as an indicator of DNA replication during cell division. We found several BrdU+/NeuN+ (neuronal nuclei) double-labeled cells, but cortical neurons, distinguished readily by their size and cytological and immunohistochemical properties, were not BrdU positive. We examined in detail the frontal cortex, where it is claimed that the largest daily addition of neurons has been made, but did not see migratory streams or any sign of addition of new neurons. Thus, we concluded that, in the normal condition, cortical neurons of adult primates, similar to other mammalian species, are neither supplemented nor renewable. 1529-2401 Journal Article},
	Author = {Koketsu, D. and Mikami, A. and Miyamoto, Y. and Hisatsune, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {J Neurosci},
	Keywords = {A pdf;Frontal Lobe/*cytology;Cell Division/physiology;Immunohistochemistry;Female;Antigens, Differentiation/biosynthesis;Macaca fascicularis;Regeneration/*physiology;Cell Count;Neurons/*cytology/metabolism;Neocortex/*cytology;Animals;Bromodeoxyuridine;Support, Non-U.S. Gov't;Age Factors;Macaca},
	Number = {3},
	Organization = {Department of Integrated Biosciences, University of Tokyo, Kashiwa, Chiba, Japan.},
	Pages = {937-42},
	Title = {Nonrenewal of neurons in the cerebral neocortex of adult macaque monkeys},
	Uuid = {55FF24D0-CDF0-11D9-B244-000D9346EC2A},
	Volume = {23},
	Year = {2003},
	url = {papers/Koketsu_JNeurosci2003.pdf}}

@article{Kokoeva:2005,
	Abstract = {Ciliary neurotrophic factor (CNTF) induces weight loss in obese rodents and humans, and for reasons that are not understood, its effects persist after the cessation of treatment. Here we demonstrate that centrally administered CNTF induces cell proliferation in feeding centers of the murine hypothalamus. Many of the newborn cells express neuronal markers and show functional phenotypes relevant for energy-balance control, including a capacity for leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3). Coadministration of the mitotic blocker cytosine-beta-d-arabinofuranoside (Ara-C) eliminates the proliferation of neural cells and abrogates the long-term, but not the short-term, effect of CNTF on body weight. These findings link the sustained effect of CNTF on energy balance to hypothalamic neurogenesis and suggest that regulated hypothalamic neurogenesis in adult mice may play a previously unappreciated role in physiology and disease.},
	Author = {Kokoeva, Maia V. and Yin, Huali and Flier, Jeffrey S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {01 Adult neurogenesis general},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5748},
	Organization = {Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 99 Brookline Avenue, Boston, MA 02215, USA.},
	Pages = {679-83},
	Pii = {310/5748/679},
	Pubmed = {16254185},
	Title = {Neurogenesis in the hypothalamus of adult mice: potential role in energy balance},
	Uuid = {EAD02836-C89B-47F9-A9B7-C19A7DB47B69},
	Volume = {310},
	Year = {2005},
	url = {papers/Kokoeva_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1115360}}

@article{Kolb:1987,
	Abstract = {Rats with complete removal of the cortex anterior to bregma in adulthood (frontal cortex) were compared behaviorally and neuroanatomically to rats with similar removals at 1, 5, or 10 days of age. The age at which animals received the cortical excision made a significant difference with respect to the development of the thalamus and the remaining cortex as well as the behavioral outcome in adulthood. There was a direct relationship between cortical thickness in adulthood and the age at surgery: the earlier the lesion the thinner the cortex. Part of this anatomical effect was acute, and could be observed within 24 h of surgery, but the major reduction in thickness was not observed until adolescence. Behaviorally, the animals were administered several tests including tongue extension, grooming, beam walking, swimming, and a spatial navigation task. Like the cortical measurements, the behavioral measurements showed a clear relationship between age at surgery and behavioral outcome: the earlier the lesion in infancy, the greater the behavioral impairments. Thus, whereas rats with lesions at 10 days of age showed behavioral sparing, relative to adult operates, on every measure, rats with lesions at 5 days of age performed at about the level of adult operates on most tests and rats with lesions at 1 day had more extensive behavioral impairments than all other groups. These results imply that the effects of cortical injury in infancy are tightly correlated with the precise level of neural maturation at the time of lesion.},
	Author = {Kolb, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0166-4328},
	Journal = {Behav Brain Res},
	Keywords = {24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Behavior, Animal;Nerve Regeneration;Female;Rats;Body Weight;Organ Size;Motor Activity;Reaction Time;Animals;Male;Thalamus;Brain;Frontal Lobe},
	Medline = {88077384},
	Month = {9},
	Nlm_Id = {8004872},
	Number = {3},
	Organization = {Department of Psychology, University of Lethbridge, Alta., Canada.},
	Pages = {205-20},
	Pubmed = {3689568},
	Title = {Recovery from early cortical damage in rats. I. Differential behavioral and anatomical effects of frontal lesions at different ages of neural maturation},
	Uuid = {BB0F0E6E-D24F-11D9-A0E9-000D9346EC2A},
	Volume = {25},
	Year = {1987}}

@article{Kolb:1991,
	Abstract = {This study examined the possibility that the presence or absence of behavioral sparing following neonatal frontal lesions might be correlated with changes in the complexity of dendritic branching. Rats were given bilateral frontal lesions in either adulthood, the day of birth, or on day 10. Ninety days later the animals were trained in a spatial navigation task. The animals' brains were then processed for Golgi-Cox staining and the dendritic branching of the pyramidal cells in the parietal cortex was analyzed. Frontal cortical lesions in newborn rats produced a severe behavioral deficit in the water task whereas frontal removal at 10 days of age allowed sparing of function relative to adult operates (that is, the Kennard effect). Analysis of dendritic arbor in sensorimotor cortex revealed that the day-10 animals exhibited a dramatic proliferation of dendritic arbor relative to control rats. In contrast, the day-1 animals had slightly less dendritic branching than control animals. Rats with frontal lesions in adulthood showed a small, but significant, increase in dendritic branching. The correlation between behavioral sparing and the increase in dendritic arborization following neonatal lesions may be illustrative of a general mechanism underlying the Kennard effect.},
	Author = {Kolb, B. and Gibb, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0166-4328},
	Journal = {Behav Brain Res},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Frontal Lobe;Rats;Neuronal Plasticity;Synaptic Transmission;Orientation;Male;Dendrites;Nerve Regeneration;Animals, Newborn;Escape Reaction;Cerebral Cortex;Discrimination Learning;Social Environment;Mental Recall;24 Pubmed search results 2008;Brain Mapping},
	Medline = {91315735},
	Month = {4},
	Nlm_Id = {8004872},
	Number = {1},
	Organization = {Department of Psychology, University of Lethbridge, Canada.},
	Pages = {51-6},
	Pubmed = {1650231},
	Title = {Sparing of function after neonatal frontal lesions correlates with increased cortical dendritic branching: a possible mechanism for the Kennard effect},
	Uuid = {3F8104D4-5411-4513-9BD3-F451714EDEF2},
	Volume = {43},
	Year = {1991}}

@article{Kolb:1996,
	Abstract = {Rats with removal of the medial prefrontal (mPFC) cortex at days 3, 6, 9, 15, or 30 were compared behaviourally and anatomically to littermate controls. In contrast to adult operates, mPFC lesions at all young ages led to the development of an abnormally thin cortical mantle. In addition, although there was an obvious cavity in brains examined in the early postoperative period, the brains of animals with lesions at day 9 or 15 had no lesion cavity in adulthood as part of the cortex appeared to regrow. The differential anatomical consequences of the lesions at days 9 and 15 was correlated with a differential behavioural outcome as well. Thus although rats in all young lesion groups showed a milder behavioural syndrome than rats with comparable lesions in adulthood, the functional outcome was best for animals with lesions at 9 days of age.},
	Author = {Kolb, B. and Petrie, B. and Cioe, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {Behav Brain Res},
	Keywords = {Foot/anatomy &histology;Body Weight/physiology;Rats;Behavior, Animal/*physiology;Female;Comparative Study;Prefrontal Cortex/growth &development/*injuries/pathology;Maze Learning/physiology;Animal;D-4;Aging/*physiology;Animals, Newborn;Support, Non-U.S. Gov't;Organ Weight/physiology;Male;Movement/physiology;Feeding Behavior/physiology},
	Number = {1-2},
	Organization = {Department of Psychology, University of Lethbridge, Canada. kolb\@hg.uleth.ca},
	Pages = {1-14.},
	Title = {Recovery from early cortical damage in rats, VII. Comparison of the behavioural and anatomical effects of medial prefrontal lesions at different ages of neural maturation},
	Uuid = {87B3E229-D23B-11D9-B244-000D9346EC2A},
	Volume = {79},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8883811}}

@article{Kolb:1997,
	Abstract = {Rats were given medial frontal lesions at 7 days of age and were tested as adults on tests of forelimb use, forelimb tactile sensitivity, tongue use, hindleg use, and in a spatial navigation task. The brains were processed with a modified Golgi-Cox procedure and dendritic arborization and spine density was measured. The animals showed recovery only on the spatial task and this was associated with an increase in the number of spines per unit length of dendrite. We also reanalyzed Golgi-Cox stained material from an experiment in which animals were depleted of cortical noradrenaline (NA) in infancy and then given frontal lesions on day 7. The NA depletion blocked the recovery from frontal lesions. Analysis of dendritic morphology showed that in otherwise intact rats, NA depletion decreased dendritic arbor but increased spine density to the level of frontal operates. Depleted frontal-operates showed no additional increase in spine density and also showed a decrease in dendritic arborization. These results suggest that recovery from neonatal cortical injury and from neonatal noradrenaline depletion may be supported by changes in both the dendritic arborization and the spine density in the remaining cortex.},
	Author = {Kolb, B. and Stewart, J. and Sutherland, R. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0166-4328},
	Journal = {Behav Brain Res},
	Keywords = {Tongue;Touch;Musculoskeletal Equilibrium;Animals;Frontal Lobe;Rats;Norepinephrine;Forelimb;Neurites;Sympatholytics;Pyramidal Cells;Male;Sympathectomy, Chemical;Body Weight;Animals, Newborn;Organ Size;Maze Learning;24 Pubmed search results 2008;Oxidopamine;Research Support, Non-U.S. Gov't},
	Medline = {98133762},
	Month = {12},
	Nlm_Id = {8004872},
	Number = {1-2},
	Organization = {Department of Psychology, University of Lethbridge, AB, Canada. Kolb\@HG.ULETH.CA},
	Pages = {61-70},
	Pubmed = {9475615},
	Title = {Recovery of function is associated with increased spine density in cortical pyramidal cells after frontal lesions and/or noradrenaline depletion in neonatal rats},
	Uuid = {5DF92B5B-920F-4E25-B133-F3EC9A6DEA95},
	Volume = {89},
	Year = {1997}}

@article{Kolb:1998,
	Abstract = {Rats were given suction lesions of the presumptive frontal cortex on embryonic day 18 (E18) and subsequently tested, as adults, on tests of spatial navigation (Morris water task, radial arm maze), motor tasks (Whishaw reaching task, beam walking), and locomotor activity. Frontal cortical lesions at E18 affected cerebral morphogenesis, producing unusual morphological structures including abnormal patches of neurons in the cortex and white matter as well as neuronal bridges between the hemispheres. A small sample of E18 operates also had hydrocephaly. The animals with E18 lesions without hydrocephalus were behaviorally indistinguishable from littermate controls. The results demonstrate that animals with focal lesions of the presumptive frontal cortex have gross abnormalities in cerebral morphology but the lesions leave the functions normally subserved by the frontal cortex in adult rats unaffected. The results are discussed in the context of a hypothesis regarding the optimal times for functional recovery from cortical injury.},
	Author = {Kolb, B. and Cioe, J. and Muirhead, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0166-4328},
	Journal = {Behav Brain Res},
	Keywords = {Research Support, Non-U.S. Gov't;Movement;Hindlimb;Touch;Musculoskeletal Equilibrium;Female;Rats;Organ Size;Motor Activity;Animals, Newborn;Maze Learning;Pregnancy;Animals;Cerebral Cortex;24 Pubmed search results 2008;Frontal Lobe},
	Medline = {98237558},
	Month = {3},
	Nlm_Id = {8004872},
	Number = {1-2},
	Organization = {Department of Psychology, University of Lethbridge, Canada. Kolb\@HG.ULETH.CA},
	Pages = {143-55},
	Pubmed = {9578447},
	Title = {Cerebral morphology and functional sparing after prenatal frontal cortex lesions in rats},
	Uuid = {00B97F60-6778-4654-839F-A64844F9E93D},
	Volume = {91},
	Year = {1998}}

@article{Kolb:1998a,
	Abstract = {The experiments described here show that the cavity left by midline frontal cortex removals at 10 days of age (P10) fills in with neural tissue. Similar changes are not found at earlier and later ages. This neuronal filling is blocked by prior pretreatment by administration of Bromodeoxyuridine (BrdU) on embryonic day 13. Administration of BrdU following the P10 lesion does not interfere with regrowth. Subsequent immunohistochemical staining for BrdU demonstrates the regrown area to be composed of newly generated cells. which include pyramidal and nonpyramidal neurons. Injections of a retrograde tracer into the striatum or posterior parietal cortex shows that the new neurons have connections similar to those of undamaged brains. The regrowth of this tissue is correlated with recovery of function in a test of forelimb use. Thus, the mammalian brain, during some privileged postnatal stages of growth. is capable of extensive reorganization that includes regeneration of lost neurons. These results are discussed in relation to the proximity of the lesion to the stem cells in the lateral ventricle and their postnatal migrational activities. 98237557 0166-4328 Journal Article},
	Author = {Kolb, B. and Gibb, R. and Gorny, G. and Whishaw, I. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0166-4328},
	Journal = {Behav Brain Res},
	Keywords = {Movement;Animals;Nerve Regeneration/*physiology;Frontal Lobe;Rats;Neural Pathways;Mitosis;Mitosis/physiology;Frontal Lobe/cytology/pathology/*physiology;Female;D both;Animal;Movement/physiology;Antimetabolites;Male;Antimetabolites/diagnostic use;Nerve Regeneration;Animals, Newborn;Support, Non-U.S. Gov't;Neural Pathways/cytology/pathology/physiology;Animals, Newborn/*physiology;Neurons;Fluorescent Antibody Technique, Direct;Immunohistochemistry;Bromodeoxyuridine/diagnostic use;Bromodeoxyuridine;Neurons/physiology;Research Support, Non-U.S. Gov't},
	Medline = {98237557},
	Month = {3},
	Nlm_Id = {8004872},
	Number = {1-2},
	Organization = {Department of Psychology, University of Lethbridge, Canada. Kolb\@HG.ULETH.CA},
	Pages = {127-41},
	Pubmed = {9578446},
	Title = {Possible regeneration of rat medial frontal cortex following neonatal frontal lesions},
	Uuid = {87B3E640-D23B-11D9-B244-000D9346EC2A},
	Volume = {91},
	Year = {1998},
	url = {papers/Kolb_BehavBrainRes1998.pdf}}

@article{Kolb:2003,
	Abstract = {Rats were given lesions of the temporal association cortex on postnatal day 4 or 10, or in adulthood. Ninety days later they were trained on two visual tasks (visual-spatial navigation; horizontal-vertical stripes discrimination). Lesion animals were compared behaviorally and neuroanatomically to littermate sham control rats. The day 4 lesions produced a larger deficit in the navigation task than day 10 or adult lesions. There were no deficits in the discrimination task. Analysis of the brains showed that the day 4 lesions produced a smaller brain and thinner cortex than day 10 lesions. The day 10 lesions produced hypertrophy in the dendritic arborization of pyramidal cells in parietal cortex. The results are consistent with the general findings that perinatal cortical injury in rats produces more severe behavioral and morphological effects than similar lesions in the second week of life and that cortical lesions around day 10 lead to an increase in cortical synaptogenesis.},
	Author = {Kolb, Bryan and Cioe, Jan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0166-4328},
	Journal = {Behav Brain Res},
	Keywords = {Motor Activity;Rats, Long-Evans;Animals;Aging;Rats;Comparative Study;Space Perception;Brain;Sex;Female;Reaction Time;Orientation;Time Factors;Dendrites;Nerve Regeneration;Body Weight;Animals, Newborn;Escape Reaction;Male;Discrimination Learning;Behavior, Animal;Organ Size;Psychomotor Performance;Temporal Lobe;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {22827283},
	Month = {9},
	Nlm_Id = {8004872},
	Number = {1-2},
	Organization = {Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Alta., Canada T1K 3M4. kolb\@uleth.ca},
	Pages = {67-76},
	Pii = {S0166432803000688},
	Pubmed = {12946596},
	Title = {Recovery from early cortical damage in rats. IX. Differential behavioral and anatomical effects of temporal cortex lesions at different ages of neural maturation},
	Uuid = {06B5E91B-6EE2-411C-A89F-9B719DF34A08},
	Volume = {144},
	Year = {2003}}

@article{Kolb:1985,
	Abstract = {Syrian golden hamsters with removals of the medial or ventral subfields of the frontal cortex at 4 days of age were compared behaviorally and neuroanatomically with hamsters with similar removals in adulthood. The behavioral results showed that hamsters with neonatal lesions show little sparing of species-typical behaviors such as hoarding and nest building. Study of the development of animals with early lesions showed that although as young juveniles the operated hamsters did not appear to be different from their littermate controls, as they developed they failed to improve in their performance as their littermates did. As adults these early operates were thus severely impaired relative to their littermates. Nonetheless, under certain environmental conditions it was possible to show that the animals were capable of performing the behaviors nearly as proficiently as normal animals. Thus, in order to thoroughly assess the extent of behavioral sparing following early neonatal lesions, it is necessary to test animals under widely varying stimulus conditions. Finally, when the brains of neonatally operated hamsters were compared with those of animals operated on in adulthood, there were striking differences; although the area of cavity appeared smaller in the neonatal operates, their brains weighed less and the remaining neocortex was thinner.},
	Author = {Kolb, B. and Whishaw, I. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0735-7044},
	Journal = {Behav Neurosci},
	Keywords = {Brain;Cerebral Cortex;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Species Specificity;Behavior, Animal;Organ Size;Mesocricetus;Nesting Behavior;Animals, Newborn;Animals;Male;Hamsters;Feeding Behavior;Frontal Lobe},
	Medline = {87298932},
	Month = {8},
	Nlm_Id = {8302411},
	Number = {4},
	Pages = {691-706},
	Pubmed = {3843735},
	Title = {Neonatal frontal lesions in hamsters impair species-typical behaviors and reduce brain weight and neocortical thickness},
	Uuid = {33C4AEE3-AB7B-40ED-9D3F-3721256842A6},
	Volume = {99},
	Year = {1985}}

@article{Kolb:1993,
	Abstract = {Rats given medial frontal lesions on Postnatal Day 1 or Day 10 were trained on the Morris water task on Days 19-21 or Days 56-58. The operated groups were equally impaired at the water task on Days 19-21, but the Day 10 rats had recovered by 56 days. Dendritic arborization and spine density were analyzed in parietal layer II-III pyramidal cells. At Day 60, but not at Day 22, the Day 10 animals had more dendritic spines per unit dendritic length than did the controls or Day 1 rats. Thus, there was functional recovery rather than sparing after frontal lesions at 10 days, and the recovery was correlated with an increase in dendritic spines.},
	Author = {Kolb, B. and Gibb, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0735-7044},
	Journal = {Behav Neurosci},
	Keywords = {Escape Reaction;24 Pubmed search results 2008;Dendrites;Research Support, Non-U.S. Gov't;Orientation;Nerve Regeneration;Female;Mental Recall;Neuronal Plasticity;Rats;Organ Size;Brain Mapping;Male;Age Factors;Animals;Neurons;Frontal Lobe},
	Medline = {94107488},
	Month = {10},
	Nlm_Id = {8302411},
	Number = {5},
	Organization = {Department of Psychology, University of Lethbridge, Alberta, Canada.},
	Pages = {799-811},
	Pubmed = {8280389},
	Title = {Possible anatomical basis of recovery of function after neonatal frontal lesions in rats},
	Uuid = {680B3703-7CE9-4BFE-89C0-F4966F6AA21C},
	Volume = {107},
	Year = {1993}}

@article{Kolb:2004,
	Abstract = {We compare the effects of psychoactive drugs such as morphine and amphetamine on the synaptic organization of neurons in the orbital frontal (OFC) and medial frontal (mPFC) regions in the rat. Both regions are altered chronically by exposure to intermittent doses of either drug but the effects are area-dependent. For example, whereas morphine produces increased spine density in OFC but decreased spine density in mPFC. The differential response of the OFC and mPFC to drugs is paralleled by an areal-dependent effect of gonadal hormones on these regions as well: males have greater dendritic arborization in the mPFC whereas females have a greater arborization in the OFC. We also compared the effects of neonatal injury to the OFC and mPFC on cognitive, motor, and social behaviors as well as on the anatomical organization of the remaining brain. Again, there were differential effects of the treatments to the OFC and mPFC. Neonatal OFC lesions allowed virtually complete functional recovery of cognitive and motor behaviors, which was correlated with mild abnormalities in cerebral development compared to the more severe deficits and morphological sequelae following mPFC lesions at the same ages. One exception was the effect of OFC on social behavior, which was severe regardless of whether the injury was in infancy or adulthood. It is proposed that both drug-induced and developmental abnormalities in the integrity of OFC neurons may lead to deficits in social behavior or other behavioral pathologies, possibly including depression.},
	Author = {Kolb, Bryan and Pellis, Sergio and Robinson, Terry E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0278-2626},
	Journal = {Brain Cogn},
	Keywords = {Neurons;Central Nervous System Stimulants;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Rats;Neuronal Plasticity;Research Support, U.S. Gov't, P.H.S.;Gonadal Steroid Hormones;Prefrontal Cortex;review, tutorial;Nerve Net;Animals;Orbit;review;Frontal Lobe},
	Month = {6},
	Nlm_Id = {8218014},
	Number = {1},
	Organization = {Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada T1K 3M4. kolb\@uleth.ca},
	Pages = {104-15},
	Pii = {S0278262603002781},
	Pubmed = {15134846},
	Title = {Plasticity and functions of the orbital frontal cortex},
	Uuid = {55F42FB7-BF07-4D88-8B05-DD17DE8EA895},
	Volume = {55},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/S0278-2626(03)00278-1}}

@article{Kolb:1994,
	Abstract = {Rats were given frontal cortical lesions at day 1 or 10 of life. Later, as adults, they were either: (1) processed with Golgi-Cox in order to analyze cortical dendritic arborization; (2) given injections of True Blue into the parietal or visual cortex, or (3) given injections of [3H]leucine into the substantia nigra. An additional group of normal rats were given injections of fluorescent dyes into the cortex on day 4 or 10 of life. The main findings were that (1) adult hemispheres with day 10 lesions had greater dendritic arbor than normal hemispheres, (2) adult hemispheres with day 1 lesions had reduced dendritic branching relative to normal hemispheres, (3) adult rats with day 10 lesions had no obvious abnormalities in cortical connections, (4) adult rats with day 1 lesions had abnormal thalamo-cortical, amygdalo-cortical, and nigro-cortical connections, and (5) many of these abnormal connections were present in the brains of 4-day-old normal rats. Since the 'abnormal' connections in the very early frontal operates were present in day 4 animals, it appears that they result from the failure of exuberant connections to retract after the lesions. The increased dendritic growth in day 10 operates does not appear related to qualitative changes in cortical afferents or efferents and may related to increased intrinsic cortical connectivity. Since rats with day 10 lesions have previously been shown to exhibit significant recovery of function, it is possible that the increased dendritic arborization is supporting the functional restitution.},
	Author = {Kolb, B. and Gibb, R. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Visual Cortex;Aging;Brain Diseases;Research Support, Non-U.S. Gov't;Dendrites;Reference Values;Rats;Neural Pathways;Fluorescent Dyes;Benzofurans;Parietal Lobe;Animals, Newborn;Animals;Injections;Rats, Inbred Strains;Male;Frontal Lobe},
	Medline = {94340407},
	Month = {5},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Department of Psychology, University of Lethbridge, Alta., Canada.},
	Pages = {85-97},
	Pubmed = {8062102},
	Title = {Neonatal frontal cortical lesions in rats alter cortical structure and connectivity},
	Uuid = {BAA1CDEB-C26D-11DA-969D-000D9346EC2A},
	Volume = {645},
	Year = {1994}}

@article{Kolb:1994a,
	Abstract = {Following bilateral removal of the medial frontal cortex, which included the medial prefrontal and adjacent midline motor cortex, 4-day-old rats were given transplants of embryonic day 17 frontal cortical tissue. Other rats were given only frontal lesions or sham operations. In adulthood, the animals were trained on a spatial navigation task and a forelimb reaching task. The transplanted tissue grew well and interacted morphologically with the host but the grafts failed to reduce the spatial navigation and motor deficits resulting from the frontal removals. The grafts also failed to reduce the anatomical sequelae of the early lesions, which included cortical thinning and thalamic shrinkage. It appears unlikely that cortical transplantation will be a viable treatment for recovery from perinatal frontal cortical injury.},
	Author = {Kolb, B. and Muirhead, D. and Cioe, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Behavior, Animal;Rats;Space Perception;Psychomotor Performance;Grooming;Body Weight;Organ Size;Animals, Newborn;Motor Activity;Forelimb;Animals;Brain;Rats, Inbred Strains;Fetal Tissue Transplantation;Frontal Lobe},
	Medline = {94349121},
	Month = {5},
	Nlm_Id = {0045503},
	Number = {1},
	Organization = {University of Lethbridge, AB, Canada.},
	Pages = {15-22},
	Pubmed = {8069698},
	Title = {Neonatal frontal cortex grafts fail to attenuate behavioural deficits or abnormal cortical morphogenesis},
	Uuid = {6E186ED3-A3A9-4976-A027-0856BFE0E4FE},
	Volume = {647},
	Year = {1994}}

@article{Kolb:2000,
	Abstract = {Rats were given bilateral lesions of the motor cortex on the day of birth (P1), tenth day of life (P10), or in adulthood. They were trained on several motor tasks (skilled forelimb reaching, beam traversing, tongue extension), general motor activity, and a test of spatial learning (Morris water task). Although all lesion groups were impaired at skilled reaching, the P10 group was less impaired than either of the other two lesion groups. Furthermore, on the other motor tests the P10 group did not differ from controls whereas both P1 and adult groups were impaired. Only the P1 lesion group was impaired at the acquisition of the Morris water task. Anatomical analyses revealed that the P1 and P10 rats had smaller brains than the other two groups as well as having a generalized decrease in cortical thickness. Dendritic analysis of layer III pyramidal cells in the parietal cortex revealed a decrease in apical arbor in the lesion groups and an increase in the basilar arbor of the P1 and adult lesion animals. The P1 and adult operated groups showed an increase in spine density in the basilar dendrites of layer V pyramidal cells. Finally, analysis of the pattern of corticospinal projections revealed that the P1 animals had a markedly wider field of corticospinal projection neurons than any of the other groups. The widespread anatomical changes in all lesion groups versus the relatively better behavioral recovery after P10 lesions suggests that day 10 represents an optimal period for adapting to brain damage and subsequent brain reorganization.},
	Author = {Kolb, B. and Cioe, J. and Whishaw, I. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Research Support, Non-U.S. Gov't;Dendrites;Motor Skills;Motor Cortex;Rats, Long-Evans;Rats;Female;Animals, Newborn;Motor Activity;Maze Learning;Animals;Parietal Lobe;Male;Age Factors;24 Pubmed search results 2008},
	Medline = {20511893},
	Month = {11},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Department of Psychology and Neuroscience, University of Lethbridge, AB T1K 3M4, Lethbridge, Canada. kolb\@uleth.ca},
	Pages = {62-74},
	Pii = {S0006899300028286},
	Pubmed = {11056185},
	Title = {Is there an optimal age for recovery from motor cortex lesions? I. Behavioral and anatomical sequelae of bilateral motor cortex lesions in rats on postnatal days 1, 10, and in adulthood},
	Uuid = {62EBC92E-F85F-4BFA-A64E-1183BC3077C2},
	Volume = {882},
	Year = {2000}}

@article{Kolb:1999,
	Abstract = {The mitotic marker 5-bromodeoxyuridine (BrdU) was injected twice daily (60 mg/kg) into pregnant hooded rats on one of embryonic days (E) 11, 12, 13, 15, 17, or 21, or into rat pups on postnatal day (P) 10. The principal findings were the following: (1) BrdU exposure on E11 produces profound effects on body morphology, and animals must be fed a special diet because of chronic tooth abnormalities; (2) BrdU exposure at E17 or earlier produces a change in coat spotting pattern, the precise pattern varying with age; (3) BrdU exposure on E15 or earlier produces a reduction in both brain and body weight; (4) BrdU exposure on E17 or earlier reduces cortical thickness; (5) BrdU exposure on E11-E13 and at P10 reduces cerebellar size relative to cerebral size; (6) spatial learning is significantly affected after injections of BrdU at E11-E17, but the largest effect is on E17; (7) the deficit in spatial learning may be related in part to a reduction in visual acuity; and (8) skilled forelimb ability is most disrupted after BrdU exposure at E15 but is also impaired after injections on E13 or earlier. BrdU thus has teratological effects on body, brain, and behavior that vary with the developmental age of the fetus or infant.},
	Author = {Kolb, B. and Pedersen, B. and Ballermann, M. and Gibb, R. and Whishaw, I. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Embryo;Aging;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Behavior, Animal;Behavioral Symptoms;Rats, Long-Evans;Rats;Abnormalities, Drug-Induced;Animals, Newborn;Drug Administration Schedule;Brain;Bromodeoxyuridine;Injections;Animals},
	Medline = {99165835},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {6},
	Organization = {Department of Psychology and Neuroscience, University of Lethbridge, Lethbridge, Canada T1K 3M4.},
	Pages = {2337-46},
	Pubmed = {10066283},
	Title = {Embryonic and postnatal injections of bromodeoxyuridine produce age-dependent morphological and behavioral abnormalities},
	Uuid = {17BC6A1F-5DDD-4A53-B5B1-988421F95431},
	Volume = {19},
	Year = {1999}}

@article{Kolb:2000a,
	Abstract = {The size of cortical removal was varied in rats that were given medial frontal lesions on postnatal day 2. In adulthood, the animals were trained on the Morris water task and Whishaw reaching task following which the brains were harvested and dendritic arborization and spine density was examined in the layer III pyramidal cells in Zilles' area Par1. There was a small relationship between lesion size and behavioral outcome as smaller lesions produced somewhat smaller deficits. In contrast, both small and large lesions produced large reductions in brain weight, dendritic arborization, and spine density. The cortex of newborn rats appears to be especially vulnerable to even restricted injury. This contrasts to the effects of similar injury a week later when animals show extensive functional recovery and anatomical compensation.},
	Author = {Kolb, B. and Cioe, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0028-3908},
	Journal = {Neuropharmacology},
	Keywords = {Research Support, Non-U.S. Gov't;Rats, Long-Evans;Animals;Frontal Lobe;Rats;Neuronal Plasticity;Appetitive Behavior;Female;Cell Count;Reaction Time;Male;Dendrites;Analysis of Variance;Animals, Newborn;Brain Injuries;Organ Size;Maze Learning;24 Pubmed search results 2008;Cerebral Decortication;Swimming},
	Medline = {20164901},
	Month = {3},
	Nlm_Id = {0236217},
	Number = {5},
	Organization = {Department of Psychology and Neuroscience, University of Lethbridge, Lethbridge, Canada. kolb\@hg.uleth.ca},
	Pages = {756-64},
	Pii = {S0028390899002609},
	Pubmed = {10699442},
	Title = {Recovery from early cortical damage in rats, VIII. Earlier may be worse: behavioural dysfunction and abnormal cerebral morphogenesis following perinatal frontal cortical lesions in the rat},
	Uuid = {784BFBB2-472A-4946-87CE-1A4D81712C0A},
	Volume = {39},
	Year = {2000}}

@article{Koliatsos:1994,
	Abstract = {The present study proposes a reproducible model of experimental degeneration of adult motor neurons in the rat. Avulsion of ventral roots in the adult lumbar cord transects motor axons at the root exit and leads to retrograde cell death of 80\%of motor neurons 2 weeks later; this result follows a series of retrograde changes, including chromatolysis, loss of transmitter phenotype, and accumulation of phosphorylated neurofilaments in perikarya. Glial cells recruited at the site of retrograde injury express both microglia-specific epitopes (as exemplified by OX-42 immunoreactivity) and macrophage-specific markers (e.g., ED-1 immunoreactivity). Macrophage-specific markers become particularly intense 7 days postaxotomy and provide additional evidence of active phagocytosis of injured neurons. Ventral root avulsion is a very useful model for assessing mechanisms of motor neuron death and testing the ability of trophic factors and other agents to preserve the phenotype and promote the survival of adult motor neurons in vivo.},
	Author = {Koliatsos, V. E. and Price, W. L. and Pardo, C. A. and Price, D. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Fluorescent Dyes;Animals;Rats;Phenotype;Models, Biological;Neurons, Afferent;Rats, Sprague-Dawley;Sciatic Nerve;Axons;Not relevant;Choline O-Acetyltransferase;11 Glia;Spinal Nerve Roots;Stilbamidines;Male;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Motor Neurons;Immunohistochemistry;Retrograde Degeneration},
	Medline = {94267079},
	Month = {4},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2196.},
	Pages = {35-44},
	Pubmed = {8207127},
	Title = {Ventral root avulsion: an experimental model of death of adult motor neurons},
	Uuid = {72B75CF9-7D3C-44AD-8898-01AC571137B1},
	Volume = {342},
	Year = {1994}}

@article{Komitova:2006,
	Abstract = {Environmental enrichment (EE) alleviates sensorimotor deficits after brain infarcts but the cellular correlates are not well-known. This study aimed to test the effects of postischemic EE on neocortical cell genesis. A neocortical infarct was caused by distal ligation of the middle cerebral artery in adult spontaneously hypertensive rats, subsequently housed in standard environment or EE. Bromodeoxyuridine (BrdU) was administered during the first postischemic week to label proliferating cells and BrdU incorporation was quantified 4 weeks later in the periinfarct, ipsilateral medial and contralateral cortex. Immunohistochemistry and confocal microscopy were used to analyze co-localization of BrdU with neuronal (calbindin D28k, calretinin, parvalbumin, glutamic acid decarboxylase, tyrosine hydroxylase), astrocytic (glial fibrillary acidic protein, glutamine synthetase, vimentin, nestin), microglia/macrophage (CD11b/Ox-42, CD68/ED-1), oligodendrocyte progenitor/polydendrocyte (NG2, platelet-derived growth factor alpha receptor) or mature oligodendrocyte (myelin basic protein) markers. BrdU positive cells were increased in all analyzed cortical regions in stroke EE rats compared with stroke standard environment rats. Newly born cells in the periinfarct cortex were mostly reactive astroglia. Occasionally, BrdU positive cells in the periinfarct cortex that were negative for glial or microglia/macrophage markers co-expressed markers typical for interneurons but did not express appropriate functional markers. The majority of BrdU positive cells in intact cortical regions, ipsi- and contralaterally, were identified as NG2 positive polydendrocytes. Perineuronally situated newly born cells and polydendrocytes were found to be brain-derived neurotrophic factor immunoreactive. In conclusion, EE enhanced newborn glial scar astroglia and NG2+ polydendrocytes in the postischemic neocortex which might be beneficial for brain repair and poststroke plasticity.},
	Author = {Komitova, and Perfilieva, and Mattsson, and Eriksson, and Johansson,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {06 Adult neurogenesis injury induced;11 Glia},
	Month = {1},
	Nlm_Id = {0370712},
	Organization = {The Arvid Carlsson Institute for Neuroscience at the Institute of Clinical Neuroscience, G{\"o}teborg University, G{\"o}teborg, Sweden.},
	Pii = {S0014-4886(05)00461-9},
	Pubmed = {16427625},
	Title = {Enriched environment after focal cortical ischemia enhances the generation of astroglia and NG2 positive polydendrocytes in adult rat neocortex},
	Uuid = {2AC7FE11-1C83-45C7-883A-6FA9E9981700},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2005.12.007}}

@article{Komitova:2002,
	Abstract = {The study aimed to elucidate the effects of cortical ischemia and postischemic environmental enrichment on hippocampal cell genesis. A cortical infarct was induced by a permanent ligation of the middle cerebral artery distal to the striatal branches in 6-month-old spontaneously hypertensive rats. Bromodeoxyuridine (BrdU) was administered as 7 consecutive daily injections starting 24 hours after surgery and animals were housed in standard or enriched environment. Four weeks after completed BrdU administration, BrdU incorporation and its co-localization with the neuronal markers NeuN and calbindin D28k, and the astrocytic marker glial fibrillary acidic protein in the granular cell layer and subgranular zone of the hippocampal dentate gyrus were determined with immunohistochemistry and were quantified stereologically. Compared with sham-operated rats, rats with cortical infarcts had a five-to sixfold ipsilateral increase in BrdU-labeled cells. About 80\%of the new cells were neurons. Differential postischemic housing did not influence significantly the total number of surviving BrdU-labeled cells or newborn neurons. However, postischemic environmental enrichment increased the ipsilateral generation of astrocytes normalizing the astrocyte-to-neuron ratio, which was significantly reduced in rats housed in standard environment postischemically. 0271-678x Journal Article},
	Author = {Komitova, M. and Perfilieva, E. and Mattsson, B. and Eriksson, P. S. and Johansson, B. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:55 -0400},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {Animals;Rats;*Cell Differentiation;Brain Ischemia/*pathology;Astrocytes/chemistry/pathology;Phenotype;Hippocampus/*pathology;Brain Infarction/pathology;Bromodeoxyuridine/analysis/metabolism;Glial Fibrillary Acidic Protein/analysis;Fluorescent Antibody Technique;Rats, Inbred SHR;Male;Support, Non-U.S. Gov't;D abstr;Neurons/chemistry/pathology;Calcium-Binding Protein, Vitamin D-Dependent/analysis;Animals, Newborn;06 Adult neurogenesis injury induced;Immunohistochemistry;Biological Markers/analysis},
	Number = {7},
	Organization = {Institute of Clinical Neuroscience, University of Goteborg, Sweden.},
	Pages = {852-60},
	Pubmed = {12142570},
	Title = {Effects of cortical ischemia and postischemic environmental enrichment on hippocampal cell genesis and differentiation in the adult rat},
	Uuid = {8B9D204E-EC81-11DA-8605-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12142570}}

@article{Kondo:2004,
	Abstract = {Cell-cell fusion generates multinucleated cells such as osteoclasts in bone, myotubes in muscle, and trophoblasts in placenta. Molecular details governing these fusion processes are still largely unknown. As a step toward identification of fusogenic genes, we tested the concept that retroviral vectors can be packaged as a result of cell-cell fusion. First, we introduced replication-deficient retroviral vectors expressing mCAT-1, which mediates fusogenic interaction with the retroviral envelope protein Env, into Chinese hamster ovary (CHO) cells to generate vector cells. Plasmids expressing virion proteins Gag, Pol, and Env were introduced into a separate culture of CHO cells to generate packaging cells. Co-culturing vector and packaging cells resulted in production of infectious retroviruses carrying the mCAT-1 gene as a consequence of cell-cell fusion. Second, we introduced a retroviral vector into primary osteoclast precursors and co-cultured them with established osteoclast precursor RAW264.7 cells, which turned out to harbor packaging activity. Packaged retroviral vector was detected in culture supernatants only where the osteoclast differentiation factor receptor activator for NF-kappaB ligand (RANKL) induced fusion between these two cell types. These data suggest that retrovirus production can occur as a result of cell-cell fusion. This provides a novel approach for isolating and characterizing fusogenic genes using retroviral expression vectors.},
	Author = {Kondo, Takako and Ikeda, Kyoji and Matsuo, Koichi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {8756-3282},
	Journal = {Bone},
	Keywords = {Hamsters;Gene Products, env;Animals;Trans-Activators;Carrier Proteins;Macrophages;Transfection;CHO Cells;Virus Assembly;Cell Fusion;Cell Line, Tumor;Cationic Amino Acid Transporter 1;Retroviridae;Giant Cells;11 Glia;Gene Products, gag;Genetic Vectors;Cricetulus;Membrane Glycoproteins;Mice;Gene Expression;Gene Products, pol;Osteoclasts;Research Support, Non-U.S. Gov't},
	Month = {11},
	Nlm_Id = {8504048},
	Number = {5},
	Organization = {Department of Geriatric Research, National Institute for Longevity Sciences (NILS), Aichi 474-8522, Japan.},
	Pages = {1120-6},
	Pii = {S8756-3282(04)00263-7},
	Pubmed = {15542037},
	Title = {Detection of osteoclastic cell-cell fusion through retroviral vector packaging},
	Uuid = {EB5B06AB-70FD-44A1-8F0A-2E0C20B087BC},
	Volume = {35},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.bone.2004.06.011}}

@article{Kondo:2001,
	Abstract = {PURPOSE: Cortical dysplasia (CD) is a frequent cause of medically intractable focal epilepsy. The mechanisms of CD-induced epileptogenicity remain unknown. The difficulty in obtaining and testing human tissue warrants the identification and characterization of animal model(s) of CD that share most of the clinical, electroencephalographic (EEG), and histopathologic characteristics of human CD. In this study, we report on the in vivo EEG characterization of the radiation-induced model of CD. METHODS: Timed-pregnant Sprague-Dawley rats were irradiated on E17 using a single dose of 145 cGy or left untreated. Their litters were identified and implanted with bifrontal epidural and hippocampal depth electrodes for prolonged continuous EEG recordings. After prolonged EEG monitoring, animals were killed and their brains sectioned and stained for histologic studies. RESULTS: In utero-irradiated rats showed frequent spontaneous interictal epileptiform spikes and spontaneous seizures arising independently from the hippocampal or the frontal neocortical structures. No epileptiform or seizure activities were recorded from age-matched control rats. Histologic studies showed the presence of multiple cortical areas of neuronal clustering and disorganization. Moreover, pyramidal cell dispersion was seen in the CA1>CA3 areas of the hippocampal formations. CONCLUSIONS: Our results further characterize the in vivo EEG characteristics of the in utero radiation model of CD using long-term EEG monitoring. This model may be used to study the molecular and cellular changes in epileptogenic CD and to test the efficacy of newer antiepileptic medications.},
	Author = {Kondo, S. and Najm, I. and Kunieda, T. and Perryman, S. and Yacubova, K. and L{\"u}ders, H. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Cerebral Cortex;Epilepsies, Partial;Electroencephalography;Rats, Sprague-Dawley;24 Pubmed search results 2008;21 Neurophysiology;21 Epilepsy;Hippocampus;Female;Rats;Evoked Potentials;Pregnancy;Animals;Disease Models, Animal;Radiation Injuries, Experimental;Neurons;Frontal Lobe},
	Medline = {21600859},
	Month = {10},
	Nlm_Id = {2983306R},
	Number = {10},
	Organization = {Section of Epilepsy, Department of Neurology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195 USA.},
	Pages = {1221-7},
	Pii = {38300},
	Pubmed = {11737155},
	Title = {Electroencephalographic characterization of an adult rat model of radiation-induced cortical dysplasia},
	Uuid = {FAAC8B58-0C2B-4F1A-B74D-9523014174C7},
	Volume = {42},
	Year = {2001}}

@article{Kontani:2005,
	Abstract = {Cell-cell fusion initiates fertilization, sculpts tissues during animal development, reprograms stem cells to new differentiated states, and may be a key step in cancer progression. While cell fusion is tightly regulated, the mechanisms that limit fusion to appropriate partners are unknown. Here, we report that the fus-1 gene is essential to repress fusion of epidermal cells in C. elegans: in severe fus-1 mutants, all epidermal cells, except the lateral seam cells, inappropriately fuse into a single large syncytium. This hyperfusion requires EFF-1, an integral membrane protein essential for fusion of epidermal cells into discrete syncytia. FUS-1 is localized to the apical plasma membrane in all epidermal cells potentiated to undergo fusion, whereas it is virtually undetectable in nonfusing seam cells. fus-1 encodes the e subunit of the vacuolar H(+)-ATPase (V-ATPase), and loss of other V-ATPase subunits also causes widespread hyperfusion. These findings raise the possibility of manipulating cell fusion by altering V-ATPase activity.},
	Author = {Kontani, Kenji and Moskowitz, Ivan P. G. and Rothman, Joel H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1534-5807},
	Journal = {Dev Cell},
	Keywords = {08 Aberrant cell cycle;11 Glia;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {101120028},
	Number = {5},
	Organization = {Department of MCD Biology, Neuroscience Research Institute, University of California, Santa Barbara, 93106, USA.},
	Pages = {787-94},
	Pii = {S1534-5807(05)00098-5},
	Pubmed = {15866168},
	Title = {Repression of cell-cell fusion by components of the C. elegans vacuolar ATPase complex},
	Uuid = {67D614CF-8BE3-4F39-B4FA-1435169C5E14},
	Volume = {8},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.devcel.2005.02.018}}

@article{Kootstra:1999,
	Abstract = {Human immunodeficiency virus type 1 (HIV-1) is considered to infect nondividing cells because nuclear localization signals (NLS) in matrix (MA, p17(Gag)) and Vpr allow active nuclear transport of the preintegration complex. Previous studies demonstrated that HIV-1 reverse transcription is successful only in cells with proliferative potential, thus restricting HIV-1 replication to cycling cells. To sort out this apparent discrepancy we compared the phenotype of a chimeric HIV-1 variant lacking a functional Vpr and MA-NLS (R7. deltaVpr.deltaNLS), and previously described to lack replicative capacity in macrophages and growth-arrested cells, with a chimera lacking a functional Vpr (R7.deltaVpr). Both variants replicated efficiently in primary macrophages, with only minimal differences in the kinetics of reverse transcription, integration, or p24 production. In agreement with our previous observation, elongation of reverse transcription was restricted to the proliferating subpopulation of macrophages. Replication of R7.deltaVpr and R7.deltaVpr.deltaNLS could also be demonstrated in aphidicolin-treated macrophages, indicating efficient nuclear transport in G1/S phase-arrested cells. In conclusion, our results confirm the dependency of the process of HIV-1 reverse transcriptase on cell proliferation in primary macrophages and exclude an important role of MA-NLS and Vpr in macrophage infection.},
	Author = {Kootstra, N. A. and Schuitemaker, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {Research Support, Non-U.S. Gov't;Viral Proteins;HIV-1;Cells, Cultured;Macrophages;Peptide Chain Elongation, Translational;Humans;Variation (Genetics);Phenotype;Gene Products, vpr;Cell Cycle;15 Retrovirus mechanism;Gene Products, gag;Kinetics;11 Glia;Mutagenesis;Nuclear Localization Signals;Nuclear Localization Signal;HIV Antigens;DNA, Viral;Cell Division;24 Pubmed search results 2008;Virus Replication;S Phase;Bromodeoxyuridine;Transcription, Genetic},
	Medline = {99119491},
	Month = {1},
	Nlm_Id = {0110674},
	Number = {2},
	Organization = {Department of Clinical Viral-Immunology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Academic Medical Centre, University of Amsterdam, Plesmanlaan 125, Amsterdam, 1066 CX, The Netherlands.},
	Pages = {170-80},
	Pii = {S004268229899482X},
	Pubmed = {9918876},
	Title = {Phenotype of HIV-1 lacking a functional nuclear localization signal in matrix protein of gag and Vpr is comparable to wild-type HIV-1 in primary macrophages},
	Uuid = {16440373-F916-4122-A16D-32602A6B2F20},
	Volume = {253},
	Year = {1999}}

@article{Kopec:2000,
	Abstract = {Nitric oxide (NO) is produced by inducible nitric oxide synthase (iNOS) in activated microglia and has been shown to participate in host defense mechanisms. However, the role of NO produced by constitutive nitric oxide synthase (cNOS) in microglia is poorly understood. In this report, NO was found to regulate phagocytosis in murine BV-2 microglial cells as quantified by flow cytometry. Addition of NO-generating compounds caused impaired phagocytosis as compared to untreated microglia. The addition of nitric oxide synthase (NOS) inhibitors to microglial cells resulted in potentiation of phagocytosis, suggesting that constitutive NO was participating in the regulation of phagocytosis. The inverse correlation between NO production and phagocytosis was also observed when Alzheimer's beta-amyloid peptide was added. With beta-amyloid treatment, constitutive NO production decreased while phagocytosis increased. Cell extracts prepared from untreated microglia were found to contain both neuronal and endothelial NOS isoforms, but not the inducible form. The correlation of spontaneous NO production with attenuated phagocytosis suggests that constitutive NOS enzymes participate in microglial regulation.},
	Author = {Kopec, K. K. and Carroll, R. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {1089-8603},
	Journal = {Nitric Oxide},
	Keywords = {Phagocytosis;Flow Cytometry;Fluorescein;11 Glia;Microglia;Nitric Oxide;Microspheres;Mice;Animals;Nitric-Oxide Synthase;Fluorescence;Isoenzymes},
	Medline = {20297117},
	Month = {4},
	Nlm_Id = {9709307},
	Number = {2},
	Organization = {Department of Neuroscience Therapeutics, Division of Warner-Lambert, Parke-Davis Pharmaceutical Research, 2800 Plymouth Road, Ann Arbor, Michigan, 48105, USA.},
	Pages = {103-11},
	Pii = {S1089860300902805},
	Pubmed = {10835290},
	Title = {Phagocytosis is regulated by nitric oxide in murine microglia},
	Uuid = {6CF5E2D0-15C8-4FA7-8DC2-A596CE053D43},
	Volume = {4},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/niox.2000.0280}}

@article{Kopen:1999,
	Abstract = {Stem cells are a valuable resource for treating disease, but limited access to stem cells from tissues such as brain restricts their utility. Here, we injected marrow stromal cells (MSCs) into the lateral ventricle of neonatal mice and asked whether these multipotential mesenchymal progenitors from bone marrow can adopt neural cell fates when exposed to the brain microenvironment. By 12 days postinjection, MSCs migrated throughout the forebrain and cerebellum without disruption to the host brain architecture. Some MSCs within the striatum and the molecular layer of the hippocampus expressed glial fibrillary acidic protein and, therefore, differentiated into mature astrocytes. MSCs also populated neuron rich regions including the Islands of Calleja, the olfactory bulb, and the internal granular layer of the cerebellum. A large number of MSCs also were found within the external granular layer of the cerebellum. In addition, neurofilament positive donor cells were found within the reticular formation of the brain stem, suggesting that MSCs also may have differentiated into neurons. Therefore, MSCs are capable of producing differentiated progeny of a different dermal origin after implantation into neonatal mouse brains. These results suggest that MSCs are potentially useful as vectors for treating a variety of central nervous system disorders.},
	Author = {Kopen, G. C. and Prockop, D. J. and Phinney, D. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Models, Biological;Cell Differentiation;Adipocytes;Chondrocytes;08 Aberrant cell cycle;Immunohistochemistry;Bone Marrow Cells;Astrocytes;Cerebellum;Bone Marrow Transplantation;Animals, Newborn;Prosencephalon;Animals;Cells, Cultured;Mice;Stromal Cells},
	Medline = {99415924},
	Month = {9},
	Nlm_Id = {7505876},
	Number = {19},
	Organization = {Center for Gene Therapy, MCP Hahnemann University, 245 North 15th Street, Philadelphia, PA 19102-1192, USA.},
	Pages = {10711-6},
	Pubmed = {10485891},
	Title = {Marrow stromal cells migrate throughout forebrain and cerebellum, and they differentiate into astrocytes after injection into neonatal mouse brains},
	Uuid = {37E7113E-D3B2-11D9-A0E9-000D9346EC2A},
	Volume = {96},
	Year = {1999}}

@article{Kornack:2001,
	Abstract = {In adult rodents, neural progenitor cells in the subependymal (SZ) zone of the lateral cerebral ventricle generate neuroblasts that migrate in chains via the rostral migratory stream (RMS) into the olfactory bulb (OB), where they differentiate into interneurons. However, the existence of this neurogenic migratory system in other mammals has remained unknown. Here, we report the presence of a homologue of the rodent SZ/RMS in the adult macaque monkey, a nonhuman Old World primate with a relatively smaller OB. Our results-obtained by using combined immunohistochemical detection of a marker for DNA replication (5- bromodeoxyuridine) and several cell type-specific markers-indicate that dividing cells in the adult monkey SZ generate neuroblasts that undergo restricted chain migration over an extended distance of more than 2 cm to the OB and differentiate into granule interneurons. These findings in a nonhuman primate extend and support the use of the SZ/RMS as a model system for studying neural regenerative mechanisms in the human brain.},
	Author = {Kornack, D. R. and Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {*Cell Movement;02 Adult neurogenesis migration;B both;Olfactory Pathways/*cytology;Immunohistochemistry;Macaca mulatta;Phenotype;Macaca fascicularis;Animal;*Cell Differentiation;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Brain/*cytology;Primates},
	Number = {8},
	Organization = {Center for Aging and Developmental Biology, Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, NY 14642, USA. david.kornack\@urmc.rochester.edu},
	Pages = {4752-7.},
	Title = {The generation, migration, and differentiation of olfactory neurons in the adult primate brain},
	Uuid = {A4E75311-F4A5-474D-B396-A1E08C3A507D},
	Volume = {98},
	Year = {2001},
	url = {papers/Kornack_ProcNatlAcadSciUSA2001}}

@article{Kornack:2001a,
	Abstract = {A recent assertion that new neurons are continually added to the neocortex of adult macaque monkeys has profound implications for understanding the cellular mechanisms of higher cognitive functions. Here we searched for neurogenesis in adult macaques by using immunofluorescent triple labeling for the DNA-replication indicator, bromodeoxyuridine (BrdU), and neuronal and glial cell markers. Although numerous BrdU-labeled cells were distributed throughout the cerebral wall, including the neocortex, these were identified as nonneuronal cells; evidence for newly generated neurons was limited to the hippocampus and olfactory bulb. Thus, our results do not substantiate the claim of neurogenesis in normal adult primate neocortex.},
	Author = {Kornack, D. R. and Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {Science},
	Keywords = {Tubulin/analysis;Fluorescent Antibody Technique;Neurons/*cytology;Microscopy, Confocal;Immunoenzyme Techniques;Neocortex/*cytology;Endothelium, Vascular/cytology;Female;Animal;Glial Fibrillary Acidic Protein/analysis;Bromodeoxyuridine/analysis/metabolism;Cell Movement;Macaca fascicularis;Microscopy, Fluorescence;Male;Nuclear Proteins/analysis;Brain/cytology;Macaca mulatta;Support, U.S. Gov't, P.H.S.;Cell Death;A pdf;Astrocytes/cytology;*Cell Division},
	Number = {5549},
	Organization = {Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.},
	Pages = {2127-30.},
	Title = {Cell proliferation without neurogenesis in adult primate neocortex},
	Uuid = {55FF2A1E-CDF0-11D9-B244-000D9346EC2A},
	Volume = {294},
	Year = {2001},
	url = {papers/Kornack_Science2001.pdf}}

@article{Kornblum:2001,
	Abstract = {The study of neural stem cell biology is hindered by the absence of well-defined markers for neural stem cells and neuronal progenitors. Without the ability to identify the relevant cell types, the analysis of how the diverse cell populations of the central nervous system are generated becomes virtually impossible.},
	Author = {Kornblum, H. I. and Geschwind, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {10 Development;F pdf},
	Number = {11},
	Organization = {Harley I. Kornblum is at the Department of Molecular and Medical Pharmacology, the Department of Pediatrics and the Crump Institute for Molecular Imaging, UCLA School of Medicine, Los Angeles, California 90095, USA.},
	Pages = {843-6.},
	Title = {Molecular markers in CNS stem cell research: hitting a moving target},
	Uuid = {0F8D7E6A-9AF9-4DFC-999C-08001209CC04},
	Volume = {2},
	Year = {2001},
	url = {papers/Kornblum_NatRevNeurosci2001.pdf}}

@article{Korr:1999,
	Abstract = {In a recent paper (Shankle et al., 1998a), post-natal neurogenesis in the human cerebral cortex was discussed. Based on re-calculations of morphometric data from the literature, the authors concluded an average 1.1\%monthly increase in post-natal cortical neuron number between post-natal months 15-72. The present paper makes clear by discussing four main assumptions done by Shankle et al., i.e. shrinkage of the tissue, morphometric features of the neurons under study, conversion of cell densities per area to number per unit volume and estimation of coefficients of variation, that their final conclusion about an increase in neuron number is unsound. Furthermore, five points are discussed here that Shankle et al. had mentioned in order to demonstrate that the pulse thymidine labeling method is less reliable than some have assumed. The present paper refute these assumptions point by point. Thus, the Shankle et al. paper does not provide scientifically valid evidence of a post-natal neurogenesis in the developing human cerebral cortex.},
	Author = {Korr, H. and Schmitz, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:25 -0400},
	Issn = {0022-5193},
	Journal = {J Theor Biol},
	Keywords = {Adolescent;Infant;Autoradiography;Models, Neurological;Cell Count;Child, Preschool;Child;Humans;Cerebral Cortex;Neurons},
	Medline = {99459024},
	Month = {10},
	Nlm_Id = {0376342},
	Number = {3},
	Organization = {Department of Anatomy and Cell Biology, RWTH University of Aachen, Pauwelsstrasse 30/Wendlingweg 2, Aachen, D-52057, Germany. korr\@post.klinikum.rwth-aachen.de},
	Pages = {291-7},
	Pii = {S002251939990992X},
	Pubmed = {10527718},
	Title = {Facts and fictions regarding post-natal neurogenesis in the developing human cerebral cortex},
	Uuid = {BAA1552F-C26D-11DA-969D-000D9346EC2A},
	Volume = {200},
	Year = {1999},
	url = {papers/Korr_JTheorBiol1999.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/jtbi.1999.0992}}

@article{Kovac:2004,
	Abstract = {Entorhinal cortex lesion (ECL) is a well described model of anterograde axonal degeneration, subsequent sprouting and reactive synaptogenesis in the hippocampus. Here, we show that such lesions induce transsynaptic degeneration of the target cells of the lesions pathway in the dentate gyrus. Peaking between 24 and 36 hours post-lesion, dying neurons were labeled with DeOlmos silver-staining and antisera against activated caspase 3 (CCP32), a downstream inductor of programmed cell death. Within caspase 3-positive neurons, fragmented nuclei were co-localized using Hoechst 33342 staining. Chromatin condensation and nuclear fragmentation were also evident in semithin sections and at the ultrastructural level, where virtually all caspase 3-positive neurons showed these hallmarks of apoptosis. There is a well-described upregulation of the apoptosis-inducing CD95/L system within the CNS after trauma, yet a comparison of caspase 3-staining patterns between CD95 (Ipr)- and CD95L (gld)-deficient with non-deficient mice (C57/bl6) provided no evidence for CD95L-mediated neuronal cell death in this setting. However, inhibition of NMDA receptors with MK-801 completely suppressed caspase 3 activation, pointing to glutamate neurotoxicity as the upstream inducer of the observed cell death. Thus, these data show that axonal injury in the CNS does not only damage the axotomized neurons themselves, but can also lethally affect their target cells, apparently by activating glutamate-mediated intracellular pathways of programmed cell death.},
	Author = {Kovac, Adam D. and Kwidzinski, Erik and Heimrich, Bernd and Bittigau, Petra and Deller, Thomas and Nitsch, Robert and Bechmann, Ingo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {1015-6305},
	Journal = {Brain Pathol},
	Keywords = {Excitatory Amino Acid Antagonists;Animals;Synapses;Enzyme Activation;Glutamic Acid;Comparative Study;Dizocilpine Maleate;Apoptosis;Entorhinal Cortex;Caspases;Perforant Pathway;11 Glia;Male;Membrane Glycoproteins;Axotomy;Neurons;Mice;Microscopy, Electron;Immunohistochemistry;Antigens, CD95;Research Support, Non-U.S. Gov't},
	Medline = {23561092},
	Month = {7},
	Nlm_Id = {9216781},
	Number = {3},
	Organization = {Institute of Anatomy, Deptment of Cell and Neurobiology, Charit{\'e}, University Medicine, Berlin, Germany.},
	Pages = {249-57},
	Pubmed = {15446579},
	Title = {Entorhinal cortex lesion in the mouse induces transsynaptic death of perforant path target neurons},
	Uuid = {36E3689F-887B-44A2-A900-8B7684B2937C},
	Volume = {14},
	Year = {2004}}

@article{Kozlowski:2000,
	Abstract = {The effects of delivering GDNF via an adenoviral vector (AdGDNF) 1 week after lesioning dopaminergic neurons in the rat substantia nigra (SN) with 6-hydroxydopamine (6-OHDA) were examined. Rats were unilaterally lesioned by injection of 6-OHDA into the striatum, resulting in progressive degeneration of dopaminergic neurons in the SN. One week later, when substantial damage had already occurred, AdGDNF or a control vector harboring beta-galactosidase (AdLacZ) was injected into either the striatum or SN (3.2 x 10(7) PFU/microl in 2 microl). Rats were examined behaviorally with the amphetamine-induced rotation test and for forelimb use for weight-bearing movements. On day 30 postlesion, the extent of nigrostriatal tract degeneration was determined by injecting a retrograde tracer (FluoroGold) bilaterally into the lesioned striatum. Five days later, rats were sacrificed within 2 h of amphetamine injection to examine amphetamine-induced Fos expression in the striatum, a measure of dopaminergic-dependent function in target neurons. AdGDNF injection in the SN rescued dopaminergic neurons in the SN and increased the number of dopaminergic neurons that maintained a connection to the striatum, compared to rats injected with AdLacZ. Further support that these spared SN cells maintained functional connections to the striatum was evidenced by increased Fos expression in striatal target neurons and a decrease in amphetamine-induced rotation. In contrast to the effects observed in rats injected with AdGDNF in the SN, rats injected with AdGDNF in the striatum did not exhibit significant ameliorative effects. This study demonstrates that experimentally increasing levels of GDNF biosynthesis near the dopaminergic neuronal soma is effective in protecting the survival of these neurons and their function even when therapy is begun after 6-OHDA-induced degeneration has commenced. Thus, GDNF gene therapy may ameliorate the consequences of Parkinson's disease through rescuing compromised dopaminergic neurons.},
	Author = {Kozlowski, D. A. and Connor, B. and Tillerson, J. L. and Schallert, T. and Bohn, M. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Fluorescent Dyes;Motor Activity;Dopamine;Nerve Degeneration;Animals;Rats;Neural Pathways;Recovery of Function;Parkinson Disease;Substantia Nigra;Nerve Growth Factors;Male;Rats, Inbred F344;Proto-Oncogene Proteins c-fos;Research Support, U.S. Gov't, P.H.S.;Neostriatum;Neurons;Gene Therapy;Tyrosine 3-Monooxygenase;24 Pubmed search results 2008;Nerve Tissue Proteins;Oxidopamine;Research Support, Non-U.S. Gov't},
	Medline = {20487523},
	Month = {11},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Pediatrics, Children's Memorial Institute for Education and Research, Chicago, Illinois 60614, USA.},
	Pages = {1-15},
	Pii = {S0014488600974636},
	Pubmed = {11031079},
	Title = {Delivery of a GDNF gene into the substantia nigra after a progressive 6-OHDA lesion maintains functional nigrostriatal connections},
	Uuid = {7EF62F54-2685-459A-90D6-43071E74A319},
	Volume = {166},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.2000.7463}}

@article{Kozorovitskiy:2003,
	Author = {Kozorovitskiy, Yevgenia and Gould, Elizabeth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {Purkinje Cells;Cell Fusion;08 Aberrant cell cycle;Stem Cells;Bone Marrow Transplantation;22 Stem cells;comment;Animals;Brain;Mice;24 Pubmed search results 2008;news},
	Month = {11},
	Nlm_Id = {100890575},
	Number = {11},
	Pages = {952-4},
	Pii = {ncb1103-952},
	Pubmed = {14593417},
	Title = {Stem cell fusion in the brain},
	Uuid = {BB56ABD9-822D-4D91-81EF-C6B23561B182},
	Volume = {5},
	Year = {2003},
	url = {papers/Kozorovitskiy_NatCellBiol2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb1103-952}}

@article{Kosel:1997,
	Abstract = {Six cases of middle cerebral artery occlusion are presented in which the cellular changes accompanying descending degeneration of the lateral corticospinal tract were studied at different time points (5 days-10 years) following the insult. Microglia and perivascular cells were found to ingest large amounts of myelin degradation products, while expressing high levels of major histocompatibility complex (MHC) class II molecules. Activation of perivascular macrophages, as indicated by increased class II expression, lasted for many years and appeared to follow down-regulation of both phagocytic activity and class II expression on parenchymal microglia. TUNEL labeling was absent from both microglia and perivascular cells at all time points investigated. Indirect evidence is presented that microglia may transfer myelin degradation products to the perivascular space. Perivascular cells which express MHC class II molecules constitutively do not appear to leave the perivascular compartment in large numbers and could release myelin degradation products into the cerebrospinal fluid. The possible immunological consequences of these findings are discussed with respect to their possible relevance for antigen presentation and autoimmune central nervous system disease.},
	Author = {K{\"o}sel, S. and Egensperger, R. and Bise, K. and Arbogast, S. and Mehraein, P. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Myelin Sheath;Humans;Macrophages;Middle Aged;Brain;Microglia;Female;11 Glia;Cerebrovascular Disorders;Male;Spinal Cord;Aged;Wallerian Degeneration;Aged, 80 and over;Arterial Occlusive Diseases;Adult;Cerebral Arterial Diseases;Histocompatibility Antigens Class II;Lipids},
	Medline = {98106759},
	Month = {12},
	Nlm_Id = {0412041},
	Number = {6},
	Organization = {Molecular Neuropathology Laboratory, Institute of Neuropathology, Ludwig-Maximilians University, Munich, Germany.},
	Pages = {532-8},
	Pubmed = {9444354},
	Title = {Long-lasting perivascular accumulation of major histocompatibility complex class II-positive lipophages in the spinal cord of stroke patients: possible relevance for the immune privilege of the brain},
	Uuid = {B75097E0-E4E7-4805-BC61-AE465760BB0F},
	Volume = {94},
	Year = {1997}}

@article{Krall:1994,
	Abstract = {Gaucher disease is an inherited lysosomal storage disease in which the loss in functional activity of glucocerebrosidase (GC) results in the storage of its lipid substrate in cells of the macrophage lineage. A gene therapy approach involving retroviral transduction of autologous bone marrow (BM) followed by transplantation has been recently approved for clinical trial. Amelioration of the disease symptoms may depend on the replacement of diseased macrophages with incoming cells expressing human GC; however, the processes of donor cell engraftment and vector gene expression have not been addressed at the cellular level in relevant tissues. Therefore, we undertook a comprehensive immunohistologic study of macrophage and microglia replacement after murine BM transplantation with retrovirus-marked BM. Serial quantitative PCR analyses were employed to provide an overview of the time course of engraftment of vector-marked cells in a panel of tissues. Following reconstitution of hematopoietic tissues with vector-marked donor cells at early stages, GC+ cells began to infiltrate the liver, lung, brain, and spinal cord by 3 months after transplant. Immunohistochemical analyses of PCR+ tissues using the 8E4 monoclonal antibody specific for human GC revealed that macrophages expressing human GC had partially reconstituted the Mac-1+ population in all tissues in a manner characteristic to each tissue type. In the brain, 20\%of the total microglia had been replaced with donor cells expressing GC by 3 to 4 months after transplant. The finding that significant numbers of donor cells expressing a retroviral gene product immigrate to the central nervous system suggests that gene therapy for neuronopathic forms of lysosomal storage diseases as well as antiviral gene therapy for AIDS may be feasible.},
	Author = {Krall, W. J. and Challita, P. M. and Perlmutter, L. S. and Skelton, D. C. and Kohn, D. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Genetic Markers;Animals;Humans;Macrophages;Bone Marrow Transplantation;Brain;Microglia;Mice, Inbred C57BL;Retroviridae;11 Glia;Male;Genetic Vectors;Research Support, U.S. Gov't, P.H.S.;Glucosylceramidase;Polymerase Chain Reaction;Mice;Immunohistochemistry;Gene Expression;Spleen;Research Support, Non-U.S. Gov't},
	Medline = {94220722},
	Month = {5},
	Nlm_Id = {7603509},
	Number = {9},
	Organization = {Division of Research Immunology and Bone Marrow Transplantation, Childrens Hospital, Los Angeles, CA 90027.},
	Pages = {2737-48},
	Pubmed = {8167352},
	Title = {Cells expressing human glucocerebrosidase from a retroviral vector repopulate macrophages and central nervous system microglia after murine bone marrow transplantation},
	Uuid = {CCE6B77F-F08D-498C-8418-609114046F07},
	Volume = {83},
	Year = {1994}}

@article{Krantic:2005,
	Abstract = {Rapid progress in understanding the molecular basis of neurodegeneration has been tightly linked with recent discoveries in the field of programmed cell death (PCD). Analysis of PCD in neuronal demise has led to identification of several associated phenomena, such as re-initiation of the cell cycle and the key role of oxidative stress, although putative causal relationships between these events are still debatable. These issues are reviewed here in the context of acute and chronic neurodegenerative processes. In addition, newly emerging concepts concerning cell-cycle re-initiation are discussed in terms of their potential impact on the development of more effective therapeutic strategies.},
	Author = {Krantic, Slavica and Mechawar, Naguib and Reix, St{\'e}phanie and Quirion, R{\'e}mi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Aging;Neurons;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;07 Excitotoxicity Apoptosis;Neurodegenerative Diseases;Reactive Oxygen Species;Apoptosis;Models, Neurological;Cell Cycle;Humans;Brain;Animals;Oxidative Stress;review},
	Month = {12},
	Nlm_Id = {7808616},
	Number = {12},
	Organization = {Institut de Neurobiologie de la M{\'e}diterran{\'e}e (INMED), Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale (INSERM), Parc Scientifique Luminy, BP13, 13 273 Marseille, France. krantic\@inmed.univ.mrs.fr},
	Pages = {670-6},
	Pii = {S0166-2236(05)00259-6},
	Pubmed = {16216345},
	Title = {Molecular basis of programmed cell death involved in neurodegeneration},
	Uuid = {194E8C79-FBF9-43DD-9C86-A921F0D6F2A7},
	Volume = {28},
	Year = {2005},
	url = {papers/Krantic_TrendsNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tins.2005.09.011}}

@article{Kreiman:2004,
	Abstract = {Sequence information and high-throughput methods to measure gene expression levels open the door to explore transcriptional regulation using computational tools. Combinatorial regulation and sparseness of regulatory elements throughout the genome allow organisms to control the spatial and temporal patterns of gene expression. Here we study the organization of cis-regulatory elements in sets of co-regulated genes. We build an algorithm to search for combinations of transcription factor binding sites that are enriched in a set of potentially co-regulated genes with respect to the whole genome. No knowledge is assumed about involvement of specific sets of transcription factors. Instead, the search is exhaustively conducted over combinations of up to four binding sites obtained from databases or motif search algorithms. We evaluate the performance on random sets of genes as a negative control and on three biologically validated sets of co-regulated genes in yeasts, flies and humans. We show that we can detect DNA regions that play a role in the control of transcription. These results shed light on the structure of transcription regulatory regions in eukaryotes and can be directly applied to clusters of co-expressed genes obtained in gene expression studies. Supplementary information is available at http://www.mit.edu/ approximately kreiman/resources/cisregul/.},
	Author = {Kreiman, Gabriel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1362-4962},
	Journal = {Nucleic Acids Res},
	Keywords = {Computational Biology;10 Development;research support, non-u.s. gov't;Binding Sites;Response Elements;Algorithms;Gene Expression Regulation;Saccharomyces cerevisiae;Drosophila melanogaster;evaluation studies;Cell Cycle;Animals;Humans;24 Pubmed search results 2008;Muscle, Skeletal;Transcription Factors},
	Nlm_Id = {0411011},
	Number = {9},
	Organization = {Center for Biological and Computational Learning, McGovern Institute for Brain Research, Massachusetts Institute of Technology, 45 Carleton Street, MIT E25-201B, Cambridge, MA 02142, USA. kreiman\@mit.edu},
	Pages = {2889-900},
	Pii = {32/9/2889},
	Pubmed = {15155858},
	Title = {Identification of sparsely distributed clusters of cis-regulatory elements in sets of co-expressed genes},
	Uuid = {78EF4B19-D067-40ED-B975-DC81187CFDA5},
	Volume = {32},
	Year = {2004},
	url = {papers/Kreiman_NucleicAcidsRes2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/nar/gkh614}}

@article{Kreutzberg:1989,
	Abstract = {Following axonal interruption, structural, metabolic and physiological parameters change in motorneurons. Also, glial cells are involved in this process. Microglia proliferate and express new proteins such as vimentin or MHC antigens. Astrocytes show hypertrophy, increased GFAP synthesis, and formation of lamellae. Both glial cell types participate in deafferentation and insulation of regenerating neurons, a process with significance for post-lesioning functional impairment.},
	Author = {Kreutzberg, G. W. and Graeber, M. B. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0885-7490},
	Journal = {Metab Brain Dis},
	Keywords = {Neuroglia;Motor Neurons;Nerve Regeneration;Not relevant;11 Glia;review, tutorial;Animals;review},
	Medline = {89201129},
	Month = {3},
	Nlm_Id = {8610370},
	Number = {1},
	Organization = {Department of Neuromorphology, Max Planck Institute for Psychiatry, Planegg-Martinsried, F.R.G.},
	Pages = {81-5},
	Pubmed = {2649780},
	Title = {Neuron-glial relationship during regeneration of motorneurons},
	Uuid = {DB0C68DC-6D86-4B68-B4DA-8D2DDCFF87AA},
	Volume = {4},
	Year = {1989}}

@article{Kriegstein:2005,
	Abstract = {Our knowledge of the proliferation, migration, and differentiation of neurons has changed dramatically over the last 10 years. Whereas traditionally it was thought that glial and neuronal cells were separate cell lines with different lineages, we now know that this is not true. Radial glia are a type of neural stem cell that generate excitatory pyramidal neurons directly through asymmetric cell division in the ventricular zone (VZ) of the telencephalon and indirectly through the symmetric division of daughter intermediate precursor cells that divide in the subventricular zone (SVZ). Moreover, pyramidal neurons, once thought to migrate only along radial guide fibers to the developing layers of the cortex, have been shown to proceed through four distinct stages of migration during which they change shape, direction, and speed. Gamma-aminobutyric acid (GABAergic) inhibitory interneurons, on the other hand, are generated not in the cortex, but in the medial ganglionic eminence and migrate tangentially to their final cortical destinations. Evidence suggests that GABA activation may play a role in coordinating the generation and migration of both pyramidal and interneuron populations. At the end of neurogenesis, radial glial cells translocate to the cortex and transform into astrocytes. Although they do not actively divide in the adult brain, astrocytes may retain the potential to generate new neurons. These new findings have increased our understanding of the mechanisms underlying certain developmental disorders and, in doing so, reveal potentially useful modes of therapeutic intervention.},
	Author = {Kriegstein, Arnold R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Epilepsy;10 Development;Neuroglia;Research Support, Non-U.S. Gov't;Pyramidal Cells;Models, Neurological;Astrocytes;Cell Division;Neocortex;Stem Cells;Interneurons;gamma-Aminobutyric Acid;Humans;Cell Movement;Neurons},
	Nlm_Id = {2983306R},
	Organization = {Department of Neurology, University of California, San Francisco, San Francisco, California 94143, USA. kreigstein\@stemcell.ucsf.edu},
	Pages = {15-21},
	Pii = {EPI304},
	Pubmed = {16201991},
	Title = {Constructing circuits: neurogenesis and migration in the developing neocortex},
	Uuid = {1556314C-B609-4380-8BCF-65E9BD7E6B2F},
	Volume = {46 Suppl 7},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1528-1167.2005.00304.x}}

@article{Kriegstein:2004,
	Abstract = {Real-time imaging of migrating neurons has changed our understanding of how newborn neurons reach their final positions in the developing cerebral cortex. The migratory routes and modes of migration are more diverse and complex than previously thought. The finding that cortical interneurons migrate to the cortex from origins in the ventral telencephalon has already markedly altered our view of cortical migration. More recent findings have demonstrated additional nuances in the migratory pattern and highlighted differences between subsets of interneurons. Moreover, radial migration of pyramidal neurons does not progress smoothly from ventricle to cortical plate, but is instead characterized by distinct migratory phases in which neurons change shape and direction of movement. Integrating these findings with the molecular machinery underlying migration will provide a more complete picture of how the cerebral cortex is assembled.},
	Author = {Kriegstein, Arnold R. and Noctor, Stephen C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {review;10 Development;Research Support, Non-U.S. Gov't;Research Support, U.S. Gov't, P.H.S.;Humans;Animals;Cerebral Cortex;Neurons;Cell Movement},
	Month = {7},
	Nlm_Id = {7808616},
	Number = {7},
	Organization = {Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA. ark17\@columbia.edu},
	Pages = {392-9},
	Pii = {S0166223604001547},
	Pubmed = {15219738},
	Title = {Patterns of neuronal migration in the embryonic cortex},
	Uuid = {0010FB9D-AEFC-46E8-A02D-59AB1B432A7A},
	Volume = {27},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tins.2004.05.001}}

@article{Kristan:2006,
	Abstract = {'Form follows function' is an architectural philosophy attributed to the great American architect Louis Sullivan , and later taken up by the Bauhaus movement. It stresses that the form of a building should reflect its function. Neuroscientists have used the connverse of this dictum to learn the functions of neural circuits, believing that if we study neural architecture, it will lead us to an understanding of how neural systems function. New tools for studying the structure of neural circuits are being developed, so it is important to discuss what the old techniques have taught us about how to derive function from the form of a neural circuit.},
	Author = {Kristan, William B. and Katz, Paul},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {9107782},
	Number = {19},
	Organization = {University of California San Diego, Division of Biological Sciences, Neurobiology Section, 9500 Gilman Drive, La Jolla, California 92093-0357, USA.},
	Pages = {R828-31},
	Pii = {S0960-9822(06)02146-4},
	Pubmed = {17027473},
	Title = {Form and function in systems neuroscience},
	Uuid = {A9A134FD-B2AF-4BC1-ABFE-0F9DE10B5E12},
	Volume = {16},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2006.08.079}}

@article{Kristensen:2003,
	Abstract = {The microtubule-disrupting agent colchicine is known to be particular toxic for certain types of neurons, including the granule cells of the dentate gyrus. In this study we investigated whether colchicine could induce such neuron-specific degeneration in developing (1 week in vitro) and mature (3 weeks in vitro) organotypic hippocampal slice cultures and whether the induced cell death was apoptotic and/or necrotic. When applied to 1-week-old cultures for 48 h, colchicine induced primarily apoptotic, but also a minor degree of necrotic cell death in the dentate granule cells, as investigated by cellular uptake of the fluorescent dye propidium iodide (PI), immunostaining for active caspase 3 and c-Jun/AP-1 (N) and fragmentation of nuclei as seen in Hoechst 33342 staining. All four markers appeared after 12 h of colchicine exposure. Two of them, active caspase 3 and c-Jun/AP-1 (N) displayed a similar time course and reached a maximum after 24 h of exposure, 24 h ahead of both PI uptake and Hoechst 33342 staining, which together displayed similar time profiles and a close correlation. In 3-week-old cultures, colchicine did not induce apoptotic or necrotic cell death. Attempts to interfere with the colchicine-induced apoptosis in 1-week-old cultures showed that colchicine-induced PI uptake and formation of apoptotic nuclei were temporarily prevented by coapplication of the protein synthesis inhibitor cycloheximide. Application of the pancaspase inhibitor z-VAD-fmk almost completely abolished the formation of active caspase 3 protein and apoptotic nuclei induced by colchicine, but the formation of necrotic nuclei increased correspondingly and the PI uptake was unaffected. We conclude that colchicine induces caspase 3-dependent apoptotic cell death of dentate granule cells in hippocampal brain slice cultures, but the apoptotic cell death is highly dependent on the developmental stage of the cultures. 0006-8993 Journal Article},
	Author = {Kristensen, B. W. and Noer, H. and Gramsbergen, J. B. and Zimmer, J. and Noraberg, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Brain Res},
	Keywords = {Fluorescent Dyes/diagnostic use;Dose-Response Relationship, Drug;Neurotoxins/*toxicity;Caspases/drug effects/metabolism;Animals;Rats;Benzimidazoles/diagnostic use;Cycloheximide/pharmacology;EE pdf;Rats, Wistar;Neuroprotective Agents/pharmacology;08 Aberrant cell cycle;Time Factors;Apoptosis/*drug effects;Dentate Gyrus/*drug effects/metabolism;Support, Non-U.S. Gov't;Colchicine/*toxicity;Protein Synthesis Inhibitors/pharmacology;Neurons/*drug effects/metabolism;Immunohistochemistry;Necrosis;Amino Acid Chloromethyl Ketones/pharmacology;Propidium/metabolism},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, Institute of Medical Biology, University of Southern Denmark, Winslowparken 21, DK-5000 C, Odense, Denmark. bkristensen\@health.sdu.dk},
	Pages = {264-78},
	Title = {Colchicine induces apoptosis in organotypic hippocampal slice cultures},
	Uuid = {4D76C49D-FB61-4229-9F3E-4ADD85218810},
	Volume = {964},
	Year = {2003},
	url = {papers/Kristensen_BrainRes2003}}

@article{Krivit:1995,
	Abstract = {Treatment and potential cure of lysosomal and peroxisomal diseases, heretofore considered fatal, has become a reality during the past decade. Bone marrow transplantation, (BMT), has provided a method for replacement of the disease-causing enzyme deficiency. Cells derived from the donor marrow continue to provide enzyme indefinitely. Several scores of patients with diseases as diverse as metachromatic leukodystrophy, adrenoleukodystrophy, globoid cell leukodystrophy, Hurler syndrome (MPS I-H), Maroteaux-Lamy (MPS VI) Gaucher disease, and fucosidosis have been successfully treated following long-term engraftment. Central nervous system (CNS) manifestations are also prevented or ameliorated in animal models of these diseases following engraftment from normal donors. The microglial cell system has been considered to be the most likely vehicle for enzyme activity following bone marrow engraftment. Microglia in the mature animal or human are derived from the newly engrafted bone marrow. Graft-v-host disease activation of the microglia is also of importance. This article will summarize some of the pertinent literature relative to the role of microglia in such transplant processes.},
	Author = {Krivit, W. and Sung, J. H. and Shapiro, E. G. and Lockman, L. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0963-6897},
	Journal = {Cell Transplant},
	Keywords = {Phagocytosis;Animals;Humans;Lysosomal Storage Diseases;Bone Marrow Transplantation;review, tutorial;Peroxisomal Disorders;review;Microglia;Female;Cell Movement;11 Glia;Male;Blood-Brain Barrier;Bone Marrow Cells;Cell Lineage;Research Support, U.S. Gov't, P.H.S.;Graft vs Host Disease;Central Nervous System},
	Medline = {96090321},
	Nlm_Id = {9208854},
	Number = {4},
	Organization = {Department of Pediatrics, University of Minnesota Medical School, Minneapolis 55455, USA.},
	Pages = {385-92},
	Pii = {096368979500021O},
	Pubmed = {7582569},
	Title = {Microglia: the effector cell for reconstitution of the central nervous system following bone marrow transplantation for lysosomal and peroxisomal storage diseases},
	Uuid = {BF60B3F9-CB4A-438B-A7A8-BBA7316F8E48},
	Volume = {4},
	Year = {1995}}

@article{Kronenberg:2003,
	Abstract = {To study how adult hippocampal neurogenesis might originate from the proliferation of stem or progenitor cells in vivo, we have used transgenic mice expressing green fluorescent protein (GFP) under the nestin promoter to identify these cells. Having described an astrocyte-like type 1 cell with low proliferative activity, a characteristic morphology, vascular end feet, and passive electrophysiological properties, we focused here on the large population of nestin-GFP-expressing type 2 cells, which lack all these features. Type 2 cells were highly proliferative and showed signs suggestive of their involvement in the neuronal lineage. They could be subclassified by the absence (type 2a) or presence (type 2b) of a coexpression of the early neuronal marker doublecortin. A third type of proliferating cells was doublecortin positive but nestin-GFP negative (type 3). We believe that type 2a, 2b, and 3 cells mirror a marker progression during earliest neuronal development. This view is supported by the increasing coexpression of the early granule cell-specific marker Prox-1. The low proliferative activity of type 1 cells showed little change over time or under "neurogenic interventions,"such as a challenge by environmental complexity (ENR) or voluntary physical activity (RUN). However, RUN led to a significant increase of type 2 cells labeled with the proliferation marker bromodeoxyuridine (BrdU). ENR did not cause increased cell proliferation or an increased number of BrdU-labeled type 2 cells, but both ENR and RUN resulted in more newly generated cells lacking nestin-GFP immunoreactivity and expressing Prox-1. These findings allow us to break down what was broadly perceived as "proliferation"in earlier experiments into the relative contribution of several cell types, representing the earliest steps of neuronal development. 0021-9967 Journal Article},
	Author = {Kronenberg, G. and Reuter, K. and Steiner, B. and Brandt, M. D. and Jessberger, S. and Yamaguchi, M. and Kempermann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Intermediate Filament Proteins/genetics/metabolism;Animals;Random Allocation;Comparative Study;Neural Cell Adhesion Molecule L1/metabolism;02 Adult neurogenesis migration;Mice, Transgenic;*Environment;Mice, Inbred C57BL;Motor Activity/physiology;Time Factors;Behavior, Animal;Neurons/classification/*physiology;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;BB pdf;Sialic Acids/metabolism;Homeodomain Proteins/metabolism;Ki-67 Antigen/metabolism;Hippocampus/*cytology/growth &development;Neuropeptides/metabolism;Mice;Cell Division;Immunohistochemistry;Bromodeoxyuridine/pharmacokinetics;Luminescent Proteins/genetics/metabolism},
	Number = {4},
	Organization = {Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch, 13125 Berlin, Germany.},
	Pages = {455-63},
	Pubmed = {14624480},
	Title = {Subpopulations of proliferating cells of the adult hippocampus respond differently to physiologic neurogenic stimuli},
	Uuid = {60780499-018E-4790-A453-31403D150336},
	Volume = {467},
	Year = {2003},
	url = {papers/Kronenberg_JCompNeurol2003.pdf}}

@article{Krueger:1987,
	Abstract = {Normal and malignant cells show differences in cell membrane lipid fluidity (CMF) which influence the expression of membrane receptors and may interfere with cell function. Friend virus (FLV) and Moloney virus (MLV) infected hematopoietic and lymphoid cells were monitored for CMF (fluorescence polarization) and for transferrin (TFC) and thymic (Thy) receptors (FITC-labelled monoclonal antibodies). CMF was modulated with cholesterol hemisuccinate (CHS), phospholipids (PL) and DMSO. Erythropoietic stem cells exhibit an increased persistent CMF within minutes after FLV infection; transferrin receptors are expressed, yet no hemoglobin is synthesized. CHS rigidification reduces TFC expression with differentiation of cells and hemoglobin synthesis, yet transformed cell populations do not react uniformly. Thymic lymphocytes, instead, do not exhibit changes in Thy expression upon CHS treatment although cell membranes become rigidified. Separate experiments showed these cells not being "transformed"per se but blocked in differentiation because of viral destruction of thymic epithelial cells with loss of thymopoietin in vivo. Thus viral cell transformation is followed by non-rigid but persistent membrane fluidization interfering with only selective receptor expression. 0258-851x Journal Article},
	Author = {Krueger, G. R. and Stolzenburg, T. and Muller, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {In Vivo},
	Keywords = {EE, DMSO, abstr;Leukemia, Experimental/genetics/*physiopathology;08 Aberrant cell cycle;Moloney murine leukemia virus/*genetics;*Cell Transformation, Neoplastic;*Membrane Fluidity;Friend murine leukemia virus/*genetics;Animals, Newborn;Receptors, Transferrin/*metabolism;Animals;Support, Non-U.S. Gov't;Mice;Mice, Inbred Strains},
	Number = {6},
	Organization = {Pathology Institute, University of Cologne, F.R.G.},
	Pages = {343-6},
	Pubmed = {2979801},
	Title = {Cell membrane lipid fluidity and receptor expression in Moloney- and Friend virus-transformed cells},
	Uuid = {15D7A82E-7FAC-49A1-A097-146BCA0B75C9},
	Volume = {1},
	Year = {1987},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2979801}}

@article{Kuan:2004,
	Abstract = {Recent studies suggest that postmitotic neurons can reenter the cell cycle as a prelude to apoptosis after brain injury. However, most dying neurons do not pass the G1/S-phase checkpoint to resume DNA synthesis. The specific factors that trigger abortive DNA synthesis are not characterized. Here we show that the combination of hypoxia and ischemia induces adult rodent neurons to resume DNA synthesis as indicated by incorporation of bromodeoxyuridine (BrdU) and expression of G1/S-phase cell cycle transition markers. After hypoxia-ischemia, the majority of BrdU- and neuronal nuclei (NeuN)-immunoreactive cells are also terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL)-stained, suggesting that they undergo apoptosis. BrdU+ neurons, labeled shortly after hypoxia-ischemia, persist for >5 d but eventually disappear by 28 d. Before disappearing, these BrdU+/NeuN+/TUNEL+ neurons express the proliferating cell marker Ki67, lose the G1-phase cyclin-dependent kinase (CDK) inhibitors p16INK4 and p27Kip1 and show induction of the late G1/S-phase CDK2 activity and phosphorylation of the retinoblastoma protein. This contrasts to kainic acid excitotoxicity and traumatic brain injury, which produce TUNEL-positive neurons without evidence of DNA synthesis or G1/S-phase cell cycle transition. These findings suggest that hypoxia-ischemia triggers neurons to reenter the cell cycle and resume apoptosis-associated DNA synthesis in brain. Our data also suggest that the demonstration of neurogenesis after brain injury requires not only BrdU uptake and mature neuronal markers but also evidence showing absence of apoptotic markers. Manipulating the aberrant apoptosis-associated DNA synthesis that occurs with hypoxia-ischemia and perhaps neurodegenerative diseases could promote neuronal survival and neurogenesis.},
	Author = {Kuan, Chia-Yi Y. and Schloemer, Aryn J. and Lu, Aigang and Burns, Kevin A. and Weng, Wei-Lan L. and Williams, Michael T. and Strauss, Kenneth I. and Vorhees, Charles V. and Flavell, Richard A. and Davis, Roger J. and Sharp, Frank R. and Rakic, Pasko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;08 Aberrant cell cycle;06 Adult neurogenesis injury induced},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {47},
	Organization = {Department of Pediatrics, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. alex.kuan\@chmcc.org},
	Pages = {10763-72},
	Pii = {24/47/10763},
	Pubmed = {15564594},
	Title = {Hypoxia-ischemia induces DNA synthesis without cell proliferation in dying neurons in adult rodent brain},
	Uuid = {325284AE-D395-11D9-A0E9-000D9346EC2A},
	Volume = {24},
	Year = {2004},
	url = {papers/Kuan_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3883-04.2004}}

@article{Kuenzel:1982,
	Abstract = {Six groups of broiler chicks, Gallus domesticus, sustained bilateral lesions to specific neural structures residing in the lateral hypothalamic and thalamic areas. In contrast to past data reported for the albino rat, the pigeon, Columba livia and barbary dove, Streptopelia risoria, bilateral destruction of the chick lateral hypothalamic area (LHy), quinto-frontal tract (QF), and stratum cellulare externum (SCE) resulted in transient aphagia and rapid recovery of lost body weight. Similarly, bilateral destruction of the nucleus reticularis superior (RS) and nucleus intercalatus (ICT) resulted in a temporary 1--3 day period of aphagia with body weight returning to pre-operative levels in approximately 4 days. Bilateral destruction of the ansa lenticularis (AL) resulted in a more prolonged period of aphagia (4 days) and an average 8-day period to recover lost body weight. Additional data suggest that more persistent aphagia can be induced following lesions to the posterior hypothalamus and midbrain. Specifically, bilateral lesions which destroyed the following combination of neural structures resulted in prolonged aphagia: AL, QF and posterior LHy; AL and posterior nucleus of the AL (ALp); and AL, ALp and QF. It is suggested that the AL and ALp contain neurons which are part of a more complex system that modulates or controls motor activity and feeding behavior in birds.},
	Author = {Kuenzel, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0031-9384},
	Journal = {Physiol Behav},
	Keywords = {24 Pubmed search results 2008;Brain Stem;Mesencephalon;Eating;Research Support, Non-U.S. Gov't;Hypothalamus;Neural Pathways;Corpus Striatum;Body Weight;Chickens;Male;Brain;Animals;Frontal Lobe},
	Medline = {82197973},
	Month = {2},
	Nlm_Id = {0151504},
	Number = {2},
	Pages = {237-44},
	Pubmed = {7079336},
	Title = {Transient aphagia produced following bilateral destruction of the lateral hypothalamic area and quinto-frontal tract of chicks},
	Uuid = {B66EFA4E-3EE3-4354-8265-5D83398DE9CD},
	Volume = {28},
	Year = {1982}}

@article{Kuhn:1996,
	Abstract = {The hippocampus is one of the few areas of the rodent brain that continues to produce neurons postnatally. Neurogenesis reportedly persists in rats up to 11 months of age. Using bromodeoxyuridine (BrdU) labeling, the present study confirms that in the adult rat brain, neuronal progenitor cells divide at the border between the hilus and the granule cell layer (GCL). In adult rats, the progeny of these cells migrate into the GCL and express the neuronal markers NeuN and calbindin-D28k. However, neurogenesis was drastically reduced in aged rats. Six-to 27-month-old Fischer rats were injected intraperitoneally with BrdU to detect newborn cells in vivo and to follow their fate in the dentate gyrus. When killed 4-6 weeks after BrdU labeling, 12- to 27- month-old rats exhibited a significant decline in the density of BrdU- positive cells in the granule cell layer compared with 6-month-old controls. Decreased neurogenesis in aging rats was accompanied by reduced immunoreactivity for poly-sialylated neural cell adhesion molecule, a molecule that is involved in migration and process elongation of developing neurons. When animals were killed immediately (12 hr) after BrdU injection, significantly fewer labeled cells were observed in the GCL and adjacent subgranular zone of aged rats, indicative of a decrease in mitotic activity of neuronal precursor cells. The reduced proliferation was not attributable to a general aged- related metabolic impairment, because the density of BrdU-positive cells was not altered in other brain regions with known mitotic activity (e.g., hilus and lateral ventricle wall). The decline in neurogenesis that occurs throughout the lifespan of an animal can thus be related to a decreasing proliferation of granule cell precursors.},
	Author = {Kuhn, H. G. and Dickinson-Anson, H. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {J Neurosci},
	Keywords = {Neural Cell Adhesion Molecules/analysis;Rats;Comparative Study;Sialic Acids/analysis;Female;Neurons/chemistry/*cytology;Animal;Polysaccharides/analysis;Aging/*physiology;Stem Cells/*cytology;Dentate Gyrus/*cytology;01 Adult neurogenesis general;Rats, Inbred F344;Support, Non-U.S. Gov't;Cell Division/physiology;A-7;Support, U.S. Gov't, P.H.S.;Cell Movement/physiology;Cell Differentiation/physiology;Immunohistochemistry;Bromodeoxyuridine;Biological Markers/analysis},
	Number = {6},
	Organization = {Laboratory of Genetics, Salk Institute, La Jolla, California 92037, USA.},
	Pages = {2027-33.},
	Title = {Neurogenesis in the dentate gyrus of the adult rat: age-related decrease of neuronal progenitor proliferation},
	Uuid = {6F91BFE5-4E8B-4F84-B75B-AB567B501497},
	Volume = {16},
	Year = {1996},
	url = {papers/Kuhn_JNeurosci1996.pdf}}

@article{Kuhn:1997,
	Abstract = {Neurons and glia are generated throughout adulthood from proliferating cells in two regions of the rat brain, the subventricular zone (SVZ) and the hippocampus. This study shows that exogenous basic fibroblast growth factor (FGF-2) and epidermal growth factor (EGF) have differential and site-specific effects on progenitor cells in vivo. Both growth factors expanded the SVZ progenitor population after 2 weeks of intracerebroventricular administration, but only FGF-2 induced an increase in the number of newborn cells, most prominently neurons, in the olfactory bulb, the normal destination for neuronal progenitors migrating from the SVZ. EGF, on the other hand, reduced the total number of newborn neurons reaching the olfactory bulb and substantially enhanced the generation of astrocytes in the olfactory bulb. Moreover, EGF increased the number of newborn cells in the striatum either by migration of SVZ cells or by stimulation of local progenitor cells. No evidence of neuronal differentiation of newborn striatal cells was found by three-dimensional confocal analysis, although many of these newborn cells were associated closely with striatal neurons. The proliferation of hippocampal progenitors was not affected by either growth factor. However, EGF increased the number of newborn glia and reduced the number of newborn neurons, similar to the effects seen in the olfactory bulb. These findings may be useful for elucidating the in vivo role of growth factors in neurogenesis in the adult CNS and may aid development of neuronal replacement strategies after brain damage.},
	Author = {Kuhn, H. G. and Winkler, J. and Kempermann, G. and Thal, L. J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {J Neurosci},
	Keywords = {Fibroblast Growth Factor, Basic/*pharmacology;Rats, Inbred F344;C-6;Stem Cells/*drug effects;Rats;Brain/*drug effects;Animal;Cell Count/*drug effects;Epidermal Growth Factor/*pharmacology;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Neurons/*drug effects;Male},
	Number = {15},
	Organization = {Laboratory of Genetics, The Salk Institute, La Jolla, California 92186, USA.},
	Pages = {5820-9.},
	Title = {Epidermal growth factor and fibroblast growth factor-2 have different effects on neural progenitors in the adult rat brain},
	Uuid = {5880393F-DEE5-45DE-A02E-D286F91864A1},
	Volume = {17},
	Year = {1997},
	url = {papers/Kuhn_JNeurosci1997.pdf}}

@article{Kulkarni:1994,
	Abstract = {Little is known about the regulation of apoptosis in fibroblasts although several model systems including serum deprivation and treatment with staurosporine or topoisomerase inhibitors have been used to induce apoptosis in vitro. To validate a reproducible in vitro model for the study of apoptosis in fibroblasts, we cultured density-inhibited monolayer cultures of Balb/c 3T3 fibroblasts in Dulbecco's modified essential medium plus 15\%fetal calf serum and then withdrew serum. Time-lapse video microscopy demonstrated that within minutes of serum withdrawal, cells lost substrate attachment and floated to the top of the liquid growth medium. There was a time-dependent increase in the number of non-adherent cells. Some of these cells regained attachment and spread momentarily, but they eventually rounded up and lost attachment permanently. In contrast to serum-containing cultures in which similar morphological changes were followed by mitosis, in serum-free cultures repeated attempts at mitosis were followed by permanent attachment loss and presumably cell death. To assess whether all the non-adherent cells were in fact dead, the percentages of cells that continued to proliferate upon return to serum-supplemented conditions was computed. After various periods of serum starvation a decreasing proportion (approx. 75\%at 30 minutes; <2\%at 24 hours) of the non-adherent cells could be rescued by addition of serum. Transmission electron microscopy of cells 3 hours after serum withdrawal showed that the majority (approximately 60\%) of non-adherent cells exhibited marked intranuclear chromatin condensation but maintained integrity of cell and nuclear membranes and cell organelles, morphological changes consistent with those of apoptotic cell death. Scanning electron microscopy of cultures 3 hours following serum withdrawal showed rounded cells with marked surface blebbing. Fluorescence and confocal microscopy revealed increased intensity of nuclear staining with DAPI while actin filaments became indistinct or collapsed around the nucleus. After cycloheximide treatment to inhibit protein synthesis, there was no reduction of apoptosis. Gel electrophoresis of DNA from both control and 3 hour-serum-deprived cells showed intact DNA with no oligonucleosomal length fragmentation. After serum withdrawal, intracellular calcium was reduced by about 32\%over 5 minutes as measured by fura2 ratio fluorimetry in single cells. Serum-starved cells showed a time-dependent shrinkage in mean cell diameter compared to trypsinized, adherent control cells (at 0 hours, mean diameter = 18.0 microns--viable; at 4 hours, mean diameter = 15.5 microns--apoptotic). Flow cytometric analysis showed increased propidium iodide staining and reduced fluorescein diacetate uptake over 3 hours, changes that were contemporaneous with the reduction of cell diameter.(ABSTRACT TRUNCATED AT 400 WORDS)},
	Author = {Kulkarni, G. V. and McCulloch, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0021-9533},
	Journal = {J Cell Sci},
	Keywords = {Microscopy, Phase-Contrast;Microscopy, Electron, Scanning;Animals;Electrophoresis, Agar Gel;07 Excitotoxicity Apoptosis;Cycloheximide;Apoptosis;Models, Biological;DNA;Mitosis;Genes, myc;Calcium;Microscopy, Fluorescence;Cell Adhesion;Support, Non-U.S. Gov't;3T3 Cells;Cell Size;Flow Cytometry;Mice;Microscopy, Electron;Culture Media;Gene Expression},
	Medline = {95014779},
	Month = {5},
	Nlm_Id = {0052457},
	Organization = {Faculty of Dentistry, University of Toronto, Ontario, Canada.},
	Pages = {1169-79},
	Pubmed = {7929626},
	Title = {Serum deprivation induces apoptotic cell death in a subset of Balb/c 3T3 fibroblasts},
	Uuid = {9F98B556-58F3-47CE-B12F-DEF9B50F7C53},
	Volume = {107 ( Pt 5)},
	Year = {1994},
	url = {papers/Kulkarni_JCellSci1994.pdf}}

@article{Kulkarni:2006,
	Abstract = {To evaluate the specificity of long dsRNAs used in high-throughput RNA interference (RNAi) screens performed at the Drosophila RNAi Screening Center (DRSC), we performed a global analysis of their activity in 30 genome-wide screens completed at our facility. Notably, our analysis predicts that dsRNAs containing >/=19-nucleotide perfect matches identified in silico to unintended targets may contribute to a significant false positive error rate arising from off-target effects. We confirmed experimentally that such sequences in dsRNAs lead to false positives and to efficient knockdown of a cross-hybridizing transcript, raising a cautionary note about interpreting results based on the use of a single dsRNA per gene. Although a full appreciation of all causes of false positive errors remains to be determined, we suggest simple guidelines to help ensure high-quality information from RNAi high-throughput screens.},
	Author = {Kulkarni, and Booker, and Silver, and Friedman, and Hong, and Perrimon, and Mathey-Prevot,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1548-7091},
	Journal = {Nat Methods},
	Keywords = {21 Neurophysiology;23 RNAi;24 Pubmed search results 2008;23 Technique},
	Month = {10},
	Nlm_Id = {101215604},
	Number = {10},
	Organization = {[1] Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. [2] Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. [3] These authors contributed equally to this work.},
	Pages = {833-838},
	Pii = {nmeth935},
	Pubmed = {16964256},
	Title = {Evidence of off-target effects associated with long dsRNAs in Drosophila melanogaster cell-based assays},
	Uuid = {FEC9BA6C-48A4-11DB-A317-000D9346EC2A},
	Volume = {3},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nmeth935}}

@article{Kumar:2006,
	Abstract = {BACKGROUND: Japanese encephalitis virus (JEV) and West Nile virus (WNV) are neurotropic flaviviruses that can cause acute encephalitis with a high fatality rate. Currently there is no effective treatment for these infections. METHODS AND FINDINGS: We tested RNA interference (RNAi)-based intervention to suppress lethal JE and WN encephalitis in mice. To induce RNAi, we used either lentivirally expressed short hairpin RNA (shRNA) or synthetic short interfering RNA (siRNA). As target, we selected the cd loop-coding sequence in domain II of the viral Envelope protein, which is highly conserved among all flaviviruses because of its essential role in membrane fusion. Using as a target a species-specific sequence in the cd loop that is conserved only among the different strains of either JEV or WNV, we could achieve specific protection against the corresponding virus. However, by targeting a cross-species conserved sequence within the cd loop, we were able to protect mice against encephalitis induced by both viruses. A single intracranial administration of lentivirally delivered shRNA or lipid-complexed siRNA before viral challenge or siRNA treatment after viral challenge was sufficient for protection against lethal encephalitis. CONCLUSIONS: RNAi-based intervention affords near complete protection from both JEV- and WNV- induced encephalitis in mice. Our results show, to our knowledge for the first time, that siRNA can be used as a broad-spectrum antiviral agent for treating encephalitis caused by multiple related viruses.},
	Author = {Kumar, Priti and Lee, Sang Kyung and Shankar, Premlata and Manjunath, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1549-1676},
	Journal = {PLoS Med},
	Keywords = {15 ERVs retroelements;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {101231360},
	Number = {4},
	Organization = {The CBR Institute for Biomedical Research and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.},
	Pages = {e96},
	Pii = {05-PLME-RA-0504R2},
	Pubmed = {16464133},
	Title = {A single siRNA suppresses fatal encephalitis induced by two different flaviviruses},
	Uuid = {A42E5F9C-F69C-45E0-84EE-B8B03833FD92},
	Volume = {3},
	Year = {2006},
	url = {papers/Kumar_PLoSMed2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pmed.0030096}}

@article{Kume:2000,
	Abstract = {Hematopoietic stem cells (HSCs) are attractive targets for gene therapy, but current gene transfer methodologies are inadequate for efficient HSC transduction and perpetual transgene expression. To improve gene transfer vectors and transduction protocols, it is vital to establish a system to evaluate transgene expression and the long-term behavior of transduced cells in vivo. For this purpose, we constructed a bicistronic retrovirus encoding the human CD24 (as the first cistron) and the enhanced green fluorescent protein (EGFP; as the second cistron). Murine bone marrow cells were transduced with this vector and the transgene expression was monitored along with hematopoietic reconstitution. Stable expression of CD24 and EGFP was demonstrated in the long-term repopulating cells for at least 6 months, and multi-parameter flow cytometry illustrated expression of both markers in all the lymphohematopoietic lineages examined (B and T lymphoid, erythroid and myeloid). Sustained expression was also shown in the secondary transplants for 6 months, suggesting that self-renewing HSCs were transduced by this vector. Overall, EGFP-tagged bicistronic retroviruses would provide powerful tools for detailed in vivo analysis of transduced hematopoietic cells, such as transgene expression in conjunction with lineage differentiation. Gene Therapy (2000) 7, 1193-1199.},
	Author = {Kume, A. and Xu, R. and Ueda, Y. and Urabe, M. and Ozawa, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Membrane Glycoproteins;Research Support, Non-U.S. Gov't;Luminescent Proteins;Transduction, Genetic;Hematopoietic Stem Cells;Bone Marrow Cells;Retroviridae;Antigens, CD;Bone Marrow Transplantation;11 Glia;Green Fluorescent Proteins;Animals;Humans;Mice},
	Medline = {20379366},
	Month = {7},
	Nlm_Id = {9421525},
	Number = {14},
	Organization = {Division of Genetic Therapeutics, Center for Molecular Medicine, Tochigi, Japan.},
	Pages = {1193-9},
	Pubmed = {10918487},
	Title = {Long-term tracking of murine hematopoietic cells transduced with a bicistronic retrovirus containing CD24 and EGFP genes},
	Uuid = {7DEE4D2B-6CE9-4E89-891D-8256222758C6},
	Volume = {7},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3301225}}

@article{Kunz:1991,
	Author = {Kunz, B. A. and Kohalmi, S. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0066-4197},
	Journal = {Annu Rev Genet},
	Keywords = {23 dNTPs-Brdu;Research Support, Non-U.S. Gov't;Mutagenesis;Deoxyribonucleotides;Animals;24 Pubmed search results 2008;23 Technique;review},
	Medline = {92255259},
	Nlm_Id = {0117605},
	Organization = {Department of Microbiology, University of Manitoba, Winnipeg, Canada.},
	Pages = {339-59},
	Pubmed = {1812810},
	Title = {Modulation of mutagenesis by deoxyribonucleotide levels},
	Uuid = {1E8E2935-7CA6-4737-BAF0-82052E057890},
	Volume = {25},
	Year = {1991},
	url = {papers/Kunz_AnnuRevGenet1991.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1146/annurev.ge.25.120191.002011}}

@article{Kuo:2006,
	Abstract = {Neural stem cells are retained in the postnatal subventricular zone (SVZ), a specialized neurogenic niche with unique cytoarchitecture and cell-cell contacts. Although the SVZ stem cells continuously regenerate, how they and the niche respond to local changes is unclear. Here we generated nestin-creER(tm) transgenic mice with inducible Cre recombinase in the SVZ and removed Numb/Numblike, key regulators of embryonic neurogenesis from postnatal SVZ progenitors and ependymal cells. This resulted in severe damage to brain lateral ventricle integrity and identified roles for Numb/Numblike in regulating ependymal wall integrity and SVZ neuroblast survival. Surprisingly, the ventricular damage was eventually repaired: SVZ reconstitution and ventricular wall remodeling were mediated by progenitors that escaped Numb deletion. Our results show a self-repair mechanism in the mammalian brain and may have implications for both niche plasticity in other areas of stem cell biology and the therapeutic use of neural stem cells in neurodegenerative diseases.},
	Author = {Kuo, Chay T. and Mirzadeh, Zaman and Soriano-Navarro, Mario and Rasin, Mladen and Wang, Denan and Shen, Jie and Sestan, Nenad and Garcia-Verdugo, Jose and Alvarez-Buylla, Arturo and Jan, Lily Y. and Jan, Yuh-Nung N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94143, USA.},
	Pages = {1253-64},
	Pii = {S0092-8674(06)01469-3},
	Pubmed = {17174898},
	Title = {Postnatal deletion of Numb/Numblike reveals repair and remodeling capacity in the subventricular neurogenic niche},
	Uuid = {44286076-FE11-407C-AA59-26415F204939},
	Volume = {127},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.10.041}}

@article{Kurant:2008,
	Abstract = {The removal of apoptotic cells by phagocytic neighbors is essential for metazoan development but remains poorly characterized. Here we report the discovery of a Drosophila phagocytosis receptor, Six-microns-under (SIMU), which is expressed in highly phagocytic cell types during development and required for efficient apoptotic cell clearance by glia in the nervous system and by macrophages elsewhere. SIMU is part of a conserved family of proteins that includes CED-1 and Draper (DRPR). Phenotypic analysis reveals that simu acts upstream of drpr in the same pathway and affects the recognition and engulfment of apoptotic cells, while drpr affects their subsequent degradation. SIMU strongly binds to apoptotic cells, presumably through its EMILIN-like domain, but requires no membrane anchoring, suggesting that it can function as a bridging molecule. Our study introduces an important factor in tissue-resident apoptotic clearance and underscores the prominent role of glia as "semiprofessional" phagocytes in the nervous system.},
	Author = {Kurant, Estee and Axelrod, Sofia and Leaman, Dan and Gaul, Ulrike},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {Phagocytosis;Animals;Apoptosis;Sequence Alignment;Cercopithecus aethiops;COS Cells;Green Fluorescent Proteins;research support, non-u.s. gov't;Receptors, Immunologic;Cell Line;Epistasis, Genetic;Neuroglia;Drosophila melanogaster;Neurons;research support, n.i.h., extramural;24 Pubmed search results 2008;Amino Acid Sequence;Central Nervous System;Molecular Sequence Data;Membrane Proteins;Drosophila Proteins},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {3},
	Organization = {Laboratory of Developmental Neurogenetics, Rockefeller University, 1230 York Avenue, New York, NY 10065-6399, USA.},
	Pages = {498-509},
	Pii = {S0092-8674(08)00446-7},
	Pubmed = {18455990},
	Title = {Six-microns-under acts upstream of Draper in the glial phagocytosis of apoptotic neurons},
	Uuid = {7A8A43A3-3D4B-45BE-BF1C-E014C4D77B4B},
	Volume = {133},
	Year = {2008},
	url = {papers/Kurant_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.02.052}}

@article{Kurpius:2007,
	Abstract = {Traumatic CNS injury activates and mobilizes resident parenchymal microglia (MG), which rapidly accumulate near injured neurons where they transform into phagocytes. The mechanisms underlying this rapid 'homing' in situ are unknown. Using time-lapse confocal imaging in acutely excised neonatal hippocampal slices, we show that rapid accumulation of MG near somata of injured pyramidal neurons in the stratum pyramidale (SP) results from directed migration from tissue regions immediately adjacent to (<200 mum from) the SP. Time-lapse sequences also reveal a 'spreading activation wave' wherein MG situated progressively farther from the SP begin to migrate later and exhibit less directional migration toward the SP. Because purines have been implicated in MG activation and chemotaxis, we tested whether ATP/ADP released from injured pyramidal neurons might account for these patterns of MG behavior. Indeed, application of apyrase, which degrades extracellular ATP/ADP, inhibits MG motility and homing to injured neurons in the SP. Moreover, bath application of exogenous ATP/ADP disrupts MG homing by inducing directional migration toward the slice exterior and away from injured neurons. These results indicate that extracellular ATP/ADP is both necessary and sufficient to induce directional migration and rapid homing of neonatal MG to injured neurons in situ. Rapid, ATP/ADP-dependent MG homing may promote clearance of dead and dying cells and help limit secondary damage during the critical first few hours after neuronal injury. (c) 2007 Wiley-Liss, Inc.},
	Author = {Kurpius, Dana and Nolley, Eric P. and Dailey, Michael E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {8806785},
	Number = {8},
	Organization = {Department of Biological Sciences, The University of Iowa, Iowa City, Iowa.},
	Pages = {873-84},
	Pubmed = {17405148},
	Title = {Purines induce directed migration and rapid homing of microglia to injured pyramidal neurons in developing hippocampus},
	Uuid = {B3CABFD1-DF74-40B8-B57C-149FA0AC9C53},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20509}}

@article{Kurre:2001,
	Abstract = {Oncoretroviral vectors require division of target cells for successful transduction. In the case of hematopoietic repopulating cells this can be achieved by cytokine stimulation using growth factor combinations which facilitate gene transfer and maintain engraftment. Interleukin-3 (IL-3) has been widely used in growth factor combinations, although more recent data in the mouse showed reduced engraftment in the presence of IL-3. Here, we used a competitive repopulation assay to study the influence of IL-3 and the early acting cytokines megakaryocyte growth and development factor (MGDF) and Flt3-ligand (Flt3-L) on gene transfer efficiency during ex vivo transduction of hematopoietic repopulating cells. In a direct comparison, baboon CD34-enriched cells were transduced on CH-296 fibronectin fragment in the presence of either IL-6, stem cell factor (SCF), Flt3-L, and MGDF or IL-3, IL-6, and SCF. Animals were followed for up to 55 weeks, and analysis of peripheral blood leukocytes by semiquantitative polymerase chain reaction showed that both cytokine combinations achieved marking of repopulating cells. A trend toward increased gene marking, especially early after transplant (P = 0.06), was seen with the combination of IL-6, SCF, Flt3-L, and MGDF. However, the highest gene marking was achieved when IL-3 was combined with early acting cytokines, suggesting that the difference observed in this study was probably due to the addition of MGDF and Flt3-L and not due to a negative effect of IL-3 on engraftment.},
	Author = {Kurre, P. and Morris, J. and Horn, P. A. and Harkey, M. A. and Andrews, R. G. and Kiem, H. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1525-0016},
	Journal = {Mol Ther},
	Keywords = {Interleukin-3;Fibronectins;Radiation-Protective Agents;Genetic Vectors;Research Support, Non-U.S. Gov't;Gene Therapy;Animals;Flow Cytometry;Research Support, U.S. Gov't, P.H.S.;Transfection;Bone Marrow Transplantation;Blotting, Southern;11 Glia;Papio;Comparative Study;Antigens, CD34;Gene Transfer Techniques;Retroviridae;Colony-Forming Units Assay;Membrane Proteins;Coculture Techniques;Bone Marrow Cells;Interleukin-6;Thrombopoietin;Polymerase Chain Reaction;Recombinant Proteins;Humans;DNA Primers;Stem Cell Factor;Helper Viruses},
	Medline = {21301864},
	Month = {6},
	Nlm_Id = {100890581},
	Number = {6},
	Organization = {Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.},
	Pages = {920-7},
	Pii = {S1525001601903284},
	Pubmed = {11407906},
	Title = {Gene transfer into baboon repopulating cells: A comparison of Flt-3 Ligand and megakaryocyte growth and development factor versus IL-3 during ex vivo transduction},
	Uuid = {98049829-20B4-41BA-A340-DA5B9A32882F},
	Volume = {3},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/mthe.2001.0328}}

@article{Kurt-Jones:2000,
	Abstract = {The innate immune system contributes to the earliest phase of the host defense against foreign organisms and has both soluble and cellular pattern recognition receptors for microbial products. Two important members of this receptor group, CD14 and the Toll-like receptor (TLR) pattern recognition receptors, are essential for the innate immune response to components of Gram-negative and Gram-positive bacteria, mycobacteria, spirochetes and yeast. We now find that these receptors function in an antiviral response as well. The innate immune response to the fusion protein of an important respiratory pathogen of humans, respiratory syncytial virus (RSV), was mediated by TLR4 and CD14. RSV persisted longer in the lungs of infected TLR4-deficient mice compared to normal mice. Thus, a common receptor activation pathway can initiate innate immune responses to both bacterial and viral pathogens.},
	Author = {Kurt-Jones, E. A. and Popova, L. and Kwinn, L. and Haynes, L. M. and Jones, L. P. and Tripp, R. A. and Walsh, E. E. and Freeman, M. W. and Golenbock, D. T. and Anderson, L. J. and Finberg, R. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1529-2908},
	Journal = {Nat Immunol},
	Keywords = {Lung;Viral Fusion Proteins;Animals;In Vitro;Humans;Respiratory Syncytial Virus Infections;Receptors, Cell Surface;Respiratory Syncytial Viruses;11 Glia;Antigens, CD14;Leukocytes, Mononuclear;Research Support, U.S. Gov't, P.H.S.;Membrane Glycoproteins;Mice, Knockout;Antibodies, Monoclonal;Inflammation Mediators;Mice;24 Pubmed search results 2008;Drosophila Proteins;Cytokines},
	Medline = {21170219},
	Month = {11},
	Nlm_Id = {100941354},
	Number = {5},
	Organization = {Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. evelyn.kurt-jones\@umassmed.edu},
	Pages = {398-401},
	Pubmed = {11062499},
	Title = {Pattern recognition receptors TLR4 and CD14 mediate response to respiratory syncytial virus},
	Uuid = {1D32CA69-0890-4509-9390-3FC9450CBD11},
	Volume = {1},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/80833}}

@article{Kusadasi:2000,
	Abstract = {In view of the limited potential for rapid hematological recovery after transplantation of umbilical cord blood cells (UCB) in adults, we have attempted to expand CD34+ selected hemopoietic stem cells (HSC) and progenitors in 2-week cultures of whole graft pools in the presence or absence of serum and stromal layers, and with various cytokine combinations including (1) FL + TPO; (2) FL + TPO plus SCF and/or IL6; or (3) SCF + IL6. Both in the input material and cultured grafts we determined the number of colony-forming cells (CFC), cobblestone area forming cells (CAFC), the NOD/SCID repopulating ability (SRA), and CD34+ CD38- subset by phenotyping. The highest fold-increase obtained for the number of nucleated cells (nc), CD34+, CD34+ CD38 cell numbers and CFC content was, respectively, 102 +/- 76, 24 +/- 19, 190 +/- 202 and 53 +/- 37 for stroma-free and 315 +/- 110, 25 +/- 3, 346 +/- 410 and 53 +/- 43 for stroma-supported cultures. CAFC week type 6 was maximally 11-fold expanded both under stroma-free and stroma-supported conditions. The FBMD-1 stromal cells supported a modest expansion of CD34+ CD38- cells (27 +/- 18-fold) and nc (6 +/- 4-fold), while a loss of CFC and CAFC subsets was observed. The stromal cells synergized with FL + TPO to give the highest expansion of hemopoietic progenitors. Stromal support could be fully replaced by complementing the FL + TPO stimulated cultures with SCF + IL6. FL + TPO were required and sufficient to give a 10- to 20-fold expansion of the ability of CD34+ UCB cells in 2-week cultures to engraft the BM of NOD/SCID mice. Stromal support, or complementation of the medium with SCF + IL6, did not significantly improve the in vivo engraftment potential. If the SRA and CAFC week 6 assays are accepted as tentative estimates of in vivo engrafting stem cells in humans, our findings may assist in the preparation of UCB grafts to meet the requirements for improved repopulation in the clinical setting.},
	Author = {Kusadasi, N. and van Soest, P. L. and Mayen, A. E. and Koevoet, J. L. and Ploemacher, R. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0887-6924},
	Journal = {Leukemia},
	Keywords = {Cell Culture Techniques;Mice, Inbred NOD;Colony-Forming Units Assay;Animals;Coculture Techniques;Humans;Cells, Cultured;Transplantation, Heterologous;Cell Separation;Recombinant Proteins;Mice, SCID;Granulocyte Colony-Stimulating Factor;Antigens, CD34;Specific Pathogen-Free Organisms;Granulocyte-Macrophage Colony-Stimulating Factor;11 Glia;Hematopoietic Stem Cell Transplantation;Radiation Chimera;Thrombopoietin;Hematopoietic Stem Cells;Infant, Newborn;Mice;Membrane Proteins;Stromal Cells;Stem Cell Factor;Cell Division;Fetal Blood},
	Medline = {20518812},
	Month = {11},
	Nlm_Id = {8704895},
	Number = {11},
	Organization = {Institute of Hematology, Erasmus University Rotterdam, The Netherlands.},
	Pages = {1944-53},
	Pubmed = {11069030},
	Title = {Successful short-term ex vivo expansion of NOD/SCID repopulating ability and CAFC week 6 from umbilical cord blood},
	Uuid = {1075DAE8-5AF0-4ABA-9B66-53A1BC7EF035},
	Volume = {14},
	Year = {2000}}

@article{Kuwabara:2004,
	Abstract = {Discovering the molecular mechanisms that regulate neuron-specific gene expression remains a central challenge for CNS research. Here, we report that small, noncoding double-stranded (ds) RNAs play a critical role in mediating neuronal differentiation. The sequence defined by this dsRNA is NRSE/RE1, which is recognized by NRSF/REST, known primarily as a negative transcriptional regulator that restricts neuronal gene expression to neurons. The NRSE dsRNA can trigger gene expression of neuron-specific genes through interaction with NRSF/REST transcriptional machinery, resulting in the transition from neural stem cells with neuron-specific genes silenced by NRSF/REST into cells with neuronal identity that can express neuronal genes. The mechanism of action appears to be mediated through a dsRNA/protein interaction, rather than through siRNA or miRNA. The discovery of small modulatory dsRNAs (smRNAs) extends the important contribution of noncoding RNAs as key regulators of cell behavior at both transcriptional and posttranscriptional levels. 0092-8674 Journal Article},
	Author = {Kuwabara, T. and Hsieh, J. and Nakashima, K. and Taira, K. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Cell},
	Keywords = {02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;C, BB pdf},
	Number = {6},
	Organization = {Laboratory of Genetics, The Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.},
	Pages = {779-93},
	Title = {A small modulatory dsRNA specifies the fate of adult neural stem cells},
	Uuid = {15140BD7-AF81-4229-9C86-94456DD99353},
	Volume = {116},
	Year = {2004},
	url = {papers/Kuwabara_Cell2004.pdf}}

@article{Kwon:2003,
	Abstract = {The colony formation assay is the most commonly used titration method for defining the concentration of replication-incompetent murine leukemia virus-derived retroviral vectors. However, titer varies with target cell type and number, transduction time, and concentration of polycation (e.g., Polybrene). Moreover, because most of the viruses cannot encounter target cells due to Brownian motion, their short half-lives, and the requirement for target cell division for activity, the actual infectious retrovirus concentration in the collected supernatant is higher than the viral titer. Here we correlate the physical viral particle concentration with the infectious virus concentration and colony formation titer with the help of a mathematical model. Ecotropic murine leukemia retrovirus supernatant, collected from the GP+E86/LNCX retroviral vector producer cell line, was concentrated by centrifugation and further purified by a sucrose density gradient. The physical concentration of purified viral vectors was determined by direct particle counting with an electron microscope. The concentrations of fresh and concentrated supernatant were determined by a quantitative reverse transcriptase activity assay. Titration of all supernatants by neomycin-resistant colony formation assay was also performed. There were 767 +/- 517 physical viral particles per infectious CFU in the crude viral supernatant. However, the infectious viral concentration determined by mathematical simulation was 143 viral particles per infectious unit, which is more consistent with the concentration determined by particle counting in purified viral solution. Our results suggest that the mathematical model can be used to extract a more accurate and reliable concentration of infectious retrovirus.},
	Author = {Kwon, Young Jik and Hung, Gene and Anderson, W. French and Peng, Ching-An A. and Yu, Hong},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Transduction, Genetic;Animals;Fluorescent Antibody Technique;Comparative Study;Models, Biological;15 Retrovirus mechanism;23 Technique;RNA-Directed DNA Polymerase;Virion;Genetic Vectors;Virology;Research Support, U.S. Gov't, P.H.S.;Moloney murine leukemia virus;3T3 Cells;Freezing;Mice;24 Pubmed search results 2008;Microscopy, Electron;Research Support, Non-U.S. Gov't},
	Medline = {22605457},
	Month = {5},
	Nlm_Id = {0113724},
	Number = {10},
	Organization = {Department of Chemical Engineering, University of Southern California, Los Angeles, California 90089, USA.},
	Pages = {5712-20},
	Pubmed = {12719564},
	Title = {Determination of infectious retrovirus concentration from colony-forming assay with quantitative analysis},
	Uuid = {612D0AFD-CE49-4325-8FC4-9073E6CAFD0F},
	Volume = {77},
	Year = {2003}}

@article{Kyrkanides:2003,
	Abstract = {The systemic effects of gene therapy have been previously described in a variety of peripheral organs following intravenous administration or intraperitoneal inoculation of viral vectors, as well as in the brain following intracranial administration. However, limited information is available on the ability of viral vectors to cross the blood-brain barrier and infect cells located within the central nervous system (CNS). We employed a VSV-G pseudotyped FIV(lacZ) vector capable of transducing dividing, growth-arrested, as well as post-mitotic cells with the reporter gene lacZ. Adult mice were injected intraperitoneally with FIV(lacZ), and the expression of beta-galactosidase was studied 5 weeks following treatment in the brain, liver, spleen and kidney by X-gal histochemistry and immunocytochemistry. Interestingly, relatively low doses of FIV(lacZ) administered intraperitoneally lead to beta-galactosidase detection in the brain and cerebellum. The identity of these cells was confirmed by double immunofluorescence, and included CD31-, CD3- and CD11b-positive cells. Fluorescent microspheres co-injected with FIV(lacZ) virus were identified within mononuclear cells in the brain parenchyma, suggesting infiltration of peripheral immune cells in the CNS. Cerebellar Purkinje neurons were also transduced in all adult-injected mice. Our observations indicate that relatively low doses of FIV(lacZ) administered intraperitoneally resulted in the transduction of immune cells in the brain, as well as a specific subset of cerebellar neurons.},
	Author = {Kyrkanides, Stephanos and Miller, Jennie H. and Federoff, Howard J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0169-328X},
	Journal = {Brain Res Mol Brain Res},
	Keywords = {Prostaglandin-Endoperoxide Synthase;Purkinje Cells;Transduction, Genetic;beta-Galactosidase;Animals;Immunodeficiency Virus, Feline;Brain;Antigens, Surface;Mice, Inbred C57BL;Chemotaxis, Leukocyte;Male;Leukocytes, Mononuclear;Blood-Brain Barrier;Genetic Vectors;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Lac Operon;Mice;Genes, Reporter;Isoenzymes;Vascular Cell Adhesion Molecule-1;Injections, Intraperitoneal},
	Medline = {22959198},
	Month = {11},
	Nlm_Id = {8908640},
	Number = {1},
	Organization = {Department of Dentistry, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. stephanos\_Kyrkanides\@urmc.rochester.edu},
	Pages = {1-9},
	Pii = {S0169328X03003681},
	Pubmed = {14597224},
	Title = {Systemic FIV vector administration: transduction of CNS immune cells and Purkinje neurons},
	Uuid = {FB425A4C-2D79-432A-BEFE-45392AF5A6FF},
	Volume = {119},
	Year = {2003},
	url = {papers/Kyrkanides_BrainResMolBrainRes2003.pdf}}

@article{LaMantia:1993,
	Abstract = {We have used an in vitro assay to identify sources of retinoic acid (RA) and transgenic mice to identify target domains in the developing forebrain. RA participates in a sequence of events that leads to the establishment of the olfactory pathway. First, the lateral cranial mesoderm activates an RA-inducible transgene in neuroepithelial cells in the olfactory placode and the ventrolateral forebrain. Then, neurons and neurites begin to differentiate in these two regions. Finally, olfactory axons grow specifically into the ventrolateral forebrain and subsequently are limited to the olfactory bulb rudiment. The coordination of these events, perhaps by common signals, implies that retinoid induction and retinoid-activated region-specific transcriptional regulation may help to define a forebrain subdivision and the peripheral neurons that provide its primary innervation. eng Journal Article},
	Author = {LaMantia, A. S. and Colbert, M. C. and Linney, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Journal = {Neuron},
	Keywords = {Olfactory Bulb/cytology/*embryology;Cell Differentiation/drug effects;Prosencephalon/cytology/*embryology;Tretinoin/*pharmacology;Neurons/cytology/drug effects/*physiology;Female;Animal;Mice, Transgenic;C abstr;Axons/physiology/ultrastructure;Male;Embryo;Neurites/drug effects/physiology/ultrastructure;Mice, Inbred Strains;Support, Non-U.S. Gov't;Olfactory Pathways/cytology/*embryology;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice},
	Number = {6},
	Organization = {Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710.},
	Pages = {1035-48.},
	Title = {Retinoic acid induction and regional differentiation prefigure olfactory pathway formation in the mammalian forebrain},
	Uuid = {3F7DC4D4-175A-4C80-A5B9-014E354A8FC8},
	Volume = {10},
	Year = {1993}}

@article{Laabs:2005,
	Abstract = {Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands. During development CSPGs pattern cell migration, axon growth pathways and axon terminations. Later in development and in adulthood CSPGs associate with some classes of neuron and control plasticity. After damage to the nervous system, CSPGs are the major axon growth inhibitory component of the glial scar tissue that blocks successful regeneration. CSPGs have a variety of roles in the nervous system, including binding to molecules and blocking their action, presenting molecules to cells and axons, localising active molecules to particular sites and presenting growth factors to their receptors.},
	Author = {Laabs, Tracy and Carulli, Daniela and Geller, Herbert M. and Fawcett, James W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Cambridge University Centre for Brain Repair, Robinson Way, Cambridge CB2 2PY, UK.},
	Pages = {116-20},
	Pii = {S0959-4388(05)00015-2},
	Pubmed = {15721753},
	Title = {Chondroitin sulfate proteoglycans in neural development and regeneration},
	Uuid = {584927E9-3371-4734-9096-B952D536BB3C},
	Volume = {15},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.01.014}}

@article{Labonia:1988,
	Abstract = {Bovine heart cytochrome c oxidase was reconstituted in phospholipid vesicles, and the effect of different non-esterified fatty acids (NEFA) was studied on its proton pump and on the proton permeability of the vesicles. Neither parameter appeared to be affected by concentrations of NEFA known to uncouple oxidative phosphorylation (10 microM). Also the permeability for K+ was not affected by them. The fatty acids caused an increase in the rate of electron transfer in the absence, but not in the presence, of uncoupler and/or valinomycin [diminution of the respiratory-control index (RCI)]. The RCI of 8.7-7.5 was decreased to about 4.5 in the presence of 0.27-10 microM-NEFA. Oleic acid was not effective at the above concentrations. Subunit III-depleted enzyme preparations gave vesicles with an RCI of about 5.5, which was decreased to 4.5 in the presence of NEFA. With both native and subunit III-depleted oxidase the RCI was never decreased to the value of 1 by NEFA, as happens with classical protonophores.},
	Author = {Labonia, N. and M{\"u}ller, M. and Azzi, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0264-6021},
	Journal = {Biochem J},
	Keywords = {Animals;Proton-Translocating ATPases;Biological Transport;Liposomes;Fatty Acids, Nonesterified;Palmitic Acids;11 Glia;Oxidation-Reduction;Cell Membrane Permeability;Potassium;Electron Transport Complex IV;Membrane Potentials;Potentiometry;Oxygen Consumption;24 Pubmed search results 2008;Palmitic Acid;Protons;Research Support, Non-U.S. Gov't},
	Medline = {89025655},
	Month = {8},
	Nlm_Id = {2984726R},
	Number = {1},
	Organization = {Institut f{\"u}r Biochemie und Molekularbiologie der Universit{\"a}t Bern, Switzerland.},
	Pages = {139-45},
	Pubmed = {2902846},
	Title = {The effect of non-esterified fatty acids on the proton-pumping cytochrome c oxidase reconstituted into liposomes},
	Uuid = {34F581FA-3395-4AD9-B2E0-63EFE0240A16},
	Volume = {254},
	Year = {1988}}

@article{Ladeby:2005,
	Abstract = {Reactive microgliosis is a highly characteristic response to neural injury and disease, which may influence neurodegenerative processes and neural plasticity. We have investigated the origin and characteristics of reactive microglia in the acute phase of their activation in the dentate gyrus following transection of the entorhino-dentate perforant path projection. To investigate the possible link between microglia and hematopoietic precursors, we analyzed the expression of the stem cell marker CD34 by lesion-reactive microglia in conjunction with the proliferation marker bromodeoxyuridine (BrdU) and the use of radiation bone marrow (BM) chimeric mice. We found that CD34 is upregulated on early-activated resident microglia, rather than by infiltrating bone marrow-derived cells. The number of CD34(+) microglia peaked at day 3 when 67\%of the resident CD11b/Mac-1(+) microglia co-expressed CD34, and all CD34(+) cells co-expressed Mac-1, and decreased sharply toward day 5, unlike Mac-1, which was maximally expressed at day 5. Approximately 80\%of the CD34(+) cells in the denervated dentate gyrus had incorporated BrdU into their nuclei at day 3. We also showed that CD34 is upregulated on early-activated microglia in the facial motor nucleus following peripheral axotomy. The results suggest lesion-reactive microglia to consist of functionally distinct subpopulations of cells; a major population of activated resident CD34(+)Mac-1(+) microglia with a high capacity for self-renewal, and a subpopulation of CD34(-)Mac-1(+) microglia which has a mixed extrinsic and intrinsic origin and whose proliferative capacity is unknown. (c) 2005 Wiley-Liss, Inc.},
	Author = {Ladeby, and Wirenfeldt, and Dalmau, and Gregersen, and Garc{\'\i}a-Ovejero, and Babcock, and Owens, and Finsen,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {8806785},
	Organization = {Medical Biotechnology Center, University of Southern Denmark, Denmark.},
	Pubmed = {15657941},
	Title = {Proliferating resident microglia express the stem cell antigen CD34 in response to acute neural injury},
	Uuid = {3CFE1A34-7A2A-4ABF-8A29-51B806C1AB1F},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20159}}

@article{Laird:2005,
	Abstract = {Stem cells are highly conserved biological units of development and regeneration. Here we formally demonstrate that stem cell lineages are also legitimate units of natural selection. In a colonial ascidian, Botryllus schlosseri, vascular fusion between genetically distinct individuals results in cellular parasitism of somatic tissues, gametes, or both. We show that genetic hierarchies of somatic and gametic parasitism following fusion can be replicated by transplanting cells between colonies. We prospectively isolate a population of multipotent, self-renewing stem cells that retain their competitive phenotype upon transplantation. Their single-cell contribution to either somatic or germline fates, but not to both, is consistent with separate lineages of somatic and germline stem cells or pluripotent stem cells that differentiate according to the niche in which they land. Since fusion is restricted to individuals that share a fusion/histocompatibility allele, these data suggest that histocompatibility genes in Botryllus evolved to protect the body from parasitic stem cells usurping asexual or sexual inheritance.},
	Author = {Laird, Diana J. and De Tomaso, Anthony W. and Weissman, Irving L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {22 Stem cells;24 Pubmed search results 2008;23 Technique},
	Month = {12},
	Nlm_Id = {0413066},
	Number = {7},
	Organization = {Department of Biological Sciences, Departments of Pathology and Developmental Biology, Stanford University Medical Center, Stanford, CA 94305, USA. diana\@stanfordalumni.org},
	Pages = {1351-60},
	Pii = {S0092-8674(05)01166-9},
	Pubmed = {16377573},
	Title = {Stem cells are units of natural selection in a colonial ascidian},
	Uuid = {5BCA6BBD-B597-4A9E-BB59-293C35369B23},
	Volume = {123},
	Year = {2005},
	url = {papers/Laird_Cell2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.10.026}}

@article{Lalancette-Hebert:2007,
	Abstract = {Here we report in vivo evidence of a neuroprotective role of proliferating microglial cells in cerebral ischemia. Using transgenic mice expressing a mutant thymidine kinase form of herpes simplex virus driven by myeloid-specific CD11b promoter and ganciclovir treatment as a tool, we selectively ablated proliferating (Mac-2 positive) microglia after transient middle cerebral artery occlusion. The series of experiments using green fluorescent protein-chimeric mice demonstrated that within the first 72 h after ischemic injury, the Mac-2 marker [unlike Iba1 (ionized calcium-binding adapter molecule 1)] was preferentially expressed by the resident microglia. Selective ablation of proliferating resident microglia was associated with a marked alteration in the temporal dynamics of proinflammatory cytokine expression, a significant increase in the size of infarction associated with a 2.7-fold increase in the number of apoptotic cells, predominantly neurons, and a 1.8-fold decrease in the levels of IGF-1. A double-immunofluorescence analysis revealed a approximately 100\%colocalization between IGF-1 positive cells and Mac-2, a marker of activated/proliferating resident microglia. Conversely, stimulation of microglial proliferation after cerebral ischemia by M-CSF (macrophage colony stimulating factor) resulted in a 1.9-fold increase in IGF-1 levels and a significant increase of Mac2+ cells. Our findings suggest that a postischemic proliferation of the resident microglial cells may serve as an important modulator of a brain inflammatory response. More importantly, our results revealed a marked neuroprotective potential of proliferating microglia serving as an endogenous pool of neurotrophic molecules such as IGF-1, which may open new therapeutic avenues in the treatment of stroke and other neurological disorders.},
	Author = {Lalancette-H{\'e}bert, M{\'e}lanie and Gowing, Genevi\`{e}ve and Simard, Alain and Weng, Yuan Cheng and Kriz, Jasna},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't;11 Glia;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {10},
	Organization = {Department of Anatomy and Physiology, Laval University, Centre de Recherche du Centre Hospitalier de l'Universit{\'e} Laval, Quebec, Canada G1V 4G2.},
	Pages = {2596-605},
	Pii = {27/10/2596},
	Pubmed = {17344397},
	Title = {Selective ablation of proliferating microglial cells exacerbates ischemic injury in the brain},
	Uuid = {AA29F0A7-7EE2-4A5D-B0BB-62F49636766E},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5360-06.2007}}

@article{Lam:2001,
	Abstract = {BACKGROUND: Ex vivo expansion of cord blood (CB) hematopoietic stem and progenitor cells increases cell dose and may reduce the severity and duration of neutropenia and thrombocytopenia after transplantation. This study's purpose was to establish a clinically applicable culture system by investigating the use of cytokines, serum-free media, and autologous plasma for the expansion of CB cells and the engraftment of expanded product in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. STUDY DESIGN AND METHODS: Enriched CB CD34+ cells were cultured in four media (Iscove's modified Dulbecco's medium with FCS, Gibco; X-Vivo-10, BioWhittaker; QBSF-60, Quality Biological; and StemSpan SFEM, Stem Cell Technologies) with four cytokine combinations (thrombopoietin [TPO], SCF, Flt-3 ligand [FL] with and without G-CSF, and/or IL-6). The effect of autologous CB plasma was also investigated. The read-out measures were evaluated on Days 8 and 12. After expansion at the optimized condition, cultured cells were transplanted into sublethally irradiated NOD/SCID mice. The engraftment of human CD45+ cells and subsets in the bone marrow, spleen, and peripheral blood was determined. RESULTS: QBSF-60 or StemSpan SFEM supported high yields of early progenitors (CD34+ cells, <or= 64.8-fold; CD34+CD38- cells, 330-fold; CFU-granulocyte erythroid macrophage megakaryocyte [GEMM], 248-fold) and CFUs of the myeloid (CFU-GM, 407-fold) and erythroid (BFU/CFU-E, 144-fold) lineages. The expansion of the megakaryocytic lineage was consistently higher in X-Vivo-10 (CFU-megakaryocyte, 684-fold). Autologous plasma promoted colony formation but reduced CD34+ cells and CFU-GEMM. The addition of G-CSF or IL-6 improved cell yields; G-CSF was more effective for committed progenitors. Expansion products from cultures in QBSF-60 with the cytokines engrafted and differentiated into the myeloid and lymphoid lineages in NOD/SCID mice. CONCLUSION: The data supported the strategy of expansion. The optimized condition may be applicable to clinical expansion for the abrogation or reduction of posttransplant cytopenia.},
	Author = {Lam, A. C. and Li, K. and Zhang, X. B. and Li, C. K. and Fok, T. F. and Chang, A. M. and James, A. E. and Tsang, K. S. and Yuen, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0041-1132},
	Journal = {Transfusion},
	Keywords = {Cell Culture Techniques;Mice, Inbred NOD;Animals;Humans;Transplantation, Heterologous;Comparative Study;Mice, SCID;Antigens, CD34;11 Glia;Hematopoietic Stem Cell Transplantation;Cell Lineage;Fetal Blood;Hematopoietic Stem Cells;Mice;Graft Survival;Culture Media;Growth Substances;Research Support, Non-U.S. Gov't},
	Medline = {21636788},
	Month = {12},
	Nlm_Id = {0417360},
	Number = {12},
	Organization = {Department of Paediatrics, Laboratory Animal Services Centre, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong.},
	Pages = {1567-76},
	Pubmed = {11778074},
	Title = {Preclinical ex vivo expansion of cord blood hematopoietic stem and progenitor cells: duration of culture; the media, serum supplements, and growth factors used; and engraftment in NOD/SCID mice},
	Uuid = {7CE819E3-630F-40B0-A671-32EC8BED262C},
	Volume = {41},
	Year = {2001}}

@article{Lamparello:2007,
	Abstract = {Focal cortical dysplasia type IIB with Ballon cells is a developmental malformation of the cerebral cortex highly associated with epilepsy. As a strategy to define the embryonic origin and neurochemical phenotype of cells in this disease, we probed specimens (n = 10) resected during epilepsy surgery with a panel of 13 antibodies recognizing proteins associated with (i) specific progenitor cell types including brain lipid binding protein (BLBP), collapsin response mediator protein 4 (CRMP4), Dlx1, Dlx2, GFAPdelta, MASH1, Otx1, Pax6, vimentin and phosphorylated vimentin and (ii) excitatory or inhibitory neurochemical phenotypes such as the vesicular glutamate transporters-1 and 2 (VGLUT-1, VGLUT-2), or the vesicular GABA transporter (VGAT). Balloon cells and large dysplastic neurons in all specimens expressed Otx1, phospho-vimentin, Pax6 and BLBP, proteins normally expressed by cells in the embryonic ventricular zone. A subpopulation of balloon cells expressed MASH-1 also expressed in the ventricular zone. Most balloon cells and dysplastic neurons were VGLUT2 immunoreactive, whereas none expressed Dlx1 or Dlx2, markers for inhibitory cells derived from the medial ganglionic eminence and few expressed VGAT, found in GABAergic interneurons. Otx1 mRNA expression and Dlx1 mRNA absence was confirmed by single cell RT-PCR. A subpopulation of balloon cells was labelled with CRMP4 and GFAPdelta, markers specific for newly generated cells derived from the adult subventricular zone. Detection of Otx1, phospho-vimentin, Pax6 and BLBP expression but absence of Dlx1/Dlx2 expression suggests that balloon cells and dysplastic neurons derive from radial glial cells in the telencephalic ventricular zone and not the medial ganglionic eminence. VGLUT expression argues that dysplastic neurons may be glutamatergic. CRMP-4 and GFAPdelta expression suggests that new cells may arrive in focal cortical dysplasia, perhaps deriving in part from the subventricular zone. These findings provide a developmental lineage model in which balloon cells and dysplastic neurons are derived from radial glial progenitor cells.},
	Author = {Lamparello, Phillip and Baybis, Marianna and Pollard, John and Hol, Elly M. and Eisenstat, David D. and Aronica, Eleonora and Crino, Peter B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1460-2156},
	Journal = {Brain},
	Keywords = {Cell Differentiation;Child, Preschool;Humans;Age of Onset;Female;Epilepsy;Infant;Cell Count;21 Dysplasia-heterotopia;RNA, Messenger;research support, non-u.s. gov't;Male;Vesicular Glutamate Transport Proteins;Vesicular Inhibitory Amino Acid Transport Proteins;Cell Lineage;Cerebral Cortex;21 Neurophysiology;Neurons;Infant, Newborn;24 Pubmed search results 2008;Stem Cells;Gene Expression;Nerve Tissue Proteins},
	Month = {9},
	Nlm_Id = {0372537},
	Number = {Pt 9},
	Organization = {PENN Epilepsy Center and Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, PA, USA.},
	Pages = {2267-76},
	Pii = {130/9/2267},
	Pubmed = {17711980},
	Title = {Developmental lineage of cell types in cortical dysplasia with balloon cells},
	Uuid = {23547B95-3AA2-437C-B617-B2B079A2C561},
	Volume = {130},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/brain/awm175}}

@article{Landen:2002,
	Abstract = {Cellular microtubules, polymers of tubulin, alternate relentlessly between phases of growth and shortening. We now show that noscapine, a tubulin-binding agent, increases the time that cellular microtubules spend idle in a paused state. As a result, most mammalian cell types observed arrest in mitosis in the presence of noscapine. We demonstrate that noscapine-treated murine melanoma B16LS9 cells do not arrest in mitosis but rather become polyploid followed by cell death, whereas primary melanocytes reversibly arrest in mitosis and resume a normal cell cycle after noscapine removal. Furthermore, in a syngeneic murine model of established s.c. melanoma, noscapine treatment resulted in an 85\%inhibition of tumor volume on day 17 when delivered by gavage compared with untreated animals (P <or= 0.01), without evidence of toxicity to the spleen, liver, duodenum, bone marrow, or peripheral blood. This inhibition was greater than that seen in vivo by paclitaxel (Taxol) alone and similar to the inhibition of tumor volume observed when noscapine was combined with paclitaxel. Importantly, noscapine also demonstrated the ability to significantly inhibit melanoma progression by 83\%on day 18 when delivered in drinking water (P <or= 0.01) and conferred a significant survival advantage (P <or= 0.01). Our results demonstrate that p.o.-administered noscapine significantly inhibits the progression of melanoma cells through alterations in microtubule dynamics, with no detected toxicity to the host. Consequently, noscapine could be a valuable chemotherapeutic agent, alone or in combination, for the treatment of advanced melanoma. 0008-5472 Journal Article},
	Author = {Landen, J. W. and Lang, R. and McMahon, S. J. and Rusan, N. M. and Yvon, A. M. and Adams, A. W. and Sorcinelli, M. D. and Campbell, R. and Bonaccorsi, P. and Ansel, J. C. and Archer, D. R. and Wadsworth, P. and Armstrong, C. A. and Joshi, H. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Cancer Res},
	Keywords = {Melanoma, Experimental/*drug therapy/metabolism/pathology;Administration, Oral;Cell Division/drug effects;EE, T abstr;Noscapine/*pharmacology/toxicity;Antineoplastic Agents/*pharmacology/toxicity;Female;08 Aberrant cell cycle;Mice, Inbred C57BL;Support, U.S. Gov't, P.H.S.;Microtubules/*drug effects/metabolism;Animals;Support, Non-U.S. Gov't;Disease Progression;Mice},
	Number = {14},
	Organization = {Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {4109-14},
	Pubmed = {12124349},
	Title = {Noscapine alters microtubule dynamics in living cells and inhibits the progression of melanoma},
	Uuid = {F7E9426A-880A-4CB4-B522-851EA8E04F8F},
	Volume = {62},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12124349}}

@article{Landis:1994,
	Author = {Landis, D. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0147-006X},
	Journal = {Annu Rev Neurosci},
	Keywords = {research support, u.s. gov't, p.h.s. ;Homeostasis;research support, non-u.s. gov't ;Astrocytes;Endothelium;14 Immune;Cerebrovascular Disorders;Animals;Humans;24 Pubmed search results 2008;review;Brain Injuries},
	Nlm_Id = {7804039},
	Organization = {Department of Neurology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.},
	Pages = {133-51},
	Pubmed = {8210172},
	Title = {The early reactions of non-neuronal cells to brain injury},
	Uuid = {3CB014A7-CF95-4E5C-9C9F-DBE96A3DEEB4},
	Volume = {17},
	Year = {1994},
	url = {papers/Landis_AnnuRevNeurosci1994.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1146/annurev.ne.17.030194.001025}}

@article{Lane:1996,
	Abstract = {During peak viremia and initial antibody response, rhesus macaques infected with pathogenic and nonpathogenic isolates of SIV show distinct differences in viral load and tissue distribution. Animals infected with pathogenic isolates of SIV invariably have virus in the CSF and brain parenchyma by two weeks postinoculation, whereas animals infected with nonpathogenic isolates do not. Mechanisms underlying neuroinvasion by SIV and HIV are unknown, but recruitment of latently infected mononuclear cells from the peripheral circulation (Trojan horse theory) is frequently proposed. Circulating monocytes, from which perivascular macrophage/microglia are derived, are a likely vehicle for cell-associated transport of virus across the blood-brain barrier. This transport and the kinetics of perivascular macrophage/microglial turnover in the CNS likely depend on endothelial and leukocyte adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), which has previously been shown to be upregulated on cerebrovascular endothelium in SIV encephalitis. To investigate the role of peripheral monocyte recruitment into the perivascular macrophage/microglial cell pool at the time of initial viral neuroinvasion, we examined the temporal relationships among perivascular macrophage/microglia density, endothelial VCAM-1 expression and localization of viral nucleic acid in the CNS of macaques acutely infected with pathogenic and nonpathogenic molecular clones of SIV. The concentration of CSF quinolinic acid, a marker of intrathecal immune and macrophage activation, was examined concurrently. We found that significant increases in the density of perivascular macrophages/microglia coincided with viral neuroinvasion and marked elevations in CSF quinolinic acid. Furthermore, combined in situ hybridization and immunohistochemistry demonstrated that infected perivascular cells were macrophages/microglia. These findings provide evidence suggesting that neuroinvasion occurs through an influx of infected monocytes which take up residence in the CNS as perivascular macrophages/microglia. VCAM-1 expression, however, was not clearly correlated with these events, thus its contribution to initial viral neuroinvasion is unclear.},
	Author = {Lane, J. H. and Sasseville, V. G. and Smith, M. O. and Vogel, P. and Pauley, D. R. and Heyes, M. P. and Lackner, A. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {1355-0284},
	Journal = {J Neurovirol},
	Keywords = {Animals;Central Nervous System Diseases;Macrophages;Image Processing, Computer-Assisted;SIV;Brain;Microglia;Lymphocyte Activation;Cerebrovascular Circulation;11 Glia;Male;Leukocyte Count;In Situ Hybridization;Macaca mulatta;Research Support, U.S. Gov't, P.H.S.;Capillaries;Quinolinic Acid;Simian Acquired Immunodeficiency Syndrome;DNA, Viral;Vascular Cell Adhesion Molecule-1;Immunohistochemistry},
	Medline = {97127674},
	Month = {12},
	Nlm_Id = {9508123},
	Number = {6},
	Organization = {New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772, USA.},
	Pages = {423-32},
	Pubmed = {8972425},
	Title = {Neuroinvasion by simian immunodeficiency virus coincides with increased numbers of perivascular macrophages/microglia and intrathecal immune activation},
	Uuid = {60334672-4B2F-4844-A98C-55E62BD8C895},
	Volume = {2},
	Year = {1996}}

@article{Lang:1993,
	Abstract = {To identify and characterize tissue remodeling processes mediated by macrophages, we have generated transgenic mice in which diphtheria toxin is expressed from a macrophage-specific transgene. Expression of the transgene disrupts subsets of mature macrophages in both the eye and the peritoneal cavity and results in the persistence of two normally transient ocular tissues, the hyaloid vasculature and the pupillary membrane. Furthermore, the cells comprising the pupillary membrane appear alive up to 14 days after the structure is normally remodeled, suggesting that the macrophage actively elicits target cell death. Thus, these transgenic mice provide direct evidence for the active involvement of macrophages in developmentally programmed tissue remodeling and identify the hyaloid vessels and the pupillary membrane in the eye as targets of macrophage-mediated remodeling.},
	Author = {Lang, R. A. and Bishop, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Animals;Diphtheria Toxin;Base Sequence;Aging;Macrophages;Humans;Phenotype;Cells, Cultured;Open Reading Frames;Restriction Mapping;Mice, Transgenic;RNA, Messenger;11 Glia;Granulocyte-Macrophage Colony-Stimulating Factor;Eye;Protein Biosynthesis;Mice;Polymerase Chain Reaction;Oligodeoxyribonucleotides;Molecular Sequence Data;Chloramphenicol O-Acetyltransferase;Cell Death;Research Support, Non-U.S. Gov't},
	Medline = {93351226},
	Month = {8},
	Nlm_Id = {0413066},
	Number = {3},
	Organization = {G. W. Hooper Foundation, University of California, San Francisco 94143-0552.},
	Pages = {453-62},
	Pii = {0092-8674(93)80047-I},
	Pubmed = {8348612},
	Title = {Macrophages are required for cell death and tissue remodeling in the developing mouse eye},
	Uuid = {CB6869B9-EE28-11DA-8605-000D9346EC2A},
	Volume = {74},
	Year = {1993}}

@article{Langenfeld:1997,
	Abstract = {The retinoids are reported to reduce incidence of second primary aerodigestive cancers. Mechanisms for this chemoprevention are previously linked to all-trans retinoic acid (RA) signaling growth inhibition at G1 in carcinogen-exposed immortalized human bronchial epithelial cells. This study investigated how RA suppresses human bronchial epithelial cell growth at the G1-S cell cycle transition. RA signaled growth suppression of human bronchial epithelial cells and a decline in cyclin D1 protein but not mRNA expression. Exogenous cyclin D1 protein also declined after RA treatment of transfected, immortalized human bronchial epithelial cells, suggesting that posttranslational mechanisms were active in this regulation of cyclin D1 expression. Findings were extended by showing treatment with ubiquitin-dependent proteasome inhibitors: calpain inhibitor I and lactacystin each prevented this decreased cyclin D1 protein expression, despite RA treatment. Treatment with the cysteine proteinase inhibitor, E-64, did not prevent this cyclin D1 decline. High molecular weight cyclin D1 protein species appeared after proteasome inhibitor treatments, suggesting that ubiquitinated species were present. To learn whether RA directly promoted degradation of cyclin D1 protein, studies using human bronchial epithelial cell protein extracts and in vitro-translated cyclin D1 were performed. In vitro-translated cyclin D1 degraded more rapidly when incubated with extracts from RA treated vs. untreated cells. Notably, this RA-signaled cyclin D1 proteolysis depended on the C-terminal PEST sequence, a region rich in proline (P), glutamate (E), serine (S), and threonine (T). Taken together, these data highlight RA-induced cyclin D1 proteolysis as a mechanism signaling growth inhibition at G1 active in the prevention of human bronchial epithelial cell transformation.},
	Author = {Langenfeld, J. and Kiyokawa, H. and Sekula, D. and Boyle, J. and Dmitrovsky, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Bronchi;Cell Transformation, Neoplastic;Research Support, Non-U.S. Gov't;Tretinoin;Cyclin D1;Gene Expression Regulation;Cell Line;Research Support, U.S. Gov't, P.H.S.;Epithelial Cells;Cysteine Endopeptidases;Multienzyme Complexes;Cell Cycle;Protein Processing, Post-Translational;Proteasome Endopeptidase Complex;Humans;Signal Transduction;24 Pubmed search results 2008},
	Medline = {98004525},
	Month = {10},
	Nlm_Id = {7505876},
	Number = {22},
	Organization = {Laboratory of Molecular Medicine, Department of Medicine, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.},
	Pages = {12070-4},
	Pubmed = {9342364},
	Title = {Posttranslational regulation of cyclin D1 by retinoic acid: a chemoprevention mechanism},
	Uuid = {F555E70E-555D-4A2B-84AE-DD8AD44D30C8},
	Volume = {94},
	Year = {1997}}

@article{Laplagne:2006,
	Abstract = {The dentate gyrus of the hippocampus contains neural progenitor cells (NPCs) that generate neurons throughout life. Developing neurons of the adult hippocampus have been described in depth. However, little is known about their functional properties as they become fully mature dentate granule cells (DGCs). To compare mature DGCs generated during development and adulthood, NPCs were labeled at both time points using retroviruses expressing different fluorescent proteins. Sequential electrophysiological recordings from neighboring neurons of different ages were carried out to quantitatively study their major synaptic inputs: excitatory projections from the entorhinal cortex and inhibitory afferents from local interneurons. Our results show that DGCs generated in the developing and adult hippocampus display a remarkably similar afferent connectivity with regard to both glutamate and GABA, the major neurotransmitters. We also demonstrate that adult-born neurons can fire action potentials in response to an excitatory drive, exhibiting a firing behavior comparable to that of neurons generated during development. We propose that neurons born in the developing and adult hippocampus constitute a functionally homogeneous neuronal population. These observations are critical to understanding the role of adult neurogenesis in hippocampal function.},
	Author = {Laplagne, and Esp{\'o}sito, and Piatti, and Morgenstern, and Zhao, and van Praag, and Gage, and Schinder,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1545-7885},
	Journal = {PLoS Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {101183755},
	Number = {12},
	Pages = {e409},
	Pii = {06-PLBI-RA-0577R3},
	Pubmed = {17121455},
	Title = {Functional Convergence of Neurons Generated in the Developing and Adult Hippocampus},
	Uuid = {B2306CB0-C956-4778-B97F-97290F88EA1B},
	Volume = {4},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0040409}}

@article{Larsson:1997,
	Abstract = {ERV3 (HERV-R) is a complete, single copy human endogenous retrovirus located on the long arm of chromosome 7. The open reading frame in its envelope gene has been conserved during evolution but the gag and pol genes contain in-frame termination codons. To find a suitable experimental model system for analysis of the functions of the ERV3 genome, an extensive screening study of different normal and neoplastic human tissues was performed. Most tissues express low levels of the ERV3 env mRNA although high expression levels are observed in placenta, sebaceous glands, adrenals, testis, bronchial, epithelium and the monocytic cell line U-937. In U-937 cells the ERV3 env expression varied in a manner related to the differentiation status of the cells; being highest in the terminally differentiated non proliferating cells. U-937 cells can be induced to differentiate from the monoblastic to the mature monocyte/macrophage stage upon stimulation by several substances such as phorbolesters (TPA), Vitamin D3, Retinoic Acid (RA) and combinations of some cytokines. We conclude that the ERV3 locus is expressed in a tissue and differentiation specific way and that the U-937 cell line is a suitable model system to further analyze the proposed functions of ERVs such as immunomodulation, cell fusion and protection against exogenous retroviral infections.},
	Author = {Larsson, E. and Venables, P. and Andersson, A. C. and Fan, W. and Rigby, S. and Botling, J. and Oberg, F. and Cohen, M. and Nilsson, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0887-6924},
	Journal = {Leukemia},
	Keywords = {Research Support, Non-U.S. Gov't;Gene Products, env;Cell Differentiation;Gene Expression Regulation, Viral;Pregnancy;Monocytes;Humans;Female;15 Retrovirus mechanism;Neoplasms;Reference Values;Retroviridae;Cholecalciferol;Genes, env;Male;Cell Line;Tetradecanoylphorbol Acetate;Organ Specificity;24 Pubmed search results 2008;15 ERVs retroelements;Tretinoin;Cytokines},
	Medline = {97353065},
	Month = {4},
	Nlm_Id = {8704895},
	Organization = {Department of Pathology, Uppsala University Hospital, Sweden.},
	Pages = {142-4},
	Pubmed = {9209323},
	Title = {Tissue and differentiation specific expression on the endogenous retrovirus ERV3 (HERV-R) in normal human tissues and during induced monocytic differentiation in the U-937 cell line},
	Uuid = {833A1C11-4326-11DB-A5D2-000D9346EC2A},
	Volume = {11 Suppl 3},
	Year = {1997}}

@article{Larsson:1994,
	Abstract = {ERV3 (HERV-R) is a complete human endogenous retrovirus located on the long arm of chromosome 7. It is expressed in several human tissues as LTR env spliced transcripts (9 and 3.5 kb). The highest level of expression is to be found in placenta and virus expression is down-regulated in choriocarcinoma cell lines. By means of in situ hybridization, the expression of ERV3 env was studied in selected human reproductive and embryonic tissues. It is concluded that (a) ERV3 env is expressed in syncytiotrophoblasts not only in the placenta but also in hydatidiform moles and choriocarcinomas (irrespective of origin) (b) ERV3 expression in placenta correlates to cell fusion but probably not to the fertilization process itself (c) ERV3 env is highly expressed in certain cells in spermatogenesis but not in the Sertoli or Leydig cells, and finally (d) ERV3 env is expressed in certain embryonic tissues such as the adrenal gland and nervous tissues.},
	Author = {Larsson, E. and Andersson, A. C. and Nilsson, B. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0300-9734},
	Journal = {Ups J Med Sci},
	Keywords = {15 ERVs retroelements;Embryo;Uterine Neoplasms;Research Support, Non-U.S. Gov't;Female;Gene Products, env;Retroviridae;Placenta;Testis;Hydatidiform Mole;Pregnancy;Choriocarcinoma;15 Retrovirus mechanism;Male;Humans;24 Pubmed search results 2008;Genes, env},
	Medline = {95232827},
	Nlm_Id = {0332203},
	Number = {2},
	Organization = {Department of Pathology, Uppsala University Hospital, Sweden.},
	Pages = {113-20},
	Pubmed = {7716822},
	Title = {Expression of an endogenous retrovirus (ERV3 HERV-R) in human reproductive and embryonic tissues--evidence for a function for envelope gene products},
	Uuid = {833A255E-4326-11DB-A5D2-000D9346EC2A},
	Volume = {99},
	Year = {1994}}

@article{Lascola:1996,
	Abstract = {Astrocytes can change shape dramatically in response to increased physiological and pathological demands, yet the functional consequences of morphological change are unknown. We report the expression of Cl- currents after manipulations that alter astrocyte morphology. Whole-cell Cl- currents were elicited after (1) rounding up cells by brief exposure to trypsin; (2) converting cells from a flat polygonal to a process-bearing (stellate) morphology by exposure to serum-free Ringer's solution; and (3) swelling cells by exposure to hypo-osmotic solution. Zero-current potentials approximated the Nernst for Cl-, and rectification usually followed that predicted by the constant-field equation. We observed heterogeneity in the activation and inactivation kinetics, as well as in the relative degree of outward versus inward rectification. Cl- conductances were inhibited by 4, 4-diisothiocyanostilbene-2,2'-disulfonic acid (200 microM) and by Zn2+ (1 mM). Whole-cell Cl- currents were not expressed in cells without structural change. We investigated whether changes in cytoskeletal actin accompanying changes in astrocytic morphology play a role in the induction of shape-dependent Cl- currents. Cytochalasins, which disrupt actin polymers by enhancing actin-ATP hydrolysis, elicited whole-cell Cl- conductances in flat, polygonal astrocytes. In stellate cells, elevated intracellular Ca2+ (2 microM), which can depolymerize actin, enhanced Cl- currents, and high intracellular ATP (5 mM), required for repolymerization, reduced Cl- currents. Modulation of Cl- current by Ca2+ and ATP was blocked by concurrent whole-cell dialysis with phalloidin and DNase, respectively. Phalloidin stabilizes actin polymers and DNase inhibits actin polymerization. Dialysis with phalloidin also prevented hypo-osmotically activated Cl- currents. These results demonstrate how the expression of astrocyte Cl- currents can be dependent on cell morphology, the structure of actin, Ca2+ homeostasis, and metabolism.},
	Author = {Lascola, C. D. and Kraig, R. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Adenosine Triphosphate;research support, non-u.s. gov't;21 Neurophysiology;Zinc;Action Potentials;Immunohistochemistry;Astrocytes;Rats;Calcium;Chloride Channels;research support, u.s. gov't, p.h.s.;Animals;Cells, Cultured;Patch-Clamp Techniques;4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {8},
	Organization = {Committee on Neurobiology, University of Chicago, Illinois 60637, USA.},
	Pages = {2532-45},
	Pubmed = {8786429},
	Title = {Whole-cell chloride currents in rat astrocytes accompany changes in cell morphology},
	Uuid = {BDEDC02A-6ACF-4EA8-9A0E-84CDDEED0C6E},
	Volume = {16},
	Year = {1996},
	url = {papers/Lascola_JNeurosci1996.pdf}}

@article{Lassmann:1993,
	Author = {Lassmann, H. and Hickey, W. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0722-5091},
	Journal = {Clin Neuropathol},
	Keywords = {Bone Marrow;Rats;Encephalomyelitis, Autoimmune, Experimental;Bone Marrow Transplantation;11 Glia;Microglia;Radiation Chimera;Spinal Cord;Animals;Brain;Rats, Inbred Strains},
	Medline = {94037713},
	Nlm_Id = {8214420},
	Number = {5},
	Organization = {Research Unit for Experimental Neuropathology, Austrian Academy of Sciences.},
	Pages = {284-5},
	Pubmed = {8222398},
	Title = {Radiation bone marrow chimeras as a tool to study microglia turnover in normal brain and inflammation},
	Uuid = {E4D0F535-EF28-4A2A-B5AD-944D8A4C60B7},
	Volume = {12},
	Year = {1993}}

@article{Lassmann:1993a,
	Abstract = {Infection of the central nervous (CNS) system by the human immunodeficiency virus (HIV) depends on the migration of infected hematogenous cells into the brain. We thus used quantitative light and electron microscopic immunocytochemistry to study the homing and turnover of bone marrow derived cells in the CNS in radiation bone marrow chimeras under normal conditions and in experimental autoimmune encephalomyelitis (EAE) as an experimental model of brain inflammation. Our studies suggest the following conclusions. First, the central nervous system is continuously patrolled by a small number of T-lymphocytes and monocytes. Meningeal and perivascular monocytes are slowly replaced by hematogenous cells under normal conditions, and this turnover is accelerated in the course of inflammation. In contrast, resident microglia represent a very stable cell pool, which in adult animals is only exceptionally replaced by hematogenous cells, even after recovery from severe brain inflammation. Second, although in bone-marrow-chimeric animals resident microglia, astrocytes, and ependymal cells are not able to present antigen to Lewis T-lymphocytes, the inflammatory reaction in EAE is qualitatively and quantitatively similar in these animals compared to fully histocompatible Lewis rats. Finally, resident microglia express the macrophage activation antigen ED1. Thus, microglia cells appear to function as effector cells in EAE lesions.},
	Author = {Lassmann, H. and Schmied, M. and Vass, K. and Hickey, W. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Histocompatibility Antigens;Bone Marrow;Neuroglia;Rats, Inbred Lew;Chimera;Research Support, Non-U.S. Gov't;Autoimmune Diseases;Research Support, U.S. Gov't, P.H.S.;Myelin Basic Proteins;Encephalomyelitis, Autoimmune, Experimental;Meninges;11 Glia;Microscopy, Electron;Encephalitis;Rats;Immunohistochemistry;Animals},
	Medline = {93138739},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Research Unit for Experimental Neuropathology, Austrian Academy of Sciences, Vienna.},
	Pages = {19-24},
	Pubmed = {7678581},
	Title = {Bone marrow derived elements and resident microglia in brain inflammation},
	Uuid = {93F8328B-E335-4779-8F2A-DAB46AFF386E},
	Volume = {7},
	Year = {1993}}

@article{Lau:2004,
	Abstract = {Reverse transcription of retroviral RNA into linear double-stranded DNA and its integration into the host cell genome are essential steps in the retroviral life cycle. The nonhomologous end-joining (NHEJ) DNA repair pathway has been implicated in protecting cells from retrovirus-induced apoptosis caused by strand breaks in host cell DNA or unintegrated linear viral DNA. In eukaryotes, both the NHEJ and homologous recombination (HR) pathways play important roles in repairing DNA double-strand breaks. Here we show that the HR repair protein RAD52 modulates the outcome of recombinant HIV-l vector infection by markedly reducing the efficiency of productive integration events. Increased retroviral integration is the first major phenotype described for a RAD52 deficiency in mammalian cells. Mutations in other HR proteins (XRCC2, XRCC3 and BRCA2) do not markedly affect retroviral transduction rates, suggesting that the HR repair pathway per se does not influence retroviral infection. Instead, the mechanism of attenuation of retroviral infection by RAD52 appears to be based upon competition between the RAD52 protein and active integration complexes for the retroviral cDNA genome.},
	Author = {Lau, Alan and Kanaar, Roland and Jackson, Stephen P. and O'Connor, Mark J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0261-4189},
	Journal = {EMBO J},
	Keywords = {15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {8208664},
	Number = {16},
	Organization = {KuDOS Pharmaceuticals Limited, 327 Cambridge Science Park, Cambridge, UK.},
	Pages = {3421-9},
	Pii = {7600348},
	Pubmed = {15297876},
	Title = {Suppression of retroviral infection by the RAD52 DNA repair protein},
	Uuid = {5B0F3138-EB95-49BA-B32A-F3B0FA93BF2B},
	Volume = {23},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.emboj.7600348}}

@article{Lauro:2006,
	Abstract = {Fractalkine/CX3CL1 and its specific receptor CX3CR1 are constitutively expressed in several regions of the CNS and are reported to mediate neuron-microglial interaction, synaptic transmission, and neuronal protection from toxic insults. CX3CL1 is released both by neuronal and astrocytic cells, whereas CX3CR1 is mainly expressed by microglial cells and neurons. Microglial cells efficiently migrate in response to CX3CL1, whereas no evidence is reported to date on CX3CL1-induced neuronal migration. For this reason, we have investigated in vitro the effects of CX3CL1 on basal migration of neurons and of the microglial and astrocytic populations, all these cells being obtained from the hippocampus and the cerebellum of newborn rats. We report that CX3CL1 stimulates microglial cell migration but efficiently reduces basal neuronal movement, regardless of the brain source. The effect of CX3CL1 is pertussis toxin (PTX) sensitive and PI3K dependent on hippocampal neurons, while it is PTX sensitive, PI3K dependent, and ERK dependent on cerebellar granules. Interestingly, CX3CL1 also increases neuron adhesion to the extracellular matrix component laminin, with mechanisms dependent on PTX-sensitive G proteins, and on the ERK and PI3K pathways. Both the reduction of migration and the increase of neuron adhesion require the activation of the beta(1) and alpha(6) integrin subunits with the exception of cerebellar neuron migration, which is only dependent on the beta(1) subunit. More importantly, in neurons, CX3CL1/CXCL12 cotreatment abolished the effect mediated by a single chemokine on chemotaxis and adhesion. In conclusion, our findings indicate that CX3CL1 reduces neuronal migration by increasing cell adhesion through integrin-dependent mechanisms in hippocampal and cerebellar neurons.},
	Author = {Lauro, Clotilde and Catalano, Myriam and Trettel, Flavia and Mainiero, Fabrizio and Ciotti, Maria Teresa and Eusebi, Fabrizio and Limatola, Cristina},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {research support, non-u.s. gov't;14 Immune;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {2985117R},
	Number = {11},
	Organization = {Istituto Pasteur-Fondazione Cenci Bolognetti and Dipartimento di Fisiologia Umana e Farmacologia, Centro di Eccellenza, Universit\`{a} La Sapienza, I-00185 Rome, Italy.},
	Pages = {7599-606},
	Pii = {177/11/7599},
	Pubmed = {17114429},
	Title = {The chemokine CX3CL1 reduces migration and increases adhesion of neurons with mechanisms dependent on the beta1 integrin subunit},
	Uuid = {3C0220B1-E9AC-4180-8DB2-17E7E071DD8B},
	Volume = {177},
	Year = {2006}}

@article{Lavdas:2006,
	Abstract = {Schwann cells, the myelin-forming cells of the PNS, are attractive candidates for remyelination therapy as they can remyelinate CNS axons. Yet their integration in CNS tissue appears hampered, at least in part, by their limited motility in the CNS environment. As the polysialylated (PSA) form of NCAM regulates migration of neural precursors in the CNS and is not expressed by developing Schwann cells, we investigated whether conferring sustained expression of PSA to Schwann cells derived from postnatal rats enhances their motility. Cells were transduced with a retrovirus encoding polysialyl-transferase STX, an enzyme that synthesizes PSA on NCAM. Migration of wild type and transduced cells expressing STX or the marker gene alkaline phosphatase was examined using a gap bridging assay in dissociated cells and by grafting cells in slice cultures of postnatal brain. Migration of PSA expressing cells was significantly increased in both models, as compared to control cells, and this effect was abolished by endoneuraminidase-N stripping of PSA. PSA-positive Schwann cells retained the ability to differentiate in vitro and expressed the Krox20 and P zero myelination markers. When grafted in neonatal cerebellar slices, STX-transduced cells started to myelinate Purkinje cell axons like control cells and make myelin internodes after 2 to 3 weeks. PSA was redistributed on the cell membrane and downregulated during differentiation in pure Schwann cell cultures and slice co-cultures. Thus, migratory properties of PNS myelin-forming cells within the CNS can be enhanced without altering their differentiation program. This finding may be beneficial for the development of remyelination therapies.},
	Author = {Lavdas, Alexandros A. and Franceschini, Isabelle and Dubois-Dalcq, Monique and Matsas, Rebecca},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Research Support, Non-U.S. Gov't;Early Growth Response Protein 2;Cell Differentiation;Transduction, Genetic;Myelin Sheath;Cells, Cultured;Up-Regulation;Rats;Animals;Myelin P0 Protein;Axons;Cell Communication;Cell Movement;Organ Culture Techniques;Genetic Vectors;Nerve Regeneration;Schwann Cells;Genetic Engineering;Sialic Acids;Animals, Newborn;Down-Regulation;Sialyltransferases;24 Pubmed search results 2008;Neural Cell Adhesion Molecule L1;Biological Markers;Peripheral Nerves},
	Month = {6},
	Nlm_Id = {8806785},
	Number = {8},
	Organization = {Laboratory of Cellular and Molecular Neurobiology, Hellenic Pasteur Institute, 127 Vas. Sofias, 11521 Athens, Greece.},
	Pages = {868-78},
	Pubmed = {16598779},
	Title = {Schwann cells genetically engineered to express PSA show enhanced migratory potential without impairment of their myelinating ability in vitro},
	Uuid = {08A63712-69BE-4FCF-A3C5-D762447B250B},
	Volume = {53},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20340}}

@article{Lavdas:1999,
	Abstract = {During development of the neocortex, the marginal zone (layer I) and the subplate (layer VII) are the first layers to form from a primordial plexiform neoropil. The cortical plate (layers II-VI) is subsequently established between these superficial and deep components of the primordial plexiform neuropil. Neurons in the early zones are thought to play important roles in the formation of the cortex: the Cajal- Retzius cells of the marginal zone are instrumental in neuronal migration and laminar formation, and cells of the subplate are involved in the formation of cortical connections. Using the fluorescent tracer 1,1'-dioctodecyl-3,3,3', 3'-tetramethylindocarbocyanine (DiI), we have shown here that a substantial proportion of neurons of the marginal zone, including cells with features of Cajal-Retzius cells, and of the subplate and lower intermediate zone are not born in the ventricular neuroepithelium but instead originate in the medial ganglionic eminence (MGE), the pallidal primordium. These neurons follow a tangential migratory route to their positions in the developing cortex. They express the neurotransmitter GABA but seem to lack the calcium binding protein calretinin; some migrating cells found in the marginal zone express reelin. In addition, migrating cells express the LIM-homeobox gene Lhx6, a characteristic marker of the MGE. It is suggested that this gene uniquely or in combination with other transcription factors may be involved in the decision of MGE cells to differentiate in situ or migrate to the neocortex.},
	Author = {Lavdas, A. A. and Grigoriou, M. and Pachnis, V. and Parnavelas, J. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;H;Gene Expression Regulation, Developmental;Rats;Neurons/*cytology;Animal;Cell Movement;Rats, Sprague-Dawley;Cerebral Cortex/cytology/*embryology;Brain/cytology/*embryology;Zinc Fingers;Support, Non-U.S. Gov't;Morphogenesis;*Fetal Development;Homeodomain Proteins/genetics;Carbocyanines;Organ Culture;12 Interneuron development},
	Number = {18},
	Organization = {Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom.},
	Pages = {7881-8.},
	Title = {The medial ganglionic eminence gives rise to a population of early neurons in the developing cerebral cortex},
	Uuid = {F05BD9D4-5A88-4154-9D64-82050001A9CA},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10479690%20http://www.jneurosci.org/cgi/content/full/19/18/7881%20http://www.jneurosci.org/cgi/content/abstract/19/18/7881}}

@article{Law:1999,
	Abstract = {A prolific neuronal progenitor cell population in the anterior portion of the neonatal rat forebrain subventricular zone, the SVZa, is specialized for the production of olfactory bulb interneurons. At all ages, SVZa-derived cells traverse a tangential migratory pathway, the rostral migratory stream (RMS), while en route to the olfactory bulb. Unlike other neuronal progenitor cells of the forebrain, migrating progeny of SVZa progenitors express neuronal-specific proteins and continue to divide into adulthood. Recent studies indicate that in the adult, migrating SVZa-derived cells are ensheathed by astrocytes, although the function of these astrocytes has not been determined. To explore the possible role(s) of astrocytes in the rat SVZa and RMS, we examined the expression of astroglial-specific genes in the postnatal SVZa and RMS using RT-PCR, in situ hybridization, and immunohistochemistry during (Postnatal Days 1-10) and after the period of peak olfactory bulb interneuron generation. We also examined the expression of neuronal-specific genes throughout the rostral-caudal extent of the postnatal subventricular zone to determine if differential cell type-specific gene expression could distinguish the neurogenic SVZa as a region distinct from the remainder of the SVZ. We found little to no astrocyte-specific gene expression in the P0-P7 SVZa, although the neuron-specific isoforms of tubulin (T alpha 1 and beta-III tubulin) were expressed abundantly in the SVZa and RMS. In contrast, astrocyte-specific genes were strongly expressed in the SVZ posterior to the SVZa. GFAP expressions begins to appear in some restricted areas of the rostral migratory stream after the first postnatal week. These data suggest that astroglia are not involved in the generation or migration of most olfactory bulb interneurons. Moreover, the scarcity of glial markers in the neonatal SVZa indicates that the forebrain subventricular zone includes a distinct neurogenic anterior region containing predominantly committed neuronal progenitor cells.},
	Author = {Law, A. K. and Pencea, V. and Buck, C. R. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Dev Biol},
	Keywords = {Astrocytes/*metabolism;Cell Differentiation;Gene Expression Regulation, Developmental;Rats;Animal;Neurons/*metabolism;02 Adult neurogenesis migration;Brain/*growth &development;Microscopy, Fluorescence;Reverse Transcriptase Polymerase Chain Reaction;*Cell Movement;In Situ Hybridization;Support, Non-U.S. Gov't;B-12;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;RNA, Messenger/metabolism;Biological Markers;Animals, Newborn/growth &development},
	Number = {2},
	Organization = {Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {622-34.},
	Title = {Neurogenesis and neuronal migration in the neonatal rat forebrain anterior subventricular zone do not require GFAP-positive astrocytes},
	Uuid = {9DE2E7ED-C579-4A37-8715-55F56CD212DB},
	Volume = {216},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10642797}}

@article{Lawson:1992,
	Abstract = {We undertook this study to determine whether the microglia, the resident macrophages of the central nervous system, turn over in the steady-state. The turnover of brain macrophages would lend support to the "Trojan Horse" hypothesis of central nervous system infection, since one origin of replacement cells is the circulating monocyte pool. We combined the immunohistochemical detection of F4/80, a specific macrophage marker, with [3H]thymidine incorporation and autoradiography in normal adult mice. We could detect double-labelled cells in the brains of mice perfused 60 min after isotope administration. Such cells were few in number, randomly scattered throughout the brain and had the morphology of typical resident cells. The labelling index at this survival time was 0.052 +/- 0.003\%. Thus resident microglia can synthesise DNA in situ. After longer survival times, we detected larger numbers of double-labelled cells. F4/80+ cells with resident morphology, mitotic figures, pairs of closely apposed (daughter) cells and cells with rounded macrophage-like morphology, all exhibited silver labelling. Twenty-four hours after isotope administration the labelling index was 0.192 +/- 0.052\%. From morphologic evidence and comparison of labelling indices at different survival times, we concluded that: (i) resident microglia can synthesise DNA and go on to divide in situ; (ii) cells are recruited from the circulating monocyte pool through an intact blood-brain barrier and rapidly differentiate into resident microglia. We estimate that the two processes contribute almost equally to the steady-state turnover of resident microglia.},
	Author = {Lawson, L. J. and Perry, V. H. and Gordon, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Mice, Inbred BALB C;Animals;Macrophages;Comparative Study;Brain;Thymidine;Female;Kinetics;DNA Replication;11 Glia;Get paper from library;Mesoderm;Mitotic Index;Organ Specificity;Mice;Tritium;Autoradiography;Research Support, Non-U.S. Gov't},
	Medline = {92293499},
	Nlm_Id = {7605074},
	Number = {2},
	Organization = {Department of Pharmacology, University of Oxford, U.K.},
	Pages = {405-15},
	Pubmed = {1603325},
	Title = {Turnover of resident microglia in the normal adult mouse brain},
	Uuid = {8112FD0B-CC45-4816-B1C6-5E59A20AA0F2},
	Volume = {48},
	Year = {1992}}

@article{Laywell:2000,
	Abstract = {The mammalian brain contains a population of neural stem cells (NSC) that can both self-renew and generate progeny along the three lineage pathways of the central nervous system (CNS), but the in vivo identification and localization of NSC in the postnatal CNS has proved elusive. Recently, separate studies have implicated ciliated ependymal (CE) cells, and special subependymal zone (SEZ) astrocytes as candidates for NSC in the adult brain. In the present study, we have examined the potential of these two NSC candidates to form multipotent spherical clones-neurospheres-in vitro. We conclude that CE cells are unipotent and give rise only to cells within the glia cell lineage, although they are capable of forming spherical clones when cultured in isolation. In contrast, astrocyte monolayers from the cerebral cortex, cerebellum, spinal cord, and SEZ can form neurospheres that give rise both to neurons and glia. However, the ability to form neurospheres is restricted to astrocyte monolayers derived during the first 2 postnatal wk, except for SEZ astrocytes, which retain this capacity in the mature forebrain. We conclude that environmental factors, simulated by certain in vitro conditions, transiently confer NSC-like attributes on astrocytes during a critical period in CNS development. 0027-8424 Journal Article},
	Author = {Laywell, E. D. and Rakic, P. and Kukekov, V. G. and Holland, E. C. and Steindler, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {02 Adult neurogenesis migration;Glial Fibrillary Acidic Protein/metabolism;03 Adult neurogenesis progenitor source;Immunohistochemistry;Microscopy, Electron;Brain/*cytology/metabolism/ultrastructure;BB both;Astrocytes/*cytology/metabolism/ultrastructure;Support, U.S. Gov't, Non-P.H.S.;Stem Cells/*cytology/metabolism/ultrastructure;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Animals;Mice;Cell Lineage},
	Number = {25},
	Organization = {Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, Memphis, TN 38163, USA. elaywell\@yahoo.com},
	Pages = {13883-8},
	Title = {Identification of a multipotent astrocytic stem cell in the immature and adult mouse brain},
	Uuid = {7710F520-68D7-11DA-A4B6-000D9346EC2A},
	Volume = {97},
	Year = {2000},
	url = {papers/Laywell_ProcNatlAcadSciUSA2000.fcgi}}

@article{Lazar:1996,
	Abstract = {We investigated the microglial reaction around cobalt-labeled degenerating neurons and nerve fibers in the frog central nervous system. The aim of these studies was to reveal the routes of migrating microglial cells during debris removal and the effect of seasonal changes on this process in a cold-blooded animal. Oculomotor and spinal motoneurons were filled with cobaltous-lysine complex through their axons. In the torus semicircularis and the isthmic nucleus, neurons were labeled with iontophoretically applied cobaltous-lysine complex through their injured dendrites and axons. The animals were left to survive for 1 to 50 days. During the summer, oculomotor neurons disintegrated by the seventh postoperative day. The debris from the neurons were phagocytosed by microglia-like cells identified by the presence of cobalt in their cytoplasm. Some of these cells were wedged between ependymoglial cells of the cerebral aqueduct, others appeared at the pial surface of the mesencephalon. The speed of this process was twice as fast during the summer as during the winter. Part of cobalt-labeled microglial cells in the torus semicircularis and the isthmic nucleus moved toward the ependyma of the optic ventricle and the cerebral aqueduct, respectively. Cobalt-loaded microglial cells did not move toward the surface in the spinal cord and the deep part of mesencephalic tegmentum, and left the brain probably via blood vessels. We conclude that microglial cells loaded with phagocytosed tissue debris may leave the brain tissue via three routes and their activity depends on the environmental temperature.},
	Author = {Lazar, G. and Pal, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:34 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Oculomotor Nerve;Nerve Degeneration;Presynaptic Terminals;Animals;Phagocytosis;Rana esculenta;Brain;Microglia;Female;Not relevant;11 Glia;Seasons;Spinal Cord;Male;Support, Non-U.S. Gov't;Histocytochemistry;Rana ridibunda;Neurons;Ependyma;Motor Neurons;Nerve Fibers;Cobalt},
	Medline = {97083323},
	Month = {2},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Anatomy, University Medical School of Pecs, Hungary.},
	Pages = {101-7},
	Pii = {10.1002/(SICI)1098-1136(199602)16:2<101::AID-GLIA2>3.0.CO;2-6},
	Pubmed = {8929897},
	Title = {Removal of cobalt-labeled neurons and nerve fibers by microglia from the frog's brain and spinal cord},
	Uuid = {0AE0E1D7-2DEB-4AF6-A3CE-B86B46720271},
	Volume = {16},
	Year = {1996}}

@article{Lazarowski:2006,
	Abstract = {Epileptogenic cortical tubers, characterized by dysplastic neurons and balloon cells, is a frequent feature of tuberous sclerosis. In severe tuberous sclerosis-affected individuals, seizures are refractory to medication. Multidrug resistance proteins (multidrug resistance protein-1 [MDR-1] and multidrug resistance-associated protein-1 [MRP-1]) have been found to be highly expressed in epileptogenic cortical tubers. However, two new proteins related to refractoriness in cancer (breast cancer resistance protein and major vault protein) have not been investigated in tuberous sclerosis and refractory epilepsy. On the same brain specimens previously describing the MDR-1 and MRP-1 expression, we investigated retrospectively breast cancer resistance protein and major vault protein by specific monoclonal antibodies and routine immunohistochemistry methods. Breast cancer resistance protein was present in vascular endothelial cells from all the vessels examined in 3 of 3 cases. Major vault protein was detected in only one case, and selectively expressed in several but not all ballooned cells. In epileptogenic cortical tubers, the additional expression of breast cancer resistance protein on vessels and major vault protein in some ballooned cells to the previously demonstrated expression of MDR-1 and MRP-1 (in vessels, astroglia, microglia, neurons, and ballooned cells) configures a brain protein pharmacoresistance map from patients with tuberous sclerosis and refractory epilepsy.},
	Author = {Lazarowski, Alberto J. and Lubieniecki, Fabiana J. and Camarero, Sandra A. and Pomata, Hugo H. and Bartuluchi, Marcelo A. and Sevlever, Gustavo and Taratuto, Ana L{\'\i}a},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0887-8994},
	Journal = {Pediatr Neurol},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {8508183},
	Number = {1},
	Organization = {Clinical Biochemistry Department, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires (UBA); Institute of Cell Biology and Neurobiology "Dr. E de Robertis", Facultad de Medicina, Universidad de Buenos Aires (UBA).},
	Pages = {20-4},
	Pii = {S0887-8994(05)00341-3},
	Pubmed = {16376273},
	Title = {New proteins configure a brain drug resistance map in tuberous sclerosis},
	Uuid = {D4B7F79E-B799-4A97-B38B-46AA0E63EFDD},
	Volume = {34},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.pediatrneurol.2005.06.008}}

@article{Lazo:2002,
	Abstract = {Small molecules provide powerful tools to interrogate biological pathways but many important pathway participants remain refractory to inhibitors. For example, Cdc25 dual-specificity phosphatases regulate mammalian cell cycle progression and are implicated in oncogenesis, but potent and selective inhibitors are lacking for this enzyme class. Thus, we evaluated 10,070 compounds in a publicly available chemical repository of the National Cancer Institute for in vitro inhibitory activity against oncogenic, full-length, recombinant human Cdc25B. Twenty-one compounds had mean inhibitory concentrations of <1 microM; >75\%were quinones and >40\%were of the para-naphthoquinone structural type. Most notable was NSC 95397 (2,3-bis-[2-hydroxyethylsulfanyl]-[1,4]naphthoquinone), which displayed mixed inhibition kinetics with in vitro K(i) values for Cdc25A, -B, and -C of 32, 96, and 40 nM, respectively. NSC 95397 was more potent than any inhibitor of dual specificity phosphatases described previously and 125- to 180-fold more selective for Cdc25A than VH1-related dual-specificity phosphatase or protein tyrosine phosphatase 1b, respectively. Modification of the bis-thioethanol moiety markedly decreased enzyme inhibitory activity, indicating its importance for bioactivity. NSC 95397 showed significant growth inhibition against human and murine carcinoma cells and blocked G(2)/M phase transition. A potential Cdc25 site of interaction was postulated based on molecular modeling with these quinones. We propose that inhibitors based on this chemical structure could serve as useful tools to probe the biological function of Cdc25. 0026-895x Journal Article},
	Author = {Lazo, J. S. and Nemoto, K. and Pestell, K. E. and Cooley, K. and Southwick, E. C. and Mitchell, D. A. and Furey, W. and Gussio, R. and Zaharevitz, D. W. and Joo, B. and Wipf, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Mol Pharmacol},
	Keywords = {Cell Division/drug effects;Tumor Cells, Cultured;Models, Molecular;Drug Evaluation, Preclinical;EE, T abstr;Kinetics;Human;Binding Sites;Amino Acid Motifs;Cell Cycle/drug effects;cdc25 Phosphatase/*antagonists &inhibitors/chemistry;08 Aberrant cell cycle;Naphthoquinones/chemistry/*pharmacology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Enzyme Inhibitors/chemistry/*pharmacology;Cell Cycle Proteins/*antagonists &inhibitors/chemistry},
	Number = {4},
	Organization = {Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA. lazo\@pitt.edu},
	Pages = {720-8},
	Pubmed = {11901209},
	Title = {Identification of a potent and selective pharmacophore for Cdc25 dual specificity phosphatase inhibitors},
	Uuid = {AA39DE2B-BD53-4746-A662-90DE0547B874},
	Volume = {61},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11901209}}

@article{Blanc:2005,
	Abstract = {During viral infection, fusion of the viral envelope with endosomal membranes and nucleocapsid release were thought to be concomitant events. We show here that for the vesicular stomatitis virus they occur sequentially, at two successive steps of the endocytic pathway. Fusion already occurs in transport intermediates between early and late endosomes, presumably releasing the nucleocapsid within the lumen of intra-endosomal vesicles, where it remains hidden. Transport to late endosomes is then required for the nucleocapsid to be delivered to the cytoplasm. This last step, which initiates infection, depends on the late endosomal lipid lysobisphosphatidic acid (LBPA) and its putative effector Alix/AIP1, and is regulated by phosphatidylinositol-3-phosphate (PtdIns(3)P) signalling via the PtdIns(3)P-binding protein Snx16. We conclude that the nucleocapsid is exported into the cytoplasm after the back-fusion of internal vesicles with the limiting membrane of late endosomes, and that this process is controlled by the phospholipids LBPA and PtdIns(3)P and their effectors.},
	Author = {Le Blanc, and Luyet, and Pons, and Ferguson, and Emans, and Petiot, and Mayran, and Demaurex, and Faur{\'e}, and Sadoul, and Parton, and Gruenberg,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {100890575},
	Number = {7},
	Organization = {[1] Biochemistry Department, University of Geneva, 30 quai E. Ansermet, 1211 Geneva 4, Switzerland. [2] Department of Molecular and Cell Biology, 16 Barker Hall, University of California, Berkeley, CA 94720-3202, USA. [3] These authors contributed equally to this work.},
	Pages = {653-664},
	Pii = {ncb1269},
	Pubmed = {15951806},
	Title = {Endosome-to-cytosol transport of viral nucleocapsids},
	Uuid = {F4A92BC6-EA30-4CC2-B1B4-666BD3A294D2},
	Volume = {7},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb1269}}

@article{Le-Borgne:2003,
	Abstract = {In Drosophila, Notch signaling regulates binary fate decisions at each asymmetric division in sensory organ lineages. Following division of the sensory organ precursor cell (pI), Notch is activated in one daughter cell (pIIa) and inhibited in the other (pIIb). We report that the E3 ubiquitin ligase Neuralized localizes asymmetrically in the dividing pI cell and unequally segregates into the pIIb cell, like the Notch inhibitor Numb. Furthermore, Neuralized upregulates endocytosis of the Notch ligand Delta in the pIIb cell and acts in the pIIb cell to promote activation of Notch in the pIIa cell. Thus, Neuralized is a conserved regulator of Notch signaling that acts as a cell fate determinant. Polarization of the pI cell directs the unequal segregation of both Neuralized and Numb. We propose that coordinated upregulation of ligand activity by Neuralized and inhibition of receptor activity by Numb results in a robust bias in Notch signaling. 1534-5807 Journal Article},
	Author = {Le Borgne, R. and Schweisguth, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Dev Cell},
	Keywords = {Trans-Activation (Genetics);10 Development;Signal Transduction;Animals;Nerve Tissue Proteins/*metabolism;Models, Biological;Mutation;Cell Polarity;Trans-Activators/metabolism;Membrane Proteins/*metabolism;*Ubiquitin-Protein Ligases;Drosophila/embryology;Support, Non-U.S. Gov't;Cell Lineage;Drosophila Proteins/metabolism;Cell Division/*physiology;Endocytosis;Juvenile Hormones/metabolism;Ligases/*metabolism;Luminescent Proteins/metabolism;F},
	Number = {1},
	Organization = {Departement de Biologie, Ecole Normale Superieure, CNRS UMR 8542, 46, rue d'Ulm 75230, Cedex, Paris, France.},
	Pages = {139-48},
	Pubmed = {12852858},
	Title = {Unequal segregation of Neuralized biases Notch activation during asymmetric cell division},
	Uuid = {81EEC7EC-06CB-4A93-A897-1ED245ECC690},
	Volume = {5},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12852858}}

@article{Lechner:2004,
	Abstract = {Several recent studies have suggested that the adult bone marrow harbors cells that can differentiate into tissues from all three germ layers. Other reports have contradicted these findings or attributed them to cell fusion. In this study, we investigated whether bone marrow-derived cells contribute to the renewal of adult pancreatic endocrine cells, in particular insulin-producing beta-cells, in vivo. To address this issue, we studied mice transplanted with green fluorescent protein (GFP)-positive, sex-mismatched bone marrow. We also extended our studies to pancreatic injury models (partial pancreatectomy and streptozotocin administration). All animals showed stable full donor chimerism in the peripheral blood and microscopic analysis at 4-6 weeks and 3 months after transplantation, indicating that the GFP(+) and Y chromosome-positive donor bone marrow contributed substantially to blood, lymphatic, and interstitial cells in the pancreas. However, after examining >100,000 beta-cells, we found only 2 beta-cells positive for GFP, both of which were in control animals without pancreatic injury. Thus our study results did not support the concept that bone marrow contributes significantly to adult pancreatic beta-cell renewal.},
	Author = {Lechner, Andreas and Yang, Yong-Guang G. and Blacken, Robyn A. and Wang, Lan and Nolan, Anna L. and Habener, Joel F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0012-1797},
	Journal = {Diabetes},
	Keywords = {Research Support, Non-U.S. Gov't;Cell Differentiation;Animals;Bone Marrow Transplantation;Female;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Time Factors;Male;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Pancreatectomy;Transplantation, Homologous;Islets of Langerhans;Mice;Luminescent Proteins;Genetic Markers},
	Month = {3},
	Nlm_Id = {0372763},
	Number = {3},
	Organization = {Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Harvard Medical School and Howard Hughes Medical Institute, Boston, Massachusetts, USA.},
	Pages = {616-23},
	Pubmed = {14988245},
	Title = {No evidence for significant transdifferentiation of bone marrow into pancreatic beta-cells in vivo},
	Uuid = {87B16BCD-FB86-4459-9337-743B86942C3D},
	Volume = {53},
	Year = {2004}}

@article{Lee:1993,
	Abstract = {Central nervous system disease is a frequent finding in both pediatric and adult AIDS. Microglia have been shown to be the major target of HIV-1 infection in the central nervous system. However, studies in vitro concerning susceptibility of human microglia to HIV-1 infection reported conflicting results; microglia from adult brain showed productive infection by HIV-1, whereas microglia from fetal brain did not. To investigate this further and to define the possible mechanisms responsible for this difference, we prepared highly purified human microglial cell cultures from fetuses of 16 to 24 weeks' gestation and exposed them to monocytotropic (HIV-1 JR-FL and HIV-1 JR-CSF) isolates of HIV-1. Culture supernatants were examined for the presence of p24 antigen for a 4-week period after viral exposure. Concurrently, potential cytopathic effects and cellular viral antigen expression (gp41 and p24) were examined by light microscopy in combination with immunocytochemistry. The results showed that human fetal microglia can be productively infected by HIV-1 as judged by p24 antigen capture assay, syncytia formation, and gp41 and p24 immunoreactivity of infected microglia. In addition, by electron microscopy, numerous viral particles characteristic of HIV-1 were present both in the intracellular and extracellular compartments. Uninfected cultures or astrocytes overgrown in the microglial cultures did not show evidence of infection under identical experimental conditions. These data demonstrate that human fetal microglia, like their adult counterparts, are susceptible to HIV-1 infection in vitro and can support the production of virus.},
	Author = {Lee, S. C. and Hatch, W. C. and Liu, W. and Kress, Y. and Lyman, W. D. and Dickson, D. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Disease Susceptibility;HIV Core Protein p24;HIV-1;Immunohistochemistry;Human;Microscopy, Electron;Microscopy, Phase-Contrast;Fetal Diseases;Research Support, U.S. Gov't, P.H.S.;11 Glia;Microglia;Support, U.S. Gov't, P.H.S.;Acquired Immunodeficiency Syndrome;Humans},
	Medline = {94027253},
	Month = {10},
	Nlm_Id = {0370502},
	Number = {4},
	Organization = {Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, New York 10461.},
	Pages = {1032-9},
	Pubmed = {8213999},
	Title = {Productive infection of human fetal microglia by HIV-1},
	Uuid = {5D47D766-BB97-4626-90AC-E49E4FDF36C5},
	Volume = {143},
	Year = {1993}}

@article{Lee:1990,
	Abstract = {Five beta-tubulin isotypes are expressed differentially during chicken brain development. One of these isotypes is encoded by the gene c beta 4 and has been assigned to an isotypic family designated as Class III (beta III). In the nervous system of higher vertebrates, beta III is synthesized exclusively by neurons. A beta III-specific monoclonal antibody was used to determine when during chick embryogenesis c beta 4 is expressed, the cellular localization of beta III, and the number of charge variants (isoforms) into which beta III can be resolved by isoelectric focusing. On Western blots, beta III is first detectable at stages 12-13. Thereafter, the relative abundance of beta III in brain increases steadily, apparently in conjunction with the rate of neural differentiation. The isotype was not detectable in non-neural tissue extracts from older embryos (days 10-14) and hatchlings. Western blots of protein separated by two-dimensional gel electrophoresis (2D-PAGE) reveal that the number of beta III isoforms increases from one to three during neural development. This evidence indicates that beta III is a substrate for developmentally regulated, multiple-site posttranslational modification. Immunocytochemical studies reveal that while c beta 4 expression is restricted predominantly to the nervous system, it is transiently expressed in some embryonic structures. More importantly, in the nervous system, immunoreactive cells were located primarily in the non-proliferative marginal zone of the neural epithelia. Regions containing primarily mitotic neuroblasts were virtually unstained. This localization pattern indicates that c beta 4 expression occurs either during or immediately following terminal mitosis, and suggests that beta III may have a unique role during early neuronal differentiation and neurite outgrowth.},
	Author = {Lee, M. K. and Tuttle, J. B. and Rebhun, L. I. and Cleveland, D. W. and Frankfurter, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0886-1544},
	Journal = {Cell Motil Cytoskeleton},
	Keywords = {Organ Specificity;10 Development;Research Support, Non-U.S. Gov't;Tubulin;Immunohistochemistry;Antibodies, Monoclonal;Research Support, U.S. Gov't, P.H.S.;Chick Embryo;Antibody Specificity;Nervous System;Protein Processing, Post-Translational;Animals;Neurons},
	Medline = {91077940},
	Nlm_Id = {8605339},
	Number = {2},
	Organization = {Neuroscience Program, University of Virginia, Charlottesville.},
	Pages = {118-32},
	Pubmed = {2257630},
	Title = {The expression and posttranslational modification of a neuron-specific beta-tubulin isotype during chick embryogenesis},
	Uuid = {FBEC0C5F-D067-11DA-8A8C-000D9346EC2A},
	Volume = {17},
	Year = {1990},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cm.970170207}}

@article{Lee:1997a,
	Abstract = {Several major advances in the understanding of the regulation of vertebrate neurogenesis by members of the basic helix-loop-helix (bHLH) protein family have been made in the past year. Specifically, a number of bHLH genes have been cloned and shown to convert non-neuronal fate to neuronal fate when expressed ectopically. In particular, studies on NeuroD and Neurogenin suggest a regulatory pathway, providing powerful molecular tools to study vertebrate neurogenesis.},
	Author = {Lee, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Curr Opin Neurobiol},
	Keywords = {F abstr;10 Development;Nervous System/*embryology;Animal;Helix-Loop-Helix Motifs/*genetics;Drosophila;Fetal Development;*Genes;Cell Differentiation/genetics},
	Number = {1},
	Organization = {Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Campus Box 347, Colorado 80309-0347, USA. jackie.lee\@colorado.edu},
	Pages = {13-20.},
	Title = {Basic helix-loop-helix genes in neural development},
	Uuid = {F04FC1DC-1253-4F93-8C71-928AD3BF586A},
	Volume = {7},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9039799%20http://www.biomednet.com/article/nb7112}}

@article{Lee:1997b,
	Abstract = {NeuroD is a basic helix-loop-helix (bHLH) transcription factor cloned from a two hybrid screen designed to search for new bHLH proteins. In our previous studies, we showed that NeuroD could convert Xenopus ectoderm into fully differentiated neurons and that it could prematurely differentiate neural precursor cells in the nervous system. Recently, an insulin transcription activator, Beta-2, was cloned from a hamster insulinoma cell line by Naya et al. [Genes Dev (1995)9:1,009- 1,019]. Sequence analysis revealed that Beta-2 is the hamster homologue of NeuroD. We are currently investigating the role that NeuroD/Beta-2 plays in vertebrate neurogenesis and pancreatic development. Using Smart Source Parsing},
	Author = {Lee, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Dev Neurosci},
	Keywords = {F abstr;10 Development;Nervous System/*embryology;Anura/embryology;Nerve Tissue Proteins/*physiology;Animal;Fetal Development;Vertebrates/embryology;Helix-Loop-Helix Motifs/physiology},
	Number = {1},
	Organization = {University of Colorado Boulder, Department of Molecular, Cellular and Developmental Biology 80309-0347, USA.},
	Pages = {27-32},
	Title = {NeuroD and neurogenesis},
	Uuid = {49BEB60F-E253-4518-B7DE-42FEFAC171C1},
	Volume = {19},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9078430}}

@article{Lee:2002b,
	Abstract = {Bis (also called Bag-3), identified as a novel Bcl-2-interacting protein, has been shown to enhance anti-cell death activity of Bcl-2. Because ischemia/reperfusion induces expression of Bcl-2, we examined the changes in the pattern of Bis expression in the adult rat hippocampus after transient forebrain ischemia. Western blot analysis with protein extracts from the hippocampus showed that, compared with controls, levels of Bis were markedly increased seven days after ischemia. An immunohistochemical study showed that the expression of Bis increased preferentially in the CA1 and the dentate hilar regions, and peaked at 3-7 days after reperfusion. The temporal and spatial patterns of expression for both Bis and glial fibrillary acidic protein (GFAP) were very similar, and double immunofluorescence histochemistry showed that Bis was expressed in reactive astrocytes, which express GFAP. Immunolabeling of adjacent sections with anti-Bcl-2 and anti-Hsp70 antibodies revealed that the pattern of Bis expression closely correlates with that of Bcl-2, but clearly differs from that of Hsp70. Coexpression of Bis and Bcl-2 in reactive astrocytes was confirmed by double immunofluorescence histochemistry. Our results demonstrate that reactive astrocytes transiently up-regulate Bis after ischemia/reperfusion in the adult rat hippocampus. However, the precise role of Bis in the astrocytic response to ischemia/reperfusion in relation to Bcl-2 remains to be determined. 0014-4886 Journal Article},
	Author = {Lee, M. Y. and Kim, S. Y. and Shin, S. L. and Choi, Y. S. and Lee, J. H. and Tsujimoto, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Exp Neurol},
	Keywords = {Carrier Proteins/analysis/immunology/*metabolism;Heat-Shock Proteins 70/analysis/immunology;Hippocampus/cytology;Rats, Sprague-Dawley;Ischemic Attack, Transient/*metabolism;Rats;06 Adult neurogenesis injury induced;Up-Regulation/physiology;Proto-Oncogene Proteins c-bcl-2/analysis/immunology/*metabolism;D pdf;Animals;Astrocytes/chemistry/*metabolism;Antibodies;Support, Non-U.S. Gov't;Male},
	Number = {2},
	Organization = {Department of Anatomy, The Catholic University of Korea, Seoul 137-701, Korea.},
	Pages = {338-46},
	Pubmed = {12061864},
	Title = {Reactive astrocytes express bis, a bcl-2-binding protein, after transient forebrain ischemia},
	Uuid = {33C96DBD-8508-47A7-9007-EF34656794EE},
	Volume = {175},
	Year = {2002},
	url = {papers/Lee_ExpNeurol2002}}

@article{Lee:2001,
	Abstract = {Human bone marrow-derived mesenchymal stem cells (hMSCs) are being investigated for a potential therapeutic role as hematopoietic support cells following chemo-radiotherapy and as vehicles of gene delivery. Although hMSCs can be safely infused into humans and experimental animals, there is limited evidence regarding their engraftment and proliferation in vivo. We developed a drug resistance gene transfer strategy to mark and selectively enrich marked hMSCs using chemotherapy. We have determined that hMSCs are markedly sensitized to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in vitro when pretreated with O(6)-benzylguanine (BG) resulting in a more than four-fold decrease in BCNU IC(90). The MFG retroviral vector encoding a bicistronic transcript for green fluorescent protein (GFP) and mutant (G156A)-methylguanine methyltransferase (G156A-MGMT), which encodes O(6)-alkylguanine-DNA alkyltransferase (AGT), conferring, BG plus BCNU resistance, transduced a high percentage of hMSCs. Transduced hMSCs had high expression of GFP and AGT and became significantly resistant to BG and BCNU. Furthermore, the proportion of GFP expressing transduced hMSCs increased from 32 +/- 14\%to 70 +/- 14\%following BG and BCNU treatment in vitro. Intravenously infused hMSCs were detected in NOD-SCID mice 8 weeks later by PCR analysis but could not be recultured from the bone marrow. GFP-expressing hMSCs inoculated into subcutaneous wounds in nonobese diabetic-severe combined immunodeficient (NOD-SCID) mouse could be recultured at a low frequency, but enriched by BG and BCNU treatment from 0.05 +/- 0.03\%to 0.55 +/- 0.4 (p = 0.028, Welch t-test). Our results indicate that hMSCs are sensitive to BG and BCNU, predicting significant toxicity to the hematopoietic microenvironment with this therapy. G156A-MGMT is a powerful selectable gene for a second marker gene in hMSCs. Drug resistance gene transfer into hMSCs may allow in vivo enrichment of hMSCs when MSC homing and engraftment into target tissues is optimized.},
	Author = {Lee, K. and Gerson, S. L. and Maitra, B. and Ko\c{c}, O. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1525-8165},
	Journal = {J Hematother Stem Cell Res},
	Keywords = {Guanine;Mice, SCID;Infusions, Intravenous;Cell Survival;Genetic Vectors;O(6)-Methylguanine-DNA Methyltransferase;Green Fluorescent Proteins;Luminescent Proteins;Dystrophin;Brain;Cells, Cultured;Animals;Flow Cytometry;Mesoderm;Research Support, U.S. Gov't, P.H.S.;DNA;Liver;Tissue Distribution;Transfection;Cell Transplantation;Spleen;11 Glia;Mice, Inbred NOD;Retroviridae;Bone Marrow Cells;Dose-Response Relationship, Drug;Antineoplastic Agents;Mutation, Missense;Recombinant Fusion Proteins;Mice;Stem Cells;Lung;Humans;Carmustine;Drug Resistance, Multiple},
	Medline = {21528902},
	Month = {10},
	Nlm_Id = {100892915},
	Number = {5},
	Organization = {Department of Medicine, Case Western Reserve University, Ireland Cancer Center of University Hospitals of Cleveland, OH 44106, USA.},
	Pages = {691-701},
	Pubmed = {11672516},
	Title = {G156A MGMT-transduced human mesenchymal stem cells can be selectively enriched by O6-benzylguanine and BCNU},
	Uuid = {1EAE6B74-95AB-48CB-81C8-C18C507AC8B0},
	Volume = {10},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/152581601753193913}}

@article{Lee:2007,
	Abstract = {Activated microglia are thought to undergo apoptosis as a self-regulatory mechanism. To better understand molecular mechanisms of the microglial apoptosis, apoptosis-resistant variants of microglial cells were selected and characterized. The expression of lipocalin 2 (lcn2) was significantly down-regulated in the microglial cells that were resistant to NO-induced apoptosis. lcn2 expression was increased by inflammatory stimuli in microglia. The stable expression of lcn2 as well as the addition of rLCN2 protein augmented the sensitivity of microglia to the NO-induced apoptosis, while knockdown of lcn2 expression using short hairpin RNA attenuated the cell death. Microglial cells with increased lcn2 expression were more sensitive to other cytotoxic agents as well. Thus, inflammatory activation of microglia may lead to up-regulation of lcn2 expression, which sensitizes microglia to the self-regulatory apoptosis. Additionally, the stable expression of lcn2 in BV-2 microglia cells induced a morphological change of the cells into the round shape with a loss of processes. Treatment of primary microglia cultures with the rLCN2 protein also induced the deramification of microglia. The deramification of microglia was closely related with the apoptosis-prone phenotype, because other deramification-inducing agents such as cAMP-elevating agent forskolin, ATP, and calcium ionophore also rendered microglia more sensitive to cell death. Taken together, our results suggest that activated microglia may secrete LCN2 protein, which act in an autocrine manner to sensitize microglia to the self-regulatory apoptosis and to endow microglia with an amoeboid form, a canonical morphology of activated microglia in vivo.},
	Author = {Lee, Shinrye and Lee, Jayoung and Kim, Sangseop and Park, Jae-Yong Y. and Lee, Won-Ha H. and Mori, Kiyoshi and Kim, Sang-Hyun H. and Kim, In Kyeom and Suk, Kyoungho},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {research support, non-u.s. gov't;11 Glia;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {2985117R},
	Number = {5},
	Organization = {Department of Pharmacology, Kyungpook National University School of Medicine, 101 Dong-in, Joong-gu, Daegu 700-422, Korea.},
	Pages = {3231-41},
	Pii = {179/5/3231},
	Pubmed = {17709539},
	Title = {A dual role of lipocalin 2 in the apoptosis and deramification of activated microglia},
	Uuid = {5CB0A68B-EA0E-4FA4-A92A-5E27D5AF0DD9},
	Volume = {179},
	Year = {2007}}

@article{Lee:2002a,
	Abstract = {The adult brain contains small populations of neural precursor cells (NPC) that can give rise to new neurons and glia, and may play important roles in learning and memory, and recovery from injury. Growth factors can influence the proliferation, differentiation and survival of NPC, and may mediate responses of NPC to injury and environmental stimuli such as enriched environments and physical activity. We now report that neurotrophin expression and neurogenesis can be modified by a change in diet. When adult mice are maintained on a dietary restriction (DR) feeding regimen, numbers of newly generated cells in the dentate gyrus of the hippocampus are increased, apparently as the result of increased cell survival. The new cells exhibit phenotypes of neurons and astrocytes. Levels of expression of brain- derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are increased by DR, while levels of expression of high-affinity receptors for these neurotrophins (trkB and trkC) are unchanged. In addition, DR increases the ratio of full-length trkB to truncated trkB in the hippocampus. The ability of a change in diet to stimulate neurotrophin expression and enhance neurogenesis has important implications for dietary modification of neuroplasticity and responses of the brain to injury and disease.},
	Author = {Lee, J. and Seroogy, K. B. and Mattson, M. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurochem},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {3},
	Organization = {Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center Baltimore, Maryland 21224, USA.},
	Pages = {539-47.},
	Title = {Dietary restriction enhances neurotrophin expression and neurogenesis in the hippocampus of adult mice},
	Uuid = {EC1ED654-A87C-413B-820C-7C833D23C933},
	Volume = {80},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11905999}}

@article{Lee:2006,
	Abstract = {After brain injury, neuroblast cells from the subventricular zone (SVZ) expand and migrate toward damaged tissue. The mechanisms that mediate these neurogenic and migratory responses remain to be fully dissected. Here, we show that bromodeoxyuridine-labeled and doublecortin-positive cells from the SVZ colocalize with the extracellular protease matrix metalloproteinase-9 (MMP-9) during the 2 week recovery period after transient focal cerebral ischemia in mice. Treatment with the broad spectrum MMP inhibitor GM6001 significantly decreases the migration of doublecortin-positive cells that extend from the SVZ into the striatum. These data suggest that MMPs are involved in endogenous mechanisms of neurogenic migration as the brain seeks to heal itself after injury.},
	Author = {Lee, Seong-Ryong R. and Kim, Hahn-Young Y. and Rogowska, Jadwiga and Zhao, Bing-Qiao Q. and Bhide, Pradeep and Parent, Jack M. and Lo, Eng H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {13},
	Organization = {Department of Neurology and Radiology, Massachusetts General Hospital, Boston, Massachusetts 02129, USA.},
	Pages = {3491-5},
	Pii = {26/13/3491},
	Pubmed = {16571756},
	Title = {Involvement of matrix metalloproteinase in neuroblast cell migration from the subventricular zone after stroke},
	Uuid = {596A2651-E881-4E98-8357-36465C0FA116},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4085-05.2006}}

@article{Lee:2000a,
	Abstract = {Endogenous calcium binding ratios (kappaS) in dendrites of cultured hippocampal neurons were estimated according to the single compartment model for transients in intracellular Ca2+ concentration ([Ca2+]). In addition, the electrophysiological characteristics of neurons were classified by their autaptic currents and intrinsic firing patterns. These data were analysed in order to determine whether a correlation between Ca2+ buffers and electrophysiological type exists. Ca2+ binding ratios of endogenous buffers were estimated by eliciting [Ca2+] transients with short depolarizations, while cells were loaded with fura-2. Two types of estimates could be obtained: one termed kappaS(tau), based on analysing time constants (tau) of [Ca2+] transients, and another termed kappaS(dCa), derived from an analysis of initial amplitudes of [Ca2+] transients. Values for kappaS(tau) and kappaS(dCa) were estimated as 57 +/- 10 (mean +/- s.d., n = 10) and 60 +/- 14 (n = 10), respectively, in excitatory neurons, and 130 +/- 50 (n = 11) and 150 +/- 70 (n = 11), respectively, in inhibitory neurons. The kappaS values of excitatory and inhibitory cells were significantly different from each other, regardless of the measurement method (Student's t test, P < 0.01). However, there was no significant difference in kappaS between the groups classified according to firing patterns. Although kappaS(tau) values were well matched to those of kappaS(dCa) in most excitatory cells, the two values did not agree in three out of the fourteen inhibitory cells investigated. In these cells, the first few [Ca2+] transients after obtaining the whole cell configuration displayed a double exponential decay, suggesting that buffers with slow binding kinetics, such as parvalbumin, are involved. This hypothesis is further explored in an accompanying paper.},
	Author = {Lee, S. H. and Rosenmund, C. and Schwaller, B. and Neher, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0022-3751},
	Journal = {J Physiol},
	Keywords = {Neurons;Dendrites;Cell Compartmentation;21 Neurophysiology;Kinetics;Hippocampus;research support, non-u.s. gov't ;Immunohistochemistry;Models, Neurological;21 Calcium imaging;Calcium;Rats;Animals;comparative study ;24 Pubmed search results 2008;Buffers;Cells, Cultured},
	Month = {6},
	Nlm_Id = {0266262},
	Organization = {Max Planck Institute for Biophysical Chemistry, Department of Membrane Biophysics, D-37077 Gottingen, Germany.},
	Pages = {405-18},
	Pii = {PHY_9975},
	Pubmed = {10835043},
	Title = {Differences in Ca2+ buffering properties between excitatory and inhibitory hippocampal neurons from the rat},
	Uuid = {32C55380-96F5-411F-827E-DAD995F2BC7C},
	Volume = {525 Pt 2},
	Year = {2000},
	url = {papers/Lee_JPhysiol2000.pdf}}

@article{Lehmann:2005,
	Abstract = {The proliferation and survival of new cells in the dentate gyrus of mammals is a complex process that is subject to numerous influences, presenting a confusing picture. We suggest regarding these processes on the level of small networks, which can be simulated in silico and which illustrate in a nutshell the influences that proliferating cells exert on plasticity and the conditions they require for survival. Beyond the insights gained by this consideration, we review the available literature on factors that regulate cell proliferation and neurogenesis in the dentate gyrus in vivo. It turns out that the rate of cell proliferation and excitatory afferents via the perforant path interactively determine cell survival, such that the best network stability is achieved when either of the two is increased whereas concurrent activation of the two factors lowers cell survival rates. Consequently, the mitotic activity is regulated by systemic parameters in compliance with the hippocampal network's requirements. The resulting neurogenesis, in contrast, depends on local factors, i.e. the activity flow within the network. In the process of cell differentiation and survival, each cell's spectrum of afferent and efferent connections decides whether it will integrate into the network or undergo apoptosis, and it is the current neuronal activity which determines the synaptic spectrum. We believe that this framework will help explain the biology of dentate cell proliferation and provide a basis for future research hypotheses.},
	Author = {Lehmann, Konrad and Butz, Markus and Teuchert-Noodt, Gertraud},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {8918110},
	Number = {12},
	Organization = {Department Neuroanatomy, Fac. Biology, University of Bielefeld, PO Box 100131, 33501 Bielefeld, Germany. Konrad.Lehmann\@uni-bielefeld.de},
	Pages = {3205-16},
	Pii = {EJN4156},
	Pubmed = {16026459},
	Title = {Offer and demand: proliferation and survival of neurons in the dentate gyrus},
	Uuid = {2491E0E2-EC2B-48D8-9117-6D550B81E16C},
	Volume = {21},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2005.04156.x}}

@article{Lehnardt:2003,
	Abstract = {Innate immunity is an evolutionarily ancient system that provides organisms with immediately available defense mechanisms through recognition of pathogen-associated molecular patterns. We show that in the CNS, specific activation of innate immunity through a Toll-like receptor 4 (TLR4)-dependent pathway leads to neurodegeneration. We identify microglia as the major lipopolysaccharide (LPS)-responsive cell in the CNS. TLR4 activation leads to extensive neuronal death in vitro that depends on the presence of microglia. LPS leads to dramatic neuronal loss in cultures prepared from wild-type mice but does not induce neuronal injury in CNS cultures derived from tlr4 mutant mice. In an in vivo model of neurodegeneration, stimulating the innate immune response with LPS converts a subthreshold hypoxic-ischemic insult from no discernable neuronal injury to severe axonal and neuronal loss. In contrast, animals bearing a loss-of-function mutation in the tlr4 gene are resistant to neuronal injury in the same model. The present study demonstrates a mechanistic link among innate immunity, TLRs, and neurodegeneration.},
	Author = {Lehnardt, Seija and Massillon, Leon and Follett, Pamela and Jensen, Frances E. and Ratan, Rajiv and Rosenberg, Paul A. and Volpe, Joseph J. and Vartanian, Timothy},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Mice, Inbred BALB C;Nerve Degeneration;Bystander Effect;Animals;Coculture Techniques;Rats;Ganglia, Spinal;Apoptosis;Microglia;Mice, Inbred C3H;Rats, Sprague-Dawley;Lipopolysaccharides;Hypoxia-Ischemia, Brain;11 Glia;Antigens, CD14;14 Immune;Spinal Cord;Research Support, U.S. Gov't, P.H.S.;Chick Embryo;Cerebral Cortex;Neurons;Mice;24 Pubmed search results 2008;Immunity, Natural;Research Support, Non-U.S. Gov't},
	Medline = {22735862},
	Month = {7},
	Nlm_Id = {7505876},
	Number = {14},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {8514-9},
	Pii = {1432609100},
	Pubmed = {12824464},
	Title = {Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway},
	Uuid = {1F636BBD-71DF-4BAC-9CD5-301D41E442FF},
	Volume = {100},
	Year = {2003},
	url = {papers/Lehnardt_ProcNatlAcadSciUSA2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.1432609100}}

@article{Leimig:2002,
	Abstract = {Protective protein/cathepsin A (PPCA), a lysosomal carboxypeptidase, is deficient in the neurodegenerative lysosomal disorder galactosialidosis (GS). PPCA(-/-) mice display a disease course similar to that of severe human GS, resulting in nephropathy, ataxia, and premature death. Bone marrow transplantation (BMT) in mutant animals using transgenic BM overexpressing the corrective enzyme in either erythroid cells or monocytes/macrophages has proven effective for the improvement of the phenotype, and encouraged the use of genetically modified BM cells for ex vivo gene therapy of GS. Here, we established stable donor hematopoiesis in PPCA(-/-) mice that received hematopoietic progenitors transduced with a murine stem cell virus (MSCV)-based, bicistronic retroviral vector overexpressing PPCA and the green fluorescent protein (GFP) marker. We observed complete correction of the disease phenotype in the systemic organs up to 10 months after transplantation. PPCA(+) BM-derived cells were detected in all tissues, with the highest expression in liver, spleen, BM, thymus, and lung. In addition, a lysosomal immunostaining was seen in nonhematopoietic cells, indicating efficient uptake of the corrective protein by these cells and cross-correction. Expression in the brain occurred throughout the parenchyma but was mainly localized on perivascular areas. However, PPCA expression in the central nervous system was apparently sufficient to delay the onset of Purkinje cell degeneration and to correct the ataxia. The long-term expression and internalization of the PPCA by cells of systemic organs and the clear improvement of the neurologic phenotype support the use of this approach for the treatment of GS in humans. (Blood. 2002;99:3169-3178)},
	Author = {Leimig, Thasia and Mann, Linda and Martin, Maria del Pilar e. l. . P. and Bonten, Erik and Persons, Derek and Knowles, James and Allay, James A. and Cunningham, John and Nienhuis, Arthur W. and Smeyne, Richard and d'Azzo, Alessandra},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Neuraminidase;Ataxia;Tissue Distribution;beta-Galactosidase;Animals;Carboxypeptidase C;Treatment Outcome;Lysosomal Storage Diseases;Central Nervous System Diseases;Mucolipidoses;11 Glia;Green Fluorescent Proteins;Hematopoietic Stem Cell Transplantation;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Mice, Knockout;Organ Specificity;Carboxypeptidases;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Kidney Diseases;Research Support, Non-U.S. Gov't},
	Medline = {21961532},
	Month = {5},
	Nlm_Id = {7603509},
	Number = {9},
	Organization = {St Jude Children's Research Hospital, Memphis, TN 38105, USA.},
	Pages = {3169-78},
	Pubmed = {11964280},
	Title = {Functional amelioration of murine galactosialidosis by genetically modified bone marrow hematopoietic progenitor cells},
	Uuid = {157BF097-6CC7-4EB4-82DE-E904BE775A25},
	Volume = {99},
	Year = {2002}}

@article{Lemasson:2005,
	Abstract = {In mammals, the olfactory bulb (OB) constitutes one of two regions of the postnatal brain with continuous neurogenesis throughout life. Despite intense explorations of neuronal replacement in the adult OB, little is known about the mechanisms that operate at earlier postnatal stages. This question is particularly pertinent, because the majority of local interneurons are born in the neonate, when olfaction controls vital functions. Here, we analyzed the recruitment of newborn cells to the granule cell (GC) layer (GCL) and found that the postnatal mouse OB is supplied with two spatiotemporally distinct populations of newborn interneurons. Early born [postnatal day 3 (P3) to P7] GCs constitute a threefold larger population compared with those generated later (P14-P60), and some of them are produced locally within the OB itself. Newborn interneurons generated at P3-P7 were predominantly targeted to the external edge of the GCL, whereas newly generated cells were positioned deeper in older mice. Additionally, although approximately 50\%of adult newborn cells were eliminated within a few weeks of reaching the OB, almost the entire population of early born GCs survived until adulthood. Importantly, early olfactory experience specifically modifies the number of newborn GCs in neonates but leaves unaltered the amount of neurons generated during adulthood. Together, these results demonstrate that early postnatal neurogenesis endows the neonate bulbar circuit with newborn GCs that differ morphologically and functionally from those produced in the adult.},
	Author = {Lemasson, Morgane and Saghatelyan, Armen and Olivo-Marin, Jean-Christophe C. and Lledo, Pierre-Marie M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration;13 Olfactory bulb anatomy},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {29},
	Organization = {Laboratory of Perception and Memory, Centre National de la Recherche Scientifique, Unit{\'e} de Recherche Associ{\'e}e 2182, Pasteur Institute, 75724 Paris Cedex 15, France.},
	Pages = {6816-25},
	Pii = {25/29/6816},
	Pubmed = {16033891},
	Title = {Neonatal and adult neurogenesis provide two distinct populations of newborn neurons to the mouse olfactory bulb},
	Uuid = {06ECAA00-B357-4FA4-9E7B-8083D364E5BB},
	Volume = {25},
	Year = {2005},
	url = {papers/Lemasson_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1114-05.2005}}

@article{Lemkine:2005,
	Abstract = {Thyroid hormones (TH) are essential for brain development. However, information on if and how this key endocrine factor affects adult neurogenesis is fragmentary. We thus investigated the effects of TH on proliferation and apoptosis of stem cells in the subventricular zone (SVZ), as well as on migration of transgene-tagged neuroblasts out of the stem cell niche. Hypothyroidism significantly reduced all three of these processes, inhibiting generation of new cells. To determine the mechanisms relaying TH action in the SVZ, we analyzed which receptor was implicated and whether the effects were played out directly at the level of the stem cell population. The alpha TH receptor (TRalpha), but not TRbeta, was found to be expressed in nestin positive progenitor cells of the SVZ. Further, use of TRalpha mutant mice showed TRalpha to be required to maintain full proliferative activity. Finally, a direct TH transcriptional effect, not mediated through other cell populations, was revealed by targeted gene transfer to stem cells in vivo. Indeed, TH directly modulated transcription from the c-myc promoter reporter construct containing a functional TH response element containing TRE but not from a mutated TRE sequence. We conclude that liganded-TRalpha is critical for neurogenesis in the adult mammalian brain.},
	Author = {Lemkine, and Raji, and Alfama, and Turque, and Hassani, and Alegria-Pr{\'e}vot, and Samarut, and Levi, and Demeneix,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8804484},
	Pii = {04-2916fje},
	Pubmed = {15728663},
	Title = {Adult neural stem cell cycling in vivo requires thyroid hormone and its alpha receptor},
	Uuid = {B998329D-CA79-476C-85CB-01E9527A0121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.04-2916fje}}

@article{Lendahl:1990,
	Abstract = {Multipotential CNS stem cells receive and implement instructions governing differentiation to diverse neuronal and glial fates. Exploration of the mechanisms generating the many cell types of the brain depends crucially on markers identifying the stem cell state. We describe a gene whose expression distinguishes the stem cells from the more differentiated cells in the neural tube. This gene was named nestin because it is specifically expressed in neuroepithelial stem cells. The predicted amino acid sequence of the nestin gene product shows that nestin defines a distinct sixth class of intermediate filament protein. These observations extend a model in which transitions in intermediate filament gene expression reflect major steps in the pathway of neural differentiation.},
	Author = {Lendahl, U. and Zimmerman, L. B. and McKay, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Research Support, Non-U.S. Gov't;10 Development;Cell Differentiation;10 Hippocampus;Animals;RNA;Base Sequence;Rats;Cloning, Molecular;Comparative Study;Genes;Gene Library;Genetic Vectors;Cell Line;Research Support, U.S. Gov't, P.H.S.;Blotting, Northern;Intermediate Filament Proteins;Nucleotide Mapping;Amino Acid Sequence;Molecular Sequence Data;Nerve Tissue Proteins;Gene Expression;Sequence Homology, Nucleic Acid;Central Nervous System},
	Medline = {90150286},
	Month = {2},
	Nlm_Id = {0413066},
	Number = {4},
	Organization = {Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02142.},
	Pages = {585-95},
	Pii = {0092-8674(90)90662-X},
	Pubmed = {1689217},
	Title = {CNS stem cells express a new class of intermediate filament protein},
	Uuid = {4380AEEE-7FED-11DA-9A2D-000D9346EC2A},
	Volume = {60},
	Year = {1990}}

@article{Lennington:2003,
	Abstract = {Presumably, the 'hard-wired'neuronal circuitry of the adult brain dissuades addition of new neurons, which could potentially disrupt existing circuits. This is borne out by the fact that, in general, new neurons are not produced in the mature brain. However, recent studies have established that the adult brain does maintain discrete regions of neurogenesis from which new neurons migrate and become incorporated into the functional circuitry of the brain. These neurogenic zones appear to be vestiges of the original developmental program that initiates brain formation. The largest of these germinal regions in the adult brain is the subventricular zone (SVZ), which lines the lateral walls of the lateral ventricles. Neural stem cells produce neuroblasts that migrate from the SVZ along a discrete pathway, the rostral migratory stream, into the olfactory bulb where they form mature neurons involved in the sense of smell. The subgranular layer (SGL) of the hippocampal dentate gyrus is another neurogenic region; new SGL neurons migrate only a short distance and differentiate into hippocampal granule cells. Here, we discuss the surprising finding of neural stem cells in the adult brain and the molecular mechanisms that regulate adult neurogenesis. 1477-7827 Journal article},
	Author = {Lennington, J. B. and Yang, Z. and Conover, J. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Reprod Biol Endocrinol},
	Keywords = {02 Adult neurogenesis migration;BB pdf;03 Adult neurogenesis progenitor source},
	Number = {1},
	Organization = {Center for Regenerative Biology and the Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269, USA. joanne.conover\@uconn.edu},
	Pages = {99},
	Pubmed = {14614786},
	Title = {Neural stem cells and the regulation of adult neurogenesis},
	Uuid = {D8AFEBAB-31FF-4F2C-8889-48B3DC1027D7},
	Volume = {1},
	Year = {2003},
	url = {papers/Lennington_ReprodBiolEndocrinol2003.pdf}}

@article{Leonardi-Essmann:2005,
	Abstract = {Fractalkine is the only known member of the CX(3)C-chemokine family, and so is its receptor CX(3)CR1. Fractalkine, typically is expressed by neurons where it is inserted in the plasma membrane ("chemokine on a stalk"). It can, however, be clipped off by a specific enzyme and diffuse into the extracellular space. CX(3)CR1 is primarily expressed by microglia, the phagocytes of the brain. This study was aimed at studying gene expression changes in cultured rat microglia upon fractalkine stimulation using gene chip technology. Six genes turned out to be upregulated, amongst which milk-fat globule EGF factor-8 protein (MFG-E8) was the most surprising, but also the most revealing one. We hypothesize that it serves as a bridging molecule between apoptotic cells (neurons) and microglia. Since the docking to microglia is, in part, mediated by members of the integrin family, six of these molecules have been-post hoc-included in real-time PCR confirmations of chip results. Two of them-integrin alpha(2) and integrin beta(5)-were upregulated as well. These data provide a much closer look into molecular mechanisms involved in apoptosis of neurons and their removal by microglia.},
	Author = {Leonardi-Essmann, Fernando and Emig, Michael and Kitamura, Yoshihisa and Spanagel, Rainer and Gebicke-Haerter, Peter J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Alpha;11 Glia},
	Month = {3},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Central Institute for Mental Health, Department of Psychopharmacology, J5, 68159 Mannheim, Germany.},
	Pages = {92-101},
	Pii = {S0165-5728(04)00415-1},
	Pubmed = {15710462},
	Title = {Fractalkine-upregulated milk-fat globule EGF factor-8 protein in cultured rat microglia},
	Uuid = {D75E7423-E05A-486D-88CC-BCBC431F88C4},
	Volume = {160},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jneuroim.2004.11.012}}

@article{Leonardo:2005,
	Abstract = {Zebra finch song is represented in the high-level motor control nucleus high vocal center (HVC) (Reiner et al., 2004) as a sparse sequence of spike bursts. In contrast, the vocal organ is driven continuously by smoothly varying muscle control signals. To investigate how the sparse HVC code is transformed into continuous vocal patterns, we recorded in the singing zebra finch from populations of neurons in the robust nucleus of arcopallium (RA), a premotor area intermediate between HVC and the motor neurons. We found that highly similar song elements are typically produced by different RA ensembles. Furthermore, although the song is modulated on a wide range of time scales (10-100 ms), patterns of neural activity in RA change only on a short time scale (5-10 ms). We suggest that song is driven by a dynamic circuit that operates on a single underlying clock, and that the large convergence of RA neurons to vocal control muscles results in a many-to-one mapping of RA activity to song structure. This permits rapidly changing RA ensembles to drive both fast and slow acoustic modulations, thereby transforming the sparse HVC code into a continuous vocal pattern.},
	Author = {Leonardo, Anthony and Fee, Michale S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Muscles;research support, n.i.h., extramural ;Finches;Animals;Neural Pathways;Sound Spectrography;research support, u.s. gov't, p.h.s. ;research support, u.s. gov't, non-p.h.s. ;Brain;Time Factors;Male;research support, non-u.s. gov't ;Vocalization, Animal;Action Potentials;21 Neurophysiology;Neurons;24 Pubmed search results 2008;Models, Neurological},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {3},
	Organization = {McGovern Institute and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.},
	Pages = {652-61},
	Pii = {25/3/652},
	Pubmed = {15659602},
	Title = {Ensemble coding of vocal control in birdsong},
	Uuid = {FC693F50-C685-40AC-956D-675B22DD57FC},
	Volume = {25},
	Year = {2005},
	url = {papers/Leonardo_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3036-04.2005}}

@article{Leonhard:2002,
	Abstract = {Resident macrophages of the peripheral nervous system have recently been shown to respond rapidly to Wallerian degeneration before the influx of blood-derived macrophages. Because resident endoneurial macrophages are slowly but incompletely exchanged from the blood within 3 months, they could potentially comprise a heterogenous cell population consisting of long-term resident cells and more mobile cells undergoing turnover. We used bone marrow chimeric mice created by transplanting bone marrow from green fluorescent protein-transgenic mice into irradiated wildtype recipients to selectively analyse the response of these two resident macrophage populations to Wallerian degeneration in sciatic nerve explant cultures. In such nerves, recently immigrated macrophages exhibit green fluorescence whereas long-term resident macrophages do not. Studies in cultures from wildtype controls revealed rapid morphological changes of resident macrophages towards a bloated phenotype, a proliferative response resulting in a 3.7-fold increase of macrophage numbers over 2 weeks, and phagocytosis of myelin basic protein-immunoreactive myelin debris. When chimeric mice were analysed, both populations of resident endoneurial macrophages participated in morphological transformation, proliferation and phagocytosis. Quantitative studies revealed a stronger proliferative and phagocytic response in long-term resident endoneurial macrophages compared with recently immigrated macrophages. Our results point towards subtle, but not principal, differences between the two macrophage populations, which might indicate different stages of macrophage differentiation rather than the existence of entirely distinct endoneurial macrophage populations. The results further underline the versatility of resident endoneurial macrophages following peripheral nerve injury, which is reminiscent of the lesion response of microglial cells within the brain.},
	Author = {Leonhard, Christine and M{\"u}ller, Marcus and Hickey, William F. and Ringelstein, Erich B. and Kiefer, Reinhard},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Peripheral Nerves;Cell Differentiation;Animals;Phagocytosis;Macrophages;Bone Marrow Transplantation;Cell Count;Mice, Transgenic;Sciatic Nerve;Cell Movement;11 Glia;Organ Culture Techniques;Time Factors;Transplantation Chimera;Wallerian Degeneration;Mice;Cell Division;Immunohistochemistry;Histocompatibility Antigens Class II;Research Support, Non-U.S. Gov't},
	Medline = {22318903},
	Month = {11},
	Nlm_Id = {8918110},
	Number = {9},
	Organization = {Department of Neurology, Universit{\"a}tsklinikum M{\"u}nster, Albert-Schweitzer-Str. 33, D-48129 M{\"u}nster, Germany.},
	Pages = {1654-60},
	Pii = {2236},
	Pubmed = {12431217},
	Title = {Lesion response of long-term and recently immigrated resident endoneurial macrophages in peripheral nerve explant cultures from bone marrow chimeric mice},
	Uuid = {6675E6E0-52CA-486C-A687-D0C7C85BD1B8},
	Volume = {16},
	Year = {2002}}

@article{Lerner-Tung:1995,
	Abstract = {Human endogenous retroviral sequences recently have been shown to be associated with breast cancer and some leukemias. These retroviral sequences have similarities to an endogenous retrovirus expressed in guinea pigs. The conditions for activation of this guinea pig retrovirus (GPRV) in cultured guinea pig embryo (GPE) cells using 5-bromo-2'-deoxyuridine (BrdU) was investigated. These studies employed the reverse transcriptase activity (RT) assay and electron microscopy (EM), in conjunction with Northern blot analysis that utilized a 2.6 kb GPRV-specific cDNA probe. Contrary to published studies, dexamethasone at concentrations ranging from 10(-8) to 10(-5) M appeared to play a minimal role in enhancing the production of GPRV. Following a 6 hr incubation with BrdU, GPRV mRNA was present in cultured GPE cells. Extracellular virion release was also observed by EM 12 hr later, although RT activity was not detected. All three methods detected viral expression at 48 hr after the addition of the drug. Additionally, after 6 hr exposure to BrdU, detectable RT and mRNA levels were maintained through 44 days after the removal of BrdU in a stationary culture condition and through 31 days in cultures that were subcultured weekly in media not containing BrdU. Low levels of extracellular viruses were detected in these cultures by electron microscopy through 49 days. Therefore, after only a 6 hr exposure to BrdU was extracellular GPRV detected 12 hr after drug removal and virus production continued for up to 49 days. This study provides information about an animal endogenous retroviral system that may be used as a model for the study of human endogenous retroviruses.},
	Author = {Lerner-Tung, M. B. and Doong, S. L. and Cheng, Y. C. and Hsiung, G. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0920-8569},
	Journal = {Virus Genes},
	Keywords = {15 ERVs retroelements;15 Retrovirus mechanism;24 Pubmed search results 2008;Guinea Pigs;Microscopy, Electron;Retroviridae;Research Support, U.S. Gov't, P.H.S.;Research Support, U.S. Gov't, Non-P.H.S.;RNA, Viral;Dexamethasone;Virus Activation;Bromodeoxyuridine;Cells, Cultured;DNA, Complementary;Animals},
	Medline = {95320966},
	Month = {2},
	Nlm_Id = {8803967},
	Number = {3},
	Organization = {Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA.},
	Pages = {201-9},
	Pubmed = {7597799},
	Title = {Characterization of conditions for the activation of endogenous guinea pig retrovirus in cultured cells by 5-bromo-2'-deoxyuridine},
	Uuid = {833A1EEC-4326-11DB-A5D2-000D9346EC2A},
	Volume = {9},
	Year = {1995}}

@article{Levine:2004,
	Abstract = {Autophagy is the major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles. It involves the rearrangement of subcellular membranes to sequester cargo for delivery to the lysosome where the sequestered material is degraded and recycled. For many decades, it has been known that autophagy occurs in a wide range of eukaryotic organisms and in multiple different cell types during starvation, cellular and tissue remodeling, and cell death. However, until recently, the functions of autophagy in normal development were largely unknown. The identification of a set of evolutionarily conserved genes that are essential for autophagy has opened up new frontiers for deciphering the role of autophagy in diverse biological processes. In this review, we summarize our current knowledge about the molecular machinery of autophagy and the role of the autophagic machinery in eukaryotic development.},
	Author = {Levine, Beth and Klionsky, Daniel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {1534-5807},
	Journal = {Dev Cell},
	Keywords = {10 Structural plasticity;10 Development;Research Support, Non-U.S. Gov't;Protein Transport;Cell Aging;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Eukaryotic Cells;Lysosomes;review, tutorial;Cell Death;Humans;Peptide Hydrolases;Animals;review;Autophagocytosis},
	Month = {4},
	Nlm_Id = {101120028},
	Number = {4},
	Organization = {Department of Medicine, Columbia University, New York, NY 10032, USA. levine\@cancercenter.columbia.edu},
	Pages = {463-77},
	Pii = {S1534580704000991},
	Pubmed = {15068787},
	Title = {Development by self-digestion: molecular mechanisms and biological functions of autophagy},
	Uuid = {F3FC63AA-DAC6-4B9C-BF80-B35D939DE827},
	Volume = {6},
	Year = {2004}}

@article{Levison:1998,
	Abstract = {Studies using transgenic mice that overexpress ciliary neurotrophic factor (CNTF), direct injection of CNTF into brain parenchyma, and ectopic expression of CNTF by an adenoviral vector have demonstrated that CNTF activates astrocytes. Paradoxically, studies to date have failed to show an effect of CNTF on the expression of GFAP by cultured astrocytes. Therefore, the goal of this study was to use nuclear hypertrophy and GFAP expression as indices of glial activation to compare the responsiveness of forebrain type 1 and type 2 astrocytes to CNTF. As reported by others, CNTF did not increase GFAP in type 1 astrocytes; however, it rapidly increased their nuclear size by 20\%. Nuclear hypertrophy was apparent within 4 h after CNTF exposure and persisted for at least 48 h. In contrast, type 2 astrocyte GFAP increased 2-fold over the course of 48 h of CNTF treatment. During this same treatment period type 2 astroglial nuclei enlarged by 25\%. We conclude that CNTF stimulates both type 1 and type 2 astrocytes directly. Together with our in vivo studies (Levison et al., 1996: Exp. Neurol. 141: 256), these data support the concept that CNTF is responsible for many of the progressive astroglial changes that appear after CNS injury and disease. 98398397 0006-8993 Journal Article},
	Author = {Levison, S. W. and Hudgins, S. N. and Crawford, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Brain Res},
	Keywords = {Ciliary Neurotrophic Factor;Prosencephalon/cytology;Rats;Nerve Tissue Proteins/*pharmacology;G abstr;Astrocytes/*drug effects/pathology;Animal;11 Glia;Glial Fibrillary Acidic Protein/*metabolism;Nerve Growth Factors/pharmacology;Animals, Newborn;Support, Non-U.S. Gov't;Cells, Cultured;Cell Nucleus/drug effects/*pathology;Hypertrophy},
	Number = {1-2},
	Organization = {Department of Neuroscience and Anatomy, H109, Pennsylvania State University, College of Medicine, P.O. Box 850, Hershey, PA 17033, USA. slevison\@psu.edu},
	Pages = {189-93},
	Pubmed = {9729376},
	Title = {Ciliary neurotrophic factor stimulates nuclear hypertrophy and increases the GFAP content of cultured astrocytes},
	Uuid = {1851C11A-9D18-4702-AFCC-EE1BAAF8CE42},
	Volume = {803},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9729376}}

@article{Levison:2000,
	Abstract = {During development, the output of the subventricular zone (SZ) becomes increasingly restricted, yet it still harbors multipotential progenitors. The output of the SZ could be gated by selectively eliminating inappropriately specified progenitors. Using in situ end- labeling (ISEL) to identify apoptotic cells, nearly 60\%of the ISEL(+) cells in the juvenile forebrain were localized to the SZ. Of these dying cells, at least 9\%could be identified as neurons, 4\%as astrocytes, and 12\%as oligodendrocytes. The remainder were negative for the stem cell marker nestin, as well as other markers evaluated. To test the hypothesis that committed progenitors were under selective pressures, neural stem/progenitor cells were allowed to differentiate in vitro in the presence or absence of the caspase 3 inhibitor z-DEVD- fmk. DEVD increased neuronal production 10-fold over control cultures. By contrast, the development of astrocytes and oligodendrocytes was not affected. Altogether, these data support the hypothesis that selective forces within the postnatal rat forebrain control the types of precursors that emerge from the germinal matrix. Furthermore, they suggest that different mechanisms control neuronal versus glial cell numbers. Using Smart Source Parsing},
	Author = {Levison, S. W. and Rothstein, R. P. and Brazel, C. Y. and Young, G. M. and Albrecht, P. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Dev Neurosci},
	Keywords = {Cell Differentiation/drug effects;Rats;Apoptosis/*physiology;Animal;Ependyma/cytology/*physiology;02 Adult neurogenesis migration;Enzyme Inhibitors/pharmacology;Rats, Sprague-Dawley;Stem Cells/cytology/metabolism;03 Adult neurogenesis progenitor source;Cell Line;Caspases/antagonists &inhibitors;BB pdf;In Situ Nick-End Labeling;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Animals, Newborn/physiology;Neuroglia/metabolism;Neurons/cytology/metabolism;Biological Markers},
	Number = {1-2},
	Organization = {Department of Neuroscience, Pennsylvania State University College of Medicine, Hershey, Pa., USA. slevison\@psu.edu},
	Pages = {106-15},
	Title = {Selective apoptosis within the rat subependymal zone: a plausible mechanism for determining which lineages develop from neural stem cells},
	Uuid = {252D46F1-C3CE-4541-B594-5B6A10791A99},
	Volume = {22},
	Year = {2000},
	url = {papers/Levison_DevNeurosci2000}}

@article{Levison:2001,
	Abstract = {Cerebral hypoxia/ischemia of the newborn has a frequency of 4/1,000 births and remains a major cause of cerebral palsy, epilepsy, and mental retardation. Despite progress in understanding the pathogenesis of hypoxic-ischemic injury, the data are incomplete regarding the mechanisms leading to permanent brain injury. Here we tested the hypothesis that cerebral hypoxia/ischemia damages stem/progenitor cells in the subventricular zone (SVZ), resulting in a permanent depletion of oligodendrocytes. We used a widely accepted rat model and examined animals at recovery intervals ranging from 4 h to 3 weeks. Within hours after the hypoxic-ischemic insult 20\%of the total cells were deleted from the SVZ. The residual damaged cells appeared necrotic. During 48 h of recovery deaths accumulated; however, these later deaths were predominantly apoptotic. Many apoptotic SVZ cells stained with a marker for immature oligodendrocytes. At 3 weeks survival, the SVZ was smaller and markedly less cellular, and it contained less than 1/4 the normal complement of neural stem cells. The corresponding subcortical white matter was dysmyelinated, relatively devoid of oligodendrocytes and enriched in astrocytes. We conclude that neural stem cells and oligodendrocyte progenitors in the SVZ are vulnerable to hypoxia/ischemia. Consequently, the developmental production of oligodendrocytes is compromised and regeneration of damaged white matter oligodendrocytes does not occur resulting in failed regeneration of CNS myelin in periventricular loci. The resulting dysgenesis of the brain that occurs subsequent to perinatal hypoxic/ischemic injury may contribute to the cognitive and motor dysfunction that results from asphyxia of the newborn. 21481710 0378-5866 Journal Article},
	Author = {Levison, S. W. and Rothstein, R. P. and Romanko, M. J. and Snyder, M. J. and Meyers, R. L. and Vannucci, S. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Dev Neurosci},
	Keywords = {Cerebrovascular Accident/pathology;Hypoxia-Ischemia, Brain/*pathology;G abstr;Female;Rats;Apoptosis;Rats, Wistar;Animal;11 Glia;Pregnancy;Cerebral Ventricles/*embryology/pathology;Support, U.S. Gov't, P.H.S.;Cerebral Palsy/pathology;Neurons/*pathology;Oligodendroglia/*pathology;Stem Cells/*pathology},
	Number = {3},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University, College of Medicine, Hershey, Pa 17033, USA. slevison\@psu.edu},
	Pages = {234-47},
	Pubmed = {11598326},
	Title = {Hypoxia/ischemia depletes the rat perinatal subventricular zone of oligodendrocyte progenitors and neural stem cells},
	Uuid = {5A825527-5F6B-44D3-9223-75271E34B105},
	Volume = {23},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11598326}}

@article{Levison:2003,
	Abstract = {The developmental origin of microglia remains a controversial subject. While it is generally accepted that primitive fetal macrophages that migrate from the yolk sac to the brain become microglia, it also has been argued that there is a second source of microglia that are of neuroectodermal lineage. To determine whether progenitors in the dorsolateral subventricular zone (SVZDL) are capable of producing microglia as well as macroglia, we infected perinatal rat SVZDL cells with a mixture of two replication-deficient retroviruses, placed these progenitors in vitro and then varied the media formulations to promote microglial differentiation. Mixed macroglial clones were obtained, but no heterogeneous clones containing microglia were observed, regardless of the media components. Among the macroglial clones, we observed every possible combination of type 1 astrocyte and O-2A lineage cells. Some clones were homogeneous and contained cells belonging to a single macroglial lineage. Other clonal clusters were heterogeneous and were comprised of type 1 astrocytes and oligodendrocytes, type 1 and type 2 astrocytes, or type 2 astrocytes and oligodendrocytes. Of 130 clones examined, where we used triple immunofluorescence with antibodies that recognize microglia, 2 clonal clusters contained OX-42+ microglia that were retrovirally labeled, but all of the cells in those clones expressed the microglial marker and none expressed either GFAP or O4. In addition, we isolated neural stem cells from the perinatal SVZDL and assessed their capacity to generate macroglia and microglia. Confirming and extending our previous analyses, neural stem cells generated homogeneous and heterogeneous macroglial clones, but they did not generate microglia. We conclude that brain macroglia and microglia do not share a common precursor, even though the neural stem cells in the SVZDL cells can produce neurons, astrocytes and oligodendrocytes. Therefore, the microglia that reside in the SVZDL are immigrants from nonneural precursors. 0378-5866 Journal Article},
	Author = {Levison, S. W. and Druckman, S. K. and Young, G. M. and Basu, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Dev Neurosci},
	Keywords = {Glial Fibrillary Acidic Protein/metabolism;Animals;Astrocytes/*cytology;Rats;Fluorescent Antibody Technique;Genetic Vectors/administration &dosage;02 Adult neurogenesis migration;Oligodendroglia/*cytology;Stem Cells/*cytology/drug effects;11 Glia;Retroviridae;Interleukin-6/pharmacology;Injections, Intraventricular;03 Adult neurogenesis progenitor source;Brain/*cytology/growth &development;BB pdf;Cell Lineage/physiology;Membrane Glycoproteins/metabolism;Support, U.S. Gov't, P.H.S.;Cell Differentiation/physiology;Immunohistochemistry;Antigens, CD45/metabolism;Clone Cells;Microglia/*cytology/metabolism},
	Number = {2-4},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University, College of Medicine, Hershey, PA 17033, USA. slevinson\@psu.edu},
	Pages = {184-96},
	Pubmed = {12966216},
	Title = {Neural stem cells in the subventricular zone are a source of astrocytes and oligodendrocytes, but not microglia},
	Uuid = {D2D212D4-1833-401F-B110-F651D5818703},
	Volume = {25},
	Year = {2003},
	url = {papers/Levison_DevNeurosci2003.pdf}}

@article{Levison:1993,
	Abstract = {Postnatal gliogenesis in the rodent forebrain was studied by infecting subventricular zone cells of either neonates or juvenile rats with replication-deficient retroviruses that encode reporter enzymes, enabling the migration and fate of these germinal zone cells to be traced over the ensuing several weeks. Neither neonatal nor juvenile subventricular zone cells migrated substantially along the rostral-caudal axis. Neonatal subventricular zone cells migrated dorsally and laterally into hemispheric gray and white matter and became both astrocytes and oligodendrocytes. Juvenile subventricular zone cells migrated into more medial areas of the subcortical white matter and on occasion appeared in the white matter of the contralateral hemisphere, but rarely migrated into the neocortex. Juvenile subventricular zone cells almost exclusively differentiated into oligodendrocytes. Thus, the migratory patterns and the developmental fates of subventricular zone cells change during the first 2 weeks of life. When either neonatal or juvenile subventricular zone cells were labeled in vivo and then removed and cultured, some generated homogeneous clones that contained either astrocytes with a 'type 1'phenotype or oligodendrocytes, but some generated heterogeneous clones that contained both glial types. These results provide additional evidence for a common progenitor for astrocytes and oligodendrocytes and strongly suggest that temporally and spatially regulated environmental signals control the destiny of glial progenitors during postnatal development. eng Journal Article},
	Author = {Levison, S. W. and Chuang, C. and Abramson, B. J. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Development},
	Keywords = {Neuroglia/*physiology;Rats, Sprague-Dawley;G abstr;Rats;Brain/*growth &development;Time Factors;Retroviridae;Cell Differentiation/physiology;11 Glia;Animal;Support, U.S. Gov't, P.H.S.;Histocytochemistry;Oligodendroglia/physiology;Cells, Cultured;Astrocytes/physiology;Cell Movement/physiology},
	Number = {3},
	Organization = {Department of Pathology, Columbia University College of Physicians and Surgeons, New York, NY 10032.},
	Pages = {611-22.},
	Title = {The migrational patterns and developmental fates of glial precursors in the rat subventricular zone are temporally regulated},
	Uuid = {A5A23E87-BD3C-45F4-BD74-B7A17987F05D},
	Volume = {119},
	Year = {1993},
	Bdsk-Url-1 = {http://www.cob.org.uk/Development/119/03/dev4131.html}}

@article{Levison:1996,
	Abstract = {CNS trauma or disease induces a constellation of changes in the glia comprising the condition known as reactive gliosis. At present, little is known regarding the nature of the injury signals and the specific consequences of their actions. Ciliary neurotrophic factor (CNTF) induces acute phase proteins in liver and increases astrocytic glial fibrillary acidic protein (GFAP) both in vitro and in vivo. The purpose of the present study was to establish whether CNTF induces other aspects of gliosis. Between 10 and 72 h after 100 ng of recombinant human CNTF was administered into the adult rat neocortex, alterations were observed in a region extending several millimeters in circumference from the injection site. Microglia in this region were more apparent and astrocytes were hypertrophic. By in situ hybridization, mRNAs for GFAP, vimentin, and clusterin were upregulated when compared to the control hemisphere (which received heat-inactivated CNTF). By immunocytochemistry, GFAP, vimentin, glutathione-S-transferase mu, S-100, and OX-42 were elevated by 48 h. By contrast, the oligodendroglial marker GSTYp, the neuronal markers MAP-2 and NSE, the intermediate filament nestin, and the stress protein alpha B-crystallin were unchanged. In addition, a greater than twofold increase in the number of proliferating cells was observed. Since CNTF induces swelling and multiple "gliotic"genes in astrocytes, increases microglial number, and stimulates cell proliferation, we conclude that CNTF is sufficient to induce multiple aspects of gliosis. These data are consistent with a model whereby CNTF (which is synthesized by astrocytes) would be released when the integrity of the astrocyte membrane is compromised, whereupon it would elicit an inflammatory response. 96424473 0014-4886 Journal Article},
	Author = {Levison, S. W. and Ducceschi, M. H. and Young, G. M. and Wood, T. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Exp Neurol},
	Keywords = {In Situ Hybridization;Rats, Sprague-Dawley;Ciliary Neurotrophic Factor;G abstr;Human;Nerve Tissue Proteins/*pharmacology;Rats;RNA, Messenger/metabolism;Female;Autoradiography;11 Glia;Animal;Nerve Growth Factors/*pharmacology;Support, Non-U.S. Gov't;Gliosis/*chemically induced},
	Number = {2},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey 17033, USA. Slevison\@Neuro.hmc.psu.edu},
	Pages = {256-68},
	Pubmed = {8812159},
	Title = {Acute exposure to CNTF in vivo induces multiple components of reactive gliosis},
	Uuid = {2116B247-4499-4572-8FFF-174BBA8DC9CA},
	Volume = {141},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8812159}}

@article{Levison:2000a,
	Abstract = {Proliferating astrocytes are frequently observed in diseased and injured brains. These newly generated astrocytes are necessary to reestablish the barriers that isolate the CNS from the rest of the body; however, they also create a matrix that inhibits regeneration and remyelination. Therefore, it is important to understand the mechanisms that enable a terminally differentiated astrocyte to reenter the cell cycle. Ciliary neurotrophic factor (CNTF), interleukin-6 (IL-6), transforming growth factor-alpha (TGF-alpha), and fibroblastic growth factor-2 (FGF-2) are four cytokines that are rapidly elevated in damaged neural tissue. These cytokines also have been implicated in glial scar formation. We sought to determine whether IL-6 and CNTF stimulate astroglial proliferation alone or in combination with other mitogens. Intraparenchymal CNTF modestly increased the number of proliferating cell nuclear antigen (PCNA) and glial fibrillary acidic protein (GFAP) double positive astrocytes when introduced by stereotactic injection into the adult rat brain. When applied directly to highly enriched rat forebrain astrocyte cultures, neither CNTF nor IL-6-stimulated DNA synthesis. Therefore, they are not astroglial mitogens. However, both cytokines synergized with epidermal growth factor (EGF), increasing its mitogenicity by approximately twofold. Astrocytes that had been "aged"for at least 3 weeks in vitro became refractory to EGF; however, when these "aged"astrocytes were pretreated with either IL-6 or CNTF for as little as 2 h, they became competent to reenter the cell cycle upon exposure to EGF. These data suggest that IL-6 type cytokines, likely by activating STAT family transcription factors, induce the expression of signaling molecules that endow resting astrocytes with the competence to respond to mitogens and to reenter the cell cycle. 20556184 0894-1491 Journal Article},
	Author = {Levison, S. W. and Jiang, F. J. and Stoltzfus, O. K. and Ducceschi, M. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Glia},
	Keywords = {*Interleukin-6;Proliferating Cell Nuclear Antigen/analysis;Prosencephalon/cytology;Cells, Cultured;Rats;Microtubule-Associated Proteins/analysis;Ciliary Neurotrophic Factor/*pharmacology;Thymidine/pharmacokinetics;Astrocytes/chemistry/*cytology/*drug effects;Animal;Epidermal Growth Factor/*pharmacology;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein/analysis;G abstr;11 Glia;DNA/biosynthesis;Support, Non-U.S. Gov't;Tritium/diagnostic use;Fibroblast Growth Factor 2/pharmacology;Cell Division/drug effects},
	Number = {3},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA. slevison\@psu.edu},
	Pages = {328-37},
	Pubmed = {11102972},
	Title = {IL-6-type cytokines enhance epidermal growth factor-stimulated astrocyte proliferation},
	Uuid = {27010CBB-9161-40EE-84C4-7434E5BDF942},
	Volume = {32},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11102972}}

@article{Levison:1991,
	Abstract = {Studies on glial cultures have demonstrated that fetal bovine serum contains a factor that induces bipotential glial precursors known as oligodendrocyte-type 2 astrocyte (O-2A) progenitors to become type 2 astroglia rather than oligodendroglia. The goal of this research project was to characterize and purify this factor, which we refer to as the astroglia-inducing molecule (AIM). Using cultures enriched in O-2A progenitors, we determined that AIM is present in human and bovine sera and that fetal bovine serum qualified as the best serum for purifying AIM. AIM is heat and trypsin labile and may be a plasma glycoprotein. A 240-fold enriched AIM preparation was produced by applying an ammonium sulfate precipitate of fetal bovine serum to heparin and then lentil lectin-agarose, followed by gel filtration chromatography. In crude preparations, AIM activity migrated at 50 kDa by gel filtration. With enrichment, activity was seen at several molecular masses, all of which were approximate multiples of 50 kDa. Treatment with 6 M guanidine hydrochloride generated an AIM with a molecular mass between 12 and 18 kDa, a result suggesting that AIM aggregates. On a preparative isoelectric focusing gel, AIM activity most frequently migrated between pH values of 3 and 4; however, proteins with isoelectric points of greater than 9 or at 6 also had activity in several experiments. These data suggest that either multiple AIMs exist or that a single AIM exists that associates with other proteins. Immunofluorescence for ganglioside GD3 and glial fibrillary acidic protein confirmed that AIM preparations induce type 2 astroglia from O-2A progenitors and suggests that AIM has little effect on type 1 astroglia. Because none of the known growth factors that have been tested to date mimics its effects. AIM may be a novel differentiation factor. 91318280 0022-3042 Journal Article},
	Author = {Levison, S. W. and McCarthy, K. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurochem},
	Keywords = {Support, U.S. Gov't, P.H.S.;Blood Proteins/*analysis/isolation &purification/physiology;Fluorescent Antibody Technique;G abstr;Rats;Astrocytes/*cytology/drug effects;Stem Cells/*cytology/drug effects;11 Glia;Animal;Cerebral Cortex/*cytology;Cell Differentiation/drug effects/physiology;Neuroglia/*cytology/drug effects;Cells, Cultured;Isoelectric Focusing;Hydrogen-Ion Concentration;Chromatography, Gel;Serum Albumin, Bovine/pharmacology},
	Number = {3},
	Organization = {Curriculum in Neurobiology, University of North Carolina, Chapel Hill 27599-7369.},
	Pages = {782-94},
	Pubmed = {1861150},
	Title = {Characterization and partial purification of AIM: a plasma protein that induces rat cerebral type 2 astroglia from bipotential glial progenitors},
	Uuid = {B0BEA641-2721-4011-80BE-C7593F35193A},
	Volume = {57},
	Year = {1991},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1861150}}

@article{Levison:1989,
	Abstract = {Cultured rat dorsal root ganglion neurons expressed ganglioside GD3 when grown in the absence of non-neuronal cells. Among the non-neuronal cells, fibroblasts, but not Schwann cells, also stained for ganglioside GD3 during the first few days in culture. When neurons were combined with non-neuronal cells the intensity of the GD3 immunoreactive neuronal processes was diminished at sites contacted by Schwann cells. This contact-mediated effect was specific for ganglioside GD3 since no difference was seen with A2B5 or JONES antibodies, which recognize different gangliosides. 90037545 0165-5728 Journal Article},
	Author = {Levison, S. W. and McCarthy, K. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neuroimmunol},
	Keywords = {Schwann Cells/*metabolism;G abstr;Rats;Antibodies, Monoclonal;Gangliosides/*analysis;Animal;11 Glia;Sciatic Nerve/cytology;Ganglia, Spinal/cytology/*metabolism;Neurons/metabolism;Cells, Cultured;Support, U.S. Gov't, P.H.S.;Rats, Inbred Strains;Fluorescent Antibody Technique},
	Number = {3},
	Organization = {Curriculum in Neurobiology, University of North Carolina, Chapel Hill 27599.},
	Pages = {223-32},
	Pubmed = {2681262},
	Title = {Schwann cells influence the expression of ganglioside GD3 by rat dorsal root ganglion neurons},
	Uuid = {8BC486A3-69B0-4E22-A32C-EFE77307A39C},
	Volume = {24},
	Year = {1989},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2681262}}

@article{Levison:1997,
	Abstract = {Developmental studies have shown that both neurons and glia arise from the subventricular zone (SVZ) but there have been no clonal analyses to determine whether a single progenitor can produce both. Therefore, we used replication deficient retroviral vectors to analyze the clonal progeny of single rat SVZ cells that were maintained in culture media permissive or non-permissive for neuronal differentiation. When maintained in medium supplemented with 5\%fetal bovine serum, all surviving progenitors generated glial cell clones. Within these glial clones we often observed both type 1 astrocytes and O-2A lineage cells. When SVZ cells were maintained in medium permissive for neurogenesis approximately 50\%of the total clones contained at least one antigenically defined neuron. Of those clones that contained neurons, 60\%contained neurons and glia. The other 50\%of the total clones were either comprised of only astrocytes, astrocytes and oligodendrocytes, or were unidentifiable. Since the culture environment permitted multilineage clone formation, yet many homogeneous neuronal or astrocytic clones were obtained, some progenitors must become developmentally restricted while they are in the germinal zone. Therefore, we conclude that the perinatal SVZ is a mosaic of multipotential, bipotential, and lineage restricted precursors, and that the lack of postnatal neocortical neurogenesis is not due to the absence of potential neuroblasts. 97276384 0360-4012 Journal Article},
	Author = {Levison, S. W. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Cell Adhesion Molecules, Neuronal/analysis/immunology;Cerebral Ventricles/*cytology;Microtubule-Associated Proteins/analysis/immunology;Cells, Cultured;Rats;Fluorescent Antibody Technique;Vimentin/analysis/immunology;Stem Cells/chemistry/*cytology;Neurons/chemistry/*cytology;Animal;Astrocytes/chemistry/*cytology;Mammals;Rats, Sprague-Dawley;11 Glia;G abstr;Retroviridae;Oligodendroglia/chemistry/*cytology;Glial Fibrillary Acidic Protein/analysis/immunology;Animals, Newborn;Antibodies, Monoclonal;Lac Operon;Cell Lineage/physiology;Support, U.S. Gov't, P.H.S.;Cell Differentiation/physiology;Genes, Reporter;Biological Markers;Intermediate Filament Proteins/analysis/immunology},
	Number = {2},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey, USA.},
	Pages = {83-94},
	Pubmed = {9130137},
	Title = {Multipotential and lineage restricted precursors coexist in the mammalian perinatal subventricular zone},
	Uuid = {59F6AA47-E68C-42CC-B64E-B21741FD9DCF},
	Volume = {48},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9130137}}

@article{Levison:1999,
	Abstract = {Gliogenesis in the mammalian central nervous system does not cease abruptly like neurogenesis. Instead, glia accumulate over a time period that extends into adulthood. To determine whether new glial cells in the adult cortex arise from resident progenitors and to determine the glial types to which these progenitors give rise to, cells in the perinatal subventricular zone (SVZ) were labeled with replication- deficient retroviral vectors, and clonal clusters of glia in the neocortex were examined from 1 week to 8 months of age. The average clonal cluster size increased during the first month of life. Interestingly, clusters containing oligodendrocyte lineage cells preferentially expanded with age, on average doubling every 3 months. Unexpectedly, the number of cells in astrocyte clusters decreased over time. In heterogeneous clusters, the numbers of oligodendroglia increased, whereas the number of astrocytes did not. Moreover, clonal clusters containing mature glia also contained less mature cells, indicating that clonally related progenitors do not differentiate synchronously in vivo. Thus, progenitors from the SVZ continue to cycle, resulting in an accumulation of oligodendroglia in the neocortex. These slowly cycling cells likely express the NG2 proteoglycan because a subset of the clonal clusters contained NG2(+) cells and these NG2(+) cells accumulated with time.},
	Author = {Levison, S. W. and Young, G. M. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Oligodendroglia/*cytology;02 Adult neurogenesis migration;Rats, Sprague-Dawley;B-11;Rats;Clone Cells/physiology;Cell Cycle/*physiology;Animal;Support, U.S. Gov't, P.H.S.;Cell Aging/*physiology;Neocortex/*cytology;Support, Non-U.S. Gov't;Stem Cells/physiology;Cell Movement/physiology},
	Number = {4},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State College of Medicine, Hershey 17033, USA. slevison\@psu.edu},
	Pages = {435-46.},
	Title = {Cycling cells in the adult rat neocortex preferentially generate oligodendroglia},
	Uuid = {2468AEEF-692C-4C25-9A4E-359D79B53940},
	Volume = {57},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10440893}}

@article{Levison:1993a,
	Abstract = {The developmental fates of subventricular zone (SVZ) cells of the postnatal rat forebrain were determined by retroviral-mediated gene transfer and immunolabeling for glial antigens. A beta-galactosidase- containing retrovirus injected stereotactically into the SVZ infected small, immature cells. By 28 days post-injection labeled cells had appeared in both gray and white matter of the ipsilateral hemisphere. White matter contained labeled oligodendrocytes, but few astrocytes, while neocortex and striatum contained both glial types, often appearing in tightly knit clusters. An analysis after simultaneously injecting alkaline phosphatase- and beta-galactosidase-containing retroviruses showed that cells in each cortical cluster were related. Most clusters contained a single cell type, but approximately 15\%contained both astrocytes and oligodendrocytes. These observations strongly suggest that a single SVZ cell can differentiate into both glial types.},
	Author = {Levison, S. W. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Neuron},
	Keywords = {Prosencephalon/*cytology;Stereotaxic Techniques;Rats;Transfection;*Cell Differentiation;Fluorescent Antibody Technique;beta-Galactosidase/analysis/genetics;Animal;Rats, Sprague-Dawley;G abstr;11 Glia;Stem Cells/*cytology;Astrocytes/*cytology/enzymology;Retroviridae/genetics;Histocytochemistry;Support, U.S. Gov't, P.H.S.;Oligodendroglia/*cytology/enzymology;Gene Expression;Alkaline Phosphatase/analysis/genetics;Genetic Markers},
	Number = {2},
	Organization = {Department of Pathology, Columbia University College of Physicians and Surgeons, New York, New York 10032.},
	Pages = {201-12},
	Title = {Both oligodendrocytes and astrocytes develop from progenitors in the subventricular zone of postnatal rat forebrain},
	Uuid = {E7A4F69A-EE2B-11DA-8605-000D9346EC2A},
	Volume = {10},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8439409}}

@article{Lewis:1994,
	Abstract = {The human immunodeficiency virus productively infects and integrates into cells that have been arrested in the cell cycle with either gamma irradiation or aphidicolin. Integration by oncoretroviruses such as the murine leukemia virus (MuLV), on the other hand, depends on cell proliferation. Although the entire cell cycle is not necessary for MuLV infection, it is essential that the infected cells pass through mitosis. The long terminal repeat circle junction, a marker for nuclear entry, is first observed in MuLV-infected cells immediately after mitosis. These results suggest that mitosis is necessary for nuclear entry of MuLV, but not human immunodeficiency virus, unintegrated proviral DNA.},
	Author = {Lewis, P. F. and Emerman, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Base Sequence;HIV-1;DNA, Circular;Research Support, Non-U.S. Gov't;S Phase;Comparative Study;Molecular Sequence Data;Research Support, U.S. Gov't, P.H.S.;Hela Cells;Aphidicolin;DNA, Viral;Mitosis;DNA, Complementary;Humans;15 Retrovirus mechanism;Leukemia Virus, Murine;Genetic Vectors},
	Medline = {94076446},
	Month = {1},
	Nlm_Id = {0113724},
	Number = {1},
	Organization = {Department of Pediatrics, University of Washington, Seattle.},
	Pages = {510-6},
	Pubmed = {8254763},
	Title = {Passage through mitosis is required for oncoretroviruses but not for the human immunodeficiency virus},
	Uuid = {E18BE20E-DFC2-11DA-AC55-000D9346EC2A},
	Volume = {68},
	Year = {1994}}

@article{Lewis:2005,
	Abstract = {PURPOSE: To compare the activation of microglia in response to retinal detachment in four species. METHODS: Experimental detachments were created in cats, rabbits, and ground squirrels and the retinas harvested 1, 3, 7, or 28 days later. Retinal reattachments of 28 days in duration were also performed in cats following a 3-day detachment. Human tissue was obtained during reattachment surgery. Microglia and macrophages were labeled with the lectins Griffonia simplicifolia and Ricinus communis and the antibody CD11b. M{\"u}ller cell and photoreceptor responses were followed immunocytochemically on the same tissue sections labeled with microglial markers. Images were collected by laser scanning confocal microscopy. RESULTS: Lightly labeled microglia were observed primarily in the inner retina of control tissue. In the cat and rabbit, a progressive increase in the number of labeled cells occurred in the outer retina beginning at 1 day of detachment. In both long term human and cat detachments numbers of microglia were elevated throughout the retina. This is in contrast to the rabbit and ground squirrel retinas where microglial activation was dramatically diminished in longer term detachments. Presumptive macrophages (anti-CD11b labeled cells) occurred only in the subretinal space. Retinal reattachment in cats significantly attenuated the response except in areas of poor outer segment regeneration. CONCLUSIONS: The robust microglial response to retinal detachment is an indicator of the importance of this cell type in the overall response of the retina. Our data suggest that the feline retina is a particularly appropriate model system for understanding this response in humans. Inhibiting the microglial response in that species should help us understand more precisely its potential role in photoreceptor survival in human pathology.},
	Author = {Lewis, Geoffrey P. and Sethi, Charanjit S. and Carter, Katrina M. and Charteris, David G. and Fisher, Steven K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {1090-0535},
	Journal = {Mol Vis},
	Keywords = {11 Glia},
	Month = {7},
	Nlm_Id = {9605351},
	Organization = {Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA.},
	Pages = {491-500},
	Pii = {v11/a57},
	Pubmed = {16052164},
	Title = {Microglial cell activation following retinal detachment: a comparison between species},
	Uuid = {E569CAA8-956E-4981-8D8A-7FD5BB4714D1},
	Volume = {11},
	Year = {2005}}

@article{Li:1995,
	Abstract = {In situ presence of numerous DNA strand breaks is a typical feature of apoptotic cells. Selective DNA strand break induction by photolysis (SBIP) at sites that contain incorporated halogenated DNA precursors has recently been proposed as a method of analysing DNA replication. Detection of DNA strand breaks, thus, enables one to identify apoptotic and/or DNA replicating cells. The current methods for DNA strand break labelling rely on the use of exogenous terminal deoxynucleotidyl transferase which either directly attaches the fluorochrome conjugated triphosphodeoxynucleotides to 3'OH ends in the breaks, or indirectly labels 3'OH ends with digoxygenin or biotin conjugated triphosphodeoxynucleotides. A limitation of these methodologies, especially restricting their routine application in the clinic, is high cost of reagents. In the present study we have tested whether relatively simple compound BrdUTP, which is approximately three orders of magnitude less expensive than dUTP conjugated to digoxygenin, can be used as marker of DNA strand breaks. Apoptosis of HL-60 cells was induced by DNA topoisomerase I inhibitor camptothecin. The incorporated BrdUTP was detected by fluoresceinated anti-BrdUrd MoAb. Cellular fluorescence was measured by flow cytometry as well as by Laser Scanning Cytometer (LSC). The data show that intensity of DNA strand break labelling with BrdUTP was nearly four- and two-fold higher than that obtained with the indirect labelling using biotin- or digoxygenin-conjugated dUTP, respectively, and over eight-fold higher than in the case of direct labelling with the fluorochrome (fluorescein or BODIPY)-conjugated deoxynucleotides. The increased labelling of DNA strand breaks with BrdUTP may reflect more efficient incorporation of this precursor by terminal transferase, compared to the nucleotides with bulky fluorochrome conjugates. DNA strand break labelling with BrdUTP, thus, offers a possibility of more sensitive (and at lower cost) detection of apoptotic or DNA replicating cells, compared to the alternative methods of DNA strand break labelling.},
	Author = {Li, X. and Darzynkiewicz, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0960-7722},
	Journal = {Cell Prolif},
	Keywords = {23 dNTPs-Brdu;Fluorescent Dyes;Humans;DNA Topoisomerases, Type I;Cell Cycle;Sensitivity and Specificity;Apoptosis;23 Technique;Boron Compounds;Fluorescein-5-isothiocyanate;Research Support, U.S. Gov't, P.H.S.;Camptothecin;DNA Damage;Cell Division;Deoxyuracil Nucleotides;Biological Markers;HL-60 Cells;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {96150267},
	Month = {11},
	Nlm_Id = {9105195},
	Number = {11},
	Organization = {Cancer Research Institute, New York Medical College, Valhalla 10523, USA.},
	Pages = {571-9},
	Pubmed = {8555370},
	Title = {Labelling DNA strand breaks with BrdUTP. Detection of apoptosis and cell proliferation},
	Uuid = {A4A6DE04-1683-41AD-BE98-3E978C95CBB3},
	Volume = {28},
	Year = {1995}}

@article{Li:2000,
	Abstract = {Bone morphogenetic proteins (BMPs) trigger neuronal differentiation of neocortical precursors within the ventricular zone (VZ) [Li et al. (1998): J Neurosci 18:8853-8862]. BMP-2/4 protein is concentrated at the VZ surface and BMPs rapidly promote the differentiation of neocortical precursors in both dissociated cell and explant cultures. Noggin binds to BMP-2/4 with high affinity, and prevents binding to cell surface receptors. In the present study, we used human recombinant noggin protein to determine whether endogenous BMP-2/4 triggers neuronal differentiation in dissociated cell culture. We find that noggin inhibits the differentiation of neocortical neurons: noggin decreases the number of MAP-2- and TUJ1-positive cells after 24 h of treatment, yet has no effect on either proliferation or cell survival. Noggin also significantly decreases neurite growth of MAP-2-positive cells. In addition, using Western blot analysis we show that noggin protein is present in developing cortex at E15. These results are consistent with previous results showing that endogenous BMPs trigger neuronal differentiation in the neocortical VZ and also indicate that a balance of noggin and BMP may regulate the differentiation of neocortical neurons in vivo.},
	Author = {Li, W. and LoTurco, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Neurons;Proteins;Embryo;10 Development;Research Support, Non-U.S. Gov't;Carrier Proteins;Embryonic and Fetal Development;Cell Differentiation;Research Support, U.S. Gov't, P.H.S.;Neocortex;Cell Survival;Cell Division;Humans;Mice;Animals;Microtubule-Associated Proteins;Cells, Cultured},
	Medline = {20125901},
	Nlm_Id = {7809375},
	Number = {1-2},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, Storrs, Conn., USA.},
	Pages = {68-73},
	Pii = {dne22068},
	Pubmed = {10657699},
	Title = {Noggin is a negative regulator of neuronal differentiation in developing neocortex},
	Uuid = {A4081506-385B-4EB3-B94A-DBA1C59ED151},
	Volume = {22},
	Year = {2000},
	url = {papers/Li_DevNeurosci2000.pdf}}

@article{Li:2005,
	Abstract = {The dentate gyrus is one of two locations with continuing neurogenesis in adult mammals. While the function of adult neurogenesis is unknown, it is believed that it is involved in learning and memory. For adult neurogenesis to occur, the dentate gyrus must maintain the appropriate precursor cell niche in the subgranular zone, which is likely to be dependent on the developmental mechanisms at play in forming the dentate gyrus. In this review, we graft a molecular framework onto the known neuroanatomic developmental plan by considering the phenotypes of several mouse mutants that have well characterized dentate gyrus developmental abnormalities. This effort reveals that there are at least six distinct developmental steps that need to occur in the formation of the dentate gyrus, which can be associated with specific gene defects: (1) defining the dentate neuroepithelium; (2) forming the primary radial glial scaffolding; (3) radial migration of granule neurons to form the primordial granule cell layer; (4) establishing the precursor pool in the hilus; (5) radial transformation of the tertiary matrix, and (6) differentiation of dentate granule cells. From this analysis, it is clear that some molecular pathways control multiple steps in the development of the dentate gyrus. For example the Wnt pathway (steps 1, 2, 4) and the chemokine receptor CXCR4 (steps 3, 4) are involved in multiple developmental steps, while the neuronal differentiation gene NeuroD (step 6) and the integrin signaling pathway (step 5) are involved only in discrete stages of the dentate gyrus morphogenesis.},
	Author = {Li, Guangnan and Pleasure, Samuel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Nlm_Id = {7809375},
	Number = {2-4},
	Organization = {Department of Neurology, Programs in Neuroscience, Developmental Biology and Epilepsy Research, University of California, San Francisco, CA 94143, USA.},
	Pages = {93-9},
	Pii = {DNE20050272_4093},
	Pubmed = {16046842},
	Title = {Morphogenesis of the dentate gyrus: what we are learning from mouse mutants},
	Uuid = {4AFD26A8-667B-11DA-A4B6-000D9346EC2A},
	Volume = {27},
	Year = {2005},
	url = {papers/Li_DevNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000085980}}

@article{Li:2001,
	Abstract = {Early after infection, the retroviral RNA genome is reverse transcribed to generate a linear cDNA copy, then that copy is integrated into a chromosome of the host cell. We report that unintegrated viral cDNA is a substrate for the host cell non-homologous DNA end joining (NHEJ) pathway, which normally repairs cellular double-strand breaks by end ligation. NHEJ activity was found to be required for an end-ligation reaction that circularizes a portion of the unintegrated viral cDNA in infected cells. Consistent with this, the NHEJ proteins Ku70 and Ku80 were found to be bound to purified retroviral replication intermediates. Cells defective in NHEJ are known to undergo apoptosis in response to retroviral infection, a response that we show requires reverse transcription to form the cDNA genome but not subsequent integration. We propose that the double-strand ends present in unintegrated cDNA promote apoptosis, as is known to be the case for chromosomal double-strand breaks, and cDNA circularization removes the pro-apoptotic signal.},
	Author = {Li, L. and Olvera, J. M. and Yoder, K. E. and Mitchell, R. S. and Butler, S. L. and Lieber, M. and Martin, S. L. and Bushman, F. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0261-4189},
	Journal = {EMBO J},
	Keywords = {Research Support, Non-U.S. Gov't;Hamsters;Animals;HIV-1;DNA-Binding Proteins;Humans;Cell Line, Transformed;Research Support, U.S. Gov't, Non-P.H.S.;Apoptosis;CHO Cells;15 Retrovirus mechanism;DNA Helicases;Research Support, U.S. Gov't, P.H.S.;Moloney murine leukemia virus;Saccharomyces cerevisiae Proteins;3T3 Cells;Antigens, Nuclear;Mice;Virus Integration;24 Pubmed search results 2008;DNA, Viral;Nuclear Proteins;Terminal Repeat Sequences;Transcription, Genetic},
	Medline = {21299385},
	Month = {6},
	Nlm_Id = {8208664},
	Number = {12},
	Organization = {Infectious Disease Laboratory, The Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.},
	Pages = {3272-81},
	Pubmed = {11406603},
	Title = {Role of the non-homologous DNA end joining pathway in the early steps of retroviral infection},
	Uuid = {08F87F4C-FC74-49A2-992F-EBBBFDCDF8E7},
	Volume = {20},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/emboj/20.12.3272}}

@article{Li:2003,
	Abstract = {Radial glia are a polarized cell type that in most neural regions appear only transiently during development. They have long been recognized as glia or glial progenitors that support neuronal migration. Recent evidence indicates that radial glia also give rise to neurons and appear to be a major population of dividing precursor cells in the embryonic cortical ventricular zone. Radial glia extend long processes from the ventricular zone to the pial surface that provide guides for neuronal migration. We reasoned that the unique morphology of radial glia is due to the composition and organization of their cytoskeleton. In this present study, we have used C6-R, a radial glial-like cell line and isolated perinatal cerebellar radial glia to ask what are the critical cytoskeletal elements in radial glial cells and how they are regulated. Treatments with nocodazole and cytochalasin D showed that microtubules, but not microfilaments, are critical for the polarized morphology of radial glia. In addition, quantitative real-time PCR indicated that certain mRNAs specific for microtubule-associated proteins (MAPs) are selectively expressed in radial glia. These results together with the known ability of microtubule affinity-regulating kinases to regulate microtubule organization suggest that microtubules and MAPs are critical for the morphology of radial glia. 0894-1491 Journal Article},
	Author = {Li, H. and Berlin, Y. and Hart, R. P. and Grumet, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Glia},
	Keywords = {Brain/growth &development/metabolism/ultrastructure;Animals;Cells, Cultured;Cell Polarity/drug effects/physiology;Rats;Protein-Serine-Threonine Kinases/*genetics;Nocodazole/pharmacology;Microtubules/drug effects/metabolism/*ultrastructure;Stem Cells/metabolism/ultrastructure;Cell Differentiation/drug effects/*physiology;Rats, Sprague-Dawley;08 Aberrant cell cycle;Cytochalasin D/pharmacology;Support, Non-U.S. Gov't;Animals, Newborn;RNA, Messenger/drug effects/metabolism;Support, U.S. Gov't, P.H.S.;Microtubule-Associated Proteins/*genetics;Cell Size/drug effects/physiology;Neuroglia/metabolism/*ultrastructure;EE, G abstr},
	Number = {1},
	Organization = {Department of Cell Biology and Neuroscience and WM Keck Center for Collaborative Neuroscience, Rutgers, State University of New Jersey, Piscataway, New Jersey 08854, USA.},
	Pages = {37-46},
	Title = {Microtubules are critical for radial glial morphology: possible regulation by MAPs and MARKs},
	Uuid = {31D292BF-5993-4694-81BE-AD113B17CDA7},
	Volume = {44},
	Year = {2003},
	url = {papers/Li_Glia2003.pdf}}

@article{Li:1999,
	Abstract = {Small, circumscribed electrolytic lesions were made in the upper cervical corticospinal tract in adult rats. In the centre of the lesion, the axons and all other tissue elements were totally destroyed. Surrounding this region of destruction is an area of tissue which is only partially damaged. In this area TUNEL positive staining of contiguous rows of tract glial cells indicates massive oligodendrocytic apoptosis at 1-3 days after operation, but axons, astrocytes and blood vessels survive. From around 4 days, the corticospinal axons in this area are demyelinated, and the microglia contain ingested myelin, identified in electron micrographs as characteristic MBP immunoreactive laminar cytoplasmic bodies. After around 3 weeks, large numbers of Schwann cells, continuous with those on the pial surface of the spinal cord, accumulate along the lesion track and selectively infiltrate the perilesional reactive area, where they mingle intimately with the phagocytic microglia. Electron micrographs show that at this time basal lamina-enclosed Schwann cell processes establish non-myelinated ensheathment of axons. From around 4 weeks after operation, prominent Schwann cell myelination is indicated by P0 immunoreactivity, and peripheral type, one-to-one myelination in electron micrographs. Thus the effect of the selective loss of oligodendrocytes is to first activate microglia, and then to induce a replacement of myelin by Schwann cells.},
	Author = {Li, Y. and Field, P. M. and Raisman, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Phagocytosis;Animals;Myelin Sheath;Rats;Myelin Basic Proteins;Apoptosis;Female;Microglia;Oligodendroglia;Rats, Inbred Strains;Cell Movement;Not relevant;11 Glia;Pyramidal Tracts;Axons;Spinal Cord Injuries;Schwann Cells;Support, Non-U.S. Gov't;In Situ Nick-End Labeling;Microscopy, Electron;Demyelinating Diseases},
	Medline = {20204293},
	Nlm_Id = {0364620},
	Number = {4-5},
	Organization = {Norman and Sadie Lee Research Centre, Division of Neurobiology, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK.},
	Pages = {417-27},
	Pubmed = {10739580},
	Title = {Death of oligodendrocytes and microglial phagocytosis of myelin precede immigration of Schwann cells into the spinal cord},
	Uuid = {37748B49-5705-4F35-9DD1-1B07C2A58F96},
	Volume = {28},
	Year = {1999}}

@article{Li:2002a,
	Abstract = {We tested the hypothesis that populations of ependymal, subependymal and choroid plexus cells proliferate and differentiate after stroke in adult rats. Rats were subjected to 2 h of middle cerebral artery occlusion (n=70) and euthanized at 1, 2, 4, 7, 14, 21 and 28 days (10 per time point). Hematoxylin and eosin staining and immunostaining were performed using antibodies against bromodeoxyuridine, neuronal nuclear antigen and glial fibrillary acidic protein after stroke. In normal nonischemic rats (n=10), single layers of ependymal and choroid plexus cells do not react with bromodeoxyuridine, neuronal nuclear antigen or glial fibrillary acidic protein. Individual subependymal cells express glial fibrillary acidic protein and bromodeoxyuridine, but not neuronal nuclear antigen. After stroke, increased bromodeoxyuridine reactivity was present in multiple layers of ependymal cells and nodules of subependymal cells and in scattered choroid plexus cells from 2 to 28 days and peaked at 7 days. Bromodeoxyuridine immunoreactivity colocalized with neural phenotypes of neuronal nuclear antigen (~0.1- 3.5\%) and glial fibrillary acidic protein (~8.6\%) immunoreactivity in cells in the ventricular zone and the subventricular zone, as well as in the choroid plexus of the ischemia affected hemisphere. Our data suggest that ependymal, subependymal and choroid plexus cells are potential neural precursor cells in the adult mammalian brain.},
	Author = {Li, Y. and Chen, J. and Chopp, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurol Sci},
	Keywords = {D abstr;06 Adult neurogenesis injury induced},
	Number = {2},
	Organization = {Department of Neurology, Henry Ford Health Sciences Center, 2799 West Grand Boulevard, 48202, Detroit, MI, USA},
	Pages = {137-46.},
	Title = {Cell proliferation and differentiation from ependymal, subependymal and choroid plexus cells in response to stroke in rats},
	Uuid = {5652C4EE-D17E-42D8-A2FD-DF6CBF7B3330},
	Volume = {193},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11790394}}

@article{Li:2002b,
	Abstract = {Many applications of hematopoietic gene therapy require selection for clones with active transgene expression. However, it was unclear whether the clonal progeny of a retrovirally transduced hematopoietic stem cell would be capable of maintaining transgene expression through serial repopulation and multilineage differentiation. Such investigations require simultaneous analyses of clonality, multilineage activity and transgene copy numbers. Using a mouse model, the present study demonstrates that a single hematopoietic stem cell expressing a marker gene from one or two insertions of a simple retroviral vector actively maintains multilineage transgene expression in the vast majority (80-99\%) of bone marrow and peripheral blood cells. Gene expression persisted through serial transplantations for at least 97 weeks post gene transfer and was observed in the lymphoid (B, T and NK cells), myeloid (CD11b(+), Gr-1(+)), erythroid (Ter119(+), mature red blood cells) and megakaryocytic (as indicated by platelets) progeny. Therefore, a single immunoselection for hematopoietic stem cells expressing the transgene in vivo was sufficient to establish a completely chimeric hematopoiesis. These observations imply that the retroviral vectors used in this study contain cis-elements that mediate expression through massive clonal expansion and multilineage differentiation, provided the insertion occurred in genetic loci permissive for expression in hematopoietic stem cells.},
	Author = {Li, Z. and Fehse, B. and Schiedlmeier, B. and D{\"u}llmann, J. and Frank, O. and Zander, A. R. and Ostertag, W. and Baum, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0887-6924},
	Journal = {Leukemia},
	Keywords = {Transgenes;Transduction, Genetic;Gene Dosage;Colony-Forming Units Assay;Humans;Chimera;Transfection;Animals;Female;Mice, Transgenic;Antigens, CD34;Retroviridae;Mice, Inbred C57BL;11 Glia;Hematopoietic Stem Cell Transplantation;Green Fluorescent Proteins;Hematopoiesis;Bone Marrow Cells;Gene Transfer Techniques;Cell Lineage;Gene Silencing;Mice;Hematopoietic Stem Cells;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22188889},
	Month = {9},
	Nlm_Id = {8704895},
	Number = {9},
	Organization = {Experimental Cell Therapy, Department of Hematology and Oncology, Hannover Medical School, Hannover, Germany.},
	Pages = {1655-63},
	Pubmed = {12200677},
	Title = {Persisting multilineage transgene expression in the clonal progeny of a hematopoietic stem cell},
	Uuid = {108C22C6-2FC3-4384-9E52-478532C6FD66},
	Volume = {16},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.leu.2402619}}

@article{Li:2002,
	Abstract = {The developmental programme of embryogenesis is controlled by both genetic and epigenetic mechanisms. An emerging theme from recent studies is that the regulation of higher-order chromatin structures by DNA methylation and histone modification is crucial for genome reprogramming during early embryogenesis and gametogenesis, and for tissue-specific gene expression and global gene silencing. Disruptions to chromatin modification can lead to the dysregulation of developmental processes, such as X-chromosome inactivation and genomic imprinting, and to various diseases. Understanding the process of epigenetic reprogramming in development is important for studies of cloning and the clinical application of stem-cell therapy.},
	Author = {Li, En},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1471-0056},
	Journal = {Nat Rev Genet},
	Keywords = {DNA Methylation;24 Pubmed search results 2008;Ectoderm;Embryonic and Fetal Development;Research Support, U.S. Gov't, P.H.S.;X Chromosome;Mammals;Trophoblasts;Models, Genetic;Chromatin;Humans;Animals;Germ Cells;review},
	Medline = {22199595},
	Month = {9},
	Nlm_Id = {100962779},
	Number = {9},
	Organization = {Cardiovascular Research Center, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA. en\@cvrc.mgh.harvard.edu},
	Pages = {662-73},
	Pii = {nrg887},
	Pubmed = {12209141},
	Title = {Chromatin modification and epigenetic reprogramming in mammalian development},
	Uuid = {C7C10AC4-D242-4144-88E6-3F99798AE719},
	Volume = {3},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrg887}}

@article{Li:2007,
	Abstract = {The neuron-specific K-Cl cotransporter, KCC2, induces a developmental shift to render GABAergic transmission from depolarizing to hyperpolarizing. Now we demonstrate that KCC2, independently of its Cl(-) transport function, is a key factor in the maturation of dendritic spines. This morphogenic role of KCC2 in the development of excitatory synapses is mediated by structural interactions between KCC2 and the spine cytoskeleton. Here, the binding of KCC2 C-terminal domain to the cytoskeleton-associated protein 4.1N may play an important role. A more general conclusion based on our data is that KCC2 acts as a synchronizing factor in the functional development of glutamatergic and GABAergic synapses in cortical neurons and networks.},
	Author = {Li, Hong and Khirug, Stanislav and Cai, Chunlin and Ludwig, Anastasia and Blaesse, Peter and Kolikova, Julia and Afzalov, Ramil and Coleman, Sarah K. and Lauri, Sari and Airaksinen, Matti S. and Kein{\"a}nen, Kari and Khiroug, Leonard and Saarma, Mart and Kaila, Kai and Rivera, Claudio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Institute of Biotechnology, University of Helsinki, Viikinkaari 4, FIN-00014, Helsinki, Finland.},
	Pages = {1019-33},
	Pii = {S0896-6273(07)00865-3},
	Pubmed = {18093524},
	Title = {KCC2 Interacts with the Dendritic Cytoskeleton to Promote Spine Development},
	Uuid = {FC15E4C7-9342-4F76-B553-D7B124DBB7CC},
	Volume = {56},
	Year = {2007},
	url = {papers/Li_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.10.039}}

@article{Li:2002c,
	Abstract = {It is now apparent that adult neurogenesis is taking place during life in the olfactory bulb (OB) of the rodent brain. In the olfactory nervous system, the precursor cells of the subventricular zone are known to continually proliferate, migrate through the rostral migratory stream (RMS) and differentiate into the bulbar neurons. The RMS, consisting of heterogeneous cell populations of the neural and neuronal precursor cells, is the unique forebrain structure that provides a long-distance migratory route for the precursor cells. The present study was undertaken to examine whether neuronal regeneration, focusing on calretinin-immunoreactive (+) cells, may proceed in the RMS following lesions induced by an excitotoxin. Two days after ibotenate injections, massive degeneration of calretinin (+) cells occurred in the RMS and its adjacent forebrains. Thereafter, calretinin (+) cells gradually increased in the RMS and reached above their control value 2 weeks after ibotenate injections. Removal of the OB also produced a marked increase in calretinin (+) cells in the RMS. Autoradiographic experiments using (3)H-thymidine showed that calretinin (+) cells were continually generated in the RMS and underwent neuronal turnover within 8 weeks in a normal condition. The results indicate that, in terms of calretinin (+) cells, neuronal differentiation and replacement is continually taking place within the RMS, and that the RMS is capable of repopulating those cells which were injured by ibotenate. 0168-0102 Journal Article},
	Author = {Li, Z. and Kato, T. and Kawagishi, K. and Fukushima, N. and Yokouchi, K. and Moriizumi, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Neurosci Res},
	Keywords = {I both;Excitatory Amino Acid Agonists/toxicity;Calcium-Binding Protein, Vitamin D-Dependent/*analysis;Neurons/chemistry/*cytology/physiology;13 Olfactory bulb anatomy;Cell Count/statistics &numerical data;Immunohistochemistry;Rats;Rats, Wistar;Cell Movement/*physiology;Support, Non-U.S. Gov't;Animals;Male;Prosencephalon/chemistry/*cytology/drug effects/*physiology;Ibotenic Acid/*toxicity},
	Number = {2},
	Organization = {Department of Anatomy, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan.},
	Pages = {123-32},
	Title = {Cell dynamics of calretinin-immunoreactive neurons in the rostral migratory stream after ibotenate-induced lesions in the forebrain},
	Uuid = {1671C3B9-E979-44BE-8B58-4E7958710F21},
	Volume = {42},
	Year = {2002},
	url = {papers/Li_NeurosciRes2002}}

@article{Li:2003a,
	Abstract = {Cells undergoing apoptosis during development are removed by phagocytes, but the underlying mechanisms of this process are not fully understood. Phagocytes lacking the phosphatidylserine receptor (PSR) were defective in removing apoptotic cells. Consequently, in PSR-deficient mice, dead cells accumulated in the lung and brain, causing abnormal development and leading to neonatal lethality. A fraction of PSR knockout mice manifested a hyperplasic brain phenotype resembling that of mice deficient in the cell death-associated genes encoding Apaf-1, caspase-3, and caspase-9, which suggests that phagocytes may also be involved in promoting apoptosis. These data demonstrate a critical role for PSR in early stages of mammalian organogenesis and suggest that this receptor may be involved in respiratory distress syndromes and congenital brain malformations. 1095-9203 Journal Article},
	Author = {Li, M. O. and Sarkisian, M. R. and Mehal, W. Z. and Rakic, P. and Flavell, R. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Science},
	Keywords = {Receptors, Cell Surface/genetics/*metabolism;Cell Nucleus/ultrastructure;Pulmonary Surfactants/metabolism;10 Development;Animals;Brain/abnormalities/cytology/*embryology;Phagocytosis;In Situ Nick-End Labeling;Neurons/cytology;Phenotype;Phosphatidylserines/metabolism;Cell Division;11 Glia;Hematopoietic Stem Cell Transplantation;Support, U.S. Gov't, P.H.S.;Necrosis;Respiratory Insufficiency/etiology;Epithelial Cells/physiology/ultrastructure;F pdf;Eye Abnormalities/etiology;Lung/cytology/*embryology/physiology;Eye/embryology;Mesoderm/ultrastructure;Mice, Knockout;Macrophages/*physiology;Support, Non-U.S. Gov't;Mice;Inflammation;Reverse Transcriptase Polymerase Chain Reaction;*Apoptosis},
	Number = {5650},
	Organization = {Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.},
	Pages = {1560-3},
	Pubmed = {14645847},
	Title = {Phosphatidylserine receptor is required for clearance of apoptotic cells},
	Uuid = {E539FCB2-EE25-11DA-8605-000D9346EC2A},
	Volume = {302},
	Year = {2003},
	url = {papers/Li_Science2003.pdf}}

@article{Lian:2006,
	Abstract = {PURPOSE OF REVIEW: The development of the cerebral cortex progresses through defined stages including neural proliferation, neuroblast migration and neuronal differentiation. Disruptions in each of these developmental stages can lead to characteristic cerebral cortical malformations. This review provides an overview of the known genetic causes of human cerebral developmental disorders and discusses the potential molecular mechanisms that contribute to these malformations. RECENT FINDINGS: Mutations in genes that are involved in neural proliferation give rise to microcephaly (small brain). Mutations in genes that direct the onset of neuroblast migration give rise to periventricular heterotopia (clusters of neurons along the ventricles of the brain). Mutations in genes that are required for neuroblast migration cause type I lissencephaly (smooth brain) and subcortical band heterotopia (smooth brain with a band of neurons beneath the cortex). Mutations in genes that direct migratory neurons to arrest in the cortex lead to type II lissencephaly (smooth brain with clusters of neurons along the surface of the brain). SUMMARY: The identification of causative genes involved in the formation of the cerebral cortex now allows for a rational approach with which to interpret the underlying mechanistic basis for many of these disorders.},
	Author = {Lian, Gewei and Sheen, Volney},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {1040-8703},
	Journal = {Curr Opin Pediatr},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {9000850},
	Number = {6},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {614-20},
	Pii = {00008480-200612000-00005},
	Pubmed = {17099359},
	Title = {Cerebral developmental disorders},
	Uuid = {B677D117-C5F1-4408-BF7F-BF686220D42C},
	Volume = {18},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1097/MOP.0b013e328010542d}}

@article{Liang:2002,
	Abstract = {Human T-lymphotropic virus type 1 (HTLV-1) Tax exerts pleiotropic effects on multiple cellular regulatory processes to bring about NF-kappaB activation, aberrant cell cycle progression, and cell transformation. Here we report that Tax stimulates cellular G(1)/S entry but blocks mitosis. Tax expression in naive cells transduced with a retroviral vector, pBabe-Tax, leads to a significant increase in the number of cells in the S phase, with an accompanying rise in the population of cells with a DNA content of 4N or more. In all cell types tested, including BHK-21, mouse NIH 3T3, and human diploid fibroblast WI-38, Tax causes an uncoupling of DNA synthesis from cell division, resulting in the formation of multinucleated giant cells and cells with decondensed, highly convoluted and lobulated nuclei that are reminiscent of the large lymphocytes with cleaved or cerebriform nuclei seen in HTLV-1-positive individuals. This contrasts with the Tax-transformed cell lines, PX1 (fibroblast) and MT4 (lymphocyte), which produce Tax at high levels, but without the accompanying late-stage cell cycle abnormalities. PX1 and MT4 may have been selected to harbor somatic mutations that allow a bypass of the Tax-induced block in mitosis. 0022-538x Journal Article},
	Author = {Liang, M. H. and Geisbert, T. and Yao, Y. and Hinrichs, S. H. and Giam, C. Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {J Virol},
	Keywords = {Hamsters;Human;Transduction, Genetic;Animals;*Mitosis/drug effects;Cell Line, Transformed;Moloney murine leukemia virus/genetics;EE pdf;*S Phase/drug effects;Giant Cells;08 Aberrant cell cycle;Genetic Vectors;Cell Line;3T3 Cells;Support, U.S. Gov't, P.H.S.;Mice;Gene Products, tax/genetics/metabolism/pharmacology/*physiology;Cell Division/drug effects},
	Number = {8},
	Organization = {Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA.},
	Pages = {4022-33},
	Title = {Human T-lymphotropic virus type 1 oncoprotein tax promotes S-phase entry but blocks mitosis},
	Uuid = {D9FA1D40-F8F8-4C43-9C3D-4661B80F4500},
	Volume = {76},
	Year = {2002},
	url = {papers/Liang_JVirol2002.pdf}}

@article{Libri:1998,
	Abstract = {The effects of the selective GABA(B) receptor antagonist [3-[[(3,4-dichlorophenyl)methyl]aminolpropyl] (diethoxymethyl) phosphinic acid (CGP 52432) on muscarinic (mAChR) and metabotropic glutamate (mGluR) responsiveness were studied in slices of piriform cortex from both immature (P16-P22) and adult (> or =P40) rats, using a conventional intracellular recording technique. In both adult and immature slices, CGP 52432 (1 microM) had no effect on neuronal membrane properties, whereas it selectively abolished the late inhibitory postsynaptic potential (IPSP) evoked by local electrical stimulation of association fibre terminals. Age-related changes in mAChR (but not mGluR) responsiveness were also detected. In adult neurones, bath-application of the mAChR agonist oxotremorine-M (OXO-M; 10 microM), or the selective mGluR agonist 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD; 10 microM) evoked similar membrane depolarization and inhibition of evoked excitatory postsynaptic potentials (EPSPs). However, while 1S,3R-ACPD and OXO-M produced indistinguishable slow excitatory effects in immature slices, during superfusion with OXO-M, neurones exhibited spontaneous paroxysmal depolarizing shifts (PDSs) that were suppressed in the presence of atropine (1 microM) or the selective GABA(B) receptor agonist beta-parachlorophenyl-gamma-aminobutyric acid [(-)baclofen; 10 microM]. Also, application of OXO-M resulted in a pronounced prolongation (rather than a decrease) of electrically evoked postsynaptic potentials (PSPs) which now exhibited recurrent superimposed spike discharges. In adult slices, in the continuous presence of CGP 52432 (1 microM; 20 min pre-incubation), a subsequent exposure to 10 microM OXO-M or 1S,3R-ACPD failed to induce any spontaneous epileptiform activity, and evoked PSPs were consistently suppressed. In contrast, in immature slices, after incubation in CGP 52432 (1 microM; 20 min), a subsequent application of a low dose of OXO-M (2.5 microM), which was inactive per se, was able to produce spontaneous PDSs and a prolongation of evoked PSPs. We conclude that a reduction in GABA(B)-mediated synaptic inhibition in immature slices (in co-operation with other factors) may contribute to the facilitation of excitatory neurotransmission and therefore play a role in the generation of mAChR-induced epileptiform activity.},
	Author = {Libri, V. and Constanti, A. and Postlethwaite, M. and Bowery, N. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0028-1298},
	Journal = {Naunyn Schmiedebergs Arch Pharmacol},
	Keywords = {Research Support, Non-U.S. Gov't;Dose-Response Relationship, Drug;Electric Stimulation;Animals;Oxotremorine;Rats;Muscarinic Agonists;Synaptic Transmission;Neuroprotective Agents;Cycloleucine;Epilepsy;Female;21 Epilepsy;Rats, Wistar;Receptors, Muscarinic;Receptors, GABA-B;Male;Cerebral Cortex;21 Neurophysiology;Phosphinic Acids;Neurons;Membrane Potentials;GABA Antagonists;24 Pubmed search results 2008;Receptors, Metabotropic Glutamate;Benzylamines;Excitatory Postsynaptic Potentials},
	Medline = {98420449},
	Month = {8},
	Nlm_Id = {0326264},
	Number = {2},
	Organization = {Department of Pharmacology, The School of Pharmacy, University of London, UK.},
	Pages = {168-74},
	Pubmed = {9750001},
	Title = {Blockade of GABA(B) receptors facilitates muscarinic agonist-induced epileptiform activity in immature rat piriform cortex in vitro},
	Uuid = {19BC0118-BD86-470D-898B-5DEABCC11617},
	Volume = {358},
	Year = {1998}}

@article{Lie:2004,
	Abstract = {New cells are continuously generated from immature proliferating cells throughout adulthood in many organs, thereby contributing to the integrity of the tissue under physiological conditions and to repair following injury. In contrast, repair mechanisms in the adult central nervous system (CNS) have long been thought to be very limited. However, recent findings have clearly demonstrated that in restricted areas of the mammalian brain, new functional neurons are constantly generated from neural stem cells throughout life. Moreover, stem cells with the potential to give rise to new neurons reside in many different regions of the adult CNS. These findings raise the possibility that endogenous neural stem cells can be mobilized to replace dying neurons in neurodegenerative diseases. Indeed, recent reports have provided evidence that, in some injury models, limited neuronal replacement occurs in the CNS. Here, we summarize our current understanding of the mechanisms controlling adult neurogenesis and discuss their implications for the development of new strategies for the treatment of neurodegenerative diseases. 0362-1642 Journal article},
	Author = {Lie, D. C. and Song, H. and Colamarino, S. A. and Ming, G. L. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {Annu Rev Pharmacol Toxicol},
	Keywords = {01 Adult neurogenesis general;A pdf},
	Organization = {1Laboratory of Genetics, The Salk Institute, La Jolla, California 92037; email: lie\@salk.edu, colamarino\@salk.edu, gage\@salk.edu, 2Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287; email: shongju1\@jhmi.edu, gming1\@jhmi.edu},
	Pages = {399-421},
	Title = {NEUROGENESIS IN THE ADULT BRAIN: New Strategies for Central Nervous System Diseases},
	Uuid = {6E7AC1A9-0F63-4775-ABB8-6BC7F0B1314D},
	Volume = {44},
	Year = {2004},
	url = {../../Volumes/Vega/Users/ackman/James/Endnotelibraries/OMEGAData/0561468416nnurev.pharmtox04.pdf}}

@article{Lieber:1973,
	Author = {Lieber, M. M. and Todaro, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0020-7136},
	Journal = {Int J Cancer},
	Keywords = {15 ERVs retroelements;Clone Cells;Chromosomes;RNA-Directed DNA Polymerase;Cell Transformation, Neoplastic;Moloney murine leukemia virus;Microscopy, Electron;Cell Line;Retroviridae;Epitopes;Radioimmunoassay;15 Retrovirus mechanism;Animals;Bromodeoxyuridine;Mice;Cells, Cultured;24 Pubmed search results 2008},
	Medline = {74173544},
	Month = {5},
	Nlm_Id = {0042124},
	Number = {3},
	Pages = {616-27},
	Pubmed = {4133949},
	Title = {Spontaneous and induced production of endogenous type-C RNA virus from a clonal line of spontaneously transformed BALB-3T3},
	Uuid = {8DFFA5E0-4328-11DB-A5D2-000D9346EC2A},
	Volume = {11},
	Year = {1973}}

@article{Lieber:2000,
	Abstract = {Moloney murine leukemia virus (MoMLV)-derived vectors require cell division for efficient transduction, which may be related to an inability of the viral DNA-protein complex to cross the nuclear membrane. In contrast, adenoviruses (Ad) can efficiently infect nondividing cells. This property may be due to the presence of multiple nuclear translocation signals in a number of Ad proteins, which are associated with the incoming viral genomes. Of particular interest is the Ad preterminal protein (pTP), which binds alone or in complex with the Ad polymerase to specific sequences in the Ad inverted terminal repeat. The goal of this study was to test whether coexpression of pTP with retroviral DNA carrying pTP-binding sites would facilitate nuclear import of the viral preintegration complex and transduction of quiescent cells. In preliminary experiments, we demonstrated that the karyophylic pTP can coimport plasmid DNA into the nuclei of growth-arrested cells. Retroviral transduction studies were performed with G(1)/S-arrested LTA cells or stationary-phase human primary fibroblasts. These studies demonstrated that pTP or pTP-Ad polymerase conferred nuclear import of retroviral DNA upon arrested cells when the retrovirus vector contained the corresponding binding motifs. However, pTP-mediated nuclear translocation of MoMLV DNA in nondividing cells was not sufficient for stable transduction. Additional cellular factors activated during S phase or DNA repair synthesis were required for efficient retroviral integration. 0022-538x Journal Article},
	Author = {Lieber, A. and Kay, M. A. and Li, Z. Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Journal = {J Virol},
	Keywords = {Human;Protein Precursors/genetics/*metabolism;Animals;Viral Proteins/genetics/*metabolism;Cells, Cultured;Transfection;Biological Transport;Cell Line, Transformed;*Virus Integration;J pdf;15 Retrovirus mechanism;Cell Nucleus/metabolism/virology;Moloney murine leukemia virus/*genetics;Adenoviruses, Human/*physiology;Plasmids;Support, Non-U.S. Gov't;DNA, Viral/*metabolism;Phosphoproteins/genetics/*metabolism;Support, U.S. Gov't, P.H.S.;Mice;Cell Division},
	Number = {2},
	Organization = {Division of Medical Genetics, University of Washington, Seattle, Washington 98195, USA. lieber00\@u.washington.edu},
	Pages = {721-34},
	Pubmed = {10623734},
	Title = {Nuclear import of moloney murine leukemia virus DNA mediated by adenovirus preterminal protein is not sufficient for efficient retroviral transduction in nondividing cells},
	Uuid = {15111441-1DD3-4845-9F8A-CC80289AB0E1},
	Volume = {74},
	Year = {2000},
	url = {papers/Lieber_JVirol2000.pdf}}

@article{Lieber:1973a,
	Author = {Lieber, M. M. and Livingston, D. M. and Todaro, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {15 ERVs retroelements;Clone Cells;RNA-Directed DNA Polymerase;Cell Transformation, Neoplastic;Kinetics;Virus Replication;Retroviridae;Gammaretrovirus;15 Retrovirus mechanism;Mice;Bromodeoxyuridine;RNA Viruses;Animals;24 Pubmed search results 2008},
	Medline = {73216982},
	Month = {8},
	Nlm_Id = {0404511},
	Number = {98},
	Pages = {443-4},
	Pubmed = {4123998},
	Title = {Superinduction of endogenous type C virus by 5-bromodeoxyuridine from transformed mouse clones},
	Uuid = {8DFFAE50-4328-11DB-A5D2-000D9346EC2A},
	Volume = {181},
	Year = {1973}}

@article{Lieberam:2005,
	Abstract = {Motor neurons, alone among neurons in the vertebrate CNS, extend axons out of the neural tube to innervate peripheral targets. Two classes of motor neurons, termed vMNs and dMNs, extend axons out of the neural tube via ventral and dorsal exit points, respectively, in accord with their homeodomain transcription factor repertoire. Downstream of these transcriptional codes, the cell surface receptors that shape initial motor axon trajectories have not been identified. We show here that the chemokine receptor Cxcr4 is expressed on the axons of vMNs as they follow their ventral trajectory, whereas its ligand, Cxcl12, is expressed by mesenchymal cells surrounding the ventral neural tube. Genetic studies reveal that Cxcl12-Cxcr4 signaling directs the ventral trajectory of spinal vMNs. In its absence, these neurons adopt a dMN-like trajectory, despite preservation of their vMN transcriptional identity. Thus, the status of Cxcr4 signaling helps to determine the initial axonal trajectory of mammalian motor neurons.},
	Author = {Lieberam, Ivo and Agalliu, Dritan and Nagasawa, Takashi and Ericson, Johan and Jessell, Thomas M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;11 Glia},
	Month = {9},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, New York, New York 10032.},
	Pages = {667-79},
	Pii = {S0896-6273(05)00653-7},
	Pubmed = {16129397},
	Title = {A cxcl12-CXCR4 chemokine signaling pathway defines the initial trajectory of Mammalian motor axons},
	Uuid = {375DF883-064B-42A8-9044-0CB5938C6451},
	Volume = {47},
	Year = {2005},
	url = {papers/Lieberam_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.08.011}}

@article{Lim:2000,
	Abstract = {Large numbers of new neurons are born continuously in the adult subventricular zone (SVZ). The molecular niche of SVZ stem cells is poorly understood. Here, we show that the bone morphogenetic protein (BMP) antagonist Noggin is expressed by ependymal cells adjacent to the SVZ. SVZ cells were found to express BMPs as well as their cognate receptors. BMPs potently inhibited neurogenesis both in vitro and in vivo. BMP signaling cell-autonomously blocked the production of neurons by SVZ precursors by directing glial differentiation. Purified mouse Noggin protein promoted neurogenesis in vitro and inhibited glial cell differentiation. Ectopic Noggin promoted neuronal differentiation of SVZ cells grafted to the striatum. We thus propose that ependymal Noggin production creates a neurogenic environment in the adjacent SVZ by blocking endogenous BMP signaling.},
	Author = {Lim, D. A. and Tramontin, A. D. and Trevejo, J. M. and Herrera, D. G. and Garcia-Verdugo, J. M. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Neuron},
	Keywords = {Cell Differentiation/drug effects;Human;Cell Survival/drug effects;inhibitors/biosynthesis/pharmacology;Brain Tissue Transplantation;Mice, Mutant Strains;Microinjections;Animal;Mice, Transgenic;Corpus Striatum/cytology/metabolism;Bone Morphogenetic Proteins/*antagonists &;Fetal Tissue Transplantation;Cell Line;C-17;Ependyma/cytology/metabolism;Receptors, Cell Surface/biosynthesis;Neurons/cytology/*metabolism/transplantation;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice;Signal Transduction/drug effects/*physiology;Gene Expression;Cell Division/drug effects;Proteins/*metabolism/pharmacology},
	Number = {3},
	Organization = {Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.},
	Pages = {713-26.},
	Title = {Noggin antagonizes BMP signaling to create a niche for adult neurogenesis},
	Uuid = {2A223AF6-9A16-4590-860F-22A046B261CF},
	Volume = {28},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11163261}}

@article{Lim:1997,
	Abstract = {The mammalian subventricular zone (SVZ) of the lateral wall of the forebrain ventricle retains a population of proliferating neuronal precursors throughout life. Neuronal precursors born in the postnatal and adult SVZ migrate to the olfactory bulb where they differentiate into interneurons. Here we tested the potential of mouse postnatal SVZ precursors in the environment of the embryonic brain: (i) a ubiquitous genetic marker, (ii) a neuron-specific transgene, and (iii) a lipophilic-dye were used to follow the fate of postnatal day 5-10 SVZ cells grafted into embryonic mouse brain ventricles at day 15 of gestation. Graft-derived cells were found at multiple levels of the neuraxis, including septum, thalamus, hypothalamus, and in large numbers in the midbrain inferior colliculus. We observed no integration into the cortex. Neuronal differentiation of graft derived cells was demonstrated by double-staining with neuron-specific beta-tubulin antibodies, expression of the neuron-specific transgene, and the dendritic arbors revealed by the lipophilic dye. We conclude that postnatal SVZ cells can migrate through and differentiate into neurons within multiple embryonic brain regions other than the olfactory bulb. 1st report of broad differentiation&migration potential of postnatalSVZ precursors transplant into embryonic brain},
	Author = {Lim, D. A. and Fishell, G. J. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {*Cell Movement;02 Adult neurogenesis migration;Cell Differentiation;03 Adult neurogenesis progenitor source;Biological Markers;Animal;Neurons/*cytology/transplantation;Cerebral Ventricles/*cytology/*embryology;Support, U.S. Gov't, P.H.S.;Mice;BB abstr},
	Number = {26},
	Organization = {The Rockefeller University, New York, NY 10021, USA.},
	Pages = {14832-6.},
	Title = {Postnatal mouse subventricular zone neuronal precursors can migrate and differentiate within multiple levels of the developing neuraxis},
	Uuid = {89C9DA53-4DF3-4504-B90A-7FDA777E62F9},
	Volume = {94},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9405699}}

@article{Lim:1999,
	Abstract = {Neurogenesis continues in the mammalian subventricular zone (SVZ) throughout life. However, the signaling and cell-cell interactions required for adult SVZ neurogenesis are not known. In vivo, migratory neuroblasts (type A cells) and putative precursors (type C cells) are in intimate contact with astrocytes (type B cells). Type B cells also contact each other. We reconstituted SVZ cell-cell interactions in a culture system free of serum or exogenous growth factors. Culturing dissociated postnatal or adult SVZ cells on astrocyte monolayers-but not other substrates-supported extensive neurogenesis similar to that observed in vivo. SVZ precursors proliferated rapidly on astrocytes to form colonies containing up to 100 type A neuroblasts. By fractionating the SVZ cell dissociates with differential adhesion to immobilized polylysine, we show that neuronal colony-forming precursors were concentrated in a fraction enriched for type B and C cells. Pure type A cells could migrate in chains but did not give rise to neuronal colonies. Because astrocyte-conditioned medium alone was not sufficient to support SVZ neurogenesis, direct cell-cell contact between astrocytes and SVZ neuronal precursors may be necessary for the production of type A cells.},
	Author = {Lim, D. A. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:52 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {B-16 both;02 Adult neurogenesis migration;Prosencephalon/*cytology/physiology;Adult;Human;Neurons/*cytology/physiology;Astrocytes/*cytology/physiology;Cell Differentiation/physiology;Support, U.S. Gov't, P.H.S.;Cells, Cultured;Cell Communication/*physiology;Cell Movement/physiology},
	Number = {13},
	Organization = {The Rockefeller University, New York, NY 10021, USA. limd\@rockvax.rockefeller.edu},
	Pages = {7526-31.},
	Title = {Interaction between astrocytes and adult subventricular zone precursors stimulates neurogenesis},
	Uuid = {513EE85C-FBD9-46D3-B47A-8F5736240ECE},
	Volume = {96},
	Year = {1999},
	url = {papers/Lim_ProcNatlAcadSciUSA1999.pdf}}

@article{Lin:2006,
	Abstract = {Neural stem and progenitor cells typically exhibit a density-dependent survival and expansion, such that critical densities are required below which clonogenic progenitors are lost. This suggests that short-range autocrine factors may be critical for progenitor cell maintenance. We report here that purines drive the expansion of ventricular zone neural stem and progenitor cells, and that purine receptor activation is required for progenitor cells to be maintained as such. Neural progenitors expressed P2Y purinergic receptors and mobilized intracellular calcium in response to agonist. Receptor antagonists suppressed proliferation and permitted differentiation into neurons and glia in vitro, while subsequent removal of purinergic inhibition restored progenitor cell expansion. Real-time bioluminescence imaging of extracellular ATP revealed that the source of extracellular nucleotides are the progenitor cells themselves, which appear to release ATP in episodic burst events. Enzyme histochemistry of the adult rat brain for ectonucleotidase activity revealed that NTDPase, which acts to degrade active ATP and thereby clears it from areas of active purinergic transmission, was selectively localized to the subventricular zone and the dentate gyrus, regions in which neuronal differentiation proceeds from the progenitor cell pool. These data suggest that purine nucleotides act as proliferation signals for neural progenitor cells, and thereby serve as negative regulators of terminal neuronal differentiation. As a result, progenitor cell-derived neurogenesis is thus associated with regions of both active purinergic signaling and modulation thereof.},
	Author = {Lin, and Takano, and Arcuino, and Wang, and Hu, and Darzynkiewicz, and Nunes, and Goldman, and Nedergaard,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {0372762},
	Organization = {Department of Cell Biology, New York Medical College, Valhalla, NY, USA.},
	Pii = {S0012-1606(06)01218-8},
	Pubmed = {17188262},
	Title = {Purinergic signaling regulates neural progenitor cell expansion and neurogenesis},
	Uuid = {5E3043F7-34AB-4E8C-9CC0-DFB260A67CE3},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2006.09.017}}

@article{Lin:2002,
	Abstract = {Antibodies against the chondroitin sulfate proteoglycan NG2 label a subpopulation of glial cells within the CNS, which have a small cell body and thin radiating processes. Physiological recordings from these small cells in acute brain slices have revealed that they possess unique properties, suggesting that they may comprise a class of glial cells distinct from astrocytes, oligodendrocytes, or microglia. NG2-expressing glial cells (abbreviated as "NG2 cells"here) have a moderate input resistance and are not dye- or tracer-coupled to adjacent cells. They express voltage-gated Na+, K+ and Ca2+ conductances, though they do not exhibit regenerative Na+ or Ca2+ action potentials due to the much larger K+ conductances present. In addition to voltage-gated conductances, they express receptors for various neurotransmitters. In the hippocampus, AMPA and GABAA receptors on these cells are activated by release of transmitter from neurons at defined synaptic junctions that are formed with CA3 pyramidal neurons and GABAergic interneurons. These rapid forms of neuron-glial communication may regulate the proliferation rate of NG2 cells or their development into mature oligodendrocytes. These depolarizing inputs may also trigger the release of neuroactive substances from NG2 cells, providing feedback regulation of signaling at neuronal synapses. Although the presence of Ca2+ permeable AMPA receptors provides a pathway to link neuronal activity to Ca2+ dependent processes within the NG2 cells, these receptors also put these cells at risk for glutamate-associated excitotoxicity. This vulnerability to the sustained elevation of glutamate may underlie ischemic induced damage to white matter tracts and contribute to cerebral palsy in premature infants. 0300-4864 Journal Article},
	Author = {Lin, S. C. and Bergles, D. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurocytol},
	Keywords = {11 Glia;G pdf},
	Number = {6-7},
	Organization = {Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe St., WBSB 813, Baltimore, MD 21205, USA.},
	Pages = {537-49},
	Pubmed = {14501222},
	Title = {Physiological characteristics of NG2-expressing glial cells},
	Uuid = {90E9978F-E2A4-4DA7-859A-144C5D9B0F26},
	Volume = {31},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14501222}}

@article{Lin:2005,
	Abstract = {Mammalian urine releases complex mixtures of volatile compounds that are used in reproduction, territoriality and conspecific recognition. To understand how such complex mixtures are represented in the main olfactory bulb, we analysed the electrophysiological responses of individual mitral cells to volatile compounds in mouse urine. In both males and females, urine volatile compounds evoke robust responses in a small subset of mitral cells. Fractionation of the volatile compounds using gas chromatography showed that out of the hundreds of compounds present, mitral cells are activated by single compounds. One cohort of mitral cells responded exclusively to male urine; these neurons were activated by (methylthio)methanethiol, a potent, previously unknown semiochemical present only in male urine. When added to urine, synthetic (methylthio)methanethiol significantly enhances urine attractiveness to female mice. We conclude that mitral cells represent natural odorant stimuli by acting as selective feature detectors, and that their activation is largely independent of the presence of other components in the olfactory stimulus.},
	Author = {Lin, and Zhang, and Block, and Katz,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:26 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0410462},
	Organization = {HHMI and Department of Neurobiology, Box 3209, Duke University Medical Center, Durham, North Carolina 27710, USA.},
	Pii = {nature03414},
	Pubmed = {15724148},
	Title = {Encoding social signals in the mouse main olfactory bulb},
	Uuid = {78BE30DA-BC2F-4899-B2BE-C551B3DF9413},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03414}}

@article{Lin:1976,
	Abstract = {Using a membrane filter assay, we have obtained results from both kinetic and competition experiments indicating that histones bind more strongly to bromodeoxyuridine-substituted DNA than to normal DNA. At 37 degrees C in our standard buffer of 0.2 M ionic strength, the rate of dissociation of histones H1, H2, and h4 from BrdU-substituted DNA is respectively 7, 4, and 2 times slower than it is from normal DNA. Competition experiments show an even greater difference between BrdU-substituted and normal DNA with respect to histone binding. The tighter binding of histones to BrdU-substituted DNA is of interest because of the known effects of BrdU on eukaryotic chromosome condensation and staining, virus induction, and the inhibition of differentiation.},
	Author = {Lin, S. and Lin, D. and Riggs, A. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:52 -0400},
	Issn = {0305-1048},
	Journal = {Nucleic Acids Res},
	Keywords = {01 Adult neurogenesis general;Protein Binding;Binding Sites;Histones;Comparative Study;DNA;Osmolar Concentration;DNA, Viral;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Plants;Filtration;Bromodeoxyuridine;Hydrogen-Ion Concentration;23 Technique},
	Medline = {77013012},
	Month = {9},
	Nlm_Id = {0411011},
	Number = {9},
	Pages = {2183-91},
	Pubmed = {9622},
	Title = {Histones bind more tightly to bromodeoxyuridine-substituted DNA than to normal DNA},
	Uuid = {A280D993-F40F-49C1-9736-16114411117B},
	Volume = {3},
	Year = {1976},
	url = {papers/Lin_NucleicAcidsRes1976.pdf}}

@article{Lindner:2003,
	Abstract = {Recommendations from experts and recently established guidelines on how to improve the face and predictive validity of animal models of stroke have stressed the importance of using older animals and long-term behavioral-functional endpoints rather than relying almost exclusively on acute measures of infarct volume in young animals. The objective of the present study was to determine whether we could produce occlusions in older rats with an acceptable mortality rate and then detect reliable, long-lasting functional deficits. A reversible intraluminar suture middle cerebral artery occlusion (MCAO) procedure was used to produce small infarcts in middle-aged rats. This resulted in an acceptable mortality rate, and robust disabilities were detected in functional assays, although the degree of total tissue loss measured 90 d after MCAO was quite modest. Infarcted animals were functionally impaired relative to sham control animals even 90 d after the occlusions, and when animals were subgrouped based on amount of tissue loss, MCAO animals with only 4\%tissue loss exhibited enduring neurological-behavioral impairments relative to sham-operated controls, and the functional impairments in the group with the largest infarcts (20\%tissue loss) were more severe than the functional impairments in the rats with 4\%tissue loss. These results suggest that this model, using reversible MCAO to produce small infarcts and long-lasting functional-behavioral deficits in older rats, may represent an advance in the relatively higher-throughput modeling of stroke and its recovery in rodents and may be useful in the development and characterization of future stroke therapies. 1529-2401 Journal Article},
	Author = {Lindner, M. D. and Gribkoff, V. K. and Donlan, N. A. and Jones, T. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci},
	Keywords = {*Disease Models, Animal;Forelimb/physiopathology;Brain/blood supply/pathology;Rats;Predictive Value of Tests;Survival Rate;Infarction, Middle Cerebral Artery/*diagnosis/pathology/*physiopathology;*Severity of Illness Index;Reproducibility of Results;Motor Activity;11 Glia;Animals;Age Factors;G pdf;*Behavior, Animal},
	Number = {34},
	Organization = {Neuroscience Drug Discovery, Bristol-Myers Squibb Pharmaceutical Research Institute, Wallingford, Connecticut 06492, USA. Mark.Lindner\@BMS.com},
	Pages = {10913-22},
	Pubmed = {14645487},
	Title = {Long-lasting functional disabilities in middle-aged rats with small cerebral infarcts},
	Uuid = {8048D81D-7D4F-4E86-93AC-5D8526087394},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14645487}}

@article{Lindner:1976,
	Abstract = {Explants and cells of nervous tissue were cultivated in the presence of aethanol, tween 80, dimethylformamid (DMF) and dimethylsulfoxid (DMSO) and the influence upon the index of area, the growth rate and fiber index was observed. They are important to solutions of drugs for tests in vitro. At the beginning of the cultivation aethanol in vitro influenced the regeneration of nerve fibers from explants and cells. A significant increase of the index of growth was observed. After a long term influence of tween 80, DMF and DMSO an inhibition of differentiation of neurons in vitro was observed. TY - JOUR M1 - 1088567 M2 - Uber die Wirkung von Athanol und anderen Losungsmitteln auf das Nervengewebe unter In-vitro-Bedingungen.},
	Author = {Lindner, G. and Grosse, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Isbn = {0044-3107},
	Journal = {Z Mikrosk Anat Forsch},
	Keywords = {Dimethylformamide;English Abstract;Polysorbates;Tissue Culture;Cell Differentiation;Ethanol;Polyethylene Glycols;Rats;Animals;Comparative Study;Dimethyl Sulfoxide;Cell Count;Telencephalon;Hippocampus;08 Aberrant cell cycle;Trigeminal Ganglion;Chick Embryo;Neurons;Heart Ventricles;Cell Division;EE abstr;Culture Media},
	Number = {3},
	Pages = {557-564},
	Title = {Action of ethanol and other solvents on the nerve tissue under in vitro conditions},
	Uuid = {6ACD2CF9-43D6-4472-9772-232F0D7D9DA6},
	Volume = {90},
	Year = {1976},
	Bdsk-Url-1 = {http://www.hubmed.org/display.cgi?issn=00443107&uids=1088567}}

@article{Lindvall:2003,
	Abstract = {0027-8424 Comment Journal Article},
	Author = {Lindvall, O. and McKay, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Dopamine/metabolism;Human;06 Adult neurogenesis injury induced;Brain/*metabolism/*physiology;D pdf;Neurons/metabolism;Animals;*Regeneration;Central Nervous System/physiology},
	Number = {13},
	Organization = {Wallenberg Neuroscience Center, Department of Clinical Neuroscience, University Hospital, Solvegatan 17 BMC A-11, 22184 Lund, Sweden.},
	Pages = {7430-1},
	Pubmed = {12810949},
	Title = {Brain repair by cell replacement and regeneration},
	Uuid = {E9FBAF76-84ED-46FF-A72C-8D0981C28B7E},
	Volume = {100},
	Year = {2003},
	url = {papers/Lindvall_ProcNatlAcadSciUSA2003.pdf}}

@article{Ling:1989,
	Abstract = {The present study describes neuronal degeneration and its accompanying non-neuronal cellular reaction in the hypoglossal nucleus following an intraneural injection of Ricinus communis agglutinin-60 (RCA-60) into the hypoglossal nerve. The first noticeable structural changes were observed in neurons in hamsters killed 3 days after the RCA injection. Drastic alterations occurred in the period extending from the 5th to the 15th postoperative day. Two forms of neuronal degeneration were observed: light and dark types. In the light type, masses of free ribosomes were observed; other changes included the dilation of Golgi saccules and the presence of abnormal mitochondria. In the dark type of degeneration, the cells became condensed with vacuoles in their cytoplasm. Axon terminals presynaptic to the degenerating cells during this period appeared to be normal. A massive influx of mononuclear leucocytes by diapedesis occurred at the large venules. Some of the infiltrated cells were clearly lymphocytes, while others were monocytes which became indistinguishable from indigenous microglia once they were in the neuropil. Neural macrophages, most probably derived both from microglia and the infiltrated monocytes, were engaged in the phagocytosis of neuronal debris. A remarkable finding in the present study was the wide-spread occurrence of dark axon terminals in the neuropil in longer surviving animals (90 and 120 days). The structural alterations, e.g., clumping and swelling of some of the synaptic vesicles in the enhanced cytoplasmic density, suggest that these were undergoing atrophic changes resulting from the long period of dysfunction following the death of postsynaptic neurons induced by RCA.},
	Author = {Ling, E. A. and Shieh, J. Y. and Wen, C. Y. and Yick, T. Y. and Wong, W. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0914-9465},
	Journal = {Arch Histol Cytol},
	Keywords = {Hamsters;Neurons;Nerve Degeneration;Lectins;Not relevant;Plant Lectins;11 Glia;Mesocricetus;Injections;Hypoglossal Nerve;Support, Non-U.S. Gov't;Male;Animals},
	Medline = {90105065},
	Month = {10},
	Nlm_Id = {8806082},
	Number = {4},
	Organization = {Department of Anatomy, Faculty of Medicine, National University of Singapore.},
	Pages = {345-54},
	Pubmed = {2513846},
	Title = {Neural degeneration and non-neuronal cellular reactions in the hypoglossal nucleus following an intraneural injection of toxic ricin},
	Uuid = {FA74EBF9-40A5-4B9A-9EEE-23E9DF588DEA},
	Volume = {52},
	Year = {1989}}

@article{Ling:1997,
	Abstract = {Studies in songbirds suggest that neurogenesis during the first few years of life is related to song learning. In this study, we examined whether postnatal neurogenesis occurs in a nonsongbird, the ring dove (Streptoplia risoria), and whether it persists to old age. Twenty-four hours after a single intramuscular injection of [3H]thymidine, labeled cells were present in the brains, particularly in the lateral wall of the lateral ventricle of juvenile (3-month and 8-month) and adult (1- year to 8-year) doves. Two months after multiple [3H]thymidine injections, there were fewer labeled cells in the ventricular zone (VZ), but many labeled cells with neuronal morphology in the parenchyma of the forebrain; labeled cells were confirmed as neurons by using neuron-specific markers, microtubule-associated protein-2 (MAP-2) and anti-neuronal nucleus (NeuN). In general, new neurons were distributed in the forebrain without clustering in any particular nucleus. During the first year of life, however, neostriatum caudale and hyperstriatum, the regions known to be essential for proper integration of sensory cues and reproductive behavior, contained more new neurons than any other brain regions. These neuronal additions showed an age-related decline; the first reduction coincided with the dove's attainment of adult physical size (about 3 months old) and the second occurred when the dove would normally attain reproductive fitness (about 1 year old). A low level of forebrain neurogenesis persisted up to 8 years of age (the oldest animals studied). These observations suggest that neurogenesis in adulthood is widespread among birds but that the biological significance of adult neurogenesis in the ring dove remains to be determined.},
	Author = {Ling, C. and Zuo, M. and Alvarez-Buylla, A. and Cheng, M. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Comp Neurol},
	Keywords = {01 Adult neurogenesis general;Cell Division/physiology;Thymidine/diagnostic use;Comparative Study;Autoradiography;Female;A abstr;Cell Count;Neurons/*cytology;Tritium/diagnostic use;Support, U.S. Gov't, P.H.S.;Aging/*physiology;Animal;Male;Birds/*physiology;Telencephalon/cytology/*growth &development;Support, Non-U.S. Gov't},
	Number = {2},
	Organization = {Department of Brain &Cognitive Science, Massachusetts Institute of Technology, Cambridge 02139, USA.},
	Pages = {300-12.},
	Title = {Neurogenesis in juvenile and adult ring doves},
	Uuid = {80D1A5B6-B2B1-4C10-B321-758E76214853},
	Volume = {379},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9050792}}

@article{Linnarsson:2000,
	Abstract = {There are two populations of neurons which are continually renewed in the adult, the dentate gyrus granule neurons and the olfactory bulb granule and periglomerular neurons. In the dentate gyrus, a secondary proliferative zone termed the subgranular zone is established along the interface between the dentate gyrus and the hilus where granule cells are born throughout life. Olfactory bulb neurons are generated in the anterior subventricular zone of the lateral ventricle and migrate via the rostral migratory stream to the olfactory bulb. We examined animals lacking brain-derived neurotrophic factor (BDNF) in order to establish whether this neurotrophin could be involved in the generation and/or survival of these neurons in vivo. We find that cells in nestin- positive regions of both the subgranular layer of the dentate gyrus and the subventricular zone of the olfactory bulb undergo apoptosis starting 2 weeks after birth in the absence of BDNF. However, increased apoptosis was not limited to precursors, as apoptotic cells were also found in the granule cell layer of the dentate gyrus and in the granule and periglomerular layers of the olfactory bulb. The excessive cell death was limited to these populations of neurons as no excessive cell death was detected in other forebrain areas. We conclude that BDNF is essential for the survival of neurons specifically in populations which are continuously being regenerated in the brain.},
	Author = {Linnarsson, S. and Willson, C. A. and Ernfors, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Brain Res Mol Brain Res},
	Keywords = {Aging;Olfactory Bulb/cytology/growth &development/*physiology;Mice, Knockout;Brain-Derived Neurotrophic Factor/deficiency/genetics/*physiology;C;Neurons/*cytology/physiology;Cerebral Ventricles/cytology/growth &development/*physiology;Nerve Regeneration/*physiology;Cell Survival;Animal;04 Adult neurogenesis factors;Support, Non-U.S. Gov't;Mice;Apoptosis/*physiology;Dentate Gyrus/cytology/growth &development/*physiology;In Situ Nick-End Labeling},
	Number = {1},
	Organization = {Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Doktorsringen 12A, 171 77, Stockholm, Sweden.},
	Pages = {61-9.},
	Title = {Cell death in regenerating populations of neurons in BDNF mutant mice},
	Uuid = {323BCDD7-7AE6-4DBF-9C00-86AAF56C0520},
	Volume = {75},
	Year = {2000},
	url = {papers/Linnarsson_BrainResMolBrainRes2000.pdf}}

@article{Lipardi:2001,
	Abstract = {In posttranscriptional gene silencing (PTGS), "quelling,"and RNA interference (RNAi), 21-25 nucleotide RNA fragments are produced from the initiating dsRNA. These short interfering RNAs (siRNAs) mediate RNAi by an unknown mechanism. Here, we show that GFP and Pp-Luc siRNAs, isolated from a protein complex in Drosophila embryo extract, target mRNA degradation in vitro. Most importantly, these siRNAs, as well as a synthetic 21-nucleotide duplex GFP siRNA, serve as primers to transform the target mRNA into dsRNA. The nascent dsRNA is degraded to eliminate the incorporated target mRNA while generating new siRNAs in a cycle of dsRNA synthesis and degradation. Evidence is presented that mRNA-dependent siRNA incorporation to form dsRNA is carried out by an RNA-dependent RNA polymerase activity (RdRP). 0092-8674 Journal Article},
	Author = {Lipardi, C. and Wei, Q. and Paterson, B. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Cell},
	Keywords = {Drosophila/embryology;*RNA Processing, Post-Transcriptional;RNA, Untranslated/*biosynthesis/metabolism;RNA, Antisense;*Gene Silencing;RNA/*metabolism;Micrococcal Nuclease/metabolism;T abstr;RNA, Double-Stranded/*metabolism;RNA, Messenger/*metabolism;Animals;RNA, Small Interfering;Polymerase Chain Reaction;23 Technique;Luminescent Proteins/genetics/metabolism},
	Number = {3},
	Organization = {Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.},
	Pages = {297-307},
	Pubmed = {11701121},
	Title = {RNAi as random degradative PCR: siRNA primers convert mRNA into dsRNAs that are degraded to generate new siRNAs},
	Uuid = {111B4059-78BB-44CE-9EED-DB1339EA65D8},
	Volume = {107},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11701121}}

@article{Lipscomb:2002,
	Abstract = {The murine olfactory system consists of two primary divisions: (1) a main olfactory system, in which olfactory sensory neurons (OSNs) located in the main olfactory epithelium (MOE) send their axons to glomeruli in the main olfactory bulb (MOB); and (2) an accessory olfactory system, in which OSNs located in the vomeronasal organ send their axons to glomeruli in the accessory olfactory bulb (AOB). In labeling studies using the lectin Ulex europaeus agglutinin (UEA), we discovered a novel subset of small neuropilar structures in the MOB that are distinct from other glomeruli both in the MOB and AOB. These "microglomeruli"are morphologically similar to MOB glomeruli in many respects: they receive innervation from processes present in the olfactory nerve layer and are isolated from other glomeruli by juxtaglomerular cells; in addition, the compartmental pattern of UEA labeling suggests the presence of UEA (-) processes within their neuropil. Microglomeruli contained processes that express the olfactory marker protein, a marker common to mature OSN axons. However, unlike other glomerular structures, the microglomeruli did not contain neural cell adhesion molecule-labeled processes. Within microglomeruli, UEA(+) processes interdigitated with MAP2(+) dendrites, some of which likely originate from interneurons, as indicated by glutamic acid decarboxylase labeling. Synaptophysin labeling in microglomeruli strongly suggested that synapses occur between UEA(+) processes and dendrites. Anterograde labeling of OSNs, by injection of rhodamine- dextran into one naris, demonstrated that UEA(+) processes in microglomeruli originated in the MOE. The unique morphology, protein expression, and location of microglomeruli have led us to hypothesize that they represent a novel class of glomerular structures in the murine olfactory system.},
	Author = {Lipscomb, B. W. and Treloar, H. B. and Greer, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci},
	Keywords = {I;13 Olfactory bulb anatomy},
	Number = {3},
	Organization = {Interdepartmental Neuroscience Graduate Program, Department of Neurosurgery, and Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.},
	Pages = {766-74.},
	Title = {Novel microglomerular structures in the olfactory bulb of mice},
	Uuid = {85181C1D-59A3-40D8-BC27-46CCE1BBBB95},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11826106%20http://www.jneurosci.org/cgi/content/full/22/3/766%20http://www.jneurosci.org/cgi/content/abstract/22/3/766}}

@article{Liu:2005a,
	Abstract = {The plant innate immune response includes the hypersensitive response (HR), a form of programmed cell death (PCD). PCD must be restricted to infection sites to prevent the HR from playing a pathologic rather than protective role. Here we show that plant BECLIN 1, an ortholog of the yeast and mammalian autophagy gene ATG6/VPS30/beclin 1, functions to restrict HR PCD to infection sites. Initiation of HR PCD is normal in BECLIN 1-deficient plants, but remarkably, healthy uninfected tissue adjacent to HR lesions and leaves distal to the inoculated leaf undergo unrestricted PCD. In the HR PCD response, autophagy is induced in both pathogen-infected cells and distal uninfected cells; this is reduced in BECLIN 1-deficient plants. The restriction of HR PCD also requires orthologs of other autophagy-related genes including PI3K/VPS34, ATG3, and ATG7. Thus, the evolutionarily conserved autophagy pathway plays an essential role in plant innate immunity and negatively regulates PCD.},
	Author = {Liu, Yule and Schiff, Michael and Czymmek, Kirk and Tall{\'o}czy, Zsolt and Levine, Beth and Dinesh-Kumar, S. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Molecular Sequence Data;Organelles;Base Sequence;Proteins;Gene Expression Regulation, Plant;Apoptosis;Research Support, U.S. Gov't, Non-P.H.S.;Plant Proteins;Tobacco;1-Phosphatidylinositol 3-Kinase;Research Support, U.S. Gov't, P.H.S.;Saccharomyces cerevisiae Proteins;Microscopy, Electron, Transmission;Tumor Suppressor Proteins;Amino Acid Sequence;Research Support, N.I.H., Extramural;Tobacco Mosaic Virus;24 Pubmed search results 2008;Immunity, Natural;Autophagocytosis},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {4},
	Organization = {Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520, USA.},
	Pages = {567-77},
	Pii = {S0092-8674(05)00240-0},
	Pubmed = {15907470},
	Title = {Autophagy regulates programmed cell death during the plant innate immune response},
	Uuid = {8AEA457A-F07E-4435-9E84-1B46663D9DEA},
	Volume = {121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.03.007}}

@article{Liu:2003a,
	Abstract = {Seizures increase dentate granule cell proliferation in adult rats but decrease proliferation in young pups. The particular period and number of perinatal seizures required to cause newborn granule cell suppression in development are unknown. Therefore, we examined cell proliferation with bromodeoxyuridine (BrdU) immunohistochemistry during the peak of neurogenesis (e.g., P6 and P9) and at later postnatal ages (e.g., P13, P20, or P30) following single and multiple episodes of perinatal status epilepticus induced by kainate (KA). Because an inverse relationship exists between glucocorticosteroids (CORT) levels and granule cell proliferation, plasma CORT levels and electroencephalographic (EEG) activity were simultaneously monitored to elucidate underlying mechanisms that inhibit cell proliferation. In control animals, the number of BrdU-labeled cells increased then declined with maturation. After 1x KA or 2x KA administered on P6 and P9, the numbers of BrdU-labeled cells were not different from age-matched controls. However, rat pups with 3x KA (on P6, P9, and P13) had marked suppression of BrdU-labeled cells 48-72 h after the last seizure (43 +/- 6.5\%of control). Cell proliferation was also significantly inhibited on P20 after 2x KA (to 56 +/- 6.9\%) or 3x KA (to 54 +/- 7.9\%) and on P30 with 3x KA (to 74.5 +/- 8.2\%of age-matched controls). Cell death was not apparent as chromatin stains showed increased basophilia of only inner cells lining the granule cell layers, in the absence of eosinophilia, argyrophilia, or terminal deoxynucleotidyl dUTP nick endlabeling (TUNEL) labeling at times examined. In P13 pups with 3x KA, electron microscopy revealed an increased number of immature granule cells and putative stem cells with irregular shape, condensed cytoplasm, and electron dense nuclei, and they were also BrdU positive. The EEG showed no relationship between neurogenesis and duration of high-synchronous ictal activity. However, endocrine studies showed a correlation with BrdU number and age, sustained increases in circulating CORT levels following 1x KA on P6 (0.7 +/- 0.1 to 2.40 +/- 0.86 microg/dl), and cumulative increases that exceeded 10 microg/dl at 4-8 h after 3x KA on P13 or P20. In conclusion, a history of only one or two perinatal seizure(s) can suppress neurogenesis if a second or third seizure recurs after a critical developmental period associated with a marked surge in CORT. During the first 2 weeks of postnatal life sustained increases in postictal circulating CORT levels but not duration or intensity of ictal activity has long-term consequences on neurogenesis. The occurrence of an increased proportion of immature granule cells and putative stem cells with irregular morphology in the absence of neurodegeneration suggests that progenitors may not differentiate properly and remain in an immature state.},
	Author = {Liu, H. and Kaur, J. and Dashtipour, K. and Kinyamu, R. and Ribak, C. E. and Friedman, L. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Fluorescent Antibody Technique, Indirect;Silver Staining;Animals;Rats;Seizures;Cell Count;Rats, Sprague-Dawley;Hippocampus;Cytoplasmic Granules;Antimetabolites;Status Epilepticus;Hydrocortisone;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;In Situ Nick-End Labeling;Glucocorticoids;Dentate Gyrus;Radioimmunoassay;24 Pubmed search results 2008;Immunohistochemistry;Microscopy, Electron;Bromodeoxyuridine;Electroencephalography},
	Medline = {22999028},
	Month = {11},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {New Jersey Neuroscience Institute, Seton Hall University, South Orange, NJ 07079, USA.},
	Pages = {196-213},
	Pii = {S0014488603002073},
	Pubmed = {14637092},
	Title = {Suppression of hippocampal neurogenesis is associated with developmental stage, number of perinatal seizure episodes, and glucocorticosteroid level},
	Uuid = {17AE3D08-D878-4CD9-AAD5-00DD2873DAF7},
	Volume = {184},
	Year = {2003}}

@article{Liu:1998a,
	Abstract = {We have examined the glial cell response, the possible expression of compounds associated with the complement cascade, including the putative complement inhibitor clusterin, and their cellular association during Wallerian degeneration in the central nervous system. Examination of the proliferation pattern revealed an overall greater mitotic activity after rhizotomy, an exclusive involvement of microglia in this proliferation after peripheral nerve injury, but, in addition, a small fraction of proliferating astrocytes after rhizotomy. Immunostaining with the phagocytic cell marker ED1 gradually became very prominent after rhizotomy, possibly reflecting a response to the extensive nerve fiber disintegration. Lumbar dorsal rhizotomy did not induce endogenous immunoglobulin G (IgG) deposition or complement expression in the spinal cord dorsal horn, dorsal funiculus, or gracile nucleus. This is in marked contrast to the situation after peripheral nerve injury, which appears to activate the entire complement cascade in the vicinity of the central sensory processes. Clusterin, a multifunctional protein with complement inhibitory effects, was markedly upregulated in the dorsal funiculus in astrocytes. In addition, there was an intense induction of clusterin expression in the degenerating white matter in oligodendrocytes, possibly reflecting a degeneration process in these cells. The findings suggest that 1) complement expression by microglial cells is intimately associated with IgG deposition; 2) axotomized neuronal perikarya, but not degenerating central fibers, undergo changes which induce such deposition; and 3) clusterin is not related to complement expression following neuronal injury but participates in regulating the state of oligodendrocytes during Wallerian degeneration.},
	Author = {Liu, L. and Persson, J. K. and Svensson, M. and Aldskogius, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Wallerian Degeneration;Brain Stem;Complement Inactivators;Complement;Sciatic Nerve;Organ Specificity;Oligodendroglia;Oligonucleotides, Antisense;Animals;Phagocytosis;Cell Division;RNA, Messenger;In Situ Hybridization;11 Glia;Molecular Chaperones;Biological Markers;Not relevant;Gene Expression Regulation;Comparative Study;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein;Neuroglia;Rats;Female;Complement Activation;Microglia;Spinal Nerve Roots;Glycoproteins;Rhizotomy;Immunoglobulin G;Support, Non-U.S. Gov't;Nerve Tissue Proteins;Astrocytes},
	Medline = {98295564},
	Month = {7},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Anatomy, Biomedical Center, Uppsala University, Sweden. li.liu\@anatomi.uu.se},
	Pages = {221-38},
	Pii = {10.1002/(SICI)1098-1136(199807)23:3<221::AID-GLIA5>3.0.CO;2-7},
	Pubmed = {9633807},
	Title = {Glial cell responses, complement, and clusterin in the central nervous system following dorsal root transection},
	Uuid = {1677A3C6-CD3E-4603-AE33-5894A0ECB285},
	Volume = {23},
	Year = {1998}}

@article{Liu:2003c,
	Abstract = {The olfactory bulb (OB) core is an extension of the rostral migratory stream and thus is a potential source of neural progenitor and neural stem cells. We characterized in vivo and in vitro neuronal progenitor and neural stem cells in the adult OB core. In mouse and rat, bromodeoxyuridine (BrdU) labeling showed that the OB core accumulates newly replicated cells. Nestin, a neuroepithelial stem cell marker, was enriched in the OB core. BrdU-positive cells were immunolabeled for nestin and TUC4, a marker for early postmitotic neurons. The distributions of cells labeled for BrdU, TUC4, and nestin were similarly concentrated in the OB core. Nestin- and TUC4-positive cells were also found in the OB of young and aged humans. Isolated and cultured OB core cells from adult rat and mouse had the capacity to generate numerous neurospheres. Adult OB core neurospheres were cryopreserved and subsequently cultured. Single cell clonal analysis of neurospheres revealed the capacity for self-renewal and multipotency. Cultured adult OB core cells differentiated into neurons, astrocytes, and oligodendrocytes. Some neurons expressed choline acetlytransferase, substance P, and glutamic acid decarboxylase. Basic fibroblast growth factor potentiated the self-renewal of cells and beta-nerve growth factor stimulated differentiation. OB-derived neural stem cells in coculture with skeletal muscle cells were induced to become neurons expressing choline acetyltransferase and substance P and formed neuromuscular synaptic junctions on myocytes displaying acetylcholinesterase-positive motor end plates. Cocultured OB-derived neural stem cells with myoblast cells also generated nonneural cell progeny. We conclude that the adult mammalian OB core is a reservoir of neural progenitor cells and pluripotent neural stem cells. 0021-9967 Journal Article},
	Author = {Liu, Z. and Martin, L. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Human;Animals;Neurons/chemistry/*cytology/drug effects;Cells, Cultured;Stem Cells/chemistry/*cytology/drug effects;Rats;Comparative Study;Cell Survival/drug effects/physiology;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Mice, Inbred C57BL;Male;Aged;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;BB pdf;Aged, 80 and over;Cell Differentiation/drug effects/physiology;Adult;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Mice;Olfactory Bulb/chemistry/*cytology/drug effects;Coculture/methods},
	Number = {4},
	Organization = {Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.},
	Pages = {368-91},
	Title = {Olfactory bulb core is a rich source of neural progenitor and stem cells in adult rodent and human},
	Uuid = {13289AF0-9881-4C21-8D64-D922E74D4A43},
	Volume = {459},
	Year = {2003},
	url = {papers/Liu_JCompNeurol2003}}

@article{Liu:1998,
	Abstract = {Neurogenesis in the dentate gyrus of adult rodents is regulated by NMDA receptors, adrenal steroids, environmental stimuli, and seizures. To determine whether ischemia affects neurogenesis, newly divided cells in the dentate gyrus were examined after transient global ischemia in adult gerbils. 5-Bromo-2'-deoxyuridine-5'-monophosphate (BrdU) immunohistochemistry demonstrated a 12-fold increase in cell birth in the dentate subgranular zone 1-2 weeks after 10 min bilateral common carotid artery occlusions. Two minutes of ischemia did not significantly increase BrdU incorporation. Confocal microscopy demonstrated that BrdU immunoreactive cells in the granule cell layer colocalized with neuron-specific markers for neuronal nuclear antigen, microtubule-associated protein-2, and calbindin D28k, indicating that the newly divided cells migrated from the subgranular zone into the granule cell layer and matured into neurons. Newborn cells with a neuronal phenotype were first seen 26 d after ischemia, survived for at least 7 months, were located only in the granule cell layer, and comprised approximately 60\%of BrdU-labeled cells in the granule cell layer 6 weeks after ischemia. The increased neurogenesis was not attributable to entorhinal cortical lesions, because no cell loss was detected in this region. Ischemic preconditioning for 2 min, which protects CA1 neurons against subsequent ischemic damage, did not prevent increased neurogenesis in the granule cell layer after a subsequent severe ischemic challenge. Thus, ischemia-induced dentate neurogenesis is not attributable to CA1 neuronal loss. Enhanced neurogenesis in the dentate gyrus may be a compensatory adaptive response to ischemia-associated injury and could promote functional recovery after ischemic hippocampal injury. 0270-6474 Journal Article},
	Author = {Liu, J. and Solway, K. and Messing, R. O. and Sharp, F. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci},
	Keywords = {Dentate Gyrus/*blood supply/*cytology;Animals;Gerbillinae;Neurons/*cytology;Thymidine/pharmacokinetics;Ischemic Attack, Transient/*physiopathology;Cell Count;Stem Cells/cytology;Antimetabolites;Male;Entorhinal Cortex/blood supply/cytology;D abstr;Cell Division/physiology;06 Adult neurogenesis injury induced;Support, U.S. Gov't, P.H.S.;Cell Differentiation/physiology;Biological Markers;Bromodeoxyuridine;Astrocytes/cytology},
	Number = {19},
	Organization = {Departments of Neurology and Neurosurgery, University of California at San Francisco and San Francisco Veterans Affairs Medical Center, San Francisco, California 94121, USA.},
	Pages = {7768-78},
	Pubmed = {9742147},
	Title = {Increased neurogenesis in the dentate gyrus after transient global ischemia in gerbils},
	Uuid = {0EDB751A-EC81-11DA-8605-000D9346EC2A},
	Volume = {18},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9742147}}

@article{Liu:2003b,
	Abstract = {Several thousand new neurons are produced each day in the adult mammalian hippocampus, among which only excitatory granule cells (GCs) have thus far been identified. In the present study, we used mutant Semliki Forest Virus vectors to express enhanced green fluorescent protein in the hippocampus, and observed that approximately 14\%of newly generated neurons in the dentate gyrus of adult rats are GABAergic basket cells (BCs). With the use of double whole-cell patch-clamp recordings from BC-GC pairs in hippocampal slices, we demonstrate that newly generated BCs in the dentate gyrus form inhibitory synapses with principal GCs. These data show for the first time that functional inhibitory neurons are recruited in the dentate gyrus of adult rats. 1529-2401 Journal Article},
	Author = {Liu, S. and Wang, J. and Zhu, D. and Fu, Y. and Lukowiak, K. and Lu, Y. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {J Neurosci},
	Keywords = {Bromodeoxyuridine;A pdf;Neurons/classification/*cytology/metabolism/virology;Animals;Rats;Phenotype;Neural Inhibition/*physiology;Patch-Clamp Techniques;Female;Cell Count;Rats, Sprague-Dawley;Excitatory Postsynaptic Potentials/physiology;Genetic Vectors/administration &dosage/physiology;Isoenzymes/analysis/biosynthesis;Male;01 Adult neurogenesis general;Support, Non-U.S. Gov't;Synaptic Transmission/physiology;Cell Division/physiology;Hippocampus/*cytology/growth &development/virology;Cell Differentiation/physiology;Immunohistochemistry;Glutamate Decarboxylase/analysis/biosynthesis;gamma-Aminobutyric Acid/metabolism;Luminescent Proteins/genetics;Semliki forest virus/genetics/physiology;Genes, Reporter},
	Number = {3},
	Organization = {Neuroscience Research Group, Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada, T2N 4N1.},
	Pages = {732-6},
	Title = {Generation of functional inhibitory neurons in the adult rat hippocampus},
	Uuid = {DDD6D9F7-CCBF-442F-A5E2-CF720E0F5F4D},
	Volume = {23},
	Year = {2003},
	url = {papers/Liu_JNeurosci2003.pdf}}

@article{Liu:2003,
	Abstract = {Interneurons in the olfactory bulb (OB) are generated not only in the developing embryo but also throughout the postnatal life of mammals from neuronal precursor cells migrating from the anterior subventricular zone (SVZa) of the mammalian forebrain. We discovered that the OB secretes a diffusible activity that attracts these neuronal precursor cells. The attractive activity is present in specific layers in the OB, including the glomerular layer but not the granule cell layer. The attractive activity and the neuronal responsiveness persist from embryonic through neonatal to adult stages. Removal of the rostral OB significantly reduces SVZa migration toward the OB, an effect that can be rescued by a transplant of the OB but not by that of the neocortex. The activity in the OB is not mimicked by the known attractants. These results provide an explanation for the continuous migration of SVZa neurons toward the OB, demonstrate an important role of the OB in neuronal migration, and reveal the existence of a new chemoattractant. 1529-2401 Journal Article},
	Author = {Liu, G. and Rao, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;Neurons/*cytology/drug effects/physiology;Signal Transduction;Animals;In Vitro;Cells, Cultured;Rats;Coculture Techniques;Stem Cells/*cytology/drug effects/physiology;B pdf;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Cell Movement;Olfactory Bulb/cytology/embryology/*metabolism;Chemotactic Factors/pharmacology/*physiology;Olfactory Bulb;Prosencephalon;Support, Non-U.S. Gov't;Research Support, U.S. Gov't, P.H.S.;Cell Movement/drug effects/physiology;Coculture;Neurons;Support, U.S. Gov't, P.H.S.;Diffusion;Chemotactic Factors;Stem Cells;Gestational Age;Signal Transduction/physiology;Prosencephalon/*cytology/embryology/physiology},
	Medline = {22761098},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {16},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.},
	Pages = {6651-9},
	Pii = {23/16/6651},
	Pubmed = {12878706},
	Title = {Neuronal migration from the forebrain to the olfactory bulb requires a new attractant persistent in the olfactory bulb},
	Uuid = {B54BBF07-8397-4C07-9AFE-6F72BA0F4B6F},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12878706}}

@article{Liu:2005,
	Abstract = {In the postnatal subventricular zone (SVZ), local cues or signaling molecules released from neuroblasts limit the proliferation of glial fibrillary acidic protein (GFAP)-expressing progenitors thought to be stem cells. However, signals between SVZ cells have not been identified. We show that depolarization of neuroblasts induces nonsynaptic SNARE-independent GABA(A) receptor currents in GFAP-expressing cells, the time course of which depends on GABA uptake in acute mouse slices. We found that GABA(A) receptors are tonically activated in GFAP-expressing cells, consistent with the presence of spontaneous depolarizations in neuroblasts that are sufficient to induce GABA release. These data demonstrate the existence of nonsynaptic GABAergic signaling between neuroblasts and GFAP-expressing cells. Furthermore, we show that GABA(A) receptor activation in GFAP-expressing cells limits their progression through the cell cycle. Thus, as GFAP-expressing cells generate neuroblasts, GABA released from neuroblasts provides a feedback mechanism to control the proliferation of GFAP-expressing progenitors by activating GABA(A) receptors.},
	Author = {Liu, Xiuxin and Wang, Qin and Haydar, Tarik F. and Bordey, Ang{\'e}lique},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Research Support, N.I.H., Extramural;Spider Venoms;24 Pubmed search results 2008;Green Fluorescent Proteins;Sodium Channel Blockers;GABA Antagonists;Immunohistochemistry;Chelating Agents;10 Development;Animals;04 Adult neurogenesis factors;03 Adult neurogenesis progenitor source;Research Support, U.S. Gov't, P.H.S.;In Vitro;Egtazic Acid;Botulinum Toxins;Cell Count;Potassium;Electric Stimulation;Bromodeoxyuridine;Lateral Ventricles;Drug Interactions;Dose-Response Relationship, Radiation;Cyclooxygenase Inhibitors;Membrane Potentials;gamma-Aminobutyric Acid;Nickel;Gene Expression Regulation;Cadmium;Comparative Study;Glial Fibrillary Acidic Protein;Enzyme Inhibitors;Tetrodotoxin;Meclofenamic Acid;Patch-Clamp Techniques;Dose-Response Relationship, Drug;Stem Cells;Animals, Newborn;Cell Proliferation;Mice;Research Support, Non-U.S. Gov't;Neurons;Mice, Transgenic},
	Month = {9},
	Nlm_Id = {9809671},
	Number = {9},
	Organization = {Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06520-8082, USA.},
	Pages = {1179-87},
	Pii = {nn1522},
	Pubmed = {16116450},
	Title = {Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP-expressing progenitors},
	Uuid = {63BEBDEF-E0E8-4922-99E1-7C281ED70367},
	Volume = {8},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1522}}

@article{Liu:2000,
	Abstract = {BETA2/NeuroD is a homologue of the Drosophila atonal gene that is widely expressed during development in the mammalian brain and pancreas. Although studies in Xenopus suggest that BETA2/NeuroD is involved in cellular differentiation, its function in the mammalian nervous system is unclear. Here we show that mutant mice homozygous for a deletion at the BETA2/NeuroD locus fail to develop a granule cell layer within the dentate gyrus, one of the principal structures of the hippocampal formation. To understand the basis of this abnormality, we analyzed dentate gyrus development by using immunocytochemical markers in BETA2/NeuroD-deficient mice. The early cell populations in the dentate gyrus, including Cajal-Retzius cells and radial glia, are present and appear normally organized. The migration of dentate precursor cells and newly born granule cells from the neuroepithelium to the dentate gyrus remains intact. However, there is a dramatic defect in the proliferation of precursor cells once they reach the dentate and a significant delay in the differentiation of granule cells. This leads to malformation of the dentate granule cell layer and excess cell death. BETA2/NeuroD null mice also exhibit spontaneous limbic seizures associated with electrophysiological evidence of seizure activity in the hippocampus and cortex. These findings thus establish a critical role of BETA2/NeuroD in the development of a specific class of neurons. Furthermore, failure to express BETA2/NeuroD leads to a stereotyped pattern of pathological excitability of the adult central nervous system.},
	Author = {Liu, M. and Pleasure, S. J. and Collins, A. E. and Noebels, J. L. and Naya, F. J. and Tsai, M. J. and Lowenstein, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Differentiation;Animals;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Trans-Activators;Mice, Mutant Strains;Phenotype;Female;Epilepsy;Mutation;Hippocampus;Mice, Inbred C57BL;Male;In Situ Hybridization;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred Strains;Neurons;Dentate Gyrus;Genotype;Mice;Cell Division;Limbic System;Research Support, Non-U.S. Gov't},
	Medline = {20105564},
	Month = {1},
	Nlm_Id = {7505876},
	Number = {2},
	Organization = {Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA.},
	Pages = {865-70},
	Pubmed = {10639171},
	Title = {Loss of BETA2/NeuroD leads to malformation of the dentate gyrus and epilepsy},
	Uuid = {3210BAF0-716F-11DA-A383-000D9346EC2A},
	Volume = {97},
	Year = {2000},
	url = {papers/Liu_ProcNatlAcadSciUSA2000.pdf}}

@article{Lo:2001,
	Author = {Lo, D. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:52 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Biomedical Technology;Gene Expression Regulation, Developmental;Drug Industry;Human;Neurosciences;Time Factors;review, tutorial;Genomic Library;Animals;Central Nervous System Diseases;review;23 Technique},
	Medline = {21547534},
	Month = {11},
	Nlm_Id = {9809671},
	Organization = {Cogent Neuroscience, Inc. 4321 Medical Park Drive Durham, NC 27704, USA.},
	Pages = {1153-4},
	Pii = {nn1101-1153},
	Pubmed = {11687820},
	Title = {Challenges for neuroscience in a post-genome world},
	Uuid = {589AB5B1-3FED-497D-8C84-6256F0A8B98D},
	Volume = {4 Suppl},
	Year = {2001},
	url = {papers/Lo_NatNeurosci2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1101-1153}}

@article{Locatelli:2003,
	Abstract = {Recent evidence suggests that cells from bone marrow can acquire neuroectodermal phenotypes in cell culture or after transplantation in animal models and in the human brain. However, isolation of the bone marrow cell subpopulation with neuronal differentiation potential remains a challenge. To isolate and expand neural progenitors from whole murine bone marrow, bone marrow was obtained from hind limb bone of C57BL6 mice and plated in culture with neuronal medium with basic fibroblast growth factor and epidermal growth factor. After 5-7 days in culture, cellular spheres similar to brain neurospheres appeared either floating or attached to culture dishes. These spheres were collected, dissociated, and expanded. The bone marrow-derived spheres were positive for nestin as assessed by immunocytochemistry and by reverse transcriptase polymerase chain reaction. Thy-1- and Sca-1-positive bone marrow cells selected by magnetic cell sorting resulted in a higher yield of nestin-positive spheres. After exposure to neuronal differentiative medium retinoic acid with and without Sonic hedgehog, cells positive for neuronal markers tubulin III (TuJ-1) and neurofilament (NF) were detected. The mRNA profile of these cells included the expression of TuJ-1, neuronal-specific enolase (NSE), and NF-light chain. To evaluate the in vivo behavior of these cells, spheres derived from bone marrow-derived cells of transgenic green fluorescent protein (GFP) mice were transplanted into newborn mouse brain. Two months later, the mouse neural cortex contained a minor proportion of GFP(+) cells co-expressing neuronal markers (TuJ-1, NF, MAP-2, NeuN). Although cell fusion phenomena with the host cells could not be ruled out, bone marrow-derived neurosphere transplantation could be a strategy for cellular mediated gene therapy.},
	Author = {Locatelli, F. and Corti, S. and Donadoni, C. and Guglieri, M. and Capra, F. and Strazzer, S. and Salani, S. and Del Bo, R. and Fortunato, F. and Bordoni, A. and Comi, G. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1525-8165},
	Journal = {J Hematother Stem Cell Res},
	Keywords = {Tretinoin;Cell Differentiation;Phosphopyruvate Hydratase;Antigens, Thy-1;Green Fluorescent Proteins;Immunohistochemistry;Luminescent Proteins;Brain;Animals;Epidermal Growth Factor;Intermediate Filament Proteins;Fibroblast Growth Factor 2;Gene Expression;Bone Marrow Transplantation;Mice, Inbred C57BL;Neurofilament Proteins;Tubulin;11 Glia;Antigens, Ly;Cell Adhesion;Proto-Oncogene Protein c-kit;Glial Fibrillary Acidic Protein;Neuroglia;Immunomagnetic Separation;Membrane Proteins;Bone Marrow Cells;Animals, Newborn;Stem Cells;Microscopy, Confocal;Mice;Research Support, Non-U.S. Gov't;Neurons;Mice, Transgenic;Reverse Transcriptase Polymerase Chain Reaction;Nerve Tissue Proteins;Trans-Activators},
	Month = {12},
	Nlm_Id = {100892915},
	Number = {6},
	Organization = {Centro Dino Ferrari, Dipartimento di Scienze Neurologiche, Universit\`{a} degli Studi di Milano, I.R.C.C.S. Ospedale Maggiore Policlinico, Milan, Italy.},
	Pages = {727-34},
	Pubmed = {14977481},
	Title = {Neuronal differentiation of murine bone marrow Thy-1- and Sca-1-positive cells},
	Uuid = {A8A7A0C0-D3A3-4E60-9FFC-3841F44311AC},
	Volume = {12},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/15258160360732740}}

@article{Loewen:2004,
	Abstract = {PURPOSE: To address a problem impeding research into glaucoma-associated genetic mutations and glaucoma gene therapy and achieve permanent, targeted transgene expression in the trabecular meshwork (TM). Lentiviral vectors are known to transduce human donor eye TM ex vivo, but efficacy in vivo has not been shown. More generally in the field of gene therapy, the authors hypothesized that distinctive properties of the intraocular aqueous circulation could facilitate solving problems of accessibility, targeting, and scale that have hindered realization of gene therapy in other settings. METHODS: A domestic cat model was developed in which long-term in vivo studies were performed. After dose-response studies in primary human TM cells, 19 cats received anterior chamber (AC) injections of stepped doses (10(6)-10(8) transduction units) of lentiviral vectors encoding different marker transgenes (beta-galactosidase, Aequorea victoria green fluorescent protein [GFP], or Renilla reniformis GFP). Animals were monitored serially for transgene expression and IOP. RESULTS: High-grade, stable transgene expression in the TM was achieved and monitored noninvasively over time in living animals. Extensive expression resulted after a single transcorneal injection, persisted for at least 10 months (time of death in the present studies), and was targeted to the TM. The initial IOP did not differ significantly from the IOP at the end of the study (P = 0.4). Aequorea GFP was superior to Renilla GFP. Vectors were effective enough to cause GFP-specific overexpression cytotoxicity at the highest dose, which was solved by dose reduction. CONCLUSIONS: High-grade transgene expression in this large-animal model persisted stably for at least 10 months after a single transcorneal lentiviral vector injection, was highly targeted, and could be monitored serially and noninvasively in living animals. These studies provide a basis for developing realistic disease models and administering glaucoma gene therapy.},
	Author = {Loewen, Nils and Fautsch, Michael P. and Teo, Wu-Lin L. and Bahler, Cindy K. and Johnson, Douglas H. and Poeschla, Eric M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0146-0404},
	Journal = {Invest Ophthalmol Vis Sci},
	Keywords = {Transgenes;Transduction, Genetic;beta-Galactosidase;Gene Targeting;Humans;Cells, Cultured;Animals;Lentivirus;Indicators and Reagents;Animals, Genetically Modified;11 Glia;Green Fluorescent Proteins;Time Factors;Genetic Vectors;Intraocular Pressure;Trabecular Meshwork;Research Support, U.S. Gov't, P.H.S.;Aqueous Humor;Luminescent Proteins;Cats;Gene Expression;Research Support, Non-U.S. Gov't},
	Month = {9},
	Nlm_Id = {7703701},
	Number = {9},
	Organization = {Molecular Medicine Program, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.},
	Pages = {3091-8},
	Pii = {45/9/3091},
	Pubmed = {15326125},
	Title = {Long-term, targeted genetic modification of the aqueous humor outflow tract coupled with noninvasive imaging of gene expression in vivo},
	Uuid = {12AB1D7D-6598-444B-9A91-E5DD606B5FDF},
	Volume = {45},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1167/iovs.04-0366}}

@article{Lois:1993,
	Abstract = {Subventricular zone (SVZ) cells proliferate spontaneously in vivo in the telencephalon of adult mammals. Several studies suggest that SVZ cells do not differentiate after mitosis into neurons or glia but die. In the present work, we show that SVZ cells labeled in the brains of adult mice with [3H]thymidine differentiate directly into neurons and glia in explant cultures. In vitro labeling with [3H]thymidine shows that 98\%of the neurons that differentiate from the SVZ explants are derived from precursor cells that underwent their last division in vivo. This report identifies the SVZ cells as neuronal precursors in an adult mammalian brain.},
	Author = {Lois, C. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Prosencephalon/*cytology;Support, Non-U.S. Gov't;02 Adult neurogenesis migration;Cell Differentiation;Cerebral Ventricles/cytology;03 Adult neurogenesis progenitor source;Cell Division;Neuroglia/*cytology;In Vitro;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Animal;Mice;Cells, Cultured;Stem Cells/cytology;BB abstr;Corpus Striatum/cytology},
	Number = {5},
	Organization = {Rockefeller University, New York, NY 10021.},
	Pages = {2074-7.},
	Title = {Proliferating subventricular zone cells in the adult mammalian forebrain can differentiate into neurons and glia},
	Uuid = {757FF8C8-F7DA-482E-9DDA-0EB28C3C5B0B},
	Volume = {90},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8446631}}

@article{Lois:1994,
	Abstract = {During the development of the mammalian brain, neuronal precursors migrate to their final destination from their site of birth in the ventricular and subventricular zones (VZ and SVZ, respectively). SVZ cells in the walls of the lateral ventricle continue to proliferate in the brain of adult mice and can generate neurons in vitro, but their fate in vivo is unknown. Here SVZ cells from adult mice that carry a neuronal-specific transgene were grafted into the brain of adult recipients. In addition, the fate of endogenous SVZ cells was examined by microinjection of tritiated thymidine or a vital dye that labeled a discrete population of SVZ cells. Grafted and endogenous SVZ cells in the lateral ventricle of adult mice migrate long distances and differentiate into neurons in the olfactory bulb.},
	Author = {Lois, C. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Science},
	Keywords = {Cerebral Ventricles/*cytology;Cell Differentiation;Neurons/*cytology/metabolism;Olfactory Bulb/*cytology;Microinjections;Brain Tissue Transplantation;beta-Galactosidase/analysis/genetics;Animal;Cell Movement;Mice, Transgenic;A-6;Brain/cytology;Mice, Inbred Strains;Support, Non-U.S. Gov't;Cell Transplantation;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Genes, Reporter},
	Number = {5162},
	Organization = {Rockefeller University, New York, NY 10021.},
	Pages = {1145-8.},
	Title = {Long-distance neuronal migration in the adult mammalian brain},
	Uuid = {120AE247-CD62-11D9-97C9-000D9346EC2A},
	Volume = {264},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8178174}}

@article{Lois:1996,
	Abstract = {In the brain of adult mice, cells that divide in the subventricular zone of the lateral ventricle migrate up to 5 millimeters to the olfactory bulb where they differentiate into neurons. These migrating cells were found to move as chains through a well-defined pathway, the rostral migratory stream. Electron microscopic analysis of serial sections showed that these chains contained only closely apposed, elongated neuroblasts connected by membrane specializations. A second cell type, which contained glial fibrillary acidic protein, ensheathed the chains of migrating neuroblasts. Thus, during chain migration, neural precursors moved associated with each other and were not guided by radial glial or axonal fibers.},
	Author = {Lois, C. and Garcia-Verdugo, J. M. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Science},
	Keywords = {Cerebral Ventricles/*cytology;Cell Differentiation;Neural Cell Adhesion Molecules/analysis;Cell Membrane/ultrastructure;B abstr;Neuroglia/chemistry/*cytology/physiology;Neurons/*cytology/ultrastructure;Mitosis;Animal;Cell Movement;02 Adult neurogenesis migration;Glial Fibrillary Acidic Protein/analysis;Male;Support, Non-U.S. Gov't;Olfactory Bulb/cytology;Support, U.S. Gov't, P.H.S.;Mice;Microscopy, Electron},
	Number = {5251},
	Organization = {Rockefeller University, New York 10021, USA.},
	Pages = {978-81.},
	Title = {Chain migration of neuronal precursors},
	Uuid = {D5824B12-8D9D-436E-82DF-65DA6355AF61},
	Volume = {271},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8584933}}

@article{Lomvardas:2006,
	Abstract = {The expression of a single odorant receptor (OR) gene from a large gene family in individual sensory neurons is an essential feature of the organization and function of the olfactory system. We have used chromosome conformation capture to demonstrate the specific association of an enhancer element, H, on chromosome 14 with multiple OR gene promoters on different chromosomes. DNA and RNA fluorescence in situ hybridization (FISH) experiments allow us to visualize the colocalization of the H enhancer with the single OR allele that is transcribed in a sensory neuron. In transgenic mice bearing additional H elements, sensory neurons that express OR pseudogenes also express a second functional receptor. These data suggest a model of receptor choice in which a single trans-acting enhancer element may allow the stochastic activation of only one OR allele in an olfactory sensory neuron.},
	Author = {Lomvardas, Stavros and Barnea, Gilad and Pisapia, David J. and Mendelsohn, Monica and Kirkland, Jennifer and Axel, Richard},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Chromosomes;In Situ Hybridization, Fluorescence;research support, n.i.h., extramural ;Animals;RNA;Gene Expression Regulation;Olfactory Receptor Neurons;DNA;09 Evolutionary dynamics;Pseudogenes;Neurons, Afferent;Mice, Transgenic;Enhancer Elements (Genetics);research support, non-u.s. gov't ;Sulfites;Alleles;Multigene Family;Receptors, Odorant;Mice;Promoter Regions (Genetics);24 Pubmed search results 2008;DNA Methylation},
	Month = {7},
	Nlm_Id = {0413066},
	Number = {2},
	Organization = {Department of Biochemistry and Molecular Biophysics and Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.},
	Pages = {403-13},
	Pii = {S0092-8674(06)00855-5},
	Pubmed = {16873069},
	Title = {Interchromosomal interactions and olfactory receptor choice},
	Uuid = {41BEF53D-8E67-4832-906F-E5785AFE3D98},
	Volume = {126},
	Year = {2006},
	url = {papers/Lomvardas_Cell2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.06.035}}

@article{Long:2007,
	Abstract = {Olfactory bulb interneuron development is a complex multistep process that involves cell specification in the ventral telencephalon, tangential migration into the olfactory bulb, and local neuronal maturation. Although several transcription factors have been implicated in this process, how or when they act remains to be elucidated. Here we explore the mechanisms that result in olfactory bulb interneuron defects in Dlx1&2-/- (distal-less homeobox 1 and 2) and Mash1-/- (mammalian achaete-schute homolog 1) mutants. We provide evidence that Dlx1&2 and Mash1 regulate parallel molecular pathways that are required for the generation of these cells, thereby providing new insights into the mechanisms underlying olfactory bulb development. The analysis also defined distinct anatomical zones related to olfactory bulb development. Finally we show that Dlx1&2 are required for promoting tangential migration to the olfactory bulb, potentially via regulating the expression of ErbB4 (v-erb-a erythroblastic leukemia viral oncogene homolog 4), Robo2 (roundabout homolog 2), Slit1 (slit homolog 1), and PK2 (prokineticin 2), which have all been shown to play essential roles in this migration.},
	Author = {Long, Jason E. and Garel, Sonia and Alvarez-Dolado, Manuel and Yoshikawa, Kazuaki and Osumi, Noriko and Alvarez-Buylla, Arturo and Rubenstein, John L. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {13 Olfactory bulb anatomy;Cell Differentiation;Signal Transduction;Animals;Transcription Factors;Mice, Mutant Strains;comparative study;Homeodomain Proteins;Cell Movement;02 Adult neurogenesis migration;Mice, Inbred C57BL;research support, non-u.s. gov't;Olfactory Bulb;Mice, Knockout;research support, n.i.h., extramural;Mice;Interneurons;24 Pubmed search results 2008;12 Interneuron development},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Nina Ireland Laboratory of Developmental Neurobiology, University of California at San Francisco, San Francisco, California 94143, USA.},
	Pages = {3230-43},
	Pii = {27/12/3230},
	Pubmed = {17376983},
	Title = {Dlx-dependent and -independent regulation of olfactory bulb interneuron differentiation},
	Uuid = {3B0B3C65-4D6B-448B-B6EA-A9ED898FCF6A},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5265-06.2007}}

@article{Lopez-Garcia:1994,
	Abstract = {In normal lizards, microglial cells populate the medial cortex (a zone homologous to the hippocampal fascia dentata), with a preferential distribution along the border between the granular cell layer and the plexiform layers. Intraperitoneal injection of the neurotoxin 3-acetylpyridine (3AP) induces a selective lesion in the medial cortex with a rapid degeneration of the granular layer and its zinc-enriched axonal projection. Within 6-8 weeks, the granular layer is, however, repopulated by a new set of neurons generated in the subjacent ependyma and the cell debris is removed. The aim of this study was to determine to what extent microglia were involved in the scavenging processes during the regeneration process. To this end we studied the brains of regenerating lizards at different times after 3AP lesion, visualising microglial cells by the nucleoside diphosphatase (NDPase) histochemical reaction. Surprisingly, we found that stained microglial cells disappeared 6-8 hours after 3AP injection and remained absent until 10-15 days after injection. One month postlesion an increased population of microglial cells was found scattered throughout all plexiform layers of the cortex. Thorough examination of semithin and ultrathin sections confirmed the absence of microglia in the medial cortex of recent lesioned animals but the presence of an exuberant population after 1 month postlesion. In the tissue, phagocytotic scavenging was carried out by radial ependymocytes, not by microglia.},
	Author = {Lopez-Garcia, C. and Nacher, J. and Castellano, B. and Luis de la Iglesia, J. A. and Molowny, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Acid Anhydride Hydrolases;Nerve Regeneration;Hippocampus;Microscopy, Electron;Pyridines;Not relevant;11 Glia;Microglia;Histocytochemistry;Lizards;Support, Non-U.S. Gov't;Animals;Phagocytosis},
	Medline = {95146147},
	Month = {9},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Facultad de Ciencias Biologicas, Universidad de Valencia, Burjasot, Spain.},
	Pages = {52-61},
	Pubmed = {7843787},
	Title = {Transitory disappearance of microglia during the regeneration of the lizard medial cortex},
	Uuid = {D39F8439-0332-4FC1-B75C-D5E9E4DE039D},
	Volume = {12},
	Year = {1994}}

@article{Lopez-Garcia:2002,
	Abstract = {The medial cerebral cortex of lizards, an area homologous to the hippocampal fascia dentata, shows delayed postnatal neurogenesis, i.e., cells in the medial cortex ependyma proliferate and give rise to immature neurons, which migrate to the cell layer. There, recruited neurons differentiate and give rise to zinc containing axons directed to the rest of cortical areas, thus resulting in a continuous growth of the medial cortex and its zinc-enriched axonal projection. This happens along the lizard life span, even in adult lizards, thus allowing one of their most important characteristics: neuronal regeneration. Experiments in our laboratory have shown that chemical lesion of the medial cortex (affecting up to 95\%of its neurons) results in a cascade of events: first, massive neuronal death and axonal-dendritic retraction and, secondly, triggered ependymal-neuroblast proliferation and subsequent neo-histogenesis and regeneration of an almost new medial cortex, indistinguishable from a normal undamaged one. This is the only case to our knowledge of the regeneration of an amniote central nervous centre by new neuron production and neo-histogenesis. Thus the lizard cerebral cortex is a good model to study neuronal regeneration and the complex factors that regulate its neurogenetic, migratory and neo-synaptogenetic events.},
	Author = {Lopez-Garcia, Carlos and Molowny, Asuncion and Nacher, Juan and Ponsoda, Xavier and Sancho-Bielsa, Francisco and Alonso-Llosa, Gregori},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0001-3765},
	Journal = {An Acad Bras Cienc},
	Keywords = {review;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Models, Animal;Nerve Regeneration;review, tutorial;Lizards;Animals;Cerebral Cortex;Neurons;Seasons},
	Medline = {21955951},
	Month = {3},
	Nlm_Id = {7503280},
	Number = {1},
	Organization = {Lab. Neurobiologia Celular, Universidad de Valencia, Burjasot, Valencia, 46100, Spain. carlos.lopez\@uv.es},
	Pages = {85-104},
	Pii = {S0001-37652002000100006},
	Pubmed = {11960178},
	Title = {The lizard cerebral cortex as a model to study neuronal regeneration},
	Uuid = {7D2759FB-FB2F-4E53-84DB-EE7E1CA9353C},
	Volume = {74},
	Year = {2002}}

@article{Lossi:2003,
	Abstract = {Apoptosis has been recognized to be an essential process during neural development. It is generally assumed that about half of the neurons produced during neurogenesis die before completion of the central nervous system (CNS) maturation, and this process affects nearly all classes of neurons. In this review, we discuss the experimental data in vivo on naturally occurring neuronal death in normal, transgenic and mutant animals, with special attention to the cerebellum as a study model. The emerging picture is that of a dual wave of apoptotic cell death affecting central neurons at different stages of their life. The first wave consists of an early neuronal death of proliferating precursors and young postmitotic neuroblasts, and appears to be closely linked to cell cycle regulation. The second wave affects postmitotic neurons at later stages, and is much better understood in functional terms, mainly on the basis of the neurotrophic concept in its broader definition. The molecular machinery of late apoptotic death of postmitotic neurons more commonly follows the mitochondrial pathway of intracellular signal transduction, but the death receptor pathway may also be involved.Undoubtedly, analysis of naturally occurring neuronal death (NOND) in vivo will offer a basis for parallel and future studies aiming to elucidate the mechanisms of pathologic neuronal loss occurring as the result of conditions such as neurodegenerative disorders, trauma or ischemia.},
	Author = {Lossi, L. and Merighi, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0301-0082},
	Journal = {Prog Neurobiol},
	Keywords = {review;Central Nervous System;Human;review, academic;Apoptosis;Not relevant;11 Glia;Necrosis;Animals;Support, Non-U.S. Gov't;Neurons;Autophagocytosis},
	Medline = {22674165},
	Month = {4},
	Nlm_Id = {0370121},
	Number = {5},
	Organization = {Department of Veterinary Morphophysiology, University of Torino, Via Leonardo da Vinci 44, I-10095 (TO), Grugliasco, Italy. laura.lossi\@unito.it},
	Pages = {287-312},
	Pii = {S0301008203000510},
	Pubmed = {12787572},
	Title = {In vivo cellular and molecular mechanisms of neuronal apoptosis in the mammalian CNS},
	Uuid = {0C760CB7-0E5F-406A-A0F9-1D0BB309CFE2},
	Volume = {69},
	Year = {2003},
	url = {../../Volumes/Vega/Users/ackman/James/Endnotelibraries/OMEGAData/Mergheri-prog04.pdf}}

@article{Lotto:2001,
	Abstract = {Many neurons die as the normal brain develops. How this is regulated and whether the mechanism involves neurotrophic molecules from target cells are unknown. We found that cultured neurons from a key forebrain structure, the dorsal thalamus, develop a need for survival factors including brain-derived neurotrophic factor (BDNF) from their major target, the cerebral cortex, at the age at which they innervate it. Experiments in vivo have shown that rates of dorsal thalamic cell death are reduced by increasing cortical levels of BDNF and are increased in mutant mice lacking functional BDNF receptors or thalamocortical projections; these experiments have also shown that an increase in the rates of dorsal thalamic cell death can be achieved by blocking BDNF in the cortex. We suggest that the onset of a requirement for cortex- derived neurotrophic factors initiates a competitive mechanism regulating programmed cell death among dorsal thalamic neurons.},
	Author = {Lotto, R. B. and Asavaritikrai, P. and Vali, L. and Price, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurosci},
	Keywords = {Prosencephalon/cytology/drug effects/embryology/*metabolism;Cells, Cultured;Gene Expression Regulation, Developmental;inhibitors/metabolism/pharmacology;Cell Survival/drug effects/genetics;Animal;Brain-Derived Neurotrophic Factor/antagonists &;Nerve Growth Factors/antagonists &inhibitors/*metabolism/pharmacology;Culture Media, Conditioned/pharmacology;Receptor, trkB/deficiency/genetics;Receptor, trkC/deficiency/genetics;In Situ Nick-End Labeling;Apoptosis/drug effects/genetics;Neurons/cytology/drug effects/*metabolism;C;Homeodomain Proteins/genetics/metabolism;04 Adult neurogenesis factors;Mice, Knockout;Mice;Thalamic Nuclei/cytology/embryology/metabolism;Neural Pathways/cytology/embryology/metabolism;Thalamus/cytology/drug effects/embryology/metabolism;Receptors, Nerve Growth Factor/deficiency/genetics/metabolism;Cerebral Cortex/cytology/metabolism;Antibodies/pharmacology;Support, Non-U.S. Gov't},
	Number = {11},
	Organization = {Genes and Development Group, Department of Biomedical Sciences, University Medical School, Edinburgh EH8 9XD, United Kingdom.},
	Pages = {3904-10.},
	Title = {Target-derived neurotrophic factors regulate the death of developing forebrain neurons after a change in their trophic requirements},
	Uuid = {CFE36093-28E5-429C-8A6C-7868412D9BC7},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11356878%20http://www.jneurosci.org/cgi/content/full/21/11/3904%20http://www.jneurosci.org/cgi/content/abstract/21/11/3904}}

@article{Louissaint:2002,
	Abstract = {Neurogenesis proceeds throughout life in the higher vocal center (HVC) of the adult songbird neostriatum. Testosterone induces neuronal addition and endothelial division in HVC. We asked if testosterone-induced angiogenesis might contribute importantly to HVC neuronal recruitment. Testosterone upregulated both VEGF and its endothelial receptor, VEGF-R2/Quek1/KDR, in HVC. This yielded a burst in local HVC angiogenesis. FACS-isolated HVC endothelial cells produced BDNF in a testosterone-dependent manner. In vivo, HVC BDNF rose by the third week after testosterone, lagging by over a week the rise in VEGF and VEGF-R2. In situ hybridization revealed that much of this induced BDNF mRNA was endothelial. In vivo, both angiogenesis and neuronal addition to HVC were substantially diminished by inhibition of VEGF-R2 tyrosine kinase. These findings suggest a causal interaction between testosterone-induced angiogenesis and neurogenesis in the adult forebrain. 0896-6273 Journal Article},
	Author = {Louissaint, A. and Rao, S. and Leventhal, C. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Neovascularization, Physiologic;Cell Movement/drug effects/physiology;Male;Receptors, Growth Factor;Vascular Endothelial Growth Factor A;Endothelial Growth Factors/biosynthesis;Receptors, Vascular Endothelial Growth Factor;Brain;Cells, Cultured;Canaries;Animals;Endothelium, Vascular/cytology/drug effects/*physiology/secretion;Brain/*blood supply/cytology/drug effects/*growth &development;03 Adult neurogenesis progenitor source;Research Support, U.S. Gov't, P.H.S.;Cell Movement;Estrogens/pharmacology;Signal Transduction;Brain-Derived Neurotrophic Factor/biosynthesis/secretion;Cell Division;Estrogens;Receptors, Growth Factor/biosynthesis;Testosterone;Signal Transduction/drug effects/physiology;Endothelial Growth Factors;Receptor Protein-Tyrosine Kinases;Support, U.S. Gov't, P.H.S.;Brain-Derived Neurotrophic Factor;Receptor Protein-Tyrosine Kinases/biosynthesis;Neurons/*cytology/drug effects/physiology;Lymphokines;Cell Division/drug effects/physiology;Canaries/*physiology;02 Adult neurogenesis migration;Lymphokines/biosynthesis;Female;Testosterone/pharmacology;Endothelium, Vascular;BB abstr;Support, Non-U.S. Gov't;Research Support, Non-U.S. Gov't;Neurons;Neovascularization, Physiologic/drug effects/*physiology;Vascular Endothelial Growth Factors},
	Medline = {22082306},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Neurology and Neuroscience, Cornell University Medical Center, 1300 York Avenue, New York, NY 10021, USA.},
	Pages = {945-60},
	Pii = {S0896627302007225},
	Pubmed = {12086642},
	Title = {Coordinated interaction of neurogenesis and angiogenesis in the adult songbird brain},
	Uuid = {1B0C3BC1-B21F-4EB4-A12C-C503D3608B1D},
	Volume = {34},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12086642}}

@article{Lovelace:2007,
	Abstract = {Cell culture analyses of growth, morphology and apoptosis commonly require counting of different cell types stained with antibodies to discriminate between them. Previously, we reported the use of l-Leucine methyl ester (l-LME) to prepare purified cultures of type 1 astrocytes with minimal microglia, and staining by GFAP and CD antibodies, respectively. Here, we demonstrate a novel use of acridine orange (AO) for rapid discrimination between these cell types using fluorescence microscopy. AO accumulates in the lysosomes and also binds strongly to nuclear DNA and cytoplasmic/nucleolar RNA. Microglia may contain abundant lysosomes due to known roles in homeostasis and immune response. AO staining of lysosomes was tested at a range of concentrations, and 2.5 microg/mL was most suitable. In agreement with previous reports, microglia treated with AO showed very intense yellow, orange or red granular cytoplasmic staining of lysosomes. Microglia contain a substantially higher number of lysosomes than astrocytes, which have a variable amount. We measured the microglia population at 5.14+/-0.50\%in mixed cultures. Thus, these results show AO is a novel discriminatory marker, as microglia were easily observed and counted in clumps on top of the monolayer of astrocytes, providing a rapid alternative to time-consuming and costly antibody-based assays.},
	Author = {Lovelace, Michael D. and Cahill, David M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {research support, non-u.s. gov't;11 Glia;24 Pubmed search results 2008;23 Technique},
	Month = {9},
	Nlm_Id = {7905558},
	Number = {2},
	Organization = {School of Life and Environmental Sciences, Deakin University, Pigdons Road, Waurn Ponds, Victoria 3217, Australia.},
	Pages = {223-9},
	Pii = {S0165-0270(07)00277-4},
	Pubmed = {17662460},
	Title = {A rapid cell counting method utilising acridine orange as a novel discriminating marker for both cultured astrocytes and microglia},
	Uuid = {6036F8F8-B5DF-49B9-B65A-B7267D6F7217},
	Volume = {165},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jneumeth.2007.06.009}}

@article{Lovell-Badge:2001,
	Abstract = {Stem cells have offered much hope by promising to greatly extend the numbers and range of patients who could benefit from transplants, and to provide cell replacement therapy to treat debilitating diseases such as diabetes, Parkinson's and Huntington's disease. The issue of stem cell research is politically charged, prompting biologists to begin engaging in ethical debates, and generating in the general public an unusually high level of interest in this aspect of biology. But excitement notwithstanding, there is a long way to go in basic research before new therapies will be established, and now the pressure is on for scientists and clinicians to deliver. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Lovell-Badge, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Nature},
	Keywords = {F abstr;Embryo/cytology;10 Development;Forecasting;Human;Research/trends;*Stem Cells;Politics;Animals},
	Number = {6859},
	Organization = {Division of Developmental Genetics, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London, UK. rlovell\@nimr.mrc.ac.uk},
	Pages = {88-91},
	Pubmed = {11689952},
	Title = {The future for stem cell research},
	Uuid = {6958CACC-5F89-4FFC-8968-AB56C3B507F9},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689952}}

@article{Lowy:1971,
	Author = {Lowy, D. R. and Rowe, W. P. and Teich, N. and Hartley, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {15 ERVs retroelements;Animals;Mice;Ultraviolet Rays;24 Pubmed search results 2008;Virus Replication;Cell Line;15 Retrovirus mechanism;Fluorescent Antibody Technique;Cells, Cultured;Idoxuridine;Bromodeoxyuridine;Antigens, Viral;Leukemia Virus, Murine},
	Medline = {72042138},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5},
	Pages = {155-6},
	Pubmed = {4330367},
	Title = {Murine leukemia virus: high-frequency activation in vitro by 5-iododeoxyuridine and 5-bromodeoxyuridine},
	Uuid = {719139FF-8E99-4AF4-8D07-F46A25FE65D6},
	Volume = {174},
	Year = {1971}}

@article{Lopez-Bendito:2008,
	Abstract = {Functioning of the cerebral cortex requires the coordinated assembly of circuits involving glutamatergic projection neurons and GABAergic interneurons. Although much is known about the migration of interneurons from the subpallium to the cortex, our understanding of the mechanisms controlling their precise integration within the cortex is still limited. Here, we have investigated in detail the behavior of GABAergic interneurons as they first enter the developing cortex by using time-lapse videomicroscopy, slice culture, and in utero experimental manipulations and analysis of mouse mutants. We found that interneurons actively avoid the cortical plate for a period of approximately 48 h after reaching the pallium; during this time, interneurons disperse tangentially through the marginal and subventricular zones. Perturbation of CXCL12/CXCR4 signaling causes premature cortical plate invasion by cortical interneurons and, in the long term, disrupts their laminar and regional distribution. These results suggest that regulation of cortical plate invasion by GABAergic interneurons is a key event in cortical development, because it directly influences the coordinated formation of appropriate glutamatergic and GABAergic neuronal assemblies.},
	Author = {L{\'o}pez-Bendito, Guillermina and S{\'a}nchez-Alca\~{n}iz, Juan Antonio and Pla, Ram{\'o}n and Borrell, V{\'\i}ctor and Pic{\'o}, Esther and Valdeolmillos, Miguel and Mar{\'\i}n, Oscar},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't;10 Development;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {7},
	Organization = {Instituto de Neurociencias de Alicante, Consejo Superior de Investigaciones Cient{\'\i}ficas and Universidad Miguel Hern{\'a}ndez, 03550 Sant Joan d'Alacant, Spain.},
	Pages = {1613-24},
	Pii = {28/7/1613},
	Pubmed = {18272682},
	Title = {Chemokine signaling controls intracortical migration and final distribution of GABAergic interneurons},
	Uuid = {78197D19-A3AC-45A4-B9A7-D533104D7936},
	Volume = {28},
	Year = {2008},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4651-07.2008}}

@article{Lower:1996,
	Abstract = {Human endogenous retroviruses (HERVs) are very likely footprints of ancient germ-cell infections. HERV sequences encompass about 1\%of the human genome. HERVs have retained the potential of other retroelements to retrotranspose and thus to change genomic structure and function. The genomes of almost all HERV families are highly defective. Recent progress has allowed the identification of the biologically most active family, HTDV/HERV-K, which codes for viral proteins and particles and is highly expressed in germ-cell tumors. The demonstrable and potential roles of HTDV/HERV-K as well as of other human elements in disease and in maintaining genome plasticity are illustrated.},
	Author = {L{\"o}wer, R. and L{\"o}wer, J. and Kurth, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {15 ERVs retroelements;Research Support, Non-U.S. Gov't;RNA-Directed DNA Polymerase;Female;Retroviridae;Genome, Human;HIV Seropositivity;Neoplasms;15 Retrovirus mechanism;Antibody Formation;Humans;Male;24 Pubmed search results 2008;Retroelements;review},
	Medline = {96224256},
	Month = {5},
	Nlm_Id = {7505876},
	Number = {11},
	Organization = {Paul-Ehrlich-Institut, Langen, Germany.},
	Pages = {5177-84},
	Pubmed = {8643549},
	Title = {The viruses in all of us: characteristics and biological significance of human endogenous retrovirus sequences},
	Uuid = {F67A3B32-EE53-11DA-8605-000D9346EC2A},
	Volume = {93},
	Year = {1996}}

@article{Lu:2002a,
	Abstract = {The oligodendrocyte lineage genes Olig1 and Olig2 encode related bHLH proteins that are coexpressed in neural progenitors. Targeted disruption of these two genes sheds light on the ontogeny of oligodendroglia and genetic requirements for their development from multipotent CNS progenitors. Olig2 is required for oligodendrocyte and motor neuron specification in the spinal cord. Olig1 has roles in development and maturation of oligodendrocytes, evident especially within the brain. Both Olig genes contribute to neural pattern formation. Neither Olig gene is required for astrocytes. These findings, together with fate mapping analysis of Olig-expressing cells, indicate that oligodendrocytes are derived from Olig-specified progenitors that give rise also to neurons. 0092-8674 Journal Article},
	Author = {Lu, Q. R. and Sun, T. and Zhu, Z. and Ma, N. and Garcia, M. and Stiles, C. D. and Rowitch, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Cell},
	Keywords = {Nerve Tissue Proteins/*deficiency/genetics/metabolism;Animals;Female;G abstr;11 Glia;Male;Body Patterning/genetics;Stem Cells/cytology/*metabolism;Motor Neurons/cytology/*metabolism;Astrocytes/cytology/metabolism;Rhombencephalon/cytology/embryology/metabolism;Oligodendroglia/cytology/*metabolism;Mutation/physiology;Cell Lineage/*genetics;Spinal Cord/cytology/*embryology/metabolism;Support, U.S. Gov't, P.H.S.;Cell Differentiation/*genetics;Mice;Mice, Knockout;Support, Non-U.S. Gov't},
	Number = {1},
	Organization = {Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.},
	Pages = {75-86},
	Pubmed = {11955448},
	Title = {Common developmental requirement for Olig function indicates a motor neuron/oligodendrocyte connection},
	Uuid = {BFF5EB76-41A4-4135-A11F-43985E82E4A8},
	Volume = {109},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11955448}}

@article{Lu:2005,
	Author = {Lu, P. and Tuszynski, M. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Month = {6},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Neurosciences, University of California at San Diego, La Jolla, CA 92093-0626, USA.},
	Pages = {273-8},
	Pii = {S0014-4886(05)00052-X},
	Pubmed = {15869931},
	Title = {Can bone marrow-derived stem cells differentiate into functional neurons?},
	Uuid = {2A74E8D9-D3A7-11D9-A0E9-000D9346EC2A},
	Volume = {193},
	Year = {2005},
	url = {papers/Lu_ExpNeurol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2005.01.031}}

@article{Lu:2006,
	Abstract = {Periventricular heterotopia (PH) is a malformation of cortical development characterized by nodules of neurons, ectopically located along the lateral ventricles of the brain. Mutations in the vesicle transport ADP-ribosylation factor guanine exchange factor 2 gene (ARFGEF2) or the actin-binding Filamin A (FLNA) gene cause PH. Previous studies have shown that FLNA expression is developmentally regulated, with strongest expression observed along the ventricular zone (VZ) and to a lesser degree in postmitotic neurons in the cortex. Here we characterize the expression patterns for ARFGEF2 within the central nervous systems of human and mouse in order to better understand their potential roles in causing PH. ARFGEF2 mRNA was widely expressed in all cortical layers, especially in the neural precursors of the ventricular and subventricular zones (SVZ) during development, with persistent but diminished expression in adulthood. ARFGEF2 encodes for the protein brefeldin-inhibited guanine exchange factor 2 (BIG2). BIG2 protein immunoreactivity was most strongly localized to the neural progenitors along the neuroependymal lining of the VZ during development, with decreased expression in adulthood. Furthermore, overlapping BIG2 and FLNA expression was greatest in these same neuroependymal cells of human embryonic brain and was co-expressed in progenitors by Western blot. Finally, transfection of a dominant-negative construct of ARFGEF2 in SHSY5Y neuroblastoma cells partially blocked FLNA transport from the Golgi apparatus to the cell membrane. These results suggest that mutations in ARFGEF2 may impair targeted transport of FLNA to the cell surface within neural progenitors along the neuroependyma and that disruption of these cells could contribute to PH formation.},
	Author = {Lu, Jie and Tiao, Grace and Folkerth, Rebecca and Hecht, Jonathon and Walsh, Christopher and Sheen, Volney},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Tissue Distribution;Animals;Humans;Gene Expression Regulation, Developmental;Microfilament Proteins;21 Epilepsy;Protein Transport;Cell Movement;Mice, Inbred C57BL;RNA, Messenger;Brain Diseases;Cerebral Ventricles;Nervous System Malformations;Cerebral Cortex;21 Neurophysiology;Neurons;Ependyma;Mice;24 Pubmed search results 2008;Contractile Proteins;Stem Cells;Choristoma;Guanine Nucleotide Exchange Factors},
	Month = {1},
	Nlm_Id = {0406041},
	Number = {3},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {476-84},
	Pubmed = {16320251},
	Title = {Overlapping expression of ARFGEF2 and Filamin A in the neuroependymal lining of the lateral ventricles: insights into the cause of periventricular heterotopia},
	Uuid = {33F04A72-67F9-4827-96F0-C62358A22C77},
	Volume = {494},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20806}}

@article{Lu:2004b,
	Abstract = {Differentiation of stem cells toward a neuronal lineage normally involves a gradually progressive restriction in developmental potential and is regulated by a diverse set of specific and temporally precise genetic events. However, recent studies have indicated that both rodent and human bone marrow stromal cells (MSCs) can be rapidly (within minutes to hours) induced to differentiate into neurons in vitro by relatively simple chemical means (using beta-mercaptoethanol [BME] or dimethylsulfoxide [DMSO] and butylated hydroxyanisol [BHA]; Woodbury et al. [ 2000] J. Neurosci. Res. 61:364-370). The ability to transdifferentiate an easily accessible cell source into neurons could have substantial potential for promoting neural repair. We therefore explored the potential of simple chemical methods to transdifferentiate other cell types, including primary rat fibroblasts, primary human keratinocytes, HEK293 cells, rat PC-12 cells, and as positive control rat bone marrow stromal (BMS) cells. Surprisingly, all cells except for keratinocytes adopted at least partial "neuron-like" pyramidal cell morphology with fine-cellular extensions resembling neurites upon stimulation with BME or DMSO/BHA. However, time-lapse microscopy indicated that the chemical exposure of MSCs did not result in new neurite growth but rather cellular shrinkage, with retraction of the majority of existing cell extensions, leaving only few, fine neurite-like processes. To determine whether the chemically induced transdifferentiation resulted from simple cellular toxicity, MSCs were exposed to various stressors, including detergents, high-molarity sodium chloride, and extremes of pH. In all cases, cellular shrinkage and adoption of pseudoneuronal morphology were observed. Concomitantly with cellular shrinkage, apparent increases in immunolabeling for the neuronal markers NSE and NeuN were detected in the cell soma that could not be confirmed by RT-PCR. Furthermore, blockade of protein synthesis with cycloheximide did not prevent cells from adopting "neuron-like" morphology after chemical induction. Thus, morphological changes and increases in immunolabeling for certain cellular markers upon "chemical induction" of MSCs are likely the result of cellular toxicity, cell shrinkage, and changes in the cytoskeleton and do not represent regulated steps in a complicated cellular differentiation process.},
	Author = {Lu, Paul and Blesch, Armin and Tuszynski, Mark H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Differentiation;Embryonic Induction;Stress;Animals;Keratinocytes;Rats;Humans;Dimethyl Sulfoxide;Fibroblasts;Phosphopyruvate Hydratase;Female;Neurites;Butylated Hydroxyanisole;PC12 Cells;08 Aberrant cell cycle;Rats, Inbred F344;Bone Marrow Cells;Cell Size;Mercaptoethanol;Cytoskeleton;Artifacts;Stromal Cells;Cytotoxins;Nerve Tissue Proteins},
	Month = {7},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, USA.},
	Pages = {174-91},
	Pubmed = {15211585},
	Title = {Induction of bone marrow stromal cells to neurons: differentiation, transdifferentiation, or artifact?},
	Uuid = {5CC5A696-1B6D-4F5F-B4EC-F2704661254D},
	Volume = {77},
	Year = {2004},
	url = {papers/Lu_JNeurosciRes2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20148}}

@article{Lu:2001,
	Abstract = {Asymmetric division is a fundamental mechanism for generating cellular diversity. In the central nervous system of Drosophila, neural progenitor cells called neuroblasts undergo asymmetric division along the apical-basal cellular axis. Neuroblasts originate from neuroepithelial cells, which are polarized along the apical-basal axis and divide symmetrically along the planar axis. The asymmetry of neuroblasts might arise from neuroblast-specific expression of the proteins required for asymmetric division. Alternatively, both neuroblasts and neuroepithelial cells could be capable of dividing asymmetrically, but in neuroepithelial cells other polarity cues might prevent asymmetric division. Here we show that by disrupting adherens junctions we can convert the symmetric epithelial division into asymmetric division. We further confirm that the adenomatous polyposis coli (APC) tumour suppressor protein is recruited to adherens junctions, and demonstrate that both APC and microtubule-associated EB1 homologues are required for the symmetric epithelial division along the planar axis. Our results indicate that neuroepithelial cells have all the necessary components to execute asymmetric division, but that this pathway is normally overridden by the planar polarity cue provided by adherens junctions.},
	Author = {Lu, B. and Roegiers, F. and Jan, L. Y. and Jan, Y. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Nature},
	Keywords = {10 Development;Cell Differentiation;Human;Adherens Junctions/*physiology;Neurons/*cytology;Mitotic Spindle Apparatus/physiology;Animal;Animals, Genetically Modified;Cell Polarity;Carrier Proteins/physiology;Support, Non-U.S. Gov't;Cell Division/*physiology;Cytoskeletal Proteins/physiology;Adenomatous Polyposis Coli Protein;Body Patterning/physiology;Drosophila;Support, U.S. Gov't, P.H.S.;Epithelial Cells/cytology;F},
	Number = {6819},
	Organization = {Howard Hughes Medical Institute and Department of Physiology, University of California at San Francisco, 94143-0725, USA.},
	Pages = {522-5.},
	Title = {Adherens junctions inhibit asymmetric division in the Drosophila epithelium},
	Uuid = {58A987C8-8E69-45BC-B2ED-C7D3C42893C7},
	Volume = {409},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11206549}}

@article{Lu:2004,
	Abstract = {The ageing of the human brain is a cause of cognitive decline in the elderly and the major risk factor for Alzheimer's disease. The time in life when brain ageing begins is undefined. Here we show that transcriptional profiling of the human frontal cortex from individuals ranging from 26 to 106 years of age defines a set of genes with reduced expression after age 40. These genes play central roles in synaptic plasticity, vesicular transport and mitochondrial function. This is followed by induction of stress response, antioxidant and DNA repair genes. DNA damage is markedly increased in the promoters of genes with reduced expression in the aged cortex. Moreover, these gene promoters are selectively damaged by oxidative stress in cultured human neurons, and show reduced base-excision DNA repair. Thus, DNA damage may reduce the expression of selectively vulnerable genes involved in learning, memory and neuronal survival, initiating a programme of brain ageing that starts early in adult life.},
	Author = {Lu, Tao and Pan, Ying and Kao, Shyan-Yuan Y. and Li, Cheng and Kohane, Isaac and Chan, Jennifer and Yankner, Bruce A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Cell Survival;Human;Gene Expression Regulation;Antioxidants;Aging;Neuronal Plasticity;Oligonucleotide Array Sequence Analysis;DNA Repair;Middle Aged;Cells, Cultured;Homeostasis;21 Neurodegenerative;Cell Line, Tumor;Calcium;08 Aberrant cell cycle;Gene Expression Profiling;Aged;Oxidative Stress;Learning;Support, Non-U.S. Gov't;Cerebral Cortex;21 Neurophysiology;Neurons;Aged, 80 and over;Adult;Support, U.S. Gov't, P.H.S.;DNA Damage;Promoter Regions (Genetics)},
	Month = {6},
	Nlm_Id = {0410462},
	Number = {6994},
	Organization = {Department of Neurology and Division of Neuroscience, The Children's Hospital and Harvard Medical School, Enders 260,300 Longwood Avenue, Boston, Massachusetts 02115, USA.},
	Pages = {883-91},
	Pii = {nature02661},
	Pubmed = {15190254},
	Title = {Gene regulation and DNA damage in the ageing human brain},
	Uuid = {CB919E08-79E0-4674-B848-F6FAB15E6886},
	Volume = {429},
	Year = {2004},
	url = {papers/Lu_Nature2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature02661}}

@article{Lu:2002,
	Abstract = {We investigated the role of the CXCR4 chemokine receptor in development of the mouse hippocampus. CXCR4 mRNA is expressed at sites of neuronal and progenitor cell migration in the hippocampus at late embryonic and early postnatal ages. mRNA for stromal cell-derived factor 1 (SDF-1), the only known ligand for the CXCR4 receptor, is expressed close to these migration sites, in the meninges investing the hippocampal primordium and the primordium itself. In mice engineered to lack the CXCR4 receptor, the morphology of the hippocampal dentate gyrus (DG) is dramatically altered. Gene expression markers for DG granule neurons and bromodeoxyuridine labeling of dividing cells revealed an underlying defect in the stream of postmitotic cells and secondary dentate progenitor cells that migrate toward and form the DG. In the absence of CXCR4, the number of dividing cells in the migratory stream and in the DG itself is reduced, and neurons appear to differentiate prematurely before reaching their target. Our findings indicate a role for the SDF-1/CXCR4 chemokine signaling system in DG morphogenesis. Finally, the DG is unusual as a site of adult neurogenesis. We find that both CXCR4 and SDF-1 are expressed in the adult DG, suggesting an ongoing role in DG morphogenesis.},
	Author = {Lu, Meiling and Grove, Elizabeth A. and Miller, Richard J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Receptors, CXCR4;Signal Transduction;Animals;Female;Culture Techniques;Hippocampus;Intracellular Fluid;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Mice, Knockout;Cerebral Cortex;Dentate Gyrus;Chemokines, CXC;Neurons;Mice;Cell Division;Gene Expression;Ligands;Research Support, Non-U.S. Gov't},
	Medline = {22008001},
	Month = {5},
	Nlm_Id = {7505876},
	Number = {10},
	Organization = {Department of Molecular Pharmacology and Biological Chemistry, Northwestern University, Chicago, IL 60611, USA.},
	Pages = {7090-5},
	Pii = {092013799},
	Pubmed = {11983855},
	Title = {Abnormal development of the hippocampal dentate gyrus in mice lacking the CXCR4 chemokine receptor},
	Uuid = {241601F4-7114-11DA-9A4D-000D9346EC2A},
	Volume = {99},
	Year = {2002},
	url = {papers/Lu_ProcNatlAcadSciUSA2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.092013799}}

@article{Lucio:1997,
	Abstract = {Previous studies have shown that hypothyroidism modifies the development of callosal connections. In particular, adult hypothyroid rats have fewer callosally projecting neurons in layers II-III of the auditory cortex and more in layer V. This might be due to disturbance in the stabilization/elimination of juvenile callosal axons, or to abnormal neuronal migration during cortical histogenesis. To distinguish between these possibilities we have studied the distribution of callosally projecting auditory neurons at different postnatal ages using retrogradely transported tracers, and the cortical neurogenetic gradients using DNA labelling with 5-bromo-2'-deoxiuridine. In hypothyroid rats, injected at postnatal day 5 (P5) and killed at P18-20, most of the neurons retrogradely labelled from the contralateral hemisphere are distributed between layers IV and VI, as in older rats. In hypothyroid rats, many neurons are at locations inappropriate for their birthdate, including the subcortical white matter, resulting in more diffuse radial neurogenetic gradients. These results indicate that early induced hypothyroidism alters neuronal migration and prevents the establishment of callosal connections from cortical layers II-III.},
	Author = {Lucio, R. A. and Garc{\'\i}a, J. V. and Ram{\'o}n Cerezo, J. and Pacheco, P. and Innocenti, G. M. and Berbel, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {Auditory Cortex;Hypothyroidism;Rats;Not relevant;Rats, Wistar;11 Glia;Histocytochemistry;Disease Models, Animal;Male;Support, Non-U.S. Gov't;Animals},
	Medline = {97321031},
	Month = {6},
	Nlm_Id = {9110718},
	Number = {4},
	Organization = {Departamento de Histolog{\'\i}a, Universidad de Alicante, Spain.},
	Pages = {303-16},
	Pubmed = {9177762},
	Title = {The development of auditory callosal connections in normal and hypothyroid rats},
	Uuid = {877BF3FE-AD94-4F90-883D-6B67A282FDD0},
	Volume = {7},
	Year = {1997}}

@article{Lue:2002,
	Abstract = {The induction of an antibody response to amyloid beta (Abeta) peptide has become a strategy for the treatment of Alzheimer's disease (AD). This has proven effective in reducing the plaque burden in transgenic mice that develop Abeta plaques similar to human AD patients. The mechanism for enhanced clearance of Abeta is partly due to the interaction of immunoglobulin Fcgamma receptor-expressing microglia and specific antibody-opsonized Abeta deposits. This interaction can stimulate Fcgamma receptor-mediated phagocytosis, but also results in inflammatory activation of these cells. Consequently, interaction of microglia with antibody-antigen complexes could exacerbate the existing inflammation in the brains of AD patients. In this study, we used substrate-bound Abeta and cultured human microglia from AD and non-demented cases to model interaction of microglia and antibody-opsonized plaques in AD brains. Enhanced production of tumor necrosis factor-alpha, macrophage colony stimulating factor, interleukin-10, and superoxide ions was detected. We also demonstrated enhanced uptake of opsonized Abeta by microglia, which was reduced significantly in the presence of excess IgG, indicative of the involvement of Fcgamma receptor-mediated mechanisms. Human microglia were shown in this study to express mRNA for Fcgamma receptors I, IIa, IIb, and III. The expression of Fcgamma receptor II was augmented by proinflammatory stimulation. These results suggest that initial interactions of human microglia with antibody-opsonized amyloid could result in increased inflammation. The consequence of this on inflammatory pathology in AD brains needs to be considered before immunization is used as a strategy for treating AD.},
	Author = {Lue, Lih-Fen F. and Walker, Douglas G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Immunotherapy;Human;Phagocytosis;Cells, Cultured;Amyloid beta-Protein;Frontal Lobe;Microglia;Superoxides;Culture Media, Conditioned;Opsonins;11 Glia;RNA, Messenger;Antibodies;Support, Non-U.S. Gov't;Peptide Fragments;Alzheimer Disease;Support, U.S. Gov't, P.H.S.;Receptors, IgG;Cytokines},
	Medline = {22292042},
	Month = {11},
	Nlm_Id = {7600111},
	Number = {4},
	Organization = {Sun Health Research Institute, Sun City, Arizona 85351, USA.},
	Pages = {599-610},
	Pubmed = {12404514},
	Title = {Modeling Alzheimer's disease immune therapy mechanisms: interactions of human postmortem microglia with antibody-opsonized amyloid beta peptide},
	Uuid = {9E4BC686-2CFF-48F3-B5D2-D9D9F99C636C},
	Volume = {70},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10422}}

@article{Lundberg:2001,
	Abstract = {The hormone leptin has been shown to be an afferent signal in a negative-feedback loop regulating body weight, and consequently, the administration of the gene product for the treatment of obesity has recently attracted considerable attention. Leptin is produced by adipocytes in response to increased trigyceride storage, and appears to affect body weight primarily through target cells in the hypothalamus. Although plasma levels of leptin correlate positively with adipose tissue mass in normal humans and animals, recent studies have shown that obese humans and animals appear to be relatively resistant to the increased plasma levels of leptin. Analysis of the levels of leptin in the cerebrospinal fluid suggests that the uptake of leptin across the blood-brain barrier may be saturable. Taken together, these results suggest that therapeutic approaches to deliver leptin through the circulation may prove to be problematic. Although recent clinical trials have suggested that peripherally administered leptin might lead to a reduction in body weight in humans, it is likely that the more effective delivery of leptin to cellular targets within the central nervous system will be necessary in order to fully reveal the therapeutic potential of the gene product. In an effort to provide a means for the delivery of leptin that obviates the need for the gene product to traverse the blood-brain barrier, we have evaluated the use of recombinant adeno-associated vectors to deliver leptin intraventricularly or directly to the hypothalamus.},
	Author = {Lundberg, C. and Jungles, S. J. and Mulligan, R. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {Obesity;Animals;Humans;Leptin;Dependovirus;Brain;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Mice, Obese;Genetic Vectors;Cerebral Ventricles;Weight Loss;Hypothalamus;Gene Therapy;Muscle, Skeletal;Recombination, Genetic;Mice;Luminescent Proteins;Genes, Reporter;Research Support, Non-U.S. Gov't},
	Medline = {21110318},
	Month = {2},
	Nlm_Id = {9604648},
	Number = {2},
	Organization = {Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {169-72},
	Pubmed = {11175734},
	Title = {Direct delivery of leptin to the hypothalamus using recombinant adeno-associated virus vectors results in increased therapeutic efficacy},
	Uuid = {1FF33080-C024-4893-B947-6725A443186C},
	Volume = {19},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/84448}}

@article{Lunyak:2005,
	Abstract = {Epigenetic strategies control the orderly acquisition and maintenance of neuronal traits. A complex network of transcriptional repressors and co-repressors mediates gene specificity for these strategies. In this issue of Cell, a study by Ballas and coworkers (Ballas et al., 2005) provides insight into the early lineage commitment events during neurogenesis. This study demonstrates that regulation of the REST/NRSF transcriptional repressor plays a fundamental role in the progression of pluripotent cells to lineage-restricted neural progenitors.},
	Author = {Lunyak, Victoria V. and Rosenfeld, Michael G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Epigenesis, Genetic;Neurons;Cell Differentiation;Gene Expression Regulation, Developmental;review;Repressor Proteins;24 Pubmed search results 2008;review, tutorial;comment;Nervous System;Animals;Humans;Pluripotent Stem Cells;Cell Lineage;Transcription Factors},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {4},
	Pages = {499-501},
	Pii = {S0092-8674(05)00445-9},
	Pubmed = {15907461},
	Title = {No rest for REST: REST/NRSF regulation of neurogenesis},
	Uuid = {3DFD3A04-9CC5-444C-AAB5-2DE80275068C},
	Volume = {121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.05.003}}

@article{Luo:2006,
	Abstract = {In the adult mouse brain, the subventricular zone (SVZ) is a neurogenic stem cell niche only 4-5 cell diameters thick. Within this narrow zone, a unique microenvironment supports stem cell self-renewal, gliogenesis or neurogenesis lineage decisions and tangential migration of newly generated neurons out of the SVZ and into the olfactory bulb. However, with aging, SVZ neurogenesis declines. Here, we examine the dynamic interplay between SVZ cytoarchitecture and neurogenesis through aging. Assembly of high-resolution electron microscopy images of corresponding coronal sections from 2-, 10- and 22-month-old mice into photomontages reveal a thinning of the SVZ with age. Following a 2-h BrdU pulse, we detect a significant decrease in cell proliferation from 2 to 22 months. Neuroblast numbers decrease with age, as do transitory amplifying progenitor cells, while both SVZ astrocytes and adjacent ependymal cells remain relatively constant. At 22 months, only residual pockets of neurogenesis remain and neuroblasts become restricted to the anterior dorsolateral horn of the SVZ. Within this dorsolateral zone many key components of the younger neurogenic niche are maintained; however, in the aged SVZ, increased numbers of SVZ astrocytes are found interposed within the ependyma. These astrocytes co-label with markers to ependymal cells and astrocytes, form intercellular adherens junctions with neighboring ependymal cells, and some possess multiple basal bodies of cilia within their cytoplasm. Together, these data reveal an age-related, progressive restriction of SVZ neurogenesis to the dorsolateral aspect of the lateral ventricle with increased numbers of SVZ astrocytes interpolated within the ependyma.},
	Author = {Luo, Jie and Daniels, Stephen B. and Lennington, Jessica B. and Notti, Ryan Q. and Conover, Joanne C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1474-9718},
	Journal = {Aging Cell},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {101130839},
	Number = {2},
	Organization = {Center for Regenerative Biology, Department of Physiology and Neurobiology, University of Connecticut, Storrs, 06250-4243, USA.},
	Pages = {139-52},
	Pii = {ACE197},
	Pubmed = {16626393},
	Title = {The aging neurogenic subventricular zone},
	Uuid = {8CA566D5-0DDB-413F-B2AB-37CF86D4DC57},
	Volume = {5},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1474-9726.2006.00197.x}}

@article{Luo:2001,
	Author = {Luo, L. and Zong, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Mosaicism;23 Technique;Gene Expression Regulation, Developmental;Central Nervous System;Human;Genetic Markers;review, tutorial;Gene Targeting;Genes, Reporter;Neurons;review},
	Medline = {21547537},
	Month = {11},
	Nlm_Id = {9809671},
	Organization = {Department of Biological Sciences, Stanford University, Stanford, California 94305, USA. lluo\@stanford.edu},
	Pages = {1158-9},
	Pii = {nn1101-1158},
	Pubmed = {11687823},
	Title = {Single neuron labeling and genetic manipulation},
	Uuid = {D2FD4A4C-658C-4703-B796-500A8B47E9E3},
	Volume = {4 Suppl},
	Year = {2001},
	url = {papers/Luo_NatNeurosci2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1101-1158}}

@article{Luskin:1994,
	Abstract = {A spatially discrete region of the anterior part of the postnatal telencephalic subventricular zone, referred to as the SVZa generates vast numbers of lineally-related neurons destined for the olfactory bulb (Luskin, 1993). The cells originating in the SVZa migrate to the olfactory bulb along a highly restricted pathway which is in a direction orthogonal to the orientation of radial glial fibers. In this study we analysed the number, distribution, orientation and rate of migration of SVZa-derived cells as they approach the olfactory bulb. In order to track the SVZa-derived cells, a retroviral lineage tracer, encoding the reporter gene E. coli beta-galactosidase (lacZ) was injected precisely into the rat SVZa at postnatal day 1 (P1). The lacZ- positive cells were visualized 1, 2 and 3 days later by X-Gal histochemistry in cryostat sections. As the number of SVZa-derived cells in the pathway increased with survival time, their distribution changed systematically. The distribution pattern of lacZ-positive cells by 2 and 3 days postinjection suggested that some of the progeny of infected progenitor cells were undergoing neurogenesis as they proceeded to the olfactory bulb; a large percentage of the lacZ- positive cells were substantially displaced from the SVZa injection site. To investigate whether lacZ-positive cells migrate in a directed fashion, their orientation preference was scored. For the majority of lacZ-positive cells (>94\%), their leading process was directed toward the olfactory bulb, possibly reflecting a response to migratory cues present along the pathway. The estimated average rate of cell migration to the olfactory bulb was 23 mu m/h, which is approximately twice the speed of radially directed neuronal migration from the telencephalic ventricular zone to the cortical plate (O'Rourke et al., 1992). Collectively, these results suggest that SVZa-derived interneurons en route to the olfactory bulb may employ a novel mode of tangential migration.},
	Author = {Luskin, M. B. and Boone, M. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Issn = {0379-864X},
	Journal = {Chem Senses},
	Keywords = {Genetic Vectors;Immunohistochemistry;Animals, Newborn/physiology;Telencephalon/*cytology/growth &development;Interneurons;Animals;beta-Galactosidase/biosynthesis/genetics;Escherichia coli/enzymology/genetics;Nerve Fibers;Research Support, U.S. Gov't, P.H.S.;Nerve Fibers/physiology;Olfactory Bulb/*cytology/growth &development;Olfactory Bulb;Support, U.S. Gov't, P.H.S.;Escherichia coli;Animal;B abstr;Rats, Sprague-Dawley;Retroviridae;beta-Galactosidase;02 Adult neurogenesis migration;Neuroglia/physiology;Rats;Neuroglia;Telencephalon;Retroviridae/genetics;Animals, Newborn;Support, Non-U.S. Gov't;Research Support, Non-U.S. Gov't;Interneurons/*physiology},
	Medline = {95253832},
	Month = {12},
	Nlm_Id = {8217190},
	Number = {6},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, GA 30322, USA.},
	Pages = {695-714.},
	Pubmed = {7735848},
	Title = {Rate and pattern of migration of lineally-related olfactory bulb interneurons generated postnatally in the subventricular zone of the rat},
	Uuid = {A19AAF07-E157-4B67-85C7-6F5487670D12},
	Volume = {19},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7735848}}

@article{Luskin:2002,
	Abstract = {For the last 10 years our laboratory has been studying the proliferation, migration and differentiation of neuronal progenitor cells located in the anterior part of the postnatal forebrain subventricular zone (SVZa). SVZa-derived cells possess a number of proliferative characteristics that distinguish them from the other progenitor cells in the central nervous system. This review summarizes our recent findings, in which we compared the pattern of cell cycle inhibitory proteins expressed by the neonatal SVZa to that of telencephalic ventricular zone cells.},
	Author = {Luskin, Marla B. and Coskun, Volkan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0379-864X},
	Journal = {Chem Senses},
	Keywords = {10 Development;Cell Differentiation;Cell Cycle Proteins;Animals;Protein p16;Humans;Cyclin-Dependent Kinase Inhibitor p19;Comparative Study;Cell Cycle;review;Cell Movement;Telencephalon;Prosencephalon;Cerebral Ventricles;03 Adult neurogenesis progenitor source;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Cyclin-Dependent Kinase Inhibitor p16;Neurons;Cell Division;Stem Cells},
	Medline = {22137523},
	Month = {7},
	Nlm_Id = {8217190},
	Number = {6},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, GA 30322, USA. luskin\@cellbio.emory.edu},
	Pages = {577-80},
	Pubmed = {12142335},
	Title = {The progenitor cells of the embryonic telencephalon and the neonatal anterior subventricular zone differentially regulate their cell cycle},
	Uuid = {47B68489-6B2C-4F38-8B40-FF97B3EBD943},
	Volume = {27},
	Year = {2002}}

@article{Luskin:1994a,
	Abstract = {Although previous studies have revealed that the prenatal rat ventricular zone contains separate progenitor cells for neurons, astrocytes, and oligodendrocytes during the development of the cerebral cortex as early as the beginning of neurogenesis (Luskin et al., 1993; Grove et al., 1993), it is still unclear whether there are bipotential progenitor cells in the neonatal telencephalic subventricular zone which give rise to both astrocytes and oligodendrocytes during the peak of gliogenesis. To investigate this possibility, discrete groups of clonally related cells, generated by infecting progenitor cells of the neonatal subventricular zone with a retroviral lineage tracer, were analyzed ultrastructurally. An intracerebral injection of retrovirus encoding the reporter gene E. coli beta-galactosidase (lacZ) was made into the subventricular zone of newborn rats. Two weeks later their brains were perfused, sectioned, and histochemically reacted with X-Gal to identify at the light microscopic level clones of lacZ-positive cells. The sections were processed for electron microscopy to enable the identity of clonally related cells to be assessed at the ultrastructural level. All of the clones analyzed contained cells of the same phenotype and could be divided into four distinct types: immature cell clones situated in the subependymal zone surrounding the lateral ventricle, oligodendrocytes clones, and white or gray matter astrocyte clones. Not all of the cells in every clone displayed ultrastructural features of a mature cell. Rather, in some glial clones the lacZ-positive cells appeared to be at different stages of differentiation. However, we never encountered clones which contained both macroglial subtypes or clones containing neurons. Although the existence of bipotential progenitor cells cannot be completely dismissed, our results indicate the absence of progenitor cells in vivo in the neonatal subventricular zone which divide and generate astrocytes and oligodendrocytes. eng Journal Article},
	Author = {Luskin, M. B. and McDermott, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Journal = {Glia},
	Keywords = {Prosencephalon/*cytology/growth &development/ultrastructure;Rats;Stem Cells/physiology;Phenotype;beta-Galactosidase/metabolism;Animal;Rats, Sprague-Dawley;G abstr;11 Glia;Cerebral Ventricles/*cytology/growth &development/ultrastructure;Histocytochemistry;Gene Transfer Techniques;Animals, Newborn/*physiology;Support, Non-U.S. Gov't;Oligodendroglia/*physiology/ultrastructure;Astrocytes/*physiology/ultrastructure;Support, U.S. Gov't, P.H.S.;Microscopy, Electron;Clone Cells},
	Number = {3},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322.},
	Pages = {211-26.},
	Title = {Divergent lineages for oligodendrocytes and astrocytes originating in the neonatal forebrain subventricular zone},
	Uuid = {C77FC097-C99F-4A3A-BAB2-28F3D2A08211},
	Volume = {11},
	Year = {1994}}

@article{Luskin:1985,
	Abstract = {The 3H-thymidine method of birth-dating was used to determine when the cells belonging to each of the principal cellular layers of the cat's primary visual cortex are generated. In order to detect systematic differences in the position of radioactively labeled cells following 3H-thymidine administration at different prenatal ages, a geometric method was devised to represent the distribution of labeled cells in the form of depth histograms. Results show that visual cortical neurogenesis occurs largely during the second half of gestation between embryonic day 31 (E31) and E57. Cells of layer 6 are generated early, between E31 and E38, whereas cells destined for successively more superficial layers are generated at progressively later times. Layer 4 cells, the principal targets of geniculocortical afferents, are generated between E37 and E44. In addition, a special population of cells embedded in the white matter below layer 6 was found to be produced throughout the week-long period immediately prior to the onset of layer 6 neurogenesis. Overall, this radial pattern of cortical neurogenesis closely resembles the inside-first, outside-last, spatiotemporal sequence of development described for the monkey's primary visual cortex (Rakic, '74). In addition to finding this pronounced gradient in the radial dimension, we were also able to detect a less pronounced gradient along the tangential dimension: neurons destined for any given layer in the anterior part of the cortex (inferior visual field representation) are generated slightly in advance of neurons destined for more posterior regions (superior visual field). However even our more quantitative histogram analysis failed to reveal a mediolateral (central to peripheral visual field) gradient within area 17. In the cat, layers 6, 5, and 4 each take about a week to be generated, although their total cell numbers and packing densities differ in the adult. About 2 weeks are required to produce the cells of layers 2 and 3 combined. Furthermore, we found that neurons belonging to different layers and different morphological classes can be generated simultaneously. This suggests that the identity of a cortical neuron is not solely a function of the time of neurogenesis. 0021-9967 Journal Article},
	Author = {Luskin, M. B. and Shatz, C. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Comp Neurol},
	Keywords = {01 Adult neurogenesis general;Thymidine/diagnostic use;Cats;Female;Neurons/analysis/*physiology;Autoradiography;Visual Cortex/anatomy &histology/*growth &development;A,F abstr;Support, U.S. Gov't, P.H.S.;*Brain Mapping/methods;Animals;Age Factors;Male;Animals, Newborn/growth &development;Injections, Intravenous},
	Number = {4},
	Pages = {611-31},
	Pubmed = {4086673},
	Title = {Neurogenesis of the cat's primary visual cortex},
	Uuid = {C3344955-15FE-4242-BF87-07AA5FF7E417},
	Volume = {242},
	Year = {1985},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=4086673}}

@article{Luskin:1998,
	Abstract = {The subventricular zone (SVZ) is the only germinal zone of the developing mammalian forebrain to persist postnatally. Although the SVZ has been known to give rise to most of the glial cells of the forebrain, several studies over the past few years have shown that the cells of the neonatal and adult SVZ can also generate neurons. Recent studies have demonstrated that a discrete region of the anterior part of the neonatal SVZ is composed exclusively of neuronal progenitor cells, whose progeny become interneurons of the olfactory bulb. This review will explore the properties that distinguish this anterior segment of the neonatal subventricular zone (SVZa) from the more posterior, gliogenic region. The cells of the SVZa, as well as its anterior extension forming the rostral migratory stream that enters the middle of the olfactory bulb, have antigenic characteristics of a neuronal phenotype, yet continue to divide during migration. In vitro, SVZa progenitor cells also retain a neuronal phenotype despite persistent division. Intriguingly, SVZa cells and their progeny migrate long distances along a highly stereotypical pathway. To better understand the guidance cues used by SVZa-derived cells during migration, both homotopic and heterotopic transplantation experiments have been conducted. SVZa cells homotopically transplanted into another animal's SVZa migrate with the recipient's endogenous SVZa cells in an indistinguishable manner, whereas those from the embryonic telencephalic ventricular zone, normally destined to follow radial glia to the cerebral cortex, fail to migrate following transplantation to the SVZa. SVZa cells transplanted heterotopically into the neonatal and adult striatum were able to disperse from their site of implantation. Thus, SVZa cells are special proliferating cells for which the rostral migratory stream is a particularly permissive pathway.},
	Author = {Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {J Neurobiol},
	Keywords = {Animals, Newborn/growth &development/*physiology;Olfactory Bulb/cytology/growth &development;02 Adult neurogenesis migration;B;Stem Cells/cytology/*physiology;Phenotype;Cell Line/physiology;Neurons/cytology/*physiology;Animal;Support, U.S. Gov't, P.H.S.;Prosencephalon/*cytology/growth &development;Support, Non-U.S. Gov't},
	Number = {2},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {221-33.},
	Title = {Neuroblasts of the postnatal mammalian forebrain: their phenotype and fate},
	Uuid = {46EA1F62-B88A-4E4F-8085-7CC8D2F8BCD0},
	Volume = {36},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9712306}}

@article{Luskin:1993,
	Abstract = {The diverse array of neurons and glia in the mammalian cerebral cortex arises from proliferating cells of the ventricular zone that surrounds the lateral ventricles of the developing brain. A fundamental but unresolved question is whether the individual cells of the ventricular zone are committed to producing progeny of only one particular phenotype or whether they generate progeny of more than one phenotype. We have begun to address this question by asking if individual cells of the ventricular zone generate exclusively neurons or glia at the onset of cortical neurogenesis in the rat. To assess the phenotypes of cells derived from a common progenitor cell, retroviral-mediated gene transfer was used to introduce the reporter gene, Escherichia coli beta-galactosidase, into ventricular zone cells at embryonic day 15 or 16. We used histochemistry to reveal beta-galactosidase-expressing cells in the mature rat cerebral cortex. Isolated clusters of beta-galactosidase-expressing cells, presumably clones, were identified in serial sections. Since the histochemical reaction product is electron dense, each cell could be examined at the ultrastructural level and assigned definitively to one of the major classes of cells in the cerebral cortex on the basis of well-established morphological criteria. This approach overcomes the problems of cell type identification encountered with light microscopy, where it is not always possible to distinguish between different cell phenotypes. We found that virtually all clones contained cells of exclusively one type: either all astrocytes, all oligodendrocytes, or all neurons. Furthermore, each particular cell type exhibited a different pattern and intensity of staining. The neuronal clones, with one exception, were composed of either all pyramidal cells (projection neurons), or all nonpyramidal cells (interneurons). The size and composition of neuronal clones did not seem related to their position in the cerebral cortex. Collectively, our observations indicate that separate progenitor cells exist for pyramidal neurons, nonpyramidal neurons, astrocytes, and oligodendrocytes. The striking phenotypic homogeneity in the clones arising from individual progenitor cells suggests that by the onset of cortical neurogenesis, at least some lineage restrictions have already occurred among the precursor cell population. Thus, our results suggest that lineage may play a pivotal role in determining some of the functionally important phenotypic attributes of cells in the cerebral cortex. eng Journal Article},
	Author = {Luskin, M. B. and Parnavelas, J. G. and Barfield, J. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {10 Development;Cerebral Cortex/*cytology/enzymology/ultrastructure;Oligodendroglia/*cytology/enzymology/ultrastructure;beta-Galactosidase;Astrocytes;beta-Galactosidase/genetics/metabolism;Rats;Animals;Neuroglia/ultrastructure;Oligodendroglia;Animal;02 Adult neurogenesis migration;Neurons/*cytology/enzymology/ultrastructure;11 Glia;BB abstr;Cell Line;03 Adult neurogenesis progenitor source;Histocytochemistry;Support, Non-U.S. Gov't;Cerebral Cortex;Neuroglia;Neurons;Lac Operon;Support, U.S. Gov't, P.H.S.;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Stem Cells/*cytology/enzymology/ultrastructure;Astrocytes/*cytology/enzymology/ultrastructure;Research Support, Non-U.S. Gov't},
	Medline = {93217553},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {4},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322.},
	Pages = {1730-50.},
	Pubmed = {8463848},
	Title = {Neurons, astrocytes, and oligodendrocytes of the rat cerebral cortex originate from separate progenitor cells: an ultrastructural analysis of clonally related cells},
	Uuid = {69307C29-DC8E-4799-B9A6-346D5A18F77C},
	Volume = {13},
	Year = {1993},
	url = {papers/Luskin_JNeurosci1993.pdf}}

@article{Luskin:1997,
	Abstract = {A discrete area of the anterior part of the subventricular zone, or SVZa, of the postnatal forebrain is composed of progenitor cells that are dissimilar to those elsewhere in the CNS. In vivo SVZa progenitor cells retain the ability for division, even though they are phenotypically neurons. To characterize further the properties of SVZa cells, we have analyzed their characteristics in vitro using cell-type specific antibodies and their proliferative capacity by the incorporation of bromodeoxyuridine. At 2 h in vitro, as well as after 1 day in vitro, virtually all SVZa cells isolated from the neonatal forebrain express TuJ1, an antibody that recognizes neuron-specific tubulin, and are GFAP-negative. Likewise, the preponderance of SVZa cells express the neuron-specific markers N-CAM and MAP-2 when examined after 1 day in culture. The majority of SVZa cells cultured for as long as 8 days also possessed a neuronal phenotype. In addition, process- bearing TuJ1-positive SVZa cells continued to proliferate throughout the entire culture period. Thus, the neuronal progenitor cells of the SVZa constitute a unique cell population with characteristics distinct from the cells of other germinal zones. Using Smart Source Parsing},
	Author = {Luskin, M. B. and Zigova, T. and Soteres, B. J. and Stewart, R. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Prosencephalon/*cytology;Neurons/*cytology/*physiology;02 Adult neurogenesis migration;Animals, Newborn/*anatomy &histology;Support, Non-U.S. Gov't;03 Adult neurogenesis progenitor source;Rats;Stem Cells/*cytology/physiology;Phenotype;Cell Division;Animal;Support, U.S. Gov't, P.H.S.;Neurites/physiology;Cells, Cultured;Telencephalon/*cytology;BB abstr;Cerebral Ventricles},
	Number = {5},
	Organization = {Department of Anatomy, Emory University School of Medicine, George Washington University Medical Center, 2300 Eye St., N.W., Atlanta, Georgia, 30322, USA. luskin\@anatomy.emory.edu},
	Pages = {351-66},
	Title = {Neuronal progenitor cells derived from the anterior subventricular zone of the neonatal rat forebrain continue to proliferate in vitro and express a neuronal phenotype},
	Uuid = {DE254ADF-4237-4775-88E4-5104143C9948},
	Volume = {8},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9073397}}

@article{Luskin:1988,
	Abstract = {To analyze cell lineage in the murine cerebral cortex, we infected progenitor cells with a recombinant retrovirus, then used the retroviral gene product to identify the descendants of infected cells. Cortices were infected on E12-E14 either in vivo or following dissociation and culture. In both cases, nearly all clones contained either neurons or glia, but not both. Thus, neuronal and glial lineages appear to diverge early in cortical development. To analyze the distribution of clonally related cells in vivo, clonal boundaries were reconstructed from serial sections. Perinatally (E18-PN0), clonally related cells were radially arrayed as they migrated to the cortical plate. Thus, clonal cohorts traverse a similar radial path. Following migration (PN7-PN23), neuronal clones generally remained radially arrayed, while glial clones were variable in orientation, suggesting that these two cell types accumulate in different ways. Neuronal clones sometimes spanned the full thickness of the cortex. Thus, a single progenitor can contribute neurons to several laminae.},
	Author = {Luskin, M. B. and Pearlman, A. L. and Sanes, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Cell Differentiation;10 Development;Neuroglia;Research Support, Non-U.S. Gov't;Retroviridae Proteins;Embryonic and Fetal Development;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Mice, Inbred C57BL;Retroviridae;15 Retrovirus mechanism;Mice;Animals;Cerebral Cortex;Neurons},
	Medline = {90166544},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {8},
	Organization = {Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110.},
	Pages = {635-47},
	Pubmed = {3272182},
	Title = {Cell lineage in the cerebral cortex of the mouse studied in vivo and in vitro with a recombinant retrovirus},
	Uuid = {AA6A06C6-2E8E-40FD-BFBA-31F2F47971AE},
	Volume = {1},
	Year = {1988}}

@article{Luskin:1993a,
	Abstract = {The subventricular zone of the postnatal forebrain produces mainly glia, although it supports limited neurogenesis. To determine whether the subventricular zone is positionally specified, the phenotype and destination of the progeny of subventricular zone cells along the anterior-posterior axis of the lateral ventricles were analyzed. A retroviral lineage tracer containing the E. coli reporter gene lacZ was injected into different parts of the subventricular zone of neonatal rat pups, and at various times thereafter, the expression of beta- galactosidase was detected histochemically or immunohistochemically in the descendants of infected cells. A discrete region of the anterior part of the subventricular zone (SVZa) generated an immense number of neurons that differentiated into granule cells and periglomerular cells of the olfactory bulb-the two major types of interneurons. Thus, the SVZa appears to constitute a specialized source of neuronal progenitor cells. To reach the olfactory bulb, neurons arising in the SVZa migrate several millimeters along a highly restricted route. Guidance cues must be involved to prohibit widespread dispersion of these migrating neurons.},
	Author = {Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Neuron},
	Keywords = {Prosencephalon/*cytology;Cell Line/physiology;Cell Differentiation;Olfactory Bulb/cytology/physiology;Rats;Phenotype;Female;Animal;Rats, Sprague-Dawley;B-3;Cell Movement;Stem Cells/cytology;Neurons/*cytology/*physiology;Male;Time Factors;Animals, Newborn;Support, Non-U.S. Gov't;Lac Operon;Support, U.S. Gov't, P.H.S.;Cell Division},
	Number = {1},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322.},
	Pages = {173-89.},
	Title = {Restricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zone},
	Uuid = {120ADD26-CD62-11D9-97C9-000D9346EC2A},
	Volume = {11},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8338665}}

@article{Luttenberg:1980,
	Author = {Luttenberg, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {0015-5640},
	Journal = {Folia Morphol (Praha)},
	Keywords = {Nerve Degeneration;Cats;Neural Pathways;Animals;24 Pubmed search results 2008;Frontal Lobe},
	Medline = {81068181},
	Nlm_Id = {0010076},
	Number = {4},
	Pages = {333-6},
	Pubmed = {7439850},
	Title = {Association systems of the cat's frontal cortex},
	Uuid = {354A35EA-8D24-4A19-9665-C5AE50892647},
	Volume = {28},
	Year = {1980}}

@article{Luthi:1994,
	Abstract = {A monoclonal antibody G39, generated against a protein extract of leech central nervous system, labels specific cell types in adult, embryonic, and regenerating preparations. The antibody stained glial cells, microglial cells, and connective tissue cells, but not neurons or muscle on cryosections. The staining pattern resembled that of an intracellular network. Affinity purification of the antigen revealed a 70 kD protein. Peptide sequencing showed significant homology of a stretch of 15 amino acids to squid neural filament protein. The same mAb G39 delineated glial cells as they formed during development of the CNS and showed that the giant neuropil glial cells appear before those in the packets. The antigen recognized by mAb G39 represents a nonneuronal intermediate filament of the leech Hirudo medicinalis found in various cell-types such as glia, microglia, and some cells of the connective tissue.},
	Author = {L{\"u}thi, T. E. and Brodbeck, D. L. and Jen{\"o}, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Mice, Inbred BALB C;Electrophoresis, Polyacrylamide Gel;Animals;Sequence Homology, Amino Acid;Decapodiformes;Hydrogen-Ion Concentration;Leeches;Neurofilament Proteins;11 Glia;Concanavalin A;Antibodies, Monoclonal;Neuroglia;Blotting, Western;Mice;Nerve Crush;Central Nervous System;Molecular Sequence Data;Amino Acid Sequence;24 Pubmed search results 2008;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {94157531},
	Month = {1},
	Nlm_Id = {0213640},
	Number = {1},
	Organization = {Department of Pharmacology, Universit{\"a}t Basel, Switzerland.},
	Pages = {70-82},
	Pubmed = {8113784},
	Title = {Identification of a 70 kD protein with sequence homology to squid neurofilament protein in glial cells of the leech CNS},
	Uuid = {33F7CBE9-60F0-4EB4-B48E-5B78092EBC32},
	Volume = {25},
	Year = {1994},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.480250107}}

@article{Lynch:1993,
	Abstract = {In this report, we have examined the role of central nervous system (CNS) development in the pathogenesis of neurodegenerative disease induced by murine retroviruses. This was accomplished by comparing the effect of delivering viruses, with either severe or marginal neurovirulence (J. L. Portis, S. Czub, C. F. Garon, and F. J. McAtee, J. Virol. 64:1648-1656, 1990), during the midgestational development of the mouse (gestation days 9 to 10). Midgestation inoculation of the marginally neurovirulent virus, 15-1, resulted in high level CNS infection, as determined by viral DNA and protein analysis. The high-level infection resulted in rapid, severe disease with 100\%incidence and an average clinical onset on postnatal day 17 (P17). The disease onset was comparable to that observed for the highly neurovirulent virus, FrCasE, when inoculated neonatally (onset ca. P16). To evaluate whether disease could be induced even earlier in CNS development, FrCasE was inoculated during midgestation. Surprisingly, neither clinical nor histological manifestations of CNS disease were accelerated but rather appeared at the same developmental time as seen for neonatally inoculated animals (onset of neuropathology at ca. P10; onset of clinical disease at ca. P15). CNS infection, on the other hand, occurred at earlier times (<P0), at higher levels, and with a broader distribution than in neonatally inoculated animals. No infection of the neurons which ultimately degenerate was observed in any regimen of virus inoculation. It was observed, however, that the gp70 viral envelope protein from the CNS showed an increase mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis compared with the envelope protein from infected spleens or purified virions. These results indicate that a postnatal developmental event must occur to allow the presence of a neurovirulent virus to precipitate spongiform degeneration and that an altered envelope protein may be participating in the process.},
	Author = {Lynch, W. P. and Portis, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Gene Products, env;Tissue Distribution;Animals;Comparative Study;Brain;Rodent Diseases;Not relevant;Get paper from library;Retroviridae;11 Glia;Time Factors;Retroviridae Infections;Animals, Newborn;Neurons;Mice;Virulence;Immunohistochemistry;Virus Replication;Central Nervous System},
	Medline = {93233225},
	Month = {5},
	Nlm_Id = {0113724},
	Number = {5},
	Organization = {Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.},
	Pages = {2601-10},
	Pubmed = {8386268},
	Title = {Murine retrovirus-induced spongiform encephalopathy: disease expression is dependent on postnatal development of the central nervous system},
	Uuid = {46DBFAD2-4C25-4DEB-881A-3723EF7F4206},
	Volume = {67},
	Year = {1993},
	url = {papers/Lynch_JVirol1993.pdf}}

@article{Lynch:1994,
	Abstract = {The observation of murine retrovirus infection of microglial cells in brain regions expressing spongiform neurodegenerative changes suggests that these cells may play an important role in pathogenesis. To evaluate this potential in vitro, murine microglial cells were infected in mixed glial cultures with the highly neurovirulent murine retrovirus, FrCasE. The microglia were then isolated from the mixed cultures on the basis of their differential adherence and shown to be approximately 98\%pure. The infected microglia expressed viral envelope protein at the plasma membrane, while viral budding was primarily intracellular. Evaluation of the viral envelope protein by immunoblotting indicated that the immunoreactive species produced was exclusively a 90-kDa precursor protein. Very little of the envelope protein was associated with particles released from these cells, and viral titers in the culture supernatant were low. Interestingly, these cells were still capable of infecting permissive target cells when seeded as infectious centers. This partially defective infection of microglial cells suggests a potential cellular means by which a neurovirulent retrovirus could disrupt normal microglia and in turn central nervous system motor system functioning.},
	Author = {Lynch, W. P. and Brown, W. J. and Spangrude, G. J. and Portis, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Virulence;Not relevant;Gammaretrovirus;11 Glia;Microglia;Protein Processing, Post-Translational;Animals;Mice;Viral Envelope Proteins},
	Medline = {94202331},
	Month = {5},
	Nlm_Id = {0113724},
	Number = {5},
	Organization = {Laboratory of Persistent Viral Diseases, National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratories, Hamilton, Montana 59840.},
	Pages = {3401-9},
	Pubmed = {8151801},
	Title = {Microglial infection by a neurovirulent murine retrovirus results in defective processing of envelope protein and intracellular budding of virus particles},
	Uuid = {0BA43F5C-3A2A-484D-9CF9-A23EE2382728},
	Volume = {68},
	Year = {1994},
	url = {papers/Lynch_JVirol1994.pdf}}

@article{Lynch:1995,
	Abstract = {FrCasE is a highly neurovirulent murine leukemia virus which causes a noninflammatory spongiform neurodegenerative disease after neonatal inoculation. The central nervous system (CNS) infection is wide-spread, involving several different cell types, whereas the lesions are localized to motor areas of the brain and spinal cord. Inoculation of FrCasE at 10 days of age (P10) results in viremia, but infection of the CNS is restricted and neurological disease is not observed (M. Czub, S. Czub, F. McAtee, and J. Portis, J. Virol. 65:2539-2544, 1991). In this study, we used this developmental resistance to restrict the extent and the distribution of FrCasE in the brain to examine whether the spongiform degeneration is a consequence of infection of cells in proximity to the lesions. Two approaches were used to infect the brain on or after P10. First, mice were inoculated with FrCasE at P10 to induce viremia and then at P17 were subjected to focal CNS injury within brain regions known to be susceptible to virus-induced spongiform degeneration. The injury resulted in local inflammation, glial activation, migration of inflammatory cells into the wound site, and high-level parenchymal infection about the wound site. However, no evidence of spongiform neurodegeneration was observed over a period of 3 months. The second approach involved the implantation of FrCasE-infected microglia into the CNS at >or = P10. This resulted in microglial engraftment and focal CNS infection unilaterally at the implantation sites and bilaterally along white matter tracts of the corpus callosum and pons and in cells of the subventricular layers of the lateral cerebral ventricles. Strikingly, focal spongiform degeneration colocalized with the sites of infection. In contrast to the wounding experiments, the implantation model was not associated with an inflammatory response or significant glial activation. Results of these studies suggest that (i) the developmental resistance of the CNS to infection lies at the blood-brain barrier and can be bypassed by direct introduction into the brain of virus-infected cells, (ii) the neuropathology induced by this virus is a consequence of local effects of the infection and does not appear to require endothelial or neuronal infection, and (iii) elements of the inflammatory response and/or glial activation may modulate the expression of neuropathology induced by neurovirulent retroviruses.},
	Author = {Lynch, W. P. and Robertson, S. J. and Portis, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Animals;Nerve Degeneration;Blood-Brain Barrier;11 Glia;Microglia;Age Factors;Mice;Nervous System Diseases;Mice, Inbred Strains;Leukemia Virus, Murine},
	Medline = {95156564},
	Month = {3},
	Nlm_Id = {0113724},
	Number = {3},
	Organization = {Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infections Diseases, Hamilton, Montana 59840.},
	Pages = {1408-19},
	Pubmed = {7853473},
	Title = {Induction of focal spongiform neurodegeneration in developmentally resistant mice by implantation of murine retrovirus-infected microglia},
	Uuid = {27C57D12-0F1B-4B8F-8FB2-AFEC1B0350A0},
	Volume = {69},
	Year = {1995},
	url = {papers/Lynch_JVirol1995.pdf}}

@article{Lynch:1996,
	Abstract = {CasBrE is a neurovirulent murine retrovirus which induces a spongiform myeloencephalopathy in susceptible mice. Genetic mapping studies have indicated that sequences responsible for neurovirulence reside within the env gene. To address the question of direct envelope protein neuroxicity in the central nervous system (CNS), we have generated chimeric mice expressing the CasBrE envelope protein in cells of neuroectodermal origin. Specifically, the multipotent neural progenitor cell line C17.2 was engineered to express the CasBrE env gene as either gp70/p15E (CasE) or gp70 alone (CasES). CasE expression in these cells resulted in complete (>10(5)) interference of superinfection with Friend murine leukemia virus clone FB29, whereas CasES expression resulted in a 1.8-log-unit decrease in FB29 titer. Introduction of these envelope-expressing C17.2 cells into the brains of highly susceptible IRW mice resulted in significant engraftment as integral cytoarchitecturally correct components of the CNS. Despite high-level envelope protein expression from the engrafted cells, no evidence of spongiform neurodegeneration was observed. To examine whether early virus replication events were necessary for pathogenesis, C17.2 cells expressing whole virus were transplanted into mice in which virus replication in the host was specifically restricted by Fv-1 to preintegration events. Again, significant C17.2 cell engraftment and infectious virus expression failed to precipitate spongiform lesions. In contrast, transplantation of virus-expressing C17.2 progenitor cells in the absence of the Fv-1 restriction resulted in extensive spongiform neurodegeneration by 2 weeks postengraftment. Cytological examination indicated that infection had spread beyond the engrafted cells, and in particular to host microglia. Spongiform neuropathology in these animals was directly correlated with CasBrE env expression in microglia rather than expression from neural progenitor cells. These results suggest that the envelope protein of CasBrE is not itself neurotoxic but that virus infectious events beyond binding and fusion in microglia are necessary for the induction of CNS disease.},
	Author = {Lynch, W. P. and Snyder, E. Y. and Qualtiere, L. and Portis, J. L. and Sharpe, A. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Central Nervous System;Animals;Prion Diseases;Base Sequence;Brain;Microglia;Gene Products, gag;Retroviridae;11 Glia;Viral Envelope Proteins;Cell Line;Research Support, U.S. Gov't, P.H.S.;Mice;DNA, Viral;Virulence;Virus Replication;Retroviridae Proteins, Oncogenic;Gene Expression;Molecular Sequence Data;Research Support, Non-U.S. Gov't},
	Medline = {97126095},
	Month = {12},
	Nlm_Id = {0113724},
	Number = {12},
	Organization = {Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. wonk\@mbcrr.harvard.edu},
	Pages = {8896-907},
	Pubmed = {8971019},
	Title = {Late virus replication events in microglia are required for neurovirulent retrovirus-induced spongiform neurodegeneration: evidence from neural progenitor-derived chimeric mouse brains},
	Uuid = {7B76721E-0ABC-42B8-A69A-D7E7A8AA0879},
	Volume = {70},
	Year = {1996},
	url = {papers/Lynch_JVirol1996.pdf}}

@article{Lynch:1999,
	Abstract = {The induction of spongiform myeloencephalopathy by murine leukemia viruses is mediated primarily by infection of central nervous system (CNS) microglia. In this regard, we have previously shown that CasBrE-induced disease requires late, rather than early, virus replication events in microglial cells (W. P. Lynch et al., J. Virol. 70:8896-8907, 1996). Furthermore, neurodegeneration requires the presence of unique sequences within the viral env gene. Thus, the neurodegeneration-inducing events could result from microglial expression of retroviral envelope protein alone or from the interaction of envelope protein with other viral structural proteins in the virus assembly and maturation process. To distinguish between these possible mechanisms of disease induction, we engineered the engraftable neural stem cell line C17-2 into packaging/producer cells in order to deliver the neurovirulent CasBrE env gene to endogenous CNS cells. This strategy resulted in significant CasBrE env expression within CNS microglia without the appearance of replication competent virus. CasBrE envelope expression within microglia was accompanied by increased expression of activation markers F4/80 and Mac-1 (CD11b) but failed to induce spongiform neurodegenerative changes. These results suggest that envelope expression alone within microglia is not sufficient to induce neurodegeneration. Rather, microglia-mediated disease appears to require neurovirulent Env protein interaction with other viral proteins during assembly or maturation. More broadly, the results presented here prove the efficacy of a novel method by which neural stem cell biology may be harnessed for genetically manipulating the CNS, not only for studying neurodegeneration but also as a paradigm for the disseminated distribution of retroviral vector-transduced genes.},
	Author = {Lynch, W. P. and Sharpe, A. H. and Snyder, E. Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Gene Transfer Techniques;Research Support, Non-U.S. Gov't;Nerve Degeneration;Research Support, U.S. Gov't, P.H.S.;Not relevant;Stem Cells;Cell Line;11 Glia;Microglia;Support, U.S. Gov't, P.H.S.;Hematopoietic Stem Cell Transplantation;Retroviridae;Animals;Mice;Support, Non-U.S. Gov't;Retroviridae Infections;Genes, env},
	Medline = {99329209},
	Month = {8},
	Nlm_Id = {0113724},
	Number = {8},
	Organization = {Department of Microbiology/Immunology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272, USA.},
	Pages = {6841-51},
	Pubmed = {10400782},
	Title = {Neural stem cells as engraftable packaging lines can mediate gene delivery to microglia: evidence from studying retroviral env-related neurodegeneration},
	Uuid = {ECC9382C-5756-43F1-BF6A-0AD45F36D4E5},
	Volume = {73},
	Year = {1999},
	url = {papers/Lynch_JVirol1999.pdf}}

@article{Lynch:2000,
	Abstract = {The wild mouse ecotropic retrovirus, Cas-Br-E, induces progressive, noninflammatory spongiform neurodegenerative disease in susceptible mice. Functional genetic analysis of the Cas-Br-E genome indicates that neurovirulence maps to the env gene, which encodes the surface glycoprotein responsible for binding and fusion of virus to host cells. To understand how the envelope protein might be involved in the induction of disease, we examined the regional and temporal expression of Cas-Br-E Env protein in the central nervous systems (CNS) of mice infected with the highly neurovirulent chimeric virus FrCas(E). We observed that multiple isoforms of Cas-Br-E Env were expressed in the CNS, with different brain regions exhibiting unique patterns of processed Env glycoprotein. Specifically, the expression of gp70 correlated with regions showing microglial infection and spongiform neurodegeneration. In contrast, regions high in neuronal infection and without neurodegenerative changes (the cerebellum and olfactory bulb) were characterized by a gp65 Env protein isoform. Sedimentation analysis of brain region extracts indicated that gp65 rather than gp70 was incorporated into virions. Biochemical analysis of the Cas-Br-E Env isoforms indicated that they result from differential processing of N-linked sugars. Taken together, these results indicate that differential posttranslational modification of the Cas-Br-E Env is associated with a failure to incorporate certain Env isoforms into virions in vivo, suggesting that defective viral assembly may be associated with the induction of spongiform neurodegeneration.},
	Author = {Lynch, W. P. and Sharpe, A. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {review;Mice;Glycosylation;Not relevant;Gammaretrovirus;Protein Isoforms;11 Glia;Support, U.S. Gov't, P.H.S.;review, tutorial;Support, Non-U.S. Gov't;Animals;Retroviridae Infections;Viral Envelope Proteins;Brain},
	Medline = {20094946},
	Month = {2},
	Nlm_Id = {0113724},
	Number = {3},
	Organization = {Department of Microbiology/Immunology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272, USA. wonk\@neoucom.edu},
	Pages = {1558-65},
	Pubmed = {10627570},
	Title = {Differential glycosylation of the Cas-Br-E env protein is associated with retrovirus-induced spongiform neurodegeneration},
	Uuid = {5DAC56DC-EA5F-46A3-B640-7B04E221DF50},
	Volume = {74},
	Year = {2000},
	url = {papers/Lynch_JVirol2000.pdf}}

@article{Lynch:1991,
	Abstract = {We have examined the pathological lesions and sites of infection in mice inoculated with a highly neurovirulent recombinant wild mouse ecotropic retrovirus (FrCasE). The spongiform lesions appeared initially as swollen postsynaptic neuronal processes, progressing to swelling in neuronal cell bodies, all in the absence of detectable gliosis. Infection of neurons in regions of vacuolation was not detected. However, high level infection of cerebellar granule neurons was observed in the absence of cytopathology, wherein viral protein was found associated with both axons and dendrites. Infection of ramified and amoeboid microglial cells was associated with cytopathology in the brain stem, and endothelial cell-pericyte infection was found throughout the CNS. No evidence of defective retroviral expression was observed. These results are consistent with an indirect mechanism of retrovirus-induced neuropathology.},
	Author = {Lynch, W. P. and Czub, S. and McAtee, F. J. and Hayes, S. F. and Portis, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Nucleic Acid Hybridization;RNA Viruses;Cerebellar Cortex;Immunohistochemistry;Gene Products, env;Reassortant Viruses;Retroviridae;Not relevant;Virus Replication;11 Glia;Support, U.S. Gov't, P.H.S.;Blood Vessels;Animals;Mice;Retroviridae Infections;Neurons;Central Nervous System Diseases},
	Medline = {92000683},
	Month = {9},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, Montana 59840.},
	Pages = {365-79},
	Pubmed = {1654946},
	Title = {Murine retrovirus-induced spongiform encephalopathy: productive infection of microglia and cerebellar neurons in accelerated CNS disease},
	Uuid = {369DB0AE-B8DB-4F32-84CE-2CA6EF114609},
	Volume = {7},
	Year = {1991},
	url = {papers/Lynch_Neuron1991.pdf}}

@article{Lyons:2007,
	Abstract = {Deficits in cognitive function are associated with neuroinflammatory changes, typified by activation of glial cells and an alteration of the pro- and anti-inflammatory cytokine balance in the brain. Although there is evidence to suggest that activation of microglia is regulated by interaction with other cell types in the brain, the mechanism(s) involved is poorly understood. Here, we provide evidence that interaction between CD200 and its receptor plays a role in modulating microglial activation under conditions of chronic and acute inflammation of the brain. We report that interleukin-4 (IL-4) plays a central role in modulating expression of CD200 and identify a mechanism by which IL-4 directly controls microglial cell activation. Our findings provide the first demonstration of a role for IL-4 in modulating CD200 expression and suggest a mechanism for regulation of microglial activation in the intact CNS under inflammatory conditions.},
	Author = {Lyons, Anthony and Downer, Eric J. and Crotty, Suzanne and Nolan, Yvonne M. and Mills, Kingston H. G. and Lynch, Marina A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Animals;Acute Disease;Rats;Interleukin-4;comparative study;Microglia;Antigens, CD;Mice, Inbred C57BL;Rats, Wistar;research support, non-u.s. gov't;11 Glia;Chronic Disease;Male;Membrane Glycoproteins;Mice;24 Pubmed search results 2008;Inflammation;Ligands},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {31},
	Organization = {Trinity College Institute for Neuroscience, Physiology Department, Trinity College, Dublin 2, Ireland.},
	Pages = {8309-13},
	Pii = {27/31/8309},
	Pubmed = {17670977},
	Title = {CD200 ligand receptor interaction modulates microglial activation in vivo and in vitro: a role for IL-4},
	Uuid = {BB7AC3FD-E4C9-44BA-8585-C9D764C9CA5A},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1781-07.2007}}

@article{Ma:2003,
	Abstract = {BACKGROUND: Despite the meridian system being an important concept in Traditional Chinese Medicine (TCM), modern biology and Western medical systems have failed to find an anatomic substrate. Since the 1960s, a variety of phenomena along meridians have been reported, among which quite a few suggest that along meridians there is a fluid pathway (but not blood vessels or lymphatics). On the other hand, perivascular space (PVS) has been demonstrated to be a body fluid pathway in addition to blood vessels and lymphatics in some mammalian tissues, such as brain, thymus, and lung. OBJECTIVES: The present study was designed to examine the relationship between PVS and the meridian. We studied characteristics of the tissues around the blood vessels along the Stomach Meridian of Foot-Yangming and the Gallbladder Meridian of Foot-shaoyang, with the goal of identifying anatomical structure corresponding to the meridian described in TCM. DESIGN AND RESULTS: Through perivascular dye injection and frozen section histology, we found that there is PVS around the blood vessels along the meridians, and it is a fluid pathway. Subsequent physiologic studies revealed that the PVS shows significantly greater electrical conductivity and significantly higher partial oxygen pressure (pO(2)) compared to medial and lateral tissues. CONCLUSIONS: The PVS along the meridians has properties offering good explanation for the meridian phenomena. The work sheds new light on the studies of meridians and may contribute to research on the mechanism of Chinese acupuncture.},
	Author = {Ma, Wentao and Tong, Hua and Xu, Weiya and Hu, Jiming and Liu, Nai and Li, Hongyi and Cao, Lianxin},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1075-5535},
	Journal = {J Altern Complement Med},
	Keywords = {Electric Conductivity;Research Support, Non-U.S. Gov't;Mice, Inbred BALB C;Female;Microscopy, Electron;Connective Tissue;Extracellular Fluid;Contrast Media;Meridians;Lymphatic Vessels;11 Glia;Rabbits;Male;Animals;Mice},
	Month = {12},
	Nlm_Id = {9508124},
	Number = {6},
	Organization = {Department of Analysis-Measurement Science, School of Life Sciences, Wuhan University, Wuhan 430-072, People's Republic of China.},
	Pages = {851-9},
	Pubmed = {14736357},
	Title = {Perivascular space: possible anatomical substrate for the meridian},
	Uuid = {A79F8A81-37D7-403C-95AD-C19BCD98ADAD},
	Volume = {9},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/107555303771952208}}

@article{Ma:2006a,
	Abstract = {RNA interference (RNAi) in both plants and animals is mediated by small RNAs of approximately 21-23 nucleotides in length for regulation of target gene expression at multiple levels through partial sequence complementarities. Combined with widespread genome sequencing, experimental use of RNAi has the potential to interrogate systematically all genes in a given organism with respect to a particular function. However, owing to a tolerance for mismatches and gaps in base-pairing with targets, small RNAs could have up to hundreds of potential target sequences in a genome, and some small RNAs in mammalian systems have been shown to affect the levels of many messenger RNAs besides their intended targets. The use of long double-stranded RNAs (dsRNAs) in Drosophila, where Dicer-mediated processing produces small RNAs inside cells, has been thought to reduce the probability of such 'off-target effects' (OTEs). Here we show, however, that OTEs mediated by short homology stretches within long dsRNAs are prevalent in Drosophila. We have performed a genome-wide RNAi screen for novel components of Wingless (Wg) signal transduction in Drosophila S2R + cells, and found few, if any, legitimate candidates. Rather, many of the top candidates exert their effects on Wg response through OTEs on known pathway components or through promiscuous OTEs produced by tandem trinucleotide repeats present in many dsRNAs and genes. Genes containing such repeats are over-represented in candidate lists from published screens, suggesting that they represent a common class of false positives. Our results suggest simple measures to improve the reliability of genome-wide RNAi screens in Drosophila and other organisms.},
	Author = {Ma, and Creanga, and Lum, and Beachy,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {23 RNAi;23 Technique},
	Month = {9},
	Nlm_Id = {0410462},
	Organization = {Howard Hughes Medical Institute, Department of Molecular Biology and Genetics.},
	Pii = {nature05179},
	Pubmed = {16964239},
	Title = {Prevalence of off-target effects in Drosophila RNA interference screens},
	Uuid = {FEC9BD16-48A4-11DB-A317-000D9346EC2A},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature05179}}

@article{Ma:2002,
	Abstract = {The Sca-1 cell surface glycoprotein is used routinely as a marker of adult hematopoietic stem cells (HSCs), allowing a >100-fold enrichment of these rare cells from the bone marrow of the adult mouse. The Sca-1 protein is encoded by the Ly-6A/E gene, a small 4-exon gene that is tightly controlled in its expression in HSCs and several hematopoietic cell types. For the ability to sort and localize HSCs directly from the mouse, we initiated a transgenic approach in which we created Ly-6A (Sca-1) green fluorescent protein (GFP) transgenic mice. We show here that a 14-kb Ly-6A expression cassette directs the transcription of the GFP marker gene in all functional repopulating HSCs in the adult bone marrow. A >100-fold enrichment of HSCs occurred by sorting for the GFP-expressing cells. Furthermore, as shown by fluorescence-activated cell sorting and histologic analysis of several hematopoietic tissues, the GFP transgene expression pattern generally corresponded to that of Sca-1. Thus, the Ly-6A GFP transgene facilitates the enrichment of HSCs and presents the likelihood of identifying HSCs in situ.},
	Author = {Ma, Xiaoqian and Robin, Catherine and Ottersbach, Katrin and Dzierzak, Elaine},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:35 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {Transgenes;Animals;Cell Separation;Bone Marrow Transplantation;Antigens, Ly;Indicators and Reagents;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Hematopoietic Stem Cell Transplantation;Mice, Inbred CBA;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Age Factors;Mice;Hematopoietic Stem Cells;Luminescent Proteins;Membrane Proteins;Biological Markers;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {22345243},
	Nlm_Id = {9304532},
	Number = {6},
	Organization = {Pathology Department, Erasmus University, Rotterdam, Netherlands.},
	Pages = {514-21},
	Pubmed = {12456959},
	Title = {The Ly-6A (Sca-1) GFP transgene is expressed in all adult mouse hematopoietic stem cells},
	Uuid = {89EFD174-8F46-4E21-BB9B-F7CBA6CC2115},
	Volume = {20},
	Year = {2002}}

@article{MacFarlane:2000,
	Abstract = {Arrest of spinal cord astrocytes at defined stages of the cell cycle clock causes significant changes in the expression of voltage-activated Na(+) and K(+) currents. Arrest of actively proliferating astrocytes in G1/G0 by all-trans-retinoic acid induces premature expression of inwardly rectifying K(+) currents (IK(IR)) typically expressed only in differentiated astrocytes. By contrast, arrest in S phase by ara-C or Aphidicolin leads to a greater than twofold increase in "delayed"outwardly rectifying currents (IK(D)) and a concomitant decrease in IK(IR). Pharmacological blockade of IK(D) by TEA and 4AP caused proliferating astrocytes to arrest in G0/G1, suggesting that activity of these channels is required for G1/S checkpoint progression. Conversely, in quiescent astrocytes, inhibition of IK(IR) by 30 microM BaCl(2) led to an increase in astrocyte proliferation and to an increase in the number of cells in S phase from 5\%to 26\%. These data suggest that a downregulation of K(IR) promotes cell cycle progression through the G1/S checkpoint. Blockade of IK(IR) in actively proliferating cells, however, leads to an accumulation in G2/M, suggesting that reappearance of this current may be critical for progression beyond DNA synthesis. Interestingly, Na(+) currents (INa(+)) are increased greater than fourfold in S phase-arrested cells, yet their pharmacological blockade by TTX has no effect on cell cycle progression. However, the resting membrane potential of S phase-arrested cells increases profoundly, and manipulation of membrane potential by the application of low concentrations of ouabain, or reduction of extracellular potassium, induces the accumulation of quiescent astrocytes in S phase of the cell cycle, suggesting that either depolarization or intracellular sodium, or both, play an important role in promoting astrocyte proliferation. 0894-1491 Journal Article},
	Author = {MacFarlane, S. N. and Sontheimer, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Glia},
	Keywords = {Electrophysiology;Sodium Channels/metabolism/physiology;Membrane Potentials/physiology;Ion Channels/*metabolism;Rats;Sodium/metabolism;Animals;Cell Cycle/physiology;G, EE pdf;Rats, Sprague-Dawley;08 Aberrant cell cycle;Astrocytes/*cytology/*metabolism;Potassium Channels/physiology;Cell Division/physiology;Potassium Channel Blockers;Spinal Cord/*cytology/*metabolism;Support, U.S. Gov't, P.H.S.;S Phase/physiology;Intracellular Fluid/metabolism/physiology},
	Number = {1},
	Organization = {Department of Neurobiology, University of Alabama, Birmingham, Alabama, USA. macfarlan\@nrc.uab.edu},
	Pages = {39-48},
	Title = {Changes in ion channel expression accompany cell cycle progression of spinal cord astrocytes},
	Uuid = {0D258350-606B-4DC2-9D9A-04AB3D843D7B},
	Volume = {30},
	Year = {2000},
	url = {papers/MacFarlane_Glia2000.pdf}}

@article{Macas:2006,
	Abstract = {The adult human brain retains the capacity to generate new neurons in the hippocampal formation (Eriksson et al., 1998) and neuronal progenitor cells (NPCs) in the forebrain (Bernier et al., 2000), but to what extent it is capable of reacting to injuries, such as ischemia, is not known. We analyzed postmortem tissue from normal and pathological human brain tissue (n = 54) to study the cellular response to ischemic injury in the forebrain. We observed that cells expressing the NPC marker polysialylated neural adhesion cell molecule (PSA-NCAM) are continuously generated in the adult human subventricular zone (SVZ) and migrate along the olfactory tracts. These cells were not organized in migrating chains as in the adult rodent rostral migratory stream, and their number was lower in the olfactory tracts of brains from old (56-81 years of age) compared with young (29 + 36 years of age) individuals. Moreover, we show that in brains of patients of advanced age (60-87 years of age), ischemia led to an elevated number of Ki-67-positive cells in the ipsilateral SVZ without concomitant apoptotic cell death. Additionally, ischemia led to an increased number of PSA-NCAM-positive NPCs close to the lateral ventricular walls, compared with brains of comparable age without obvious neuropathologic changes. These results suggest that the adult human brain retains a capacity to respond to ischemic injuries and that this capacity is maintained even in old age.},
	Author = {Macas, Jadranka and Nern, Christian and Plate, Karl H. and Momma, Stefan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Aging;Cell Differentiation;research support, non-u.s. gov't;Adult;Aged;Aged, 80 and over;Cell Proliferation;Stem Cells;Middle Aged;Lateral Ventricles;comparative study;Prosencephalon;Humans;Cell Movement;24 Pubmed search results 2008;Neurons},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {50},
	Organization = {Institute of Neurology (Edinger Institute), University of Frankfurt, D-60528 Frankfurt, Germany.},
	Pages = {13114-9},
	Pii = {26/50/13114},
	Pubmed = {17167100},
	Title = {Increased generation of neuronal progenitors after ischemic injury in the aged adult human forebrain},
	Uuid = {4A808686-54FC-4917-978E-68460A4BC331},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4667-06.2006}}

@article{Macdonald:2006,
	Abstract = {Neuron-glia communication is central to all nervous system responses to trauma, yet neural injury signaling pathways remain poorly understood. Here we explore cellular and molecular aspects of neural injury signaling in Drosophila. We show that transected Drosophila axons undergo injury-induced degeneration that is morphologically similar to Wallerian degeneration in mammals and can be suppressed by the neuroprotective mouse Wld(s) protein. Axonal injury elicits potent morphological and molecular responses from Drosophila glia: glia upregulate expression of the engulfment receptor Draper, undergo dramatic changes in morphology, and rapidly recruit cellular processes toward severed axons. In draper mutants, glia fail to respond morphologically to axon injury, and severed axons are not cleared from the CNS. Thus Draper appears to act as a glial receptor for severed axon-derived molecular cues that drive recruitment of glial processes to injured axons for engulfment.},
	Author = {Macdonald, Jennifer M. and Beach, Margaret G. and Porpiglia, Ermelinda and Sheehan, Amy E. and Watts, Ryan J. and Freeman, Marc R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Neuroglia;Wallerian Degeneration;Membrane Proteins;research support, non-u.s. gov't ;Animals, Genetically Modified;Drosophila Proteins;Nerve Tissue Proteins;Drosophila;10 Structural plasticity;Animals;comparative study ;24 Pubmed search results 2008;Axons},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605.},
	Pages = {869-81},
	Pii = {S0896-6273(06)00319-9},
	Pubmed = {16772169},
	Title = {The Drosophila cell corpse engulfment receptor draper mediates glial clearance of severed axons},
	Uuid = {D7312C6C-E02E-40AF-9EEE-E44E934C0848},
	Volume = {50},
	Year = {2006},
	url = {papers/Macdonald_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.04.028}}

@article{Macklis:1993,

@article{Mackowiak:2007,
	Abstract = {Recent evidence indicates that the polysialylated neural cell adhesion molecule (PSA-NCAM) is involved in hippocampal plasticity. On the other hand, CB1 receptor activation is known to disturb some hippocampal processes involving plastic changes, such as learning and memory. Therefore, the present study investigated the effect of HU-210, a CB1 receptor agonist, on the expression of PSA-NCAM protein in the dentate gyrus (DG) and CA3 region of the rat hippocampus. It was found that at a dose of 0.1 mg/kg i.p. of HU-210, the number of PSA-NCAM immunoreactive (IR) cells in the DG declined in a time-dependent manner. The decrease in PSA-NCAM expression was observed at 1 and 2 days (ca. 21\%and 30\%, respectively), but not after 4 h and 4 days following HU-210 administration. However, HU-210 treatment did not change the length density of PSA-NCAM immunopositive processes in CA3 mossy fibers at all the time points measured. The effect observed in the DG on day 2 was blocked by AM-251 (1 mg/kg, i.p.), a CB1 receptor antagonist, given 30 min before HU-210. Neither the number of Ki-67 (IR) cells (a marker of proliferation) nor the number of doublecortin-IR cells (a marker of immature neurons) was affected by HU-210 (0.1 mg/kg, i.p.) treatment at any of the time points. An analysis of co-localization of CB1 receptor protein with PSA-NCAM protein revealed that both proteins were not present in the same population of neurons in the subgranular layer of the DG. The observed changes in PSA-NCAM expression were not related to the reduction of proliferation or differentiation of newly born cells, but were possible due to alternations in the synaptic activity in the DG. However, such alteration in the PSA-NCAM expression may change the timing of the functional maturation of newly born neurons. Moreover, the above finding suggests that acute activation of CB1 receptors may result in the stiffening of the hippocampal structure and susceptibility to plastic changes and may lead to functional impairment governed by alterations in the hippocampal structure.},
	Author = {Ma\'{c}kowiak, and Chocyk, and Markowicz-Kula, and Wdzony,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {02 Adult neurogenesis migration;04 Adult neurogenesis factors;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0045503},
	Organization = {Laboratory of Pharmacology and Brain Biostructure, Institute of Pharmacology, Polish Academy of Sciences, 31-343 Krak{\'o}w, 12 Smtna Street, Poland.},
	Pii = {S0006-8993(07)00343-5},
	Pubmed = {17355876},
	Title = {Acute activation of CB1 cannabinoid receptors transiently decreases PSA-NCAM expression in the dentate gyrus of the rat hippocampus},
	Uuid = {F3DDE5C9-A991-45E3-AF7B-67E3FE47B800},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainres.2007.02.014}}

@article{Madaule:1998,
	Abstract = {During mitosis, a ring containing actin and myosin appears beneath the equatorial surface of animal cells. This ring then contracts, forms a cleavage furrow and divides the cell, a step known as cytokinesis. The two daughter cells often remain connected by an intercellular bridge which contains a refringent structure known as the midbody. How the appearance of this ring is regulated is unclear, although the small GTPase Rho, which controls the formation of actin structures, is known to be essential. Protein kinases are also thought to participate in cytokinesis. We now show that a splice variant of a Rho target protein, named citron, contains a protein kinase domain that is related to the Rho-associated kinases ROCK14 and ROK, which regulate myosin-based contractility. Citron kinase localizes to the cleavage furrow and midbody of HeLa cells; Rho is also localized in the midbody. We find that overexpression of citron mutants results in the production of multinucleate cells and that a kinase-active mutant causes abnormal contraction during cytokinesis. We propose that citron kinase regulates cytokinesis at a step after Rho in the contractile process. 98361238 0028-0836 Journal Article},
	Author = {Madaule, P. and Eda, M. and Watanabe, N. and Fujisawa, K. and Matsuoka, T. and Bito, H. and Ishizaki, T. and Narumiya, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Nature},
	Keywords = {GTP-Binding Proteins/*physiology;GTP Phosphohydrolases/*physiology;Transfection;Sequence Homology, Amino Acid;Molecular Sequence Data;Hela Cells;Human;Proteins/chemistry/genetics/*physiology;Alternative Splicing;CK;Amino Acid Sequence;Protein-Serine-Threonine Kinases/chemistry/metabolism;Cell Division/*physiology;Support, Non-U.S. Gov't;rho GTP-Binding Proteins},
	Number = {6692},
	Organization = {Department of Pharmacology, Kyoto University Faculty of Medicine, Japan.},
	Pages = {491-4},
	Title = {Role of citron kinase as a target of the small GTPase Rho in cytokinesis},
	Uuid = {AD8AF47C-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {394},
	Year = {1998},
	url = {papers/Madaule_Nature1998}}

@article{Madsen:2000,
	Abstract = {BACKGROUND: Electroconvulsive therapy (ECT) is a widely used and efficient treatment modality in psychiatry, although the basis for its therapeutic effect is still unknown. Past research has shown seizure activity to be a regulator of neurogenesis in the adult brain. This study examines the effect of a single and multiple electroconvulsive seizures on neurogenesis in the rat dentate gyrus. METHODS: Rats were given either a single or a series of 10 electroconvulsive seizures. At different times after the seizures, a marker of proliferating cells, Bromodeoxyuridine (BrdU), was administered to the animals. Subsequently, newborn cells positive for BrdU were counted in the dentate gyrus. Double staining with a neuron-specific marker indicated that the newborn cells displayed a neuronal phenotype. RESULTS: A single electroconvulsive seizure significantly increased the number of new born cells in the dentate gyrus. These cells survived for at least 3 months. A series of seizures further increased neurogenesis, indicating a dose-dependent mechanism. CONCLUSIONS: We propose that generation of new neurons in the hippocampus may be an important neurobiologic element underlying the clinical effects of electroconvulsive seizures.},
	Author = {Madsen, T. M. and Treschow, A. and Bengzon, J. and Bolwig, T. G. and Lindvall, O. and Tingstr{\"o}m, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0006-3223},
	Journal = {Biol Psychiatry},
	Keywords = {Animals;Rats;Microscopy, Confocal;Phenotype;Apoptosis;Electroconvulsive Therapy;Cell Count;Rats, Wistar;Antimetabolites;Male;Neurons;Dentate Gyrus;Fluorescent Antibody Technique, Direct;Cell Division;Immunohistochemistry;Bromodeoxyuridine;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {20322947},
	Month = {6},
	Nlm_Id = {0213264},
	Number = {12},
	Organization = {Neuropsychiatry Laboratory, Department of Psychiatry, H:S Rigshospitalet, (TMM, TGB), Copenhagen, Denmark.},
	Pages = {1043-9},
	Pii = {S0006322300002286},
	Pubmed = {10862803},
	Title = {Increased neurogenesis in a model of electroconvulsive therapy},
	Uuid = {99B37E3F-3704-4A0B-A6CC-F4CE3E6A1D25},
	Volume = {47},
	Year = {2000}}

@article{Madsen:2003,
	Abstract = {The generation of new neurons in the adult mammalian brain has been documented in numerous recent reports. Studies undertaken so far indicate that adult hippocampal neurogenesis is related in a number of ways to hippocampal function.Here, we report that subjecting adult rats to fractionated brain irradiation blocked the formation of new neurons in the dentate gyrus of the hippocampus. At different time points after the termination of the irradiation procedure, the animals were tested in two tests of short-term memory that differ with respect to their dependence on hippocampal function. Eight and 21 days after irradiation, the animals with blocked neurogenesis performed poorer than controls in a hippocampus-dependent place-recognition task, indicating that the presence of newly generated neurons may be necessary for the normal function of this brain area. The animals were never impaired in a hippocampus-independent object-recognition task. These results are in line with other reports documenting the functional significance of newly generated neurons in this region. As our irradiation procedure models prophylactic cranial irradiation used in the treatment of different cancers, we suggest that blocked neurogenesis contributes to the reported deleterious side effects of this treatment, consisting of memory impairment, dysphoria and lethargy. 0306-4522 Journal Article},
	Author = {Madsen, T. M. and Kristjansen, P. E. and Bolwig, T. G. and Wortwein, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Neuroscience},
	Keywords = {Cell Division/physiology/*radiation effects;Maze Learning/physiology/radiation effects;Exploratory Behavior/physiology/radiation effects;Dentate Gyrus/growth &development/*physiopathology/*radiation effects;Neurons/physiology/*radiation effects;Memory Disorders/*etiology/pathology/physiopathology;Rats;Immunohistochemistry;Rats, Wistar;06 Adult neurogenesis injury induced;Radiotherapy/*adverse effects;D pdf;Animals;Support, Non-U.S. Gov't;Bromodeoxyuridine/diagnostic use;Male;Stem Cells/physiology/*radiation effects},
	Number = {3},
	Organization = {Laboratory of Neuropsychiatry, Department of Psychiatry O-6102, H:S Rigshospitalet, Blegdamsvej 9, 2100, Copenhagen, Denmark.},
	Pages = {635-42},
	Pubmed = {12809684},
	Title = {Arrested neuronal proliferation and impaired hippocampal function following fractionated brain irradiation in the adult rat},
	Uuid = {B5B155C1-A944-4583-825E-CA871C4C660C},
	Volume = {119},
	Year = {2003},
	url = {papers/Madsen_Neuroscience2003}}

@article{Magavi:2000,
	Abstract = {Neurogenesis normally only occurs in limited areas of the adult mammalian brain--the hippocampus, olfactory bulb and epithelium, and at low levels in some regions of macaque cortex. Here we show that endogenous neural precursors can be induced in situ to differentiate into mature neurons, in regions of adult mammalian neocortex that do not normally undergo any neurogenesis. This differentiation occurs in a layer- and region-specific manner, and the neurons can re-form appropriate corticothalamic connections. We induced synchronous apoptotic degeneration of corticothalamic neurons in layer VI of anterior cortex of adult mice and examined the fates of dividing cells within cortex, using markers for DNA replication (5-bromodeoxyuridine; BrdU) and progressive neuronal differentiation. Newly made, BrdU- positive cells expressed NeuN, a mature neuronal marker, in regions of cortex undergoing targeted neuronal death and survived for at least 28 weeks. Subsets of BrdU+ precursors expressed Doublecortin, a protein found exclusively in migrating neurons, and Hu, an early neuronal marker. Retrograde labelling from thalamus demonstrated that BrdU+ neurons can form long-distance corticothalamic connections. Our results indicate that neuronal replacement therapies for neurodegenerative disease and CNS injury may be possible through manipulation of endogenous neural precursors in situ.},
	Author = {Magavi, S. S. and Leavitt, B. R. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Transcription Factors;Nerve Degeneration;Cell Differentiation;Animals;Neocortex/cytology/*physiology;Aging;Transcription Factors/immunology/metabolism;Neurons/*cytology;Antigens, Differentiation/metabolism;Antigens, Differentiation;Neocortex;Aging/physiology;D-12;Animal;Cell Movement;Apoptosis;Nerve Regeneration;Bromodeoxyuridine/metabolism;Support, Non-U.S. Gov't;Research Support, U.S. Gov't, P.H.S.;Neurons;Support, U.S. Gov't, P.H.S.;Mice;Bromodeoxyuridine;Research Support, Non-U.S. Gov't},
	Medline = {20335883},
	Month = {6},
	Nlm_Id = {0410462},
	Number = {6789},
	Organization = {Division of Neuroscience, Children's Hospital, and Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {951-5.},
	Pubmed = {10879536},
	Title = {Induction of neurogenesis in the neocortex of adult mice},
	Uuid = {BAA16A96-C26D-11DA-969D-000D9346EC2A},
	Volume = {405},
	Year = {2000},
	url = {papers/Magavi_Nature2000.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35016083}}

@article{Magavi:2001,
	Abstract = {Over the past three decades, research exploring potential neuronal replacement therapies have focused on replacing lost neurons by transplanting cells or grafting tissue into diseased regions of the brain. Over most of the past century of modern neuroscience, it was thought that the adult brain was completely incapable of generating new neurons. However, in the last decade, the development of new techniques has resulted in an explosion of new research showing that neurogenesis, the birth of new neurons, normally occurs in two limited and specific regions of the adult mammalian brain, and that there are significant numbers of multipotent neural precursors in many parts of the adult mammalian brain. Recent findings from our lab demonstrate that it is possible to induce neurogenesis de novo in the adult mammalian brain, particularly in the neocortex where it does not normally occur, and that it may become possible to manipulate endogenous multipotent precursors in situ to replace lost or damaged neurons. Elucidation of the relevant molecular controls may allow the development of neuronal replacement therapies for neurodegenerative disease and other CNS injuries that do not require transplantation of exogenous cells.},
	Author = {Magavi, S. S. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Neuropsychopharmacology},
	Keywords = {Stem Cells/*physiology;Neurons/*physiology;Epithelium/physiology;Olfactory Bulb/physiology;Human;D;06 Adult neurogenesis injury induced;Animal;Hippocampus/cytology/growth &development/physiology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Mice;Vertebrates/physiology;Neocortex/cytology/*growth &development/physiology},
	Number = {6},
	Organization = {Division of Neuroscience, Children's Hospital, Department of Neurology and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {816-35.},
	Title = {Manipulation of neural precursors in situ: induction of neurogenesis in the neocortex of adult mice},
	Uuid = {A0E7C1DA-618A-4314-AAF8-02DBBE3BFE80},
	Volume = {25},
	Year = {2001},
	url = {papers/Magavi_Neuropsychopharmacology2001.pdf}}

@article{Mager:1985,
	Abstract = {The properties of clonogenic and leukemic cells, derived from mice infected with different helper virus pseudotypes of the polycythemic strain of Friend spleen focus-forming virus (SFFVp), have been analyzed. Four different replication-competent murine leukemia viruses (MuLVs) were used as helpers for the defective SFFVp genome: the Friend MuLVs, Moloney MuLV, and an amphotropic MuLV. Three different biological parameters were measured: (i) the kinetics of emergence of clonogenic cells characteristic of the late stages of Friend erythroleukemia; (ii) the ability of cells in these colonies to give rise to secondary colonies (self-renewal capacity); and (iii) the capacity of cell lines derived from these colonies to respond to inducers of erythroid differentiation. The properties of these cells was found to be independent of the helper virus used, suggesting that it is the SFFVp genome, not the helper virus, that plays a determinant role in the late stages of erythroleukemia. 0042-6822 Journal Article},
	Author = {Mager, D. L. and Bernstein, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:56 -0400},
	Journal = {Virology},
	Keywords = {Friend murine leukemia virus/physiology;Cell Differentiation;Animals;Helper Viruses/*physiology;Erythropoiesis;Erythropoietin/pharmacology;Leukemia Virus, Murine/*genetics/*physiology;EE, DMSO, abstr;08 Aberrant cell cycle;Dimethyl Sulfoxide/pharmacology;Cell Line;Genes, Viral;Support, Non-U.S. Gov't;Moloney murine leukemia virus/physiology;Hematopoietic Stem Cells/*pathology;Hemoglobins/biosynthesis;Spleen/pathology;Cell Division;Mice;Spleen Focus-Forming Viruses/*genetics/physiology;Clone Cells;Leukemia, Erythroblastic, Acute/*microbiology/pathology},
	Number = {2},
	Pages = {337-41},
	Pubmed = {3002024},
	Title = {Induction of clonogenic and erythroleukemic cells by different helper virus pseudotypes of Friend spleen focus-forming virus},
	Uuid = {0148F92C-A095-4FAC-84B3-2A3AB5861B92},
	Volume = {141},
	Year = {1985},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3002024}}

@article{Mainen:1999,
	Abstract = {Two-photon excitation laser scanning microscopy (TPLSM) has become the tool of choice for high-resolution fluorescence imaging in intact neural tissues. Compared with other optical techniques, TPLSM allows high-resolution imaging and efficient detection of fluorescence signal with minimal photobleaching and phototoxicity. The advantages of TPLSM are especially pronounced in highly scattering environments such as the brain slice. Here we describe our approaches to imaging various aspects of synaptic function in living brain slices. To combine several imaging modes together with patch-clamp electrophysiological recordings we found it advantageous to custom-build an upright microscope. Our design goals were primarily experimental convenience and efficient collection of fluorescence. We describe our TPLSM imaging system and its performance in detail. We present dynamic measurements of neuronal morphology of neurons expressing green fluorescent protein (GFP) and GFP fusion proteins as well as functional imaging of calcium dynamics in individual dendritic spines. Although our microscope is a custom instrument, its key advantages can be easily implemented as a modification of commercial laser scanning microscopes.},
	Author = {Mainen, Z. F. and Maletic-Savatic, M. and Shi, S. H. and Hayashi, Y. and Malinow, R. and Svoboda, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1046-2023},
	Journal = {Methods},
	Keywords = {Lasers;Fluorescent Dyes;Microscopy, Video;Animals;Synapses;In Vitro;Rats;Equipment Design;Microscopy, Confocal;Synaptic Transmission;Brain;Rats, Sprague-Dawley;Hippocampus;Pyramidal Cells;Recombinant Fusion Proteins;Green Fluorescent Proteins;Dissection;Dendrites;Research Support, U.S. Gov't, P.H.S.;21 Neurophysiology;Photons;24 Pubmed search results 2008;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {99286365},
	Month = {6},
	Nlm_Id = {9426302},
	Number = {2},
	Organization = {Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA.},
	Pages = {231-9, 181},
	Pii = {S1046-2023(99)90776-4},
	Pubmed = {10356355},
	Title = {Two-photon imaging in living brain slices},
	Uuid = {75832941-D788-40E1-ABE0-4D503019DB23},
	Volume = {18},
	Year = {1999},
	url = {papers/Mainen_Methods1999.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/meth.1999.0776}}

@article{Mainland:2002,
	Abstract = {0028-0836 Clinical Trial Controlled Clinical Trial Journal Article},
	Author = {Mainland, J. D. and Bremner, E. A. and Young, N. and Johnson, B. N. and Khan, R. M. and Bensafi, M. and Sobel, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:53 -0400},
	Journal = {Nature},
	Keywords = {*Perception/drug effects;Human;Female;Nose/*physiology;Androstenes/administration &dosage/pharmacology;I pdf;Smell/drug effects/*physiology;Male;*Neuronal Plasticity/drug effects;13 Olfactory bulb anatomy},
	Number = {6909},
	Organization = {Helen Wills Neuroscience Institute, University of California at Berkeley, Berkeley, California 94720, USA. mainland\@uclink.berkeley.edu},
	Pages = {802},
	Title = {Olfactory plasticity: one nostril knows what the other learns},
	Uuid = {00C7A6CC-39EB-47CA-8332-3CCDCD7B6478},
	Volume = {419},
	Year = {2002},
	url = {papers/Mainland_Nature2002.pdf}}

@article{Majed:2006,
	Abstract = {Microglia exist under physiological conditions in a resting state but become activated after neuronal injury. Recent studies have highlighted the reciprocal role of neurons in controlling both the number and activity of microglia. In this study, microglia derived from newborn rat cortices were cultured and activated by interferon-gamma (IFNgamma) treatment, then exposed to recombinant Sema3A or conditioned medium derived from stressed embryonic cortical neurons. We found that activation of microglia by IFNgamma induced differential upregulation of the semaphorin receptors Plexin-A1 and Neuropilin-1. This result was confirmed by Northern blotting, reverse transcription-PCR, and Western blotting. Furthermore, recombinant Sema3A induced apoptosis of microglia when added to the in vitro culture, and a similar result was obtained on activated microglia when Sema3A was produced by stressed neurons. Using an in vivo model of microglia activation by striatal injection of lipopolysaccharide demonstrated a corresponding upregulation of Plexin-A1 and Neuropilin-1 in activated microglia and enhanced production of Sema3A by stressed adult neurons. These results suggest a novel semaphorin-mediated mechanism of neuroprotection whereby stressed neurons can protect themselves from further damage by activated microglia.},
	Author = {Majed, Henry H. and Chandran, Siddharthan and Niclou, Simone P. and Nicholas, Richard S. and Wilkins, Alastair and Wing, Mark G. and Rhodes, Kate E. and Spillantini, Maria Grazia and Compston, Alastair},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {6},
	Organization = {Department of Clinical Neurosciences, Centre for Brain Repair, University of Cambridge, Forvie Site, Cambridge CB2 2PY, United Kingdom.},
	Pages = {1730-8},
	Pii = {26/6/1730},
	Pubmed = {16467521},
	Title = {A novel role for Sema3A in neuroprotection from injury mediated by activated microglia},
	Uuid = {E3B5B916-4959-11DB-8404-000D9346EC2A},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0702-05.2006}}

@article{Majewska:2006,
	Abstract = {Although plastic changes are known to occur in developing and adult cortex, it remains unclear whether these changes require remodeling of cortical circuitry whereby synapses are formed and eliminated or whether they rely on changes in the strength of existing synapses. To determine the structural stability of dendritic spines and axon terminals in vivo, we chose two approaches. First, we performed time-lapse two-photon imaging of dendritic spine motility of layer 5 pyramidal neurons in juvenile [postnatal day 28 (P28)] mice in visual, auditory, and somatosensory cortices. We found that there were differences in basal rates of dendritic spine motility of the same neuron type in different cortices, with visual cortex exhibiting the least structural dynamics. Rewiring visual input into the auditory cortex at birth, however, failed to alter dendritic spine motility, suggesting that structural plasticity rates might be intrinsic to the cortical region. Second, we investigated the persistence of both the presynaptic (axon terminals) and postsynaptic (dendritic spine) structures in young adult mice (P40-P61), using chronic in vivo two-photon imaging in different sensory areas. Both terminals and spines were relatively stable, with >80\%persisting over a 3 week period in all sensory regions. Axon terminals were more stable than dendritic spines. These data suggest that changes in network function during adult learning and memory might occur through changes in the strength and efficacy of existing synapses as well as some remodeling of connectivity through the loss and gain of synapses.},
	Author = {Majewska, Ania K. and Newton, Jessica R. and Sur, Mriganka},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't ;24 Pubmed search results 2008;Inferior Colliculus;Green Fluorescent Proteins;Auditory Pathways;Luminescent Proteins;10 Structural plasticity;10 Development;Animals;Presynaptic Terminals;Genes, Reporter;Visual Pathways;Visual Cortex;Synapses;Mice, Inbred C57BL;research support, n.i.h., extramural ;21 Circuit structure-function;Dendrites;Motion;Neuronal Plasticity;Axons;Bacterial Proteins;Learning;Auditory Cortex;Pyramidal Cells;21 Activity-development;Denervation;Geniculate Bodies;21 Neurophysiology;Microscopy, Confocal;Mice;Somatosensory Cortex;Memory;Mice, Transgenic},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {11},
	Organization = {Department of Brain and Cognitive Sciences, Picower Center for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. ania\_majewska\@urmc.rochester.edu},
	Pages = {3021-9},
	Pii = {26/11/3021},
	Pubmed = {16540580},
	Title = {Remodeling of synaptic structure in sensory cortical areas in vivo},
	Uuid = {FBE9C75E-05EB-40D2-BD0F-D690CBF97A7F},
	Volume = {26},
	Year = {2006},
	url = {papers/Majewska_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4454-05.2006}}

@article{Mak:2007,
	Abstract = {The regulation of female reproductive behaviors may involve memories of male pheromone signatures, formed in part by neural circuitry involving the olfactory bulb and hippocampus. These neural structures are the principal sites of adult neurogenesis; however, previous studies point to their independent regulation by sensory and physiological stimuli. Here we report that the pheromones of dominant (but not subordinate) males stimulate neuronal production in both the olfactory bulb and hippocampus of female mice, which are independently mediated by prolactin and luteinizing hormone, respectively. Neurogenesis induced by dominant-male pheromones correlates with a female preference for dominant males over subordinate males, whereas blocking neurogenesis with the mitotic inhibitor cytosine arabinoside eliminated this preference. These results suggest that male pheromones are involved in regulating neurogenesis in both the olfactory bulb and hippocampus, which may be important for female reproductive success.},
	Author = {Mak, Gloria K. and Enwere, Emeka K. and Gregg, Christopher and Pakarainen, Tomi and Poutanen, Matti and Huhtaniemi, Ilpo and Weiss, Samuel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Receptors, Prolactin;Sexual Behavior, Animal;Animals;Receptors, LH;Brain;Female;Mice, Inbred C57BL;research support, non-u.s. gov't;Behavior, Animal;Cell Proliferation;Immunosuppressive Agents;Mice, Inbred ICR;Male;Cytarabine;In Situ Nick-End Labeling;Mice, Knockout;Neurons;Sex Attractants;Social Dominance;Zinc Sulfate;Mice;24 Pubmed search results 2008;Bromodeoxyuridine;Nerve Tissue Proteins;Astringents},
	Month = {8},
	Nlm_Id = {9809671},
	Number = {8},
	Organization = {Hotchkiss Brain Institute, Department of Cell Biology & Anatomy, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada.},
	Pages = {1003-11},
	Pii = {nn1928},
	Pubmed = {17603480},
	Title = {Male pheromone-stimulated neurogenesis in the adult female brain: possible role in mating behavior},
	Uuid = {98853858-5A97-4F01-A8CD-2B62468B859D},
	Volume = {10},
	Year = {2007},
	url = {papers/Mak_NatNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1928}}

@article{Makar:2002,
	Abstract = {The peripheral delivery of interferon-beta (IFN-beta) for the treatment of central nervous system (CNS) diseases is only partially effective because of the blood-brain barrier (BBB). To circumvent this problem, we evaluated the feasibility of genetically altering bone marrow cells ex vivo and using them as vehicles to transfer the IFN-beta cDNA into the mouse CNS. An IFN-beta retroviral expression vector (pLXSN-IFNbeta) was used to stably transfect PA317 cells. The supernatant from these producer cells, which expressed IFN-beta mRNA and protein, were used to infect bone marrow cells. When transplanted into irradiated mice, IFN-beta-engineered marrow cells accessed the CNS and expressed IFN-beta mRNA and protein. Marrow cells transduced with a control neomycin vector entered the brain and expressed the neomycin but not the IFN-beta gene. In the CNS, IFN-beta delivered by marrow cells induced the mRNA expression of 2',5'-oligoadenylate synthetase (2',5'-OAS), indicating biologic activity. Our findings demonstrating that bone marrow cells can serve as a delivery system for IFN-beta cDNA into the CNS could have implications for the treatment of neurologic disorders, such as multiple sclerosis (MS), viral encephalitis, and brain tumors.},
	Author = {Makar, Tapas Kumar and Wilt, Susan and Dong, Zhongyun and Fishman, Paul and Mouradian, M. Maral and Dhib-Jalbut, Suhayl},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1079-9907},
	Journal = {J Interferon Cytokine Res},
	Keywords = {Animals;Feasibility Studies;Transfection;Bone Marrow Transplantation;Research Support, U.S. Gov't, Non-P.H.S.;Brain;Enzyme Induction;Kanamycin Kinase;Specific Pathogen-Free Organisms;2',5'-Oligoadenylate Synthetase;Recombinant Fusion Proteins;Blood-Brain Barrier;Genes, Synthetic;11 Glia;Research Support, U.S. Gov't, P.H.S.;RNA, Messenger;Genetic Vectors;Gene Therapy;DNA, Complementary;Mice;Genes, Reporter;Interferon-beta;Research Support, Non-U.S. Gov't},
	Medline = {22172979},
	Month = {7},
	Nlm_Id = {9507088},
	Number = {7},
	Organization = {Department of Neurology, University of Maryland, and Department of Veterans Affairs, Baltimore, MD 21201, USA.},
	Pages = {783-91},
	Pubmed = {12184916},
	Title = {IFN-beta gene transfer into the central nervous system using bone marrow cells as a delivery system},
	Uuid = {4620A9EC-1589-4012-A77F-FA327B9893BA},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/107999002320271378}}

@article{Makranz:2004,
	Abstract = {Complement-receptor-3 (CR3/MAC-1), scavenger-receptor-AI/II (SRAI/II) and Fcgamma-receptor (FcgammaR) can mediate phagocytosis of degenerated myelin in macrophages and microglia. However, CR3/MAC-1 and SRAI/II, but not FcgammaR, mediate phagocytosis after axonal injury. We tested for phosphatidylinositol 3-kinase (PI3K), phosphoinositide-specific phospholipase-Cgamma (PLCgamma) and protein kinase-C (PKC) signaling in myelin phagocytosis mediated by CR3/MAC-1 alone and by CR3/MAC-1 combined with SRAI/II. Phagocytosis was inhibited by PI3K inhibitors wortmannin and LY-294002, PLCgamma inhibitor U-73122, classical PKC (cPKC) inhibitor Go-6976, general PKC inhibitors Ro-318220 and calphostin-C, and BAPTA/AM which chelates intracellular Ca(2+) required for cPKC activation. PKC activator PMA augmented phagocytosis and further alleviated inhibitions induced by PI3K and PLCgamma inhibitors. Overall, altering PKC activity modulated phagocytosis 4- to 6-fold between inhibition and augmentation. PLCgamma activation did not require tyrosine phosphorylation. Thus, signaling of myelin phagocytosis mediated by CR3/MAC-1 alone and by CR3/MAC-1 combined with SRAI/II involves PI3K, PLCgamma and cPKC, the cascade PI3K-->PLCgamma-->cPKC, and wide-range modulation by PKC. This pathway may thus be targeted for in vivo modulation, which may explain differences in the efficiency of CR3/MAC-1-mediated myelin phagocytosis in different pathological conditions.},
	Author = {Makranz, Chen and Cohen, Goni and Baron, Ayellet and Levidor, Lital and Kodama, Tatsuhiko and Reichert, Fanny and Rotshenker, Shlomo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0969-9961},
	Journal = {Neurobiol Dis},
	Keywords = {Mice, Inbred BALB C;Signal Transduction;Protein Kinase C;Nerve Degeneration;Myelin Sheath;Protein Subunits;Macrophages;Enzyme Inhibitors;Animals;Phosphorylation;Phagocytosis;Axons;Cell Line, Tumor;Phospholipase C;Not relevant;11 Glia;1-Phosphatidylinositol 3-Kinase;Nerve Regeneration;Chelating Agents;Support, Non-U.S. Gov't;Macrophage-1 Antigen;Mice, Knockout;Antigens, CD36;Mice;Demyelinating Diseases},
	Month = {3},
	Nlm_Id = {9500169},
	Number = {2},
	Organization = {Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School and the Eric Roland Center for Neurodegenerative Diseases, Jerusalem, Israel.},
	Pages = {279-86},
	Pii = {S0969996103002456},
	Pubmed = {15006698},
	Title = {Phosphatidylinositol 3-kinase, phosphoinositide-specific phospholipase-Cgamma and protein kinase-C signal myelin phagocytosis mediated by complement receptor-3 alone and combined with scavenger receptor-AI/II in macrophages},
	Uuid = {A134BE99-4BE7-424E-BBF1-A5EB194051CD},
	Volume = {15},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.nbd.2003.11.007}}

@article{Malatesta:2000,
	Abstract = {The developing central nervous system of vertebrates contains an abundant cell type designated radial glial cells. These cells are known as guiding cables for migrating neurons, while their role as precursor cells is less clear. Since radial glial cells express a variety of astroglial characteristics and differentiate as astrocytes after completing their guidance function, they have been considered as part of the glial lineage. Using fluorescence-activated cell sorting, we show here that radial glial cells also are neuronal precursors and only later, after neurogenesis, do they shift towards an exclusive generation of astrocytes. These results thus demonstrate a novel function for radial glial cells, namely their ability to generate two major cell types found in the nervous system, neurons and astrocytes.},
	Author = {Malatesta, P. and Hartfuss, E. and G{\"o}tz, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Glial Fibrillary Acidic Protein;Cell Differentiation;Animals;Astrocytes;Cell Separation;Rats;Recombinant Proteins;Mice, Transgenic;ATP-Binding Cassette Transporters;Rats, Wistar;Mice, Inbred C57BL;Green Fluorescent Proteins;Amino Acid Transport System X-AG;Male;Cerebral Cortex;Neurons;Neuroglia;Flow Cytometry;Promoter Regions (Genetics);Mice;Luminescent Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {20530480},
	Month = {12},
	Nlm_Id = {8701744},
	Number = {24},
	Organization = {Max-Planck Institute of Neurobiology, Am Klopferspitz 18A, D-82152 Planegg-Martinsried, Germany.},
	Pages = {5253-63},
	Pubmed = {11076748},
	Title = {Isolation of radial glial cells by fluorescent-activated cell sorting reveals a neuronal lineage},
	Uuid = {AE860997-71C2-11DA-A383-000D9346EC2A},
	Volume = {127},
	Year = {2000},
	url = {papers/Malatesta_Development2000.pdf}}

@article{Malatesta:2003,
	Abstract = {The precursor function of the ubiquitous glial cell type in the developing central nervous system (CNS), the radial glia, is largely unknown. Using Cre/loxP in vivo fate mapping studies, we found that radial glia generate virtually all cortical projection neurons but not the interneurons originating in the ventral telencephalon. In contrast to the cerebral cortex, few neurons in the basal ganglia originate from radial glia, and in vitro lineage analysis revealed intrinsic differences in the potential of radial glia from the dorsal and ventral telencephalon. This shows that the progeny of radial glia not only differs profoundly between brain regions but also includes the majority of neurons in some parts of the CNS. 22516608 0896-6273 Journal Article},
	Author = {Malatesta, P. and Hack, M. A. and Hartfuss, E. and Kettenmann, H. and Klinkert, W. and Kirchhoff, F. and Gotz, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Neuron},
	Keywords = {10 Development;Integrase/analysis/biosynthesis/genetics;Glial Fibrillary Acidic Protein/analysis/biosynthesis/genetics;Neural Pathways/chemistry/embryology/growth &development/metabolism;Cerebral Cortex/chemistry/embryology/growth &development/metabolism;Neurons/*chemistry/physiology;Viral Proteins/analysis/biosynthesis/genetics;Mice, Inbred C57BL;Animal;Mice, Transgenic;F;Neuroglia/*chemistry/physiology;Cells, Cultured;Support, Non-U.S. Gov't;Mice;Basal Ganglia/chemistry/embryology/growth &development/metabolism},
	Number = {5},
	Organization = {Max-Planck Institute of Neurobiology, Am Klopferspitz 18A, D-82152 Planegg-Martinsried, Germany.},
	Pages = {751-64},
	Pubmed = {12628166},
	Title = {Neuronal or glial progeny: regional differences in radial glia fate},
	Uuid = {74035A95-54E7-4E61-9700-E2ADDCAB33FC},
	Volume = {37},
	Year = {2003},
	url = {papers/Malatesta_Neuron2003.pdf}}

@article{Male:2001,
	Author = {Male, D. and Rezaie, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0079-6123},
	Journal = {Prog Brain Res},
	Keywords = {Central Nervous System;Cell Adhesion Molecules;Stem Cells;Chemokines;11 Glia;Microglia;review, tutorial;Blood Vessels;Animals;Humans;review},
	Medline = {21428568},
	Nlm_Id = {0376441},
	Organization = {Immunology Section, Department of Biological Sciences, Open University, Milton Keynes MK7 6AA, UK. d.k.male\@open.ac.uk},
	Pages = {81-93},
	Pubmed = {11545033},
	Title = {Colonisation of the human central nervous system by microglia: the roles of chemokines and vascular adhesion molecules},
	Uuid = {BA6DC32A-F039-48D7-AB1C-F187DECA5CE2},
	Volume = {132},
	Year = {2001}}

@article{Maletic-Savatic:1995,
	Abstract = {Hippocampal neurons are highly plastic in their excitable properties, both during development and in the adult brain. As voltage-sensitive K+ channels are major determinants of membrane excitability, one mechanism for generating plasticity is through regulation of K+ channel activity. To gain insights into the regulation of K+ channels in the hippocampus, we have analyzed the spatiotemporal expression patterns of five K+ channel polypeptides in rat hippocampal neurons developing in situ and in vitro. Delayed rectifier-type channels (Kv1.5, Kv2.1, and Kv2.2) are expressed on all neuronal somata and proximal dendrites, while A-type channels (Kv1.4 and Kv4.2) are present distally on distinct subpopulations of neurons. The development of these patterns in situ is monotonic; that is, while the time and spatial development varies among the channels, each K+ channel subtype initially appears in its adult pattern, suggesting that the mechanisms underlying spatial patterning operate through development. Immunoblots confirm the differential temporal expression of K+ channels in the developing hippocampus, and demonstrate developmentally regulated changes in the microheterogeneity of some K+ channel polypeptide species. Temporal expression patterns of all five K+ channels observed in situ are retained in vitro, while certain aspects of cellular and subcellular localization are altered for some of the K+ channel polypeptides studied. Similarities in K+ channel polypeptide expression in situ and in vitro indicate that the same regulatory mechanisms are controlling spatiotemporal patterning in both situations. However, differences between levels of expression for all subtypes studied except Kv2.1 indicate additional mechanisms operating in situ but absent in vitro that are important in determining polypeptide abundance.},
	Author = {Maletic-Savatic, M. and Lenn, N. J. and Trimmer, J. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:53 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Fetus;13 Olfactory bulb anatomy;Electrophoresis, Polyacrylamide Gel;Animals;In Vitro;Cells, Cultured;Aging;Rats;Comparative Study;Cell Membrane;Rats, Sprague-Dawley;Hippocampus;Pyramidal Cells;Immunoblotting;Dendrites;Animals, Newborn;Support, Non-U.S. Gov't;Potassium Channels;Neurons;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Gene Expression},
	Medline = {95271336},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {5 Pt 2},
	Organization = {Department of Neurology, State University of New York, Stony Brook, New York 11794, USA.},
	Pages = {3840-51},
	Pubmed = {7751950},
	Title = {Differential spatiotemporal expression of K+ channel polypeptides in rat hippocampal neurons developing in situ and in vitro},
	Uuid = {A54A7FD3-F248-4FB5-86E6-2B20CF31EACC},
	Volume = {15},
	Year = {1995},
	url = {papers/Maletic-Savatic_JNeurosci1995.pdf}}

@article{Malik:1995,
	Abstract = {Gene transfer into human hematopoietic stem cells with expression targeted to the maturing myelomonocytic progeny has applications for gene therapy of genetic diseases affecting granulocytes and macrophages. We hypothesized that promoters of myeloid-specific genes that are upregulated with myelomonocytic differentiation would also upregulate expression of an exogenous gene in a retroviral vector. Moloney murine leukemia virus (MoMuLV)-based retroviral vectors using promoters from hematopoietic genes (CD11b, CD18, and CD34) were compared with vectors with viral promoters (MoMuLV long terminal repeat [LTR], cytomegalovirus [CMV], and simian virus 40 [SV40]). Human glucocerebrosidase (GC) cDNA was the reporter gene. HL60 cells were transduced with these vectors and vector-derived GC activity was compared in undifferentiated HL-60 cells and the same cells differentiated into granulocytes using dimethyl sulfoxide or monocyte/macrophages using phorbol myristate acetate. In undifferentiated HL-60 cells, vector-derived GC activity was the highest when it was controlled by the MoMuLV LTR. In HL-60 cells differentiated into granulocytes, vector-derived GC activity transcribed from the CD11b, MoMuLV LTR, and CMV promoters was equivalent to 1.7, 1.5, and 1.5 times the normal endogenous GC activity, respectively, and 0.8, 2.0, and 3.6 times the normal GC activity, respectively, in those differentiated into macrophages. With granulocytic differentiation, the CD11b promoter showed maximal induction in GC activity (8-fold); with macrophage differentiation, the CD11b promoter showed a fourfold induction in GC expression. The CD11b promoter also generated significant levels of GC activity in the myelomonocytic progeny of transduced CD34+ cells. Expression from the CD11b promoter, unlike that from the CMV or the MoMuLV LTR promoters, was relatively myelomonocyte-specific, with minimal expression observed in Jurkat T cells or HeLa carcinoma cells. The induction of expression from the CD11b promoter with differentiation in HL-60 cells correlates with the developmental regulation of the CD11b gene. Retroviral vectors using the CD11b promoter have potential utility for gene therapy of disorders affecting the myelomonocytic lineage. 0006-4971 Journal Article},
	Author = {Malik, P. and Krall, W. J. and Yu, X. J. and Zhou, C. and Kohn, D. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Blood},
	Keywords = {*Genetic Vectors;Human;Cell Differentiation;DNA, Complementary/genetics;T-Lymphocytes/drug effects;Glucosylceramidase/genetics;Leukemia, T-Cell, Acute;Repetitive Sequences, Nucleic Acid;*Gene Expression Regulation, Neoplastic;Macrophage-1 Antigen/*genetics;Moloney murine leukemia virus/*genetics;*Promoter Regions (Genetics);EE, DMSO, abstr;08 Aberrant cell cycle;Hematopoietic Stem Cells/*metabolism;Antigens, CD34/*genetics;Recombinant Fusion Proteins/biosynthesis;Dimethyl Sulfoxide/pharmacology;Hela Cells/drug effects;Support, Non-U.S. Gov't;*Gene Transfer Techniques;Organ Specificity;Tumor Cells, Cultured;Support, U.S. Gov't, P.H.S.;HL-60 Cells/drug effects;Tetradecanoylphorbol Acetate/pharmacology;Genes, Reporter;Antigens, CD18/*genetics},
	Number = {8},
	Organization = {Division of Research Immunology/Bone Marrow Transplantation, Childrens Hospital, Los Angeles, University of Southern California School of Medicine, USA.},
	Pages = {2993-3005},
	Pubmed = {7579392},
	Title = {Retroviral-mediated gene expression in human myelomonocytic cells: a comparison of hematopoietic cell promoters to viral promoters},
	Uuid = {717F1A5D-6A3A-4ECE-9EB6-F4EE62689F8E},
	Volume = {86},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7579392}}

@article{Mallat:2005,
	Abstract = {Cell corpses generated during CNS development are eliminated through phagocytosis performed by a variety of cells, including mesenchyme-derived macrophages and microglia, or glial cells originating in the neurogenic ectoderm. Mounting evidence indicates that in different species, phagocytes not only clear cell corpses but also engulf still-living neural cells or axons, and thereby promote cell death or axon pruning. Knowledge of the mechanisms of corpse recognition by engulfing cells provides molecular signals to this new role for phagocytes. These observations support a conserved and instructive role for phagocytosis in the execution of regressive events during neurogenesis.},
	Author = {Mallat, Michel and Mar{\'\i}n-Teva, Jos{\'e} Luis and Ch{\'e}ret, Cyril},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Central Nervous System;Apoptosis;11 Glia;Humans;Animals;Phagocytosis;review;Neurons},
	Month = {2},
	Nlm_Id = {9111376},
	Number = {1},
	Organization = {Biologie des Interactions Neurone-glie, INSERM U.495, IFR 70, UPMC, H\^{o}pital de la Salp\^{e}tri\`{e}re, 47 boulevard de l'H\^{o}pital, 75013 Paris, France. michel.mallat\@infobiogen.fr},
	Pages = {101-7},
	Pii = {S0959-4388(05)00007-3},
	Pubmed = {15721751},
	Title = {Phagocytosis in the developing CNS: more than clearing the corpses},
	Uuid = {BCEDC80F-00B3-11DB-9E68-000D9346EC2A},
	Volume = {15},
	Year = {2005},
	url = {papers/Mallat_CurrOpinNeurobiol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2005.01.006}}

@article{Manaka:1972,
	Author = {Manaka, S. and Sato, S. and Fuchinoue, T. and Sekino, H. and Nagai, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0006-8969},
	Journal = {No To Shinkei},
	Keywords = {Epilepsy;Electroencephalography;Adult;Female;Humans;Psychosurgery;Brain},
	Medline = {72145055},
	Month = {3},
	Nlm_Id = {0413550},
	Number = {3},
	Pages = {311-8},
	Pubmed = {5067047},
	Title = {[Successfully treated case of ectopic gray matter as a cause of uncontrollable epilepsy]},
	Uuid = {961AF4BA-4963-4F38-BE45-5B27B9BAA9F4},
	Volume = {14},
	Year = {1972}}

@article{Mander:2006,
	Abstract = {Microglia are resident brain macrophages that become activated and proliferate following brain damage or stimulation by immune mediators, such as IL-1beta or TNF-alpha. We investigated the mechanisms by which microglial proliferation is regulated in primary cultures of rat glia. We found that basal proliferation of microglia was stimulated by proinflammatory cytokines IL-1beta or TNF-alpha, and this proliferation was completely inhibited by catalase, implicating hydrogen peroxide as a mediator of proliferation. In addition, inhibitors of NADPH oxidase (diphenylene iodonium or apocynin) also prevented microglia proliferation, suggesting that this may be the source of hydrogen peroxide. IL-1beta and TNF-alpha rapidly stimulated the rate of hydrogen peroxide produced by isolated microglia, and this was inhibited by diphenylene iodonium, implying that the cytokines were acting directly on microglia to stimulate the NADPH oxidase. Low concentrations of PMA or arachidonic acid (known activators of NADPH oxidase) or xanthine/xanthine oxidase or glucose oxidase (generating hydrogen peroxide) also increased microglia proliferation and this was blocked by catalase, showing that NADPH oxidase activation or hydrogen peroxide was sufficient to stimulate microglia proliferation. In contrast to microglia, the proliferation of astrocytes was unaffected by the presence of catalase. In conclusion, these findings indicate that microglial proliferation in response to IL-1beta or TNF-alpha is mediated by hydrogen peroxide from NADPH oxidase.},
	Author = {Mander, Palwinder K. and Jekabsone, Aiste and Brown, Guy C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {2985117R},
	Number = {2},
	Organization = {Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom.},
	Pages = {1046-52},
	Pii = {176/2/1046},
	Pubmed = {16393992},
	Title = {Microglia proliferation is regulated by hydrogen peroxide from NADPH oxidase},
	Uuid = {D934E02E-901F-4BCB-B24E-9AB58C5542D8},
	Volume = {176},
	Year = {2006}}

@article{Manev:2001,
	Abstract = {5-Lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) are two enzymes that are critical for the synthesis of eicosanoids, the inflammatory metabolites of arachidonic acid. Both 5-LOX and COX-2 are expressed in the brain, including in CNS neurons. The physiologic role of these proteins in neuronal functioning is not clear. In non-neuronal tissues these two enzymes often assume similar roles: in addition to their function in inflammation, 5-LOX and COX-2 appear to be associated with cell proliferation, that is, with tumor growth. High 5-LOX expression has been noticed in the proliferating brain or pancreatic tumor cells; reduction in tumor cell proliferation and/or destruction of tumor cells was achieved with 5-LOX inhibitors. Proliferation of immature neurons/neuroblasts is an important component of mitotic neurogenesis. We investigated the role of 5-LOX in proliferation using cultures of human neuronal precursor cells, NT2. We found that these cells express 5-LOX mRNA and we used 3H-thymidine incorporation as a measure of cell proliferation; this was reduced by treating the cultures with 5-LOX inhibitor AA-861. We propose that the 5-LOX pathway plays a crucial role in mitotic neurogenesis. Additional studies should explore whether 5-LOX may participate in neurogenesis related pathologies and whether it should be considered a target for procedures aimed at altering neurogenesis for therapeutic purposes. eng Journal Article},
	Author = {Manev, H. and Uz, T. and Manev, R. and Zhang, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {Neurons/*drug effects/*physiology;Neuroprotective Agents/metabolism;Human;Cell Line;Lipoxygenase Inhibitors/*pharmacology;Animal;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Benzoquinones/*pharmacology;Arachidonate 5-Lipoxygenase/*drug effects/metabolism;RNA, Messenger/drug effects/metabolism;C abstr},
	Organization = {Psychiatric Institute, Department of Psychiatry, University of Illinois at Chicago, 1601 West Taylor Street, MC912, Chicago, IL 60612, USA. HManev\@psych.uic.edu},
	Pages = {45-51.},
	Title = {Neurogenesis and neuroprotection in the adult brain. A putative role for 5-lipoxygenase?},
	Uuid = {E587D2AD-CAC9-4DDD-8D46-7417BBE6D5DF},
	Volume = {939},
	Year = {2001}}

@article{Manfra:2001,
	Abstract = {Transgenic mice expressing green fluorescent protein (GFP) were generated to provide a source of labeled leukocytes for cell transfer studies. The transgene comprises the GFP coding region under the transcriptional control of the chicken ss-actin promoter and human cytomegalovirus enhancer. Mice expressing this GFP transgene were generated in the B6D2 and in the 129SvEv backgrounds. Flow cytometric analysis of cells from the blood, spleen, and bone marrow of these transgenic mice revealed that most leukocytes, including dendritic cells and memory T cells, express GFP. In allogeneic cell transfers, donor GFP+ splenocytes were detected in the spleen and mesenteric lymph nodes of recipient mice within 2 hours after transfer and for at least 9 days thereafter. In syngeneic experiments using 129-derived GFP+ donor splenocytes, donor cells were detected in multiple tissues of 129 recipients from 2 hours to 3 weeks after transfer. In bone-marrow transplantation experiments using irradiated allogeneic recipients, the percent of GFP+ donor cells in recipients at 3 weeks was comparable to that seen in similar tissues of GFP+ donor mice. These data demonstrate that GFP+ transgenic mice provide a ready source of GFP-expressing primary cells that can be easily monitored after their transfer to recipient animals.},
	Author = {Manfra, D. J. and Chen, S. C. and Yang, T. Y. and Sullivan, L. and Wiekowski, M. T. and Abbondanzo, S. and Vassileva, G. and Zalamea, P. and Cook, D. N. and Lira, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Animals;Bone Marrow Transplantation;Female;Mice, Transgenic;Adoptive Transfer;Recombinant Fusion Proteins;Mice, Inbred C57BL;11 Glia;Microscopy, Fluorescence;Green Fluorescent Proteins;Male;Bone Marrow Cells;Mice, Inbred Strains;Leukocytes;Mice, Inbred DBA;Mice;Luminescent Proteins;Gene Expression;Spleen},
	Medline = {20580890},
	Month = {1},
	Nlm_Id = {0370502},
	Number = {1},
	Organization = {Department of Immunology, Schering-Plough Research Institute, Kenilworth, NJ 07033, USA.},
	Pages = {41-7},
	Pubmed = {11141477},
	Title = {Leukocytes expressing green fluorescent protein as novel reagents for adoptive cell transfer and bone marrow transplantation studies},
	Uuid = {2CD570BE-2F25-4B16-9410-E50C1F107499},
	Volume = {158},
	Year = {2001}}

@article{Mangale:2008,
	Abstract = {The earliest step in creating the cerebral cortex is the specification of neuroepithelium to a cortical fate. Using mouse genetic mosaics and timed inactivations, we demonstrated that Lhx2 acts as a classic selector gene and essential intrinsic determinant of cortical identity. Lhx2 selector activity is restricted to an early critical period when stem cells comprise the cortical neuroepithelium, where it acts cell-autonomously to specify cortical identity and suppress alternative fates in a spatially dependent manner. Laterally, Lhx2 null cells adopt antihem identity, whereas medially they become cortical hem cells, which can induce and organize ectopic hippocampal fields. In addition to providing functional evidence for Lhx2 selector activity, these findings show that the cortical hem is a hippocampal organizer.},
	Author = {Mangale, Vishakha S. and Hirokawa, Karla E. and Satyaki, Prasad R. V. and Gokulchandran, Nandini and Chikbire, Satyadeep and Subramanian, Lakshmi and Shetty, Ashwin S. and Martynoga, Ben and Paul, Jolly and Mai, Mark V. and Li, Yuqing and Flanagan, Lisa A. and Tole, Shubha and Monuki, Edwin S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {10 Development;Embryonic Induction;Animals;Transcription Factors;Gene Expression Regulation, Developmental;Chimera;Epithelium;Homeodomain Proteins;Mutation;Telencephalon;Hippocampus;Pyramidal Cells;Neuroepithelial Cells;research support, non-u.s. gov't;Organizers, Embryonic;Prosencephalon;Embryonic Stem Cells;10 genetics malformation;Cerebral Cortex;Mice, Knockout;Cell Aggregation;Dentate Gyrus;Recombination, Genetic;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008},
	Mid = {UKMS1965},
	Month = {1},
	Nlm_Id = {0404511},
	Number = {5861},
	Organization = {Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai 400005, India.},
	Pages = {304-9},
	Pii = {319/5861/304},
	Pmc = {PMC2494603},
	Pubmed = {18202285},
	Title = {Lhx2 selector activity specifies cortical identity and suppresses hippocampal organizer fate},
	Uuid = {1D3F8C0E-E5F7-4492-B285-5EA34C534417},
	Volume = {319},
	Year = {2008},
	url = {papers/Mangale_Science2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1151695}}

@article{Manganas:2007,
	Abstract = {The identification of neural stem and progenitor cells (NPCs) by in vivo brain imaging could have important implications for diagnostic, prognostic, and therapeutic purposes. We describe a metabolic biomarker for the detection and quantification of NPCs in the human brain in vivo. We used proton nuclear magnetic resonance spectroscopy to identify and characterize a biomarker in which NPCs are enriched and demonstrated its use as a reference for monitoring neurogenesis. To detect low concentrations of NPCs in vivo, we developed a signal processing method that enabled the use of magnetic resonance spectroscopy for the analysis of the NPC biomarker in both the rodent brain and the hippocampus of live humans. Our findings thus open the possibility of investigating the role of NPCs and neurogenesis in a wide variety of human brain disorders.},
	Author = {Manganas, Louis N. and Zhang, Xueying and Li, Yao and Hazel, Raphael D. and Smith, S. David and Wagshul, Mark E. and Henn, Fritz and Benveniste, Helene and Djuric, Petar M. and Enikolopov, Grigori and Maletic-Savatic, Mirjana},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Cell Differentiation;Animals;Humans;Signal Processing, Computer-Assisted;Rats;Algorithms;Brain;Adult Stem Cells;Female;Child;Hippocampus;research support, non-u.s. gov't;Male;Embryonic Stem Cells;Brain Chemistry;Magnetic Resonance Spectroscopy;Neurons;Fatty Acids;Adult;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Biological Markers;Stem Cells;research support, u.s. gov't, non-p.h.s.;Protons;Adolescent},
	Month = {11},
	Nlm_Id = {0404511},
	Number = {5852},
	Organization = {SUNY Stony Brook, Stony Brook, NY 11794, USA.},
	Pages = {980-5},
	Pii = {318/5852/980},
	Pubmed = {17991865},
	Title = {Magnetic resonance spectroscopy identifies neural progenitor cells in the live human brain},
	Uuid = {973E3224-E7DB-4537-B879-672D758038D3},
	Volume = {318},
	Year = {2007},
	url = {papers/Manganas_Science2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1147851}}

@article{Mao:2001a,
	Abstract = {Neural progenitor cells are present in the rodent brain throughout adulthood, and can proliferate and differentiate into new neurons and/or glia to repair injury. To explore the repair processes mediated by brain progenitor cells, a selective lesion of the nigrostriatal dopaminergic pathway was induced in young adult mice by repeated administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). A thymidine analog, bromodeoxyuridine (BrdU), was used as a tracer for DNA synthesis to label the dividing cells and their terminal progeny following injury. Three days after MPTP treatments (25 mg/kg, once daily for 5 days), an 8-fold increase in the number of BrdU-labeled newborn cells was observed in the dorsal striatum. A 5-fold increase was also seen in the substantia nigra (SN). Newborn cells in the striatum survived beyond 60 days after their birth whereas newborn cells in the SN survived for less than 31 days. The vast majority of newborn cells in the striatum differentiated into astroglia according to their radial morphology and co-expression with an astroglial marker, S100beta, within 10 days after birth. In contrast, most BrdU-positive cells in the SN failed to co-express S100beta. Little or none of BrdU-labeled cells in both the striatum and SN were found to co-localize with a neuronal marker, neuronal nuclear antigen, or tyrosine hydroxylase during the full course of survival days surveyed (3 to 60 days). Repeated MPTP also decreased dopamine content and uptake in the striatum, which showed a significant recovery 31 days after MPTP lesion. These results demonstrate a rapid and profound astrogenesis in the striatum of young adult mice in response to toxic dopaminergic insult. The lack of neurogenesis in the two affected brain areas indicates the relative importance of glial cell regeneration in repairing MPTP injury.},
	Author = {Mao, L. and Lau, Y. S. and Petroske, E. and Wang, J. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0165-3806},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Cell Survival;Cell Differentiation;MPTP Poisoning;Astrocytes;Dopamine;Animals;Dopamine Agents;3,4-Dihydroxyphenylacetic Acid;Substantia Nigra;Mice, Inbred C57BL;1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine;Male;Research Support, U.S. Gov't, P.H.S.;Neostriatum;Tyrosine 3-Monooxygenase;Age Factors;Mice;Cell Division;24 Pubmed search results 2008;Bromodeoxyuridine;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {21575786},
	Month = {11},
	Nlm_Id = {8908639},
	Number = {1-2},
	Organization = {Division of Pharmacology, School of Pharmacy, University of Missouri-Kansas City, 2411 Holmes Street, M3-225, Kansas City, MO, USA},
	Pages = {57-65},
	Pii = {S0165380601002607},
	Pubmed = {11718836},
	Title = {Profound astrogenesis in the striatum of adult mice following nigrostriatal dopaminergic lesion by repeated MPTP administration},
	Uuid = {EA4AC4AC-945B-44F0-8380-71CB1C396E6D},
	Volume = {131},
	Year = {2001}}

@article{Margolis:1972,
	Author = {Margolis, F. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Hamsters;Rabbits;Immune Sera;13 Olfactory bulb anatomy;I;Rats;Goats;Female;Animal;Species Specificity;Male;Immunoelectrophoresis;Brain Chemistry;Ammonium Sulfate;Immunodiffusion;Organ Specificity;Limbic System/*analysis;Olfactory Bulb/analysis;Chromatography, DEAE-Cellulose;Mice;Electrophoresis, Disc;Molecular Weight;Guinea Pigs;Precipitin Tests;Chickens;Nerve Tissue Proteins/*isolation &purification},
	Number = {5},
	Pages = {1221-4.},
	Title = {A brain protein unique to the olfactory bulb},
	Uuid = {435F6C0D-02F6-4355-9D62-0E7B58217F9A},
	Volume = {69},
	Year = {1972},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=4624756}}

@article{Marin-Teva:2004,
	Abstract = {The loss of neuronal cells, a prominent event in the development of the nervous system, involves regulated triggering of programmed cell death, followed by efficient removal of cell corpses. Professional phagocytes, such as microglia, contribute to the elimination of dead cells. Here we provide evidence that, in addition to their phagocytic activity, microglia promote the death of developing neurons engaged in synaptogenesis. In the developing mouse cerebellum, Purkinje cells die, and 60\%of these neurons that already expressed activated caspase-3 were engulfed or contacted by spreading processes emitted by microglial cells. Apoptosis of Purkinje cells in cerebellar slices was strongly reduced by selective elimination of microglia. Superoxide ions produced by microglial respiratory bursts played a major role in this Purkinje cell death. Our study illustrates a mammalian form of engulfment-promoted cell death that links the execution of neuron death to the scavenging of dead cells.},
	Author = {Mar{\'\i}n-Teva, Jos{\'e} Luis and Dusart, Isabelle and Colin, Catherine and Gervais, Annie and van Rooijen, Nico and Mallat, Michel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Apoptosis/*physiology;Purkinje Cells/cytology/*physiology;Cell Communication/*physiology;Cell Differentiation;Apoptosis;Cell Survival;Caspases/metabolism;Alpha;Signal Transduction/*physiology;Animals;Presynaptic Terminals/physiology;Antibodies/pharmacology;Presynaptic Terminals;Cerebellar Cortex;In Vitro;Signal Transduction;Caspases;Free Radical Scavengers/pharmacology;Cell Respiration/drug effects/physiology;Purkinje Cells;Mice, Inbred C57BL;Cell Differentiation/physiology;Receptors, Tumor Necrosis Factor/antagonists &inhibitors/metabolism;Cell Communication;Not relevant;Cell Survival/drug effects/physiology;Enzyme Inhibitors;Receptors, Tumor Necrosis Factor;Cerebellar Cortex/cytology/*growth &development;Enzyme Inhibitors/pharmacology;Cell Respiration;EE, G pdf;Microglia;Mice, Knockout;Mice;Antibodies;Microglia/cytology/*physiology;Support, Non-U.S. Gov't;Free Radical Scavengers},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Biologie des Interactions Neurone-glie, INSERM U.495, IFR 70, UPMC, 47 Bd de l'h\^{o}pital, 75013 Paris, France.},
	Pages = {535-47},
	Pii = {S0896627304000698},
	Pubmed = {14980203},
	Title = {Microglia promote the death of developing Purkinje cells},
	Uuid = {79AF5F34-D3BA-11D9-A0E9-000D9346EC2A},
	Volume = {41},
	Year = {2004}}

@article{Markakis:1999,
	Abstract = {The subgranule zone of the dentate gyrus in rats has been shown to be proliferative into adulthood and senescence. However, the connectivity of newly generated, identified neurons in the adult has not been definitively described. In the present study, 9 weeks after a series of intraperitoneal injections of 5-bromo-2'-deoxyuridine (BrdU), animals received stereotaxic iontophoretic injections of Fluoro-Gold (FG) into field CA3. Three weeks after FG injections, sections were analyzed for BrdU immunoreactivity (proliferative label), FG retrograde label, and either calbindin-D28k or synaptophysin immunohistochemistry. A large proportion (up to 44\%) of BrdU-labeled cells in the dentate gyrus within regions of FG retrograde label incorporated FG. All of the doubly labeled (BrdU-FG) neurons also immunolabeled with the antibody to calbindin-D28k. Many doubly labeled (BrdU-FG) cells were also surrounded in three planes by synaptophysin immunoreactivity. We conclude that newly generated neurons in the dentate gyrus have the correct immunohistochemical profile, send appropriate axonal projections to field CA3, and are surrounded by profiles containing synaptic vesicle proteins.},
	Author = {Markakis, E. A. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Fluorescent Dyes;Neural Pathways/chemistry/ultrastructure;Synaptic Vesicles/*chemistry/ultrastructure;Rats;Iontophoresis;Dentate Gyrus/*chemistry/cytology;Animal;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Nerve Tissue Proteins/analysis;Axons/*chemistry/ultrastructure;Synaptophysin/analysis;Male;Calcium-Binding Protein, Vitamin D-Dependent/analysis;B;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Bromodeoxyuridine;Neurons/*chemistry/ultrastructure},
	Number = {4},
	Organization = {The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California 92037, USA.},
	Pages = {449-60.},
	Title = {Adult-generated neurons in the dentate gyrus send axonal projections to field CA3 and are surrounded by synaptic vesicles},
	Uuid = {22E070E4-C6EA-4209-B831-D929468E4ED0},
	Volume = {406},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10205022}}

@article{Markakis:2004,
	Abstract = {We report the first isolation of progenitor cells from the hypothalamus, a derivative of the embryonic basal plate that does not exhibit neurogenesis postnatally. Neurons derived from hypothalamic progenitor cells were compared with those derived from progenitor cultures of hippocampus, an embryonic alar plate derivative that continues to support neurogenesis in vivo into adulthood. Aside from their different embryonic origins and their different neurogenic potential in vivo, these brain regions were chosen because they are populated with cells of three different categories: Category I cells are generated in both hippocampus and hypothalamus, Category II cells are generated in the hypothalamus but are absent from the hippocampus, and Category III is a cell type generated in the olfactory placode that migrates into the hypothalamus during development. Stem-like cells isolated from other brain regions, with the ability to generate neurons and glia, produce neurons of several phenotypes including gabaergic, dopaminergic, and cholinergic lineages. In the present study, we extended our observations into neuroendocrine phenotypes. The cultured neural precursors from 7-week-old rat hypothalamus readily generated neuropeptide-expressing neurons. Hippocampal and hypothalamic progenitor cultures converged to indistinguishable populations and produced neurons of all three categories, confirming that even short-term culture confers or selects for immature progenitors with enough plasticity to elaborate neuronal phenotypes usually inhibited in vivo by the local microenvironment. The range of phenotypes generated from neuronal precursors in vitro now includes the peptides found in the neuroendocrine system: corticotropin-releasing hormone, growth hormone-releasing hormone, gonadotropin-releasing hormone, oxytocin, somatostatin, thyrotropin-releasing hormone, and vasopressin.},
	Author = {Markakis, Eleni A. and Palmer, Theo D. and Randolph-Moore, Lynne and Rakic, Pasko and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Cell Separation;Cells, Cultured;Rats;Neurosecretory Systems;Comparative Study;Phenotype;Antigens, Differentiation;Cell Count;Rats, Sprague-Dawley;Hippocampus;RNA, Messenger;Corticotropin-Releasing Hormone;Male;Reverse Transcriptase Polymerase Chain Reaction;Neuropeptides;Rats, Inbred F344;Hypothalamus;Support, Non-U.S. Gov't;Neurons;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Stem Cells},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.},
	Pages = {2886-97},
	Pii = {24/12/2886},
	Pubmed = {15044527},
	Title = {Novel neuronal phenotypes from neural progenitor cells},
	Uuid = {B9D50436-CB07-4FA2-86B8-0184D7B67599},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4161-03.2004}}

@article{Marodon:2003,
	Abstract = {Achieving cell-specific expression of a therapeutic transgene by gene transfer vectors represents a major goal for gene therapy. To achieve specific expression of a transgene in CD4(+) cells, we have generated lentiviral vectors expressing the enhanced green fluorescent protein (eGFP) reporter gene under the control of regulatory sequences derived from the CD4 gene--a minimal promoter and the proximal enhancer, with or without the silencer. Both lentiviral vectors could be produced at high titers (more than 10(7) infectious particles per milliliter) and were used to transduce healthy murine hematopoietic stem cells (HSCs). On reconstitution of RAG-2-deficient mice with transduced HSCs, the specific vectors were efficiently expressed in T cells, minimally expressed in B cells, and not expressed in immature cells of the bone marrow. Addition of the CD4 gene-silencing element in the vector regulatory sequences led to further restriction of eGFP expression into CD4(+) T cells in reconstituted mice and in ex vivo-transduced human T cells. Non-T CD4(+) dendritic and macrophage cells derived from human CD34(+) cells in vitro expressed the transgene of the specific vectors, albeit at lower levels than CD4(+) T cells. Altogether, we have generated lentiviral vectors that allow specific targeting of transgene expression to CD4(+) cells after differentiation of transduced mice HSCs and human mature T cells. Ultimately, these vectors may prove useful for in situ injections for in vivo gene therapy of HIV infection or genetic immunodeficiencies.},
	Author = {Marodon, Gilles and Mouly, Enguerran and Blair, Emma J. and Frisen, Charlotte and Lemoine, Fran\c{c}ois M. and Klatzmann, David},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Cell Differentiation;Transduction, Genetic;Animals;DNA-Binding Proteins;Gene Expression Regulation;Humans;Lentivirus;Antigens, CD4;Mice, Inbred C57BL;Recombinant Fusion Proteins;11 Glia;Green Fluorescent Proteins;Radiation Chimera;Genes, Synthetic;Genetic Vectors;Bone Marrow Cells;Cell Lineage;Thymus Gland;Mice, Knockout;Adult;Regulatory Sequences, Nucleic Acid;Mice;CD4-Positive T-Lymphocytes;Luminescent Proteins;Genes, Reporter;Hematopoietic Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {22592439},
	Month = {5},
	Nlm_Id = {7603509},
	Number = {9},
	Organization = {Centre National de la Recherche Scientifique UMR-7087, Biologie et Th{\'e}rapeutique des Pathologies Immunitaires, Centre d'Etude et de Recherche en Virologie et en Immunologie, H\^{o}pital La Piti{\'e}-S\^{a}lp{\'e}tri\`{e}re, Paris, France.},
	Pages = {3416-23},
	Pii = {2002-02-0578},
	Pubmed = {12511423},
	Title = {Specific transgene expression in human and mouse CD4+ cells using lentiviral vectors with regulatory sequences from the CD4 gene},
	Uuid = {A54BF6A1-6B32-4BDF-969A-FB71EE636972},
	Volume = {101},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2002-02-0578}}

@article{Marshall:2003,
	Abstract = {The subventricular zone (SVZ) of the perinatal forebrain gives rise to both neurons and glia. The mechanisms governing the phenotypic specification of progenitors within this heterogeneous germinal zone are unclear. However, the characterization of subpopulations of SVZ cells has given us a better understanding of the basic architecture of the SVZ and presents us with the opportunity to ask more detailed questions regarding phenotype specification and cell fate. Recent work demonstrating the embryonic origins of SVZ cells is summarized, and a model describing the formation of the perinatal SVZ, noting contributions of cells from pallial as well as subpallial germinal zones, is presented. We further address differences among classes of SVZ cells based on molecular profile, phenotype, and migration behavior and present a model summarizing the organization of perinatal SVZ cells along coronal, sagittal, and horizontal axes. A detailed description of the SVZ in the adult, outlining classes of cells based on morphology, molecular profile, and proliferative behavior, was recently reported by Doetsch et al. (Proc Natl Acad Sci USA 93:14895-14900, 1997). Potential relationships among cells within the perinatal and adult SVZ will be discussed. GLIA 43:52-61, 2003. 0894-1491 Journal Article Review Review, Academic},
	Author = {Marshall, C. A. and Suzuki, S. O. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {Glia},
	Keywords = {Prosencephalon/cytology/*embryology/*growth &development;02 Adult neurogenesis migration;Lateral Ventricles/cytology/*embryology/growth &development;Neuroglia/*cytology/physiology;Neurons/*cytology/physiology;Stem Cells/*cytology/physiology;Human;03 Adult neurogenesis progenitor source;Biological Markers;BB both;Cell Lineage/physiology;Cell Differentiation/physiology;Support, U.S. Gov't, P.H.S.;Animals;Cell Movement/physiology},
	Number = {1},
	Organization = {Center for Neurobiology and Behavior, Division of Neuropathology, Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA.},
	Pages = {52-61},
	Pubmed = {12761867},
	Title = {Gliogenic and neurogenic progenitors of the subventricular zone: who are they, where did they come from, and where are they going?},
	Uuid = {32DAD1B5-4469-4245-863F-08049F5F04D0},
	Volume = {43},
	Year = {2003},
	url = {papers/Marshall_Glia2003}}

@article{Martens:2002,
	Abstract = {Stem cells isolated from the fourth ventricle and spinal cord form neurospheres in vitro in response to basic fibroblast growth factor (FGF2)+heparin (H) or epidermal growth factor (EGF)+FGF2 together. To determine whether these growth factor conditions are sufficient to induce stem cells within the fourth ventricle and spinal cord to proliferate and expand their progeny in vivo, we infused EGF and FGF2, alone or together, with or without H, into the fourth ventricle for 6 days via osmotic minipumps. Animals were injected with bromodeoxyuridine (BrdU) on days 4, 5 and 6 of infusion in order to label cells proliferating in response to the growth factors. Infusions of EGF+FGF2+H into the fourth ventricle resulted in the largest proliferative effect, a 10.8-fold increase in the number of BrdU+ cells around the fourth ventricle, and a 33.5-fold increase in the number of BrdU+ cells around the central canal of the spinal cord, as compared to vehicle infused controls. The majority of the cells were nestin+ after 6 days of infusion. Seven weeks post-infusion, 22 and 30\%of the number of BrdU+ cells induced to proliferate after 6 days of EGF+FGF2+H infusions were still detected around the fourth ventricle and central canal of the spinal cord, respectively. Analysis of the fates of the remaining cells showed that a small percentage of BrdU+ cells around the fourth ventricle and in the white matter of the spinal cord differentiated into astrocytes and oligodendrocytes. BrdU+ neurons were not found in the brainstem or in the grey matter of the cervical spinal cord 7 weeks post-infusion. These results show that endogenous stem cells and progenitors around the fourth ventricle and central canal of the spinal cord proliferate in response to exogenously applied growth factors, but unlike in the lateral ventricle where they generate some new neurons, they only produce new astrocytes and oligodendrocytes at 7 weeks post-infusion. 0953-816x Journal Article},
	Author = {Martens, D. J. and Seaberg, R. M. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {Heparin/pharmacology;Animals;Lateral Ventricles/cytology/drug effects/metabolism;Cells, Cultured;Fourth Ventricle/*cytology/drug effects/metabolism;Spinal Cord/*cytology/drug effects/metabolism;Growth Substances/*pharmacology;Male;Injections, Intraventricular;Stem Cells/*cytology/drug effects/metabolism;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Mice, Inbred Strains;Neuroglia/cytology/drug effects/metabolism;Neurons/*cytology/drug effects/metabolism;Cell Division/drug effects/*physiology;04 Adult neurogenesis factors;Fibroblast Growth Factor 2/pharmacology;Mice;Immunohistochemistry;C pdf;Rhombencephalon/*cytology/drug effects/metabolism;Up-Regulation/drug effects/physiology},
	Number = {6},
	Organization = {Department of Anatomy and Cell Biology, Faculty of Medicine, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada. djmartens\@sympatico.ca},
	Pages = {1045-57},
	Pubmed = {12383233},
	Title = {In vivo infusions of exogenous growth factors into the fourth ventricle of the adult mouse brain increase the proliferation of neural progenitors around the fourth ventricle and the central canal of the spinal cord},
	Uuid = {107B0C44-E370-4A89-9EA8-3B0B14EB88C3},
	Volume = {16},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12383233}}

@article{Martens:2000,
	Abstract = {The embryonic forebrain germinal zone contains two separate and additive populations of epidermal growth factor (EGF)- and fibroblast growth factor (FGF)-responsive stem cells that both exhibit self-renewal and multipotentiality. Although cumulative S phase labeling studies have investigated the proliferation kinetics of the overall population of precursor cells within the forebrain germinal zone through brain development, little is known about when and how (symmetrically or asymmetrically) the small subpopulations of stem cells are proliferating in vivo. This has been determined by injecting timed-pregnant mice with high doses of tritiated thymidine ((3)H-thy) to kill any stem cells proliferating within the striatal germinal zone in vivo and then by assaying for neurosphere formation in vitro. Injections of 0.8 mCi of (3)H-thy given every 2 hr for 12 hr to timed-pregnant mice at E11, E14, and E17 resulted in significant depletions in the number of neurospheres generated by FGF-responsive stem cells at E11 and by EGF-responsive and FGF-responsive stem cells at E14 and E17. With increasing embryonic age, the depletions observed in the number of neurospheres generated in vitro in response to FGF2 after exposure to (3)H-thy in vivo decreased, suggesting there is an increase in the length of the cell cycle of FGF-responsive neural stem cells through embryonic development. The results suggest that the FGF-responsive stem cell population expands between E11 and E14 by dividing symmetrically, but switches to primarily asymmetric division between E14 and E17. The EGF-responsive stem cells arise after E11, and their population expands through symmetric divisions and through asymmetric divisions of FGF-responsive stem cells. 20115704 1529-2401 Journal Article},
	Author = {Martens, D. J. and Tropepe, V. and van Der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {J Neurosci},
	Keywords = {Prosencephalon/*embryology;Drug Administration Schedule;Neurons/*cytology/metabolism;Embryo/cytology/metabolism;Stem Cells/*cytology/metabolism;Epidermal Growth Factor/*pharmacology;Animal;Cell Count;Kinetics;Corpus Striatum/embryology;Fibroblast Growth Factors/*pharmacology;DNA/metabolism;Cell Division/drug effects/physiology;Thymidine/administration &dosage/metabolism;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Mice;Injections;C-18},
	Number = {3},
	Organization = {University of Toronto, Department of Anatomy and Cell Biology, Toronto, Ontario M5S 1A8, Canada. david.martens\@utoronto.ca},
	Pages = {1085-95},
	Pubmed = {10648714},
	Title = {Separate proliferation kinetics of fibroblast growth factor-responsive and epidermal growth factor-responsive neural stem cells within the embryonic forebrain germinal zone},
	Uuid = {87E9034E-01B1-4B29-8BA5-954DA67FD3E5},
	Volume = {20},
	Year = {2000},
	url = {papers/Martens_JNeurosci2000.pdf}}

@article{Martin:2001,

@article{Martinez-Marcos:2005,
	Abstract = {The location of neurogenesis and the direction of migration of neurons in the adult mouse vomeronasal organ is controversial. Cell division occurs at the center, and particularly, at the edges of the epithelium. Newly generated cells at the center of the epithelium participate in neurogenesis, however, it is unknown to what extent dividing cells at the edges participate in growth, become apoptotic or mature into neurons. Premitotic cells were labeled with bromodeoxyuridine (BrdU) in adult mice and animals allowed to survive for different postinjection periods. The terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end-labeling (TUNEL) method was used to show the distribution of apoptotic cells. The vertical and horizontal position of BrdU-labeled cells was analyzed as a function of postinjection survival time. Vertical and horizontal migration of BrdU-labeled cells were detected. Cells in the central portions of the epithelium migrated vertically to become neurons as demonstrated by co-expression of olfactory marker protein. Cells at the edges migrated horizontally very slowly (less than 10\%of the distance from the edge to the center of the epithelium per month), thus indicating that these cells participate in cell renewal exclusively in marginal regions. Neural turnover in the mouse vomeronasal epithelium, therefore appears to occur through a process of vertical migration. Data on the distribution of apoptotic cells indicate that a number of dividing cells throughout the epithelium, but particularly at the edges, die before becoming functional neurons. Accordingly, most dividing cells at the edges probably constitute a reservoir of stem cells dying before differentiation. (c) 2005 Wiley Periodicals, Inc. J Neurobiol, 2005.},
	Author = {Martinez-Marcos, and Jia, and Quan, and Halpern,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0213640},
	Organization = {Departamento de Ciencias M{\'e}dicas, Facultad de Medicina, Centro Regional de Investigaci{\'o}n Biom{\'e}dica, Universidad de Castillala Mancha, Avda. Almansa S/N, 02006 Albacete, Spain.},
	Pubmed = {15729685},
	Title = {Neurogenesis, migration, and apoptosis in the vomeronasal epithelium of adult mice},
	Uuid = {A3849F76-97AC-46FB-BA62-6E106AB8D53A},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.20128}}

@article{Martin:2001a,
	Abstract = {Human immunodeficiency virus type 1 (HIV-1) infects and induces syncytium formation in microglial cells from the central nervous system (CNS). A primary isolate (HIV-1(BORI)) was sequentially passaged in cultured microglia, and the isolate recovered (HIV-1(BORI-15)) showed high levels of fusion and replicated more efficiently in microglia (J. M. Strizki, A. V. Albright, H. Sheng, M. O'Connor, L. Perrin, and F. Gonz{\'a}lez-Scarano, J. Virol. 70:7654-7662, 1996). The parent and adapted viruses used CCR5 as coreceptor. Recombinant viruses demonstrated that the syncytium-inducing phenotype was associated with four amino acid differences in the V1/V2 region of the viral gp120 (J. T. C. Shieh, J. Martin, G. Baltuch, M. H. Malim, and F. Gonz{\'a}lez-Scarano, J. Virol. 74:693-701, 2000). We produced luciferase-reporter, env-pseudotyped viruses using plasmids containing env sequences from HIV-1(BORI), HIV-1(BORI-15), and the V1/V2 region of HIV-1(BORI-15) in the context of HIV-1(BORI) env (named rBORI, rB15, and rV1V2, respectively). The pseudotypes were used to infect cells expressing various amounts of CD4 and CCR5 on the surface. In contrast to the parent recombinant, the rB15 and rV1V2 pseudotypes retained their infectability in cells expressing low levels of CD4 independent of the levels of CCR5, and they infected cells expressing CD4 with a chimeric coreceptor containing the third extracellular loop of CCR2b in the context of CCR5 or a CCR5 Delta4 amino-terminal deletion mutant. The VH-rB15 and VH-rV1V2 recombinant viruses were more sensitive to neutralization by a panel of HIV-positive sera than was VH-rBORI. Interestingly, the CD4-induced 17b epitope on gp120 was more accessible in the rB15 and rV1V2 pseudotypes than in rBORI, even before CD4 binding, and concomitantly, the rB15 and rV1V2 pseudotypes were more sensitive to neutralization with the human 17b monoclonal antibody. Adaptation to growth in microglia--cells that have reduced expression of CD4 in comparison with other cell types--appears to be associated with changes in gp120 that modify its ability to utilize CD4 and CCR5. Changes in the availability of the 17b epitope indicate that these affect conformation. These results imply that the process of adaptation to certain tissue types such as the CNS directly affects the interaction of HIV-1 envelope glycoproteins with cell surface components and with humoral immune responses.},
	Author = {Mart{\'\i}n, J. and LaBranche, C. C. and Gonz{\'a}lez-Scarano, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Immune Sera;HIV-1;Adaptation, Biological;Cells, Cultured;Humans;Transfection;Brain;Microglia;HIV Antibodies;Serial Passage;Antigens, CD4;11 Glia;Cell Line;Research Support, U.S. Gov't, P.H.S.;Sequence Deletion;Chimeric Proteins;Antibodies, Monoclonal;Receptors, Chemokine;Epitopes;Neutralization Tests;Receptors, CCR5;Enzyme-Linked Immunosorbent Assay;Genes, Reporter;HIV Envelope Protein gp120;Luciferases},
	Medline = {21165267},
	Month = {4},
	Nlm_Id = {0113724},
	Number = {8},
	Organization = {Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.},
	Pages = {3568-80},
	Pubmed = {11264346},
	Title = {Differential CD4/CCR5 utilization, gp120 conformation, and neutralization sensitivity between envelopes from a microglia-adapted human immunodeficiency virus type 1 and its parental isolate},
	Uuid = {9F7628F0-2472-4F89-8263-7987F5A6F2F6},
	Volume = {75},
	Year = {2001},
	url = {papers/Martín_JVirol2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.75.8.3568-3580.2001}}

@article{Martin-Garcia:2006,
	Abstract = {We previously described envelope glycoproteins of an HIV-1 isolate adapted in vitro for growth in microglia that acquired a highly fusogenic phenotype and lower CD4 dependence, as well as resistance to inhibition by anti-CD4 antibodies. Here, we investigated whether similar phenotypic changes are present in vivo. Envelope clones from the brain and spleen of an HIV-1-infected individual with neurological disease were amplified, cloned, and sequenced. Phylogenetic analysis demonstrated clustering of sequences according to the tissue of origin, as expected. Functional clones were then used in cell-to-cell fusion assays to test for CD4 and co-receptor utilization and for sensitivity to various antibodies and inhibitors. Both brain- and spleen-derived envelope clones mediated fusion in cells expressing both CD4 and CCR5 and brain envelopes also used CCR3 as co-receptor. We found that the brain envelopes had a lower CD4 dependence, since they efficiently mediated fusion in the presence of low levels of CD4 on the target cell membrane, and they were significantly more resistant to blocking by anti-CD4 antibodies than the spleen-derived envelopes. In contrast, we observed no difference in sensitivity to the CCR5 antagonist TAK-779. However, brain-derived envelopes were significantly more resistant than those from spleen to the fusion inhibitor T-1249 and concurrently showed slightly greater fusogenicity. Our results suggest an increased affinity for CD4 of brain-derived envelopes that may have originated from in vivo adaptation to replication in microglial cells. Interestingly, we note the presence of envelopes more resistant to a fusion inhibitor in the brain of an untreated, HIV-1-infected individual.},
	Author = {Mart{\'\i}n-Garc{\'\i}a, Julio and Cao, Wei and Varela-Rohena, Angel and Plassmeyer, Matthew L. and Gonz{\'a}lez-Scarano, Francisco},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {HIV Fusion Inhibitors;Receptors, HIV;HIV Infections;Molecular Sequence Data;HIV-1;Membrane Fusion;AIDS Dementia Complex;HIV Envelope Protein gp41;Research Support, N.I.H., Extramural;Amino Acid Sequence;Antigens, CD4;11 Glia;Humans;Brain;Spleen;Drug Resistance, Viral;HIV Envelope Protein gp120},
	Month = {3},
	Nlm_Id = {0110674},
	Number = {1},
	Organization = {Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. julio.martin-garcia\@drexelmed.edu},
	Pages = {169-79},
	Pii = {S0042-6822(05)00726-9},
	Pubmed = {16309726},
	Title = {HIV-1 tropism for the central nervous system: Brain-derived envelope glycoproteins with lower CD4 dependence and reduced sensitivity to a fusion inhibitor},
	Uuid = {6BEF24CF-6A1E-4CFB-8FA2-DCF80FE7AA86},
	Volume = {346},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.virol.2005.10.031}}

@article{Martinez-Cerdeno:2006,
	Abstract = {The vertebrate cerebral cortex varies from the 3-layered dorsal cortex of reptiles to the 6-layered lissencephalic cortex characteristic of rodents and to the 6-layered gyrencephalic cortex typical of carnivores and primates. Distinct developmental mechanisms may have evolved independently to account for the radial expansion that produced the multilayered cortex of mammals and for the tangential expansion of cortical surface area that resulted in gyrencephalic cortex. Recent evidence shows that during the late stages of cortical development, radial glial cells divide asymmetrically in the ventricular zone to generate radial glial cells and intermediate progenitor (IP) cells and that IP cells subsequently divide symmetrically in the subventricular zone to produce multiple neurons. We propose that the evolution of this two-step pattern of neurogenesis played an important role in the amplification of cell numbers underlying the radial and tangential expansion of the cerebral cortex.},
	Author = {Mart{\'\i}nez-Cerde\~{n}o, Ver{\'o}nica and Noctor, Stephen C. and Kriegstein, Arnold R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {9110718},
	Number = {Suppl 1},
	Organization = {Department of Neurology and the Institute for Stem Cell and Tissue Biology, University of California-San Francisco, San Francisco, CA 94143, USA.},
	Pages = {i152-i161},
	Pii = {16/suppl_1/i152},
	Pubmed = {16766701},
	Title = {The role of intermediate progenitor cells in the evolutionary expansion of the cerebral cortex},
	Uuid = {57B58582-BADF-4786-81A4-0B48D42B7ED1},
	Volume = {16},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhk017}}

@article{Martinez-Contreras:2002,
	Abstract = {Recent studies confirm that astrocytes and neurons are associated with the synaptic transmission, particularly with the regulation of glutamate (Glu) levels. Therefore, they have the capacity to modulate the Glu released from neurons into the extracellular space. It has also been demonstrated an intense astrocytic and microglia response to physical or chemical lesions of the central nervous system. However, the persistence of the response of the glial cells in adult brain had not been previously reported, after the excitotoxic damage caused by neonatal dosage of monosodium glutamate (MSG) to newborn rats. In this study, 4 mg/g body weight of MSG were administered to newborn rats at 1, 3, 5, and 7 days after birth, at the age of 60 days the astrocytes and the microglia cells were analyzed with immunohistochemical methods in the fronto-parietal cortex. Double labeling to glial fibrillary acidic protein (GFAP) and BrdU, or isolectin-B(4) and BrdU identified astrocytes or microglia cells that proliferated; immunoblotting and immunoreactivity to vimentin served for assess immaturity of astrocytic intermediate filaments. The results show that the neonatal administration of MSG-induced reactivity of astrocytes and microglia cells in the fronto-parietal cortex, which was characterized by hyperplasia; an increased number of astrocytes and microglia cells that proliferated, hypertrophy; increased complexity of the cytoplasm extension of both glial cells and expression of RNAm to vimentin, with the presence of vimentin-positive astrocytes. This glial response to neuroexcitotoxic stimulus of Glu on the immature brain, which persisted to adulthood, suggests that the neurotransmitter Glu could trigger neuro-degenerative illnesses.},
	Author = {Mart{\'\i}nez-Contreras, A. and Huerta, M. and Lopez-Perez, S. and Garc{\'\i}a-Estrada, J. and Luqu{\'\i}n, S. and Beas Z{\'a}rate, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Research Support, Non-U.S. Gov't;Neurotoxins;Astrocytes;Animals;Aging;Rats;Fluorescent Antibody Technique;Glutamic Acid;Synaptic Transmission;Microglia;Female;Vimentin;Rats, Wistar;Disease Models, Animal;Male;Animals, Newborn;Cerebral Cortex;Gliosis;Neurodegenerative Diseases;Cell Division;24 Pubmed search results 2008;Stem Cells;Bromodeoxyuridine;Lectins;Glial Fibrillary Acidic Protein},
	Medline = {21642404},
	Month = {1},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Lab de Neuroqu{\'\i}mica, Div de Neurociencias, C.I.B.O., Guadalajara Jal., Mexico.},
	Pages = {200-10},
	Pii = {10.1002/jnr.10093},
	Pubmed = {11782964},
	Title = {Astrocytic and microglia cells reactivity induced by neonatal administration of glutamate in cerebral cortex of the adult rats},
	Uuid = {3944E797-5B2A-42E6-84CF-994951B8224E},
	Volume = {67},
	Year = {2002}}

@article{Masahira:2006,
	Abstract = {Motoneurons and oligodendrocytes in the embryonic spinal cord are produced from a restricted domain of the ventral ventricular zone, termed the pMN domain. The pMN domain is the site of expression of two basic helix-loop-helix transcription factors, Olig1 and Olig2, which are essential for motoneuron and oligodendrocyte development. Previous lineage-tracing experiments using Olig1-Cre and Olig2-GFP mice suggested that motoneurons and oligodendrocytes, but not astrocytes, are produced from the pMN domain. However, important questions remain, including the fate of neuroepithelial cells in the pMN domain, and specifically whether motoneurons and oligodendrocytes are the only types of cells produced in the pMN domain. We performed lineage-tracing experiments using a tamoxifen-inducible Cre-recombinase inserted into the Olig2 locus. We demonstrated that motoneurons and oligodendrocyte progenitors are derived from the Olig2(+) progenitors in the pMN domain, and also found that a subset of astrocytes at the ventral surface of the spinal cord and ependymal cells at the ventricular surface are also produced from the pMN domain. These findings demonstrate that motoneurons and oligodendrocytes are not the only cell types originating from this domain.},
	Author = {Masahira, and Takebayashi, and Ono, and Watanabe, and Ding, and Furusho, and Ogawa, and Nabeshima, and Alvarez-Buylla, and Shimizu, and Ikenaka,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {0372762},
	Organization = {Division of Neurobiology and Bioinformatics, National Institute for Physiological Sciences, 5-1 Higashiyama, Myodaiji, Okazaki 444-8787, Japan; Department of Neurosurgery, Kochi Medical School, Nankoku 783-8505, Japan.},
	Pii = {S0012-1606(06)00126-6},
	Pubmed = {16581057},
	Title = {Olig2-positive progenitors in the embryonic spinal cord give rise not only to motoneurons and oligodendrocytes, but also to a subset of astrocytes and ependymal cells},
	Uuid = {BD702F19-08AE-461D-B96C-6BEA64DA9FDB},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2006.02.029}}

@article{Maslov:2004,
	Abstract = {The mammalian brain contains neural stem cells (NSCs) that allow continued neurogenesis throughout the life of the animal. However, neurogenesis is known to decline during aging and, to the extent that neurogenesis is required for normal CNS function, this may contribute to neurodegenerative disease. Decreased neurogenesis could result from loss of NSCs or dysfunction at some later step, and distinguishing these possibilities is important for understanding the cause of the decline. However, because of the inability to distinguish NSCs from their rapidly dividing progeny in situ, it has not been possible to quantitatively assess the NSC populations in young and old animals. In this report we show that the G1 phase-specific expression of the replication factor Mcm2 is a useful marker for detecting slowly cycling putative NSCs in situ and confirm the identity of these cells using both cytosine beta-D-arabinofuranoside (Ara-C) treatment and a double nucleoside analog-labeling technique. The ability to distinguish NSCs from proliferative progenitors has allowed characterization of the expression of several markers including Nestin, Musashi, and GFAP in these different cell types. Furthermore, comparison of the NSC populations in the subventricular zones of young (2-4 months) and old (24-26 months) mice demonstrates an approximately twofold reduction in the older mice. A similar twofold reduction is also observed in the number of neurospheres recovered in culture from old relative to young animals. The reduction in the neural stem cell population documented here is sufficient to account for the reduced level of neurogenesis in old animals. 1529-2401 Journal Article},
	Author = {Maslov, A. Y. and Barone, T. A. and Plunkett, R. J. and Pruitt, S. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Journal = {J Neurosci},
	Keywords = {B pdf;02 Adult neurogenesis migration},
	Number = {7},
	Organization = {Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.},
	Pages = {1726-33},
	Title = {Neural stem cell detection, characterization, and age-related changes in the subventricular zone of mice},
	Uuid = {9486AD80-D4D3-4A47-B89D-9E3572EA82AE},
	Volume = {24},
	Year = {2004},
	url = {papers/Maslov_JNeurosci2004.pdf}}

@article{Maslov:2007,
	Abstract = {Previous studies have demonstrated expression of the minichromosome maintenance protein Mcm2 in cells that remain competent to divide, including stem/progenitor cells of the subventricular zone (SVZ) within the brain. Here, a transgenic mouse line in which the Mcm2 gene drives expression of enhanced green fluorescent protein (EGFP) was constructed by insertion of an internal ribosomal entry site (IRES)-EGFP cassette into the last exon of the gene, 3' to the stop codon. In these mice, expression of EGFP is observed in the SVZ and several other tissues with high proliferative activity, including the spleen, intestine, hair follicles, and bone marrow. These observations suggest that EGFP fluorescence in this mouse line provides an index of the proliferative capacity of different tissues. Immunohistological analysis demonstrates a direct concordance between expression of EGFP and Mcm2, consistent with a transcriptional level downregulation of Mcm2 expression in postmitotic cells. To test the utility of EGFP expression for recovery of live cells retaining the capacity to divide, EGFP-expressing and -nonexpressing cells from bone marrow and brain were isolated from an adult Mcm2(IRES-EGFP) mouse by fluorescence-activated cell sorting and assayed for clonal growth. The EGFP-positive fraction contained the entire clonogenic population of the bone marrow and greater than 90\%of neurosphere-forming cells from the brain. Brain-derived clonogenic cells were shown to remain competent to differentiate towards all three neural lineages. These studies demonstrate that the Mcm2(IRES-EGFP) transgenic line constructed here can be used for recovery of proliferation competent cells from different tissue types.},
	Author = {Maslov, Alexander Y. and Bailey, Kimberly J. and Mielnicki, Lawrence M. and Freeland, Amy L. and Sun, Xiaolei and Burhans, William C. and Pruitt, Steven C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {9304532},
	Number = {1},
	Organization = {Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, New York, New York 14263, USA. steven.pruitt\@roswellpark.org.},
	Pages = {132-8},
	Pii = {2006-0032},
	Pubmed = {17008428},
	Title = {Stem/Progenitor cell-specific enhanced green fluorescent protein expression driven by the endogenous mcm2 promoter},
	Uuid = {50C3CA8B-6A51-4A8A-A535-89C22D2DB78D},
	Volume = {25},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1634/stemcells.2006-0032}}

@article{Massague:2000,
	Author = {Massague, J. and Blain, S. W. and Lo, R. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Cell},
	Keywords = {Models, Biological;Neoplasms/etiology;Hereditary Diseases/etiology;Human;Cell Division/genetics;C-15;Signal Transduction/*genetics;Transforming Growth Factor beta/*metabolism;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Cell Differentiation/genetics},
	Number = {2},
	Organization = {Cell Biology Program, Howard Hughes Medical Institute, Memorial Sloan- Kettering Cancer Center, New York, New York 10021, USA. j- massague\@ski.mskcc.org},
	Pages = {295-309.},
	Title = {TGFbeta signaling in growth control, cancer, and heritable disorders},
	Uuid = {60143CA6-F0DE-4ADB-B81D-C542065B2BA5},
	Volume = {103},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11057902}}

@article{Massengale:2005,
	Abstract = {Several studies have reported that bone marrow (BM) cells may give rise to neurons and astrocytes in vitro and in vivo. To further test this hypothesis, we analyzed for incorporation of neural cell types expressing donor markers in normal or injured brains of irradiated mice reconstituted with whole BM or single, purified c-kit(+)Thy1.1(lo)Lin(-)Sca-1(+) (KTLS) hematopoietic stem cells (HSCs), and of unirradiated parabionts with surgically anastomosed vasculature. Each model showed low-level parenchymal engraftment of donor-marker(+) cells with 96-100\%immunoreactivity for panhematopoietic (CD45) or microglial (Iba1 or Mac1) lineage markers in all cases studied. Other than one arborizing structure in the olfactory bulb of one BM-transplanted animal, possibly representing a neuronal or glial cell process, we found no donor-marker-expressing astrocytes or non-Purkinje neurons among >10,000 donor-marker(+) cells from 21 animals. These data strongly suggest that HSCs and their progeny maintain lineage fidelity in the brain and do not adopt neural cell fates with any measurable frequency.},
	Author = {Massengale, Mei and Wagers, Amy J. and Vogel, Hannes and Weissman, Irving L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-1007},
	Journal = {J Exp Med},
	Keywords = {08 Aberrant cell cycle;22 Stem cells},
	Month = {5},
	Nlm_Id = {2985109R},
	Number = {10},
	Organization = {Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305.},
	Pages = {1579-89},
	Pii = {jem.20050030},
	Pubmed = {15897275},
	Title = {Hematopoietic cells maintain hematopoietic fates upon entering the brain},
	Uuid = {BFCE77E0-DB37-4096-8A56-49C3D9776C2D},
	Volume = {201},
	Year = {2005},
	url = {papers/Massengale_JExpMed2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1084/jem.20050030}}

@article{Masuda-Nakagawa:1994,
	Abstract = {The principal aim of the present experiments has been to analyze the properties of microglial cells and their role in nerve regeneration. In the leech, damage to the CNS has been shown to be followed by accumulation of laminin and microglial cells at the site of injury (Masuda-Nakagawa et al., 1990. Proc. R. Soc. Lond. B. 241:201-206; and 1993. Proc. Natl. Acad. Sci. USA 90:4966-4970). Procedures were devised for isolating these small, wandering cells from the CNS of the leech. In culture, they were reliably identified by their sizes, shapes, and phagocytotic activity. Their morphology, motility, and interactions with neurons were influenced by the substrate molecules on which they were plated. On the plant lectin concanavalin A (Con A) microglia had a rounded shape and remained stationary. By contrast on extracts of leech extracellular matrix (ECM) enriched with laminin the cells were mobile and spindle-shaped with long processes. On Con A, neuronal growth cones avoided microglial cells, whereas on ECM extract the presence of a microglial cell did not influence neurite growth. Microglial cells showed immunoreactivity on both substrates when stained with a monoclonal antibody against leech laminin. Together these results suggest that microglial cells are influenced in their properties by molecules in the environment and that they could contribute to neuronal outgrowth at the site of an injury.},
	Author = {Masuda-Nakagawa, L. M. and Walz, A. and Brodbeck, D. and Neely, M. D. and Grumbacher-Reinert, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:27 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Microscopy, Electron, Scanning;Phagocytosis;Animals;Cells, Cultured;Microglia;Axons;Neurites;Leeches;Not relevant;11 Glia;Laminin;Concanavalin A;Extracellular Matrix;Support, Non-U.S. Gov't;Antibodies, Monoclonal;Neurons;Freeze Drying;24 Pubmed search results 2008;Immunohistochemistry;Culture Media;Research Support, Non-U.S. Gov't},
	Medline = {94157532},
	Month = {1},
	Nlm_Id = {0213640},
	Number = {1},
	Organization = {Department of Pharmacology, Universit{\"a}t Basel, Switzerland.},
	Pages = {83-91},
	Pubmed = {8113785},
	Title = {Substrate-dependent interactions of leech microglial cells and neurons in culture},
	Uuid = {B3F0B75C-A48A-4C51-9AD4-6A2CAD78E05A},
	Volume = {25},
	Year = {1994},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.480250108}}

@article{Mato:1996,
	Abstract = {The transport of solutes between blood and brain is regulated by a specific barrier. Capillary endothelial cells of brain are known to mediate barrier function and facilitate transport. Here we report that specific cells surrounding arterioles, known as Mato's fluorescent granular perithelial (FGP) cells or perivascular microglial cells, contribute to the barrier function. Immunohistochemical and in situ hybridization studies indicate that, in normal brain cortex, type I and type II macrophage scavenger receptors are expressed only in FGP/perivascular microglial cells, and surface markers of macrophage lineage are also detected on them. These cells mediate the uptake of macromolecules, including modified low density lipoprotein, horseradish peroxidase, and ferritin injected either into the blood or into the cerebral ventricles. Accumulation of scavenged materials with aging or after the administration of a high-fat diet results in the formation of honeycomb-like foam cells and the narrowing of the lumen of arterioles in the brain cortex. These results indicate involvement of FGP/perivascular microglial cells in the barrier and scavenger functions in the central nervous system.},
	Author = {Mato, M. and Ookawara, S. and Sakamoto, A. and Aikawa, E. and Ogawa, T. and Mitsuhashi, U. and Masuzawa, T. and Suzuki, H. and Honda, M. and Yazaki, Y. and Watanabe, E. and Luoma, J. and Yla-Herttuala, S. and Fraser, I. and Gordon, S. and Kodama, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Human;Ferritin;Animals;Biological Transport, Active;In Vitro;Macrophages;Aging;Rats;Receptors, Cell Surface;Microglia;Rats, Wistar;Not relevant;Vitamin E Deficiency;Lipoproteins, LDL;Blood-Brain Barrier;Aged;11 Glia;Arterioles;Male;Cerebral Cortex;Horseradish Peroxidase;Adult;Mice;Immunohistochemistry;Microscopy, Electron;Dietary Fats},
	Medline = {96194956},
	Month = {4},
	Nlm_Id = {7505876},
	Number = {8},
	Organization = {Department of Anatomy, Jichi Medical School, Tochigi, Japan.},
	Pages = {3269-74},
	Pubmed = {8622926},
	Title = {Involvement of specific macrophage-lineage cells surrounding arterioles in barrier and scavenger function in brain cortex},
	Uuid = {6888F5A0-E029-49F3-B833-669E78A95FB1},
	Volume = {93},
	Year = {1996}}

@article{Matsuda:2008,
	Abstract = {Microglia are believed to play an important role in the regulation of phagocytosis, neuronal survival, neuronal cell death, and inflammation. Recent studies have demonstrated that microglia are multipotential stem cells that give rise to neurons, astrocytes, and oligodendrocytes. However, the functional properties of neurons derived from microglia are poorly understood. In this study, we investigated the possibility that microglia differentiate into functional neurons. Immunocytochemical study demonstrated that microtubule-associated protein 2 (MAP2)-positive cells were derived from microglia under differentiation conditions. Intracellular Ca(2+) imaging study demonstrated that KCl caused no significant changes in [Ca(2+)](i) in microglia, whereas it caused a remarkable increase in [Ca(2+)](i) in microglia-derived cells. Furthermore, electrophysiological study demonstrated that the spike waveform, firing rate, and tetrodotoxin sensitivity of extracellular action potentials evoked by 4-aminopyridine from microglia-derived MAP2-positive cells were nearly identical to those from cultured cortical neurons. These results suggest that microglia-derived MAP2-positive cells possess properties of functional neurons.},
	Author = {Matsuda, and Niidome, and Nonaka, and Goto, and Fujimura, and Kato, and Nakanishi, and Akaike, and Kihara, and Sugimoto,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1090-2104},
	Journal = {Biochem Biophys Res Commun},
	Keywords = {01 Adult neurogenesis general;10 Development;08 Aberrant cell cycle;11 Glia;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0372516},
	Organization = {Department of Neuroscience for Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, Yoshida-Shimoadachi-cho, Sakyo-ku, Kyoto 606-8501, Japan.},
	Pii = {S0006-291X(08)00270-2},
	Pubmed = {18284917},
	Title = {Microtubule-associated protein 2-positive cells derived from microglia possess properties of functional neurons},
	Uuid = {121A8EEF-A3DC-4ABE-990C-830DA8BEABE8},
	Year = {2008},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.bbrc.2008.02.038}}

@article{Matsuda:2007,
	Abstract = {In vivo electroporation is a powerful technique for the introduction of genes into organisms. Temporal and spatial regulation of expression of introduced genes, or of RNAi, would further enhance the utility of this method. Here we demonstrate conditional regulation of gene expression from electroporated plasmids in the postnatal rat retina and the embryonic mouse brain. For temporal regulation, Cre/loxP-mediated inducible expression vectors were used in combination with a vector expressing a conditionally active form of Cre recombinase, which is activated by 4-hydroxytamoxifen. Onset of gene expression was regulated by the timing of 4-hydroxytamoxifen administration. For spatial regulation, transgenes were expressed by using promoters specific for rod photoreceptors, bipolar cells, amacrine cells, M{\"u}ller glia or progenitor cells. Combinations of these constructs will facilitate a variety of experiments, including cell-type-specific gene misexpression, conditional RNAi, and fate mapping of progenitor and precursor cells.},
	Author = {Matsuda, Takahiko and Cepko, Constance L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {7505876},
	Number = {3},
	Organization = {Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.},
	Pages = {1027-32},
	Pii = {0610155104},
	Pubmed = {17209010},
	Title = {Controlled expression of transgenes introduced by in vivo electroporation},
	Uuid = {CCB8B11B-E842-429E-868F-D312B7143B35},
	Volume = {104},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0610155104}}

@article{Matsugami:2006,
	Abstract = {Previous in vitro studies have shown that the neurotransmitter glutamate is important in brain development. Paradoxically, loss-of-function mouse models of glutamatergic signaling that are generated by genetic deletion of glutamate receptors or glutamate release show normal brain assembly. We examined the direct consequences on brain development of extracellular glutamate buildup due to the depletion of the glutamate transporters GLAST and GLT1. GLAST/GLT1 double knockout mice show multiple brain defects, including cortical, hippocampal, and olfactory bulb disorganization with perinatal mortality. Here, we report abnormal formation of the neocortex in GLAST/GLT1 mutants. Several essential aspects of neuronal development, such as stem cell proliferation, radial migration, neuronal differentiation, and survival of SP neurons, were impaired. These results provide direct in vivo evidence that GLAST and GLT1 are necessary for brain development through regulation of extracellular glutamate concentration and show that an important mechanism is likely to be maintenance of glutamate-mediated synaptic transmission.},
	Author = {Matsugami, Toshiko R. and Tanemura, Kentaro and Mieda, Michihiro and Nakatomi, Reiko and Yamada, Keiko and Kondo, Takashi and Ogawa, Masaharu and Obata, Kunihiko and Watanabe, Masahiko and Hashikawa, Tsutomu and Tanaka, Kohichi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Neurons;Excitatory Amino Acid Transporter 1;Mutation;Dendrites;Mice, Knockout;24 Pubmed search results 2008;Heterozygote;Gene Deletion;research support, non-u.s. gov't ;Excitatory Amino Acid Transporter 2;Mice, Transgenic;Animals;Brain;Cerebral Cortex;Glutamic Acid;Mice},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {32},
	Organization = {Laboratory of Molecular Neuroscience, School of Biomedical Science and Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.},
	Pages = {12161-6},
	Pii = {0509144103},
	Pubmed = {16880397},
	Title = {From the Cover: Indispensability of the glutamate transporters GLAST and GLT1 to brain development},
	Uuid = {56869094-BB45-4CEE-8146-0F1F9973CC81},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0509144103}}

@article{Matsumoto:2007,
	Abstract = {There is increasing evidence that heparan sulfate (HS) plays an essential role in various axon guidance processes. These observations, however, have not addressed whether HS is required cell autonomously as an axonal coreceptor or as an environmental factor that modulates the localization of guidance molecules in the terrain in which growing axons navigate. Here we demonstrate that netrin-1-mediated commissural axon guidance requires cell-autonomous expression of HS in commissural neurons in vivo. We used the Wnt1-Cre transgene to drive region-specific ablation of Ext1, which encodes an enzyme essential for HS synthesis, in the dorsal part of the spinal cord. Remarkably, Wnt1-Cre-mediated ablation of Ext1 causes commissural axon pathfinding defects that share similarities with those of Netrin-1-deficient and DCC (deleted in colorectal cancer)-deficient mice. Neither Ext1-deficient dorsal spinal cord explants nor wild-type explants in which HS expression was ablated could extend axons in response to netrin-1. Intracellular signaling downstream of netrin-1 and DCC was defective in Ext1-deficient commissural neurons and in DCC-transfected HEK293T cells from which HS was removed. These results demonstrate that the expression of HS by commissural neurons is essential for these neurons to transduce netrin-1 signals, thus providing evidence for a cell-autonomous role of HS in netrin-1/DCC-mediated axon guidance.},
	Author = {Matsumoto, Yoshihiro and Irie, Fumitoshi and Inatani, Masaru and Tessier-Lavigne, Marc and Yamaguchi, Yu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {16},
	Organization = {Developmental Neurobiology Program, Burnham Institute for Medical Research, La Jolla, California 92037, USA.},
	Pages = {4342-50},
	Pii = {27/16/4342},
	Pubmed = {17442818},
	Title = {Netrin-1/DCC signaling in commissural axon guidance requires cell-autonomous expression of heparan sulfate},
	Uuid = {BCBF83D2-223A-4D71-8C87-5C20320F8347},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0700-07.2007}}

@article{Matsumura:2001,
	Abstract = {Phosphorylation of regulatory light chain (RMLC) of myosin II at Ser19/Thr18 is likely to play important roles in controlling the morphological changes seen during cell division of cultured mammalian cells. Phosphorylation of RMLC regulates the activity of myosin II, an essntial motor for cytokinesis, and phosphorylation of RMLC shows dramatic changes during mitosis. Two exzymes, myosin phosphatase and kinase, control phosphorvlation of RMLC. Myosin phosphatase is activated during mitosis, apparently as a result of mitosis-specific phosphorylation of the myosin phosphatase targeting subunit (MYPT). This activation of myosin phosphatase is likely to result in RMLC dephosphorylation, causing the disassemly of stress fibers and focal adhesions during prophase. The phosphorylation of MYPT is lost in cyotokinesis, which would decrease myosin phosphatase activity. At the same time, ROCK (Rho-kinase) probably phosphorylates MYPT at its inhibitory sites, further decreasing the activity of myosin phosphatase. These changes in MYPT phosphorylation would raise RMLC phosphorylation, leading to the activation of myosin II for cyotokinesis. RMLC phosphorylation is also regulated by several RMLC kinases including ROCK (Rho-kinase), MLCK and citron kinase, all of which are localized at cleavage furrows. Future studies should examine whether these multiple kinases are redundant or whether they control distinct aspects of cell division. 21939132 0386-7196 Journal Article Review Review, Tutorial},
	Author = {Matsumura, F. and Totsukawa, G. and Yamakita, Y. and Yamashiro, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Cell Struct Funct},
	Keywords = {Immunohistochemistry;Myosin-Light-Chain Kinase/metabolism;CK;Phosphoprotein Phosphatase/metabolism;Myosin Light Chains/*metabolism;Animal;Cell Division/*physiology;Phosphorylation;05 Citron Kinase flathead;Protein-Serine-Threonine Kinases/metabolism},
	Number = {6},
	Organization = {Department of Molecular Biology &Biochemistry, Rutgers University, Piscataway, NJ 08855, USA. matsumura\@mbcl.rutgers.edu},
	Pages = {639-44},
	Title = {Role of myosin light chain phosphorylation in the regulation of cytokinesis},
	Uuid = {BF2B1080-1977-4F01-A3F8-A59ADD6A763F},
	Volume = {26},
	Year = {2001},
	url = {papers/Matsumura_CellStructFunct2001.pdf}}

@article{Matthaei:2007,
	Abstract = {Although genetic manipulations in mice have provided a powerful tool for investigating gene function in vivo, recent studies have uncovered a number of developmental phenomena that complicate the attribution of phenotype to the specific genetic change. A more realistic approach has been to modulate gene expression and function in a temporal and tissue-specific manner. The most common of these methods, the CreLoxP and tetracycline response systems, are surveyed here and their recently identified shortcomings discussed, along with a less well known system based on the E. coli lac operon and modified for use in mammals. The potential for further complications in interpretation due to hitherto unexpected epigenetic effects involving transfer of RNA or protein in oocytes or sperm is also explored. Given these problems we reiterate the necessity for the use of completely reversible methods that will allow each experimental group of animals to act as their own control. Using these methods with a number of specific modifications to eliminate non-specific effects from random insertion sites and inducer molecules, the full potential of genetic manipulation studies should be realized.},
	Author = {Matthaei, Klaus I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0022-3751},
	Journal = {J Physiol},
	Keywords = {Tissue Distribution;Animals;Trans-Activators;Aging;Tetracycline;review;Embryo, Mammalian;Integrases;Mice, Transgenic;Gene Deletion;Protein Synthesis Inhibitors;Animals, Newborn;Genetic Engineering;Epigenesis, Genetic;Escherichia coli;Lac Operon;Mice;24 Pubmed search results 2008;Gene Expression;Transgenes},
	Month = {7},
	Nlm_Id = {0266262},
	Number = {Pt 2},
	Organization = {Gene Targeting Laboratory, The John Curtin School of Medical Research, GPO Box 334, Canberra City, ACT 0200, Australia. klaus.matthaei\@anu.edu.au},
	Pages = {481-8},
	Pii = {jphysiol.2007.134908},
	Pmc = {PMC2075346},
	Pubmed = {17495035},
	Title = {Genetically manipulated mice: a powerful tool with unsuspected caveats},
	Uuid = {18D8B6EF-4F03-4B09-AD4B-440FD0913D0A},
	Volume = {582},
	Year = {2007},
	url = {papers/Matthaei_JPhysiol2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1113/jphysiol.2007.134908}}

@article{Mattia:1995,
	Abstract = {Application of the convulsant drug 4-aminopyridine (50 to 100 microM) induced spontaneous seizure-like discharges (duration = 76.3 +/- 46.8 sec, mean +/- SD; interval of occurrence = 225.2 +/- 87.9 sec) in slices of neocortex obtained from patients with a diagnosis of focal neuronal migration disorders during neurosurgical procedures for relief of drug-resistant seizures. Similar epileptiform discharges could also be elicited in these slices by single-shock stimuli delivered in the underlying white matter or within the gray matter. By contrast, neocortical slices obtained from patients suffering from temporal lobe epilepsy (which is characterized by Ammon's horn sclerosis but relatively normal neocortex) did not generate any epileptiform activity during 4-aminopyridine application. Thus, our study is the first to provide experimental evidence for the intrinsic epileptogenicity that characterizes neuronal migration disorders.},
	Author = {Mattia, D. and Olivier, A. and Avoli, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0028-3878},
	Journal = {Neurology},
	Keywords = {Epilepsies, Partial;Research Support, Non-U.S. Gov't;21 Neurophysiology;4-Aminopyridine;Action Potentials;Cells, Cultured;Humans;Cerebral Cortex;24 Pubmed search results 2008;21 Epilepsy},
	Medline = {95342419},
	Month = {7},
	Nlm_Id = {0401060},
	Number = {7},
	Organization = {Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, PQ, Canada.},
	Pages = {1391-5},
	Pubmed = {7617202},
	Title = {Seizure-like discharges recorded in human dysplastic neocortex maintained in vitro},
	Uuid = {15AAED9A-9C4A-46E2-8FD3-B26561EBF651},
	Volume = {45},
	Year = {1995}}

@article{Mattson:2004,
	Author = {Mattson, Mark P. and Taub, Dennis D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {15 ERVs retroelements;Pregnancy Proteins;Endogenous Retroviruses;Multiple Sclerosis;Cytokines;Encephalitis;Gene Products, env;Astrocytes;Reactive Oxygen Species;11 Glia;comment;15 Retrovirus mechanism;Humans;24 Pubmed search results 2008;Oxidative Stress;news},
	Month = {10},
	Nlm_Id = {9809671},
	Number = {10},
	Pages = {1021-3},
	Pii = {nn1004-1021},
	Pubmed = {15452568},
	Title = {Ancient viral protein enrages astrocytes in multiple sclerosis},
	Uuid = {E410D850-3650-4B2B-B169-10EFFF15EF48},
	Volume = {7},
	Year = {2004},
	url = {papers/Mattson_NatNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1004-1021}}

@article{Mattsson:1997,
	Abstract = {BACKGROUND AND PURPOSE: The purpose of this study was to evaluate whether grafting of fetal neocortical tissue 1 week after focal brain ischemia improved behavioral outcome and reduced secondary thalamic atrophy. METHODS: One week after distal ligation of the right middle cerebral artery in spontaneously hypertensive male rats, blocks of fetal neocortex (embryonic day 17) were homografted to rats housed in standard or enriched environments. Control infarcted nongrafted rats were housed in the enriched environment. Behavioral outcome was repeatedly tested until the rats were killed 20 weeks after the ligation. Ten days earlier, a mixture of 2\%Fluoro-Gold and 10\%biotinylated dextran amine was injected into the transplants for retrograde and anterograde tracing of graft-host connections. RESULTS: Grafted and nongrafted rats with enriched housing performed significantly better than grafted rats with standard housing on a rotating pole and a prehensile traction test. Grafted "enriched"rats were moreover significantly better than grafted "standard"rats and nongrafted enriched rats in a rotation test and a postural and locomotor tail position test. In the latter test, nongrafted enriched rats performed significantly better than grafted standard rats. The lesion-induced atrophy in posterior thalamus with its major sensorimotor cortex relay nuclei was significantly reduced in grafted enriched rats compared with nongrafted enriched rats. Afferent and efferent graft-host connections were identified in both grafted groups. Graft volumes did not differ. CONCLUSIONS: Neural grafting enhanced functional outcome and reduced thalamic atrophy only when combined with housing in enriched environments. 0039-2499 Journal Article},
	Author = {Mattsson, B. and Sorensen, J. C. and Zimmer, J. and Johansson, B. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Stroke},
	Keywords = {Fetus;17 Transplant Regeneration;Rats;L abstr;Housing, Animal;Cerebral Infarction/pathology/*physiopathology/*surgery;*Environment;Atrophy;Rats, Inbred SHR;Thalamus/*pathology;Animals;Support, Non-U.S. Gov't;Male;Cerebral Cortex/*transplantation;*Behavior, Animal},
	Number = {6},
	Organization = {Laboratory for Experimental Neurology, Wallenberg Neuroscience Center, Lund University Hospital, Sweden.},
	Pages = {1225-31; discussion 1231-2},
	Pubmed = {9183356},
	Title = {Neural grafting to experimental neocortical infarcts improves behavioral outcome and reduces thalamic atrophy in rats housed in enriched but not in standard environments},
	Uuid = {873928BF-EC80-11DA-8605-000D9346EC2A},
	Volume = {28},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9183356}}

@article{Matute-Bello:2004,
	Abstract = {To determine the time required to repopulate mouse lungs with donor alveolar macrophages following total body irradiation (TBI) and bone marrow transplantation (BMT), C57Bl/6 mice were subjected to TBI with 900 cGy, followed by transplantation of bone marrow cells from mice expressing green fluorescent protein (GFP) in their somatic cells. The mice were euthanized at either 30 (n=5), 60 (n=5) or 90 (n=5) days following BMT. Thirty days following transplantation, 87.8 +/- 3.9\%(mean +/- S.E.M.) circulating leukocytes in recipient mice were derived from the donor, as determined by fluorescence activated cell sorting (FACS) analysis for GFP. However, only 46.9 +/- 7.4\%of the resident alveolar cells expressed GFP, indicating incomplete repopulation. By day 60 post-transplantation, the percentage of bronchoalveolar lavage fluid (BALF) cells expressing GFP reached 74.5 +/- 2.4\%, remaining stable 90 days after transplantation (80.4 +/- 1.9\%). We conclude that 60 days after TBI with 900 cGy and bone marrow transplantation, the majority of the lung resident alveolar macrophages is of donor origin. This study provides useful information regarding the time of reconstitution with donor alveolar macrophages in the pulmonary airspaces of recipient mice following marrow transplantation.},
	Author = {Matute-Bello, Gustavo and Lee, Janet S. and Frevert, Charles W. and Liles, W. Conrad and Sutlief, Steven and Ballman, Kimberly and Wong, Venus and Selk, Amy and Martin, Thomas R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0022-1759},
	Journal = {J Immunol Methods},
	Keywords = {Macrophages, Alveolar;Adoptive Transfer;Luminescent Proteins;Research Support, U.S. Gov't, P.H.S.;Time Factors;Mice, Inbred C57BL;Bone Marrow Transplantation;11 Glia;Whole-Body Irradiation;Animals;Mice;Green Fluorescent Proteins},
	Month = {9},
	Nlm_Id = {1305440},
	Number = {1-2},
	Organization = {Pulmonary and Critical Care Division, Department of Medicine, University of Washington, Seattle, WA 98108, USA.},
	Pages = {25-34},
	Pii = {S0022-1759(04)00203-0},
	Pubmed = {15350509},
	Title = {Optimal timing to repopulation of resident alveolar macrophages with donor cells following total body irradiation and bone marrow transplantation in mice},
	Uuid = {2A23F70E-F4D1-4AA9-A8A7-50944B37C2EB},
	Volume = {292},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jim.2004.05.010}}

@article{Mautes:2000,
	Abstract = {Oxidative stress contributes to secondary injury after spinal cord trauma. Among the consequences of oxidative stress is the induction of heme oxygenase-1 (HO-1), an inducible isozyme that metabolizes heme to iron, biliverdin, and carbon monoxide. Here we examine the induction of HO-1 in the hemisected spinal cord, a model that results in reproducible degeneration in the ipsilateral white matter. HO-1 was induced in microglia and macrophages from 24 h to at least 42 days after injury. Within the first week after injury, HO-1 was induced in both the gray and the white matter. Thereafter, HO-1 expression was limited to degenerating fiber tracts. HSP70, a heat shock protein induced mainly by the presence of denatured proteins, was consistently colocalized with HO-1 in the microglia and macrophages. This study to demonstrates long-term induction of HO-1 and HSP70 in microglia and macrophages after traumatic injury and an association between induction of HO-1 and Wallerian degeneration. White matter degeneration is characterized by phagocytosis of cellular debris and remodeling of surviving tissue. This results in the metabolism, synthesis, and turnover of heme and heme proteins. Thus, sustained induction of HO-1 and HSP70 in microglia and macrophages suggests that tissue degeneration is an ongoing process, lasting 6 weeks and perhaps even longer.},
	Author = {Mautes, A. E. and Bergeron, M. and Sharp, F. R. and Panter, S. S. and Weinzierl, M. and Guenther, K. and Noble, L. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Animals;Astrocytes;Myelitis;Macrophages;Rats;Anterior Horn Cells;Heat-Shock Proteins 70;Microglia;Axons;Rats, Sprague-Dawley;Not relevant;11 Glia;Male;Spinal Cord Injuries;Oxidative Stress;Heme Oxygenase (Decyclizing);Support, Non-U.S. Gov't;Wallerian Degeneration;Support, U.S. Gov't, P.H.S.},
	Medline = {20539894},
	Month = {12},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Neurosurgery, University of California at San Francisco, San Francisco, California, 94143, USA.},
	Pages = {254-65},
	Pii = {S0014488600975204},
	Pubmed = {11085891},
	Title = {Sustained induction of heme oxygenase-1 in the traumatized spinal cord},
	Uuid = {FF8E1D55-98AC-4E0D-A4C0-4AE4C1FE916B},
	Volume = {166},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.2000.7520}}

@article{Mayne:2003,
	Abstract = {Due to their phagocytic and poorly proliferative nature, it has been difficult to transfect human monocytes and macrophages. Adenoviral vectors have recently allowed transduction of a high percentage of human macrophages, but only after CSF upregulation of the integrins, alphavbeta3 or alphavbeta5, during culture for 48 h, a time allowing significant monocyte to macrophage differentiation. In our hands, after 24-h incubation with M-CSF (20 ng/ml) and a further 24-h incubation with an adenoviral vector encoding green fluorescent protein (AdV-GFP) [multiplicity of infection (MOI)=50:1], only 35\%of CD14-positive cells express GFP. We report that centrifugation of these cells with AdV-GFP at 2000 x g for 1 h at 37 degrees C significantly enhanced the number of cells expressing GFP (to 65\%) and the level of GFP expression per transduced cell (fivefold). The viability of the cells was not compromised (<5 \%CD14-positive cells were 7-aminoactinomycin D (7AAD)-positive after 24 h AdV-GFP exposure at MOI=50:1). Centrifugation allowed efficient transduction of monocytes and macrophages with an MOI at least tenfold lower than otherwise required and did not activate the transduced cells or affect their ability to produce TNFalpha or IL-1beta in response to lipopolysaccharide (LPS). This methodology was also suitable for transducing large numbers of in vitro monocyte-derived macrophages (MDMac) and macrophages isolated from synovial fluids with up to 75-80\%of CD14-positive cells transduced after 24-h exposure to AdV-GFP (50:1) and centrifugation (2000 x g). This methodology should provide significant expression of transgenes in human monocytes and macrophages.},
	Author = {Mayne, George C. and Borowicz, Romana A. and Greeneklee, Kate V. L. and Finlay-Jones, John J. and Williams, Keryn A. and Hart, Prue H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0022-1759},
	Journal = {J Immunol Methods},
	Keywords = {Cell Survival;Transduction, Genetic;Animals;Monocytes;Macrophages;Humans;Integrins;Tumor Necrosis Factor-alpha;Receptors, Vitronectin;Extracellular Space;11 Glia;Green Fluorescent Proteins;Centrifugation;Genetic Vectors;Integrin alphaVbeta3;Interleukin-1;Flow Cytometry;Adenoviridae;Luminescent Proteins;Synovial Fluid;Research Support, Non-U.S. Gov't},
	Medline = {22838810},
	Month = {7},
	Nlm_Id = {1305440},
	Number = {1-2},
	Organization = {Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, GPO Box 2100, Adelaide 5001, Australia.},
	Pages = {45-56},
	Pii = {S0022175903002291},
	Pubmed = {12957395},
	Title = {Centrifugation facilitates transduction of green fluorescent protein in human monocytes and macrophages by adenovirus at low multiplicity of infection},
	Uuid = {B96728CB-A2B5-47AE-9883-32D31887F444},
	Volume = {278},
	Year = {2003}}

@article{Maysinger:1996,
	Abstract = {The aim of this study was to develop delivery systems for administration of CSF-1 to remedy the systemic deficiency of this cytokine in osteopetrotic op/op mice and to study the microglial response and neuronal survival in op/op mice following cerebral cortex ischemic lesion. Unilateral cerebral cortex ischemic lesions were produced in homozygous op/op mice and either microencapsulated rhCSF-1 or LM-10 fibroblast-like cells producing CSF-1 were administered either locally, at the site and time of the lesioning, or into the peritoneum 2 weeks before the lesion was made. Physical properties (shape, size, integrity) and kinetics of rhCSF-1 release were assessed prior to the experiments in situ. Depending on the characteristics of the biodegradable polymer (e.g., chitosan with different densities or poly-L-lactic-poly-glycolic acid), remarkable differences in survival of encapsulated cells were observed. Cellular integrity following encapsulation and metabolic activity was regularly assessed for a period of 1 month. The best level of viability was achieved with highly viscous chitosan (311). The results from these studies demonstrate that: (1) rhCSF-1 incorporated into biodegradable spheres can be released and retain its biological activity; (2) microencapsulated LM-10 cells which produce CSF-1 can survive and constitutively release CSF-1 in alginate-chitosan spheres for different lengths of time depending on the physical properties of the chitosan used; and (3) CSF-1 is an important growth factor in the central nervous system where it can both strongly alter morphological changes of microglia and enhance survival of neurons in injured brain.},
	Author = {Maysinger, D. and Berezovskaya, O. and Fedoroff, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cell Survival;Human;Animals;Capsules;Osteopetrosis;Mice, Mutant Strains;Recombinant Proteins;Fibroblasts;Brain;Cell Count;11 Glia;Nerve Growth Factors;Cell Line;Biopolymers;Microspheres;Support, Non-U.S. Gov't;Macrophage Colony-Stimulating Factor;Mice;Drug Delivery Systems;Microscopy, Electron},
	Medline = {96390694},
	Month = {9},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.},
	Pages = {47-56},
	Pii = {S0014488696901387},
	Pubmed = {8797667},
	Title = {The hematopoietic cytokine colony stimulating factor 1 is also a growth factor in the CNS: (II). Microencapsulated CSF-1 and LM-10 cells as delivery systems},
	Uuid = {52E5AB29-6EE8-4DF7-A34A-E25E63F0E0C4},
	Volume = {141},
	Year = {1996}}

@article{Mazzoni:1994,
	Abstract = {The presence and binding properties of epidermal growth-factor receptors (EGF-Rs) in different cell types purified from the rat medial septal area in culture were investigated. We report that astrocytes, oligodendrocytes and neurons from this area possess EGF-Rs while microglia do not. EGF-binding sites are detectable on astrocytes derived from the medial septum of both embryonic and neonatal rats. Scatchard analysis of the data for astrocytes from the fetal rats show that EGF specifically binds to both high- (Kd = 7.21 x 10(-10) M, Bmax = 3602 receptors/cell) and low-affinity (Kd = 3.99 x 10(-8) M, Bmax = 86,265 receptors/cell) receptors on these cells. On the other hand, astrocytes purified from neonatal tissue possess a greater number of high-affinity receptors (Bmax = 10,938 receptors/cell) when compared with the embryonic astroglia. With time in culture, the number of both types of receptors on neonatal astrocytes decreases. Oligodendrocytes also possess high- and low-affinity EGF-Rs with dissociation constants of 3.25 x 10(-10) M and 3.85 x 10(-8) M, respectively. The number of receptors on oligodendrocytes is significantly lower than those of neonatal astrocytes (Bmax = 1185 and 25,081 receptors/cell for high- and low-affinity binding sites, respectively). Finally, neurons from this area also exhibit two different EGF-R types with dissociation constants similar to those described for astrocytes. As the number of receptors/neuron (Bmax = 136 and 1159 receptors/cell for high- and low-affinity binding sites, respectively) appears to be extremely low, it is possible that EGF specifically binds only to a subpopulation of neurons from this area. These studies demonstrate which cell types in the developing medial septal area possess EGF-Rs and provide a detailed characterization of these binding sites. These EGF-R-bearing cells may be potential targets for this growth factor or for transforming growth factor alpha in this brain area.},
	Author = {Mazzoni, I. E. and Kenigsberg, R. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Animals;Receptor, Epidermal Growth Factor;Astrocytes;Cells, Cultured;Rats;Microglia;Oligodendroglia;Iodine Radioisotopes;Rats, Sprague-Dawley;Kinetics;11 Glia;Septal Nuclei;Alpha;Neuroglia;Epidermal Growth Factor;Neurons;Isotope Labeling;Immunohistochemistry;Lectins;Research Support, Non-U.S. Gov't},
	Medline = {95103258},
	Month = {9},
	Nlm_Id = {0045503},
	Number = {1},
	Organization = {Department of Physiology, University of Montreal, Que., Canada.},
	Pages = {115-26},
	Pubmed = {7804824},
	Title = {Localization and characterization of epidermal growth-factor receptors in the developing rat medial septal area in culture},
	Uuid = {4DD506E9-6CE1-45F1-A385-5C56A25C36E8},
	Volume = {656},
	Year = {1994}}

@article{Maurer:2003,
	Abstract = {Macrophages have recently been shown to be critically involved in the pathogenesis of genetically determined demyelination in mice heterozygously deficient for P0 (P0(+-)). Since little is known about the origin of these cells, we created chimeric P0(+-) mice by transplanting bone marrow from green fluorescent protein (GFP)-transgenic mice into irradiated P0(+-) mice. When analyzing chimeric P0(+-) mice, we could determine two populations (GFP(+) and GFP(-)) of endoneurial macrophages that became phagocytic for myelin and increased in number. We found that both GFP(-) resident macrophages and GFP(+) macrophages proliferated in peripheral nerves of P0(+-) mice but not in nerves of chimeric or nonchimeric P0(++) mice. These findings demonstrate a so far poorly recognized role of resident endoneurial macrophages in demyelinating neuropathies. Surprisingly, we also found GFP(+) cells that unequivocally showed the morphological characteristics of fibroblasts. These blood-borne fibroblast-like cells express the common hematopoetic stem cell marker CD34 and might comprise another cell type of potential importance for immune regulation in hereditary demyelinating neuropathies.},
	Author = {M{\"a}urer, Mathias and M{\"u}ller, Marcus and Kobsar, Igor and Leonhard, Christine and Martini, Rudolf and Kiefer, Reinhard},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Peripheral Nerves;Phagocytosis;Animals;Myelin Sheath;Microscopy, Immunoelectron;Macrophages;Bone Marrow Transplantation;Phenotype;Fibroblasts;Cell Movement;Mice, Transgenic;Mice, Inbred C57BL;Green Fluorescent Proteins;Transplantation Chimera;Disease Models, Animal;11 Glia;Spinal Nerve Roots;Peripheral Nervous System Diseases;Mice;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22722092},
	Month = {7},
	Nlm_Id = {9100095},
	Number = {3},
	Organization = {Department of Neurology, Bayerische Julius-Maximilians-Universit{\"a}t W{\"u}rzburg, D-97080 W{\"u}rzburg, Germany.},
	Pages = {351-9},
	Pii = {S1044743103000551},
	Pubmed = {12837620},
	Title = {Origin of pathogenic macrophages and endoneurial fibroblast-like cells in an animal model of inherited neuropathy},
	Uuid = {46F301AD-28D9-4511-BD13-F1FCA0E1C40E},
	Volume = {23},
	Year = {2003}}

@article{McBride:2004,
	Abstract = {The present study investigated the neuroanatomical and behavioral effects of human stem cell transplants into the striatum of quinolinic acid (QA)-lesioned rats. Twenty-four rats received unilateral QA (200 nM/microl) injections into the striatum. One week later, rats were transplanted with stem cells derived from human fetal cortex (12 weeks postconception) that were either 1) pretreated in culture media with the differentiating cytokine ciliary neurotrophic factor (CNTF; n = 9) or 2) allowed to grow in culture media alone (n=7). Each rat was injected with a total of 200,000 cells. A third group of rats (n=8) was given a sham injection of vehicle. Rats transplanted with human stem cells performed significantly better over the 8 weeks of testing on the cylinder test compared with those treated with vehicle (P < or = 0.001). Stereological striatal volume analyses performed on Nissl-stained sections revealed that rats transplanted with CNTF-treated neurospheres had a 22\%greater striatal volume on the lesioned side compared with those receiving transplants of untreated neurospheres (P = 0.0003) and a 26\%greater striatal volume compared with rats injected with vehicle (P < or = 0.0001). Numerous human nuclei-positive cells were visualized in the striatum in both transplantation groups. Grafted cells were also observed in the globus pallidus, entopeduncular nucleus, and substantia nigra pars reticulata, areas of the basal ganglia receiving striatal projections. Some of the human nuclei-positive cells coexpressed glial fibrillary acidic protein and NeuN, suggesting that they had differentiated into neurons and astrocytes. Taken together, these data demonstrate that striatal transplants of human fetal stem cells elicit behavioral and anatomical recovery in a rodent model of Huntington's disease.},
	Author = {McBride, Jodi L. and Behrstock, Soshana P. and Chen, Er-Yun Y. and Jakel, Rebekah J. and Siegel, Irwin and Svendsen, Clive N. and Kordower, Jeffrey H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Glial Fibrillary Acidic Protein;Movement;Cell Differentiation;Rats, Inbred Lew;Ciliary Neurotrophic Factor;Astrocytes;Corpus Striatum;Treatment Outcome;Rats;Transplantation, Heterologous;Recovery of Function;Cells, Cultured;Humans;Animals;Stem Cell Transplantation;Disease Models, Animal;Male;Nerve Regeneration;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Neurons;Quinolinic Acid;Huntington Disease;24 Pubmed search results 2008;Graft Survival;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA.},
	Pages = {211-9},
	Pubmed = {15211462},
	Title = {Human neural stem cell transplants improve motor function in a rat model of Huntington's disease},
	Uuid = {B13E991D-9ED7-4351-9243-DDD6C6E83E80},
	Volume = {475},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20176}}

@article{McCaffrey:2002,
	Abstract = {RNA interference is an evolutionarily conserved surveillance mechanism that responds to double-stranded RNA by sequence-specific silencing of homologous genes. Here we show that transgene expression can be suppressed in adult mice by synthetic small interfering RNAs and by small-hairpin RNAs transcribed in vivo from DNA templates. We also show the therapeutic potential of this technique by demonstrating effective targeting of a sequence from hepatitis C virus by RNA interference in vivo. 0028-0836 Journal Article},
	Author = {McCaffrey, A. P. and Meuse, L. and Pham, T. T. and Conklin, D. S. and Hannon, G. J. and Kay, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:53 -0400},
	Journal = {Nature},
	Keywords = {Hepacivirus/*genetics;Human;Liver/metabolism;Luciferase/biosynthesis/genetics;RNA, Untranslated/chemistry/*genetics/*metabolism;Aging/*genetics;Animals;Recombinant Fusion Proteins/biosynthesis/genetics;Genes, Reporter/genetics;T pdf;23 Technique;RNA, Small Interfering;RNA, Viral/genetics/metabolism;Substrate Specificity;*Gene Silencing;RNA, Double-Stranded/chemistry/genetics/metabolism;Mice;Viral Nonstructural Proteins/biosynthesis/genetics;Transgenes/genetics},
	Number = {6893},
	Organization = {Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305-5208, USA.},
	Pages = {38-9},
	Title = {RNA interference in adult mice},
	Uuid = {FF057C67-E1CD-4C22-A9E5-7733A5E720BB},
	Volume = {418},
	Year = {2002},
	url = {papers/McCaffrey_Nature2002.pdf}}

@article{McCann:1996,
	Abstract = {We have investigated the response of astrocytes and microglia to trimethyl tin intoxication in the septum, hippocampus, olfactory bulb, and pyriform cortex of the rat. Microglia were studied qualitatively using lectin histochemistry, and astrocytes were examined both qualitatively with immunohistochemistry, and quantitatively using an immunoassay for glial fibrillary acidic protein. Our results show that activated microglia first appeared 2 days after trimethyl tin intoxication in the lateral septum and hippocampus. Four days after trimethyl tin intoxication, the same regions revealed a most intense microglial reaction characterized by microglial hypertrophy and the formation of phagocytic clusters. By day 7, microglial activation in the septum and hippocampus had lessened, suggesting that the cells were reverting to the resting phenotype. The microglial response in the pyriform cortex and olfactory bulb, while being later in onset than in the septum and hippocampus, showed a similar progression of microglial changes reaching maximal intensity 7 days after trimethyl tin intoxication. Significant increases in the expression of glial fibrillary acidic protein were observed in all regions examined and typically occurred after microglial activation was already underway. We conclude that microglial and astroglial reactions which occur in response to trimethyl tin-induced neuronal necrosis are separated in time, with microglial activation preceding astrogliosis. In addition, our study stresses the importance of microglia as an endogenous source of CNS macrophages, and illustrates the merit of histochemical analysis with microglial markers for the early delineation of neurotoxicant-induced brain damage.},
	Author = {McCann, M. J. and O'Callaghan, J. P. and Martin, P. M. and Bertram, T. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Macrophage Activation;Glial Fibrillary Acidic Protein;Nerve Degeneration;Trimethyltin Compounds;Comparative Study;Immunohistochemistry;Astrocytes;Rats;Not relevant;11 Glia;Microglia;Horseradish Peroxidase;Animals;Enzyme-Linked Immunosorbent Assay;Brain;Male},
	Medline = {96295043},
	Month = {5},
	Nlm_Id = {7605074},
	Number = {1},
	Organization = {Procter and Gamble Company, Miami Valley Laboratories, Cincinnati, OH 45239, USA.},
	Pages = {273-81},
	Pii = {0306452295005269},
	Pubmed = {8730724},
	Title = {Differential activation of microglia and astrocytes following trimethyl tin-induced neurodegeneration},
	Uuid = {C9150240-66AA-4F93-8C58-292F10E4AF46},
	Volume = {72},
	Year = {1996}}

@article{McCarthy:2002,
	Abstract = {The longitudinal evolution of HIV-1 phenotypes was studied in a cohort of six vertically infected children with early onset and rapid progression of clinical disease. Among 30 viral isolates obtained from peripheral blood, tropisms for both human blood-derived cells (macrophages, T-lymphocytes), and for human neural (brain-derived) cells (microglia, astrocytes) were determined, as was chemokine co-receptor usage. All children harbored from birth macrophage-tropic isolates using the CCR5 co-receptor. Two children later developed T-cell tropic isolates with CXCR4 and CCR3 usage. While all six patients developed neurological abnormalities, only three produced neural cell tropic isolates, which used CCR5. However, early and persistent finding of both astrocyte- and microglia-tropic isolates in one patient did associate with the most rapid progression to brain atrophy among the six patients. Viral phenotypic properties determined in cell culture did not specifically predict clinical features or course, and the development of AIDS did not coincide with, or depend on, the appearance T-tropic, syncytia-inducing viruses.},
	Author = {McCarthy, Micheline and He, Jun and Auger, Denise and Geffin, Rebeca and Woodson, Cristina and Hutto, Cecelia and Wood, Charles and Scott, Gwendolyn},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0146-6615},
	Journal = {J Med Virol},
	Keywords = {Receptors, CXCR4;Human;Prospective Studies;HIV-1;CD4 Lymphocyte Count;Astrocytes;Child, Preschool;Disease Progression;Humans;Cells, Cultured;Research Support, U.S. Gov't, Non-P.H.S.;Microglia;Female;Nervous System Diseases;Receptors, HIV;Infant;Disease Transmission, Vertical;11 Glia;Time Factors;Male;HIV Infections;Research Support, U.S. Gov't, P.H.S.;Receptors, Chemokine;Viral Load;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Receptors, CCR5},
	Medline = {21918115},
	Month = {5},
	Nlm_Id = {7705876},
	Number = {1},
	Organization = {Department of Veterans Affairs Medical Center, Miami, Florida 33125, USA. mmccarth\@med.miami.edu},
	Pages = {1-8},
	Pii = {10.1002/jmv.2185},
	Pubmed = {11920811},
	Title = {Cellular tropisms and co-receptor usage of HIV-1 isolates from vertically infected children with neurological abnormalities and rapid disease progression},
	Uuid = {F8B1A6DC-B546-436A-A3DD-54B7E6255F81},
	Volume = {67},
	Year = {2002}}

@article{McCubrey:1982,
	Abstract = {The frequency of ecotropic murine leukemia virus (MuLV) production in cells induced with halogenated pyrimidines has been investigated in several low leukemic strains of mice. Very few BALB/c or C57BL/6 (B6) induced embryo cells produce MuLV; this low frequency increases 10 to 50 fold in cells of the BALB/c x B6 F1 hybrid. Data from back-crosses of the F1 hybrid to each parent and from BALB/c x B6 recombinant inbred strains indicate that the phenotype of enhanced MuLV production results from interaction of two unlinked loci, dominant (+/+) alleles of which are carried by either parent. Genetic tests with BALB/c x B6 recombinant inbred strains confirm this two-locus model. The loci are designated Inc-1 and Inb-1 to signify their phenotypic detection by induction and the BALB/c or B6 strain of origin, respectively. Examination of hybrids of BALB/c and of B6 with other strains indicates that strains related in pedigree to BALB/c carry Inc-1, whereas those related to B6 carry Inb-1. Identification of genetic loci that specifically interact to enhance MuLV production after exposure to halogenated pyrimidines indicates the existence of mechanisms that regulate the induction or intracellular expression of endogenous MuLV.},
	Author = {McCubrey, J. and Risser, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Mice, Inbred BALB C;Idoxuridine;Animals;Cells, Cultured;Phenotype;Leukemia;15 Retrovirus mechanism;Virus Activation;Crosses, Genetic;Embryo;Leukemia Virus, Murine;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred Strains;Mice;24 Pubmed search results 2008;Plaque Assay;15 ERVs retroelements;Research Support, Non-U.S. Gov't},
	Medline = {82233707},
	Month = {4},
	Nlm_Id = {0413066},
	Number = {4},
	Pages = {881-8},
	Pii = {0092-8674(82)90067-8},
	Pubmed = {6284378},
	Title = {Genetic interactions in induction of endogenous murine leukemia virus from low leukemic mice},
	Uuid = {8DFFB311-4328-11DB-A5D2-000D9346EC2A},
	Volume = {28},
	Year = {1982}}

@article{McElhaney:1994,
	Abstract = {The purpose of this study was to identify cellular sources of nitric oxide (NO) after injury to rat facial motor neurons using NADPH-diaphorase histochemistry. We employed intraneural injections of either saline or toxic ricin, followed by nerve crush, in order to produce regeneration or degeneration of facial motor neurons (FMNs), respectively. Reactive astrocytes responding to ricin-induced degeneration of FMNs showed increased NADPH-diaphorase activity while reactive astrocytes responding to axotomy (saline injection) did not. Reactive microglial cells were found not to express NADPH-diaphorase in either one of these two paradigms. We conclude that irreversible neuron injury resulting in neurodegeneration causes increased production of NO by reactive astrocytes.},
	Author = {McElhaney, M. R. and Chandler, L. J. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Nerve Degeneration;Astrocytes;Ricin;Animals;Rats;Microglia;Rats, Sprague-Dawley;Not relevant;11 Glia;Male;Nerve Regeneration;NADPH Dehydrogenase;Support, Non-U.S. Gov't;Histocytochemistry;Support, U.S. Gov't, P.H.S.;Motor Neurons;Nerve Crush;Facial Nerve;Ligands},
	Medline = {95183230},
	Month = {10},
	Nlm_Id = {7600130},
	Number = {1},
	Organization = {Department of Comparative and Experimental Pathology, College of Veterinary Medicine, University of Florida, Gainesville 32610.},
	Pages = {67-70},
	Pubmed = {7877765},
	Title = {Astrocytes but not microglia express NADPH-diaphorase activity after motor neuron injury in the rat},
	Uuid = {77F92E3E-C615-4542-9F2E-372211CD07ED},
	Volume = {180},
	Year = {1994}}

@article{McGeer:1998,
	Abstract = {Lesions in such chronic neurodegenerative disorders as Alzheimer disease, Parkinson disease, the parkinsonism dementia complex of Guam and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. This is particularly true of Alzheimer disease where inflammatory reactions are thought to be important contributors to the neuronal loss. They include complement proteins, complement inhibitors, acute phase reactants, inflammatory cytokines, proteases and protease inhibitors. Studies of cultured human astrocytes and microglia, obtained from postmortem brain, have established that nearly all of these proteins are produced by one or another of these cell types. Human neurons also produce many inflammatory proteins and their inhibitors, creating complex interactions. Accumulations of amyloid and extracellular tangles apparently act as irritants, causing the activation of complement, the initiation of reactive changes in microglia, and the release of potentially neurotoxic products. Such products include the membrane attack complex, oxygen free radicals and excess glutamate. Twenty epidemiological studies that have been published to data indicate that populations taking antiinflammatory drugs have a significantly reduced prevalence of Alzheimer disease or a slower mental decline. One small clinical trial with indomethacin showed arrest of the disease over a 6 month period. Therapeutic intervention in key inflammatory processes holds great promise for the amelioration of Alzheimer disease and possibly other neurodegenerative disorders.},
	Author = {McGeer, P. L. and McGeer, E. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0303-6995},
	Journal = {J Neural Transm Suppl},
	Keywords = {Human;Inflammation;Models, Neurological;Astrocytes;Models, Immunological;Microglia;review, tutorial;Alzheimer Disease;Parkinson Disease;Support, Non-U.S. Gov't;Brain;11 Glia;Neurons;review},
	Medline = {99067910},
	Nlm_Id = {0425126},
	Organization = {Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada.},
	Pages = {159-66},
	Pubmed = {9850924},
	Title = {Mechanisms of cell death in Alzheimer disease--immunopathology},
	Uuid = {32FC2B8F-19B3-414B-B040-902C82B5A8A2},
	Volume = {54},
	Year = {1998}}

@article{McGuire:2001,
	Abstract = {In this issue of Neuron, report that forebrain-specific Presenilin-1 conditional knockout mice show defects in enrichment-induced neurogenesis in the dentate gyrus. This defect in neurogenesis is associated with enhanced fear memory of contextual cues when animals are subjected to enrichment between training and testing. The authors suggest that neurogenesis in the adult dentate gyrus may serve to clear out old memory traces from the hippocampus, thus leaving the hippocampus available for new memory processing.},
	Author = {McGuire, S. E. and Davis, R. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Neuron},
	Keywords = {Memory/*physiology;Alzheimer Disease/drug therapy/metabolism;Human;Membrane Proteins/*metabolism;Animal;Prosencephalon/*metabolism;04 Adult neurogenesis factors;C abstr},
	Number = {5},
	Organization = {Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.},
	Pages = {763-5.},
	Title = {Presenilin-1 and memories of the forebrain},
	Uuid = {A9A66685-FEBC-4469-9779-40C9B46BE822},
	Volume = {32},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11738022}}

@article{McKay:2004,
	Abstract = {The vitamin biotin is an endogenous molecule that acts as an important cofactor for several carboxylases in the citric acid cycle. Disorders of biotin metabolism produce neurological symptoms that range from ataxia to sensory loss, suggesting the presence of biotin in specific functional systems of the CNS. Although biotin has been described in some cells of nonmammalian nervous systems, the distribution of biotin in mammalian CNS is virtually unknown. We report the presence of biotin in select regions of rat CNS, as revealed with a monoclonal antibody directed against biotin and with avidin- and streptavidin-conjugated labels. Detectable levels of biotin were primarily found caudal to the diencephalon, with greatest expression in the cerebellar motor system and several brainstem auditory nuclei. Biotin was found as a somatic label in cerebellar Purkinje cells, in cell bodies and proximal dendrites of cerebellar deep nuclear neurons, and in red nuclear neurons. Biotin was detected in cells of the spiral ganglion, somata and proximal dendrites of cells in the cochlear nuclei, superior olivary nuclei, medial nucleus of the trapezoid body, and nucleus of the lateral lemniscus. Biotin was further found in pontine nuclei and fiber tracts, the substantia nigra pars reticulata, lateral mammillary nucleus, and a small number of hippocampal interneurons. Biotin was detected in glial cells of major tract systems throughout the brain but was most prominent in tracts of the hindbrain. Biotin is thus expressed in select regions of rat CNS with a distribution that correlates to the known clinical sequelae associated with biotin deficiencies.},
	Author = {McKay, Bruce E. and Molineux, Michael L. and Turner, Ray W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Avidin;Streptavidin;Tissue Distribution;Rats, Sprague-Dawley;Central Nervous System;Comparative Study;Immunohistochemistry;Rats;Biotin;Histocytochemistry;Support, Non-U.S. Gov't;Male;Animals;Neurons;23 Technique},
	Month = {5},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Neuroscience Research Group, University of Calgary, Calgary, Alberta T2N 4N1, Canada.},
	Pages = {86-96},
	Pubmed = {15067720},
	Title = {Biotin is endogenously expressed in select regions of the rat central nervous system},
	Uuid = {E878B101-02EA-43BC-97C8-9FFA24C3143D},
	Volume = {473},
	Year = {2004},
	url = {papers/McKay_JCompNeurol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20109}}

@article{McLaren:2001,
	Abstract = {Much recent interest has focused on whether stem cell therapy could alleviate or even cure common degenerative diseases. This has been accompanied by debate on the ethics of destructive research on early human embryos. Stem cells derived from various sources raise different ethical issues, but their contribution to medical research could be immense. Any use of stem cells should be subject to appropriate scientific and ethical review. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {McLaren, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Nature},
	Keywords = {*Bioethics;Morals;Embryo/cytology;10 Development;F abstr;Public Policy;Human;*Research/legislation &jurisprudence/standards;*Stem Cells;Sociology;*Ethics, Medical},
	Number = {6859},
	Organization = {Wellcome/CRC Institute, University of Cambridge, UK. a.mclaren\@welc.cam.ac.uk},
	Pages = {129-31},
	Pubmed = {11689959},
	Title = {Ethical and social considerations of stem cell research},
	Uuid = {9CE01674-47C0-48F3-8630-1846EA6E40EC},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689959}}

@article{McMahon:2007,
	Abstract = {During development there is a clear correlation between position of dividing progenitor cells, mode of division and developmental potential, suggesting that the local environment of progenitor cells may influence their cell fate [ 17 (6), 639-647]. The contribution of these conditions was investigated here by transplantation of radial glial progenitor cells into isotopic, isochronic, heterotopic and heterochronic environment conditions. Neuronal cells were removed from E14 spinal cords using negative immunoselection. The remaining radial glia were transplanted into the ventricular system of host embryos and pups. Distance of migration as well as morphological and antigenic phenotype of transplanted radial glia was examined after various survival times post transplantation. Host age clearly influenced migration and differentiation of transplant cells, with transplant cells migrating further in younger hosts and differentiating earlier in older aged host environments. Evidence is presented showing that most transplanted spinal cord radial glia give rise to astrocytes. In addition some transplanted radial glia were shown to give rise to neurons in spinal cord regions. Radial glia did not appear to generate neurons in the brains of host animals until postnatal ages, perhaps because transplanted radial glia were isolated from spinal cord and thus may not have been influenced to behave as endogenous radial glia in the brain which commonly produce neurons.},
	Author = {McMahon, Siobhan S. and McDermott, Kieran W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Anatomy and Biosciences Institute, University College Cork, Cork, Ireland.},
	Pages = {128-36},
	Pii = {S0014-4886(06)00467-5},
	Pubmed = {17010971},
	Title = {Developmental potential of radial glia investigated by transplantation into the developing rat ventricular system in utero},
	Uuid = {8ADF0455-442F-4185-8257-23294969647E},
	Volume = {203},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2006.07.029}}

@article{McMahon:2002,
	Abstract = {The contribution of peripheral macrophage was assessed in cuprizone intoxication, a model of demyelination and remyelination in which the blood-brain barrier remains intact. Flow cytometry of brain cells isolated from cuprizone-treated mice revealed an increase in the percentage of Mac-1(+)/CD45(hi) peripheral macrophage. To confirm these results in situ, C57BL/6 mice were lethally irradiated, transplanted with bone marrow from GFP-transgenic mice, and exposed to cuprizone. GFP(+) peripheral macrophages were seen in the CNS after 2 weeks of treatment, and infiltration continued through 6 weeks. While the peripheral macrophages were far outnumbered by the resident microglia, their recruitment across the blood-brain barrier alludes to a potentially important role.},
	Author = {McMahon, Eileen J. and Suzuki, Kinuko and Matsushima, Glenn K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Antigens, CD45;Animals;Macrophages;Bone Marrow Transplantation;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Chemotaxis, Leukocyte;Disease Models, Animal;Blood-Brain Barrier;Antigens, CD3;Radiation Chimera;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Macrophage-1 Antigen;Male;Demyelinating Autoimmune Diseases, CNS;Flow Cytometry;Mice;Central Nervous System;Research Support, Non-U.S. Gov't},
	Medline = {22213662},
	Month = {9},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Microbiology and Immunology, University of North Carolina, 27599, Chapel Hill, NC, USA},
	Pages = {32-45},
	Pii = {S0165572802002059},
	Pubmed = {12225886},
	Title = {Peripheral macrophage recruitment in cuprizone-induced CNS demyelination despite an intact blood-brain barrier},
	Uuid = {B60654D4-FDC9-49CF-B8F6-160A01A4CD0F},
	Volume = {130},
	Year = {2002}}

@article{McMillian:1994,
	Abstract = {Reactive gliosis is a powerful response to brain injury and subsequent neuronal damage in vivo. Neuronal cell cultures are now well established as assays to study this process in vitro. However, equivalent studies of purified glial cell populations have only recently been achieved, following the realization that glial cells produce many of the neuropeptides, transmitters and growth factors that are produced also by neurons. There is now scope for studies in vitro that use mixed, identified populations of glial and neuronal cells to dissect the interactions between the two. Such cultures also lend themselves to assays for potential therapeutic strategies for brain injury that take account of all the different cell types found in the brain.},
	Author = {McMillian, M. K. and Thai, L. and Hong, J. S. and O'Callaghan, J. P. and Pennypacker, K. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {11 Glia;Neurotransmitters;Nerve Tissue Proteins;Astrocytes;Neuropeptides;Gliosis;Rats;Growth Substances;Microglia;Animals, Suckling;Cell Death;Growth Inhibitors;Animals;Cells, Cultured;review, tutorial;Neurons;review},
	Medline = {94295082},
	Month = {4},
	Nlm_Id = {7808616},
	Number = {4},
	Organization = {Laboratory of Molecular and Integrative Neurosciences, National Institute of Environmental Health Sciences, National Institutes of Health.},
	Pages = {138-42},
	Pubmed = {7517589},
	Title = {Brain injury in a dish: a model for reactive gliosis},
	Uuid = {50CADAB1-EA03-499A-95C6-990AABE2A2B0},
	Volume = {17},
	Year = {1994}}

@article{McNamara:2000,
	Abstract = {We have previously shown that the myristoylated alanine-rich C kinase substrate, a primary protein kinase C substrate in brain that binds and cross-links filamentous actin, is enriched in neuronal growth cones and is developmentally regulated in brain. Here we examined myristoylated alanine-rich C kinase substrate expression in the facial motor nucleus during axonal regeneration following facial nerve axotomy or facial nerve resection lesions, which impede regeneration, or following motor neuron degeneration induced by the retrograde neurotoxin ricin. For comparative purposes, the protein kinase C substrates myristoylated alanine-rich C kinase substrate-like protein and growth-associated protein-43 were examined in parallel. Myristoylated alanine-rich C kinase substrate messenger RNA exhibited a robust increase in both neurons and non-neuronal cells in the facial motor nucleus beginning four days after axotomy, peaked at seven days (2.5-fold), and declined back to baseline levels by 40 days. Myristoylated alanine-rich C kinase substrate protein similarly exhibited a twofold elevation in the facial motor nucleus determined four and 14 days post-axotomy. Following nerve resection, myristoylated alanine-rich C kinase substrate messenger RNA levels increased at seven days and returned to baseline levels by 40 days. Unlike myristoylated alanine-rich C kinase substrate messenger RNA, myristoylated alanine-rich C kinase substrate-like messenger RNA levels did not increase in the facial motor nucleus at any time point following nerve axotomy or resection, whereas growth-associated protein-43 messenger RNA exhibited a rapid (one day) and prolonged (40 days) elevation in facial motor nucleus neurons following either nerve axotomy or resection. Ricin-induced degeneration of facial motor neurons elevated myristoylated alanine-rich C kinase substrate and myristoylated alanine-rich C kinase substrate-like messenger RNAs in both microglia (lectin-positive) and astrocytes (glial fibrillary acidic protein-positive).Collectively, these data demonstrate that myristoylated alanine-rich C kinase substrate exhibits a unique expression profile in the facial motor nucleus following facial nerve lesions, and it is proposed that myristoylated alanine-rich C kinase substrate may serve to mediate actin-membrane cytoskeletal plasticity in both neurons and glial cells in response to protein kinaseC-mediated signaling during nerve regeneration and degeneration.},
	Author = {McNamara, R. K. and Jiang, Y. and Streit, W. J. and Lenox, R. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {GAP-43 Protein;Nerve Degeneration;Animals;Up-Regulation;Rats;Proteins;RNA, Messenger;Not relevant;11 Glia;Male;Nerve Regeneration;Support, Non-U.S. Gov't;Axotomy;Neuroglia;Support, U.S. Gov't, P.H.S.;Motor Neurons;Membrane Proteins;Facial Nerve},
	Medline = {20291264},
	Nlm_Id = {7605074},
	Number = {3},
	Organization = {Department of Psychiatry, University of Pennsylvania School of Medicine, Clinical Research Building, Philadelphia, PA 19104-6140, USA. rkm\@mail.med.upenn.edu},
	Pages = {581-9},
	Pii = {S0306452200000397},
	Pubmed = {10828540},
	Title = {Facial motor neuron regeneration induces a unique spatial and temporal pattern of myristoylated alanine-rich C kinase substrate expression},
	Uuid = {45BF0640-8455-4E2A-B483-E932DCA725A5},
	Volume = {97},
	Year = {2000}}

@article{McNeill:1988,
	Abstract = {Loss of dopaminergic neurons from the pars compacta of the substantia nigra is the pathological hallmark of Parkinson's disease (PD) and results in a partial deafferentation to the striatum. Since deafferentation is known to induce transynaptic atrophy of postsynaptic cells, we examined by Golgi impregnation the morphology of medium spiny I (MSI) striatal neurons, the principal target population for both nigrostriatal and corticostriatal fibers. Our quantitative data indicate that the dendritic arbor of MSI neurons in the putamen is significantly reduced in both length and number and MSI neurons are morphologically characterized by truncated dendrites with few dendritic spines and irregular, bulbous swellings. These data provide morphological evidence for the atrophy of striatal dendrites in PD and may explain, in part, the declining efficacy of chronic L-DOPA replacement therapy in advanced PD.},
	Author = {McNeill, T. H. and Brown, S. A. and Rafols, J. A. and Shoulson, I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Reference Values;10 Development;Dendrites;Aged;Aged, 80 and over;10 Spiny stellate;Research Support, U.S. Gov't, P.H.S.;Corpus Striatum;Atrophy;11 Glia;Parkinson Disease;10 Structural plasticity;Humans;G;24 Pubmed search results 2008;Neurons},
	Medline = {88327382},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {1},
	Organization = {Department of Neurology, University of Rochester, NY 14642.},
	Pages = {148-52},
	Pubmed = {3416180},
	Title = {Atrophy of medium spiny I striatal dendrites in advanced Parkinson's disease},
	Uuid = {AE810627-6F60-4E7B-AB48-66B533AFB704},
	Volume = {455},
	Year = {1988}}

@article{McQuiston:2001,
	Abstract = {In the mammalian olfactory bulb, glomeruli are surrounded by a heterogeneous population of interneurons called juxtaglomerular neurons. As they receive direct input from olfactory receptor neurons and connect with mitral cells, they are involved in the initial stages of olfactory information processing, but little is known about their detailed physiological properties. Using whole cell patch-clamp techniques, we recorded from juxtaglomerular neurons in rat olfactory bulb slices. Based on their response to depolarizing pulses, juxtaglomerular neurons could be divided into two physiological classes: bursting and standard firing. When depolarized, the standard firing neurons exhibited a range of responses: accommodating, nonaccommodating, irregular firing, and delayed to firing patterns of action potentials. Although the firing pattern was not rigorously predictive of a particular neuronal morphology, most short axon cells fired accommodating trains of action potentials, while most delayed to firing cells were external tufted cells. In contrast to the standard firing neurons, bursting neurons produced a calcium-channel-dependent low-threshold spike when depolarized either by current injection or by spontaneous or evoked postsynaptic potentials. Bursting neurons also could oscillate spontaneously. Most bursting cells were either periglomerular cells or external tufted cells. Based on their mode of firing and placement in the bulb circuit, these bursting cells are well situated to drive synchronous oscillations in the olfactory bulb. 21486690 0022-3077 Journal Article},
	Author = {McQuiston, A. R. and Katz, L. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {J Neurophysiol},
	Keywords = {Quinoxalines/pharmacology;2-Amino-5-phosphonovalerate/pharmacology;13 Olfactory bulb anatomy;Rats;Excitatory Amino Acid Antagonists/pharmacology;Nickel/pharmacology;Animal;Cell Size/physiology;Patch-Clamp Techniques;Action Potentials/drug effects/physiology;Nootropic Agents/pharmacology;Periodicity;Rats, Sprague-Dawley;Male;Olfactory Bulb/cytology/*physiology;Interneurons/cytology/*physiology;Anesthetics, Local/pharmacology;Excitatory Postsynaptic Potentials/drug effects/physiology;Lidocaine/*analogs &derivatives/pharmacology;I both;Choline/pharmacology},
	Number = {4},
	Organization = {Howard Hughes Medical Institute and Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA.},
	Pages = {1899-907},
	Title = {Electrophysiology of interneurons in the glomerular layer of the rat olfactory bulb},
	Uuid = {5A557FE3-8D3D-4C59-8ECB-4887A1E338A2},
	Volume = {86},
	Year = {2001},
	url = {papers/McQuiston_JNeurophysiol2001.pdf}}

@article{McTigue:1998,
	Abstract = {Functional loss after spinal cord injury (SCI) is caused, in part, by demyelination of axons surviving the trauma. Neurotrophins have been shown to induce oligodendrogliagenesis in vitro, but stimulation of oligodendrocyte proliferation and myelination by these factors in vivo has not been examined. We sought to determine whether neurotrophins can induce the formation of new oligodendrocytes and myelination of regenerating axons after SCI in adult rats. In this study, fibroblasts producing neurotrophin-3 (NT-3), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor, nerve growth factor, basic fibroblast growth factor, or beta-galactosidase (control grafts) were transplanted subacutely into the contused adult rat spinal cord. At 10 weeks after injury, all transplants contained axons. NT-3 and BDNF grafts, however, contained significantly more axons than control or other growth factor-producing grafts. In addition, significantly more myelin basic protein-positive profiles were detected in NT-3 and BDNF transplants, suggesting enhanced myelination of ingrowing axons within these neurotrophin-producing grafts. To determine whether augmented myelinogenesis was associated with increased proliferation of oligodendrocyte lineage cells, bromodeoxyuridine (BrdU) was used to label dividing cells. NT-3 and BDNF grafts contained significantly more BrdU-positive oligodendrocytes than controls. The association of these new oligodendrocytes with ingrowing myelinated axons suggests that NT-3- and BDNF-induced myelinogenesis resulted, at least in part, from expansion of oligodendrocyte lineage cells, most likely the endogenous oligodendrocyte progenitors. These findings may have significant implications for chronic demyelinating diseases or CNS injuries.},
	Author = {McTigue, D. M. and Horner, P. J. and Stokes, B. T. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {J Neurosci},
	Keywords = {Myelin Sheath/*physiology;Fibroblasts/drug effects;Nerve Growth Factors/*pharmacology;Rats;Schwann Cells/drug effects;Spinal Cord Injuries/*drug therapy;Female;Animal;Brain-Derived Neurotrophic Factor/*pharmacology;Oligodendroglia/cytology/drug effects;Neurotrophin 3;G abstr;11 Glia;Rats, Inbred F344;Cell Lineage;Cell Division/physiology;Support, Non-U.S. Gov't;Contusions/*drug therapy;Nerve Regeneration/*drug effects;Support, U.S. Gov't, P.H.S.;Axons/drug effects},
	Number = {14},
	Organization = {Department of Physiology, Ohio State University, Columbus, Ohio 43210, USA.},
	Pages = {5354-65.},
	Title = {Neurotrophin-3 and brain-derived neurotrophic factor induce oligodendrocyte proliferation and myelination of regenerating axons in the contused adult rat spinal cord},
	Uuid = {6A320F65-A359-4D2A-AE81-9091E757CFA8},
	Volume = {18},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9651218%20http://www.jneurosci.org/cgi/content/full/18/14/5354}}

@article{Meeker:1999,
	Abstract = {Microglia are thought to play an important role in neurodegenerative changes due to infection with human or animal immunodeficiency viruses. Using feline immunodeficiency virus and cat neural cultures, we observed a dramatic increase in the accumulation of microglia from a basal rate of 5-7\%day(-1) to 25-126\%day(-1). Both live virus and heat-inactivated virus induced proliferation. Negligible proliferation was seen in purified microglial cultures. Conditioned medium from astrocytes or mixed neural cultures treated with feline immunodeficiency virus stimulated the proliferation of purified microglia. Disease progression may be facilitated by early non-infectious interactions of lentiviruses with neural tissue that promote the activation and proliferation of microglia.},
	Author = {Meeker, R. B. and Azuma, Y. and Bragg, D. C. and English, R. V. and Tompkins, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Cats;Female;AIDS Dementia Complex;Astrocytes;Cell Division;Tumor Necrosis Factor-alpha;Microglia;Pregnancy;Immunodeficiency Virus, Feline;11 Glia;Cells, Cultured;Bromodeoxyuridine;Cerebral Cortex;Animals;24 Pubmed search results 2008},
	Medline = {20046776},
	Month = {11},
	Nlm_Id = {8109498},
	Number = {1},
	Organization = {Department of Neurology, University of North Carolina, Chapel Hill 27599, USA.},
	Pages = {15-26},
	Pii = {S0165572899001265},
	Pubmed = {10580809},
	Title = {Microglial proliferation in cortical neural cultures exposed to feline immunodeficiency virus},
	Uuid = {02F4E76B-8278-4B68-94AD-F2309D79021F},
	Volume = {101},
	Year = {1999},
	url = {papers/Meeker_JNeuroimmunol1999.pdf}}

@article{Mehmet:2000,
	Author = {Mehmet, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Nature},
	Keywords = {Amyloid beta-Protein/metabolism;Receptors, Cytoplasmic and Nuclear/metabolism;07 Excitotoxicity Apoptosis;Alzheimer Disease/enzymology;*Apoptosis;Calcium-Binding Proteins/metabolism;E-13;Caspases/*metabolism;Animal;Receptors, Peptide/metabolism;Endoplasmic Reticulum/*metabolism;Mice},
	Number = {6765},
	Pages = {29-30.},
	Title = {Caspases find a new place to hide},
	Uuid = {A2C589B2-034F-4818-BDFB-CC9807681025},
	Volume = {403},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10638735}}

@article{Mehta:2005,
	Abstract = {The exocyst is a complex of proteins originally identified in yeast that has been implicated in polarized secretion. Components of the exocyst have been implicated in neurite outgrowth, cell polarity, and cell viability. We have isolated an exocyst component, sec15, in a screen for genes required for synaptic specificity. Loss of sec15 causes a targeting defect of photoreceptors that coincides with mislocalization of specific cell adhesion and signaling molecules. Additionally, sec15 mutant neurons fail to localize other exocyst members like Sec5 and Sec8, but not Sec6, to neuronal terminals. However, loss of sec15 does not cause cell lethality in contrast to loss of sec5 or sec6. Our data suggest a role of Sec15 in an exocyst-like subcomplex for the targeting and subcellular distribution of specific proteins. The data also show that functions of other exocyst components persist in the absence of sec15, suggesting that different exocyst components have separable functions.},
	Author = {Mehta, Sunil Q. and Hiesinger, P. Robin and Beronja, Slobodan and Zhai, R. Grace and Schulze, Karen L. and Verstreken, Patrik and Cao, Yu and Zhou, Yi and Tepass, Ulrich and Crair, Michael C. and Bellen, Hugo J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Exocytosis;Animals;Synapses;Humans;Sequence Homology, Amino Acid;comparative study;Protein Transport;Mutation;research support, non-u.s. gov't;research support, u.s. gov't, p.h.s.;Blotting, Western;Neurons;Drosophila;Microscopy, Electron, Transmission;Polymerase Chain Reaction;Amino Acid Sequence;24 Pubmed search results 2008;Molecular Sequence Data;Membrane Proteins;Immunohistochemistry},
	Month = {4},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Program in Developmental Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.},
	Pages = {219-32},
	Pii = {S0896-6273(05)00237-0},
	Pubmed = {15848801},
	Title = {Mutations in Drosophila sec15 reveal a function in neuronal targeting for a subset of exocyst components},
	Uuid = {B66795D8-162A-45CA-BB67-F4D5377536D0},
	Volume = {46},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.02.029}}

@article{Meikle:2007,
	Abstract = {Tuberous sclerosis (TSC) is a hamartoma syndrome caused by mutations in TSC1 or TSC2 in which cerebral cortical tubers and seizures are major clinical issues. We have engineered mice in which most cortical neurons lose Tsc1 expression during embryonic development. These Tsc1 mutant mice display several neurological abnormalities beginning at postnatal day 5 with subsequent failure to thrive and median survival of 35 d. The mice also display clinical and electrographic seizures both spontaneously and with physical stimulation, and some seizures end in a fatal tonic phase. Many cortical and hippocampal neurons are enlarged and/or dysplastic in the Tsc1 mutant mice, strongly express phospho-S6, and are ectopic in multiple sites in the cortex and hippocampus. There is a striking delay in myelination in the mutant mice, which appears to be caused by an inductive neuronal defect. This new TSC brain model replicates several features of human TSC brain lesions and implicates an important function of Tsc1/Tsc2 in neuronal development.},
	Author = {Meikle, Lynsey and Talos, Delia M. and Onda, Hiroaki and Pollizzi, Kristen and Rotenberg, Alexander and Sahin, Mustafa and Jensen, Frances E. and Kwiatkowski, David J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;Animals;Seizures;comparative study;Tuberous Sclerosis;Female;Mice, Transgenic;Mice, Inbred C57BL;research support, non-u.s. gov't;Disease Models, Animal;Male;Mice, Inbred CBA;Survival Rate;10 genetics malformation;Neurons;research support, n.i.h., extramural;Mice;Tumor Suppressor Proteins;24 Pubmed search results 2008;Demyelinating Diseases},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {21},
	Organization = {Division of Translational Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.},
	Pages = {5546-58},
	Pii = {27/21/5546},
	Pubmed = {17522300},
	Title = {A mouse model of tuberous sclerosis: neuronal loss of Tsc1 causes dysplastic and ectopic neurons, reduced myelination, seizure activity, and limited survival},
	Uuid = {C191DE96-E574-48C5-9CD7-E609857BA655},
	Volume = {27},
	Year = {2007},
	url = {papers/Meikle_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5540-06.2007}}

@article{Mekel-Bobrov:2005,
	Abstract = {The gene ASPM (abnormal spindle-like microcephaly associated) is a specific regulator of brain size, and its evolution in the lineage leading to Homo sapiens was driven by strong positive selection. Here, we show that one genetic variant of ASPM in humans arose merely about 5800 years ago and has since swept to high frequency under strong positive selection. These findings, especially the remarkably young age of the positively selected variant, suggest that the human brain is still undergoing rapid adaptive evolution.},
	Author = {Mekel-Bobrov, Nitzan and Gilbert, Sandra L. and Evans, Patrick D. and Vallender, Eric J. and Anderson, Jeffrey R. and Hudson, Richard R. and Tishkoff, Sarah A. and Lahn, Bruce T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Sequence Analysis, DNA;10 Development;Animals;Adaptation, Biological;Humans;Research Support, U.S. Gov't, Non-P.H.S.;Brain;Pan troglodytes;Phylogeny;Models, Genetic;Gene Conversion;19 Neocortical evolution;Time;Haplotypes;Polymorphism, Genetic;Evolution;African Continental Ancestry Group;Gene Frequency;Recombination, Genetic;Asian Continental Ancestry Group;Genotype;Organ Size;Linkage Disequilibrium;Nerve Tissue Proteins;European Continental Ancestry Group;Selection (Genetics);Research Support, Non-U.S. Gov't},
	Month = {9},
	Nlm_Id = {0404511},
	Number = {5741},
	Organization = {Howard Hughes Medical Institute, Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA.},
	Pages = {1720-2},
	Pii = {309/5741/1720},
	Pubmed = {16151010},
	Title = {Ongoing adaptive evolution of ASPM, a brain size determinant in Homo sapiens},
	Uuid = {4371E42B-804D-40F6-BF83-1114EB210557},
	Volume = {309},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1116815}}

@article{Meletis:2006,
	Abstract = {There is increasing evidence that tumors are heterogeneous and that a subset of cells act as cancer stem cells. Several proto-oncogenes and tumor suppressors control key aspects of stem cell function, suggesting that similar mechanisms control normal and cancer stem cell properties. We show here that the prototypical tumor suppressor p53, which plays an important role in brain tumor initiation and growth, is expressed in the neural stem cell lineage in the adult brain. p53 negatively regulates proliferation and survival, and thereby self-renewal, of neural stem cells. Analysis of the neural stem cell transcriptome identified the dysregulation of several cell cycle regulators in the absence of p53, most notably a pronounced downregulation of p21 expression. These data implicate p53 as a suppressor of tissue and cancer stem cell self-renewal.},
	Author = {Meletis, Konstantinos and Wirta, Valtteri and Hede, Sanna-Maria M. and Nist{\'e}r, Monica and Lundeberg, Joakim and Fris{\'e}n, Jonas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {03 Adult neurogenesis progenitor source;22 Stem cells;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8701744},
	Number = {2},
	Organization = {Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institute, SE-171 77 Stockholm, Sweden.},
	Pages = {363-9},
	Pii = {133/2/363},
	Pubmed = {16368933},
	Title = {p53 suppresses the self-renewal of adult neural stem cells},
	Uuid = {FF1EBD28-0472-4C97-AD6B-79CB678D4769},
	Volume = {133},
	Year = {2006},
	url = {papers/Meletis_Development2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.02208}}

@article{Menezes:1998,
	Abstract = {The anterior subventricular zone (SVZa) is the site for postnatal neurogenesis of interneurons of the olfactory bulb (OB). Concurrently or after proliferation, neuronal precursors therein migrate within it to reach the OB, an event known as the rostral migratory stream (RMS). We used bromodeoxyuridine (BrdU) incorporation with short survival times to investigate the distribution of S-phase nuclei in the SVZa/RMS of the postnatal mouse. We observed that they were distributed along a radial, outside-in, decreasing gradient that persisted until postnatal day 10 (P10), then faded away to finally disappear by P16. After longer post-injection survival times labeled cell distribution became homogeneous. GFAP-positive glia are present at the periphery but not at the core of the SVZa. Our results represent the first evidence of a discrete spatial organization of a cell cycle phase within the SVZ, and also suggests a segregation of proliferating and migrating cells in the rostral migratory stream of the early postnatal mouse.},
	Author = {Menezes, J. R. and Dias, F. and Garson, A. V. and Lent, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Anat Embryol (Berl)},
	Keywords = {Neuroglia/cytology/metabolism;Glial Fibrillary Acidic Protein/metabolism;BB;Cerebral Ventricles/*cytology/growth &development;Animal;02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;Bromodeoxyuridine/metabolism;Support, Non-U.S. Gov't;Cell Division/physiology;Animals, Newborn;Olfactory Bulb/cytology/growth &development;Interneurons/cytology;Mice;Cell Movement/physiology;Immunohistochemistry;Prosencephalon/*cytology/growth &development;S Phase/*physiology},
	Number = {3},
	Organization = {Departamento de Anatomia, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Brazil. jmenezes\@anato.ufrj.br},
	Pages = {205-11.},
	Title = {Restricted distribution of S-phase cells in the anterior subventricular zone of the postnatal mouse forebrain},
	Uuid = {F6BD7F45-162C-4C6D-89B7-1E4A93A728EB},
	Volume = {198},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9764975}}

@article{Menezes:1995,
	Abstract = {In the mammalian forebrain most neurons originate from proliferating cells in the ventricular zone lining the lateral ventricles. These neurons become postmitotic before they undergo migration to their final destinations. In this study we examined the proliferative and migratory properties of cells destined for the olfactory bulb that arise postnatally from progenitor cells situated at the anterior extent of the subventricular zone (SVZa). The SVZa-derived cells migrate along a stereotypical pathway to the olfactory bulb where they become interneurons. Using lineage tracers and the cell proliferation marker BrdU, we have demonstrated that SVZa-derived cells in the rat retain the capacity for division after migrating away from their initial site of generation. These cells also express a neuron-specific tubulin, recognized by the antibody TuJ1. These results suggest that, unlike other immature neurons, these SVZa-derived cells have made a commitment to become neurons before becoming postmitotic.},
	Author = {Menezes, J. R. and Smith, C. M. and Nelson, K. C. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Olfactory Bulb/cytology/physiology;Cell Differentiation;Recombinant Proteins/analysis/biosynthesis;Neurons/*cytology/physiology;Transfection;Rats;Mitosis;Animal;Cell Movement;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Interneurons/cytology/physiology;03 Adult neurogenesis progenitor source;Animals, Newborn;beta-Galactosidase/analysis/biosynthesis;BB abstr;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Stem Cells/*cytology/physiology;Cell Division;Prosencephalon/*cytology/physiology;Immunohistochemistry},
	Number = {6},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {496-508.},
	Title = {The division of neuronal progenitor cells during migration in the neonatal mammalian forebrain},
	Uuid = {2DE28CFB-95CC-4488-AA25-39EB693E9321},
	Volume = {6},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8742267}}

@article{Menn:2006,
	Abstract = {Glial fibrillary acidic protein (GFAP)-positive astrocytes (type B cells) in the subventricular zone (SVZ) generate large numbers of new neurons in the adult brain. SVZ stem cells can also generate oligodendrocytes in vitro, but it is not known whether these adult primary progenitors generate oligodendrocytes in vivo. Myelin repair and oligodendrocyte formation in the adult brain is instead associated with glial-restricted progenitors cells, known as oligodendrocyte progenitor cells (OPCs). Here we show that type B cells also generate a small number of nonmyelinating NG2-positive OPCs and mature myelinating oligodendrocytes. Some type B cells and a small subpopulation of actively dividing type C (transit-amplifying) cells expressed oligodendrocyte lineage transcription factor 2 (Olig2), suggesting that oligodendrocyte differentiation in the SVZ begins early in the lineage. Olig2-positive, polysialylated neural cell adhesion molecule-positive, PDGF receptor alpha-positive, and beta-tubulin-negative cells originating in the SVZ migrated into corpus callosum, striatum, and fimbria fornix to differentiate into the NG2-positive nonmyelinating and mature myelinating oligodendrocytes. Furthermore, primary clonal cultures of type B cells gave rise to oligodendrocytes alone or oligodendrocytes and neurons. Importantly, the number of oligodendrocytes derived from type B cells in vivo increased fourfold after a demyelinating lesion in corpus callosum, indicating that SVZ astrocytes participate in myelin repair in the adult brain. Our work identifies SVZ type B cells as progenitors of oligodendrocytes in normal and injured adult brain.},
	Author = {Menn, B{\'e}n{\'e}dicte and Garcia-Verdugo, Jose Manuel and Yaschine, Cynthia and Gonzalez-Perez, Oscar and Rowitch, David and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Aging;24 Pubmed search results 2008;Cell Differentiation;research support, n.i.h., extramural ;Basic Helix-Loop-Helix Transcription Factors;research support, non-u.s. gov't ;Nerve Tissue Proteins;Stem Cells;Animals;Brain;Cerebral Ventricles;Mice;Oligodendroglia},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {30},
	Organization = {Department of Neurosurgery and Developmental and Stem Cell Biology Program, University of California at San Francisco, San Francisco, California 94143, USA.},
	Pages = {7907-18},
	Pii = {26/30/7907},
	Pubmed = {16870736},
	Title = {Origin of oligodendrocytes in the subventricular zone of the adult brain},
	Uuid = {FFCE7325-9713-4024-9DF9-1E1A32FA2D93},
	Volume = {26},
	Year = {2006},
	url = {papers/Menn_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1299-06.2006}}

@article{Mercier:2002,
	Abstract = {Cytogenesis in adult peripheral organs, and in all organs during development, occurs nearby basal laminae (BL) overlying connective tissue. Paradoxically, cytogenesis in the adult brain occurs primarily in the subependymal layer (SEL), a zone where no particular organization of BL and connective tissue has been described. We have reinvestigated the anatomy of the area considered the most neurogenic in the adult brain, the SEL of the lateral ventricle, in zones adjacent to the caudate putamen, corpus callosum, and lateral septal nucleus. Here, we report structural (confocal microscopy using laminin as a marker) and ultrastructural evidence for highly organized extravascular BL, unique to the SEL. The extravascular BL, termed fractones because of their fractal organization, were regularly arranged along the SEL and consisted of stems terminating in bulbs immediately underneath the ependyma. Fractones contacted local blood vessels by means of their stems. An individual fractone engulfed in its folds numerous processes of astrocytes, ependymocytes, microglial cells, and precursor cell types. The attachment site (base) of stems to blood vessels was extensively folded, overlying large perivascular macrophages that belong to a fibroblast/macrophage network coursing in the perivascular layer and through the meninges. In addition, collagen-1, which is associated with BL and growth factors during developmental morphogenetic inductions, was immunodetected in the SEL and particularly regionalized within fractones. Because macrophages and fibroblasts produce cytokines and growth factors that may concentrate in and exert their effect from the BL, we suggest that the structure described is implicated in adult neurogenesis, gliogenesis, and angiogenesis.},
	Author = {Mercier, Frederic and Kitasako, John T. and Hatton, Glenn I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Animals;Macrophages;Image Processing, Computer-Assisted;Rats;Microscopy, Confocal;Neuronal Plasticity;Brain;Fibroblasts;Rats, Sprague-Dawley;Male;Fractals;03 Adult neurogenesis progenitor source;Research Support, U.S. Gov't, P.H.S.;Nerve Net;Cerebral Ventricles;Collagen Type I;Immunohistochemistry;Microscopy, Electron;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {22198815},
	Month = {9},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Department of Cell Biology and Neuroscience, University of California, Riverside, California 92521, USA. fmercier\@pop.ucr.edu},
	Pages = {170-88},
	Pubmed = {12209835},
	Title = {Anatomy of the brain neurogenic zones revisited: fractones and the fibroblast/macrophage network},
	Uuid = {A9017865-A677-4B1B-B3AD-050049E09EE7},
	Volume = {451},
	Year = {2002},
	url = {papers/Mercier_JCompNeurol2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10342}}

@article{Mergliano:2003,
	Abstract = {Programmed cell death plays an essential role during Drosophila embryonic development. A stereotypic series of cellular changes occur during apoptosis, most of which are initiated by a caspase cascade that is triggered by a trio of proteins, RPR, HID and GRIM. The final step in apoptosis is engulfment of the cell corpse. To monitor cell engulfment in vivo, we developed a fluorogenic beta-galactosidase substrate that is cleaved by an endogenous, lysosomal beta-galactosidase activity. The pattern of cell engulfment in wild-type embryos correlated well with the known pattern of apoptosis. Surprisingly, the pattern of cell engulfment persisted in apoptosis-deficient embryos. We provide evidence for a caspase-independent engulfment process that affects the majority of cells expected to die in developing Drosophila embryos.},
	Author = {Mergliano, Jaime and Minden, Jonathan S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Gene Expression Regulation, Developmental;Research Support, U.S. Gov't, P.H.S.;Acridine Orange;Fluorescent Dyes;Biological Markers;Drosophila melanogaster;Endocytosis;beta-Galactosidase;Cell Death;Animals;Caspases;24 Pubmed search results 2008;Transgenes},
	Medline = {22934560},
	Month = {12},
	Nlm_Id = {8701744},
	Number = {23},
	Organization = {Department of Biological Sciences and Science and Technology Center for Light Microscope Imaging and Biotechnology, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA 15213, USA.},
	Pages = {5779-89},
	Pii = {dev.00824},
	Pubmed = {14534140},
	Title = {Caspase-independent cell engulfment mirrors cell death pattern in Drosophila embryos},
	Uuid = {DBDC98DA-6824-4D3D-B505-84EFE2F9B74F},
	Volume = {130},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.00824}}

@article{Merkle:2006,
	Abstract = {Neural stem cells (NSCs) are primary progenitors that give rise to neurons and glia in the embryonic, neonatal and adult brain. In recent years, we have learned three important things about these cells. First, NSCs correspond to cells previously thought to be committed glial cells. Second, embryonic and adult NSCs are lineally related: they transform from neuroepithelial cells into radial glia, then into cells with astroglial characteristics. Third, NSCs divide asymmetrically and often amplify the number of progeny they generate via symmetrically dividing intermediate progenitors. These advances challenge our traditional perceptions of glia and stem cells, and provide the foundation for understanding the molecular basis of mammalian NSC behavior.},
	Author = {Merkle, Florian T. and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0955-0674},
	Journal = {Curr Opin Cell Biol},
	Keywords = {Neurons;Transcription Factors;Cell Differentiation;research support, non-u.s. gov't;Central Nervous System;Gene Expression Regulation, Developmental;Neuroglia;24 Pubmed search results 2008;Stem Cells;research support, u.s. gov't, non-p.h.s.;research support, n.i.h., extramural;Animals;Cell Movement;Humans;review;Cell Lineage},
	Month = {12},
	Nlm_Id = {8913428},
	Number = {6},
	Organization = {Department of Neurological Surgery and Program in Developmental and Stem Cell Biology, University of California, San Francisco, Box 0525, HSW 1201A, San Francisco, California 94143, USA.},
	Pages = {704-9},
	Pii = {S0955-0674(06)00153-0},
	Pubmed = {17046226},
	Title = {Neural stem cells in mammalian development},
	Uuid = {2714E463-3C81-4E2D-9423-E6FC1B8F3C07},
	Volume = {18},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ceb.2006.09.008}}

@article{Merkle:2004,
	Abstract = {Neural stem cells with the characteristics of astrocytes persist in the subventricular zone (SVZ) of the juvenile and adult brain. These cells generate large numbers of new neurons that migrate through the rostral migratory stream to the olfactory bulb. The developmental origin of adult neural stem cells is not known. Here, we describe a lox-Cre-based technique to specifically and permanently label a restricted population of striatal radial glia in newborn mice. Within the first few days after labeling, these radial glial cells gave rise to neurons, oligodendrocytes, and astrocytes, including astrocytes in the SVZ. Remarkably, the rostral migratory stream contained labeled migratory neuroblasts at all ages examined, including 150-day-old mice. Labeling dividing cells with the S-phase marker BrdUrd showed that new neurons continue to be produced in the adult by precursors ultimately derived from radial glia. Furthermore, both radial glia in neonates and radial glia-derived cells in the adult lateral ventricular wall generated self-renewing, multipotent neurospheres. These results demonstrate that radial glial cells not only serve as progenitors for many neurons and glial cells soon after birth but also give rise to adult SVZ stem cells that continue to produce neurons throughout adult life. This study identifies and provides a method to genetically modify the lineage that links neonatal and adult neural stem cells.},
	Author = {Merkle, Florian T. and Tramontin, Anthony D. and Garc{\'\i}a-Verdugo, Jos{\'e} Manuel and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {01 Adult neurogenesis general;03 Adult neurogenesis progenitor source},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {50},
	Organization = {Department of Neurological Surgery, Developmental and Stem Cell Biology Program, Box 0525, University of California-San Francisco, San Francisco, CA 94143, USA.},
	Pages = {17528-32},
	Pii = {0407893101},
	Pubmed = {15574494},
	Title = {Radial glia give rise to adult neural stem cells in the subventricular zone},
	Uuid = {7710F98A-68D7-11DA-A4B6-000D9346EC2A},
	Volume = {101},
	Year = {2004},
	url = {papers/Merkle_ProcNatlAcadSciUSA2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0407893101}}

@article{Mestres:1980,
	Abstract = {In order to analyse whether or not surface morphology and intracellular skeleton are interdependent, Cytochalasin B (CB), an agent which interferes with microfilaments, was introduced ino the brain ventricular system of adult rats. Following intraventricular application of CB for different periods of time (up to 6h) the animals were sacrificed and the ventricular wall examined with both transmission and scanning electron microscopes. The first signs of cellular alteration after short periods of CB application were an increase in the number of microfilaments within the cytoplasm and the appearance of a multitude of small knobs on the surface of the cilia of the cuboidal ependymal cells, whereas the tanycytes exhibited extensive blebbing at their apical poles. When the duration of CB perfusion was lengthened, entire ciliated cells became rounded up and were loosened from the epithelium, especially in the transition zone of the third ventricle where the ependyma is composed of both tanycytes and ciliated cells. The significance of the CB-induced changes in the ependyma are discussed in relation to the ependymal surface modifications seen under physiological and other experimental conditions. 0586-5581 Journal Article},
	Author = {Mestres, P. and Garfia, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Scan Electron Microsc},
	Keywords = {Cell Adhesion/drug effects;Biological Transport/drug effects;Rats;Microscopy, Electron, Scanning;08 Aberrant cell cycle;Cytochalasin B/*pharmacology;Hypothalamus/*drug effects;EE, G abstr;Ependyma/cytology/*drug effects;Cytoskeleton/drug effects;Animals;Male;Cell Membrane/ultrastructure;Cilia/ultrastructure},
	Number = {3},
	Pages = {465-74},
	Pubmed = {7191139},
	Title = {Effects of cytochalasin B on the ependyma},
	Uuid = {2CBD9D02-1850-4ADC-8B72-4DB766E3CC25},
	Year = {1980},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7191139}}

@article{Metin:1996,
	Abstract = {In the nervous system of many species, growing axons associate transiently with cellular groupings along their path. Whether this mechanism applies to the development of corticothalamic and thalamocortical projections is unknown. Using carbocyanine dyes, we studied the early growth of both corticofugal and thalamocortical fibers in hamster embryos. At embryonic day 11.5 (E11.5), corticofugal fibers invade the lateral ganglionic eminence (LGE), and thalamocortical fibers invade the medial ganglionic eminence (MGE). At this age, both sets of fibers are not yet in contact with each other. At the same time, neurons in each subdivision of the GE grow toward the cortex and thalamus. During the next 24 hr, corticofugal and thalamocortical fibers remain within the confines of the GE, where they course at different radial levels and bear large and complex growth cones. In the LGE, corticofugal fibers are often found in close association with cells that are likely to be neuronal. Starting on E13.5, both early projections from the GE decrease, and corticothalamic and thalamocortical fibers invade their definitive target regions. To test whether the GE specifically orients the growth and trajectories of cortical fibers even in the absence of the reciprocal thalamic projection, we cocultured explants of cortex and GE from either hamster or mouse embryos. These experiments showed that the GE, but not other tested brain regions, is able specifically to orient the growth of cortical axons. We therefore suggest that the GE may be an intermediate target in the pathfinding of axons between the cortex and the thalamus. 0270-6474 Journal Article},
	Author = {Metin, C. and Godement, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {J Neurosci},
	Keywords = {Cerebral Cortex/*anatomy &histology;Axons/*physiology;Thalamus/*anatomy &histology;Immunohistochemistry;Neural Pathways/physiology;Mice, Inbred C57BL;N;Ganglia/*anatomy &histology;Support, Non-U.S. Gov't;Animals;Hamsters;Mice;19 Neocortical evolution},
	Number = {10},
	Organization = {Institut Alfred Fessard, Centre National de la Recherche Scientifique UPR 2212, Gif-sur-Yvette, France.},
	Pages = {3219-35},
	Pubmed = {8627360},
	Title = {The ganglionic eminence may be an intermediate target for corticofugal and thalamocortical axons},
	Uuid = {C888318E-EE6E-4C00-BD7E-6F5A10CEEB35},
	Volume = {16},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8627360}}

@article{Meucci:2000,
	Abstract = {Recent in vitro and in vivo studies have shown that the chemokine fractalkine is widely expressed in the brain and localized principally to neurons. Central nervous system expression of CX(3)CR1, the only known receptor for fractalkine, has been demonstrated exclusively on microglia and astrocytes. Thus, it has been proposed that fractalkine regulates cellular communication between neurons (that produce fractalkine) and microglia (that express its receptor). Here we show, for the first time, that hippocampal neurons also express CX(3)CR1. Receptor activation by soluble fractalkine induces activation of the protein kinase Akt, a major component of prosurvival signaling pathways, and nuclear translocation of NF-kappaB, a downstream effector of Akt. Fractalkine protects hippocampal neurons from the neurotoxicity induced by the HIV-1 envelope protein gp120(IIIB), an effect blocked by anti-CX(3)CR1 antibodies. Experiments with two different inhibitors of the phosphatidylinositol 3-kinase, a key enzyme in the activation of Akt, and with a phospholipid activator of Akt demonstrate that Akt activation is responsible for the neuroprotective effects of fractalkine. These data show that neuronal CX(3)CR1 receptors mediate the neurotrophic effects of fractalkine, suggesting that fractalkine and its receptor are involved in a complex network of both paracrine and autocrine interactions between neurons and glia.},
	Author = {Meucci, O. and Fatatis, A. and Simen, A. A. and Miller, R. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Survival;Signal Transduction;Animals;Astrocytes;DNA-Binding Proteins;Rats;NF-kappa B;Phosphatidylinositols;Recombinant Proteins;Culture Techniques;Receptors, HIV;Hippocampus;Protein-Serine-Threonine Kinases;11 Glia;1-Phosphatidylinositol 3-Kinase;Chemokines, CX3C;Research Support, U.S. Gov't, P.H.S.;I-kappa B;Neurons;Chemokines, CXC;24 Pubmed search results 2008;Proto-Oncogene Proteins;Membrane Proteins;Receptors, Cytokine},
	Medline = {20345114},
	Month = {7},
	Nlm_Id = {7505876},
	Number = {14},
	Organization = {Department of Neurobiology, Pharmacology, and Physiology, and Committee on Neurobiology, University of Chicago, Chicago, IL 60637, USA.},
	Pages = {8075-80},
	Pii = {090017497},
	Pubmed = {10869418},
	Title = {Expression of CX3CR1 chemokine receptors on neurons and their role in neuronal survival},
	Uuid = {2ACA9BFB-DA87-4C70-9115-EA9DF6C7A7E9},
	Volume = {97},
	Year = {2000},
	url = {papers/Meucci_ProcNatlAcadSciUSA2000.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.090017497}}

@article{Meuth:1974,
	Author = {Meuth, M. and Green, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {15 ERVs retroelements;Animals;24 Pubmed search results 2008;DNA;Deoxycytidine;Cell Survival;Cell Aggregation;15 Retrovirus mechanism;Cells, Cultured;Bromodeoxyuridine;Ribonucleotide Reductases;Bromouracil;Mice},
	Medline = {75129340},
	Month = {6},
	Nlm_Id = {0413066},
	Number = {2},
	Pages = {109-12},
	Pii = {0092-8674(74)90099-3},
	Pubmed = {4477047},
	Title = {Induction of a deoxycytidineless state in cultured mammalian cells by bromodeoxyuridine},
	Uuid = {8DFFAC32-4328-11DB-A5D2-000D9346EC2A},
	Volume = {2},
	Year = {1974}}

@article{Mey:2005,
	Abstract = {Retinoic acid (RA) promotes growth and differentiation in many developing tissues but less is known about its influence on CNS regeneration. We investigated the possible involvement of RA in rat spinal cord injury (SCI) using the New York University (NYU) impactor to induce mild or moderate spinal cord contusion injury. Changes in RA at the lesion site were determined by measuring the activity of the enzymes for its synthesis, the retinaldehyde dehydrogenases (RALDHs). A marked increase in enzyme activity occurred by day 4 and peaked at days 8-14 following the injuries. RALDH2 was the only detectable RALDH present in the control or injured spinal cord. The cellular localization of RALDH2 was identified by immunostaining. In the noninjured spinal cord, RALDH2 was detected in oligodendroglia positive for the markers RIP and CNPase. Expression was also intense in the arachnoid membrane surrounding the spinal cord. After SCI the increase in RALDH2 was independent of the RIP- and CNPase-positive cells, which were severely depleted. Instead, RALDH2 was present in a cell type not previously identified as capable of synthesizing RA, that expressed NG2 and that was negative for markers of astrocytes, oligodendroglia, microglia, neurons, Schwann cells and immature lymphocytes. We postulate that the RALDH2- and NG2-positive cells migrate into the injured sites from the adjacent arachnoid membrane, where the RALDH2-positive cells proliferate substantially following SCI. These findings indicate that close correlations exist between RA synthesis and SCI and that RA may play a role in the secondary events that follow acute SCI.},
	Author = {Mey, J{\"o}rg and J Morassutti, Dante and Brook, Gary and Liu, Rong-Huan H. and Zhang, Yi-Ping P. and Koopmans, Guido and McCaffery, Peter},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Rats, Sprague-Dawley;Research Support, Non-U.S. Gov't;Spinal Cord Injuries;Comparative Study;Rats;Research Support, U.S. Gov't, P.H.S.;Aldehyde Oxidoreductases;Tretinoin;Antigens;Research Support, N.I.H., Extramural;11 Glia;Male;Proteoglycans;Animals},
	Month = {3},
	Nlm_Id = {8918110},
	Number = {6},
	Organization = {Institute of Biology II, RWTH Aachen, Germany.},
	Pages = {1555-68},
	Pii = {EJN3928},
	Pubmed = {15845083},
	Title = {Retinoic acid synthesis by a population of NG2-positive cells in the injured spinal cord},
	Uuid = {39EC210E-C63C-4B45-BA3C-538AE5A74031},
	Volume = {21},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2005.03928.x}}

@article{Mezey:2003,
	Abstract = {Adult bone marrow stem cells seem to differentiate into muscle, skin, liver, lung, and neuronal cells in rodents and have been shown to regenerate myocardium, hepatocytes, and skin and gastrointestinal epithelium in humans. Because we have demonstrated previously that transplanted bone marrow cells can enter the brain of mice and differentiate into neurons there, we decided to examine postmortem brain samples from females who had received bone marrow transplants from male donors. The underlying diseases of the patients were lymphocytic leukemia and genetic deficiency of the immune system, and they survived between 1 and 9 months after transplant. We used a combination of immunocytochemistry (utilizing neuron-specific antibodies) and fluorescent in situ hybridization histochemistry to search for Y chromosome-positive cells. In all four patients studied we found cells containing Y chromosomes in several brain regions. Most of them were nonneuronal (endothelial cells and cells in the white matter), but neurons were certainly labeled, especially in the hippocampus and cerebral cortex. The youngest patient (2 years old), who also lived the longest time after transplantation, had the greatest number of donor-derived neurons (7 in 10,000). The distribution of the labeled cells was not homogeneous. There were clusters of Y-positive cells, suggesting that single progenitor cells underwent clonal expansion and differentiation. We conclude that adult human bone marrow cells can enter the brain and generate neurons just as rodent cells do. Perhaps this phenomenon could be exploited to prevent the development or progression of neurodegenerative diseases or to repair tissue damaged by infarction or trauma.},
	Author = {Mezey, Eva and Key, Sharon and Vogelsang, Georgia and Szalayova, Ildiko and Lange, G. David and Crain, Barbara},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Microscopy, Confocal;In Situ Hybridization, Fluorescence;Cell Differentiation;Adult;Infant;Immunohistochemistry;Female;Bone Marrow Cells;Cell Division;Bone Marrow Transplantation;22 Stem cells;Microscopy, Fluorescence;Child;Male;Brain;Humans;Neurons},
	Medline = {22457179},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {3},
	Organization = {National Institutes of Health (NIH)/National Institute of Neurological Disorders and Stroke (NINDS)/In situ Hybridization Facility (ISHF), Bethesda, MD 20892, USA. mezey\@codon.nih.gov},
	Pages = {1364-9},
	Pii = {0336479100},
	Pubmed = {12538864},
	Title = {Transplanted bone marrow generates new neurons in human brains},
	Uuid = {37E716AA-D3B2-11D9-A0E9-000D9346EC2A},
	Volume = {100},
	Year = {2003},
	url = {papers/Mezey_ProcNatlAcadSciUSA2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0336479100}}

@article{Mezey:2000,
	Abstract = {Bone marrow stem cells give rise to a variety of hematopoietic lineages and repopulate the blood throughout adult life. We show that, in a strain of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone marrow cells migrated into the brain and differentiated into cells that expressed neuron-specific antigens. These findings raise the possibility that bone marrow-derived cells may provide an alternative source of neurons in patients with neurodegenerative diseases or central nervous system injury.},
	Author = {Mezey, E. and Chandross, K. J. and Harta, G. and Maki, R. A. and McKercher, S. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Cell Differentiation;Animals;Stem Cell Transplantation;Bone Marrow Transplantation;Microscopy, Confocal;Immunoenzyme Techniques;Brain;Phosphopyruvate Hydratase;Female;Cell Movement;Male;Research Support, U.S. Gov't, P.H.S.;Antigens;Bone Marrow Cells;Mice, Knockout;Intermediate Filament Proteins;Neurons;Mice;Y Chromosome;Stem Cells;Biological Markers;Nerve Tissue Proteins},
	Medline = {20553650},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5497},
	Organization = {Basic Neuroscience Program, Laboratory of Developmental Neurogenetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. mezey\@codon.nih.gov},
	Pages = {1779-82},
	Pii = {9025},
	Pubmed = {11099419},
	Title = {Turning blood into brain: cells bearing neuronal antigens generated in vivo from bone marrow},
	Uuid = {ED9BE605-99B6-4936-86D6-B08EF3B9C7BD},
	Volume = {290},
	Year = {2000},
	url = {papers/Mezey_Science2000.pdf}}

@article{Mi:2000,
	Abstract = {Many mammalian viruses have acquired genes from their hosts during their evolution. The rationale for these acquisitions is usually quite clear: the captured genes are subverted to provide a selective advantage to the virus. Here we describe the opposite situation, where a viral gene has been sequestered to serve an important function in the physiology of a mammalian host. This gene, encoding a protein that we have called syncytin, is the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W. We find that the major sites of syncytin expression are placental syncytiotrophoblasts, multinucleated cells that originate from fetal trophoblasts. We show that expression of recombinant syncytin in a wide variety of cell types induces the formation of giant syncytia, and that fusion of a human trophoblastic cell line expressing endogenous syncytin can be inhibited by an anti-syncytin antiserum. Our data indicate that syncytin may mediate placental cytotrophoblast fusion in vivo, and thus may be important in human placental morphogenesis.},
	Author = {Mi, S. and Lee, X. and Li, X. and Veldman, G. M. and Finnerty, H. and Racie, L. and LaVallie, E. and Tang, X. Y. and Edouard, P. and Howes, S. and Keith, J. C. and McCoy, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Interleukin-12;Gene Products, env;Tissue Distribution;Animals;Humans;Sequence Homology, Amino Acid;Transfection;15 Retrovirus mechanism;Cell Fusion;Trophoblasts;Endogenous Retroviruses;COS Cells;Giant Cells;Hela Cells;Green Fluorescent Proteins;Proviruses;Genes, Viral;Tumor Cells, Cultured;Pregnancy Proteins;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;15 ERVs retroelements;Luminescent Proteins;Gene Expression},
	Medline = {20155476},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {6771},
	Organization = {Genetics Institute, Inc., Cambridge, Massachusetts 02140, USA.},
	Pages = {785-9},
	Pubmed = {10693809},
	Title = {Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis},
	Uuid = {A12D8DB6-EE4C-11DA-8605-000D9346EC2A},
	Volume = {403},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35001608}}

@article{Michaels:1988,
	Abstract = {The autopsied brains of three homosexual men with acquired immune deficiency syndrome (AIDS), progressive encephalopathy and widespread multinucleated giant cell encephalitis were investigated by lectin and immunohistochemical methods to ascertain the cellular distribution of a human immunodeficiency virus (HIV) core protein, p25. Abundant viral antigen was present in all brains, limited to perivascular macrophages, microglial and multinucleated cells, some bearing elongated cytoplasmic processes. The multinucleated cells were consistently labelled by the lectin Ricinus communis agglutinin-1, a marker for microglia, which demonstrated process-bearing variants of these cells. The prominent staining of microglia for viral antigen and the morphological suggestion that they fuse with other microglia and/or macrophages to form the multinucleated cells characteristic of HIV encephalitis indicate that microglia are probably direct targets of HIV infection and serve to propagate and amplify this retroviral encephalitis.},
	Author = {Michaels, J. and Price, R. W. and Rosenblum, M. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Ricin;Neuroglia;Research Support, Non-U.S. Gov't;Aged;Encephalitis;Adult;Research Support, U.S. Gov't, P.H.S.;HIV Antigens;Viral Core Proteins;Middle Aged;Homosexuality;Acquired Immunodeficiency Syndrome;11 Glia;Humans;Male;HIV},
	Medline = {89021907},
	Nlm_Id = {0412041},
	Number = {4},
	Organization = {Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.},
	Pages = {373-9},
	Pubmed = {3176903},
	Title = {Microglia in the giant cell encephalitis of acquired immune deficiency syndrome: proliferation, infection and fusion},
	Uuid = {F0C6C354-2299-4372-85CF-9CEA7B7B48B6},
	Volume = {76},
	Year = {1988}}

@article{Migheli:1999,
	Abstract = {A missense mutation in the gene coding for the G-protein-activated inwardly rectifying potassium (GIRK) channel, GIRK2, is responsible for apoptosis in the external germinal layer (EGL) of the cerebellum and a nonapoptotic death of midbrain dopaminergic neurons in the weaver (wv) mouse. Failure of axonogenesis and migration are considered to be the primary consequences of GIRK2 channel malfunction in the cerebellum. We investigated whether a disruption of the cell cycle precedes the failure of migration and axonogenesis and leads to massive apoptosis. To this end, immunohistochemistry and immunoblotting for PCNA, Cdk4, cyclin D, cyclin A, and the Cdk inhibitor p27/kip1, as well as in situ end-labeling for apoptotic DNA fragmentation, were applied to cerebella of P7-P21+/+, wv/+, and wv/wv mice. In +/+ and wv/+ mice, the expression of cell cycle proteins was limited to the outer, premigratory zone of the EGL. Antibodies to p27, a marker of cell differentiation, gave a reverse staining pattern. Due to migration delay, patches of p27-positive cells persisted in the outer EGL in P21 wv/+ mice. On the contrary, marked cell cycle up-regulation and absence of p27 occurred throughout the EGL at all ages in wv/wv mice, indicating an inability to switch off the cell cycle. Mitotic index evaluation showed that cell cycle activation was unrelated to proliferative events. Cell cycle proteins were not expressed in the substantia nigra, suggesting that nonapoptotic death of mature dopaminergic neurons is not preceded by abortive cell cycle re-entry. Our data show that abnormalities of the cell cycle in wv/wv cerebellum represent a major and early consequence of GIRK2 channel malfunction and may strongly influence the susceptibility of EGL cells to apoptosis. These observations may help in understanding the pathogenesis of human neurological channelopathies. 0002-9440 Journal Article},
	Author = {Migheli, A. and Piva, R. and Casolino, S. and Atzori, C. and Dlouhy, S. R. and Ghetti, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Am J Pathol},
	Keywords = {Potassium Channels/metabolism;Human;Animals;Cyclins/analysis/*metabolism;Ion Channels/physiology;*Cell Cycle Proteins;Mitosis;EE pdf;*Tumor Suppressor Proteins;Cyclin-Dependent Kinases/analysis/antagonists &inhibitors/*metabolism;08 Aberrant cell cycle;Substantia Nigra/anatomy &histology/physiology;Microtubule-Associated Proteins/analysis/*metabolism;*Mice, Neurologic Mutants;In Situ Hybridization;Support, Non-U.S. Gov't;*Apoptosis;*Cell Cycle;Mitotic Index;DNA Damage;Genotype;Support, U.S. Gov't, P.H.S.;Mice;Immunohistochemistry;Proliferating Cell Nuclear Antigen/*analysis/*metabolism;Cerebellum/*metabolism/*physiology;DNA Fragmentation;Cyclin A/analysis/*metabolism},
	Number = {2},
	Organization = {Department of Neuroscience, Laboratory of Neuropathology, University of Turin, Italy.},
	Pages = {365-73},
	Title = {A cell cycle alteration precedes apoptosis of granule cell precursors in the weaver mouse cerebellum},
	Uuid = {77F51F59-226A-43C8-B65D-88D45D67BC23},
	Volume = {155},
	Year = {1999},
	url = {papers/Migheli_AmJPathol1999.pdf}}

@article{Mignone:2004,
	Abstract = {Neural stem cells generate a wide spectrum of cell types in developing and adult nervous systems. These cells are marked by expression of the intermediate filament nestin. We used the regulatory elements of the nestin gene to generate transgenic mice in which neural stem cells of the embryonic and adult brain are marked by the expression of green fluorescent protein (GFP). We used these animals as a reporter line for studying neural stem and progenitor cells in the developing and adult nervous systems. In these nestin-GFP animals, we found that GFP-positive cells reflect the distribution of nestin-positive cells and accurately mark the neurogenic areas of the adult brain. Nestin-GFP cells can be isolated with high purity by using fluorescent-activated cell sorting and can generate multipotential neurospheres. In the adult brain, nestin-GFP cells are approximately 1,400-fold more efficient in generating neurospheres than are GFP-negative cells and, despite their small number, give rise to 70 times more neurospheres than does the GFP-negative population. We characterized the expression of a panel of differentiation markers in GFP-positive cells in the nestin-GFP transgenics and found that these cells can be divided into two groups based on the strength of their GFP signal: GFP-bright cells express glial fibrillary acidic protein (GFAP) but not betaIII-tubulin, whereas GFP-dim cells express betaIII-tubulin but not GFAP. These two classes of cells represent distinct classes of neuronal precursors in the adult mammalian brain, and may reflect different stages of neuronal differentiation. We also found unusual features of nestin-GFP-positive cells in the subgranular cell layer of the dentate gyrus. Together, our results indicate that GFP-positive cells in our transgenic animals accurately represent neural stem and progenitor cells and suggest that these nestin-GFP-expressing cells encompass the majority of the neural stem cells in the adult brain.},
	Author = {Mignone, John L. and Kukekov, Valery and Chiang, Ann-Shyn S. and Steindler, Dennis and Enikolopov, Grigori},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Green Fluorescent Proteins;Immunohistochemistry;Luminescent Proteins;Animals;Cells, Cultured;Brain;Flow Cytometry;Hippocampus;Gene Expression Regulation, Developmental;Research Support, U.S. Gov't, P.H.S.;Stem Cell Transplantation;Proteins;Cell Count;Intermediate Filament Proteins;Bromodeoxyuridine;Tubulin;11 Glia;Comparative Study;Glial Fibrillary Acidic Protein;Time Factors;Embryo;Stem Cells;Indicators and Reagents;Microscopy, Confocal;Mice;Research Support, Non-U.S. Gov't;Neurons;Mice, Transgenic;Reverse Transcriptase Polymerase Chain Reaction;Nerve Tissue Proteins},
	Month = {2},
	Nlm_Id = {0406041},
	Number = {3},
	Organization = {Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.},
	Pages = {311-24},
	Pubmed = {14730584},
	Title = {Neural stem and progenitor cells in nestin-GFP transgenic mice},
	Uuid = {6A7851D4-B1E3-41B4-978F-762F33AF7919},
	Volume = {469},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10964}}

@article{Mikhailov:1998,
	Abstract = {Microtubules (MTs) contribute to the directional locomotion of many cell types through an unknown mechanism. Previously, we showed that low concentrations (<200 nM) of nocodazole or taxol reduced the rate of locomotion of NRK fibroblasts over 60\%without altering MT polymer level [Liao et al., 1995: J. Cell Sci. 108:3473-3483]. In this paper, we directly measured the dynamics of MTs in migrating NRK cells injected with rhodamine tubulin and treated with low concentrations of nocodazole or taxol. Both drug treatments caused statistically significant reductions (approx. twofold) in growth and shortening rates and less dramatic effects on rescue and catastrophe transition frequencies. The percent time MTs were inactive (i.e., paused) increased greater than twofold in nocodazole- and taxol-treated cells, while the percent time growing was substantially reduced. Three parameters of MT dynamics were linearly related to the rates of locomotion determined previously: rate of shortening, percent time pausing and percent time growing. The number of MTs that came within 1 microm of the leading edge was reduced in drug-treated cells, suggesting that reduced MT dynamics may affect actin arrays necessary for cell locomotion. We examined two such structures, lamellipodium and adhesion plaques, and found that lamellipodia area was coordinately reduced with MT dynamics. No effect was detected on adhesion plaque density or distribution. In time-lapse recordings, MTs did not penetrate into the lamellipodium of untreated cells, suggesting that MTs affect lamellipodia either through their interaction with factors at the base of the lamellipodium or by releasing factors that diffuse into the lamellipodia. In support of the latter hypothesis, when all MTs were rapidly depolymerized by 20 microM nocodazole, we detected the rapid formation of exaggerated protrusions from the leading edge of the cell. Our results show for the first time a linear relationship between MT dynamics and the formation of the lamellipodium and support the idea that MT dynamics may contribute to cell locomotion by regulating the size of the lamellipodium, perhaps through diffusable factors. 0886-1544 Journal Article},
	Author = {Mikhailov, A. and Gundersen, G. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Cell Motil Cytoskeleton},
	Keywords = {Cell Movement/drug effects/physiology;EE, T abstr;EE, T pdf;Paclitaxel/*pharmacology;Image Processing, Computer-Assisted;Cell Adhesion;Cell Line;08 Aberrant cell cycle;Dose-Response Relationship, Drug;Tyrosine;Support, U.S. Gov't, P.H.S.;Animals;Support, Non-U.S. Gov't;Microtubules/drug effects/*physiology;Nocodazole/*pharmacology},
	Number = {4},
	Organization = {Department of Pathology, Columbia University, New York, New York 10032, USA.},
	Pages = {325-40},
	Pubmed = {9858157},
	Title = {Relationship between microtubule dynamics and lamellipodium formation revealed by direct imaging of microtubules in cells treated with nocodazole or taxol},
	Uuid = {922E92A0-243A-43D8-8363-D4394451C121},
	Volume = {41},
	Year = {1998},
	url = {papers/Mikhailov_CellMotilCytoskeleton1998}}

@article{Mikita:1988,
	Abstract = {Cytosine arabinoside (araC) is a potent antileukemic agent that is misincorporated into DNA in the course of its action. We have developed a chemical synthetic method that allows site-specific introduction of araC into synthetic DNA oligomers. We describe here the utilization of these oligomers as primer/template substrates for in vitro DNA synthesis reactions and as fragments for DNA ligation. These studies were undertaken to investigate the manner in which sites of araC misincorporation constitute sites of DNA dysfunction. AraCMP at the primer terminus dramatically reduced the rate of next nucleotide addition for Escherichia coli polymerase I (Klenow fragment) (Pol I), T4 polymerase, HeLa cell polymerase alpha 2 (Pol alpha 2), and AMV reverse transcriptase. Polymerases with associated 3'-5'exonuclease activity preferentially excised araCMP from the primer terminus prior to chain elongation. AraCMP-terminated fragments were ligated more slowly than control fragments by T4 DNA ligase. AraCMP located at an internucleotide site in the template markedly slowed replicative bypass for Pol I, T4 polymerase, and Pol alpha 2, but not for reverse transcriptase. Synthesis was partially arrested after insertion of the correct nucleotide opposite the lesion site. These results suggest a complex mechanism for the inhibition of DNA replication by araC when it is misincorporated into DNA. 0006-2960 Journal Article},
	Author = {Mikita, T. and Beardsley, G. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Biochemistry},
	Keywords = {Base Sequence;RNA-Directed DNA Polymerase/metabolism;*DNA Damage;Human;DNA Polymerase II/metabolism;08 Aberrant cell cycle;DNA Polymerase I/metabolism;Hela Cells/enzymology;EE abstr;DNA-Directed DNA Polymerase/*metabolism;Escherichia coli/enzymology;Oligodeoxyribonucleotides/chemical synthesis;DNA/*chemical synthesis;Support, U.S. Gov't, P.H.S.;Templates, Genetic;*Cytarabine},
	Number = {13},
	Organization = {Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06510.},
	Pages = {4698-705},
	Pubmed = {2458756},
	Title = {Functional consequences of the arabinosylcytosine structural lesion in DNA},
	Uuid = {B9F64701-A6C7-4111-8B4E-D9447F819D36},
	Volume = {27},
	Year = {1988},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2458756}}

@article{Miller:1988,
	Abstract = {The use of an exogenously administered thymidine analog, 5-bromo-2'-deoxyuridine (BrdU), for studies of the proliferation, migration and time of origin of cells in the cerebral cortex was investigated and compared with [3H]thymidine [( 3H]dT) autoradiography. Pregnant rats or mice were injected with BrdU and/or [3H]dT and processed by standard immunohistochemical techniques using a primary antibody directed against BrdU in single-stranded DNA, autoradiographic methods, or both. In animals that survived only 1 h after the injection, BrdU-positive cells were distributed in the proliferative zones throughout the central nervous system (CNS). In animals killed 1-3 days after the BrdU injection, intensely immunoreactive cells were in the superficial cortical plate and less intensely labeled cells were scattered throughout the deep cortical plate, the intermediate zone, and the germinal zones. In adult animals, 60 days or more after an injection of BrdU on GD 19, BrdU-positive cells were located in layer II/III of neocortex, the hippocampal pyramidal layer, and the granule layer of the dentate gyrus. In the double-labeling studies, the distribution of BrdU-immunoreactive cells was identical to that of autoradiographically labeled cells, and all autoradiographically labeled neurons were BrdU positive. Thus, BrdU immunohistochemistry is suitable for developmental studies of the CNS; moreover, it provides several advantages over [3H]dT autoradiography.},
	Author = {Miller, M. W. and Nowakowski, R. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Pregnancy;Cell Differentiation;Animals;Rats;Comparative Study;Brain;Thymidine;Female;Cell Movement;23 Technique;Rats, Inbred Strains;Time Factors;01 Adult neurogenesis general;Research Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Immunohistochemistry;Autoradiography;Bromodeoxyuridine;Research Support, Non-U.S. Gov't},
	Medline = {89002086},
	Month = {8},
	Nlm_Id = {0045503},
	Number = {1},
	Organization = {Department of Anatomy, School of Osteopathic Medicine, University of Medicine and Dentistry of New Jersey, Piscataway 08854.},
	Pages = {44-52},
	Pii = {0006-8993(88)90055-8},
	Pubmed = {3167568},
	Title = {Use of bromodeoxyuridine-immunohistochemistry to examine the proliferation, migration and time of origin of cells in the central nervous system},
	Uuid = {01DF6DA8-42A3-11DB-A5D2-000D9346EC2A},
	Volume = {457},
	Year = {1988}}

@article{Miller:1993,
	Abstract = {Postmitotic neurons migrate from a zone(s) near the ventricles to the neocortex. During this migration, neurons associate with radial glia. After serving their role as guides for neuronal migration, the radial glia transform into astrocytes. Prenatal exposure to ethanol causes abnormal neuronal migration. We examined the effects of gestational exposure to ethanol on radial glia and astrocytes. Radial glia were stained immunohistochemically with the antibody RAT-401, and astrocytes were labeled with an antibody directed against glial fibrillary acidic protein (GFAP). The subjects were the offspring of rats fed an ethanol- containing liquid diet (Et), pair-fed a liquid control diet (Ct), or fed chow and water (Ch). During the first postnatal week, radial glial fibers (in Et-treated rats and controls) stretched from the ventricular surface through the developing cerebral wall to the pial surface. In the Et-treated rats, the radial processes were less dense and more poorly fasciculated than they were in the Ch- and Ct-treated rats. Moreover, by postnatal day (P) 5, there was a significant reduction in RAT-401 immunostaining in the Et-treated rats, particularly in the superficial cortex. A similar reduction in control rats did not begin until P10. In all three treatment groups, GFAP-immunoreactive astrocytes were in the cortex throughout the period from P1 to P45. In neonates, GFAP-positive cells were distributed in the marginal zone (layer I) and the intermediate zone (the white matter). The number of GFAP-positive cells in the cortical plate increased steadily with time so that, by P26, GFAP-immunoreactive astrocytes were distributed evenly through all cortical laminae. Interestingly, between P5 and P12, the number of astrocytes was significantly greater in Et-treated rats than in controls. Thus prenatal exposure to ethanol induces the premature loss of RAT-401-positive processes and the precocious increase in GFAP immunostaining. These ethanol-induced changes in glial development indicate that ethanol accelerates the transformation of radial glia into astrocytes. Moreover, the ethanol-induced premature degradation of the network of radial glial fibers may underlie the migration of late- generated neurons to ectopic sites.},
	Author = {Miller, M. W. and Robertson, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Rats, Sprague-Dawley;Prenatal Exposure Delayed Effects;Neuroglia/*drug effects;Female;Rats;Glial Fibrillary Acidic Protein/immunology/metabolism;Ethanol/*pharmacology;Astrocytes/*drug effects;11 Glia;Animal;Pregnancy;Support, U.S. Gov't, P.H.S.;G;Cerebral Cortex/*cytology/drug effects/*growth &development},
	Number = {2},
	Organization = {Research Service, Veterans Affairs Medical Center, Iowa City, Iowa 52246.},
	Pages = {253-66.},
	Title = {Prenatal exposure to ethanol alters the postnatal development and transformation of radial glia to astrocytes in the cortex},
	Uuid = {40A39CF4-74CA-4B85-AD7D-1B7C379A735E},
	Volume = {337},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8276999}}

@article{Miller:2007,
	Abstract = {DNA methylation is a covalent chemical modification of DNA catalyzed by DNA methyltransferases (DNMTs). DNA methylation is associated with transcriptional silencing and has been studied extensively as a lifelong molecular information storage mechanism put in place during development. Here we report that DNMT gene expression is upregulated in the adult rat hippocampus following contextual fear conditioning and that DNMT inhibition blocks memory formation. In addition, fear conditioning is associated with rapid methylation and transcriptional silencing of the memory suppressor gene PP1 and demethylation and transcriptional activation of the synaptic plasticity gene reelin, indicating both methyltransferase and demethylase activity during consolidation. DNMT inhibition prevents the PP1 methylation increase, resulting in aberrant transcription of the gene during the memory-consolidation period. These results demonstrate that DNA methylation is dynamically regulated in the adult nervous system and that this cellular mechanism is a crucial step in memory formation.},
	Author = {Miller, Courtney A. and Sweatt, J. David},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Phosphoprotein Phosphatase;Animals;Fear;Rats;Enzyme Inhibitors;Memory;DNA;Models, Biological;Rats, Sprague-Dawley;Hippocampus;Cell Adhesion Molecules, Neuronal;Azacitidine;research support, non-u.s. gov't;Behavior, Animal;Gene Expression Regulation, Enzymologic;Reverse Transcriptase Polymerase Chain Reaction;Male;Serine Endopeptidases;Extracellular Matrix Proteins;Conditioning, Classical;21 Neurophysiology;DNA (Cytosine-5-)-Methyltransferase;research support, n.i.h., extramural;24 Pubmed search results 2008;Nerve Tissue Proteins;DNA Methylation},
	Month = {3},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Neurobiology and the Evelyn F. McKnight Brain Institute,University of Alabama at Birmingham, Birmingham, AL 35294, USA.},
	Pages = {857-69},
	Pii = {S0896-6273(07)00142-0},
	Pubmed = {17359920},
	Title = {Covalent modification of DNA regulates memory formation},
	Uuid = {B2347B89-1B63-4C82-9C78-3F0A365CF6B0},
	Volume = {53},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.02.022}}

@article{Miller:2007a,
	Abstract = {During development of the mammalian nervous system, neural stem cells generate neurons first and glia second, thereby allowing the initial establishment of neural circuitry, and subsequent matching of glial numbers and position to that circuitry. Here, we have reviewed work addressing the mechanisms underlying this timed cell genesis, with a particular focus on the developing cortex. These studies have defined an intriguing interplay between intrinsic epigenetic status, transcription factors, and environmental cues, all of which work together to establish this fascinating and complex biological timing mechanism.},
	Author = {Miller, Freda D. and Gauthier, Andr{\'e}e S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Developmental & Stem Cell Biology, Hospital for Sick Children, Toronto M5G 1X8, Canada; Department of Molecular & Medical Genetics, University of Toronto, Toronto M5S 1A8, Canada; Department of Physiology, University of Toronto, Toronto M5S 1A8, Canada.},
	Pages = {357-69},
	Pii = {S0896-6273(07)00298-X},
	Pubmed = {17481390},
	Title = {Timing Is Everything: Making Neurons versus Glia in the Developing Cortex},
	Uuid = {FE52E7C9-5829-4E58-BE62-118B159DF3E2},
	Volume = {54},
	Year = {2007},
	url = {papers/Miller_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.04.019}}

@article{Miller:2006,
	Author = {Miller, Greg},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Mice;Mutation;Neurons;Methyl-CpG-Binding Protein 2;Phosphorylation;24 Pubmed search results 2008;Female;Gene Silencing;Rett Syndrome;Brain-Derived Neurotrophic Factor;Mental Disorders;Animals;Brain;Corticotropin-Releasing Hormone;Humans;news},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {5805},
	Pages = {1536-7},
	Pii = {314/5805/1536},
	Pubmed = {17158303},
	Title = {Neuroscience. Getting a read on Rett syndrome},
	Uuid = {94669E2F-9585-41E0-8FDC-4DA747AD87B8},
	Volume = {314},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.314.5805.1536}}

@article{Milligan:1991,
	Abstract = {Brain macrophages and microglia play important roles in central nervous system (CNS) development, especially during regressive events in which particular neuronal and glial constituents are eliminated. The purpose of this study is to provide a complete map of brain macrophage and microglia distribution in all regions of the neuraxis from birth to sexual maturity. We have utilized morphology and immunostaining with the specific antibodies OX-42 and ED1 to distinguish between brain macrophages and microglia. Brain macrophages are large, round cells, 10-15 microns in diameter, with few or no cytoplasmic processes; these cells are ED1- and OX-42-immunopositive. Microglia have small cell bodies with numerous, ramified cytoplasmic processes. These cells are OX-42-positive, and ED1-negative. We found a specific pattern of distribution of brain macrophages, targeting specific cortical and subcortical areas transiently, including developing fiber tracts. These cells disappeared completely by the third postnatal week. In contrast, OX-42-positive microglia exhibited a gradual increase in number and were distributed uniformly throughout gray matter and within white matter tracts. These cells remain in the adult CNS, constituting the resident microglia population. We suggest that these two distinct phagocytic cell populations perform unique functions in the developing brain, including remodeling of restricted CNS areas by brain macrophages that is part of a normal morphological process.},
	Author = {Milligan, C. E. and Cunningham, T. J. and Levitt, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:36 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Neuroglia;Immunohistochemistry;Antibodies, Monoclonal;Rats;11 Glia;Animals, Newborn;Macrophages;Support, U.S. Gov't, P.H.S.;Animals;Brain},
	Medline = {92184999},
	Month = {12},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129.},
	Pages = {125-35},
	Pubmed = {1797868},
	Title = {Differential immunochemical markers reveal the normal distribution of brain macrophages and microglia in the developing rat brain},
	Uuid = {34DBBCE6-B9F4-11DA-93EA-000D9346EC2A},
	Volume = {314},
	Year = {1991}}

@article{Milne:2005,
	Abstract = {Ischaemia induces activation of resident microglia and infiltration of peripheral monocyte/macrophage cells into the central nervous system. The role of scavenger receptors, receptors critical to the recognition and clearance of cell debris, has not been investigated during cerebral ischaemia. MARCO is an inducible member of the scavenger receptor family unique to cells of monocytic lineage and is a cell surface marker that plays a critical role in the differentiation of monocytes to dendritic cells. To understand the role of MARCO in cerebral ischaemia, we investigated its expression in mice following middle cerebral artery (MCA) occlusion. No MARCO mRNA expression was observed in naive mouse brain. There was no significant increase in expression of MARCO mRNA following transient occlusion (60min) of the MCA at any time point up to 24 h. However, a significant, marked increase in MARCO mRNA expression was observed at 24 h in the cortex of mouse brains after a permanent occlusion of the MCA. The increased expression of MARCO mRNA at 24 h after prolonged ischaemia is consistent with its putative role in the clearance of debris and/or degenerating cells after severe ischaemia and supports previous publications showing the presence of dendritic cells around permanently occluded lesions.},
	Author = {Milne, Stuart A. and McGregor, Ailsa L. and McCulloch, James and Sharkey, John},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {11 Glia},
	Nlm_Id = {7600130},
	Number = {1-2},
	Organization = {Astellas CNS in Edinburgh, The University of Edinburgh, UK. stuart.miline\@ed.ac.uk},
	Pages = {58-62},
	Pii = {S0304-3940(05)00355-1},
	Pubmed = {15936512},
	Title = {Increased expression of macrophage receptor with collagenous structure (MARCO) in mouse cortex following middle cerebral artery occlusion},
	Uuid = {8BD875D7-32DC-4BDC-A231-773F389979F6},
	Volume = {383},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neulet.2005.03.065}}

@article{Milward:2005,
	Abstract = {The phenomenon of colossal magnetoresistance in manganites is generally agreed to be a result of competition between crystal phases with different electronic, magnetic and structural order; a competition which can be strong enough to cause phase separation between metallic ferromagnetic and insulating charge-modulated states. Nevertheless, closer inspection of phase diagrams in many manganites reveals complex phases where the two order parameters of magnetism and charge modulation unexpectedly coexist. Here we show that such experiments can be naturally explained within a phenomenological Ginzburg-Landau theory. In contrast to models where phase separation originates from disorder or as a strain-induced kinetic phenomenon, we argue that magnetic and charge modulation coexist in new thermodynamic phases. This leads to a rich diagram of equilibrium phases, qualitatively similar to those seen experimentally. The success of this model argues for a fundamental reinterpretation of the nature of charge modulation in these materials, from a localized to a more extended 'charge-density wave' picture. The same symmetry considerations that favour textured coexistence of charge and magnetic order may apply to many electronic systems with competing phases. The resulting 'electronically soft' phases of matter with incommensurate, inhomogeneous and mixed order may be general phenomena in correlated systems.},
	Author = {Milward, G. C. and Calder{\'o}n, M. J. and Littlewood, P. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {7026},
	Organization = {Cavendish Laboratory, Cambridge University, Madingley Road, Cambridge CB3 0HE, UK. gcm24\@cam.ac.uk},
	Pages = {607-10},
	Pii = {nature03300},
	Pubmed = {15703740},
	Title = {Electronically soft phases in manganites},
	Uuid = {B7949D53-7E27-4899-8396-5F3F818677C9},
	Volume = {433},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03300}}

@article{Miragall:1982,
	Abstract = {The time interval between the incorporation of [3H]thymidine and the appearance of olfactory marker protein (OMP) in autoradiographically labeled neurons which have differentiated from stem cells, has been determined by autoradiographic and immunohistochemical techniques. The first [3H]thymidine-labeled, OMP-containing elements have been observed 7 days after administration of the radioactive thymidine. This result allows some speculation on the potential function of the olfactory marker protein.},
	Author = {Miragall, F. and Monti Graziadei, G. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Brain Res},
	Keywords = {13 Olfactory bulb anatomy;I;Cell Differentiation;Neurons/*physiology;Tritium;Fluorescent Antibody Technique;Kinetics;Autoradiography;Animal;Support, U.S. Gov't, Non-P.H.S.;DNA Replication;Nerve Tissue Proteins/*analysis;Support, Non-U.S. Gov't;Male;Mice;Mice, Inbred Strains;Olfactory Bulb/*physiology},
	Number = {1},
	Pages = {245-50.},
	Title = {Experimental studies on the olfactory marker protein. II. Appearance of the olfactory marker protein during differentiation of the olfactory sensory neurons of mouse: an immunohistochemical and autoradiographic study},
	Uuid = {C409DE67-CB5A-4BDD-8AC2-C0979B305563},
	Volume = {239},
	Year = {1982},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7046875}}

@article{Mirescu:2006,
	Abstract = {Prolonged sleep deprivation is stressful and has been associated with adverse consequences for health and cognitive performance. Here, we show that sleep deprivation inhibits adult neurogenesis at a time when circulating levels of corticosterone are elevated. Moreover, clamping levels of this hormone prevents the sleep deprivation-induced reduction of cell proliferation. The recovery of normal levels of adult neurogenesis after chronic sleep deprivation occurs over a 2-wk period and involves a temporary increase in new neuron formation. This compensatory increase is dissociated from glucocorticoid levels as well as from the restoration of normal sleep patterns. Collectively, these findings suggest that, although sleep deprivation inhibits adult neurogenesis by acting as a stressor, its compensatory aftereffects involve glucocorticoid-independent factors.},
	Author = {Mirescu, Christian and Peters, Jennifer D. and Noiman, Liron and Gould, Elizabeth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {7505876},
	Number = {50},
	Organization = {Department of Psychology, Princeton University, Princeton, NJ 08544.},
	Pages = {19170-5},
	Pii = {0608644103},
	Pubmed = {17135354},
	Title = {Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids},
	Uuid = {A011A288-C511-4D32-8570-83CE33B10304},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0608644103}}

@article{Mischel:1995,
	Author = {Mischel, P. S. and Nguyen, L. P. and Vinters, H. V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {10 Development;Child, Preschool;Humans;review;Female;Epilepsy;Infant;Severity of Illness Index;21 Dysplasia-heterotopia;Child;Male;10 genetics malformation;21 Neurophysiology;research support, u.s. gov't, p.h.s.;Adult;Cerebral Cortex;Infant, Newborn;24 Pubmed search results 2008;Immunohistochemistry;Adolescent},
	Month = {3},
	Nlm_Id = {2985192R},
	Number = {2},
	Organization = {Department of Pathology and Laboratory Medicine, UCLA Medical Center 90024-1732.},
	Pages = {137-53},
	Pubmed = {7876884},
	Title = {Cerebral cortical dysplasia associated with pediatric epilepsy. Review of neuropathologic features and proposal for a grading system},
	Uuid = {D436FF9A-1D63-4DE0-813D-FFD84D47B092},
	Volume = {54},
	Year = {1995}}

@article{Mishima:2007,
	Abstract = {Glial cells have traditionally been considered to play supportive roles in the central nervous system. As recent experimental evidence suggests glial cells' participation in neural information processing, there has been a need to monitor the physiology of glial cells in vivo in the matured brain. Concurrently, identification and classification of the recorded glial cells is essential as there are at least several different kinds of glial cells. Past studies have achieved in vivo intracellular electrophysiological recording of glial cells using sharp glass microelectrodes, however, morphological recovery and identification of the recorded cells have hardly been done, due to technical difficulties. We demonstrate that use of large fragment biotinylated dextran amine (BDA) is an effective way to label a single glial cell recorded with a sharp microelectrode in vivo. Furthermore, the tracer signal amplification was achieved by a combination of avidin biotinylated horseradish peroxidase macromolecular complex (ABC) and tyramide-based methods, making multiple immunohistochemistry feasible. Using the method described in this study, we have successfully recorded and labeled cortical glial cells including astrocytes, oligodendrocytes, and microglia.},
	Author = {Mishima, Tsuneko and Sakatani, Seiichi and Hirase, Hajime},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008;23 Technique},
	Month = {10},
	Nlm_Id = {7905558},
	Number = {1},
	Organization = {Hirase Research Unit, Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.},
	Pages = {32-40},
	Pii = {S0165-0270(07)00306-8},
	Pubmed = {17686526},
	Title = {Intracellular labeling of single cortical astrocytes in vivo},
	Uuid = {CDD2AE2A-3CDB-4782-B5AB-2045533EA757},
	Volume = {166},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jneumeth.2007.06.021}}

@article{Mission:1991,
	Abstract = {Three cell forms of astroglial lineage populate the prenatal and early postnatal murine cerebral wall. In the present review we consider the ontogeny of these cell forms with respect to histogenetic events of the perinatal period. Classic bipolar radial glial cells predominate prior to E17. The bipolar coexist with monopolar radial forms in the perinatal period. Both bipolar and monopolar radial forms coexist with multipolar astrocytes in the course of the first postnatal week and are ultimately succeeded by the multipolar cells. The shift from bipolar to monopolar radial forms is initially coincident with translocation of somata of bipolar cells from the ventricular zone to the upper intermediate zone and cortical strata. Arborization appears to occur both at the growing tips and along the shaft of the processes of both bipolar and monopolar radial cell types. As arborization continues, the processes of the monopolar radial cells come to resemble those of the multipolar astrocytes. Eventually the radial cells are fully transformed into the multipolar astrocytic forms. During this period of transition, radial processes in the cortex appear to be degenerating, suggesting that regressive processes contribute to the cytologic transformation. This sequence of transformations begins late in the period of neuronal migration and continues through the early stages of growth and differentiation in the murine cerebral cortex. The signals that induce these changes may arise from differentiating neurons within the cortex. These transformations occur at a time when radial glial fibers are no longer required as guides for neuronal migration, and the glial population assumes new roles related to the development and operation of cortical neuronal circuits. Using Smart Source Parsing},
	Author = {Mission, J. P. and Takahashi, T. and Caviness, V. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Glia},
	Keywords = {Staining and Labeling;Cell Differentiation;Cerebral Cortex/*cytology/embryology/growth &development;Antibodies, Monoclonal/diagnostic use;Astrocytes/chemistry/*cytology;Biological Markers;Animal;11 Glia;Fetal Development;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;G;Mice;Nerve Tissue Proteins/analysis;Glycogen/analysis},
	Number = {2},
	Organization = {Department of Neurology, Developmental Neurobiology, Massachusetts General Hospital, Harvard Medical School, Boston 02114.},
	Pages = {138-48},
	Title = {Ontogeny of radial and other astroglial cells in murine cerebral cortex},
	Uuid = {A1E1E51E-94DC-4F2E-8011-B961E0894BCF},
	Volume = {4},
	Year = {1991},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1709615}}

@article{Mitchell:2001a,
	Abstract = {Flathead is a rat neurological mutant which is phenotypically characterized by a flattened cranium, resting tremor, ataxia, progressive paralysis of the hind limbs, and death at 3-4 weeks after birth. Previous studies showed that rats homozygous for the mutation have a dramatically reduced brain size caused by a burst of apoptosis that begins after embryonic day 16 (E16) and which peaks at about E18. Late-developing structures such as the dentate gyrus, internal granule layer of the cerebellum, and superficial layers of the neocortex are severely depleted of cells. In the present study we have found that neurons and glia are both affected by the mutation. Immunohistochemical analysis with TAG-1, a marker for migratory neurons, revealed reduced staining in Fh neocortex and cerebellum, indicating that the mutation affects neuronal migration or a developmental event prior to it. Analysis of acutely dissociated neocortical cultures showed an accumulation of nestin-positive progenitor cells. Moreover, a substantial proportion of these progenitor cells were multinucleated with the nuclei organized as rosettes. Such multinucleated cells were also found in intact sections of the neocortex and the cerebellum where their presence was restricted to proliferative zones. Within the neocortex, the abundance of multinucleated progenitors is highest at E18 and decreases thereafter, thus correlating with the profile of cell death. This, along with the dramatically higher frequency of apoptosis among multinucleated cells, suggests that the aberrant cell death in Fh is due to defective cytokinesis that occurs in progenitor cells during late stages of brain development. 21441449 0165-3806 Journal Article},
	Author = {Mitchell, B. D. and Gibbons, B. and Allen, L. R. and Stella, J. and D'Mello, S. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Rats;Giant Cells/chemistry/cytology;Neocortex/*abnormalities/pathology;Stem Cells/chemistry/*cytology;Neurons/chemistry/*cytology;Animal;Membrane Glycoproteins/analysis;CK;DNA/biosynthesis;Cerebellum/*abnormalities/pathology;Cell Division/genetics;In Situ Nick-End Labeling;Support, Non-U.S. Gov't;Skull/abnormalities;Intermediate Filament Proteins/analysis;Apoptosis/*genetics;Neuroglia/cytology;Rats, Mutant Strains},
	Number = {1},
	Organization = {Department of Molecular and Cell Biology, University of Texas at Dallas, 2601 North Floyd Road, Richardson, TX 75083, USA.},
	Pages = {53-63},
	Title = {Aberrant apoptosis in the neurological mutant Flathead is associated with defective cytokinesis of neural progenitor cells},
	Uuid = {8850E816-6D6B-11DA-A4FE-000D9346EC2A},
	Volume = {130},
	Year = {2001},
	url = {papers/Mitchell_BrainResDevBrainRes2001}}

@article{Mitchell:2004,
	Abstract = {Over most of the past century of modern neuroscience, it was thought that the adult brain was completely incapable of generating new neurons. During the past 3 decades, research exploring potential neuronal replacement therapies has focused on replacing lost neurons by transplanting cells or grafting tissue into diseased regions of the brain. However, in the last decade, the development of new techniques has resulted in an explosion of new research showing that neurogenesis, the birth of new neurons, normally occurs in two limited and specific regions of the adult mammalian brain and that there are significant numbers of multipotent neural precursors in many parts of the adult mammalian brain. Recent advances in our understanding of related events of neural development and plasticity, including the role of radial glia in developmental neurogenesis and the ability of endogenous precursors present in the adult brain to be induced to produce neurons and partially repopulate brain regions affected by neurodegenerative processes, have led to fundamental changes in the views about how the brain develops as well as to approaches by which endogenous precursors might be recruited to repair the adult brain. Recruitment of new neurons can be induced in a region-specific, layer-specific and neuronal-type-specific manner, and, in some cases, newly recruited neurons can form long-distance connections to appropriate targets. Elucidation of the relevant molecular controls may both allow control over transplanted precursor cells and potentially allow the development of neuronal replacement therapies for neurodegenerative disease and other CNS injuries that do not require transplantation of exogenous cells.},
	Author = {Mitchell, Bartley D. and Emsley, Jason G. and Magavi, Sanjay S. P. and Arlotta, Paola and Macklis, Jeffrey D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Cell Lineage;01 Adult neurogenesis general;Stem Cell Transplantation;Cell Differentiation;Central Nervous System Diseases;Research Support, Non-U.S. Gov't;17 Transplant Regeneration;Mammals;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Animals;Brain;Humans;review;Neurons},
	Nlm_Id = {7809375},
	Number = {2-4},
	Organization = {MGH-HMS Center for Nervous System Repair, Department of Neurosurgery, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.},
	Pages = {101-17},
	Pii = {DNE20040262_4101},
	Pubmed = {15711054},
	Title = {Constitutive and induced neurogenesis in the adult mammalian brain: manipulation of endogenous precursors toward CNS repair},
	Uuid = {636C848A-659B-4E35-A7C4-10A34EAB5351},
	Volume = {26},
	Year = {2004},
	url = {papers/Mitchell_DevNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000082131}}

@article{Mitchell:1999,
	Abstract = {OBJECTIVE: To examine the nature and frequency of anterior temporal lobe (AT) abnormalities that occur in intractable temporal lobe epilepsy (TLE). METHODS: We reviewed the MR scans and clinical histories of 50 consecutive patients with intractable TLE. Histopathology was available in 42 surgically treated cases. RESULTS: MRI demonstrated loss of the gray-white matter differentiation and decreased T1- and increased T2-weighted signal in the ipsilateral AT in 58\%of the 50 patients. This appearance was observed in 64\%of the 36 patients with hippocampal sclerosis (HS) but was also seen in patients without HS. These changes were associated with temporal lobe atrophy, a higher hippocampal T2 relaxation time, and a history of febrile convulsions. Pathologic examination showed that the MRI appearances were not caused by dysplasia, degenerative abnormalities, or inflammatory change. Histologic quantitation showed increased glial cell nuclei counts in the intractable TLE cases compared with controls. There was no difference in glial cell numbers between cases with AT abnormality and those without this appearance. Presence or absence of changes was not predictive of preoperative neuropsychology, postoperative change in neuropsychology, or seizure outcome after surgery. CONCLUSIONS: These frequently seen ipsilateral changes are not caused by gliosis and may reflect a nonspecific increase in water content in the temporal lobe. This may be due to myelin abnormalities or some other as yet unidentified pathologic factor.},
	Author = {Mitchell, L. A. and Jackson, G. D. and Kalnins, R. M. and Saling, M. M. and Fitt, G. J. and Ashpole, R. D. and Berkovic, S. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0028-3878},
	Journal = {Neurology},
	Keywords = {Neuropsychological Tests;Adolescent;Magnetic Resonance Imaging;Child, Preschool;Humans;Treatment Outcome;Middle Aged;Female;Child;Atrophy;clinical trial;Male;Analysis of Variance;controlled clinical trial;Epilepsy, Temporal Lobe;Adult;Temporal Lobe;Research Support, Non-U.S. Gov't},
	Medline = {99129732},
	Month = {1},
	Nlm_Id = {0401060},
	Number = {2},
	Organization = {Brain Imaging Research Institute, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia.},
	Pages = {327-36},
	Pubmed = {9932952},
	Title = {Anterior temporal abnormality in temporal lobe epilepsy: a quantitative MRI and histopathologic study},
	Uuid = {AD8B2A63-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {52},
	Year = {1999}}

@article{Mitrasinovic:2005,
	Abstract = {Microglia with increased expression of the macrophage colony-stimulating factor receptor (M-CSFR; c-fms) are found surrounding plaques in Alzheimer's disease (AD) and in mouse models for AD and after ischemic or traumatic brain injury. Increased expression of M-CSFR causes microglia to adopt an activated state that results in proliferation, release of cytokines, and enhanced phagocytosis. To determine whether M-CSFR-induced microglial activation affects neuronal survival, we assembled a coculture system consisting of BV-2 microglia transfected to overexpress the M-CSFR and hippocampal organotypic slices treated with NMDA. Twenty-four hours after assembly of the coculture, microglia overexpressing M-CSFR proliferated at a higher rate than nontransfected control cells and exhibited enhanced migration toward NMDA-injured hippocampal cultures. Surprisingly, coculture with c-fms-transfected microglia resulted in a dramatic reduction in NMDA-induced neurotoxicity. Similar results were observed when cocultures were treated with the teratogen cyclophosphamide. Biolistic overexpression of M-CSFR on microglia endogenous to the organotypic culture also rescued neurons from excitotoxicity. Furthermore, c-fms-transfected microglia increased neuronal expression of macrophage colony-stimulating factor (M-CSF), the M-CSFR, and neurotrophin receptors in the NMDA-treated slices, as determined with laser capture microdissection. In the coculture system, direct contact between the exogenous microglia and the slice was necessary for neuroprotection. Finally, blocking expression of the M-CSF ligand by exogenous c-fms-transfected microglia with a hammerhead ribozyme compromised their neuroprotective properties. These results demonstrate a protective role for microglia overexpressing M-CSFR in our coculture system and suggest under certain circumstances, activated microglia can help rather than harm neurons subjected to excitotoxic and teratogen-induced injury.},
	Author = {Mitrasinovic, Olivera M. and Grattan, Alicia and Robinson, Christopher C. and Lapustea, Nicolae B. and Poon, Clara and Ryan, Heather and Phong, Connie and Murphy, Greer M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Neuroscience Research Laboratories, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.},
	Pages = {4442-51},
	Pii = {25/17/4442},
	Pubmed = {15858070},
	Title = {Microglia overexpressing the macrophage colony-stimulating factor receptor are neuroprotective in a microglial-hippocampal organotypic coculture system},
	Uuid = {8050F9BD-2870-4960-9BD5-352AC3044BC2},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0514-05.2005}}

@article{Mitrasinovic:2003,
	Abstract = {Macrophage colony stimulating factor (M-CSF) and its receptor are upregulated in the brain in Alzheimer's disease. M-CSF induces activation and proliferation of microglial cells and expression of proinflammatory cytokines. Amyloid beta (Abeta) immunization experiments suggest that microglia have the capacity to aggressively clear Abeta from the brain under certain circumstances. We examined the role of M-CSF in phagocytosis of fluorescent microspheres and Abeta by cultured microglia. M-CSF treatment increased microglial cell phagocytosis of both microspheres and of Abeta. Antibody neutralization of M-CSF inhibited Abeta uptake induced by overexpression of the M-CSF receptor on microglia. These results suggest that M-CSF could be important in promoting microglial clearance of abnormal protein aggregates such as Abeta.},
	Author = {Mitrasinovic, Olivera M. and Vincent, Valerie A. M. and Simsek, Dilek and Murphy, Greer M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Amyloid beta-Protein;Flow Cytometry;Peptide Fragments;Research Support, Non-U.S. Gov't;Macrophage Colony-Stimulating Factor;Cell Line;Research Support, U.S. Gov't, P.H.S.;Fluorescent Dyes;11 Glia;Microglia;Microspheres;Animals;Mice;Phagocytosis},
	Medline = {22697620},
	Month = {7},
	Nlm_Id = {7600130},
	Number = {3},
	Organization = {Neuroscience Research Laboratories, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305-5485, USA.},
	Pages = {185-8},
	Pii = {S0304394003004749},
	Pubmed = {12812836},
	Title = {Macrophage colony stimulating factor promotes phagocytosis by murine microglia},
	Uuid = {F92DE338-4087-4D1D-AA79-394774E93B0C},
	Volume = {344},
	Year = {2003},
	url = {papers/Mitrasinovic_NeurosciLett2003.pdf}}

@article{Miyakoshi:2001,
	Abstract = {Neurons from the anterior subventricular zone (SVZ) of the cerebral cortex migrate tangentially to become interneurons in the olfactory bulb during development and in adult rodents. This migration was defined as neuronophilic, independent of a radial glial substrate. The cortical SVZ and the rostral migratory stream to the olfactory bulb were shown to be rich in 9-O-acetyl GD3 gangliosides (9-O-acGD3), which have been previously shown to be implicated in gliophilic migration in the rodent cerebral cortex and cerebellum. In the present study, we performed SVZ explant cultures using rats during their first postnatal week to analyze the expression of these gangliosides in chain migration of neuronal precursors. We characterized migrating chains of these neuroblasts through morphological analysis and immunocytochemistry for the neural cell adhesion molecule. By using the Jones monoclonal antibody which binds specifically to 9-O-acGD3 we showed that migrating chains from the SVZ explants express 9-O-acGD3 which is distributed in a punctate manner in individual cells. 9-O-acGD3 is also present in migrating chains that form in the absence of radial glia, typical of the neuronophilic chain migration of the SVZ. Our data indicate that 9- O-acetylated gangliosides may participate in neuronophilic as well as gliophilic migration.},
	Author = {Miyakoshi, L. M. and Mendez-Otero, R. and Hedin-Pereira, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Braz J Med Biol Res},
	Keywords = {Neurons/*metabolism/ultrastructure;Cerebral Ventricles/cytology;Rats;Olfactory Bulb/*metabolism;C pdf;Animal;Gangliosides/analysis/*metabolism;Neuroglia/cytology;Cell Movement/*physiology;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Cerebral Cortex/cytology/*metabolism},
	Number = {5},
	Organization = {Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brasil.},
	Pages = {669-73.},
	Title = {The 9-O-acetyl GD3 gangliosides are expressed by migrating chains of subventricular zone neurons in vitro},
	Uuid = {89D39105-291F-4F77-8FAE-1A882D2D66FD},
	Volume = {34},
	Year = {2001},
	url = {papers/Miyakoshi_BrazJMedBiolRes2001}}

@article{Miyata:2004,
	Abstract = {Mature neocortical layers all derive from the cortical plate (CP), a transient zone in the dorsal telencephalon into which young neurons are continuously delivered. To understand cytogenetic and histogenetic events that trigger the emergence of the CP, we have used a slice culture technique. Most divisions at the ventricular surface generated paired cycling daughters (P/P divisions) and the majority of the P/P divisions were asymmetric in daughter cell behavior; they frequently sent one daughter cell to a non-surface (NS) position, the subventricular zone (SVZ), within a single cell-cycle length while keeping the other mitotic daughter for division at the surface. The NS-dividing cells were mostly Hu+ and their daughters were also Hu+, suggesting their commitment to the neuronal lineage and supply of early neurons at a position much closer to their destiny than from the ventricular surface. The release of a cycling daughter cell to SVZ was achieved by collapse of the ventricular process of the cell, followed by its NS division. Neurogenin2 (Ngn2) was immunohistochemically detected in a certain cycling population during G1 phase and was further restricted during G2-M phases to the SVZ-directed population. Its retroviral introduction converted surface divisions to NS divisions. The asymmetric P/P division may therefore contribute to efficient neuron/progenitor segregation required for CP initiation through cell cycle-dependent and lineage-restricted expression of Ngn2.},
	Author = {Miyata, Takaki and Kawaguchi, Ayano and Saito, Kanako and Kawano, Masako and Muto, Tetsuji and Ogawa, Masaharu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {10 Development;Transcription Factors;Animals;Gene Expression Regulation, Developmental;Epithelial Cells;Cell Cycle;Mitosis;Ki-67 Antigen;Models, Biological;Brain;Telencephalon;Cell Movement;Retroviridae;G2 Phase;Time Factors;Green Fluorescent Proteins;Cell Lineage;Cerebral Cortex;Neurons;Mice;Cell Division;G1 Phase;Immunohistochemistry;Collagen;Nerve Tissue Proteins;Stem Cells;Luminescent Proteins},
	Month = {7},
	Nlm_Id = {8701744},
	Number = {13},
	Organization = {Laboratory for Cell Culture Development, Brain Science Institute, RIKEN, Saitama 351-0198, Japan. tmiyata\@med.nagoya-u.ac.jp},
	Pages = {3133-45},
	Pii = {dev.01173},
	Pubmed = {15175243},
	Title = {Asymmetric production of surface-dividing and non-surface-dividing cortical progenitor cells},
	Uuid = {AB69CE3F-EB35-4EE7-B7D3-43D587AAAB71},
	Volume = {131},
	Year = {2004},
	url = {papers/Miyata_Development2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.01173}}

@article{Miyata:1999,
	Abstract = {NeuroD, a bHLH transcription factor, is implicated in differentiation of neurons and pancreatic beta cells. NeuroD-null mice die shortly after birth due to severe neonatal diabetes. To examine if there is postnatal neuronal phenotype in these mice, we rescued them from neonatal lethality by introducing a transgene encoding the mouse neuroD gene under the insulin promoter. These mice survive to adulthood but display severe neurological phenotype due to neuronal deficit in the granule layers of the cerebellum and hippocampus. We show here that NeuroD is required for these postnatally generated microneurons to undergo proper differentiation, the absence of which results in cell death.},
	Author = {Miyata, T. and Maeda, T. and Lee, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0890-9369},
	Journal = {Genes Dev},
	Keywords = {Research Support, Non-U.S. Gov't;10 Development;Cell Differentiation;Animals;10 Hippocampus;Phenotype;Apoptosis;Cell Count;Mice, Transgenic;Hippocampus;Recombinant Fusion Proteins;Mice, Neurologic Mutants;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Mice, Knockout;Neurons;In Situ Nick-End Labeling;Insulin;Cerebellum;Mice;Promoter Regions (Genetics);Nerve Tissue Proteins;Transgenes},
	Medline = {99328891},
	Month = {7},
	Nlm_Id = {8711660},
	Number = {13},
	Organization = {Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Boulder, Colorado 80309-0347, USA.},
	Pages = {1647-52},
	Pubmed = {10398678},
	Title = {NeuroD is required for differentiation of the granule cells in the cerebellum and hippocampus},
	Uuid = {33538635-E001-4773-86E0-B13136723BFD},
	Volume = {13},
	Year = {1999},
	url = {papers/Miyata_GenesDev1999.pdf}}

@article{Miyata:2001,
	Abstract = {Recent studies demonstrated the neuronogenic role of radial glial cells (RGCs) in the rodent. To reveal the fate of radial glial processes, we intensively monitored divisions of RGCs in DiI-labeled slices from the embryonic day 14 mouse cortex. During RGC division, each pia-connected fiber becomes thin but is neither lost nor divided; it is inherited asymmetrically by one daughter cell. In divisions that produce a neuron and a progenitor, the neuron inherits the pial fiber, also grows a thick ventricular process for several hours, and is therefore indistinguishable from the progenitor RGC. The ventricular process in the radial glial-like neuron ("radial neuron") then collapses, leading to ascent of the neuron by using the "recycled"radial fiber. 21453756 0896-6273 Journal Article},
	Author = {Miyata, T. and Kawaguchi, A. and Okano, H. and Ogawa, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Neuron},
	Keywords = {Fetus;10 Development;Neurons/*cytology/metabolism;Cerebral Cortex/cytology/*embryology/metabolism;Cell Movement/*physiology;Stem Cells/*cytology/metabolism;Aging/physiology;Animal;Cell Size/physiology;Cell Compartmentation/physiology;Cell Differentiation/*physiology;Mice, Inbred ICR;Support, Non-U.S. Gov't;Cell Division/*physiology;Body Patterning/physiology;Neuroglia/*cytology/metabolism;Nerve Tissue Proteins/metabolism;Cell Lineage/physiology;Mice;Immunohistochemistry;Neurites/metabolism/ultrastructure;Organ Culture;F},
	Number = {5},
	Organization = {Laboratory for Cell Culture Development, Brain Science Institute, RIKEN, 351-0198, Saitama, Japan. tmiyata\@brain.riken.go.jp},
	Pages = {727-41},
	Pubmed = {11567613},
	Title = {Asymmetric inheritance of radial glial fibers by cortical neurons},
	Uuid = {7CC4274D-7D83-421E-BEED-90D39FD09A02},
	Volume = {31},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11567613}}

@article{Mizrahi:2003,
	Abstract = {In many regions of the adult mammalian brain, pronounced changes in synaptic input caused by lesions or severe sensory deprivation induce marked sprouting or retraction of neuronal dendrites. In the adult olfactory bulb, adult neurogenesis produces less pronounced, but continuously ongoing synapse turnover. To test the structural stability of adult dendrites in this context, we used two-photon microscopy to image dendrites of mitral and tufted (M/T) cells over prolonged periods in adult mice. Although pharmacologically increased activity could elicit morphological changes, under natural conditions such as ongoing neurogenesis, an odor-enriched environment or olfactory-based learning, M/T cell dendrites remained highly stable. Thus, in a context of ongoing adult synaptogenesis, dendritic stability could serve as a structural scaffold to maintain the organization of local circuits. 1097-6256 Journal Article},
	Author = {Mizrahi, A. and Katz, L. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Probability;Microscopy, Confocal/methods;Synapses/*physiology;Acetophenones/pharmacology;I pdf;Olfactory Bulb/*cytology/drug effects/physiology;Imaging, Three-Dimensional/instrumentation/methods;Animals;Electrophysiology;Aldehydes/pharmacology;Bacterial Proteins/genetics;Conditioning, Classical;Transfection/veterinary;Behavior, Animal;Dendrites/*physiology;Photons;Odors;Support, U.S. Gov't, P.H.S.;Luminescent Proteins/genetics;Comparative Study;13 Olfactory bulb anatomy;Nerve Net/*physiology;Action Potentials/drug effects;Time Factors;Neurons, Afferent/physiology/virology;Bicuculline/pharmacology;Dose-Response Relationship, Drug;Stimulation, Chemical;Discrimination Learning/physiology;Mice;Support, Non-U.S. Gov't;GABA Antagonists/pharmacology;Mice, Transgenic;Neuronal Plasticity/*physiology},
	Number = {11},
	Organization = {Howard Hughes Medical Institute and the Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA. mizrahi\@neuro.duke.edu},
	Pages = {1201-7},
	Pubmed = {14528309},
	Title = {Dendritic stability in the adult olfactory bulb},
	Uuid = {7C6D760F-1DF7-4224-9388-3C6697F79983},
	Volume = {6},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14528309}}

@article{Mizrahi:2006,
	Abstract = {As a consequence of adult neurogenesis, the olfactory bulb (OB) receives a continuous influx of newborn neurons well into adulthood. However, their rates of generation and turnover, the factors controlling their survival, and how newborn neurons intercalate into adult circuits are largely unknown. To visualize the dynamics of adult neurogenesis, we produced a line of transgenic mice expressing GFP in approximately 70\%of juxtaglomerular neurons (JGNs), a population that undergoes adult neurogenesis. Using in vivo two-photon microscopy, time-lapse analysis of identified JGN cell bodies revealed a neuronal turnover rate of approximately 3\%of this population per month. Although new neurons appeared and older ones disappeared, the overall number of JGNs remained constant. This approach provides a dynamic view of the actual appearance and disappearance of newborn neurons in the vertebrate central nervous system, and provides an experimental substrate for functional analysis of adult neurogenesis.},
	Author = {Mizrahi, Adi and Lu, Jing and Irving, Ryan and Feng, Guoping and Katz, Lawrence C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration;13 Olfactory bulb anatomy},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {6},
	Organization = {*Howard Hughes Medical Institute and Department of Neurobiology, Duke University Medical Center, Durham, NC 27710.},
	Pages = {1912-7},
	Pii = {0506297103},
	Pubmed = {16446451},
	Title = {In vivo imaging of juxtaglomerular neuron turnover in the mouse olfactory bulb},
	Uuid = {C171D912-302A-4B1F-A80A-7B660E3BA20E},
	Volume = {103},
	Year = {2006},
	url = {papers/Mizrahi_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0506297103}}

@article{Mizumoto:2003,
	Abstract = {Neural progenitor cells isolated from the brains of neonatal GFP transgenic mice were grafted to the retina of RCS rats and rds and B6 mice. Expression of GFP and differentiation markers was evaluated at 1-4 weeks post-transplantation. Grafted cells maintained transgene expression throughout the 4-week period. At 1 week there was widespread migration of GFP+cells within the host retina and at 2 weeks evidence of neuronal differentiation (as shown by both marker expression and cell morphology), although integration at 4 weeks was limited to syngeneic recipients. Because brain-derived neural progenitor cells exhibit both neuronal and astrocytic differentiation in diseased and normal host retina, these cells provide a useful tool for studies of retinal regeneration.},
	Author = {Mizumoto, Hiroyuki and Mizumoto, Keiko and Shatos, Marie A. and Klassen, Henry and Young, Michael J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0042-6989},
	Journal = {Vision Res},
	Keywords = {Retina;Mice, Inbred BALB C;Cell Differentiation;Animals;Stem Cell Transplantation;Rats;Transplantation, Heterologous;Brain;Indicators and Reagents;11 Glia;Green Fluorescent Proteins;Cell Line;Research Support, U.S. Gov't, P.H.S.;Mice;Luminescent Proteins;Stem Cells;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {22704539},
	Month = {7},
	Nlm_Id = {0417402},
	Number = {16},
	Organization = {The Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.},
	Pages = {1699-708},
	Pii = {S0042698903002359},
	Pubmed = {12818339},
	Title = {Retinal transplantation of neural progenitor cells derived from the brain of GFP transgenic mice},
	Uuid = {5DB7385D-9645-4E6C-9FD9-14645F907A31},
	Volume = {43},
	Year = {2003}}

@article{Mizuno:1999,
	Abstract = {Telencephalin (TLCN) is a neuronal surface glycoprotein whose expression is restricted to the telencephalon, the most rostral segment of the brain. TLCN binds to lymphocyte function-associated antigen-1 (LFA-1) integrin. In the central nervous system, LFA-1 is selectively and constitutively expressed by microglia, suggesting that TLCN/LFA-1 binding may mediate cell-cell interactions between telencephalic neurons and microglia. In the present study, we investigated the effects of recombinant TLCN protein on the morphology of microglia. TLCN induced an intensive spreading of lamellipodia, causing a rapid change in microglial morphology. In contrast, TLCN induced no significant change in morphology of neuroblastoma and fibroblasts. Furthermore, the TLCN-induced spreading of microglia was accompanied by a clustering of LFA-1 on cell surface membrane. These results provide evidence that TLCN binding to the surface of microglia transduces signals into microglia that mediate or accelerate cell spreading and LFA-1 redistribution, implying that neuronal TLCN may control the state and/or function of microglia in both physiological and pathological conditions.},
	Author = {Mizuno, T. and Yoshihara, Y. and Kagamiyama, H. and Ohsawa, K. and Imai, Y. and Kohsaka, S. and Mori, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Research Support, Non-U.S. Gov't;Neuroblastoma;Animals;Cells, Cultured;Diencephalon;Recombinant Proteins;Microglia;L Cells (Cell Line);Tumor Suppressor Protein p53;Telencephalon;Genes, p53;Cell Movement;Animals, Newborn;Mice, Inbred Strains;Membrane Glycoproteins;Mice, Knockout;Tumor Cells, Cultured;Mice;24 Pubmed search results 2008;Nerve Tissue Proteins;Lymphocyte Function-Associated Antigen-1;Neural Cell Adhesion Molecules},
	Medline = {20074697},
	Month = {12},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Laboratory for Neurobiology of Synapse, RIKEN Brain Science Institute, Wako, Japan.},
	Pages = {58-66},
	Pii = {S0006-8993(99)01984-8},
	Pubmed = {10592287},
	Title = {Neuronal adhesion molecule telencephalin induces rapid cell spreading of microglia},
	Uuid = {628A3CB3-16B7-4C52-A72A-0D5D480936F6},
	Volume = {849},
	Year = {1999}}

@article{Mizutani:2007,
	Abstract = {During brain development, neurons and glia are generated from a germinal zone containing both neural stem cells (NSCs) and more limited intermediate neural progenitors (INPs). The signalling events that distinguish between these two proliferative neural cell types remain poorly understood. The Notch signalling pathway is known to maintain NSC character and to inhibit neurogenesis, although little is known about the role of Notch signalling in INPs. Here we show that both NSCs and INPs respond to Notch receptor activation, but that NSCs signal through the canonical Notch effector C-promoter binding factor 1 (CBF1), whereas INPs have attenuated CBF1 signalling. Furthermore, whereas knockdown of CBF1 promotes the conversion of NSCs to INPs, activation of CBF1 is insufficient to convert INPs back to NSCs. Using both transgenic and transient in vivo reporter assays we show that NSCs and INPs coexist in the telencephalic ventricular zone and that they can be prospectively separated on the basis of CBF1 activity. Furthermore, using in vivo transplantation we show that whereas NSCs generate neurons, astrocytes and oligodendrocytes at similar frequencies, INPs are predominantly neurogenic. Together with previous work on haematopoietic stem cells, this study suggests that the use or blockade of the CBF1 cascade downstream of Notch is a general feature distinguishing stem cells from more limited progenitors in a variety of tissues.},
	Author = {Mizutani, Ken-ichi and Yoon, Keejung and Dang, Louis and Tokunaga, Akinori and Gaiano, Nicholas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {24 Pubmed search results 2008;research support, non-u.s. gov't;Telencephalon;Basic Helix-Loop-Helix Leucine Zipper Transcription Factors;Signal Transduction;Stem Cells;research support, n.i.h., extramural;Green Fluorescent Proteins;Animals;Cells, Cultured;Mice;Neurons;Receptors, Notch},
	Month = {9},
	Nlm_Id = {0410462},
	Number = {7160},
	Organization = {Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.},
	Pages = {351-5},
	Pii = {nature06090},
	Pubmed = {17721509},
	Title = {Differential Notch signalling distinguishes neural stem cells from intermediate progenitors},
	Uuid = {AB97042F-AD1E-4F32-875F-BB008B72DBA1},
	Volume = {449},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06090}}

@article{Moffett:1997,
	Abstract = {Experimental tumors of the central nervous system were investigated with antibodies to quinolinate to assess the cellular distribution of this endogenous neurotoxin. In advanced F98 and RG-2 glioblastomas and E367 neuroblastomas in the striatum of rats, variable numbers of quinolinate immunoreactive cells were observed in and around the tumors, with the majority being present within tumors, rather than brain parenchyma. The stained cells were morphologically variable, including round, complex, rod-shaped, and sparsely dendritic cells. Neuroblastoma and glioma cells were unstained, as were neurons, astrocytes, oligodendrocytes, ependymal cells, endothelial cells, and cells of the choroid plexus and leptomeninges. Glial fibrillary acidic protein immunoreactivity was strongly elevated in astrocytes surrounding the tumors. Dual labeling immunohistochemistry with antibodies to quinolinate and glial fibrillary acidic protein demonstrated that astrocytes and the cells containing quinolinate immunoreactivity were morphologically disparate and preferentially distributed external and internal to the tumors, respectively, and no dual labeled cells were observed. Lectin histochemistry with Griffonia simplicifolia B4 isolectin and Lycopersicon esculentum lectin demonstrated numerous phagocytic macrophages and reactive microglia in and around the tumors whose distribution was similar to that of quinolinate immunoreactive cells, albeit much more numerous. Dual labeling studies with antibodies to quinolinate and the lectins demonstrated partial codistribution of these markers, with most double-labeled cells having the morphology of phagocytes. The present findings suggest the possibility that quinolinate may serve a functional role in a select population of inflammatory cell infiltrates during the immune response to brain neoplasms.},
	Author = {Moffett, J. R. and Els, T. and Espey, M. G. and Walter, S. A. and Streit, W. J. and Namboodiri, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Lectins;Neuroblastoma;Plant Lectins;Astrocytes;Corpus Striatum;Macrophages;Rats;Animals;Neoplasm Transplantation;Microglia;Female;Rats, Wistar;11 Glia;Not relevant;Brain Neoplasms;Tumor Stem Cells;Male;Glioblastoma;Rats, Inbred F344;Antibody Specificity;Quinolinic Acid;Organ Specificity;Support, U.S. Gov't, P.H.S.;Biological Markers;Inflammation;Nerve Tissue Proteins;Tryptophan Oxygenase;Glial Fibrillary Acidic Protein},
	Medline = {97312389},
	Month = {4},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Biology, Georgetown University, Washington, DC 20057-1229, USA.},
	Pages = {287-301},
	Pii = {S0014488696963657},
	Pubmed = {9168830},
	Title = {Quinolinate immunoreactivity in experimental rat brain tumors is present in macrophages but not in astrocytes},
	Uuid = {F40CE37D-6170-4736-A653-0F901FF77EAF},
	Volume = {144},
	Year = {1997},
	url = {papers/Moffett_ExpNeurol1997.pdf}}

@article{Moga:2005,
	Abstract = {Annexin 7 (ANX7), also termed synexin, is a member of the annexin family of calcium-binding proteins. In the present study, we examined the distribution and cellular localization of ANX7-immunoreactivity in the rat hippocampus and its response to adrenalectomy (ADX). ANX7 was co-localized with OX42 in microglia distributed throughout the hippocampus of both control and ADX animals. ANX7-immunoreactivity was not detected in GFAP-positive astrocytes or in hippocampal neurons. At 1-week and 4-weeks following ADX, we observed a population of large, ameboid, ANX7-immunopositive microglia ("reactive microglia") which were largely confined to the granule cell layer of the dentate gyrus throughout its rostrocaudal extent. No reactive microglia were present in the hippocampus of sham-ADX or ADX + corticosterone treated animals. In 4-weeks ADX animals but not 1-week ADX, ANX7-immunostaining was significantly increased in the mossy fiber layer of CA3, due to the presence of many small, dark-staining "activated microglia". Our results show that ANX7 is abundantly expressed in the rat hippocampus by different microglial forms (e.g., ramified, activated and reactive microglia), suggesting an important role for this calcium-binding protein in microglial Ca2+-dependent processes.},
	Author = {Moga, Margaret M. and Dempah, Dominique and Zhou, Dan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Research Support, Non-U.S. Gov't;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein;Immunohistochemistry;Hippocampus;Comparative Study;Time Factors;Rats;Annexin A7;Microglia;Antigens, CD11b;11 Glia;Animals;Male;Adrenalectomy},
	Nlm_Id = {7600130},
	Number = {1-2},
	Organization = {Department Anatomy and Cell Biology, Indiana University School of Medicine, Terre Haute, IN 47809, USA. mmoga\@medicine.indstate.edu},
	Pages = {42-7},
	Pii = {S0304-3940(05)00022-4},
	Pubmed = {15854748},
	Title = {Annexin 7-immunoreactive microglia in the hippocampus of control and adrenalectomized rats},
	Uuid = {8FC8F2DD-86CE-45DB-8D05-1563ADC16D78},
	Volume = {380},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neulet.2005.01.022}}

@article{Molofsky:2003,
	Abstract = {Stem cells persist throughout life by self-renewing in numerous tissues including the central and peripheral nervous systems. This raises the issue of whether there is a conserved mechanism to effect self-renewing divisions. Deficiency in the polycomb family transcriptional repressor Bmi-1 leads to progressive postnatal growth retardation and neurological defects. Here we show that Bmi-1 is required for the self-renewal of stem cells in the peripheral and central nervous systems but not for their survival or differentiation. The reduced self-renewal of Bmi-1-deficient neural stem cells leads to their postnatal depletion. In the absence of Bmi-1, the cyclin-dependent kinase inhibitor gene p16Ink4a is upregulated in neural stem cells, reducing the rate of proliferation. p16Ink4a deficiency partially reverses the self-renewal defect in Bmi-1-/- neural stem cells. This conserved requirement for Bmi-1 to promote self-renewal and to repress p16Ink4a expression suggests that a common mechanism regulates the self-renewal and postnatal persistence of diverse types of stem cell. Restricted neural progenitors from the gut and forebrain proliferate normally in the absence of Bmi-1. Thus, Bmi-1 dependence distinguishes stem cell self-renewal from restricted progenitor proliferation in these tissues. 1476-4687 Journal Article},
	Author = {Molofsky, A. V. and Pardal, R. and Iwashita, T. and Park, I. K. and Clarke, M. F. and Morrison, S. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Nature},
	Keywords = {Cell Survival;Cell Differentiation;Animals;Protein p16/metabolism;Apoptosis;Stem Cells/*cytology/*metabolism;Mice, Inbred C57BL;Support, Non-U.S. Gov't;Cell Lineage;Neural Crest/cytology/metabolism;Proto-Oncogene Proteins/deficiency/genetics/*metabolism;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Neurons/*cytology/*metabolism;C pdf;Nuclear Proteins/deficiency/genetics/*metabolism;Nervous System/*cytology/*metabolism},
	Number = {6961},
	Organization = {Howard Hughes Medical Institute, and Departments of Internal Medicine and Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109-0934, USA.},
	Pages = {962-7},
	Pubmed = {14574365},
	Title = {Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation},
	Uuid = {4DA326E9-F3C9-40D6-9A96-9A24B6E9F11D},
	Volume = {425},
	Year = {2003},
	url = {papers/Molofsky_Nature2003.pdf}}

@article{Monckton:1980,
	Abstract = {Several B-lymphocyte mitogens have been previously characterized as efficient inducers of endogenous C-type viruses in mouse spleen cell cultures. We now report that foetal calf serum is also capable of inducing C-type virus release in such cultures. While virus induction by B-cell mitogens was found to be serum independent, the combined effects of serum and mitogens were found to be additive and, with some serum batches, synergistic. The kinetics of induction of virus release by serum was very similar to the established pattern using mitogens. The effect of serum was concentration-dependent. The serum lipoprotein fraction prepared by density ultracentrifugation contained virus-inducing activity. By co-cultivation with mink CCL64 cells, stable lines of mouse xenotropic C-type virus could be recovered from cultures which contained serum, serum lipoprotein fraction or mitogens, but not from control cultures. Preliminary evidence indicates that human sera contained a similar virus-inducing activity in the lipoprotein fraction.},
	Author = {Monckton, R. P. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0022-1317},
	Journal = {J Gen Virol},
	Keywords = {Lipoproteins;Mice, Inbred BALB C;Blood;Animals;Cells, Cultured;Lymphocytes;Lipopolysaccharides;Mice, Inbred C3H;15 Retrovirus mechanism;RNA-Directed DNA Polymerase;Retroviridae;Mitogens;Virus Activation;Mice;Fetal Blood;24 Pubmed search results 2008;Bromodeoxyuridine;Virus Replication;15 ERVs retroelements;Spleen;Mice, Inbred AKR},
	Medline = {80161930},
	Month = {3},
	Nlm_Id = {0077340},
	Number = {1},
	Pages = {59-66},
	Pubmed = {6154125},
	Title = {Foetal calf serum acts as an inducer of endogenous C-type virus in mouse lymphoid cells},
	Uuid = {1FE44D3D-5C0D-4DFA-B762-30310693919C},
	Volume = {47},
	Year = {1980}}

@article{Monier:2006,
	Abstract = {We describe the topographical distribution of microglial subpopulations during development of the human diencephalon and telencephalon. Brains from embryos and fetuses age 5-23.5 gestational weeks (gw) were subjected to single- and double-immunolabeling for lectin RCA-1 (Ricinus Communis Agglutinin 1), Iba1 (a microglial marker), CD68 (specific of macrophages), CD45 (marker for mononucleate cells of hematopoietic lineage), CD34 (expressed on endothelial cells), and MIB1 and Ki67 (markers for cell proliferation). At 5.5 gw the first intracerebral microglial cells were seen close to the meninges and choroid plexus near the di-telencephalic fissure. They were amoeboid and positive for Iba1, CD45, and RCA-1, whereas cells in the deep parenchyma expressed Iba1/CD68/RCA-1 and constituted clusters. In the developing diencephalon, microglial clusters were located in junctional regions of the white matter anlagen, most notably at the junctions of the internal capsule with the thalamic projections, the external capsule, and the cerebral peduncle. In the cortical anlagen, Iba1+/RCA-1/CD68+/CD45+ cells accumulated at 10-12 gw, constituting a tangential band at the junction between the cortical plate and the subplate. Between 10 and 16 gw microglial clusters increased markedly in size and cellular density. Contact between Iba1+ microglia and CD34+ blood vessels was clearly visible from 10-12 gw onward, first in microglial clusters of the white matter anlagen and subsequently throughout the parenchyma. From the middle of the second trimester onward microglial cells colonized the entire cerebral parenchyma, developed a ramified morphology, and downregulated their surface antigens, but remained more numerous in the white matter.},
	Author = {Monier, Anne and Evrard, Philippe and Gressens, Pierre and Verney, Catherine},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Embryo;Cell Differentiation;research support, non-u.s. gov't;Fetus;Pregnancy Trimester, Second;Female;Immunohistochemistry;11 Glia;Microglia;Pregnancy;Humans;Brain;Pregnancy Trimester, First;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {Inserm, U676, Paris, F-75019 France.},
	Pages = {565-82},
	Pubmed = {17029271},
	Title = {Distribution and differentiation of microglia in the human encephalon during the first two trimesters of gestation},
	Uuid = {93B11D64-44E2-4B97-A7EB-058E61C4977C},
	Volume = {499},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.21123}}

@article{Monje:2002,
	Abstract = {In both pediatric and adult patients, cranial radiation therapy causes a debilitating cognitive decline that is poorly understood and currently untreatable. This decline is characterized by hippocampal dysfunction, and seems to involve a radiation-induced decrease in postnatal hippocampal neurogenesis. Here we show that the deficit in neurogenesis reflects alterations in the microenvironment that regulates progenitor-cell fate, as well as a defect in the proliferative capacity of the neural progenitor-cell population. Not only is hippocampal neurogenesis ablated, but the remaining neural precursors adopt glial fates and transplants of non-irradiated neural precursor cells fail to differentiate into neurons in the irradiated hippocampus. The inhibition of neurogenesis is accompanied by marked alterations in the neurogenic microenvironment, including disruption of the microvascular angiogenesis associated with adult neurogenesis and a marked increase in the number and activation status of microglia within the neurogenic zone. These findings provide clear targets for future therapeutic interventions. 1078-8956 Journal Article},
	Author = {Monje, M. L. and Mizumatsu, S. and Fike, J. R. and Palmer, T. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {Nat Med},
	Keywords = {Cell Differentiation;DNA Repair/radiation effects;Animals;Cells, Cultured;Microglia/radiation effects;Rats;Cell Division/radiation effects;Stem Cell Transplantation;Female;Bromodeoxyuridine/analysis/metabolism;D pdf;Stem Cells/*radiation effects;Neovascularization, Pathologic;Rats, Inbred F344;Support, Non-U.S. Gov't;06 Adult neurogenesis injury induced;Cell Transplantation;Astrocytes/radiation effects;Neurons/*radiation effects;Support, U.S. Gov't, P.H.S.;Brain/*pathology/*radiation effects},
	Number = {9},
	Organization = {Department of Neurosurgery, Stanford University, Stanford, California, USA.},
	Pages = {955-62},
	Title = {Irradiation induces neural precursor-cell dysfunction},
	Uuid = {5405B9C8-D938-407C-9285-2701474788BF},
	Volume = {8},
	Year = {2002},
	url = {papers/Monje_NatMed2002.pdf}}

@article{Monsonego:2003,
	Abstract = {Although neurodegenerative diseases such as Alzheimer's disease are not classically considered mediated by inflammation or the immune system, in some instances the immune system may play an important role in the degenerative process. Furthermore, it has become clear that the immune system itself may have beneficial effects in nervous system diseases considered neurodegenerative. Immunotherapeutic approaches designed to induce a humoral immune response have recently been developed for the treatment of Alzheimer's disease. These studies have led to human trials that resulted in both beneficial and adverse effects. In animal models, it has also been shown that immunotherapy designed to induce a cellular immune response may be of benefit in central nervous system injury, although T cells may have either a beneficial or detrimental effect depending on the type of T cell response induced. These areas provide a new avenue for exploring immune system-based therapy of neurodegenerative diseases and will be discussed here with a primary focus on Alzheimer's disease. We will also discuss how these approaches affect microglia activation, which plays a key role in therapy of such diseases.},
	Author = {Monsonego, Alon and Weiner, Howard L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:54 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Immunotherapy;T-Lymphocytes;Human;Animals;Antigen-Presenting Cells;Amyloid beta-Protein;review, tutorial;Alzheimer Vaccines;review;Microglia;Antibody Formation;Lymphocyte Activation;21 Neurodegenerative;Clinical Trials;Alzheimer Disease;21 Neurophysiology;Immunization;Immunity, Mucosal;Immunity, Natural;Central Nervous System;Nitric Oxide},
	Medline = {22954848},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5646},
	Organization = {Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. amonsonego\@rics.bwh.harvard.edu},
	Pages = {834-8},
	Pii = {302/5646/834},
	Pubmed = {14593170},
	Title = {Immunotherapeutic approaches to Alzheimer's disease},
	Uuid = {4193E8A4-1F11-41AD-B948-B2ACE071736F},
	Volume = {302},
	Year = {2003},
	url = {papers/Monsonego_Science2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1088469}}

@article{Monuki:2001a,
	Abstract = {The organizing centers and molecules that pattern the cerebral cortex have been elusive. Here we show that cortical patterning involves regulation of the Lhx2 homeobox gene by the roof plate. Roof plate ablation results in reduced cortical size and Lhx2 expression defects that implicate roof plate signals in the bimodal regulation of Lhx2 in vivo. Bimodal Lhx2 regulation can be recapitulated in explants using two roof plate-derived signaling molecules, Bmp4 and Bmp2. Loss of Lhx2 function results in profound losses of cortical progenitors and neurons, but Lhx2 mutants continue to generate cortical neurons from dorsal sources that may include the roof plate region itself. These findings provide evidence for the roof plate as an organizing center of the developing cortex and for a roof plate-Lhx2 pathway in cortical patterning.},
	Author = {Monuki, E. S. and Porter, F. D. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;10 Hippocampus;Animals;Transcription Factors;Cells, Cultured;Gene Expression Regulation, Developmental;Pregnancy;Transforming Growth Factor beta;Female;Homeodomain Proteins;Bone Morphogenetic Proteins;Male;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Mice, Knockout;Neurons;Cerebral Cortex;Mice;Growth Substances;Research Support, Non-U.S. Gov't},
	Medline = {21576527},
	Month = {11},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Division of Neurogenetics, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.},
	Pages = {591-604},
	Pii = {S0896-6273(01)00504-9},
	Pubmed = {11719201},
	Title = {Patterning of the dorsal telencephalon and cerebral cortex by a roof plate-Lhx2 pathway},
	Uuid = {0530A234-C1AB-4FC9-B071-BF3BAD333AF5},
	Volume = {32},
	Year = {2001}}

@article{Moore:2002,
	Abstract = {The repair of oxidative DNA lesions (ODLs) in the nucleus of ischemic cortical brain cells was examined following experimentally induced stroke by occluding the right middle cerebral artery and both common carotid arteries for 60-90 min followed by reperfusion in male long-Evans hooded rats. The control group consisted of sham-operated animals undergoing the same surgery without vessel occlusion. Using a gene-specific assay based upon the presence of Escherichia coli Fpg protein-sensitive sites, we noted that animals with stroke exhibited six and four ODLs per gene in the actin and DNA polymerase-beta genes, respectively. This was increased from one per four copies of each gene in the sham-operated control (p <0.01). One half of the initial ODLs was repaired within 30 min, and 83\%of them were repaired as early as 45 min of reperfusion. There was no further increase when gene repair was measured again at 2 h of reperfusion. The rates of active repair within 45 min of reperfusion were the same in these two genes (p = 0.103, ANOVA). BrdU (10 mg/kg) was administered via intraperitoneal injection at least one day before surgery. We observed that there was no significant incorporation of BrdU triphosphates into genomic DNA during active repair, but there were significant amounts of BrdU triphosphate in nuclear DNA after active repair. The result indicates that genomic repair of ODLs in the brain did not significantly incorporate BrdU, and the initiation of neurogenesis probably starts after the completion of repair in the brain. 0022-3042 Journal Article},
	Author = {Moore, N. and Okocha, F. and Cui, J. K. and Liu, P. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Journal = {J Neurochem},
	Keywords = {DNA/metabolism;EE pdf;Cerebrovascular Accident/*genetics;Brain/*physiopathology/surgery;Rats, Long-Evans;Rats;Bromodeoxyuridine/metabolism;Sutures;*DNA Repair;Cell Nucleus/*physiology;Support, U.S. Gov't, P.H.S.;Animals;Male;Brain Injuries/etiology/metabolism},
	Number = {1},
	Organization = {Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.},
	Pages = {111-8},
	Title = {Homogeneous repair of nuclear genes after experimental stroke},
	Uuid = {F865814F-CDF0-11D9-B244-000D9346EC2A},
	Volume = {80},
	Year = {2002},
	url = {papers/Moore_JNeurochem2002.pdf}}

@article{Moran:2004a,
	Abstract = {Experimental models such as the facial nerve axotomy paradigm in rodents allow the systematic and detailed study of the response of neurones and their microenvironment to various types of challenges. Well-studied experimental examples include peripheral nerve trauma, the retrograde axonal transport of neurotoxins and locally enhanced inflammation following the induction of experimental autoimmune encephalomyelitis in combination with axotomy. These studies have led to novel insights into the regeneration programme of the motoneurone, the role of microglia and astrocytes in synaptic plasticity and the biology of glial cells. Importantly, many of the findings obtained have proven to be valid in other functional systems and even across species barriers. In particular, microglial expression of major histocompatibility complex molecules has been found to occur in response to various types of neuronal damage and is now regarded as a characteristic component of "glial inflammation". It is found in the context of numerous neurodegenerative disorders including Parkinson's and Alzheimer's disease. The detachment of afferent axonal endings from the surface membrane of regenerating motoneurones and their subsequent displacement by microglia ("synaptic stripping") and long-lasting insulation by astrocytes have also been confirmed in humans. The medical implications of these findings are significant. Also, the facial nerve system of rats and mice has become the best studied and most widely used test system for the evaluation of neurotrophic factors.},
	Author = {Moran, Linda B. and Graeber, Manuel B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0165-0173},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {Nerve Regeneration;Facial Nerve Injuries;11 Glia;review, tutorial;Axotomy;Animals;Disease Models, Animal;review;Humans},
	Month = {3},
	Nlm_Id = {8908638},
	Number = {2-3},
	Organization = {Department of Neuropathology, Division of Neuroscience and Psychological Medicine, Faculty of Medicine, Imperial College London, Charing Cross Campus, Fulham Palace Road, London W6 8RF, UK.},
	Pages = {154-78},
	Pii = {S0165017303002595},
	Pubmed = {15003391},
	Title = {The facial nerve axotomy model},
	Uuid = {FF13CCF2-EE26-11DA-8605-000D9346EC2A},
	Volume = {44},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainresrev.2003.11.004}}

@article{Moran:2004,
	Abstract = {This study provides an expression signature of interferon-gamma (IFN-gamma)-activated microglia. Microglia are macrophage precursor cells residing in the brain and spinal cord. The microglial phenotype is highly plastic and changes in response to numerous pathological stimuli. IFN-gamma has been established as a strong immunological activator of microglial cells both in vitro and in vivo. Affymetrix RG\_U34A microarrays were used to determine the effect of IFN-gamma stimulation on migroglia cells isolated from newborn Lewis rat brains. More than 8,000 gene sequences were examined, i.e., 7,000 known genes and 1,000 expressed sequence tag (EST) clusters. Under baseline conditions, microglia expressed 326 of 8,000 genes examined (approximately 4\%of all genes, 182 known and 144 ESTs). Transcription of only 34 of 7,000 known genes and 8 of 1,000 ESTs was induced by IFN-gamma stimulation. The majority of the newly expressed genes encode pro-inflammatory cytokines and components of the MHC-mediated antigen presentation pathway. The expression of 60 of 182 identified genes and of 9 of 144 ESTs was increased by IFN-gamma, whereas 29 of 182 known genes and 7 of 144 ESTs were down-regulated or undetectable in IFN-gamma-stimulated cultures. Overall, the activating effect of IFN-gamma on the microglial transcriptome showed restriction to pathways involved in antigen presentation, protein degradation, actin binding, cell adhesion, apoptosis, and cell signaling. In comparison, down-regulatory effects of IFN-gamma stimulation appeared to be confined to pathways of growth regulation, remodeling of the extracellular matrix, lipid metabolism, and lysosomal processing. In addition, transcriptomic profiling revealed previously unknown microglial genes that were de novo expressed, such as calponin 3, or indicated differential regulatory responses, such as down-regulation of cathepsins that are up-regulated in response to other microglia stimulators.},
	Author = {Moran, L. B. and Duke, D. C. and Turkheimer, F. E. and Banati, R. B. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1364-6745},
	Journal = {Neurogenetics},
	Keywords = {Down-Regulation;Research Support, Non-U.S. Gov't;Rats, Inbred Lew;Rats;Oligonucleotide Array Sequence Analysis;Interferon Type II;Gene Expression;Transcription, Genetic;Up-Regulation;Reproducibility of Results;Microglia;Animals;Antineoplastic Agents;Cells, Cultured;11 Glia},
	Month = {6},
	Nlm_Id = {9709714},
	Number = {2},
	Organization = {University Department of Neuropathology, Neurosciences Division, Faculty of Medicine, Imperial College London, London, UK.},
	Pages = {95-108},
	Pubmed = {15042428},
	Title = {Towards a transcriptome definition of microglial cells},
	Uuid = {9A72A57B-72B9-4EF4-A20D-46E257DA915E},
	Volume = {5},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s10048-004-0172-5}}

@article{Mordelet:2002,
	Abstract = {Transplantation of ex vivo gene-corrected autologous cells represents an attractive therapeutic approach for brain diseases. Among the cells of the central nervous system, brain macrophages are promising candidates due to their role in tissue homeostasis and their implication in several neurological diseases. Up to now, gene transfer into macrophages has proven difficult by most currently available gene delivery methods. We describe herein, an efficient transduction of rat bone marrow-derived and brain macrophages with an HIV-1-derived vector containing a central DNA flap and encoding the GFP reporter gene (TRIP-DeltaU3-GFP). In primary cultures of macrophages our results show that more than 90\%of the cells were transduced by the TRIP vector and that GFP expression remained stable for 1 month without cytopathic effect. In vivo, transplants of transduced macrophages into the striatum of adult rats exhibited long-term expression of GFP up to 3 months. Transduced macrophages were observed around the brain injection site and exhibited the brain macrophage/microglia phenotype. There was no significant sign of astrogliosis around the graft. These results confirm the potential of lentiviral vectors for efficient and stable ex vivo transduction of macrophages. Moreover, transduced autologous macrophages appear as a valuable vehicle for long-term and localized gene expression into the brain.},
	Author = {Mordelet, E. and Kissa, K. and Calvo, C-F F. and Lebastard, M. and Milon, G. and van der Werf, S. and Vidal, C. and Charneau, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;HIV-1;Rats, Long-Evans;Astrocytes;Rats;Macrophages;Animals;Brain;Rats, Wistar;11 Glia;Green Fluorescent Proteins;Brain Diseases;Time Factors;Male;Genetic Vectors;Bone Marrow Cells;Gene Therapy;Transplantation, Autologous;Luminescent Proteins;Gene Expression;Cell Death;Research Support, Non-U.S. Gov't},
	Medline = {21838676},
	Month = {1},
	Nlm_Id = {9421525},
	Number = {1},
	Organization = {Unite de Genetique Moleculaire des Virus Respiratoires, Institut Pasteur, Paris, France.},
	Pages = {46-52},
	Pubmed = {11850722},
	Title = {Brain engraftment of autologous macrophages transduced with a lentiviral flap vector: an approach to complement brain dysfunctions},
	Uuid = {A6C77A52-275E-401A-9BC9-EA1789FAA060},
	Volume = {9},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301591}}

@article{Moreau-Gaudry:2001,
	Abstract = {Use of oncoretroviral vectors in gene therapy for hemoglobinopathies has been impeded by low titer vectors, genetic instability, and poor expression. Fifteen self- inactivating (SIN) lentiviral vectors using 4 erythroid promoters in combination with 4 erythroid enhancers with or without the woodchuck hepatitis virus postregulatory element (WPRE) were generated using the enhanced green fluorescent protein as a reporter gene. Vectors with high erythroid-specific expression in cell lines were tested in primary human CD34(+) cells and in vivo in the murine bone marrow (BM) transplantation model. Vectors containing the ankyrin-1 promoter showed high-level expression and stable proviral transmission. Two vectors containing the ankyrin-1 promoter and 2 erythroid enhancers (HS-40 plus GATA-1 or HS-40 plus 5-aminolevulinate synthase intron 8 [I8] enhancers) and WPRE expressed at levels higher than the HS2/beta-promoter vector in bulk unilineage erythroid cultures and individual erythroid blast-forming units derived from human BM CD34(+) cells. Sca1(+)/lineage(-) Ly5.1 mouse hematopoietic cells, transduced with these 2 ankyrin-1 promoter vectors, were injected into lethally irradiated Ly5.2 recipients. Eleven weeks after transplantation, high-level expression was seen from both vectors in blood (63\%-89\%of red blood cells) and erythroid cells in BM (70\%-86\%engraftment), compared with negligible expression in myeloid and lymphoid lineages in blood, BM, spleen, and thymus (0\%-4\%). The I8/HS-40-containing vector encoding a hybrid human beta/gamma-globin gene led to 43\%to 113\%human gamma-globin expression/copy of the mouse alpha-globin gene. Thus, modular use of erythroid-specific enhancers/promoters and WPRE in SIN-lentiviral vectors led to identification of high-titer, stably transmitted vectors with high-level erythroid-specific expression for gene therapy of red cell diseases.},
	Author = {Moreau-Gaudry, F. and Xia, P. and Jiang, G. and Perelman, N. P. and Bauer, G. and Ellis, J. and Surinya, K. H. and Mavilio, F. and Shen, C. K. and Malik, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Gene Expression;Transduction, Genetic;Animals;Humans;Gene Expression Regulation, Viral;Bone Marrow Transplantation;Comparative Study;Lentivirus;Antigens, CD34;11 Glia;Green Fluorescent Proteins;Enhancer Elements (Genetics);Genetic Vectors;Bone Marrow Cells;RNA Processing, Post-Transcriptional;Hepatitis B Virus, Woodchuck;Mice;Erythroid Progenitor Cells;Luminescent Proteins;Promoter Regions (Genetics);Models, Animal;Gamma-Globulins;Hematopoietic Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {21531304},
	Month = {11},
	Nlm_Id = {7603509},
	Number = {9},
	Organization = {Children's Hospital Los Angeles, University of Southern California School of Medicine, Los Angeles 90027, USA.},
	Pages = {2664-72},
	Pubmed = {11675336},
	Title = {High-level erythroid-specific gene expression in primary human and murine hematopoietic cells with self-inactivating lentiviral vectors},
	Uuid = {607AA673-A3F0-4F05-AA24-7AAD86A2E836},
	Volume = {98},
	Year = {2001}}

@article{Moreno-Lopez:2000,
	Abstract = {The subventricular zone (SVZ) of the adult mouse brain retains the capacity to generate new neurons from stem cells. The neuronal precursors migrate tangentially along the rostral migratory stream (RMS) towards the olfactory bulb, where they differentiate as periglomerular and granular interneurons. In this study, we have investigated whether nitric oxide (NO), a signaling molecule in the nervous system with a role in embryonic neurogenesis, may be produced in the proximity of the progenitor cells in the adult brain, as a prerequisite to proposing a functional role for NO in adult neurogenesis. Proliferating and immature precursor cells were identified by immunohistochemistry for bromo-deoxyuridine (BrdU) and PSA-NCAM, respectively, and nitrergic neurons by either NADPH- diaphorase staining or immunohistochemical detection of neuronal NO synthase (NOS I). Nitrergic neurons with long varicose processes were found in the SVZ, intermingled with chains of cells expressing PSA-NCAM or containing BrdU. Neurons with similar characteristics surrounded the RMS all along its caudo-rostral extension as far as the core of the olfactory bulb. No expression of NOS I by precursor cells was detected either in the proliferation or in the migration zones. Within the olfactory bulb, many small cells in the granular layer and around the glomeruli expressed either PSA-NCAM or NOS I and, in some cases, both markers. Colocalization was also found in a few isolated cells at a certain distance from the neurogenesis areas. The anatomical disposition shown indicates that NO may be released close enough to the neuronal progenitors to allow a functional influence of this messenger in adult neurogenesis.},
	Author = {Moreno-Lopez, B. and Noval, J. A. and Gonzalez-Bonet, L. G. and Estrada, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Brain Res},
	Keywords = {Mice, Inbred Strains;Neural Cell Adhesion Molecules/metabolism;Nitric Oxide/*metabolism;Sialic Acids/metabolism;Cell Differentiation/*physiology;Neurons/cytology/*metabolism;04 Adult neurogenesis factors;Olfactory Bulb/cytology/growth &development/metabolism;Animal;C-14;Stem Cells/cytology/*metabolism;Cell Division/*physiology;Support, Non-U.S. Gov't;Brain/cytology/*growth &development/metabolism;Mice;Male;Cell Movement/physiology},
	Number = {1-2},
	Organization = {Area de Fisiologia, Facultad de Medicina, Universidad de Cadiz, Plaza Fragela 9, 11003, Cadiz, Spain.},
	Pages = {244-50.},
	Title = {Morphological bases for a role of nitric oxide in adult neurogenesis},
	Uuid = {64C3BA69-EE85-4FE4-AAE3-ABC05CC75703},
	Volume = {869},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10865083}}

@article{Moreno-Lopez:2004,
	Abstract = {The subventricular zone of the rodent brain retains the capacity of generating new neurons in adulthood. The newly formed neuroblasts migrate rostrally toward the olfactory bulb, where they differentiate as granular and periglomerular interneurons. The reported presence of differentiated neurons expressing the neuronal isoform of nitric oxide synthase (NOS) in the periphery of the neurogenic region and the organization of their varicose axons as a network in which the precursors are immersed raised the hypothesis that endogenous nitric oxide (NO) may participate in the control of neurogenesis in the subventricular zone. Systemic administration of the NOS inhibitors N(omega)-nitro-L-arginine methyl ester or 7-nitroindazole to adult mice produced a dose- and time-dependent increase in the number of mitotic cells in the subventricular zone, rostral migratory stream, and olfactory bulb, but not in the dentate gyrus of the hippocampus, without affecting apoptosis. In the subventricular zone, this effect was exerted selectively on a precursor subpopulation expressing nestin but not neuronal or glial cell-specific proteins. In addition, in the olfactory bulb, analysis of maturation markers in the newly generated neurons indicated that chronic NOS inhibition caused a delay in neuronal differentiation. Postmitotic cell survival and migration were not affected when NO production was impaired. Our results suggest that NO, produced by nitrergic neurons in the adult mouse subventricular zone and olfactory bulb, exerts a negative control on the size of the undifferentiated precursor pool and promotes neuronal differentiation. 1529-2401 Journal Article},
	Author = {Moreno-Lopez, B. and Romero-Grimaldi, C. and Noval, J. A. and Murillo-Carretero, M. and Matarredona, E. R. and Estrada, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {J Neurosci},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {1},
	Organization = {Area de Fisiologia, Facultad de Medicina, Universidad de Cadiz, 11003 Cadiz, Spain.},
	Pages = {85-95},
	Pubmed = {14715941},
	Title = {Nitric oxide is a physiological inhibitor of neurogenesis in the adult mouse subventricular zone and olfactory bulb},
	Uuid = {6AE54247-7A77-48F2-8C47-05E8E9C56E38},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14715941}}

@article{Morgenstern:2003,
	Abstract = {We have investigated expression of the axon growth-inhibitory proteoglycan NG2 in peripheral nerve. In the adult, NG2 was present on endoneurial and perineurial fibroblasts, but not on Schwann cells. At birth, peripheral nerve NG2 was heavily glycanated, but was much less so in the adult. In vitro, sciatic nerve fibroblasts also produced heavily glycanated NG2. After peripheral nerve injury in rats and humans, an accumulation of NG2-positive cells was observed at the injury site. In the rat, there was an increase in NG2 glycanation for at least 2 weeks following injury. In mixed cultures of Schwann cells and peripheral nerve fibroblasts, the axons preferred to grow on the Schwann cells and seldom crossed onto the fibroblasts. Three-dimensional cultures of sciatic nerve fibroblasts were inhibitory to the growth of dorsal root ganglion axons. Inhibition of proteoglycan synthesis made the cells more permissive. NG2 may play a part in blocking axon regeneration through scar tissue in injured human peripheral nerve. 1044-7431 Journal Article},
	Author = {Morgenstern, D. A. and Asher, R. A. and Naidu, M. and Carlstedt, T. and Levine, J. M. and Fawcett, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {G abstr;11 Glia},
	Number = {3},
	Organization = {Centre for Brain Repair, University of Cambridge, Robinson Way, Cambridge CB2 2PY, UK.},
	Pages = {787-802},
	Pubmed = {14664826},
	Title = {Expression and glycanation of the NG2 proteoglycan in developing, adult, and damaged peripheral nerve},
	Uuid = {E565655C-09DD-4E1A-B96B-B2D4EF0D40E7},
	Volume = {24},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14664826}}

@article{Morioka:1992,
	Abstract = {The appearance and cellular distribution of major histocompatibility complex (MHC), as well as lymphocytic and macrophage antigens has been studied in a fully developed experimental rat forebrain glioma. Activated microglial cells and microglia-derived macrophages expressing CR3 complement receptor molecules and MHC class II (Ia) antigen were found throughout the tumor, and with increased density along the tumor's periphery. MHC class I antigen expression was entirely absent from tumor cells, and found only occasionally on microglia. The expression of leukocyte common antigen, and CD4 and CD8 antigens was conspicuous throughout the tumor, and associated with lymphocytes, perivascular cells, and microglia. Cells expressing the ED2 macrophage epitope were almost exclusively of the perivascular type and revealed a distribution dissimilar to that of cells positive for Ia antigen. The ED2 epitope was found sporadically on ramified microglial cells. The results show that despite heavy infiltration with blood mononuclear and CNS microglial cells, the tumor showed no evidence of destruction caused by inflammatory cells. Possible mechanisms of tumor immunosuppressive activity preventing the full immunological activation of microglia and blood mononuclear cells are discussed.},
	Author = {Morioka, T. and Baba, T. and Black, K. L. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Neuroglia;Glioma;Rats;Female;Phenotype;Antibodies, Monoclonal;Not relevant;Leukocytes;11 Glia;Nervous System Neoplasms;Neoplasms, Experimental;Animals;Rats, Inbred Strains;Major Histocompatibility Complex;Support, Non-U.S. Gov't},
	Medline = {92343307},
	Nlm_Id = {0412041},
	Number = {6},
	Organization = {Department of Neurological Surgery, University of Florida, Gainesville 32610.},
	Pages = {590-7},
	Pubmed = {1636377},
	Title = {Immunophenotypic analysis of infiltrating leukocytes and microglia in an experimental rat glioma},
	Uuid = {D8A95923-DBF5-4FD2-AC51-0BB188B8F911},
	Volume = {83},
	Year = {1992}}

@article{Morioka:1992a,
	Abstract = {We show a differential up-regulation of immunomolecules in the rat dorsal hippocampus accompanying neuronal cell death as a consequence of transient forebrain ischemia (four-vessel occlusion model). Using a panel of monoclonal antibodies (mAbs), we have examined the time course of expression of major histocompatibility complex (MHC) antigens class I (OX-18) and class II (OX-6), leukocyte common antigen (OX-1), CD4 (W3/25) and CD8 (OX-8) antigens, CR3 complement receptor (OX-42), as well as brain macrophage antigen (ED2). The study was performed at time intervals ranging from 1 to 28 days after reperfusion. Throughout all post-ischemic time periods, strongly enhanced immunoreactivity on microglial cells in the CA1 region and dentate hilus and, to a lesser extent, in CA3 was demonstrated with mAb OX-42. MHC class I-positive cells (OX-18) appeared on day 2, whereas cells immunoreactive with OX-1 and W3/25 became evident in the CA1 and hilar regions on post-ischemic day 6. In contrast, MHC class II (Ia) antigen was first detected on indigenous microglia by day 13. In some animals, the OX-8 antibody resulted in the labelling of scattered CD8-positive lymphocytes, but perivascular inflammatory infiltrates were absent. No changes in the expression of ED2 immunoreactivity on perivascular cells could be observed. The results show that following ischemic injury, microglial cells demonstrate a time-dependent up-regulation and de novo expression of certain immunomolecules, indicative of their immunocompetence. The findings are compared with those obtained in other models of brain injury.},
	Author = {Morioka, T. and Kalehua, A. N. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Animals;Up-Regulation;Rats;Lymphocytes;Female;Antigens, CD4;Hippocampus;Rats, Inbred Strains;Not relevant;11 Glia;Prosencephalon;Receptors, Complement;Antibodies, Monoclonal;Neuroglia;Antigens, CD8;Support, U.S. Gov't, P.H.S.;Ischemic Attack, Transient;Complement 3;Histocompatibility Antigens Class I;Histocompatibility Antigens Class II},
	Medline = {92214062},
	Nlm_Id = {0412041},
	Number = {2},
	Organization = {Department of Neurological Surgery, University of Florida Health Science Center, Gainesville 32610-0244.},
	Pages = {149-57},
	Pubmed = {1557947},
	Title = {Progressive expression of immunomolecules on microglial cells in rat dorsal hippocampus following transient forebrain ischemia},
	Uuid = {E4528A1F-2BD8-4B6B-8E3F-257B6415B852},
	Volume = {83},
	Year = {1992}}

@article{Morioka:1992b,
	Abstract = {The response of indigenous CNS microglia to an experimentally induced glioma has been studied in rat brain using lectin histochemistry with the Griffonia simplicifolia B4-isolectin. The study was undertaken 2 weeks after tumor cell injection when tumor size was near maximal. Reactive microglial cells formed a dense band that surrounded most of the well-circumscribed tumor mass, and extended along the corpus callosum into the contralateral cerebral hemisphere. From the periphery inward, reactive microglia extended into the tumor tissue, where large numbers of them were found to be present as microglia-derived macrophages. The lectin stain, which also labels endothelial cells, revealed a highly vascularized tumor with ongoing neovascularization apparent as vascular sprouts. Moderate numbers of lectin-stained blood monocytes were localized primarily inside the vessel lumina. Our results show that microglial cells react to brain tumors; however, it remains to be determined whether the microglial response represents an active antitumor defense mechanism that could be manipulated during immunotherapeutic approaches.},
	Author = {Morioka, T. and Baba, T. and Black, K. L. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Neuroglia;Glioma;Rats;Lectins;Not relevant;Transplantation, Homologous;11 Glia;Neoplasm Transplantation;Brain Neoplasms;Histocytochemistry;Support, Non-U.S. Gov't;Horseradish Peroxidase;Animals},
	Medline = {92380742},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Department of Neurological Surgery, University of Florida, Gainesville 32610.},
	Pages = {75-9},
	Pubmed = {1387388},
	Title = {Response of microglial cells to experimental rat glioma},
	Uuid = {77A3B746-7632-42A0-B88D-899C84913AF0},
	Volume = {6},
	Year = {1992}}

@article{Morioka:1991,
	Abstract = {We have examined the distribution and time course of the microglial reaction in the rat dorsal hippocampus after 25-min transient forebrain ischemia (four-vessel occlusion model). Microglial cells were visualized in brain sections using lectin staining with the Griffonia simplicifolia B4-isolectin following intervals of reperfusion ranging from 20 min to 4 weeks. Increased staining of microglial cells was detected in the dentate hilus and area CA1 as early as 20 min after reperfusion. These same regions demonstrated more intense microglial staining after 24 h. The strongest microglial reaction was observed 4-6 days after reperfusion when reactive microglia were abundant throughout all laminae of CA1 and the dentate hilus. Following longer reperfusion intervals, the microglial reaction became less intense; however, it remained above normal levels until the end of the fourth week. At all time points examined, microglial reactivity in the CA3 pyramidal and dentate granule cell layers was considerably lower than that observed in CA1 and dentate hilus. Our results are consistent with the known serial pathological changes associated with cerebral ischemia, but, in addition, show that the examination of the microglial reaction provides an extremely sensitive indicator of subtle and morphologically nonapparent neuronal damage during the early stages of injury.},
	Author = {Morioka, T. and Kalehua, A. N. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0271-678X},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {Staining and Labeling;Neuroglia;Female;Lectins;Hippocampus;Time Factors;Not relevant;Rats;11 Glia;Support, U.S. Gov't, P.H.S.;Cell Death;Prosencephalon;Animals;Rats, Inbred Strains;Ischemic Attack, Transient;Neurons},
	Medline = {92042381},
	Month = {11},
	Nlm_Id = {8112566},
	Number = {6},
	Organization = {Department of Neurological Surgery, University of Florida, Gainesville 32610.},
	Pages = {966-73},
	Pubmed = {1719009},
	Title = {The microglial reaction in the rat dorsal hippocampus following transient forebrain ischemia},
	Uuid = {4B59A5F0-5EF3-4B40-A5DA-75A182A19EF6},
	Volume = {11},
	Year = {1991}}

@article{Morioka:1993,
	Abstract = {We have studied the microglial reaction that accompanies cortical infarction induced by middle cerebral artery occlusion (MCAO). Lectin histochemistry with the B4-isolectin from Griffonia simplicifolia as well as immunocytochemistry with a panel of monoclonal antibodies directed against major histocompatibility complex (MHC) and lymphocytic antigens were performed. Principal attention was focused on neocortical and thalamic regions, representative of primary and secondary ischemic damage, respectively. With the lectin procedure, activated microglial cells were abundant in the neocortex 24 hours after MCAO. In contrast, microglial activation in the thalamus was not apparent until day 2 after MCAO. On day 5, MHC class II antigen was expressed by reactive microglia in fiber tracts traversing the striatum, but was absent from activated microglia in the primary cortical infarction area. MHC class I and lymphocytic antigens were expressed differentially on microglia with class I antigens appearing early and lymphocytic antigens appearing late in the time course after focal ischemia. The findings are compatible with previous studies during global ischemia and confirm the early activation and the progressive nature of immunomolecule expression on activated microglia after an ischemic insult. In addition to neocortical and thalamic sites, our results showed an early microglial activation to be present also in forebrain regions outside of the middle cerebral artery (MCA) territory, such as the contralateral cortex and hippocampus. A unilateral microglial reaction was also detectable after long-term survival (>or = 4 weeks) in the pyramidal tracts, as well as in the corticospinal tracts at cervical but not lumbar spinal cord levels. Ischemia-induced neuronal damage, as evaluated by Nissl staining, was found only in cortical and thalamic regions. We conclude that the demonstration of reactive microglia indicates not only imminent ischemic neuronal damage within MCA territory but can also delineate extra-focal disturbances, possibly reflecting subtle and transitory changes in neuronal activity.},
	Author = {Morioka, T. and Kalehua, A. N. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Neuroglia;Immunophenotyping;Rats;Inflammation;Lymphocytes;Rats, Wistar;Cerebral Infarction;11 Glia;Arterial Occlusive Diseases;Not relevant;Gliosis;Cerebral Arterial Diseases;Animals},
	Medline = {93163419},
	Month = {1},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Neurological Surgery, University of Florida, Gainesville 32610-0244.},
	Pages = {123-32},
	Pubmed = {8432904},
	Title = {Characterization of microglial reaction after middle cerebral artery occlusion in rat brain},
	Uuid = {1945975B-7C81-4086-85AB-A8E50F5BD568},
	Volume = {327},
	Year = {1993}}

@article{Morioka:1992c,
	Abstract = {We have studied the cellular immune response that accompanies primary and metastatic brain cancers induced experimentally in rats by inoculation of RG-2 glioma and Walker 256 (W256) carcinoma cells, respectively. The inflammatory cell infiltrates were characterized with lectin histochemistry to visualize microglial cells and macrophages and with immunohistochemistry, using a panel of monoclonal antibodies, to detect major histocompatibility complex (MHC), lymphocytic, and macrophage antigens. The metastatic tumor was composed of a loose stroma with multiple, often large, necrotic areas, whereas the RG-2 glioma was composed of a dense collection of tumor cells showing only rare necrotic foci. Both tumor types were heavily infiltrated with microglia and/or macrophages, and these were positive for MHC Class II (Ia) antigens. Expression of MHC Class I antigens was absent from RG-2 glioma cells, but it was present in W256 metastatic carcinoma cells. The metastatic tumor was also characterized by a much heavier infiltrate of lymphocytes, as shown by the presence of cells positive for CD4, CD8, and leukocyte common antigens. These lymphocytic markers were absent from reactive microglia in the W256 carcinoma, whereas they were present in the RG-2 glioma. Polymorphonuclear leukocytes were seen only in the metastatic tumor. Our study delineates differences between the inflammatory cell infiltrates found in metastatic brain tumors and those found in primary brain tumors. The differences in cell composition and immunophenotype may indicate a more effective antitumor response in the metastatic tumor that could account for the observed tissue destruction.},
	Author = {Morioka, T. and Baba, T. and Black, K. L. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0148-396X},
	Journal = {Neurosurgery},
	Keywords = {Neuroglia;Immunophenotyping;Glioma;Rats;Female;Not relevant;T-Lymphocytes;11 Glia;Neoplasm Transplantation;Macrophages;Brain Neoplasms;Carcinoma 256, Walker;Support, Non-U.S. Gov't;Animals;Phagocytosis},
	Medline = {92310646},
	Month = {6},
	Nlm_Id = {7802914},
	Number = {6},
	Organization = {Department of Neurological Surgery, University of Florida, Gainesville.},
	Pages = {891-6},
	Pubmed = {1614593},
	Title = {Inflammatory cell infiltrates vary in experimental primary and metastatic brain tumors},
	Uuid = {7007F65B-3162-4048-9985-CF5A7992F5FA},
	Volume = {30},
	Year = {1992}}

@article{Moroni:1978,
	Abstract = {Lipoprotein E. coli, a B-cell mitogen, is identified as a new agent inducing the release of endogenous C-type virus from mouse spleen cells. Like lipopolysaccharide, a previously identified inducer, this compound has a synergistic effect with 5-bromo-2'-deoxyuridine. Induced virus has the characteristic density as well as morphology of C-type viruses. Budding viruses are detected on cultured BALB/c cells by electron microscopy 2 to 4 days following culturing in the presence of lipoprotein. Pokeweed mitogen, a compound mitogenic for T- and B-cells was negative when tested for virus induction, both alone and in combination with 5-bromo-2'-deoxyuridine. Dextran sulphate, another B-cell mitogen, was negative for induction as well. However, when, combined with lipopolysaccharide, it enhanced the virus release induced by this mitogen. In contrast, no additive effects were observed either by combining dextran sulphate with other virus amplifying mitogens or by combinations of mitogens which both have virus-inducing ability. This finding is discussed with respect to B-cell differentiation.},
	Author = {Moroni, C. and Schumann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0022-1317},
	Journal = {J Gen Virol},
	Keywords = {Mice, Inbred BALB C;Drug Synergism;Polysaccharides, Bacterial;Animals;Bacterial Proteins;Dextrans;Lipopolysaccharides;15 Retrovirus mechanism;Retroviridae;Mitogens;Cell Line;Escherichia coli;Mice;Virus Replication;Bromodeoxyuridine;24 Pubmed search results 2008;15 ERVs retroelements;Lectins;Lipoproteins},
	Medline = {78131923},
	Month = {3},
	Nlm_Id = {0077340},
	Number = {3},
	Pages = {497-503},
	Pubmed = {204733},
	Title = {Mitogen induction of murine C-type viruses. IV. Effects of lipoprotein E. coli, pokeweed mitogen and dextran sulphate},
	Uuid = {00F878C3-3CF0-485B-942C-F0AA89BF4DBB},
	Volume = {38},
	Year = {1978}}

@article{Moroni:1975,
	Author = {Moroni, C. and Schumann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {15 ERVs retroelements;Lipopolysaccharides;Animals;Mice, Inbred BALB C;RNA-Directed DNA Polymerase;Virus Replication;Lectins;Retroviridae;Mitogens;Concanavalin A;15 Retrovirus mechanism;Polynucleotides;Spleen;Mice;24 Pubmed search results 2008;Templates, Genetic;Cells, Cultured},
	Medline = {75100417},
	Month = {3},
	Nlm_Id = {0410462},
	Number = {5495},
	Pages = {60-1},
	Pubmed = {46591},
	Title = {Lipopolysaccharide induces C-type virus in short term cultures of BALB/c spleen cells},
	Uuid = {AD3D0EED-B499-43AE-9E0E-2AE095DADB50},
	Volume = {254},
	Year = {1975}}

@article{Moroni:1977,
	Author = {Moroni, C. and Schumann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {15 ERVs retroelements;Genes, Viral;Retroviridae;Immunosuppression;15 Retrovirus mechanism;Antibody Formation;Cells, Cultured;Spleen;Antigen-Antibody Reactions;Antibodies, Viral;24 Pubmed search results 2008},
	Medline = {78031209},
	Month = {10},
	Nlm_Id = {0410462},
	Number = {5629},
	Pages = {600-1},
	Pubmed = {199846},
	Title = {Are endogenous C-type viruses involved in the immune system?},
	Uuid = {3C2F634B-E422-4714-BB95-F9419BF28D4D},
	Volume = {269},
	Year = {1977}}

@article{Moroni:1975a,
	Abstract = {In short-term cultures of BALB/c spleen cells, treatment with a combination of 5-bromo-2'-deoxyuridine (BrdU) and either lipopolysaccharide W. Escherichia coli or concanavalin A resulted in release of C-type virus into the medium. Only lipopolysaccharide induced virus release when given alone. This could be potentiated by a combined treatment with BrdU. In contrast, phytohemagglutinin at mitogenic concentration had no effect with or without BrdU, suggesting that inducibility may vary between various mitogen-responsive spleen cell populations. In AKR mice, spontaneous virus release was detectable in nonstimulated spleen cell cultures. This could be potentiated by lipopolysaccharide, whereas no further increase occurred upon additional BrdU treatment. The induced viruses had C-type characteristics in that they contained reverse transcriptase that could be distinguished from cellular enzymes by template-primer preference experiments. Furthermore, the enzyme activities were particle-associated, banding in isopycnic sucrose gradients at 1.15-1.17 g/cm-3. The presence of C-type viruses was confirmed by electron microscopy.},
	Author = {Moroni, C. and Schumann, G. and Robert-Guroff, M. and Suter, E. R. and Martin, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Mice, Inbred BALB C;Polysaccharides, Bacterial;Animals;Gammaretrovirus;Cells, Cultured;DNA;Lipopolysaccharides;Thymidine;15 Retrovirus mechanism;RNA-Directed DNA Polymerase;Retroviridae;Mitogens;Concanavalin A;Mice;Virus Replication;Bromodeoxyuridine;24 Pubmed search results 2008;15 ERVs retroelements;Spleen;Lectins},
	Medline = {75139495},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {2},
	Pages = {535-8},
	Pubmed = {47632},
	Title = {Induction of endogenous murine C-type virus in spleen cell cultures treated with mitogens and 5-bromo-2'-deoxyuridine},
	Uuid = {1BA03DBE-BDB8-11DA-969D-000D9346EC2A},
	Volume = {72},
	Year = {1975}}

@article{Moroni:1980,
	Abstract = {Goat and rat antisera directed against Friend leukemia virus (anti-FLV) were found to be B-lymphocyte mitogens stimulating DNA synthesis in these cells but not in T lymphocytes. Membrane fluorescence microscopy showed that anti-FLV reacts with a subset of B lymphocytes of which the majority express immunoglobulin mu chains. The mitogenic effect was found with all mouse strains tested including 129 and AKR. Absorption experiments with purified viruses indicated that the mitogenic effect is specific for an antigen present in murine leukemia viruses of the FMR subgroup. In absorption experiments with viable cells, the antigen involved in mitogenicity was found to be expressed on Friend erythroleukemia cell lines (4/4) and on myelomas (2/2) but not on normal thymus T lymphomas (0/2) or on rabbit or mink cells infected with BALB/c xenotropic virus. Preincubation of spleen cells with anti-gp70 antiserum inhibited the mitogenic effect of anti-FLV but not of lipopolysaccharide.},
	Author = {Moroni, C. and Forni, L. and Hunsmann, G. and Schumann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {15 ERVs retroelements;Lymphocyte Activation;Antibodies, Viral;B-Lymphocytes;DNA;Mitogens;Antigens, Surface;Friend murine leukemia virus;Thymus Gland;Helper Viruses;15 Retrovirus mechanism;Mice;Spleen;24 Pubmed search results 2008;Animals;Antigen-Antibody Reactions},
	Medline = {80190078},
	Month = {3},
	Nlm_Id = {7505876},
	Number = {3},
	Pages = {1486-90},
	Pubmed = {6966399},
	Title = {Antibody directed against Friend leukemia virus stimulates DNA synthesis in a subpopulation of mouse B lymphocytes},
	Uuid = {5F86876A-7DCD-4D77-9B06-FA22C3D5CA3C},
	Volume = {77},
	Year = {1980}}

@article{Moroni:1976,
	Author = {Moroni, C. and Schumann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {Lysogeny;Polysaccharides, Bacterial;Tuberculin;Animals;Comparative Study;DNA;Lipopolysaccharides;15 Retrovirus mechanism;RNA-Directed DNA Polymerase;B-Lymphocytes;Cross Reactions;Mitogens;Retroviridae;Rauscher Virus;Cell Line;Escherichia coli;Salmonella;Mice;24 Pubmed search results 2008;Virus Replication;Bromodeoxyuridine;15 ERVs retroelements},
	Medline = {76272705},
	Month = {8},
	Nlm_Id = {0110674},
	Number = {1},
	Pages = {17-22},
	Pubmed = {60824},
	Title = {Mitogen induction of murine C-type viruses. II. Effect of B-lymphocyte mitogens},
	Uuid = {F5D84104-8ADE-4D33-A6BA-4C74BB2DC16D},
	Volume = {73},
	Year = {1976}}

@article{Morozov:2002,
	Abstract = {Several techniques enable to inject intracellularly neurons with dyes and to use light and electron microscopy to correlate the physiological data with the morphological properties of the neuron. However, the ultrastructure of the neuron is usually obscured by the injected dye thus notably precluding the analysis of the postsynaptic specialisation and that of the other organelles. To overcome this problem, we have developed a technique based on fluorophore- and ultra small gold-conjugated streptavidins. We report, that this method facilitates the identification of intracellular organelles of the biocytin-filled neuron and of postsynaptic densities. This method is valid for the study of early postnatal neurons that are particularly refractory to this type of analysis. The procedure introduced here consists of the following steps: (1) injection of biocytin into the neuron by a patch-clamp pipette, (2) aldehyde fixation, (3) reaction with a fluorophore-conjugated streptavidin, (4) analysis with a fluorescence microscope, (5) formation of avidin-biotin complexes (ABC), (6) reaction with an ultra small gold-conjugated streptavidin, (7) silver enhancement of gold, (8) postfixation with osmium tetroxide and embedding in resin, (9) ultrathin sectioning and analysis with an electron microscope. Using this method, we show that in early postnatal hippocampal neurons, that have been injected with biocytine, it is possible to determine the morphology of the dendritic and axonal trees (including very thin details such as spines and filopodia) and to identify the localisation of the symmetric and asymmetric synapses on dendrites of the injected neuron.},
	Author = {Morozov, Youri and Khalilov, Ilgam and Ben-Ari, Yehezkel and Represa, Alfonso},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {Fluorescent Dyes;Synaptic Membranes;Lysine;Organelles;Animals;Rats;21 Epilepsy;Neuroanatomy;Axons;Hippocampus;Pyramidal Cells;Organ Culture Techniques;Microscopy, Fluorescence;Tissue Embedding;Dendrites;Animals, Newborn;Neurons;21 Neurophysiology;Streptavidin;Interneurons;24 Pubmed search results 2008;Microscopy, Electron;Immunohistochemistry;Tissue Fixation;Fixatives},
	Medline = {22079920},
	Month = {5},
	Nlm_Id = {7905558},
	Number = {1},
	Organization = {INMED/INSERM U29, 163 Route de Luminy, BP 13, 13009 Marseille, France.},
	Pages = {81-5},
	Pii = {S0165027002000766},
	Pubmed = {12084567},
	Title = {Correlative fluorescence and electron microscopy of biocytin-filled neurons with a preservation of the postsynaptic ultrastructure},
	Uuid = {B443D284-8446-451B-BF37-081407F038A1},
	Volume = {117},
	Year = {2002}}

@article{Morris:2001,
	Abstract = {Though the cytomechanics of spectrin have been explored only for erythrocytes, it is thought that the spectrin skeleton acts universally to support the otherwise mechanically vulnerable cell surface bilayer. Evidence for this role is beginning to accumulate and is reviewed here. Compared to that for erythrocytes, cells whose simplicity facilitates biophysical approaches, the evidence is indirect. One way that membrane skeleton/bilayer interactions have been probed is via the behavior of mechanosusceptible ion channels - channel whose gating is perturbed by abnormally high bilayer tension. These initially unresponsive channels become progressively more mechanoresponsive as stretch and chemical reagents damage the membrane skeleton. The straightforward implication is that the intact membrane skeleton is mechanoprotective. In non-erythroid cells there is continual trafficking of bilayer to and from the plasma membrane. Some of the traffic involves spectrin-lined vacuolar membrane. Several lines of evidence suggest that when neurons elongate and remodel their neurites, membrane skeleton-based mechanoprotection allows the dynamic vacuoles and the plasma membrane to participate in mechanosensitive surface area expansion and retrieval.},
	Author = {Morris, C. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {1425-8153},
	Journal = {Cell Mol Biol Lett},
	Keywords = {Cell Membrane;Neurites;Cytoskeleton;Ion Channels;Human;Spectrin;Not relevant;Growth Cones;11 Glia;Vacuoles;review, tutorial;Electrophysiology;Stress, Mechanical;Animals;Biological Transport;review;Neurons},
	Medline = {21481651},
	Nlm_Id = {9607427},
	Number = {3},
	Organization = {Neurosciences, Ottawa Health Research Institute, Ottawa Hospital, 725 Parkdale Ave, Ottawa, Ontario, Canada K1Y 4K9.},
	Pages = {703-20},
	Pubmed = {11598643},
	Title = {Mechanoprotection of the plasma membrane in neurons and other non-erythroid cells by the spectrin-based membrane skeleton},
	Uuid = {F7B4ADBD-D818-4496-8067-4912B19A659F},
	Volume = {6},
	Year = {2001}}

@article{Morrison:2000,
	Abstract = {The genesis of vertebrate peripheral ganglia poses the problem of how multipotent neural crest stem cells (NCSCs) can sequentially generate neurons and then glia in a local environment containing strong instructive neurogenic factors, such as BMP2. Here we show that Notch ligands, which are normally expressed on differentiating neuroblasts, can inhibit neurogenesis in NCSCs in a manner that is completely dominant to BMP2. Contrary to expectation, Notch activation did not maintain these stem cells in an uncommitted state or promote their self-renewal. Rather, even a transient activation of Notch was sufficient to cause a rapid and irreversible loss of neurogenic capacity accompanied by accelerated glial differentiation. These data suggest that Notch ligands expressed by neuroblasts may act positively to instruct a cell-heritable switch to gliogenesis in neighboring stem cells. 0092-8674 Journal Article},
	Author = {Morrison, S. J. and Perez, S. E. and Qiao, Z. and Verdi, J. M. and Hicks, C. and Weinmaster, G. and Anderson, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Cell},
	Keywords = {Neuregulin-1/metabolism;Cell Differentiation;Human;Signal Transduction;Receptors, Cell Surface/*metabolism;Animals;Neurons/*cytology;Fibroblasts/cytology;Solubility;Cell Line, Transformed;10 Development;Immunoglobulins, Fc/metabolism;Membrane Proteins/*metabolism;Stem Cells/*cytology;Neural Crest/*cytology;Support, Non-U.S. Gov't;Chick Embryo;Support, U.S. Gov't, P.H.S.;Bone Morphogenetic Proteins/metabolism;Mice;Neuroglia/*cytology;F;Recombinant Fusion Proteins/genetics/metabolism},
	Number = {5},
	Organization = {Department of Internal Medicine, University of Michigan, Ann Arbor 48109, USA.},
	Pages = {499-510},
	Pubmed = {10850492},
	Title = {Transient Notch activation initiates an irreversible switch from neurogenesis to gliogenesis by neural crest stem cells},
	Uuid = {305DEE6E-2151-4CE4-B1E4-90F6DE769EDE},
	Volume = {101},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10850492}}

@article{Morrison:2001,
	Abstract = {Recent results suggest that stem cells from one tissue can give rise to cells from developmentally unrelated tissues. These results strongly support the idea that certain progenitors retain much broader developmental potentials than expected, and other progenitors may be able to acquire broader potentials in culture.},
	Author = {Morrison, S. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {Stem Cells;review, tutorial;Cell Lineage;review},
	Medline = {21109566},
	Month = {1},
	Nlm_Id = {9107782},
	Number = {1},
	Organization = {Howard Hughes Medical Institute, Department of Internal Medicine, 3215 CCGC, University of Michigan, Ann Arbor, Michigan 48109-0934, USA.},
	Pages = {R7-9},
	Pii = {S0960982200000336},
	Pubmed = {11166187},
	Title = {Stem cell potential: can anything make anything?},
	Uuid = {BAA1C70C-C26D-11DA-969D-000D9346EC2A},
	Volume = {11},
	Year = {2001},
	url = {papers/Morrison_CurrBiol2001.pdf}}

@article{Morshead:1998,
	Abstract = {The adult mammalian forebrain contains a population of multipotential neural stem cells in the subependyma of the lateral ventricles whose progeny are the constitutively proliferating cells, which divide actively throughout life. The adult mammalian brain is ideal for examining the kinetics of the stem cells due to their strict spatial localization and the limited and discrete type of progeny generated (constitutively proliferating cells). Clonal lineage analyses 6 days after retrovirus infection revealed that under baseline conditions 60\%of the constitutively proliferating cells undergo cell death, 25\%migrate to the olfactory bulb and 15\%remain confined to the lateral ventricle subependyma (where they reside for approximately 15 days). Analysis of single cell clones 31 days after retroviral infection revealed that the stem cell divides asymmetrically to self-renew and give rise to constitutively proliferating cells. Following repopulation of the depleted subependyma the average clone size is 2.8 times larger than control, yet the absolute number of cells migrating to the olfactory bulb is maintained and the stem cell retains its asymmetric mode of division. The number of neural stem cells in the adult forebrain 33 days after repopulation of the subependyma was estimated using bromodeoxyuridine labeling of subepenydmal cells. There were calculated to be 1200-1300 cells between the rostral corpus callosum and rostral anterior commissure; these data support a lineage model similar to those based on stem cell behavior in other tissue types.},
	Author = {Morshead, C. M. and Craig, C. G. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Development},
	Keywords = {Prosencephalon/*cytology;Ependyma/cytology;BB;Animal;Cell Count;02 Adult neurogenesis migration;Retroviridae/physiology;Kinetics;Cell Movement;Male;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;Cell Lineage;Olfactory Bulb/cytology;Stem Cells/*cytology/virology;Mice;Cell Division;Clone Cells;Cell Death},
	Number = {12},
	Organization = {Neurobiology Research Group, Department of Anatomy and Cell Biology, University of Toronto, Toronto, Ontario M5S 1A8, Canada. cinci.morshead\@utoronto.ca},
	Pages = {2251-61.},
	Title = {In vivo clonal analyses reveal the properties of endogenous neural stem cell proliferation in the adult mammalian forebrain},
	Uuid = {6563A2A8-31D6-4AE3-94F8-2B176785FB68},
	Volume = {125},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9584124%20http://www.biologists.com/Development/125/12/dev1261.html}}

@article{Moscona:1992,
	Abstract = {Cells can be persistently infected with human parainfluenza virus type 3 (HPF3) by using a high multiplicity of infection (MOI) (>or = 5 PFU per cell). The persistently infected cells exhibit no cytopathic effects and do not fuse with each other, yet they readily fuse with uninfected cells. We have previously shown that the failure of the persistently infected cells to fuse with each other is due to the lack of a receptor on these cells for the viral hemagglutinin-neuraminidase glycoprotein, and we have established that both fusion and hemagglutinin-neuraminidase proteins are needed for cell fusion mediated by HPF3. We then postulated that the generation of persistent infection and the failure of cells infected with HPF3 at high MOI to form syncytia are both due to the action of viral neuraminidase in the high-MOI inoculum. In this report, we describe experiments to test this hypothesis and further investigate the receptor requirements for HPF3 infection and cell fusion. A normally cytopathic low-MOI HPF3 infection can be converted into a noncytopathic infection by the addition of exogenous neuraminidase, either in the form of a purified enzyme or as UV-inactivated HPF3 virions. Evidence is presented that the receptor requirements for an HPF3 virus particle to infect a cell are different from those for fusion between cells. By treating infected cells in culture with various doses of neuraminidase, we demonstrate that virus spreads from cell to cell in the complete absence of cell-cell fusion. We compare the outcome of HPF3 infection in the presence of excess neuraminidase with that of another paramyxovirus (simian virus 5) and provide evidence that these two viruses differ in their receptor requirements for mediating fusion.},
	Author = {Moscona, A. and Peluso, R. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Neuraminidase;Viral Fusion Proteins;Human;Cells, Cultured;N-Acetylneuraminic Acid;Retroviruses, Simian;Models, Biological;15 Retrovirus mechanism;Cell Fusion;11 Glia;08 Aberrant cell cycle;Support, Non-U.S. Gov't;Sialic Acids;Hemagglutinins, Viral;Membrane Fusion;Support, U.S. Gov't, P.H.S.;Receptors, Virus;Virus Replication;Parainfluenza Virus 3, Human},
	Medline = {93021352},
	Month = {11},
	Nlm_Id = {0113724},
	Number = {11},
	Organization = {Department of Pediatrics and Cell Biology, Mount Sinai School of Medicine, New York, New York 10029-6574.},
	Pages = {6280-7},
	Pubmed = {1328668},
	Title = {Fusion properties of cells infected with human parainfluenza virus type 3: receptor requirements for viral spread and virus-mediated membrane fusion},
	Uuid = {1F24ABE8-37B8-42B6-BAD0-B81906397345},
	Volume = {66},
	Year = {1992},
	url = {papers/Moscona_JVirol1992.pdf}}

@article{Mott:2004,
	Abstract = {Although considered an immunologically privileged site, the central nervous system (CNS) can display significant inflammatory responses, which may play a pathogenic role in a number of neurological diseases. Microglia appear to be particularly important for initiating and sustaining CNS inflammation. These cells exist in a quiescent form in the normal CNS, but acquire macrophage-like properties (including active phagocytosis, upregulation of proteins necessary for antigen presentation, and production of proinflammatory cytokines) after stimulation with inflammatory substances such as lipopolysaccharide (LPS). Recent studies have focused on elucidating the role of neurons in the regulation of microglial inflammatory responses. In the present study, we demonstrate, using neuron-microglial cocultures, that neurons are capable of inhibiting LPS-induced tumor necrosis factor-alpha (TNF-alpha) production by microglia. This inhibition appears to be dependent on secretion of substances at axon terminals, as treatment with the presynaptic calcium channel blocker omega-conotoxin abolishes this inhibitory effect. Moreover, we show that conditioned medium from neuronal cultures similarly inhibits microglial TNF-alpha production, which provides additional evidence that neurons secrete inhibitory substances. We previously demonstrated that the transmembrane protein-tyrosine phosphatase CD45 plays an important role in negatively regulating microglial activation. The recent characterization of CD22 as an endogenous ligand of this receptor led us to investigate whether neurons express this protein. Indeed, we were able to demonstrate CD22 mRNA and protein expression in cultured neurons and mouse brain, using reverse transcriptase-polymerase chain reaction and antibody-based techniques. Furthermore, we show that neurons secrete CD22, which functions as an inhibitor of microglial proinflammatory cytokine production.},
	Author = {Mott, Ryan T. and Ait-Ghezala, Ghania and Town, Terrence and Mori, Takashi and Vendrame, Martina and Zeng, Jin and Ehrhart, Jared and Mullan, Michae and Tan, Jun},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Antigens, CD45;Tumor Necrosis Factor;Presynaptic Terminals;Antigens, Differentiation, B-Lymphocyte;Feedback, Biochemical;Animals;Cells, Cultured;Calcium Channel Blockers;Dose-Response Relationship, Drug;Brain;Microglia;Lipopolysaccharides;Cell Communication;Antigens, CD;Culture Media, Conditioned;RNA, Messenger;Not relevant;11 Glia;Support, Non-U.S. Gov't;Coculture;Neurons;Support, U.S. Gov't, P.H.S.;Mice;Lectins;Ligands;Cytokines},
	Month = {5},
	Nlm_Id = {8806785},
	Number = {4},
	Organization = {Department of Pathology, Duke University Medical Center, Durham, North Carolina, USA.},
	Pages = {369-79},
	Pubmed = {15095367},
	Title = {Neuronal expression of CD22: novel mechanism for inhibiting microglial proinflammatory cytokine production},
	Uuid = {19AACB03-0982-4A67-8FCB-201D55B80A63},
	Volume = {46},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20009}}

@article{Mount:2007,
	Abstract = {Growing evidence implicates microglia in the loss of dopaminergic neurons in Parkinson's disease (PD). However, factors mediating microglial activation in PD are poorly understood. Proinflammatory cytokines, such as interferon-gamma (IFN-gamma), orchestrate the actions of microglia. We report here that PD patients express significantly elevated levels of IFN-gamma in their blood plasma. After this initial finding, we found that IFN-gamma-deficient mice displayed attenuated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced substantia nigra pars compacta dopaminergic cell loss along with reduced loss of striatal tyrosine hydroxylase and dopamine transporter fiber density. MPTP-induced depletion of striatal dopamine and its metabolite DOPAC (3,4-dihydroxyphenylacetic acid), as well as deltaFosB, a marker of postsynaptic dysfunction, were also attenuated in these knock-out mice. Consistent with the role for IFN-gamma in microglial activation, MPTP-induced morphological activation of microglia was abrogated compared with wild-type mice. To examine more mechanistically the role of IFN-gamma in microglial activation, we evaluated the interactions between microglia and dopaminergic neurons in an in vitro mixed microglia/midbrain neuron rotenone-induced death paradigm. In this in vitro paradigm, dopaminergic neurons are selectively damaged by rotenone. Exogenous IFN-gamma ligand alone and without rotenone resulted in dopaminergic cell loss, but only in the presence of microglia. The addition of an IFN-gamma neutralizing antibody attenuated neuronal loss as a result of rotenone treatment. The presence of only wild-type microglia and not those deficient in IFN-gamma receptor elicited significant dopaminergic cell loss when exposed to rotenone. Neurons deficient in IFN-gamma receptor, however, did not display increased resistance to death. Finally, levels of IFN-gamma message increased in microglia in response to rotenone. Together, these data suggest that IFN-gamma participates in death of dopaminergic neurons by regulating microglial activity.},
	Author = {Mount, Matthew P. and Lira, Arman and Grimes, David and Smith, Patrice D. and Faucher, Sylvie and Slack, Ruth and Anisman, Hymie and Hayley, Shawn and Park, David S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Dopamine;Animals;Cells, Cultured;Coculture Techniques;Middle Aged;comparative study;Humans;Interferon Type II;Microglia;Cell Count;21 Neurodegenerative;Parkinson Disease;Mice, Inbred C57BL;11 Glia;research support, non-u.s. gov't;Male;Aged;Mice, Knockout;21 Neurophysiology;Neurons;Adult;Mice;24 Pubmed search results 2008;Cell Death;research support, u.s. gov't, non-p.h.s.},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Ottawa Health Research Institute, Neuroscience Group, Ottawa, Ontario, Canada K1H 8M5.},
	Pages = {3328-37},
	Pii = {27/12/3328},
	Pubmed = {17376993},
	Title = {Involvement of interferon-gamma in microglial-mediated loss of dopaminergic neurons},
	Uuid = {8C2B1810-AC1C-4A65-AD0E-ACDD6FCB0C87},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5321-06.2007}}

@article{Mourzina:2006,
	Abstract = {A spatially resolved delivery of substances integrated with cell culture substrates shows promise for application in pharmacological assays, bioanalytical studies on cell signaling pathways and cell-based biosensors, where control over the extracellular biochemical environment with a cellular resolution is desirable. In this work, we studied a biohybrid system where rat embryonic cortical neuronal networks are reconstructed on microstructured silicon chips and interfaced to microfluidics. The design of cell-cell and cell-medium interactions in confined geometries is presented. We developed an aligned microcontact printing technique (AmicroCP) for poly(lysine)-extracellular matrix proteins on microstructured chips, which allows a high degree of geometrical control over the network architecture and alignment of the neuronal network with the microfluidic features of a substrate. Spatially resolved on-chip delivery of compounds with a cellular resolution is demonstrated by chemical stimulation of patterned rat cortical neurons within a network with a number of solutions of excitatory neurotransmitter glutamate delivered via microfluidics. The combination of the system described with a patch-clamp technique allowed both modulation of the biochemical environment on a cellular level and the monitoring of electrophysiological properties in the reconstructed rat embryonic cortical networks changed by this microenvironment.},
	Author = {Mourzina, Yulia and Kaliaguine, Dmitry and Schulte, Petra and Offenh{\"a}usser, Andreas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:28 -0400},
	Issn = {1873-4324},
	Journal = {Anal Chim Acta},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {0370534},
	Number = {2},
	Organization = {Institute of Bio- and Nanosystems and Center of Nanoelectronic Systems for Information Technology, Research Center J{\"u}lich, 52425 J{\"u}lich, Germany. y.mourzina\@fz-juelich.de},
	Pages = {281-9},
	Pii = {S0003-2670(06)01225-6},
	Pubmed = {17723603},
	Title = {Patterning chemical stimulation of reconstructed neuronal networks},
	Uuid = {3E81D06E-3ACD-43F0-ABC6-477BF0661217},
	Volume = {575},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.aca.2006.06.010}}

@article{Mozdziak:2000,
	Abstract = {5-Bromo-2'-deoxyuridne (BrdU) and 3H-thymidine label mitotically active cells, but they do not adequately mark the progeny of dividing cells for long term study. An alternative method is to label cells using the replication-defective CXL retroviral vector, which carries the lacZ gene encoding beta-galactosidase; however, the ability of the CXL retroviral vector to pulse-label mitotically active cells selectively is not known. Cultures of proliferating muscle cells were simultaneously incubated with the CXL retrovirus and BrdU (10 microM) for 2 hr. After removing the retrovirus containing medium, the cells were maintained for an additional 24 hr in vitro before they were stained to detect beta-galactosidase and BrdU simultaneously. More than 95\%of beta-galactosidase positive cells were also BrdU positive suggesting that the majority of beta-galactosidase positive cells were in the S-phase of the cell cycle at the time of CXL retroviral administration. Therefore, the CXL retroviral vector is an appropriate pulse marker for dividing cells, and it is useful when it is desirable to know the fate of the progeny of a particular cell following a mitotic event.},
	Author = {Mozdziak, P. and Schultz, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {1052-0295},
	Journal = {Biotech Histochem},
	Keywords = {beta-Galactosidase;Animals;Cells, Cultured;Injections, Intramuscular;DNA;Research Support, U.S. Gov't, Non-P.H.S.;Sensitivity and Specificity;15 Retrovirus mechanism;Turkeys;Staining and Labeling;Retroviridae;Get paper from library;Genetic Vectors;Defective Viruses;evaluation studies;Muscle, Skeletal;Lac Operon;Cell Division;24 Pubmed search results 2008;Biological Markers;Bromodeoxyuridine},
	Medline = {20405109},
	Month = {5},
	Nlm_Id = {9107378},
	Number = {3},
	Organization = {Department of Poultry Science, North Carolina State University, Raleigh, North Carolina 27695, USA. pemozdzi\@unity.ncsu.edu},
	Pages = {141-6},
	Pubmed = {10950176},
	Title = {Retroviral labeling is an appropriate marker for dividing cells},
	Uuid = {862545B3-05CC-4950-8017-AA46684F4C09},
	Volume = {75},
	Year = {2000}}

@article{Moller:1996,
	Abstract = {Thrombospondin (TSP) is a multifunctional extracellular matrix protein that plays a role in neuronal migration and axonal outgrowth in the developing central nervous system. In the current study we have examined the localization and regulation of TSP immunoreactivity (TSP-IR) during neuronal regeneration in the axotomized facial motor nucleus using Western blotting and light and electron microscopy. Transection of the facial nerve led to a gradual increase in TSP-IR in the regenerating motoneurons, peaking 4-7 days after injury (DAI). In addition to regenerating neurons, axotomy also caused a rapid upregulation of TSP-IR on activated microglia throughout the facial nucleus, with a maximum of 2-3 DAI, and a second increase at 14-21 DAI on microglial aggregates surrounding degenerating motoneurons and in neuronophagic microglia. In summary, injury leads to the induction of thrombospondin on axotomized neurons and activated microglia, peaking at the times of maximal posttraumatic microglial proliferation and during neuronal phagocytosis. Since thrombospondin is a multimodal extracellular matrix protein with a variety of cell attachment sites, thrombospondin might serve to link microglia and injured neurons, followed by microglial proliferation and removal of the neuronal debris.},
	Author = {M{\"o}ller, J. C. and Klein, M. A. and Haas, S. and Jones, L. L. and Kreutzberg, G. W. and Raivich, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Membrane Glycoproteins;Thrombospondins;Motor Neurons;Facial Nerve;Immunohistochemistry;Microscopy, Electron;Regeneration;Time Factors;Not relevant;11 Glia;Mice;Animals;Mice, Inbred Strains},
	Medline = {96372786},
	Month = {6},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Neuromorphology, Max-Planck Institute for Psychiatry, Martinsried, Germany.},
	Pages = {121-32},
	Pii = {10.1002/(SICI)1098-1136(199606)17:2<121::AID-GLIA4>3.0.CO;2-5},
	Pubmed = {8776579},
	Title = {Regulation of thrombospondin in the regenerating mouse facial motor nucleus},
	Uuid = {4EE7A346-AC66-455B-978A-A5088032D1CC},
	Volume = {17},
	Year = {1996}}

@article{Mueller:2003,
	Abstract = {Whereas local microglial cells of the CNS rapidly respond to injury, little is known about the functional role of resident macrophages of the peripheral nervous system in nerve pathology. Using bone marrow chimeric rats, we recently identified individual resident endoneurial macrophages that rapidly became activated after nerve injury. However, the extent of local macrophage activation and its quantitative contribution to the total macrophage response is unknown. We now have created chimeric mice by transplanting bone marrow from green fluorescent protein (GFP)-transgenic mice into irradiated wild-type mice, allowing easy differentiation and quantification of hematogenous and resident endoneurial macrophages. After sciatic nerve crush injury, both GFP(-) and GFP(+) resident macrophages, the latter having undergone physiological turnover from the blood before injury, rapidly underwent morphological alterations and increased in number. Proliferating GFP(-) and GFP(+) resident macrophages were abundant and peaked 3 days after injury. A major lesion-induced influx of hematogenous macrophages with a disproportionate increase of GFP(+) macrophages was not observed until Day 4. Throughout all time points examined, GFP(-) resident macrophages were strikingly frequent, reaching maximum numbers 9.5-fold above baseline. There was also a notable proportion of GFP(-) resident endoneurial macrophages phagocytosing myelin and expressing major histocompatibility complex class II. Our results demonstrate for the first time that the rapid response of resident endoneurial macrophages to nerve injury is quantitatively important and that local macrophages contribute significantly to the total endoneurial macrophage pool during Wallerian degeneration.},
	Author = {Mueller, Marcus and Leonhard, Christine and Wacker, Karin and Ringelstein, E. Bernd and Okabe, Masaru and Hickey, William F. and Kiefer, Reinhard},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0023-6837},
	Journal = {Lab Invest},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Macrophages;Bone Marrow Transplantation;Apoptosis;Indicators and Reagents;Mice, Transgenic;Sciatic Nerve;Mice, Inbred C57BL;11 Glia;Cell Count;Green Fluorescent Proteins;Radiation Chimera;Wallerian Degeneration;Mice;Nerve Crush;Luminescent Proteins;Peripheral Nerves},
	Medline = {22482723},
	Month = {2},
	Nlm_Id = {0376617},
	Number = {2},
	Organization = {Department of Neurology, Universit{\"a}tsklinikum M{\"u}nster, M{\"u}nster, Germany.},
	Pages = {175-85},
	Pubmed = {12594233},
	Title = {Macrophage response to peripheral nerve injury: the quantitative contribution of resident and hematogenous macrophages},
	Uuid = {76AC1DD9-052C-4BD6-B7A5-546BD0F54363},
	Volume = {83},
	Year = {2003}}

@article{Mujtaba:1998,
	Abstract = {We have previously shown that interferon-tau (IFN-tau) pretreatment inhibits the development of both acute and chronic mouse experimental allergic encephalomyelitis (EAE), an animal model for the human demyelinating disease multiple sclerosis (MS). IFN-tau is a type I IFN that has pregnancy recognition hormone activity in ruminants. Here we show that IFN-tau induced remission in SJL/J mice that had ongoing chronic active EAE disease and protected mice against secondary relapses. IFN-tau treatment reversed lymphocyte infiltration and microglial activation in the central nervous system. Mice that were treated with IFN-tau had lower levels of anti-MBP antibodies than untreated mice in both chronic and acute forms of EAE. MBP induced proliferation in B cells from EAE mice, but treatment with IFN-tau either in vivo or in vitro blocked activation. Furthermore, IFN-tau inhibited MBP activation of T cells from EAE mice. Thus, IFN-tau inhibits the humoral arm as well as the cellular arm of the autoimmune disease EAE. The data presented here show that IFN-tau inhibits both B cell and T cell responses in EAE as well as active, chronic EAE, and this may help explain the effectiveness of type I IFNs in treatment of MS.},
	Author = {Mujtaba, M. G. and Streit, W. J. and Johnson, H. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0008-8749},
	Journal = {Cell Immunol},
	Keywords = {T-Lymphocytes;Animals;Encephalomyelitis, Experimental Autoimmune;Paralysis;Interferon Type I;Myelin Basic Proteins;Microglia;Antibody Formation;Sheep;B-Lymphocytes;Not relevant;11 Glia;Antibodies;Cell Line;Cattle;Immunity, Cellular;Pregnancy Proteins;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Recurrence},
	Medline = {98330574},
	Month = {6},
	Nlm_Id = {1246405},
	Number = {2},
	Organization = {Department of Microbiology, University of Florida, Gainesville 32611, USA.},
	Pages = {94-102},
	Pii = {S0008874998913004},
	Pubmed = {9665751},
	Title = {IFN-tau suppresses both the autoreactive humoral and cellular immune responses and induces stable remission in mice with chronic experimental allergic encephalomyelitis},
	Uuid = {5C78D478-4FAD-4CC4-AFAA-14257F725385},
	Volume = {186},
	Year = {1998}}

@article{Mullen:1992,
	Abstract = {A battery of monoclonal antibodies (mAbs) against brain cell nuclei has been generated by repeated immunizations. One of these, mAb A60, recognizes a vertebrate nervous system- and neuron-specific nuclear protein that we have named NeuN (Neuronal Nuclei). The expression of NeuN is observed in most neuronal cell types throughout the nervous system of adult mice. However, some major cell types appear devoid of immunoreactivity including cerebellar Purkinje cells, olfactory bulb mitral cells, and retinal photoreceptor cells. NeuN can also be detected in neurons in primary cerebellar cultures and in retinoic acid-stimulated P19 embryonal carcinoma cells. Immunohistochemically detectable NeuN protein first appears at developmental timepoints which correspond with the withdrawal of the neuron from the cell cycle and/or with the initiation of terminal differentiation of the neuron. NeuN is a soluble nuclear protein, appears as 3 bands (46-48 x 10(3) M(r)) on immunoblots, and binds to DNA in vitro. The mAb crossreacts immunohistochemically with nervous tissue from rats, chicks, humans, and salamanders. This mAb and the protein recognized by it serve as an excellent marker for neurons in the central and peripheral nervous systems in both the embryo and adult, and the protein may be important in the determination of neuronal phenotype.},
	Author = {Mullen, R. J. and Buck, C. R. and Smith, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {10 Development;Animals;Nervous System;Brain;23 Technique;Immunoblotting;01 Adult neurogenesis general;Research Support, U.S. Gov't, P.H.S.;Brain Chemistry;Antibodies, Monoclonal;Neurons;Cell Nucleus;Nuclear Proteins;24 Pubmed search results 2008;Immunohistochemistry;Nerve Tissue Proteins;Biological Markers;Vertebrates},
	Medline = {93130769},
	Month = {9},
	Nlm_Id = {8701744},
	Number = {1},
	Organization = {Department of Anatomy, University of Utah School of Medicine, Salt Lake City 84132.},
	Pages = {201-11},
	Pubmed = {1483388},
	Title = {NeuN, a neuronal specific nuclear protein in vertebrates},
	Uuid = {B1852397-B1C4-41B1-8224-E56CDB663096},
	Volume = {116},
	Year = {1992}}

@article{Muller:1977,
	Abstract = {The rational design of antitumor and antiviral agents must ultimately take advantage of biochemical differences between normal host cells and transformed cells. The initial experiments must be performed with subcellular or cellular model systems. For the studies with arabinosyl nucleosides we have chosen those enzyme systems, synthesizing DNA and RNA; being precursor analogues, the different arabinosyl nucleosides have been added in the triphosphate state to the different DNA- and RNA polymerase assays. 1-beta-D-Arabinofuranosylcytosine-5'-triphosphate has been found to inhibit the RNA-dependent DNA polymerases (isolated from oncogenic RNA viruses) 200-fold more sensitively than viral and cellular DNA-dependent DNA polymerases. Recent results, showing that RNA-leukemia-virus-related sequences are present in DNA of some human leukemia patients might support the assumption that the efficacy of this antimetabolite in the treatment of acute leukemia is due to its, at least relative selective inhibitory activity on reverse transcriptase. 9-beta-D-Arabinofuranosyladenine-5'-triphosphate is a strong inhibitor of cellular DNA polymerases with the cytological consequence of an inhibition of cell proliferation. The clinical benefit of the compound in treatment of tumors is dependent on their levels of adenosine deaminase. The triphosphate of this compound is a 100-fold more sensitive inhibitor of the herpesvirus DNA polymerase compared to the cellular replicative DNA polymerase. In addition the analogue, incorporated into herpesvirus DNA, acts as chain terminator. These effects are the biochemical basis for the highly selective antiherpesvirus activity of this antimetabolite. The anomer 9-alpha-D-arabinofuranosyladenine-5'-triphosphate only inhibits cellular replicative DNA polymerase and has no effect on herpesvirus DNA polymerase. Consequently this agent acts only cytostatically and not antivirally. Concerning 1-beta-D-arabinofuranosyluracil and 1-beta-D-arabinofuranosylthymine no pronounced antitumor or antiviral effect is known. 0368-2781 Journal Article},
	Author = {Muller, W. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Jpn J Antibiot},
	Keywords = {Nucleosides/isolation &purification/*pharmacology;Rabbits;Animals;Cells, Cultured;Vidarabine/pharmacology/therapeutic use;Herpesviridae;DNA-Directed DNA Polymerase/antagonists &inhibitors;Virus Diseases/drug therapy;Models, Biological;DNA-Directed RNA Polymerases/antagonists &inhibitors;Arabinose/pharmacology/therapeutic use;Cytarabine/pharmacology/therapeutic use;08 Aberrant cell cycle;Chemistry;*Antineoplastic Agents;Research Design;*Antiviral Agents;Mice;EE abstr},
	Pages = {104-20},
	Pubmed = {612702},
	Title = {Rational design of arabinosyl nucleosides as antitumor and antiviral agents},
	Uuid = {5CBB1B60-4ECD-4CF8-94D6-7538D3C10549},
	Volume = {30 Suppl},
	Year = {1977},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=612702}}

@article{Muller:1996,
	Abstract = {Hippocampal organotypic slice cultures maintained 10-20 days in vitro express a high level of the polysialylated embryonic form of neural cell adhesion molecule (NCAM) (PSA-NCAM). Treatment of the cultures with endoneuraminidase-N selectively removed polysialic acid (PSA) from NCAM and completely prevented induction of long-term potentiation (LTP) and long-term depression (LTD) without affecting cellular or synaptic parameters. Similarly, slices prepared from transgenic mice lacking the NCAM gene exhibited a decaying LTP. No inhibition of N-methyl-D-aspartic acid receptor-dependent synaptic responses was detected. Washout of the enzyme resulted in reexpression of PSA immunoreactivity which correlated with a complete recovery of LTP and LTD. This reexpression was blocked by TTX and low calcium and enhanced by bicuculline. Taken together, these results indicate that neuronal activity regulates the expression of PSA-NCAM at the synapse and that this expression is required for the induction of synaptic plasticity.},
	Author = {Muller, D. and Wang, C. and Skibo, G. and Toni, N. and Cremer, H. and Calaora, V. and Rougon, G. and Kiss, J. Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Long-Term Potentiation;Neural Cell Adhesion Molecules;Electrophysiology;Microscopy, Immunoelectron;Synapses;Animals;Rats;Neuronal Plasticity;N-Acetylneuraminic Acid;Mice, Mutant Strains;Glycoside Hydrolases;Rats, Sprague-Dawley;Hippocampus;Organ Culture Techniques;Animals, Newborn;Mice;Immunohistochemistry;Receptors, N-Methyl-D-Aspartate;24 Pubmed search results 2008;Neural Inhibition;Research Support, Non-U.S. Gov't},
	Medline = {96413551},
	Month = {9},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Morphology Centre M{\'e}dical Universitaire, Geneva, Switzerland.},
	Pages = {413-22},
	Pii = {S0896-6273(00)80174-9},
	Pubmed = {8816705},
	Title = {PSA-NCAM is required for activity-induced synaptic plasticity},
	Uuid = {DDCCF3A8-4A20-44A3-9C6B-8C1657AD3728},
	Volume = {17},
	Year = {1996}}

@article{Munirathinam:1997,
	Abstract = {Neuronal regeneration following early postnatal olfactory tract transection (OTS) was investigated in newborn Wistar rats. Olfactory tract lesioned rats were sacrificed at different time periods and the brains processed for Nissl staining. This was used to study the neural cell architecture; fiber tracts (myelinated fibers) were examined with Luxol Fast Blue staining. In addition, a neuronal tracing technique (i.e., retrograde labeling) was employed to study the reestablishment of connections with the target sites following transection of the tract. Degeneration of the olfactory tract was evident at the 7th day following lesion. Regeneration of the tract was not apparent even up to 60 days following transection. However, by 240 days, the olfactory tract had regenerated and the tract fibers had reestablished connection. This was confirmed by retrograde labeling of mitral cells of the olfactory bulb with Fast Blue (FB) injected into the piriform cortex, the target site of these neurons. In this study, we show that mammalian olfactory tract can regenerate spontaneously if the olfactory tract is lesioned neonatally. The results suggest that the olfactory tract is an excellent model to investigate some issues related to central nervous system regeneration.},
	Author = {Munirathinam, S. and Rao, M. S. and Mohan, Y. R. and Raju, T. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Dyes;Indoles;Olfactory Pathways;Nerve Degeneration;Nerve Regeneration;Rats;Female;Time Factors;Rats, Wistar;Fluorescent Dyes;Denervation;Animals, Newborn;Male;Animals;24 Pubmed search results 2008;Central Nervous System Diseases;Amidines},
	Medline = {97271217},
	Month = {3},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bangalore, India.},
	Pages = {174-82},
	Pii = {S0014488697964190},
	Pubmed = {9126168},
	Title = {Regeneration of the olfactory tract following neonatal lesion in rats},
	Uuid = {B1DE1A5A-68E0-4516-9806-8A5B6B75EE57},
	Volume = {144},
	Year = {1997}}

@article{Munoz-Elias:2004,
	Abstract = {We recently differentiated adult rat and human bone marrow stromal cells (MSCs) into presumptive neurons in cell culture. To determine whether the MSCs assume neuronal functions in vivo, we now characterize for the first time engraftment, migration, phenotypic expression, and long-term survival after infusion into embryonic day 15.5 (E15.5) rat ventricles in utero. By E17.5, donor cells formed discrete spheres in periventricular germinal zones, suggesting preferential sites of engraftment. The cells expressed progenitor vimentin and nestin but not mature neuronal markers. By E19.5, a subset assumed elongated migratory morphologies apposed to radial nestin-positive fibers running through the cortical white matter and plate, suggesting migration along radial glial processes. Cells remaining in germinal zones extended long, vimentin-positive fibers into the parenchyma, suggesting that the MSCs generated both migratory neurons and guiding radial glia. Consistent with this suggestion, >50\%of cultured mouse MSCs expressed the neuroprecursor/radial glial protein RC2. From E19.5 to postnatal day 3, MSCs populated distant areas, including the neocortices, hippocampi, rostral migratory stream, and olfactory bulbs. Whereas donor cells confined to the subventricular zone continued to express nestin, cells in the neocortex and midbrain expressed mature neuronal markers. The donor cells survived for at least 2 months postnatally, the longest time examined. Confocal analysis revealed survival of thousands of cells per cubic millimeter in the frontal cortex and olfactory bulb at 1 month. In the cortex and bulb, 98.6 and 77.3\%were NeuN (neuronal-specific nuclear protein) positive, respectively. Our observations suggest that transplanted adult MSCs differentiate in a regionally and temporally specific manner.},
	Author = {Mu\~{n}oz-Elias, Guillermo and Marcus, Akiva J. and Coyne, Thomas M. and Woodbury, Dale and Black, Ira B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Cell Differentiation;Animals;Cells, Cultured;Frontal Lobe;Rats;Neuronal Plasticity;Phenotype;Brain;Antigens, Differentiation;Female;Vimentin;Rats, Sprague-Dawley;Cell Movement;08 Aberrant cell cycle;Time Factors;Olfactory Bulb;Research Support, U.S. Gov't, P.H.S.;Bone Marrow Cells;Neurons;Intermediate Filament Proteins;Neuroglia;Graft Survival;Nerve Tissue Proteins;Stromal Cells;Research Support, Non-U.S. Gov't},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {19},
	Organization = {Department of Neuroscience and Cell Biology and the Stem Cell Research Center, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5635, USA.},
	Pages = {4585-95},
	Pii = {24/19/4585},
	Pubmed = {15140930},
	Title = {Adult bone marrow stromal cells in the embryonic brain: engraftment, migration, differentiation, and long-term survival},
	Uuid = {37E71A42-D3B2-11D9-A0E9-000D9346EC2A},
	Volume = {24},
	Year = {2004},
	url = {papers/Munoz-Elias_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5060-03.2004}}

@article{Munoz-Elias:2003,
	Abstract = {To define relationships among marrow stromal cells (MSCs), multipotential progenitors, committed precursors, and derived neurons, we examined differentiation, mitosis, and apoptosis in vitro. Neural induction medium morphologically converted over 70\%of MSCs to typical neurons, which expressed tau, neuronal nuclear antigen, neuron-specific enolase, and TUC-4 within 24 hours. A subset decreased fibronectin expression, consistent with mesenchymal to neuroectodermal conversion. More than 35\%of differentiating neurons incorporated bromodeoxyuridine (BrdU) and divided, increasing cell number by 60\%, while another subpopulation differentiated without incorporating BrdU or dividing. Inhibition of mitosis and DNA synthesis did not prevent neural differentiation, with 70\%of blocked cells expressing tau and displaying neuronal morphologies. By deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay, less than 1\%of cells underwent apoptosis at 36 and 72 hours, suggesting differentiation without cell-selective mechanisms. Apparently, MSCs may directly differentiate into neurons without passing through a mitotic stage, suggesting that distinctions among stem cells, progenitors, and precursors are more flexible than formerly recognized.},
	Author = {Mu\~{n}oz-El{\'\i}as, Guillermo and Woodbury, Dale and Black, Ira B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {Cell Differentiation;Animals;Rats;Phenotype;DNA;Apoptosis;Female;Mitosis;Rats, Sprague-Dawley;08 Aberrant cell cycle;Time Factors;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Fibronectins;In Situ Nick-End Labeling;Neurons;Immunohistochemistry;Bromodeoxyuridine;Stromal Cells;Biotin;Research Support, Non-U.S. Gov't},
	Medline = {22717324},
	Nlm_Id = {9304532},
	Number = {4},
	Organization = {University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, Piscataway 08854, USA.},
	Pages = {437-48},
	Pubmed = {12832697},
	Title = {Marrow stromal cells, mitosis, and neuronal differentiation: stem cell and precursor functions},
	Uuid = {D7682BB3-8686-4877-8E42-B109E2D96B1B},
	Volume = {21},
	Year = {2003},
	url = {papers/Munoz-Elías_StemCells2003.pdf}}

@article{Muotri:2005,
	Abstract = {Revealing the mechanisms for neuronal somatic diversification remains a central challenge for understanding individual differences in brain organization and function. Here we show that an engineered human LINE-1 (for long interspersed nuclear element-1; also known as L1) element can retrotranspose in neuronal precursors derived from rat hippocampus neural stem cells. The resulting retrotransposition events can alter the expression of neuronal genes, which, in turn, can influence neuronal cell fate in vitro. We further show that retrotransposition of a human L1 in transgenic mice results in neuronal somatic mosaicism. The molecular mechanism of action is probably mediated through Sox2, because a decrease in Sox2 expression during the early stages of neuronal differentiation is correlated with increases in both L1 transcription and retrotransposition. Our data therefore indicate that neuronal genomes might not be static, but some might be mosaic because of de novo L1 retrotransposition events.},
	Author = {Muotri, Alysson R. and Chu, Vi T. and Marchetto, Maria C. N. and Deng, Wei and Moran, John V. and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Cell Differentiation;Research Support, N.I.H., Extramural;24 Pubmed search results 2008;Green Fluorescent Proteins;Mosaicism;Animals;Cells, Cultured;Brain;Transcription, Genetic;Research Support, U.S. Gov't, P.H.S.;15 Retrovirus mechanism;Promoter Regions (Genetics);Transcription Factors;Molecular Sequence Data;RNA, Messenger;15 ERVs retroelements;DNA-Binding Proteins;Retroelements;Gene Expression Regulation;Cell Lineage;Rats;Long Interspersed Nucleotide Elements;HMGB Proteins;Recombination, Genetic;Mice;Stem Cells;Research Support, Non-U.S. Gov't;Neurons;Humans;Mice, Transgenic;Nerve Tissue Proteins},
	Month = {6},
	Nlm_Id = {0410462},
	Number = {7044},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.},
	Pages = {903-10},
	Pii = {nature03663},
	Pubmed = {15959507},
	Title = {Somatic mosaicism in neuronal precursor cells mediated by L1 retrotransposition},
	Uuid = {5AC0AB3A-6C70-442F-9B17-4C32198FCFAA},
	Volume = {435},
	Year = {2005},
	url = {papers/Muotri_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03663}}

@article{Muraille:2001,
	Abstract = {The germinative ventricular zone of embryonic brain contains neural lineage progenitor cells that give rise to neurons, astrocytes and oligodendrocytes. The ability to generate neurons persists at adulthood in restricted brain areas. During development, many growth factors exert their effects by interacting with tyrosine kinase receptors and activate the phosphatidylinositol 3-kinase and the Ras/MAP kinase pathways. By its ability to modulate these pathways, the recently identified Src homology 2 domain-containing inositol polyphosphate 5- phosphatase 2, SHIP2, has the potential to regulate neuronal development. Using in situ hybridization technique with multiple synthetic oligonucleotides, we demonstrated that SHIP2 mRNA was highly expressed in the ventricular zone at early embryonic stages and subventricular zones at latter stages of brain and spinal cord and in the sympathetic chain. No significant expression was seen in differentiated fields. This restricted expression was maintained from embryonic day 11.5 to birth. In the periphery, large expression was detected in muscle and kidney and moderate expression in thyroid, pituitary gland, digestive system and bone. In the adult brain, SHIP2 was mainly restricted in structures containing neural stem cells such as the anterior subventricular zone, the rostral migratory stream and the olfactory tubercle. SHIP2 was also detected in the choroid plexuses and the granular layer of the cerebellum. The specificity of SHIP2 expression in neural stem cells was further demonstrated by (i) the dramatic increase in SHIP2 mRNA signal in neural cell adhesion molecule (N-CAM)-deficient mice, which present an accumulation of progenitor cells in the anterior subventricular zone and the rostral migratory stream, (ii) the abundant expression of 160-kDa SHIP2 by western blotting in proliferating neurospheres in culture and its downregulation in non-proliferating differentiated neurospheres.In conclusion, the close correlation between the pattern of SHIP2 expression in the brain and the proliferative and early differentiative events suggests that the phosphatase SHIP2 may have important roles in neural development. Using Smart Source Parsing},
	Author = {Muraille, E. and Dassesse, D. and Vanderwinden, J. M. and Cremer, H. and Rogister, B. and Erneux, C. and Schiffmann, S. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Neuroscience},
	Keywords = {C pdf;04 Adult neurogenesis factors},
	Number = {4},
	Pages = {1019-30},
	Title = {The SH2 domain-containing 5-phosphatase SHIP2 is expressed in the germinal layers of embryo and adult mouse brain: increased expression in N-CAM-deficient mice},
	Uuid = {188E89B6-95A6-4CA4-B27E-7A3FCC1A15EF},
	Volume = {105},
	Year = {2001},
	url = {papers/Muraille_Neuroscience2001}}

@article{Murase:2002,
	Abstract = {Macrophage colony stimulating factor (M-CSF) is known to be the most effective growth factor for macrophage and microglial proliferation. In the brain tissue system, M-CSF is mainly produced in astrocytes and microglia, but is not known to occur in neurons. In the present paper, we examined the distribution of neurons expressing M-CSF in the mouse brain by immunohistochemistry and in situ hybridization. We observed M-CSF immunoreactivity in both the cerebellum and the olfactory bulb. These positive cells were found to be Purkinje cells in the cerebellum, and mitral cells in the olfactory bulb. M-CSF mRNA expression was also confirmed to occur in these cells. Purkinje cells of reeler and weaver mutants showed M-CSF expression as seen in wild-type mice; however, those in the staggerer mutant did not. This expression in wild-type mice first appeared at postnatal day 7 and continued stably thereafter. When Purkinje cells were deprived of their climbing fibre innervation by inferior cerebellar pedunculotomy or by transplantation of cerebellar anlagen into the anterior eye chamber, the expression of M-CSF remained unchanged. These data indicate that expression of M-CSF in Purkinje cells is controlled by an intrinsic mechanism and could, therefore, be a new marker of postnatal development in rodent cerebella. The absence of M-CSF expression in the staggerer mutant is possibly due to developmental arrest in the early postnatal period.},
	Author = {Murase, Shin-ichi and Hayashi, Yokichi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0018-2214},
	Journal = {Histochem J},
	Keywords = {Purkinje Cells;Animals;Mutation;RNA, Messenger;11 Glia;Mice, Neurologic Mutants;Male;Embryo;Olfactory Bulb;In Situ Hybridization;Fetal Tissue Transplantation;Blotting, Western;Neurons;Macrophage Colony-Stimulating Factor;Mice;Cerebellum;24 Pubmed search results 2008;Immunohistochemistry;Nerve Fibers},
	Medline = {22251859},
	Nlm_Id = {0163161},
	Number = {1-2},
	Organization = {Department of Anatomy, Keio University School of Medicine, Tokyo, Japan.},
	Pages = {85-95},
	Pubmed = {12365804},
	Title = {Neuronal expression of macrophage colony stimulating factor in Purkinje cells and olfactory mitral cells of wild-type and cerebellar-mutant mice},
	Uuid = {0526A742-563B-4381-926A-56CFD8B9C665},
	Volume = {34},
	Year = {2002}}

@article{Murray:2004,
	Abstract = {I discuss advances in the cell cycle in the 21 years since cyclin was discovered. The surprising redundancy amongst the classical cyclins (A, B, and E) and cyclin-dependent kinases (Cdk1 and Cdk2) show that the important differences between these proteins are when and where they are expressed rather than the proteins they phosphorylate. Although the broad principles of the cell cycle oscillator are widely accepted, we are surprisingly ignorant of its detailed mechanism. This is especially true of the anaphase promoting complex (APC), the machine that triggers chromosome segregation and the exit of mitosis by targeting securin and mitotic cyclins for destruction. I discuss how a cyclin/Cdk-based engine could have evolved to assume control of the cell cycle from other, older protein kinases. 0092-8674 Journal Article Review Review, Academic},
	Author = {Murray, A. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Cell},
	Keywords = {Models, Biological;EE pdf;*Cell Cycle;Mitotic Spindle Apparatus/physiology;Human;08 Aberrant cell cycle;Time Factors;Support, U.S. Gov't, P.H.S.;Mitosis;Animals;Phosphorylation;Cyclins/*physiology},
	Number = {2},
	Organization = {Department of Molecular and Cellular Biology, Biological Laboratories, Harvard University, Cambridge, MA 02138, USA. amurray\@mcb.harvard.edu},
	Pages = {221-34},
	Title = {Recycling the cell cycle: cyclins revisited},
	Uuid = {1452B089-5B68-482E-B1B9-42C8AE09B4C0},
	Volume = {116},
	Year = {2004},
	url = {papers/Murray_Cell2004.pdf}}

@article{Murrell:1999,
	Abstract = {The site for interactions between the nervous system and much of the chemical world is in the olfactory sensory neuron (OSN). Odorant receptor proteins (ORPs) are postulated to mediate these interactions. However, the function of most ORPs has not been demonstrated in vivo or in vitro. For this and other reasons, we created a conditionally immortalized cell line derived from the OSN lineage, which we term odora. Odora cells, under control conditions, are phenotypically similar to the OSN progenitor, the globose basal cell. After differentiation, odora cells more closely resemble OSNs. Differentiated odora cells express neuronal and olfactory markers, including components of the olfactory signal transduction pathway. Unlike other cell lines, they also efficiently target exogenous ORPs to their surface. Strikingly, differentiated odora cells expressing ORPs respond to odorants, as measured by an influx of calcium. In particular, cells expressing one ORP demonstrate a specific response to only one type of tested odorant. Odora cells, therefore, are ideal models to examine the genesis and function of olfactory sensory neurons.},
	Author = {Murrell, J. R. and Hunter, D. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {J Neurosci},
	Keywords = {13 Olfactory bulb anatomy;I;Cell Differentiation;Reverse Transcriptase Polymerase Chain Reaction;Rats;Cell Culture/methods;Cell Line;Signal Transduction;*Odors;Animal;Olfactory Mucosa/*cytology;Animals, Newborn;Support, Non-U.S. Gov't;Olfactory Receptor Neurons/*cytology/*physiology;Receptors, Odorant/*genetics/*physiology;Nerve Tissue Proteins/analysis;Ion Channels/*genetics},
	Number = {19},
	Organization = {Program in Cell, Molecular, and Developmental Biology, Department of Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.},
	Pages = {8260-70.},
	Title = {An olfactory sensory neuron line, odora, properly targets olfactory proteins and responds to odorants},
	Uuid = {583F42E2-B6C1-4D75-BBCB-7B347B1B361F},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10493727%20http://www.jneurosci.org/cgi/content/full/19/19/8260%20http://www.jneurosci.org/cgi/content/abstract/19/19/8260}}

@article{Muller:2007,
	Abstract = {The chemokine receptor CXCR3 promotes the trafficking of activated T and NK cells in response to three ligands, CXCL9, CXCL10, and CXCL11. Although these chemokines are produced in the CNS in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), their role in the pathogenesis of CNS autoimmunity is unresolved. We examined the function of CXCR3 signaling in EAE using mice that were deficient for CXCR3 (CXCR3(-/-)). The time to onset and peak disease severity were similar for CXCR3(-/-) and wild-type (WT) animals; however, CXCR3(-/-) mice had more severe chronic disease with increased demyelination and axonal damage. The inflammatory lesions in WT mice consisted of well-demarcated perivascular mononuclear cell infiltrates, mainly in the spinal cord and cerebellum. In CXCR3(-/-) mice, these lesions were more widespread throughout the CNS and were diffused and poorly organized, with T cells and highly activated microglia/macrophages scattered throughout the white matter. Although the number of CD4(+) and CD8(+) T cells infiltrating the CNS were similar in CXCR3(-/-) and WT mice, Foxp3(+) regulatory T cells were significantly reduced in number and dispersed in CXCR3(-/-) mice. The expression of various chemokine and cytokine genes in the CNS was similar in CXCR3(-/-) and WT mice. The genes for the CXCR3 ligands were expressed predominantly in and/or immediately surrounding the mononuclear cell infiltrates. We conclude that in EAE, CXCR3 signaling constrains T cells to the perivascular space in the CNS and augments regulatory T cell recruitment and effector T cell interaction, thus limiting autoimmune-mediated tissue damage.},
	Author = {M{\"u}ller, Marcus and Carter, Sally L. and Hofer, Markus J. and Manders, Peter and Getts, Daniel R. and Getts, Meghan T. and Dreykluft, Angela and Lu, Bao and Gerard, Craig and King, Nicholas J. C. and Campbell, Iain L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {research support, non-u.s. gov't;14 Immune;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {2985117R},
	Number = {5},
	Organization = {School of Molecular and Microbial Biosciences, School of Medical Sciences, University of Sydney, Sydney, Australia.},
	Pages = {2774-86},
	Pii = {179/5/2774},
	Pubmed = {17709491},
	Title = {CXCR3 signaling reduces the severity of experimental autoimmune encephalomyelitis by controlling the parenchymal distribution of effector and regulatory T cells in the central nervous system},
	Uuid = {FBD7AAD8-4CA5-4DD8-8CDB-3313BCE7D3C6},
	Volume = {179},
	Year = {2007}}

@article{Munch:2003,
	Abstract = {Activation of glial cells has been proposed to contribute to neuronal dysfunction and neuronal cell death in Alzheimer's disease. In this study, we attempt to determine some of the effects of secreted factors from activated murine N-11 microglia on viability and morphology of neurons using the differentiated neuroblastoma cell line Neuro2a. Microglia were activated either by lipopolysaccharide (LPS), bacterial cell wall proteoglycans, or advanced glycation endproducts (AGEs), protein-bound sugar oxidation products. At high LPS or AGE concentrations, conditioned medium from microglia caused neuronal cell death in a dose-dependent manner. At sublethal LPS or AGE concentrations, conditioned media inhibited retinoic acid-induced neurite outgrowth and stimulated retraction of already extended neurites. Among the many possible secreted factors, the contribution of NO or NO metabolites in the cytotoxicity of conditioned medium was investigated. Cell death and changes in neurite morphology were partly reduced when NO production was inhibited by nitric oxide synthase inhibitors. The results suggest that even in the absence of significant cell death, inflammatory processes, which are partly transmitted via NO metabolites, may affect intrinsic functions of neurons such as neurite extension that are essential components of neuronal morphology and thus may contribute to degenerative changes in Alzheimer's disease.},
	Author = {M{\"u}nch, Gerald and Gasic-Milenkovic, Jovana and Dukic-Stefanovic, Sladjana and Kuhla, Bj{\"o}rn and Heinrich, Katrin and Riederer, Peter and Huttunen, Henri J. and Founds, Hank and Sajithlal, Gangadharan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0014-4819},
	Journal = {Exp Brain Res},
	Keywords = {Cell Survival;Dose-Response Relationship, Drug;Cell Differentiation;Neuroblastoma;Animals;Proteoglycans;Microglia;Lipopolysaccharides;Neurites;Culture Media, Conditioned;Not relevant;11 Glia;Support, Non-U.S. Gov't;Alzheimer Disease;Tumor Cells, Cultured;Gliosis;Mice;Inflammation;Nitric Oxide;Tretinoin;Cell Death;Glycosylation End Products, Advanced},
	Medline = {22583643},
	Month = {5},
	Nlm_Id = {0043312},
	Number = {1},
	Organization = {Neuroimmunological Cell Biology Unit, Leipzig, Germany. mueg\@medizin.uni-leipzig.de},
	Pages = {1-8},
	Pubmed = {12698210},
	Title = {Microglial activation induces cell death, inhibits neurite outgrowth and causes neurite retraction of differentiated neuroblastoma cells},
	Uuid = {B15E5C36-3CED-42BB-9B67-4BC6D7E908BE},
	Volume = {150},
	Year = {2003},
	url = {papers/Münch_ExpBrainRes2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00221-003-1389-5}}

@article{Myslobodski:1968,
	Author = {Myslobodski, M. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0031-2991},
	Journal = {Patol Fiziol Eksp Ter},
	Keywords = {Epilepsy;21 Neurophysiology;Humans;24 Pubmed search results 2008;21 Epilepsy;review},
	Medline = {70265267},
	Nlm_Id = {0376421},
	Number = {4},
	Pages = {80-6},
	Pubmed = {4915997},
	Title = {[Provocation of epileptiform activity by physical factors]},
	Uuid = {5F369D47-28AD-4FDA-A85C-80C228B8464F},
	Volume = {12},
	Year = {1968}}

@article{Nacher:2001,
	Abstract = {Doublecortin (DCX) is a protein required for normal neuronal migration in the developing cerebral cortex, where it is widely expressed in both radially and tangentially migrating neuroblasts. Moreover, it has been observed in the adult rostral migratory stream, which contains the neuronal precursors traveling to the olfactory bulb. We have performed DCX immunocytochemistry in the adult rat brain to identify precisely the neuronal populations expressing this protein. Our observations confirm the presence of DCX immunoreactive cells with the characteristic morphology of migrating neuroblasts in the subventricular zone, rostral migratory stream and the main and accessory olfactory bulbs. We have also found putative migratory cells expressing DCX in regions were no adult neuronal migration has been described, as the corpus callosum, the piriform cortex layer III/endopiriform nucleus and the striatum. Surprisingly, many cells with the phenotype of differentiated neurons were DCX immunoreactive; e.g. certain granule neurons in the hilar border of the granular layer of the dentate gyrus, some neuronal types in the piriform cortex layer II, granule and periglomerular neurons in the main and accessory olfactory bulbs, and isolated cells in the striatum. Almost all DCX immunoreactive cells also express the polysialylated form of neural cell adhesion molecule and have a similar distribution to rat collapsin receptor-mediated protein-4, two molecules involved in neuronal structural plasticity. Given these results, we hypothesize that DCX expression in differentiated neurons could be related to its capacity for microtubule reorganization and that this fact could be linked to axonal outgrowth or synaptogenesis.},
	Author = {Nacher, J. and Crespo, C. and McEwen, B. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {B pdf;02 Adult neurogenesis migration},
	Number = {4},
	Organization = {Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY 10021, USA; Neurobiology, Cell Biology Department, Universitat de Valencia, E-46100, Spain.},
	Pages = {629-44.},
	Title = {Doublecortin expression in the adult rat telencephalon},
	Uuid = {0606CEF5-2480-4700-BC97-F5CFD2BD87E6},
	Volume = {14},
	Year = {2001},
	url = {papers/Nacher_EurJNeurosci2001}}

@article{Nacher:1999,
	Abstract = {Intraperitoneal injection of the neurotoxin 3-acetylpyridine (3AP) induces a rapid degeneration of the medial cerebral cortex (lizard fascia dentata) granular layer and of its zinc enriched axonal projection (lizard mossy fibres). After 6-8 weeks post-lesion the cell debris have been removed and the granular layer is repopulated by neurons generated in the subjacent ependyma. Both processes, neuron incorporation and debris removal, seem to be crucial for successful regeneration. Scavenging processes in the lesioned mammalian CNS are usually carried out by microglia and/or astrocytes. In the lizard cerebral cortex there are no free astrocytes and the only glial fibrillary acid (GFAP) immunoreactive cells are radial glia-ependymocytes, similar to those present during mammalian CNS development. Ependymocytes, in addition to their help in vertical migrations of just generated immature neurons, built the cortical glial scaffold, insulate the blood capillaries, form the outer glial limiting membrane, thus playing an essential role in the lizard cortical blood-brain barrier. In this study, by means of GFAP-immunocytochemistry and electron microscopy, we have shown that radial glial cells participate actively in the removal/phagocytosis of cellular debris generated in the lesion process: mainly degenerated synapses, but interestingly, also some neuronal somata. Cell debris taken up by ependymocyte lateral processes seem to be progressively transported to either distal (pial) or proximal (ventricular) poles of the cell, where they result in lipofuscin accumulations. The hypothetical subsequent exchange of debris from ependymoglia by microglia/macrophages and Kolmer cells is discussed.},
	Author = {Nacher, J. and Ram{\'\i}rez, C. and Palop, J. J. and Molowny, A. and Luis de la Iglesia, J. A. and L{\'o}pez-Garc{\'\i}a, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0213-3911},
	Journal = {Histol Histopathol},
	Keywords = {Neuroglia;Glial Fibrillary Acidic Protein;Microscopy, Electron;Dentate Gyrus;Not relevant;Pyridines;Neurotoxins;11 Glia;Regeneration;Time Factors;Immunoenzyme Techniques;Lizards;Support, Non-U.S. Gov't;Animals;Cerebral Cortex},
	Medline = {99142127},
	Month = {1},
	Nlm_Id = {8609357},
	Number = {1},
	Organization = {Faculty of Biological Sciences, University of Valencia, Spain.},
	Pages = {89-101},
	Pubmed = {9987654},
	Title = {Radial glia and cell debris removal during lesion-regeneration of the lizard medial cortex},
	Uuid = {91B44A68-3C6A-4B98-B516-6AF953CB9567},
	Volume = {14},
	Year = {1999}}

@article{Nacher:2003,
	Abstract = {The production of new neurons declines during adulthood and persists, although at very low levels, in the aged hippocampus. Since neurogenesis in young adults has been related to learning and memory, its reduction may contribute to the age-related impairments in these abilities. Adrenalectomy (ADX) enhances neurogenesis in the aged hippocampus, although it also induces neuronal cell death. Since the administration of an NMDA receptor antagonist enhances neurogenesis in young adult rats without deleterious morphological effects, we have tested whether neurogenesis could be reactivated in aged rats. Our study shows that cell proliferation, cell death, neurogenesis and the number of radial glia-like nestin immunoreactive cells decrease in middle-age (10 months) and remain very low in the aged hippocampus. Injection of the NMDA receptor antagonist to aged rats increases significantly the number of proliferating cells, new neurons and radial glia-like cells in the hippocampus. 0197-4580 Journal Article},
	Author = {Nacher, J. and Alonso-Llosa, G. and Rosell, D. R. and McEwen, B. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Neurobiol Aging},
	Keywords = {Bromodeoxyuridine;Animals;Cell Survival/drug effects;Rats;Excitatory Amino Acid Antagonists/pharmacology;Female;Neurons/chemistry/*cytology;Receptors, N-Methyl-D-Aspartate/*antagonists &inhibitors;Adrenalectomy;Aging/*physiology;Nerve Tissue Proteins/analysis;Dentate Gyrus/*cytology;Antimetabolites;Rats, Inbred F344;Support, Non-U.S. Gov't;Neuropeptides/analysis;Support, U.S. Gov't, Non-P.H.S.;Cell Death/drug effects;Support, U.S. Gov't, P.H.S.;04 Adult neurogenesis factors;Immunohistochemistry;Biological Markers;C pdf;Neuroglia/cytology;Cell Division/drug effects;2-Amino-5-phosphonovalerate/*analogs &derivatives/pharmacology},
	Number = {2},
	Organization = {Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. nacher\@uv.es},
	Pages = {273-84},
	Pubmed = {12498961},
	Title = {NMDA receptor antagonist treatment increases the production of new neurons in the aged rat hippocampus},
	Uuid = {10E00C3F-AABE-459B-9B27-DBE929973B7E},
	Volume = {24},
	Year = {2003},
	url = {papers/Nacher_NeurobiolAging2003}}

@article{Nacimiento:1995,
	Abstract = {Structural changes in lumbosacral ventral horn neurons and their synaptic input were studied at 3, 10, 21, 42, and 90 days following low thoracic cord hemisection in adult rats by light microscopic examination of synaptophysin immunoreactivity (SYN-IR) and by electron microscopy. There was an ipsilateral transient decrease in SYN-IR at the somal and proximal dendritic surfaces of anterior horn neurons which extended caudally from the site of injury over a postoperative (p.o.) period of 42 days. Concomitantly, at 21 days p.o., perineuronal SYN-IR started to recover in upper lumbar segments. By 90 days p.o., a normal staining pattern of SYN was noted in upper and mid lumbar segments, but the perineuronal SYN-IR was still slightly below normal levels in low lumbar and sacral segments. Electron microscopy revealed ultrastructural changes coincident with the alterations in SYN-IR. At 3 days p.o., phagocytosis of degenerating axon terminals by activated microglial cells was observed at the somal and proximal dendritic surfaces of ventral horn neurons. These changes were most prominent up to two segments caudal to the lesion. At 10 days p.o., advanced stages of bouton phagocytosis were still detectable in all lumbosacral motor nuclei. Additionally, abnormal axon terminals, with a few dispersed synaptic vesicles and accumulations of large mitochondria, appeared at the scalloped somal surfaces of anterior horn neurons. At 21 days p.o., several large lumbosacral motoneurons had developed chromatolysis-like ultrastructural alterations and motoneuronal cell bodies had become partially covered by astrocytic lamellae. At 42 days p.o., there was a transient appearance of polyribosomes in some M-type boutons. In addition, at 42 and 90 days p.o., a few degenerating motoneurons were detected in all lumbosacral segments, but most displayed normal neuronal cell bodies contacted by numerous intact synapses as well as by astrocytic processes. In contrast to these striking alterations of synaptic input at somal and proximal dendritic surfaces of motoneurons, relatively few degenerating boutons were detected in the neuropil of motor nuclei at all the p.o. times studied. We suggest that the preferential disturbance of the predominantly inhibitory axosomatic synapses on ventral horn neurons may be involved in the mechanisms which influence the well-established increase in motoneuronal excitability after spinal cord injury.},
	Author = {Nacimiento, W. and Sappok, T. and Brook, G. A. and T{\'o}th, L. and Schoen, S. W. and Noth, J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Phagocytosis;Presynaptic Terminals;Animals;Synapses;Rats;Mitochondria;Female;Microglia;Synaptophysin;Fibrosis;Not relevant;11 Glia;Spinal Cord;Spinal Cord Injuries;Support, Non-U.S. Gov't;Neurons;Gliosis;Immunohistochemistry;Microscopy, Electron},
	Medline = {96191752},
	Nlm_Id = {0412041},
	Number = {6},
	Organization = {Depart of Neurology, Technical University, School of Medicine, Aachen, Germany.},
	Pages = {552-64},
	Pubmed = {8615075},
	Title = {Structural changes of anterior horn neurons and their synaptic input caudal to a low thoracic spinal cord hemisection in the adult rat: a light and electron microscopic study},
	Uuid = {DA99FEBA-9C42-420B-B7EC-2573C21766A1},
	Volume = {90},
	Year = {1995}}

@article{Nadler:1980,
	Abstract = {Degeneration of hippocampal CA3 pyramidal cells was investigated by light and electron microscopy after intraventricular injection of the potent convulsant, kainic acid. Electron microscopy revealed evidence of pyramidal cell degeneration within one hour. The earliest degenerative changes were confined to the cell body and proximal dendritic shafts. These included an increased incidence of lysosomal structures, deformation of the perikaryal and nuclear outlines, some increase in background electron density, and dilation of the cisternae of the endoplasmic reticulum accompanied by detachment of polyribosomes. Within the next few hours the pyramidal cells atrophied and became electron dense. Then these cells became electron lucent once more as ribosomes disappeared and their membranes and organelles broke up and disintegrated. Light microscopic changes correlated with these ultrastructural observations. The dendritic spines and the initial portion of the dendritic shaft became electron dense within four hours and degenerated rapidly, whereas the intermediate segment of the dendrites swelled moderately and became more electron lucent. No degenerative changes were evident in pyramidal cell axons and boutons until one day after kainic acid treatment. Less than one hour after kainic acid administration, astrocytes in the CA3 area swelled, initially in the vicinity of the cell body and mossy fiber layers. It is suggested that the paroxysmal discharges initiated in CA3 pyramidal cells by kainic acid served as the stimulus for this response. Phagocytosis commenced between one and three days after kainic acid administration, but remained incomplete at survival times of 6-8 weeks. Astrocytes, microglia, and probably oligodendroglia phagocytized the degenerating material. These results point to the pyramidal cell body and possibly also the dendritic spines as primary targets of kainic acid neurotoxicity. In conjunction with other data, they support the view that lesions made by intraventricular kainic acid can serve as models of epileptic brain damage.},
	Author = {Nadler, J. V. and Perry, B. W. and Gentry, C. and Cotman, C. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Pyrrolidines;Synapses;Dendrites;Neuroglia;Nerve Degeneration;Hippocampus;Rats;Not relevant;11 Glia;Support, U.S. Gov't, Non-P.H.S.;Injections, Intraventricular;Kainic Acid;Support, U.S. Gov't, P.H.S.;Male;Animals;Neurons;Axons},
	Medline = {80250039},
	Month = {7},
	Nlm_Id = {0406041},
	Number = {2},
	Pages = {333-59},
	Pubmed = {7400401},
	Title = {Degeneration of hippocampal CA3 pyramidal cells induced by intraventricular kainic acid},
	Uuid = {D1E9F199-FFC4-48AD-BBBA-345DA517E55B},
	Volume = {192},
	Year = {1980}}

@article{Nagano:2004,
	Abstract = {In the developing neocortex, most excitatory neurons are supplied and arranged through radial migration. Because neurons show global morphological changes and complicated behavior during that migration, precise regulation of cell shape and polarity is essential for proper migration and correct neocortical formation; however, how cell shape and polarity are regulated in migrating neuron remains elusive. We show here that Filamin A, a well known actin-binding protein, determines the shape of neocortical neurons during radial migration in vivo. Dysfunction of Filamin A, caused by a mutant Filamin A expression, prevents cells from acquiring consistent polarity toward specific direction and decreases motility in the subventricular and intermediate zones. In contrast, Filamin A overexpression, achieved by a short interfering RNA for Filamin A-interacting protein that induces Filamin A degradation (FILIP), promotes the development and maintenance of a bipolar shape also in the subventricular and intermediate zones. These results suggest that the amount of Filamin A helps migrating neurons determine their mode of migration, multipolar or bipolar, before entering the cortical plate and that FILIP is responsible, at least in part, for Filamin A content. In addition, our results also give a possible clue to understanding the pathogenesis of human malformation periventricular heterotopia, which is caused by various "loss-of-function" mutations in the filamin A gene.},
	Author = {Nagano, Takashi and Morikubo, Soichi and Sato, Makoto},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Pregnancy;Animals;Tissue Culture Techniques;Carrier Proteins;Rats;Transfection;Microfilament Proteins;21 Epilepsy;Neocortex;Female;Cell Movement;Cell Polarity;RNA Interference;Mice, Inbred C57BL;Rats, Wistar;Gene Transfer Techniques;21 Neurophysiology;Mice;24 Pubmed search results 2008;Contractile Proteins;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {43},
	Organization = {Division of Cell Biology and Neuroscience, Department of Morphological and Physiological Sciences, Faculty of Medical Sciences, University of Fukui, Matsuoka, Fukui 910-1193, Japan.},
	Pages = {9648-57},
	Pii = {24/43/9648},
	Pubmed = {15509752},
	Title = {Filamin A and FILIP (Filamin A-Interacting Protein) regulate cell polarity and motility in neocortical subventricular and intermediate zones during radial migration},
	Uuid = {05245B5A-B74D-444A-9DD3-CA16452CB3D9},
	Volume = {24},
	Year = {2004},
	url = {papers/Nagano_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2363-04.2004}}

@article{Nagano:2002,
	Abstract = {Precisely regulated radial migration out of the ventricular zone is essential for corticogenesis. Here, we identify a mechanism that can tether ventricular zone cells in situ. FILIP interacts with Filamin A, an indispensable actin-binding protein that is required for cell motility, and induces its degradation in COS-7 cells. Degradation of Filamin A is identified in the cortical ventricular zone, where filip mRNA is localized. Furthermore, most ventricular zone cells that overexpress FILIP fail to migrate in explants. These results demonstrate that FILIP functions through a Filamin A F-actin axis to control the start of neocortical cell migration from the ventricular zone.},
	Author = {Nagano, Takashi and Yoneda, Takunari and Hatanaka, Yumiko and Kubota, Chikara and Murakami, Fujio and Sato, Makoto},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Carrier Proteins;Rats;Microfilament Proteins;21 Epilepsy;Neocortex;Cell Movement;COS Cells;Rats, Wistar;In Situ Hybridization;21 Neurophysiology;Cytoskeleton;Contractile Proteins;Molecular Sequence Data;Amino Acid Sequence;24 Pubmed search results 2008;Actins;Cytoskeletal Proteins},
	Medline = {22100428},
	Month = {7},
	Nlm_Id = {100890575},
	Number = {7},
	Organization = {Department of Anatomy 2, Fukui Medical University, 23 Shimoaizuki, Matsuoka, Fukui 910-1193, Japan.},
	Pages = {495-501},
	Pii = {ncb808},
	Pubmed = {12055638},
	Title = {Filamin A-interacting protein (FILIP) regulates cortical cell migration out of the ventricular zone},
	Uuid = {AF740D8E-9E4C-432B-A525-13C70BF1CE81},
	Volume = {4},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb808}}

@article{Nait-Oumesmar:2007,
	Abstract = {In multiple sclerosis (MS), oligodendrocyte and myelin destruction lead to demyelination with subsequent axonal loss. Experimental demyelination in rodents has highlighted the activation of the subventricular zone (SVZ) and the involvement of progenitor cells expressing the polysialylated form of neural cell adhesion molecule (PSA-NCAM) in the repair process. In this article, we studied the distribution of early PSA-NCAM(+) progenitors in the SVZ and MS lesions in human postmortem brains. Compared with controls, MS SVZ showed a 2- to 3-fold increase in cell density and proliferation, which correlated with enhanced numbers of PSA-NCAM(+) and glial fibrillary acidic protein-positive (GFAP(+)) cells. PSA-NCAM(+) progenitors mainly were Sox9(+), and a few expressed Sox10 and Olig2, markers of oligodendroglial specification. PSA-NCAM(+) progenitors expressing Sox10 and Olig2 also were detected in demyelinated MS lesions. In active and chronic active lesions, the number of PSA-NCAM(+) progenitors was 8-fold higher compared with chronic silent lesions, shadow plaques, and normal-appearing white matter. In active and chronic active lesions, PSA-NCAM(+) progenitors were more frequent in periventricular lesions (30-50\%) than in lesions remote from the ventricular wall. These data indicate that, as in rodents, activation of gliogenesis in the SVZ occurs in MS and suggest the mobilization of SVZ-derived early glial progenitors to periventricular lesions, where they could give rise to oligodendrocyte precursors. These early glial progenitors could be a potential target for therapeutic strategies designed to promote myelin repair in MS.},
	Author = {Nait-Oumesmar, Brahim and Picard-Riera, Nathalie and Kerninon, Christophe and Decker, Laurence and Seilhean, Danielle and H{\"o}glinger, G{\"u}nter U. and Hirsch, Etienne C. and Reynolds, Richard and Baron-Van Evercooren, Anne},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {02 Adult neurogenesis migration;11 Glia;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7505876},
	Number = {11},
	Organization = {*Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale, Unit{\'e} 546, 75013 Paris, France.},
	Pages = {4694-9},
	Pii = {0606835104},
	Pubmed = {17360586},
	Title = {Activation of the subventricular zone in multiple sclerosis: Evidence for early glial progenitors},
	Uuid = {2B68AA16-D116-4214-B909-6EB87C57A877},
	Volume = {104},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0606835104}}

@article{Nakagawa:2000,
	Abstract = {PURPOSE: Mitogenic effects of seizures on granule cell progenitors in the dentate gyrus were studied in two rat models of epilepsy. We investigated which stage of epileptogenesis is critical for eliciting progenitor cell division and whether seizure-induced neuronal degeneration is responsible for the enhancement of progenitor cell division. METHODS: Seizures were induced by either kainic acid (KA) administration or electrical kindling. Neurogenesis of dentate granule cells was evaluated using the bromodeoxyuridine (BrdU) labeling method, and neuronal degeneration was assessed by in situ DNA fragmentation analysis. RESULTS: After injection of KA, the number of BrdU-positive granule cells began to increase at day 3 after the treatment, peaked at day 5, and returned to baseline at day 10. By day 13, the values were lower than control. After kindling, the number of BrdU-positive cells began to increase after five consecutive experiences of stage I seizures. The increase occurred from day 1 to day 3 after the last electrical stimulation, but returned to baseline by day 7. After generalized seizures were well established, repeated stimulation did not facilitate division of granule cell progenitors. DNA fragmentation was noted in pyramidal neurons in the CA1, CA3, and hilus regions at 18 h after KA injection, but not in the kindling model. CONCLUSIONS: These observations indicate that a mechanism in epileptogenesis boosts dentate progenitor cell division, but progenitor cells may become unreactive to prolonged generalized seizures. Pyramidal neuronal degeneration is not necessary for triggering the upregulation. It is suggested that newly born granule cells may play a role in the network reorganization that occurs during epileptogenesis.},
	Author = {Nakagawa, E. and Aimi, Y. and Yasuhara, O. and Tooyama, I. and Shimada, M. and McGeer, P. L. and Kimura, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:57 -0400},
	Journal = {Epilepsia},
	Keywords = {Male;Dentate Gyrus/*pathology;Rats, Sprague-Dawley;Rats;Immunohistochemistry;D;Time Factors;Limbic System/*pathology;Animal;Seizures/*pathology;06 Adult neurogenesis injury induced;Support, Non-U.S. Gov't;Bromodeoxyuridine/diagnostic use;Disease Models, Animal;DNA Fragmentation;Stem Cells/*pathology},
	Number = {1},
	Organization = {Molecular Neuroscience Research Center, and Department of Pediatrics, Shiga University of Medical Science, Otsu, Japan. eijin\@interchange.ubc.ca},
	Pages = {10-8.},
	Title = {Enhancement of progenitor cell division in the dentate gyrus triggered by initial limbic seizures in rat models of epilepsy},
	Uuid = {553ECD85-0FC4-49EC-BA3D-280D52B3A8EE},
	Volume = {41},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10643917}}

@article{Nakahira:2005,
	Abstract = {Neuronal migration defects in the hippocampus during development are thought to be involved in various mental disorders. Studies of neural cell migration in the developing cerebrum have focused mainly on the neocortex, but those that have been performed on the developing hippocampal formation have not been adequately carried out. In the present study, the morphological differentiation of immature neurons that form the laminar structure of the hippocampus was investigated by labeling ventricular surface cells with the expression vector of the enhanced-green-fluorescent-protein (EGFP) gene. Vector DNA was transfected into spatially and temporally restricted neuroepithelium of the hippocampal primordium by in utero electroporation, and the morphology of EGFP-labeled migratory neurons and their interrelationships with the radial glial arrangement were observed. Pyramidal cells of Ammon's horn began to migrate radially along glial processes from a broad area of neuroepithelium on embryonic day (E)14. Large numbers of multipolar cells were found in the intermediate zone in the initial stage and stratified pyramidal cells appeared later. Dentate granule cells were labeled later than (E)16 and originated from a restricted area of neuroepithelium adjacent to the fimbria. Their initial migration was rapid and independent of radial glial fibers. Subsequent tangential migration in the subpial space and their ultimate settling into the forming dentate gyrus were closely associated with the radial glia. These findings indicate that distinct cellular mechanisms are involved in the development of the cortical layer of Ammon's horn and dentate gyrus.},
	Author = {Nakahira, Eiko and Yuasa, Shigeki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Research Support, Non-U.S. Gov't;10 Development;Cell Differentiation;Animals;10 Hippocampus;Pregnancy;Comparative Study;Female;Cell Count;Electroporation;Embryonic Development;Hippocampus;Green Fluorescent Proteins;Cell Movement;Male;Embryo;Mice, Inbred ICR;Gene Transfer Techniques;Neuroglia;Neurons;Age Factors;Mice;Immunohistochemistry;Uterus},
	Month = {3},
	Nlm_Id = {0406041},
	Number = {3},
	Organization = {Department of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan. nakahira\@ncnp.go.jp},
	Pages = {329-40},
	Pubmed = {15682392},
	Title = {Neuronal generation, migration, and differentiation in the mouse hippocampal primoridium as revealed by enhanced green fluorescent protein gene transfer by means of in utero electroporation},
	Uuid = {7C9505F9-616E-4FD0-99DA-67F14FB0072D},
	Volume = {483},
	Year = {2005},
	url = {papers/Nakahira_JCompNeurol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20441}}

@article{Nakajima:1998,
	Abstract = {Although the physiological role of neurotrophins in neuronal development and survival has been extensively investigated, their role in glial cell physiology remains to be elucidated. In the present study, we investigated the effects of neurotrophins on cultured microglia from newborn rat brain. All of the neurotrophins tested nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4), increased the secretion of plasminogen and urokinase type-plasminogen activator and specific activity of acid phosphatase, but suppressed the release of constitutively-produced and lipopolysaccharide-stimulated nitric oxide (NO) from microglia. The reverse transcription-polymerase chain reaction, immunocytochemical staining, and Western blotting revealed that cultured microglia express Trk A, B, and C, and low-affinity NGF receptor, LNGFRp75. Neurotrophin was found to phosphorylate Trk A and B, and the neurotrophin-induced enhancement of plasminogen-secretion was suppressed by protein kinase inhibitor, K252a. Furthermore, neurotrophins caused an activation of transcription factor, NF-kappaB. These results indicate that the neurotrophin family regulate the function of microglia through Trk and/or LNGFRp75-mediated signal transduction.},
	Author = {Nakajima, K. and Kikuchi, Y. and Ikoma, E. and Honda, S. and Ishikawa, M. and Liu, Y. and Kohsaka, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Animals;Cells, Cultured;Acid Phosphatase;Rats;Phosphorylation;NF-kappa B;5'-Nucleotidase;Brain-Derived Neurotrophic Factor;Microglia;Neurotrophin 3;Culture Media, Conditioned;RNA, Messenger;Nerve Growth Factors;Not relevant;11 Glia;Reverse Transcriptase Polymerase Chain Reaction;Blotting, Southern;Receptors, Nerve Growth Factor;Plasminogen;Animals, Newborn;Support, Non-U.S. Gov't;Blotting, Western;Receptor Protein-Tyrosine Kinases;Cell Division;Urinary Plasminogen Activator;Nitric Oxide},
	Medline = {98446874},
	Month = {11},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Neurochemistry, National Institute of Neuroscience, Kodaira, Tokyo, Japan.},
	Pages = {272-89},
	Pii = {10.1002/(SICI)1098-1136(199811)24:3<272::AID-GLIA2>3.0.CO;2-4},
	Pubmed = {9775979},
	Title = {Neurotrophins regulate the function of cultured microglia},
	Uuid = {8E3E6573-3B7C-434E-9DCD-2C55BD3D6FA3},
	Volume = {24},
	Year = {1998},
	url = {papers/Nakajima_Glia1998.pdf}}

@article{Nakajima:2001,
	Abstract = {Because microglia have been suggested to produce neurotrophins, we tested this ability in vitro. Rat primary microglia were found to constitutively secrete a limited amount of brain-derived neurotrophic factor (BDNF), but nerve growth factor (NGF) and neurotrophin-3 (NT-3) were undetectable in the conditioned medium. Stimulation of the cells with lipopolysaccharide (LPS) increased BDNF secretion, and induced NGF secretion. As a first step to examine this regulation system, the association of protein kinase C (PKC) was pharmacologically analyzed. A PKC activator, phorbol-12-myristate-13-acetate, enhanced the secretion of BDNF. Pre-treatment of microglia with a PKC inhibitor, bisindolylmaleimide, suppressed LPS-stimulated BDNF secretion as well as the constitutive one. These results suggest that the PKC signaling cascade is closely associated with BDNF secretion. Among PKC isoforms, PKCalpha probably plays a role in BDNF secretion, based on the results of experiments using a specific PKC activator, 1-oleoyl-2-acetyl-sn-glycerol, and a specific PKC inhibitor, G{\"o} 6976, and by immunoblotting. Taken together, these findings suggest that the secretion of BDNF from microglia is regulated through PKCalpha-associated signal transduction mechanism.},
	Author = {Nakajima, K. and Honda, S. and Tohyama, Y. and Imai, Y. and Kohsaka, S. and Kurihara, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Protein Kinase C;Animals;Cells, Cultured;Nerve Growth Factor;Rats;Enzyme Inhibitors;Diglycerides;Brain-Derived Neurotrophic Factor;Microglia;Neurotrophin 3;Maleimides;Lipopolysaccharides;Culture Media, Conditioned;Nerve Growth Factors;Indoles;Not relevant;11 Glia;Antibodies;Support, Non-U.S. Gov't;Carcinogens;Tetradecanoylphorbol Acetate;Cerebral Cortex;Carbazoles;Isoenzymes},
	Medline = {21385486},
	Month = {8},
	Nlm_Id = {7600111},
	Number = {4},
	Organization = {Institute of Life Science, Soka University, 1-236, Tangi-machi, Hachioji, Tokyo 192-8577. nakajima\@t.soka.ac.jp},
	Pages = {322-31},
	Pubmed = {11494368},
	Title = {Neurotrophin secretion from cultured microglia},
	Uuid = {3F07A720-6995-4C85-BFD3-BD6E35454D22},
	Volume = {65},
	Year = {2001}}

@article{Nakamichi:2005,
	Abstract = {During neurotropic virus infection, microglia act as a source of chemokines, thereby regulating the recruitment of peripheral leukocytes and the multicellular immune response within the CNS. Herein, we present a comprehensive study on the chemokine production by microglia in response to double-stranded RNA (dsRNA), a conserved molecular pattern of virus infection. Transcriptional analyses of chemokine genes revealed that dsRNA strongly induces the expression of CXC chemokine ligand 10 (CXCL10) and CC chemokine ligand 5 (CCL5) in microglia. We also observed that the dsRNA stimulation triggered the activation of signaling pathways mediated by nuclear factor kappaB (NF-kappaB) and mitogen-activated protein kinases (MAPK), including extracellular signal-regulated kinases 1 and 2 (ERK1/2), p38, and c-Jun N-terminal kinase (JNK). The microglial CXCL10 response to dsRNA was induced via NF-kappaB, p38, and JNK pathways, whereas the dsRNA-induced CCL5 production was dependent on JNK, but not on the other signal-transducing molecules tested. In addition, the acidic environment of intracellular vesicles was required for the activation of cellular signaling in response to dsRNA. Taken together, these results suggest that the recognition of dsRNA structure selectively induces the CXCL10 and CCL5 responses in microglia through vacuolar pH-dependent activation of NF-kappaB and MAPK signaling pathways.},
	Author = {Nakamichi, and Saiki, and Sawada, and Yamamuro, and Morimoto, and Kurane,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {07 Excitotoxicity Apoptosis;11 Glia;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {2985190R},
	Organization = {Department of Virology 1, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan.},
	Pii = {JNC3354},
	Pubmed = {16086695},
	Title = {Double-stranded RNA stimulates chemokine expression in microglia through vacuolar pH-dependent activation of intracellular signaling pathways},
	Uuid = {94FA5E83-9FA5-417B-A70E-8E5F542DB6E2},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1471-4159.2005.03354.x}}

@article{Nakano:2001,
	Abstract = {BACKGROUND: Bone marrow transplantation is reportedly effective in preventing the progression of neurological deterioration in lysosomal storage disorders, although the mechanism underlying the therapeutic effects remains to be elucidated. Recent research on stem cell biology suggests that bone marrow cells contain nonhematopoietic stem cells, including brain precursor cells. To evaluate the contribution of bone marrow cells as carriers for cell and gene therapy of neurological disorders, we studied the fate of transplanted bone marrow cells in the adult mouse brain. METHODS: Bone marrow cells were genetically marked with a retroviral vector containing the green fluorescence protein gene and then transplanted into irradiated mice by either systemic infusion or direct injection. To identify cell types, brain sections were stained with specific antibodies against neuronal cell markers-neuron specific enolase for neurons, glial fibrillary acidic protein (GFAP) for astrocytes, carbonic anhydrase II (CAII) for oligodendrocytes, and ionized calcium binding adaptor molecule 1 (Iba1) for microglia-and then examined under a confocal microscope. RESULTS: Twenty-four weeks after systemic infusion, transplanted cells expressed Iba1 but none of the other brain cell markers. Conversely, 12 weeks after direct injection, transplanted cells were stained with antibodies against GFAP, CAII, and Iba1. CONCLUSIONS: Bone marrow contains cells capable of differentiating into oligodendrocytes, astrocytes, and microglia when exposed to the brain microenvironment. Autologous bone marrow cells may be useful as carriers for ex vivo gene therapy for lysosomal disorders with neurological symptoms.},
	Author = {Nakano, K. and Migita, M. and Mochizuki, H. and Shimada, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0041-1337},
	Journal = {Transplantation},
	Keywords = {Cell Differentiation;Transduction, Genetic;Animals;Stereotaxic Techniques;Corpus Striatum;Bone Marrow Transplantation;Brain;Indicators and Reagents;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Bone Marrow Cells;Neuroglia;Mice;Injections, Intravenous;Luminescent Proteins;Injections;Research Support, Non-U.S. Gov't},
	Medline = {21348760},
	Month = {6},
	Nlm_Id = {0132144},
	Number = {12},
	Organization = {Department of Biochemistry and Molecular Biology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.},
	Pages = {1735-40},
	Pubmed = {11455251},
	Title = {Differentiation of transplanted bone marrow cells in the adult mouse brain},
	Uuid = {847107A0-7F61-4EC6-BD71-7B4EF3477D37},
	Volume = {71},
	Year = {2001}}

@article{Nakatomi:2002,
	Abstract = {The adult brain is extremely vulnerable to various insults. The recent discovery of neural progenitors in adult mammals, however, raises the possibility of repairing damaged tissue by recruiting their latent regenerative potential. Here we show that activation of endogenous progenitors leads to massive regeneration of hippocampal pyramidal neurons after ischemic brain injury. Endogenous progenitors proliferate in response to ischemia and subsequently migrate into the hippocampus to regenerate new neurons. Intraventricular infusion of growth factors markedly augments these responses, thereby increasing the number of newborn neurons. Our studies suggest that regenerated neurons are integrated into the existing brain circuitry and contribute to ameliorating neurological deficits. These results expand the possibility of novel neuronal cell regeneration therapies for stroke and other neurological diseases. 22190657 0092-8674 Journal Article},
	Author = {Nakatomi, H. and Kuriu, T. and Okabe, S. and Yamamoto, S. and Hatano, O. and Kawahara, N. and Tamura, A. and Kirino, T. and Nakafuku, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Cell},
	Keywords = {D},
	Number = {4},
	Organization = {Department of Neurobiology, The University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, 113-0033, Tokyo, Japan},
	Pages = {429},
	Title = {Regeneration of hippocampal pyramidal neurons after ischemic brain injury by recruitment of endogenous neural progenitors},
	Uuid = {BAA16E92-C26D-11DA-969D-000D9346EC2A},
	Volume = {110},
	Year = {2002},
	url = {papers/Nakatomi_Cell2002.pdf}}

@article{Naldini:1996,
	Abstract = {We describe the construction of a safe, replication-defective and efficient lentiviral vector suitable for in vivo gene delivery. The reverse transcription of the vector was found to be a rate-limiting step; therefore, promoting the reaction inside the vector particles before delivery significantly enhanced the efficiency of gene transfer. After injection into the brain of adult rats, sustained long-term expression of the transgene was obtained in the absence of detectable pathology. A high proportion of the neurons in the areas surrounding the injection sites of the vector expressed the transduced beta-galactosidase gene. This pattern was invariant in animals sacrificed several months after a single administration of the vector. Transduction occurs by integration of the vector genome, as it was abolished by a single amino acid substitution in the catalytic site of the integrase protein incorporated in the vector. Development of clinically acceptable derivatives of the lentiviral vector may thus enable the sustained delivery of significant amounts of a therapeutic gene product in a wide variety of somatic tissues.},
	Author = {Naldini, L. and Bl{\"o}mer, U. and Gage, F. H. and Trono, D. and Verma, I. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {beta-Galactosidase;Animals;Kidney;Cytomegalovirus;Rats;Humans;research support, u.s. gov't, p.h.s. ;Lentivirus;Safety;15 Retrovirus mechanism;Animals, Genetically Modified;Genes, gag;Brain;Genes, pol;Genetic Vectors;research support, non-u.s. gov't ;Cell Line;Gene Transfer Techniques;Neurons;Lac Operon;Virus Integration;Genes, Reporter},
	Month = {10},
	Nlm_Id = {7505876},
	Number = {21},
	Organization = {Salk Institute for Biological Studies, San Diego, CA 92186-5800, USA.},
	Pages = {11382-8},
	Pubmed = {8876144},
	Title = {Efficient transfer, integration, and sustained long-term expression of the transgene in adult rat brains injected with a lentiviral vector},
	Uuid = {39E6E80D-45DB-4D22-A1D7-FBD0535676E1},
	Volume = {93},
	Year = {1996},
	url = {papers/Naldini_ProcNatlAcadSciUSA1996.pdf}}

@article{Nam:2007,
	Abstract = {Neuroblasts migrate long distances in the postnatal subventricular zone (SVZ) and rostral migratory stream (RMS) to the olfactory bulbs. Many fundamental features of SVZ migration are still poorly understood, and we addressed several important questions using two-photon time-lapse microscopy of brain slices from postnatal and adult eGFP(+) transgenic mice. 1) Longitudinal arrays of neuroblasts, so-called chain migration, have never been dynamically visualized in situ. We found that neuroblasts expressing doublecortin-eGFP (Dcx-eGFP) and glutamic acid decarboxylase-eGFP (Gad-eGFP) remained within arrays, which maintained their shape for many hours, despite the fact that there was a wide variety of movement within arrays. 2) In the dorsal SVZ, neuroblasts migrated rostrocaudally as expected, but migration shifted to dorsoventral orientations throughout ventral regions of the lateral ventricle. 3) Whereas polarized bipolar morphology has been a gold standard for inferring migration in histologic sections, our data indicated that migratory morphology was not predictive of motility. 4) Is there local motility in addition to long distance migration? 5) How fast is SVZ migration? Unexpectedly, one-third of motile neuroblasts moved locally in complex exploratory patterns and at average speeds slower than long distance movement. 6) Finally, we tested, and disproved, the hypothesis that all motile cells in the SVZ express doublecortin, indicating that Dcx is not required for migration of all SVZ cell types. These data show that cell motility in the SVZ and RMS is far more complex then previously thought and involves multiple cell types, behaviors, speeds, and directions. J. Comp. Neurol. 505:190-208, 2007. (c) 2007 Wiley-Liss, Inc.},
	Author = {Nam, Sang Chae and Kim, Yongsoo and Dryanovski, Dilyan and Walker, Avery and Goings, Gwendolyn and Woolfrey, Kevin and Kang, Seong Su and Chu, Chris and Chenn, Anjen and Erdelyi, Ferenc and Szabo, Gabor and Hockberger, Philip and Szele, Francis G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Chonnam National University Medical School, Gwangju, Republic of Korea 501-746.},
	Pages = {190-208},
	Pubmed = {17853439},
	Title = {Dynamic features of postnatal subventricular zone cell motility: A two-photon time-lapse study},
	Uuid = {26B91A4C-3096-401B-BFA3-2F731D5B6E2C},
	Volume = {505},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.21473}}

@article{Namba:2005,
	Abstract = {In the dentate gyrus neurons continue to be generated from late embryonic to adult stage. Recent extensive studies have unveiled several key aspects of the adult neurogenesis, but only few attempts have so far been made on the analysis of the early postnatal neurogenenesis, a transition state between the embryonic and adult neurogenesis. Here, we focus on the early postnatal neurogenesis and examine the nature and development of neural progenitor cells in Wistar rats. Immunohistochemistry for Ki67, a cell cycle marker, and 5-bromo-2-deoxyuridine (BrdU) labelling show that cell proliferation occurs mainly in the hilus and partly in the subgranular zone. A majority of the proliferating cells express S100beta and astrocyte-specific glutamate transporter (GLAST) and the subpopulation are also positive for glial fibrillary acidic protein (GFAP) and nestin. Tracing with BrdU and our modified retrovirus vector carrying enhanced green fluorescent protein (GFP) indicate that a substantial population of the proliferating cells differentiate into proliferative neuroblasts and immature neurons in the hilus, which then migrate to the granule cell layer (66.8\%), leaving a long axon-like process behind in the hilus, and the others mainly become star-shaped astrocytes (12.0\%) and radial glia-like cells (4.7\%) in the subgranular zone. These results suggest that the progenitors of the granule cells expressing astrocytic and radial glial markers, proliferate and differentiate into neurons mainly in the hilus during the early postnatal period.},
	Author = {Namba, Takashi and Mochizuki, Hideki and Onodera, Masafumi and Mizuno, Yoshikuni and Namiki, Hideo and Seki, Tatsunori},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;10 Development;10 Hippocampus;Animals;Gene Expression Regulation, Developmental;Rats;Fluorescent Antibody Technique;Comparative Study;Hu Paraneoplastic Encephalomyelitis Antigens;Ki-67 Antigen;Zidovudine;Models, Biological;Cell Count;Rats, Wistar;Green Fluorescent Proteins;Cell Proliferation;Nerve Growth Factors;Animals, Newborn;Excitatory Amino Acid Transporter 1;Neuroglia;Intermediate Filament Proteins;Neurons;Age Factors;Dentate Gyrus;Stem Cells;Nerve Tissue Proteins;S100 Proteins;Glial Fibrillary Acidic Protein},
	Month = {10},
	Nlm_Id = {8918110},
	Number = {8},
	Organization = {Department of Anatomy, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo 113-8421, Japan.},
	Pages = {1928-41},
	Pii = {EJN4396},
	Pubmed = {16262632},
	Title = {The fate of neural progenitor cells expressing astrocytic and radial glial markers in the postnatal rat dentate gyrus},
	Uuid = {1C9A8DB4-1B79-411B-A11A-F82D52C6E8D5},
	Volume = {22},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2005.04396.x}}

@article{Nanmoku:2003,
	Abstract = {Moloney murine leukemia retroviral vectors are more suitable as tools for gene delivery in vivo in comparison to other vectors due to their stable expression and absence of cytotoxicity. However, because of their low titers and poor proliferation rate in the adult nervous system, the application of retroviral vectors to the nervous system has been limited. To overcome this disadvantage, we have attempted to achieve higher viral titers and apply them to the embryonic mouse brain. By utilizing our improved packaging cell line and concentrating the viral supernatant by the low-speed centrifugation method, we have successfully increased the retroviral titer up to 10(12) cfu/ml. This titer is over 10(6)-fold greater than routinely achieved retroviral titers, and is comparable to, or even higher than, those of adenoviral vectors. We investigated the efficacy of gene transfer into the nervous system, which has thus far proven quite recalcitrant to genetic transfer by characteristically low retroviral titers. Using our retroviral preparation, we have demonstrated the highly efficient delivery and long-term expression of a foreign gene into neural cells both in vitro and in vivo. Moreover, we demonstrated that predominant gene delivery into the neurons of one cortical layer can be achieved by choosing an appropriate date of retroviral infection. 0378-5866 Journal Article},
	Author = {Nanmoku, K. and Kawano, M. and Iwasaki, Y. and Ikenaka, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Dev Neurosci},
	Keywords = {Transduction, Genetic/*methods;15 Retrovirus mechanism;Embryo;J pdf;Animals, Newborn;Brain/*physiology;Neurons/physiology;Female;Moloney murine leukemia virus/*genetics;Pregnancy;3T3 Cells;Injections, Intraventricular;Fibroblasts/physiology;Support, Non-U.S. Gov't;Animals;Mice;Genetic Vectors/administration &dosage},
	Number = {2-4},
	Organization = {Laboratory of Neural Information, National Institute for Physiological Sciences, Okazaki, Aichi, Japan.},
	Pages = {152-61},
	Pubmed = {12966213},
	Title = {Highly efficient gene transduction into the brain using high-titer retroviral vectors},
	Uuid = {B5B6E11E-5A03-4F90-AD60-F2BDCB30B56D},
	Volume = {25},
	Year = {2003},
	url = {papers/Nanmoku_DevNeurosci2003.pdf}}

@article{Narasimhan:2005,
	Author = {Narasimhan, Kalyani},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Brain Injuries;Adenosine Triphosphate;Brain Diseases;Phagocytosis;Signal Transduction;Gliosis;11 Glia;Microglia;comment;Mice;Animals;Humans;Receptors, Purinergic P2;news},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Pages = {707},
	Pii = {nn0605-707},
	Pubmed = {15917834},
	Title = {Brain's guard cells show their agility},
	Uuid = {3DA0C994-99E2-4621-9787-56001C0D7E05},
	Volume = {8},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn0605-707}}

@article{Nataf:2001,
	Abstract = {Expression of the C5a receptor in the central nervous system has been demonstrated on microglia, astrocytes and neurons. In the present study, we demonstrate C5aR expression in vitro by rat and murine O2-A progenitor cells and oligodendrocytes. We also observed that in vitro differentiation of O2-A progenitors into mature oligodendrocytes is accompanied by down-regulation of C5aR mRNA expression. These results suggest that the C5aR may be a marker for oligodendroglial differentiation and play a role in oligodendrocyte function. 21149821 0006-8993 Journal Article},
	Author = {Nataf, S. and Levison, S. W. and Barnum, S. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Brain Res},
	Keywords = {In Situ Hybridization;Flow Cytometry;Stem Cells/cytology/physiology;G abstr;Gene Expression/physiology;Rats;Cell Differentiation/physiology;Cell Lineage/physiology;RNA, Messenger/analysis;11 Glia;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Cells, Cultured;Oligodendroglia/cytology/*physiology;Receptors, Complement/*genetics;Antigens, CD/*genetics},
	Number = {2},
	Organization = {Department of Microbiology, University of Alabama at Birmingham, 35294, USA.},
	Pages = {321-6},
	Pubmed = {11251209},
	Title = {Expression of the anaphylatoxin C5a receptor in the oligodendrocyte lineage},
	Uuid = {94F762E2-99FE-4D18-8D59-2A5102D77165},
	Volume = {894},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11251209}}

@article{Nathan:2001,
	Abstract = {Apolipoprotein E (apoE), a lipid transporting protein, has been postulated to participate in nerve regeneration. To better clarify apoE function in the olfactory system, we evaluated the amount and distribution of apoE in the olfactory bulb following olfactory nerve lesion in mice. Olfactory nerve was lesioned in 2- to 4-month-old mice by intranasal irrigation with Triton X-100. Olfactory bulbs were collected at 0, 3, 7, 21, 42, and 56 days postlesion, and both apoE concentrations and apoE distribution were determined. ApoE levels, as determined by immunoblot analysis, were twofold greater than normal during nerve degeneration at 3 days. ApoE levels remained elevated by approximately 1.5 times normal levels at 7 through 21 days after injury and returned to baseline by 56 days. Immunocytochemical studies supported these observations. ApoE immunoreactivity was prominent on the olfactory nerve at 3 days after lesion and decreased to baseline levels at later time periods. Double-labeling immunocytochemical studies confirmed that both reactive astroglia and microglia produced detectable amounts of apoE following the lesion. Return of apoE expression to baseline paralleled measures of olfactory nerve maturation as measured by olfactory marker protein. These data suggest that apoE increases concurrent with nerve degeneration. ApoE may facilitate efficient regeneration perhaps by recycling lipids from degenerating fibers for use by growing axons. The association of apoE genotype with dementing illnesses may represent a diminished ability to support a lifetime of nerve regeneration. Copyright 2001 Academic Press.},
	Author = {Nathan, B. P. and Nisar, R. and Randall, S. and Short, J. and Sherrow, M. and Wong, G. K. and Struble, R. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Exp Neurol},
	Keywords = {I abstr;13 Olfactory bulb anatomy},
	Number = {1},
	Organization = {Department of Biological Sciences, Eastern Illinois University, 600 Lincoln Avenue, Charleston, Illinois, 61920},
	Pages = {128-36.},
	Title = {Apolipoprotein e is upregulated in olfactory bulb glia following peripheral receptor lesion in mice},
	Uuid = {4A26FBA8-342B-4A3B-9779-57766212D424},
	Volume = {172},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11681846}}

@article{Nedivi:1998,
	Abstract = {Activity-independent and activity-dependent mechanisms work in concert to regulate neuronal growth, ensuring the formation of accurate synaptic connections. CPG15, a protein regulated by synaptic activity, functions as a cell-surface growth-promoting molecule in vivo. In Xenopus laevis, CPG15 enhanced dendritic arbor growth in projection neurons, with no effect on interneurons. CPG15 controlled growth of neighboring neurons through an intercellular signaling mechanism that requires its glycosylphosphatidylinositol link. CPG15 may represent a new class of activity-regulated, membrane-bound, growth-promoting proteins that permit exquisite spatial and temporal control of neuronal structure.},
	Author = {Nedivi, E. and Wu, G. Y. and Cline, H. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Signal Transduction;Animals;Image Processing, Computer-Assisted;Neuronal Plasticity;Microscopy, Confocal;Recombinant Proteins;research support, non-u.s. gov't;Genetic Vectors;Dendrites;Xenopus laevis;Superior Colliculus;21 Neurophysiology;Vaccinia virus;research support, u.s. gov't, p.h.s.;Neurons;Interneurons;24 Pubmed search results 2008;Membrane Proteins;Nerve Tissue Proteins;Glycosylphosphatidylinositols;Ligands},
	Month = {9},
	Nlm_Id = {0404511},
	Number = {5384},
	Organization = {Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA. nedivi\@cshl.org},
	Pages = {1863-6},
	Pubmed = {9743502},
	Title = {Promotion of dendritic growth by CPG15, an activity-induced signaling molecule},
	Uuid = {0E3393CA-3F59-4980-83D5-37B60631ABD1},
	Volume = {281},
	Year = {1998}}

@article{Negishi:2003,
	Abstract = {We established selective primary cultures of neurons, astrocytes, and microglial cells from cryopreserved fetal cerebral cortex of cynomolgus monkeys (Macaca fascicularis). At 14 days in serum-containing medium, the cell cultures of the fetal cerebral cortex consisted primarily of neurons, astrocytes, and floating microglial cells. At 21 days, we observed a small number of myelin basic protein (MBP)-positive oligodendrocytes. The addition of cytosine arabinoside (a selective DNA synthesis inhibitor) at 2 days in culture eliminated proliferative glial cells, allowing adequate numbers of neurons to survive selectively. A chemically defined serum-free medium successfully supported neuronal survival at a level equivalent to that supported by the serum-containing medium. Brain-derived neurotrophic factor (BDNF) significantly affected the survival of primate neurons. Glutamate induced a significant degree of neuronal cell death against primate neurons and MK-801, a selective N-methyl-D-aspartate receptor (NMDAR) antagonist, blocked cell death, which suggests that primate cortical neurons have NMDAR and the glutamate-induced cell toxicity is mediated by NMDAR. In the serum-free medium, type-1 astrocytes responded to dibutyryl cyclic AMP and showed a process-bearing morphology. The growth of type-1 astrocytes in the serum-free medium was stimulated by epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and hydrocortisone, which are known growth factors in rat type-1 astrocytes. Cultured microglial cells expressed CD68, a monocyte marker. Macrophage-colony stimulating factor (M-CSF) stimulated microglial cell growth in the serum-free medium. These selective primary culture systems of primate cerebral cortical cells will be useful in issues involving species specificity in neuroscience.},
	Author = {Negishi, Takayuki and Ishii, Yoshiyuki and Kyuwa, Shigeru and Kuroda, Yoichiro and Yoshikawa, Yasuhiro},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {Fetus;Dose-Response Relationship, Drug;Excitatory Amino Acid Antagonists;Animals;Culture Media, Serum-Free;Antigens, Differentiation, Myelomonocytic;Astrocytes;Cells, Cultured;Glutamic Acid;Comparative Study;Myelin Basic Proteins;Dizocilpine Maleate;Microglia;Microtubule-Associated Proteins;Antigens, CD;Macaca fascicularis;11 Glia;Immunosuppressive Agents;Cytarabine;Cyclic CMP;Cerebral Cortex;Neurons;Epidermal Growth Factor;Fibroblast Growth Factors;Cell Division;Cell Culture;Immunohistochemistry;Cell Death;Glial Fibrillary Acidic Protein},
	Month = {12},
	Nlm_Id = {7905558},
	Number = {1-2},
	Organization = {Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan. taka-u\@yayoi.club.ne.jp},
	Pages = {133-40},
	Pii = {S0165027003002681},
	Pubmed = {14659833},
	Title = {Primary culture of cortical neurons, type-1 astrocytes, and microglial cells from cynomolgus monkey (Macaca fascicularis) fetuses},
	Uuid = {9CA6F93F-572B-4D60-BFCB-6AE05199CCE2},
	Volume = {131},
	Year = {2003},
	url = {papers/Negishi_JNeurosciMethods2003.pdf}}

@article{Ness:2001,
	Abstract = {Hypoxia-ischemia (HI) is a leading cause of white matter damage, a major contributor to cerebral palsy in premature infants. Preferential white matter damage is believed to result from vulnerability of the immature oligodendrocyte (the pro-OL) to factors elevated during ischemic damage, such as oxygen free radicals and glutamate. In order to determine whether pro-OLs undergo apoptotic death after HI, we analyzed periventricular white matter OLs in P7 rats 4, 12 and 24 h after HI to analyze the time course and mode of cell death. DNA fragmentation was seen at 12 and 24 h of recovery after HI, representing a 17-fold increase over control. In addition, caspase-3 activation was found in NG2+ pro-OLs at 12 h. Electron-microscopic analysis of cell death in the white matter revealed a transition from early necrotic deaths to hybrid cell deaths to classical apoptosis between 4 and 24 h of recovery from HI. The delayed time course of apoptosis in pro-OLs supports the feasibility of interventions to improve clinical outcomes for newborns surviving birth asphyxia. 21481705 0378-5866 Journal Article},
	Author = {Ness, J. K. and Romanko, M. J. and Rothstein, R. P. and Wood, T. L. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Dev Neurosci},
	Keywords = {Pregnancy;Caspases/metabolism;Neurotoxins;Hypoxia-Ischemia, Brain/*pathology;Rats;Female;Animal;Rats, Wistar;G abstr;11 Glia;Oligodendroglia/enzymology/*pathology/ultrastructure;Cerebral Ventricles/pathology;Stem Cells/enzymology/*pathology/ultrastructure;*Apoptosis;Support, Non-U.S. Gov't;Cerebral Palsy/pathology;Support, U.S. Gov't, P.H.S.;Microscopy, Electron},
	Number = {3},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University, College of Medicine, Hershey, Pa 17033, USA.},
	Pages = {203-8},
	Pubmed = {11598321},
	Title = {Perinatal hypoxia-ischemia induces apoptotic and excitotoxic death of periventricular white matter oligodendrocyte progenitors},
	Uuid = {4988609D-536E-4216-8AE7-12E4DDA8A8F3},
	Volume = {23},
	Year = {2001},
	url = {papers/Ness_DevNeurosci2001.pdf}}

@article{Neuhaus:1994,
	Abstract = {Microglia develop in cultures initiated from disaggregated neopallial cells of newborn C3H/HeJ mice when the cultures are subjected to nutritional deprivation for 10 or more days (Hao et al: Int J Dev Neurosci 9:1-14, 1991). In the present experiments, the cultures were pulsed with BrdU for 3 hours at different times during incubation and then the cells were immunoreacted with antibodies against BrdU, GFAP, and CR3 receptor. The dividing cells (BrdU+) were found to be either GFAP+ or GFAP-, but not Mac-1+/BrdU+. Infection of proliferating cells after 2 or more days of incubation with replication-deficient retroviral vector containing E. coli lacZ reporter gene resulted in many labeled astroglia cell clones but no labeled microglia. However, when cells were infected right after disaggregation of neopallium, labeled Mac-1+ microglia were found. When Mac-1+ cells in a suspension of disaggregated neopallial cells were killed using complement mediated lysis before setting up the cultures, Mac-1+ microglia developed, in spite of the treatment. We conclude that in cultures initiated from mouse neopallium there are MAC-1-/GFAP- microglia progenitor cells which do not divide in nutritionally deprived cultures but can transform into Mac-1+ microglia under the influence of astroglia-derived trophic factors. Microglia, which become Mac-1+ (i.e., express CR3 receptor), proliferate extensively in the presence of CSF-1 (which is produced by astroglia).},
	Author = {Neuhaus, J. and Fedoroff, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Mice;Clone Cells;Globus Pallidus;Research Support, Non-U.S. Gov't;Glial Fibrillary Acidic Protein;Astrocytes;Retroviridae;Cell Division;Stem Cells;11 Glia;Microglia;Culture Media;Mice, Inbred C3H;Bromodeoxyuridine;24 Pubmed search results 2008;Animals;Escherichia coli},
	Medline = {94350462},
	Month = {5},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Department of Anatomy, University of Saskatchewan, Saskatoon, Canada.},
	Pages = {11-7},
	Pubmed = {8070891},
	Title = {Development of microglia in mouse neopallial cell cultures},
	Uuid = {9CB07530-796B-4B0A-A4F7-C7852F5D8ACD},
	Volume = {11},
	Year = {1994},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.440110104}}

@article{Neuhuber:2004,
	Abstract = {Bone marrow stromal cells (MSC), which represent a population of multipotential mesenchymal stem cells, have been reported to undergo rapid and robust transformation into neuron-like phenotypes in vitro following treatment with chemical induction medium including dimethyl sulfoxide (DMSO; Woodbury et al. [2002] J. Neurosci. Res. 96:908). In this study, we confirmed the ability of cultured rat MSC to undergo in vitro osteogenesis, chondrogenesis, and adipogenesis, demonstrating differentiation of these cells to three mesenchymal cell fates. We then evaluated the potential for in vitro neuronal differentiation of these MSC, finding that changes in morphology upon addition of the chemical induction medium were caused by rapid disruption of the actin cytoskeleton. Retraction of the cytoplasm left behind long processes, which, although strikingly resembling neurites, showed essentially no motility and no further elaboration during time-lapse studies. Similar neurite-like processes were induced by treating MSC with DMSO only or with actin filament-depolymerizing agents. Although process formation was accompanied by rapid expression of some neuronal and glial markers, the absence of other essential neuronal proteins pointed toward aberrantly induced gene expression rather than toward a sequence of gene expression as is required for neurogenesis. Moreover, rat dermal fibroblasts responded to neuronal induction by forming similar processes and expressing similar markers. These studies do not rule out the possibility that MSC can differentiate into neurons; however, we do want to caution that in vitro differentiation protocols may have unexpected, misleading effects. A dissection of molecular signaling and commitment events may be necessary to verify the ability of MSC transdifferentiation to neuronal lineages.},
	Author = {Neuhuber, Birgit and Gallo, Gianluca and Howard, Linda and Kostura, Lisa and Mackay, Alastair and Fischer, Itzhak},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Biological Markers;Cell Differentiation;Embryonic Induction;Animals;Cells, Cultured;Gene Expression Regulation, Developmental;Rats;Phenotype;Fibroblasts;Osteogenesis;Chondrogenesis;Neurites;08 Aberrant cell cycle;Microfilaments;Research Support, U.S. Gov't, P.H.S.;Bone Marrow Cells;Cell Lineage;Neurons;Actins;Adipocytes;Culture Media;Stromal Cells;Nerve Tissue Proteins;Growth Substances},
	Month = {7},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania 19129, USA.},
	Pages = {192-204},
	Pubmed = {15211586},
	Title = {Reevaluation of in vitro differentiation protocols for bone marrow stromal cells: disruption of actin cytoskeleton induces rapid morphological changes and mimics neuronal phenotype},
	Uuid = {4A92069A-85B0-4580-9B9F-7A7E2C3F64FD},
	Volume = {77},
	Year = {2004},
	url = {papers/Neuhuber_JNeurosciRes2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20147}}

@article{Neumann:2006,
	Abstract = {Many neurological insults are accompanied by a marked acute inflammatory reaction, involving the activation of microglia. Using a model of exogenous application of fluorescence-labeled BV2 microglia in pathophysiologically relevant concentrations onto organotypic hippocampal slice cultures, we investigated the specific effects of microglia on neuronal damage after ischemic injury. Neuronal cell death after oxygen-glucose deprivation (OGD) was determined by propidium iodide incorporation and Nissl staining. Migration and interaction with neurons were analyzed by time resolved 3-D two-photon microscopy. We show that microglia protect against OGD-induced neuronal damage and engage in close physical cell-cell contact with neurons in the damaged brain area. Neuroprotection and migration of microglia were not seen with integrin regulator CD11a-deficient microglia or HL-60 granulocytes. The induction of migration and neuron-microglia interaction deep inside the slice was markedly increased under OGD conditions. Lipopolysaccharide-prestimulated microglia failed to provide neuroprotection after OGD. Pharmacological interference with microglia function resulted in a reduced neuroprotection. Microglia proved to be neuroprotective even when applied up to 4 h after OGD, thus defining a "protective time window." In acute injury such as trauma or stroke, appropriately activated microglia may primarily have a neuroprotective role. Anti-inflammatory treatment within the protective time window of microglia would therefore be counterintuitive.},
	Author = {Neumann, and Gunzer, and Gutzeit, and Ullrich, and Reymann, and Dinkel,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {8804484},
	Pii = {05-4882fje},
	Pubmed = {16473887},
	Title = {Microglia provide neuroprotection after ischemia},
	Uuid = {624E6294-B752-4B99-A930-7F6968E54294},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.05-4882fje}}

@article{Neumann:2006a,
	Abstract = {Metachromatic leukodystrophy (MLD) is a lysosomal storage disease caused by deficiency of the enzyme arylsulfatase A (ARSA). MLD is characterized by progressive demyelination and neurological deficits. Treatment of MLD is still a challenge due to the fact that the blood-brain barrier is a major obstacle for most therapeutic substances. In this issue of the JCI, Biffi et al. report that genetically modified hematopoietic precursor cells transduced to overexpress ARSA and transplanted into mice with a targeted disruption of the murine Arsa gene (Arsa(-/-) mice) migrated into the CNS and cross-corrected brain ARSA deficiency (see the related article beginning on page 3070). Microglia served as a cellular vehicle to effectively deliver the enzyme to other brain cells while hepatocytes overexpressing ARSA increased plasma ARSA levels but failed to deliver ARSA into the CNS.},
	Author = {Neumann, Harald},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0021-9738},
	Journal = {J Clin Invest},
	Keywords = {Cell Differentiation;research support, non-u.s. gov't;Central Nervous System;Blood-Brain Barrier;Hematopoietic Stem Cells;11 Glia;Microglia;comment;Gene Therapy;Animals;Leukodystrophy, Metachromatic;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {7802877},
	Number = {11},
	Organization = {Neural Regeneration Unit, Institute of Reconstructive Neurobiology, University of Bonn, and LIFE & BRAIN Center and Hertie Foundation, Bonn, Germany. hneuman1\@uni-bonn.de},
	Pages = {2857-60},
	Pubmed = {17080190},
	Title = {Microglia: a cellular vehicle for CNS gene therapy},
	Uuid = {6C3D6D31-1EB2-4000-893E-6883E0479859},
	Volume = {116},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1172/JCI30230}}

@article{Neumann:2002,
	Abstract = {In response to injury and inflammation of the CNS, brain cells including microglia and astrocytes secrete tumor necrosis factor-alpha (TNF). This pro-inflammatory cytokine has been implicated in both neuronal cell death and survival. We now provide evidence that TNF affects the formation of neurites. Neurons cultured on astrocytic glial cells exhibited reduced outgrowth and branching of neurites after addition of recombinant TNF or prestimulation of glial cells to secrete TNF. This effect was absent in neurons of TNF receptor-deficient mice cultured on prestimulated glia of wild-type mice and was reverted by blocking TNF with soluble TNF receptor IgG fusion protein. TNF activated in neurons the small GTPase RhoA. By inactivating Rho with C3 transferase, the inhibitory effect of TNF on neurite outgrowth and branching was abolished. These results suggest that glia-derived TNF, as part of an injury or inflammatory process, can inhibit neurite elongation and branching during development and regeneration.},
	Author = {Neumann, Harald and Schweigreiter, Rudiger and Yamashita, Toshihide and Rosenkranz, Katja and Wekerle, Hartmut and Barde, Yves-Alain A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Research Support, Non-U.S. Gov't;Animals;Cells, Cultured;Coculture Techniques;Tumor Necrosis Factor-alpha;Beta;Interferon Type II;Antigens, CD;Cell Count;Neurites;Hippocampus;Mice, Inbred C57BL;11 Glia;Receptors, Tumor Necrosis Factor;Reverse Transcriptase Polymerase Chain Reaction;rhoA GTP-Binding Protein;Receptors, Tumor Necrosis Factor, Type II;Mice, Knockout;Neuroglia;Interleukin-1;Neurons;Botulinum Toxins;Mice;ADP Ribose Transferases;Receptors, Tumor Necrosis Factor, Type I},
	Medline = {21683824},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {3},
	Organization = {Departments of Neuroimmunology and Neurobiochemistry, Max-Planck Institute of Neurobiology, 82152 Martinsried, Germany.},
	Pages = {854-62},
	Pii = {22/3/854},
	Pubmed = {11826115},
	Title = {Tumor necrosis factor inhibits neurite outgrowth and branching of hippocampal neurons by a rho-dependent mechanism},
	Uuid = {A699FC32-F904-4A3E-AF33-E2C61752CECD},
	Volume = {22},
	Year = {2002}}

@article{Neumann:2008,
	Abstract = {Microglial cells maintain the immunological integrity of the healthy brain and can exert protection from traumatic injury. During ischemic tissue damage such as stroke, peripheral immune cells acutely infiltrate the brain and may exacerbate neurodegeneration. Whether and how microglia can protect from this insult is unknown. Polymorphonuclear neutrophils (PMNs) are a prominent immunologic infiltrate of ischemic lesions in vivo. Here, we show in organotypic brain slices that externally applied invading PMNs massively enhance ischemic neurotoxicity. This, however, is counteracted by additional application of microglia. Time-lapse imaging shows that microglia exert protection by rapid engulfment of apoptotic, but, strikingly, also viable, motile PMNs in cell culture and within brain slices. PMN engulfment is mediated by integrin- and lectin-based recognition. Interference with this process using RGDS peptides and N-acetyl-glucosamine blocks engulfment of PMNs and completely abrogates the neuroprotective function of microglia. Thus, engulfment of invading PMNs by microglia may represent an entirely new mechanism of CNS immune privilege.},
	Author = {Neumann, Jens and Sauerzweig, Steven and R{\"o}nicke, Raik and Gunzer, Frank and Dinkel, Klaus and Ullrich, Oliver and Gunzer, Matthias and Reymann, Klaus G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Neurons;Phagocytosis;24 Pubmed search results 2008;research support, non-u.s. gov't;Central Nervous System;Rats;Rats, Wistar;Microglia;comparative study;Neutrophils;Animals;Cell Movement;Cells, Cultured;Immunity, Cellular;Mice},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {23},
	Organization = {Leibniz Institute for Neurobiology, Project Group Neuropharmacology, Otto von Guericke University Magdeburg, 39118 Magdeburg, Germany. jens.neumann\@sciencetoday.de},
	Pages = {5965-75},
	Pii = {28/23/5965},
	Pubmed = {18524901},
	Title = {Microglia cells protect neurons by direct engulfment of invading neutrophil granulocytes: a new mechanism of CNS immune privilege},
	Uuid = {9C7C341F-3891-479C-94D2-D8C691A75BFB},
	Volume = {28},
	Year = {2008},
	url = {papers/Neumann_JNeurosci2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0060-08.2008}}

@article{Neves:2008,
	Abstract = {The role of cell size and shape in controlling local intracellular signaling reactions, and how this spatial information originates and is propagated, is not well understood. We have used partial differential equations to model the flow of spatial information from the beta-adrenergic receptor to MAPK1,2 through the cAMP/PKA/B-Raf/MAPK1,2 network in neurons using real geometries. The numerical simulations indicated that cell shape controls the dynamics of local biochemical activity of signal-modulated negative regulators, such as phosphodiesterases and protein phosphatases within regulatory loops to determine the size of microdomains of activated signaling components. The model prediction that negative regulators control the flow of spatial information to downstream components was verified experimentally in rat hippocampal slices. These results suggest a mechanism by which cellular geometry, the presence of regulatory loops with negative regulators, and key reaction rates all together control spatial information transfer and microdomain characteristics within cells.},
	Author = {Neves, Susana R. and Tsokas, Panayiotis and Sarkar, Anamika and Grace, Elizabeth A. and Rangamani, Padmini and Taubenfeld, Stephen M. and Alberini, Cristina M. and Schaff, James C. and Blitzer, Robert D. and Moraru, Ion I. and Iyengar, Ravi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {Models, Biological;Cyclic AMP;Fetus;Hippocampus;Rats;Metabolic Networks and Pathways;Feedback, Biochemical;Aplysia;research support, n.i.h., extramural;Cell Shape;MAP Kinase Signaling System;Animals;Isoproterenol;Receptors, Adrenergic, beta-2;Neurons;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {4},
	Organization = {Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1215, New York, NY 10029, USA.},
	Pages = {666-80},
	Pii = {S0092-8674(08)00517-5},
	Pubmed = {18485874},
	Title = {Cell shape and negative links in regulatory motifs together control spatial information flow in signaling networks},
	Uuid = {7AAAD56D-CD98-4D9F-A4CD-F07D5AE104AD},
	Volume = {133},
	Year = {2008},
	url = {papers/Neves_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.04.025}}

@article{Ng:2001,
	Abstract = {PURPOSE: To explore the effects of light exposure and deprivation on the distribution and function of microglia in the subretinal space of mice. METHODS: Using a monoclonal antibody, 5D4, that identifies resting, ramified microglia, the distribution and density of microglia in the retina, and the subretinal space were determined by confocal microscopy and by immunohistochemistry of cryopreserved sections of eyes of albino and pigmented mice exposed to diverse levels of light, ranging from complete darkness to intense brightness. Axotomized retinal ganglion cells were retrograde labeled by fluorescent tracer to determine whether the marker colocalizes to 5D4+ cells. Electron microscopy was used to evaluate microglia for evidence of phagocytosis. RESULTS: 5D4+ microglia in pigmented eyes were limited to the inner retinal layers, but in albino eyes 5D4+ cells were found in the outer retinal layers and subretinal space as well. The subretinal space of eyes of albino mice raised from birth in complete darkness contained few 5D4+ cells, but exposure to light caused the rapid accumulation of 5D4+ cells at this site. 5D4+ cell density in the subretinal space correlated directly with intensity of ambient light. Retrograde labeling of axotomized ganglion cells resulted in 5D4+ cells in the subretinal space that contained the retrograde label. Subretinal microglia contained phagocytized rod outer segment discs. On intense light exposure, 5D4+ cells adopted an active morphology, but failed to express class II major histocompatibility complex (MHC) molecules. CONCLUSIONS: Light exposure induced retinal microglia migration into the subretinal space in albino mice. Subretinal microglia appeared to augment through phagocytosis the capacity of pigment epithelium to take up the photoreceptor debris of light toxicity. The unexpected presence of these cells in the subretinal space raises questions concerning their potential contribution to immune privilege in this space and to the fate of retinal transplants.},
	Author = {Ng, T. F. and Streilein, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0146-0404},
	Journal = {Invest Ophthalmol Vis Sci},
	Keywords = {Retina;Phagocytosis;Animals;Microglia;Cell Count;Cell Movement;Reference Values;Not relevant;11 Glia;Eye Color;Support, Non-U.S. Gov't;Mice, Inbred Strains;Antibodies, Monoclonal;Light;Albinism;Support, U.S. Gov't, P.H.S.;Mice;Dose-Response Relationship, Radiation},
	Medline = {21583626},
	Month = {12},
	Nlm_Id = {7703701},
	Number = {13},
	Organization = {Department of Ophthalmology, Schepens Eye Research Institute, 20 Staniford Street, Boston, MS 02114, USA.},
	Pages = {3301-10},
	Pubmed = {11726637},
	Title = {Light-induced migration of retinal microglia into the subretinal space},
	Uuid = {E32E389B-D247-4842-B2D2-4D0DC7FDF83E},
	Volume = {42},
	Year = {2001}}

@article{Ng:2005,
	Abstract = {Neurogenesis persists in the olfactory bulb (OB) of the adult mammalian brain. New interneurons are continually added to the OB from the subventricular zone (SVZ) via the rostral migratory stream (RMS). Here we show that secreted prokineticin 2 (PK2) functions as a chemoattractant for SVZ-derived neuronal progenitors. Within the OB, PK2 may also act as a detachment signal for chain-migrating progenitors arriving from the RMS. PK2 deficiency in mice leads to a marked reduction in OB size, loss of normal OB architecture, and the accumulation of neuronal progenitors in the RMS. These findings define an essential role for G protein-coupled PK2 signaling in postnatal and adult OB neurogenesis.},
	Author = {Ng, Kwan L. and Li, Jia-Da D. and Cheng, Michelle Y. and Leslie, Frances M. and Lee, Alex G. and Zhou, Qun-Yong Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Signal Transduction;Animals;Dopamine;Coculture Techniques;Rats;Chemotaxis;Apoptosis;Brain;Cell Count;Rats, Sprague-Dawley;Receptors, G-Protein-Coupled;Mice, Inbred C57BL;Gastrointestinal Hormones;Cell Proliferation;Neuropeptides;Olfactory Bulb;Cerebral Ventricles;Cell Adhesion;Cell Line;Neurons;Mice;Interneurons;24 Pubmed search results 2008;Chemotactic Factors;Stem Cells;Gene Expression},
	Month = {6},
	Nlm_Id = {0404511},
	Number = {5730},
	Organization = {Department of Pharmacology, University of California-Irvine (UCI), Irvine, CA 92697, USA.},
	Pages = {1923-7},
	Pii = {308/5730/1923},
	Pubmed = {15976302},
	Title = {Dependence of olfactory bulb neurogenesis on prokineticin 2 signaling},
	Uuid = {E3D2E2D6-3C03-44E0-8527-F4624628DFED},
	Volume = {308},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1112103}}

@article{Nguyen-Ba-Charvet:2004,
	Abstract = {The subventricular zone (SVZ) contains undifferentiated cells, which proliferate and generate olfactory bulb (OB) interneurons. Throughout life, these cells leave the SVZ and migrate along the rostral migratory stream (RMS) to the OB where they differentiate. In vitro, the septum and the choroid plexus (CP) secrete repulsive factors that could orient the migration of OB precursors. Slit1 and Slit2, two known chemorepellents for developing axons, can mimic this effect. We show here that the Slit receptors Robo2 and Robo3/Rig-1 are expressed in the SVZ and the RMS and that Slit1 and Slit2 are still present in the adult septum. Using Slit1/2-deficient mice, we found that Slit1 and Slit2 are responsible for both the septum and the CP repulsive activity in vitro. In adult mice lacking Slit1, small chains of SVZ-derived cells migrate caudally into the corpus callosum, supporting a role for Slits in orienting the migration of SVZ cells. Surprisingly, in adult mice, Slit1 was also expressed by type A and type C cells in the SVZ and RMS, suggesting that Slit1 could act cell autonomously. This hypothesis was tested using cultures of SVZ explants or isolated neurospheres from Slit1-/- or Slit1+/- mice. In both types of cultures, the migration of SVZ cells was altered in the absence of Slit1. This suggests that the regulation of the migration of OB precursors by Slit proteins is complex and not limited to repulsion. 1529-2401 Journal Article},
	Author = {Nguyen-Ba-Charvet, K. T. and Picard-Riera, N. and Tessier-Lavigne, M. and Baron-Van Evercooren, A. and Sotelo, C. and Chedotal, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {J Neurosci},
	Keywords = {B pdf;02 Adult neurogenesis migration},
	Number = {6},
	Organization = {Institut National de la Sante et de la Recherche Medicale U106, Batiment de Pediatrie, Hopital de la Salpetriere, 75013 Paris, France.},
	Pages = {1497-506},
	Title = {Multiple roles for slits in the control of cell migration in the rostral migratory stream},
	Uuid = {09FE2BF0-E474-4AE0-9A05-BF4AF1F5AA94},
	Volume = {24},
	Year = {2004},
	url = {papers/Nguyen-Ba-Charvet_JNeurosci2004.pdf}}

@article{Nicholas:2002,
	Abstract = {Biodegradable microspheres made with poly-[D,L-lactide-co-glycolide] represent an evolving technology for drug delivery into the central nervous system. Even though these microspheres have been shown to be engulfed by astrocytes in vitro, the purpose of the present study was to track the fate of biodegradable microspheres in vivo. This was accomplished using microspheres containing the fluorescent dye coumarin-6 followed 1 day, 1 week and 1 month after intracerebral injections of this material were made into the rat brain. Using dual color immunohistochemistry and antisera against glial fibrillary acidic protein for astrocytes versus phosphotyrosine for microglia, results demonstrate that phagocytosis of small coumarin-containing microspheres <7.5 microm in diameter was primarily by microglia in vivo during the first week post-injection. In contrast, only a small minority of these microspheres appeared to be engulfed by astrocytes.},
	Author = {Nicholas, Anthony P. and McInnis, Carey and Gupta, Kiran B. and Snow, William W. and Love, Darryl F. and Mason, David W. and Ferrell, Teresa M. and Staas, Jay K. and Tice, Thomas R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Biocompatible Materials;Research Support, Non-U.S. Gov't;Rats, Sprague-Dawley;Lactic Acid;Polyglycolic Acid;Rats;Polymers;Astrocytes;11 Glia;Injections, Intraventricular;Microspheres;Animals;Brain;Male},
	Medline = {21948072},
	Month = {4},
	Nlm_Id = {7600130},
	Number = {2},
	Organization = {Department of Neurology, University of Alabama at Birmingham and the Birmingham Veterans Administration Medical Center, 619 19th Street South, Birmingham, AL 35249-7340, USA. tony\@email.neuro.uab.edu},
	Pages = {85-8},
	Pii = {S0304394001025344},
	Pubmed = {11950499},
	Title = {The fate of biodegradable microspheres injected into rat brain},
	Uuid = {E7C81010-1129-4B6A-9F18-FE00AA8DA8A7},
	Volume = {323},
	Year = {2002}}

@article{Nicole:2001,
	Abstract = {The glial cell line-derived neurotrophic factor (GDNF) is first characterized for its trophic activity on dopaminergic neurons. Recent data suggested that GDNF could modulate the neuronal death induced by ischemia. The purpose of this study was to characterize the influence of GDNF on cultured cortical neurons subjected to two paradigms of injury (necrosis and apoptosis) that have been identified during cerebral ischemia and to determine the molecular mechanisms involved. First, we demonstrated that both neurons and astrocytes express the mRNA and the protein for GDNF and its receptor complex (GFRalpha-1 and c-Ret). Next, we showed that the application of recombinant human GDNF to cortical neurons and astrocytes induces the activation of the MAP kinase (MAPK) pathway, as visualized by an increase in the phosphorylated forms of extracellular signal-regulated kinases (ERKs). Thereafter, we demonstrated that GDNF fails to prevent apoptotic neuronal death but selectively attenuates slowly triggered NMDA-induced excitotoxic neuronal death via a direct effect on cortical neurons. To further characterize the neuroprotective mechanisms of GDNF against NMDA-mediated neuronal death, we showed that a pretreatment with GDNF reduces NMDA-induced calcium influx. This effect likely results from a reduction of NMDA receptor activity rather than an enhanced buffering or extrusion capacity for calcium. Finally, we also demonstrated that an ERKs activation pathway is necessary for GDNF-mediated reduction of the NMDA-induced calcium response. Together, these results describe a novel mechanism by which the activation of MAPK induced by GDNF modulates NMDA receptor activity, a mechanism that could be responsible for the neuroprotective effect of GDNF in acute brain injury.},
	Author = {Nicole, O. and Ali, C. and Docagne, F. and Plawinski, L. and MacKenzie, E. T. and Vivien, D. and Buisson, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;Brain Ischemia/metabolism;Calcium/*metabolism;Glycosylphosphatidylinositols/metabolism;Apoptosis/drug effects;Mitogen-Activated Protein Kinases/metabolism;Nerve Tissue Proteins/genetics/*metabolism/pharmacology;07 Excitotoxicity Apoptosis;Animal;N-Methylaspartate/antagonists &inhibitors/*metabolism/toxicity;Membrane Proteins/metabolism;MAP Kinase Signaling System/drug effects/*physiology;Receptor Protein-Tyrosine Kinases/genetics/metabolism;Neurons/cytology/drug effects/metabolism;Chelating Agents;Mice, Inbred Strains;Oxidation-Reduction/drug effects;Neuroprotective Agents/*metabolism/pharmacology;Proto-Oncogene Proteins/genetics/metabolism;Support, Non-U.S. Gov't;Phosphorylation/drug effects;Astrocytes/cytology/drug effects/metabolism;C;Cerebral Cortex/cytology/drug effects/metabolism;04 Adult neurogenesis factors;Mice;RNA, Messenger/metabolism;Necrosis},
	Number = {9},
	Organization = {Universite de Caen, Unite Mixte de Recherche, Centre National de la Recherche Scientifique 6551, 14074 Caen Cedex, France.},
	Pages = {3024-33.},
	Title = {Neuroprotection mediated by glial cell line-derived neurotrophic factor: involvement of a reduction of NMDA-induced calcium influx by the mitogen-activated protein kinase pathway},
	Uuid = {1BCEA2D0-EE23-42A0-BE2D-67A2F1775D38},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11312287%20http://www.jneurosci.org/cgi/content/full/21/9/3024%20http://www.jneurosci.org/cgi/content/abstract/21/9/3024}}

@article{Nicolini:2002,
	Abstract = {Transfer of therapeutic genes to human hematopoietic stem cells (HSCs) using complex vectors at clinically relevant efficiencies remains a major challenge. Recently we described a stable retroviral vector that sustains long-term expression of green fluorescent protein (GFP) and a human beta-globin gene in the erythroid progeny of transduced murine HSCs. We now report the efficient transduction of primitive human CD34(+) fetal liver or cord blood cells with this vector and expression of the beta-globin transgene in the erythroid progeny of these human cells for at least 2 months. After growth factor prestimulation and then a 2- to 3-day exposure to the virus, 35\%to 55\%GFP(+) progeny were seen in assays of transduced colony-forming cells, primitive erythroid precursors that generate large numbers of glycophorin A(+) cells in 3-week suspension cultures, and 6-week long-term culture-initiating cells. In immunodeficient mice injected with unselected infected cells, 5\%to 15\%of the human cells regenerated in the marrow (including the erythroid cells) were GFP(+) 3 and 6 weeks after transplantation. Importantly, the numbers of GFP(+) human lymphoid and either granulopoietic or erythroid cells in individual mice 6 weeks after transplantation were significantly correlated, indicative of the initial transduction of human multipotent cells with in vivo repopulating activity. Expression of the transduced beta-globin gene in human cells obtained directly from the mice or after their differentiation into erythroid cells in vitro was demonstrated by reverse transcriptase-polymerase chain reaction using specific primers. These experiments represent a significant step toward the realization of a gene therapy approach for human beta-globin gene disorders.},
	Author = {Nicolini, Franck E. and Imren, Suzan and Oh, Il-Hoan H. and Humphries, R. Keith and Leboulch, Philippe and Fabry, Mary E. and Nagel, Ronald L. and Eaves, Connie J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Erythrocytes;Transgenes;Cell Differentiation;Animals;Globins;Cells, Cultured;Humans;Transfection;Liver;Retroviridae;Antigens, CD34;11 Glia;Reverse Transcriptase Polymerase Chain Reaction;Hematopoietic Stem Cell Transplantation;Green Fluorescent Proteins;Research Support, U.S. Gov't, P.H.S.;Genetic Vectors;Gene Therapy;Mice;Erythroid Progenitor Cells;Luminescent Proteins;Fetal Blood;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {22144000},
	Month = {8},
	Nlm_Id = {7603509},
	Number = {4},
	Organization = {Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada.},
	Pages = {1257-64},
	Pubmed = {12149206},
	Title = {Expression of a human beta-globin transgene in erythroid cells derived from retrovirally transduced transplantable human fetal liver and cord blood cells},
	Uuid = {539FF2CB-6977-403F-AD4A-54DC75F9E36C},
	Volume = {100},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2002-02-0599}}

@article{Nieoullon:2005,
	Abstract = {We previously showed that deletion of the cell surface molecule mCD24 resulted in an increased proliferation in adult subventricular zone (SVZ). Here, we report an increased PSA-NCAM+/TuJ1- population in the mCD24-/- in vivo SVZ as well as in vitro neurospheres. Isolated in vitro, these cells were able to generate neurospheres. Proliferation studies, using BrdU incorporation, showed an increased proliferation in P7 mCD24-/- SVZ and neurospheres. Using electron microscopy, the same cell types were identified in the in vivo SVZ as well as in vitro neurospheres from the WT and mCD24-/- mice. In mixed neurospheres, formed with WT and EGFP/KO cells (enhanced green fluorescent protein mCD24-/-), the WT environment was able to control the proliferation rate of the mCD24-/- cells, but was unable to regulate their differentiation. We concluded that mCD24 acts cell nonautonomously to regulate transit-amplifying cells proliferation and/or differentiation.},
	Author = {Nieoullon, Vincent and Belvindrah, Richard and Rougon, Genevi\`{e}ve and Chazal, Genevi\`{e}ve},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Cell Differentiation;Animals;Cells, Cultured;Tubulin;Antigens, CD;Mice, Inbred C57BL;Green Fluorescent Proteins;Cell Proliferation;Male;P-Selectin;Antigens, CD24;Animals, Newborn;Cell Lineage;Membrane Glycoproteins;Mice, Knockout;Neurons;Sialic Acids;Microscopy, Electron, Transmission;Mice;Neural Cell Adhesion Molecule L1;24 Pubmed search results 2008;Stem Cells;Lateral Ventricles;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {9100095},
	Number = {3},
	Organization = {Neurogen\`{e}se et Morphogen\`{e}se dans le D{\'e}veloppement et chez l'Adulte/Institut de Biologie du D{\'e}veloppement de Marseille, Centre National de la Recherche Scientifique, Marseilles, France.},
	Pages = {462-74},
	Pii = {S1044-7431(04)00248-9},
	Pubmed = {15737737},
	Title = {mCD24 regulates proliferation of neuronal committed precursors in the subventricular zone},
	Uuid = {6828E463-2981-4F9F-A7EA-500D01A5F239},
	Volume = {28},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2004.10.007}}

@article{Niewmierzycka:2005,
	Abstract = {Integrin-linked kinase (Ilk) is a scaffold and kinase that links integrin receptors to the actin cytoskeleton and to signaling pathways involved in cell adhesion, migration, and extracellular matrix deposition. Targeted deletion of Ilk from embryonic mouse dorsal forebrain neuroepithelium results in severe cortical lamination defects resembling cobblestone (type II) lissencephaly. Defects in adult mutants include neuronal invasion of the marginal zone, downward displacement of marginal zone components, fusion of the cerebral hemispheres, and scalloping of the dentate gyrus. These lesions are associated with abundant astrogliosis and widespread fragmentation of the basal lamina at the cortical surface. During cortical development, neuronal ectopias are associated with severe disorganization of radial glial processes and displacement of Cajal-Retzius cells. Lesions are not seen when Ilk is specifically deleted from embryonic neurons. Interestingly, targeted Ilk deletion has no effect on proliferation or survival of cortical cells or on phosphorylation of two Ilk substrates, Pkb/Akt and Gsk-3beta, suggesting that Ilk does not regulate cortical lamination via these enzymes. Instead, Ilk acts in vivo as a major intracellular mediator of integrin-dependent basal lamina formation. This study demonstrates a critical role for Ilk in cortical lamination and suggests that Ilk-associated pathways are involved in the pathogenesis of cobblestone lissencephalies.},
	Author = {Niewmierzycka, Agnieszka and Mills, Julia and St-Arnaud, Rene and Dedhar, Shoukat and Reichardt, Louis F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {30},
	Organization = {Department of Pathology, University of California, San Francisco, California 94143, USA.},
	Pages = {7022-31},
	Pii = {25/30/7022},
	Pubmed = {16049178},
	Title = {Integrin-linked kinase deletion from mouse cortex results in cortical lamination defects resembling cobblestone lissencephaly},
	Uuid = {AD8B1558-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {25},
	Year = {2005},
	url = {papers/Niewmierzycka_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1695-05.2005}}

@article{Ninkovic:2007,
	Abstract = {Adult neurogenesis is restricted to two distinct areas of the mammalian brain: the olfactory bulb (OB) and the dentate gyrus (DG). Despite its spatial restriction, adult neurogenesis is of crucial importance for sensory processing and learning and memory. Although it has been shown that tens of thousands of new neurons arrive in the OB and DG every day with about half of them surviving after integration, the total contribution of adult neurogenesis to the pre-existing network remains mostly unknown. This is because of previous approaches labeling only a small proportion of adult-generated neurons. Here, we used genetic fate mapping to follow the majority of adult-generated neurons over long periods. Our data demonstrate two distinct modes of neuron addition to the pre-existing network. In the glomerular layer of the OB, there is a constant net addition of adult-generated neurons reaching a third of the total neuronal population within 9 months. In contrast, adult neurogenesis contributes to only a minor fraction of the entire neuronal network in the granular cell layer of the OB and the DG. Although the fraction of adult generated neurons can be further increased by an enriched environment, it still remains a minority of the neuronal network in the DG. Thus, neuron addition is distinct and tightly regulated in the neuronal networks that incorporate new neurons life long.},
	Author = {Ninkovic, Jovica and Mori, Tetsuji and G{\"o}tz, Magdalena},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {40},
	Organization = {Institute for Stem Cell Research, Gesellschaft f{\"u}r Strahlenforschung-National Research Institute for Environment and Health, 85764 Neuherberg/Munich, Germany.},
	Pages = {10906-11},
	Pii = {27/40/10906},
	Pubmed = {17913924},
	Title = {Distinct modes of neuron addition in adult mouse neurogenesis},
	Uuid = {2090195B-EEBC-4C7D-BA9C-212F3FEE12AB},
	Volume = {27},
	Year = {2007},
	url = {papers/Ninkovic_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2572-07.2007}}

@article{Nishikura:2001,
	Abstract = {One of the many intriguing features of gene silencing by RNA interference is the apparent catalytic nature of the phenomenon. New biochemical and genetic evidence now shows that an RNA-directed RNA polymerase chain reaction, primed by siRNA, amplifies the interference caused by a small amount of "trigger"dsRNA. 0092-8674 Journal Article Review Review, Tutorial},
	Author = {Nishikura, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Cell},
	Keywords = {Drosophila melanogaster/embryology/genetics;Gene Targeting;Animals;Plant Proteins/physiology;RNA, Untranslated/genetics/*physiology;Polymerase Chain Reaction/methods;Endoribonucleases/physiology;RNA Replicase/*physiology;23 Technique;Models, Genetic;Insect Proteins/physiology;RNA, Small Interfering;RNA, Messenger/*antagonists &inhibitors/genetics/metabolism;RNA Processing, Post-Transcriptional;RNA, Double-Stranded/pharmacology/physiology;T abstr;Cell-Free System;Sequence Homology, Nucleic Acid;Gene Silencing/*physiology;Ribonuclease III},
	Number = {4},
	Organization = {The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA. kazuko\@wistar.upenn.edu},
	Pages = {415-8},
	Pubmed = {11719182},
	Title = {A short primer on RNAi: RNA-directed RNA polymerase acts as a key catalyst},
	Uuid = {E6DF3360-200D-42C2-822D-BAFF630C7C68},
	Volume = {107},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11719182}}

@article{Nishiyama:2002,
	Abstract = {Cells that express the NG2 proteoglycan (NG2+ cells) comprise a unique population of glial cells in the central nervous system. While there is no question that some NG2+ cells differentiate into oligodendrocytes during development, the persistence of numerous NG2+ cells in the mature CNS has raised questions about their identity, relation to other CNS cell types, and functions besides their progenitor role. NG2+ cells also express the alpha receptor for platelet-derived growth factor (PDGF alphaR), a receptor that mediates oligodendrocyte progenitor proliferation during development. Antigenically, NG2+ cells are distinct from fibrous and protoplasmic astrocytes, resting microglia, and mature oligodendrocytes. Therefore, we propose the term polydendrocytes to refer to all NG2-expressing glial cells in the CNS parenchyma. This distinguishes them from the classical glial cell types and identifies them as the fourth major glial population in the CNS. Recent observations suggest that polydendrocytes are complex cells that physically and functionally interact with other cell types in the CNS. Committed oligodendrocyte progenitor cells arise from restricted foci in the ventral ventricular zone in both spinal cord and brain. It remains to be clarified whether there are multiple sources of oligodendrocytes, and if so whether polydendrocytes (NG2+ cells) represent progenitor cells of all oligodendrocyte lineages. Proliferation of NG2+ cells during early development appears to be dependent on PDGF, but the regulatory mechanisms that govern NG2+ cell proliferation in the mature CNS remain unknown. Pulse-chase labeling with bromodeoxyuridine indicates that polydendrocytes that proliferate in the postnatal spinal cord differentiate into oligodendrocytes. Novel experimental approaches are being developed to further elucidate the functional properties and differentiation potential of polydendrocytes. 0300-4864 Journal Article},
	Author = {Nishiyama, A. and Watanabe, M. and Yang, Z. and Bu, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neurocytol},
	Keywords = {11 Glia;G pdf},
	Number = {6-7},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, 3107 Horsebarn Hill Road, Unit 4156, Storrs, CT 06269-4156, USA. akiko.nishiyama\@uconn.edu},
	Pages = {437-55},
	Pubmed = {14501215},
	Title = {Identity, distribution, and development of polydendrocytes: NG2-expressing glial cells},
	Uuid = {157B3793-5E2D-4E12-959A-07E8A17571B0},
	Volume = {31},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14501215}}

@article{Nishiyama:1999,
	Abstract = {We describe a major glial cell population in the central nervous system (CNS) that can be identified by the expression of 2 cell surface molecules, the NG2 proteoglycan and the alpha receptor for platelet-derived growth factor (PDGF alphaR). In vitro and in the developing brain in vivo, NG2 and PDGF alphaR are expressed on oligodendrocyte progenitor cells but are down-regulated as the progenitor cells differentiate into mature oligodendrocytes. In the mature CNS, numerous NG2+/PDGF alphaR+ cells with extensive arborization of their cell processes are found ubiquitously long after oligodendrocytes are generated. NG2+ cells in the mature CNS do not express antigens specific to mature oligodendrocytes, astrocytes, microglia, or neurons, suggesting that they are a novel population of glial cells. Recently NG2+ cells in the adult CNS have been shown to undergo proliferation and morphological changes in response to a variety of stimuli, such as demyelination and inflammation, suggesting that they are dynamic cells capable of responding to changes in the environment. Furthermore, high levels of NG2+ and PDGF alphaR are expressed on oligodendroglioma cells, raising the possibility that the NG2+/PDGF alphaR+ cells in the mature CNS contribute to glial neoplasm. 0022-3069 Journal Article Review Review, Tutorial},
	Author = {Nishiyama, A. and Chang, A. and Trapp, B. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Proteoglycans/*analysis;Antigens/*analysis;Brain Diseases/pathology;Brain/*cytology/pathology;Neuroglia/*chemistry/*cytology;11 Glia;Mice, Jimpy;Support, U.S. Gov't, P.H.S.;Animals;Support, Non-U.S. Gov't;Age Factors;Mice;G},
	Number = {11},
	Organization = {Department of Neurosciences, The Lerner Research Institute, Cleveland Clinic Foundation, Ohio, USA.},
	Pages = {1113-24},
	Pubmed = {10560654},
	Title = {NG2+ glial cells: a novel glial cell population in the adult brain},
	Uuid = {EE9FA190-1B87-4E50-B5CF-539E62A333C5},
	Volume = {58},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10560654}}

@article{Niwa:1983,
	Abstract = {Expression and DNA methylation of the Moloney murine leukemia virus (M-MuLV) genome were investigated in murine teratocarcinoma cells after virus infection. The newly acquired viral genome was devoid of methylation, yet its expression was repressed. The integrated viral genome in undifferentiated teratocarcinoma cells was methylated within 15 days after infection. Although 5-azacytidine decreased the level of DNA methylation, it did not activate M-MuLV in undifferentiated cells. Activation by 5-azacytidine occurred only in differentiated teratocarcinoma cells. Thus two independent mechanisms seem to regulate gene expression during the course of differentiation. The first mechanism operates in undifferentiated cells to block expression of M-MuLV and other exogeneously acquired viral genes, such as SV40 and polyoma virus, and does not depend on DNA methylation. The second mechanism relates only to differentiated cells and represses expression of genes in which DNA is methylated.},
	Author = {Niwa, O. and Yokota, Y. and Ishida, H. and Sugahara, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Transcription, Genetic;Teratoma;Cell Differentiation;Animals;Gene Expression Regulation;Transfection;Cell Cycle;15 Retrovirus mechanism;Methylation;Azacitidine;Genes, Viral;Cell Line;Moloney murine leukemia virus;Recombination, Genetic;DNA, Viral;Mice;24 Pubmed search results 2008;Bromodeoxyuridine;Tretinoin;Research Support, Non-U.S. Gov't},
	Medline = {83180409},
	Month = {4},
	Nlm_Id = {0413066},
	Number = {4},
	Pages = {1105-13},
	Pii = {0092-8674(83)90294-5},
	Pubmed = {6188535},
	Title = {Independent mechanisms involved in suppression of the Moloney leukemia virus genome during differentiation of murine teratocarcinoma cells},
	Uuid = {43FB7583-F3B3-4A0D-9E94-CF3B304B9937},
	Volume = {32},
	Year = {1983}}

@article{Noble:2003,
	Abstract = {Studies on the development of cortical oligodendrocytes indicate that although general principles that apply to other parts of the CNS are applicable, there are important differences that appear to be critical to the analysis of this lineage in the cortex. Herein, we review previous studies demonstrating that oligodendrocyte-type-2 astrocyte progenitor cells (or oligodendrocyte precursor cells; aka O-2A/OPCs) of the developing postnatal cortex exhibit a striking cell-intrinsic bias towards undergoing prolonged self-renewal in the relative absence of oligodendrocyte generation [Power et al., Dev Biol 2002;245:362-375]. This phenotype is quite distinct from that observed in comparable cells isolated from the optic tract. This predilection for self-renewal is associated with a lessened response to inducers of oligodendrocyte generation and of possible mechanistic importance in regards to these other properties. We also review studies on stem/progenitor cells isolated from the embryonic cortex that are able to generate oligodendrocytes. As for the studies on O-2A/OPCs, important differences also distinguish these early cells from those studied in other CNS regions in their response to signaling molecules and expression of the Dlx family of transcriptional regulators [He et al., J Neurosci 2001;21:8854-8862; Yung et al., Proc Natl Acad Sci USA 2002;99:16273-16278]. We also present new data on clonal analysis of A2B5+ precursor cells isolated from the E13.5 cortex, demonstrating that this tissue appears to contain a cell similar in properties to the tripotential glial-restricted precursor cell that has been isolated from embryonic spinal cord [Rao et al., Proc Natl Acad Sci USA 1998;95:3996-4001]. Moreover, the A2B5+ precursor cells isolated from embryonic cortex are much more heterogeneous than is seen in the spinal cord at this age, even to the point of including an A2B5/PSA-NCAM double-positive cell that can generate neurons.},
	Author = {Noble, M. and Arhin, A. and Gass, D. and Mayer-Pr{\"o}schel, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;Comparative Study;Research Support, U.S. Gov't, P.H.S.;Stem Cells;11 Glia;Spinal Cord;Animals;Oligodendroglia;Cerebral Cortex;Cell Lineage;Humans},
	Medline = {22845919},
	Nlm_Id = {7809375},
	Number = {2-4},
	Organization = {Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY 14642, USA. Mark\_Noble\@urmc.rochester.edu},
	Pages = {217-33},
	Pii = {DNE20030252_4217},
	Pubmed = {12966219},
	Title = {The cortical ancestry of oligodendrocytes: common principles and novel features},
	Uuid = {250CAF47-382C-4D1B-A9FA-CAB0BE55C147},
	Volume = {25},
	Year = {2003},
	url = {papers/Noble_DevNeurosci2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000072270}}

@article{Noctor:2002,
	Abstract = {The embryonic ventricular zone (VZ) of the cerebral cortex contains migrating neurons, radial glial cells, and a large population of cycling progenitor cells that generate newborn neurons. The latter two cell classes have been assumed for some time to be distinct in both function and anatomy, but the cellular anatomy of the progenitor cell type has remained poorly defined. Several recent reports have raised doubts about the distinction between radial glial and precursor cells by demonstrating that radial glial cells are themselves neuronal progenitor cells (Malatesta et al., 2000; Hartfuss et al., 2001; Miyata et al., 2001; Noctor et al., 2001). This discovery raises the possibility that radial glia and the population of VZ progenitor cells may be one anatomical and functional cell class. Such a hypothesis predicts that throughout neurogenesis almost all mitotically active VZ cells and a substantial percentage of VZ cells overall are radial glia. We have therefore used various anatomical, immunohistochemical, and electrophysiological techniques to test these predictions. Our data demonstrate that the majority of VZ cells, and nearly all mitotically active VZ cells during neurogenesis, both have radial glial morphology and express radial glial markers. In addition, intracellular dye filling of electrophysiologically characterized progenitor cells in the VZ demonstrates that these cells have the morphology of radial glia. Because the vast majority cycling cells in the cortical VZ have characteristics of radial glia, the radial glial precursor cell may be responsible for both the production of newborn neurons and the guidance of daughter neurons to their destinations in the developing cortex. 21940963 1529-2401 Journal Article},
	Author = {Noctor, S. C. and Flint, A. C. and Weissman, T. A. and Wong, W. S. and Clinton, B. K. and Kriegstein, A. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;F;Cerebral Ventricles/*cytology;Biolistics;In Vitro;Rats;Mitosis;Stem Cells/*cytology/metabolism;Patch-Clamp Techniques;Animal;Rats, Sprague-Dawley;Microspheres;Support, Non-U.S. Gov't;Retroviridae/genetics;Vimentin/biosynthesis;Cerebral Cortex/*cytology/*embryology;Support, U.S. Gov't, P.H.S.;Pyramidal Cells/cytology/metabolism;Cell Division;Immunohistochemistry;S Phase;Antigens, Differentiation/biosynthesis;Neuroglia/*cytology;Cell Differentiation/physiology;Luminescent Proteins/biosynthesis/genetics},
	Number = {8},
	Organization = {Department of Neurology, Columbia College of Physicians and Surgeons, New York, New York 10032, USA.},
	Pages = {3161-73},
	Pubmed = {11943818},
	Title = {Dividing precursor cells of the embryonic cortical ventricular zone have morphological and molecular characteristics of radial glia},
	Uuid = {AE860DC7-71C2-11DA-A383-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	url = {papers/Noctor_JNeurosci2002.pdf}}

@article{Noctor:2004,
	Abstract = {Precise patterns of cell division and migration are crucial to transform the neuroepithelium of the embryonic forebrain into the adult cerebral cortex. Using time-lapse imaging of clonal cells in rat cortex over several generations, we show here that neurons are generated in two proliferative zones by distinct patterns of division. Neurons arise directly from radial glial cells in the ventricular zone (VZ) and indirectly from intermediate progenitor cells in the subventricular zone (SVZ). Furthermore, newborn neurons do not migrate directly to the cortex; instead, most exhibit four distinct phases of migration, including a phase of retrograde movement toward the ventricle before migration to the cortical plate. These findings provide a comprehensive and new view of the dynamics of cortical neurogenesis and migration. 1097-6256 Journal Article},
	Author = {Noctor, S. C. and Martinez-Cerdeno, V. and Ivic, L. and Kriegstein, A. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Nat Neurosci},
	Keywords = {10 Development;F pdf},
	Number = {2},
	Organization = {Department of Neurology, Columbia University College of Physicians &Surgeons, 630 W. 168th Street, New York, New York 10032, USA.},
	Pages = {136-44},
	Pubmed = {14703572},
	Title = {Cortical neurons arise in symmetric and asymmetric division zones and migrate through specific phases},
	Uuid = {A13EE4C4-CF6F-4CC8-93FB-FA1D0D695968},
	Volume = {7},
	Year = {2004},
	url = {papers/Noctor_NatNeurosci2004.pdf}}

@article{Noctor:2001,
	Abstract = {The neocortex of the adult brain consists of neurons and glia that are generated by precursor cells of the embryonic ventricular zone. In general, glia are generated after neurons during development, but radial glia are an exception to this rule. Radial glia are generated before neurogenesis and guide neuronal migration. Radial glia are mitotically active throughout neurogenesis, and disappear or become astrocytes when neuronal migration is complete. Although the lineage relationships of cortical neurons and glia have been explored, the clonal relationship of radial glia to other cortical cells remains unknown. It has been suggested that radial glia may be neuronal precursors, but this has not been demonstrated in vivo. We have used a retroviral vector encoding enhanced green fluorescent protein to label precursor cells in vivo and have examined clones 1-3 days later using morphological, immunohistochemical and electrophysiological techniques. Here we show that clones consist of mitotic radial glia and postmitotic neurons, and that neurons migrate along clonally related radial glia. Time-lapse images show that proliferative radial glia generate neurons. Our results support the concept that a lineage relationship between neurons and proliferative radial glia may underlie the radial organization of neocortex.},
	Author = {Noctor, S. C. and Flint, A. C. and Weissman, T. A. and Dammerman, R. S. and Kriegstein, A. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Nature},
	Keywords = {Clone Cells;Cell Differentiation;Luminescent Proteins;Rats, Sprague-Dawley;Rats;Antigens, Differentiation/biosynthesis;Microscopy, Video;Neuroglia/*cytology;Animal;Neurons/*cytology;F;Mitosis;Neocortex/*cytology;Support, Non-U.S. Gov't;Cell Movement;Support, U.S. Gov't, P.H.S.},
	Number = {6821},
	Organization = {Department of Neurology, Columbia University College of Physicians &Surgeons, New York, New York 10032, USA.},
	Pages = {714-20.},
	Title = {Neurons derived from radial glial cells establish radial units in neocortex},
	Uuid = {AE861032-71C2-11DA-A383-000D9346EC2A},
	Volume = {409},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11217860}}

@article{Nolte:1997,
	Abstract = {Epidermal growth factor (EGF) and its receptor are present in the central nervous system and modulate a variety of neural functions. Here we show that microglial cells, the brain-intrinsic macrophages, express the receptor for EGF and migrate in response to EGF. Transcripts encoding the EGF receptor could be detected in purified microglial cultures obtained from newborn mouse cortex. More specifically, cDNA fragments derived from EGF receptor mRNA could be amplified from 21\%of electrophysiologically characterized microglial cells by the use of a single-cell reverse transcription-polymerase chain reaction method. Expression of the protein was confirmed on rat microglia by flow cytometry. EGF dose-dependently stimulated chemotactic migration, as revealed with a microchemotaxis assay. The dose-response curve peaked-at 10 ng/ml EGF, reaching a 3-fold increase in migration over the unstimulated control; migration was about half of that induced by complement 5a (10 nM), a previously described microglial chemoattractant. Chequerboard analysis showed that EGF-induced motility was composed of both chemotaxis and chemokinesis. In contrast to its pronounced effect on cell motility, EGF (0.01-10 ng/ml) was not a mitotic signal for microglia, as shown by lack of bromodeoxyuridine incorporation. Acute and chronic pathological processes within the brain stimulate the synthesis and release of immunoregulators and growth factors (including EGF) that play a major role in the brain's response to injury. EGF may serve as a paracrine factor to direct microglial cells to the lesion site. Moreover, since EGF is secreted by activated microglia themselves in vivo, it may act as an autocrine modulator of microglial cell function.},
	Author = {Nolte, C. and Kirchhoff, F. and Kettenmann, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Patch-Clamp Techniques;Mice, Inbred Strains;Receptor, Epidermal Growth Factor;Research Support, Non-U.S. Gov't;Alpha;Rats;Epidermal Growth Factor;Rats, Wistar;Cell Division;11 Glia;Microglia;Mitosis;Cells, Cultured;Animals;Chemotaxis;Mice;Cell Movement},
	Medline = {97429473},
	Month = {8},
	Nlm_Id = {8918110},
	Number = {8},
	Organization = {Max Delbr{\"u}ck Centre for Molecular Medicine, Berlin, Germany.},
	Pages = {1690-8},
	Pubmed = {9283823},
	Title = {Epidermal growth factor is a motility factor for microglial cells in vitro: evidence for EGF receptor expression},
	Uuid = {472A3D1B-1BC8-454C-830A-4C46ED31416D},
	Volume = {9},
	Year = {1997}}

@article{Nona:1998,
	Abstract = {In crushed goldfish optic nerve, regenerating axons cross the site of lesion within 10 days following injury. Some 30 days later, Schwann cells accumulate at the lesion, where they myelinate the new axons. In this study, we have used immunohistochemistry and electron microscopy to examine the cellular environment of the crush site prior to the establishment of Schwann cells in order to learn more about the early events that contribute to axonal regeneration. During the first week following injury, macrophages enter the site of lesion and efficiently phagocytose the debris. The infiltration of macrophages precedes the arrival of regenerating axons that abut and surround these phagocytes. Based on EM morphology and phagocytic capacity, macrophages of the type observed at the site of lesion are not present in the degenerating distal nerve segment, where debris clearance is shared between conventional microglia and astrocytes over a period of several weeks. During this period, axon bundles emerging distally from the injury zone become enwrapped by astrocyte processes, thereby re-establishing the characteristic fascicular cytoarchitecture of the optic nerve. The process of fasciculation also leads to the displacement of myelin debris to the margins of the fiber bundles, where it is trapped by the astrocytes. Our results suggest that the early robust appearance of macrophages at the lesion, and their effectiveness as phagocytes compared with the microglia distally, may contribute to the vigorous axonal regeneration across the crush, beyond which axons--excepting the pioneers--extend through newly formed debris-free channels delineated by astrocyte processes.},
	Author = {Nona, S. N. and Thomlinson, A. M. and Stafford, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:37 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Goldfish;Nerve Regeneration;Microscopy, Electron;Not relevant;11 Glia;Macrophages;Optic Nerve;Nerve Crush;Support, Non-U.S. Gov't;Cell Movement;Animals;Phagocytosis;Axons},
	Medline = {99382397},
	Month = {11},
	Nlm_Id = {0364620},
	Number = {11},
	Organization = {Neuroscience Group, Department of Optometry &Vision Sciences, UMIST, Manchester M60 1QD, UK.},
	Pages = {791-803},
	Pubmed = {10451426},
	Title = {Temporary colonization of the site of lesion by macrophages is a prelude to the arrival of regenerated axons in injured goldfish optic nerve},
	Uuid = {0F27F310-D697-45BB-8314-E055C5CE7BF4},
	Volume = {27},
	Year = {1998}}

@article{Nossal:2003,
	Abstract = {The immune system can recognize and produce antibodies to virtually any molecule in the Universe. This enormous diversity arises from the ingenious reshuffling of DNA sequences encoding components of the immune system. Immunology is an example of a field completely transformed during the past 50 years by the discovery of the structure of DNA and the emergence of DNA technologies that followed. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Nossal, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Nature},
	Keywords = {DNA/chemistry/genetics/*metabolism;Vaccines, DNA/immunology;10 Development;Lymphocytes/immunology/metabolism;Human;Gene Rearrangement/*genetics;Antibody Diversity/*genetics;Animals;F pdf;Autoimmunity;Receptors, Antigen, T-Cell/*genetics;Lymphoma/genetics/immunology},
	Number = {6921},
	Organization = {Department of Pathology, The University of Melbourne, Victoria 3010, Australia.},
	Pages = {440-4},
	Pubmed = {12540919},
	Title = {The double helix and immunology},
	Uuid = {EF4596FE-3B14-42AA-B3FF-CD4FB8FED108},
	Volume = {421},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12540919}}

@article{Nosten-Bertrand:2008,
	Abstract = {Patients with Doublecortin (DCX) mutations have severe cortical malformations associated with mental retardation and epilepsy. Dcx knockout (KO) mice show no major isocortical abnormalities, but have discrete hippocampal defects. We questioned the functional consequences of these defects and report here that Dcx KO mice are hyperactive and exhibit spontaneous convulsive seizures. Changes in neuropeptide Y and calbindin expression, consistent with seizure occurrence, were detected in a large proportion of KO animals, and convulsants, including kainate and pentylenetetrazole, also induced seizures more readily in KO mice. We show that the dysplastic CA3 region in KO hippocampal slices generates sharp wave-like activities and possesses a lower threshold for epileptiform events. Video-EEG monitoring also demonstrated that spontaneous seizures were initiated in the hippocampus. Similarly, seizures in human patients mutated for DCX can show a primary involvement of the temporal lobe. In conclusion, seizures in Dcx KO mice are likely to be due to abnormal synaptic transmission involving heterotopic cells in the hippocampus and these mice may therefore provide a useful model to further study how lamination defects underlie the genesis of epileptiform activities.},
	Author = {Nosten-Bertrand, Marika and Kappeler, Caroline and Dinocourt, C{\'e}line and Denis, C{\'e}cile and Germain, Johanne and Phan Dinh Tuy, Fran\c{c}oise and Verstraeten, Soraya and Alvarez, Chantal and M{\'e}tin, Christine and Chelly, Jamel and Giros, Bruno and Miles, Richard and Depaulis, Antoine and Francis, Fiona},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1932-6203},
	Journal = {PLoS ONE},
	Keywords = {Epilepsy;research support, non-u.s. gov't;Mice, Knockout;Hippocampus;Neuropeptides;Animals;Convulsants;Mice;Microtubule-Associated Proteins;24 Pubmed search results 2008},
	Nlm_Id = {101285081},
	Number = {6},
	Organization = {INSERM, U513, Universit{\'e} Pierre et Marie Curie, Paris, France.},
	Pages = {e2473},
	Pmc = {PMC2429962},
	Pubmed = {18575605},
	Title = {Epilepsy in Dcx knockout mice associated with discrete lamination defects and enhanced excitability in the hippocampus},
	Uuid = {3E817120-20BF-4C6F-A38D-5227F88C0697},
	Volume = {3},
	Year = {2008},
	url = {papers/Nosten-Bertrand_PLoSONE2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pone.0002473}}

@article{Nottebohm:2002,
	Author = {Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;Cell Survival/physiology;Neurons/*cytology/physiology;Female;Regeneration/*physiology;Aging/physiology;A both;Cell Count;Animal;Memory/physiology;Brain/*cytology/growth &development;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Songbirds;Male;Research Design},
	Number = {3},
	Organization = {The Rockefeller University, Field Research Center, Millbrook, New York 12545, USA. nottebo\@mail.rockefeller.edu},
	Pages = {624-8.},
	Title = {Why are some neurons replaced in adult brain?},
	Uuid = {6AE6B57F-4AAC-4EEE-9AC9-442EBAF62A9B},
	Volume = {22},
	Year = {2002},
	url = {papers/Nottebohm_JNeurosci2002.pdf}}

@article{Nygren:2006,
	Abstract = {BACKGROUND AND PURPOSE: Cells proliferate continuously in the adult mammalian brain, and in rodents, cell genesis is affected by housing conditions and brain injury. Increase in neurogenesis after brain ischemia has been postulated to be linked to functional recovery after stroke. Housing rodents in an enriched environment improves motor function after stroke injury. We have investigated whether changes in cell genesis can explain the beneficial effects of an enriched environment. METHODS: Intact mice and mice subjected to transient occlusion of the middle cerebral artery were exposed to an enriched environment for 1 month. Bromodeoxyuridine was injected daily to label proliferating cells during the first postischemic week. Newborn cells were analyzed immunohistochemically after 4 weeks. RESULTS: The enriched environment increased neurogenesis in the dentate gyrus in both intact and stroke-injured animals. An increased number of newborn cells was found in the subventricular zone of stroke-injured mice, but not in injured mice exposed to an enriched environment. Also, the number of newborn astrocytes (BrdU+/S-100beta+ cells), neuroblasts (dcx+ cells), and reactive astrocytes (vimentin mRNA) in the striatum ipsilateral to the ischemic injury was markedly attenuated and new adult neurons (BrdU+/NeuN+) were not found. The enriched environment did not affect infarct size or mortality. CONCLUSIONS: An enriched environment after experimental stroke increased neurogenesis in the hippocampus, whereas there was a decreased cell genesis and migration of neuroblasts and newborn astrocytes in the striatum.},
	Author = {Nygren, Josefine and Wieloch, Tadeusz and Pesic, Jelena and Brundin, Patrik and Deierborg, Tomas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1524-4628},
	Journal = {Stroke},
	Keywords = {Male;Mice;Brain Ischemia;Cell Differentiation;research support, non-u.s. gov't ;Environment;Mice, Inbred C57BL;Stem Cells;Corpus Striatum;Cell Count;Animals;comparative study ;24 Pubmed search results 2008;Cell Movement;Cerebral Ventricles},
	Month = {11},
	Nlm_Id = {0235266},
	Number = {11},
	Organization = {Experimental Brain Research, Wallenberg Neuroscience Center, Lund University, Lund, Sweden.},
	Pages = {2824-9},
	Pii = {01.STR.0000244769.39952.90},
	Pubmed = {17008628},
	Title = {Enriched environment attenuates cell genesis in subventricular zone after focal ischemia in mice and decreases migration of newborn cells to the striatum},
	Uuid = {1A7761B1-F051-40C3-AEE6-865C0870EC84},
	Volume = {37},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.STR.0000244769.39952.90}}

@article{ORourke:1996,
	Author = {O'Rourke, N. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Neuron},
	Keywords = {Neurons/*physiology;02 Adult neurogenesis migration;Animal;Olfactory Bulb/*physiology;B abstr;Neural Pathways/*anatomy &histology},
	Number = {6},
	Organization = {Department of Biological Sciences, Stanford University, California 94305, USA.},
	Pages = {1061-4.},
	Title = {Neuronal chain gangs: homotypic contacts support migration into the olfactory bulb},
	Uuid = {99643B5B-1AA9-4152-BE60-9727AB841FC2},
	Volume = {16},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8663980}}

@article{Oberto:2001,
	Abstract = {ErbB-4 is expressed by the periglomerular and the mitral/tufted cells of the adult mouse olfactory bulb (OB) and in the present work we tested whether this expression is regulated by the olfactory nerve input to the OB. Reversible zinc sulphate lesions of the olfactory mucosa were made in adult mice and the deafferented OB analysed by immunohistochemistry, Western blotting and semiquantitative RT-PCR. Following deafferentation, the expression of erbB-4, erbB-2 and neuregulin-1 (NRG-1) mRNAs in the OB was altered. At early stages (7-14 days) after lesion the levels of expression of olfactory marker protein (OMP), tyrosine hydroxylase (TH), erbB-4 and NRG-1 mRNAs were decreased, whilst expression of erbB-2 increased and that of NRG-2 was not significantly altered. We observed at least two distinct time courses for these expression changes. The lowest amounts of mRNA for erbB-4 and NRG-1 were observed at day 7 after lesion, whilst mRNAs for TH and OMP were lowest at day 14. At day 28 after the lesion, when olfactory receptor neuron axons had reinnervated the olfactory bulb, the expression levels of OMP, TH, erbB-2, erbB-4 and NRG-1 were identical to control values. These results indicate that the expression of erbB-4 mRNA and protein in periglomerular and mitral cells is controlled by peripheral olfactory innervation. The tight correlation in NRG-1 and erbB-4 expression levels also suggests a possible functional link that deserves further exploration.},
	Author = {Oberto, M. and Soncin, I. and Bovolin, P. and Voyron, S. and De Bortoli, M. and Dati, C. and Fasolo, A. and Perroteau, I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {I pdf;13 Olfactory bulb anatomy},
	Number = {3},
	Organization = {Department of Human and Animal Biology, University of Turin, via Accademia Albertina 13, Torino10123, Italy.},
	Pages = {513-21.},
	Title = {ErbB-4 and neuregulin expression in the adult mouse olfactory bulb after peripheral denervation},
	Uuid = {E22B0764-ADA8-4398-BCB0-E6C9D85F30C5},
	Volume = {14},
	Year = {2001},
	url = {papers/Oberto_EurJNeurosci2001}}

@article{Odenwald:2005,
	Abstract = {One of the longstanding goals of neurobiologists is to describe, in molecular terms, how a neural progenitor cell (NPC) can generate an ordered series of uniquely fated neurons and glia. Recent studies reveal that many, or all, neural-subtype identities can be linked to sequentially changing regulatory programs within NPCs. Two new studies, in this issue of Developmental Cell, provide novel insights into the molecular details of how Drosophila NPCs transition from one offspring identity program to the next.},
	Author = {Odenwald, Ward F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1534-5807},
	Journal = {Dev Cell},
	Keywords = {10 Development},
	Month = {2},
	Nlm_Id = {101120028},
	Number = {2},
	Pages = {133-4},
	Pii = {S1534-5807(05)00007-9},
	Pubmed = {15691753},
	Title = {Changing fates on the road to neuronal diversity},
	Uuid = {A5597378-95F8-4D4B-955F-9562B5BFC8F5},
	Volume = {8},
	Year = {2005},
	url = {papers/Odenwald_DevCell2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.devcel.2005.01.005}}

@article{Oehmichen:1982,
	Abstract = {According to recent submicroscopic, cytokinetics, and functional (particularly cytoimmunologic) investigations, no relationship exists between "resting" microglia (the small argyrophilic cells appearing in undamaged brain tissue, first described by Rio Hortega) and "reactive" microglia (the argyrophilic cells appearing under pathologic conditions). While "resting" microglia are apparently cells of neuro-ectodermal origin, all observations tend to indicate that "reactive" microglia are derived from extravasated blood monocytes and should be called brain macrophages. In the intact brain parenchyma, no macrophages are demonstrable. Free subarachnoidal cells in the cerebrospinal fluid (CSF), perivascular cells, and epiplexus and/or supraependymal cells in the CSF-containing spaces of the normal central nervous system are cells of the mononuclear phagocyte system and must be considered as CSF macrophages. According to rough estimates, the normal adult central nervous system contains a maximum of 280,000 CSF macrophages.},
	Author = {Oehmichen, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0171-2985},
	Journal = {Immunobiology},
	Keywords = {Rabbits;Cell Differentiation;Animals;Phagocytosis;Monocytes;Macrophages;Bone Marrow Transplantation;Mitosis;Brain;review;Mammals;Wounds, Stab;11 Glia;Phagocytes;Brain Injuries;Cell Adhesion;Cerebrospinal Fluid;Receptors, Fc;Mice},
	Medline = {82238040},
	Month = {4},
	Nlm_Id = {8002742},
	Number = {3-4},
	Pages = {246-54},
	Pubmed = {7047372},
	Title = {Are resting and/or reactive microglia macrophages?},
	Uuid = {43CFF1E2-9352-48B7-AC5E-126061607A41},
	Volume = {161},
	Year = {1982}}

@article{Ogle:2004,
	Abstract = {Human cells can fuse with damaged or diseased somatic cells in vivo. Whether human cells fuse in vivo in the absence of disease and with cells of disparate species is unknown. Such a question is of current interest because blood exchanges between species through direct physical contact, via insect vectors or parasitism, are thought to underlie the transmission of zoonotic agents. In a model of human-pig chimerism, we show that some human hematopoietic stem cells engrafted in pigs contain both human and porcine chromosomal DNA. These hybrid cells divide, express human and porcine proteins, and contribute to porcine nonhematopoietic tissues. In addition, the hybrid cells contain porcine endogenous retroviral DNA sequences and are able to transmit this virus to uninfected human cells in vitro. Thus, spontaneous fusion can occur in vivo between the cells of disparate species and in the absence of disease. The ability of these cell hybrids to acquire and transmit retroviral elements together with their ability to integrate into tissues could explain genetic recombination and generation of novel pathogens. * differentiation * fusion * retrovirus},
	Author = {Ogle, Brenda M. and Butters, Kim A. and Plummer, Timothy B. and Ring, Kevin R. and Knudsen, Bruce E. and Litzow, Mark R. and Cascalho, Marilia and Platt, Jeffrey L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {Cell Differentiation;Transplantation Chimera;Genetic Markers;Cell Line;24 Pubmed search results 2008;Ploidies;Organ Specificity;DNA, Viral;Kidney;Animals;Endogenous Retroviruses;Herpesvirus 4, Human;15 Retrovirus mechanism;Swine;Blood Transfusion, Intrauterine;Hybrid Cells;Hematopoietic Stem Cells;Chromosome Banding;Species Specificity;Skin;Transplantation, Heterologous;Hematopoietic Stem Cell Transplantation;15 ERVs retroelements;Comparative Study;Graft Survival;Retroviridae Infections;Cell Lineage;Genes, pol;Fibroblasts;B-Lymphocytes;Cell Line, Transformed;Cell Fusion;Humans},
	Month = {3},
	Nlm_Id = {8804484},
	Number = {3},
	Organization = {Transplantation Biology, Mayo Clinic, Rochester, Minnesota 55905, USA.},
	Pages = {548-50},
	Pii = {03-0962fje},
	Pubmed = {14715691},
	Title = {Spontaneous fusion of cells between species yields transdifferentiation and retroviral transfer in vivo},
	Uuid = {6A461CA7-71DF-494C-B3D6-1E8697EE059F},
	Volume = {18},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.03-0962fje}}

@article{Ogle:2005,
	Abstract = {Until recently, cells were thought to be integral and discrete components of tissues, and their state was determined by cell differentiation. However, under some conditions, stem cells or their progeny can fuse with cells of other types, mixing cytoplasmic and even genetic material of different (heterotypic) origins. The fusion of heterotypic cells could be of central importance for development, repair of tissues and the pathogenesis of disease.},
	Author = {Ogle, Brenda M. and Cascalho, Marilia and Platt, Jeffrey L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1471-0072},
	Journal = {Nat Rev Mol Cell Biol},
	Keywords = {Aging;Models, Biological;Cell Differentiation;Cell Fusion;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Research Support, N.I.H., Extramural;Humans;Animals;24 Pubmed search results 2008;review},
	Month = {7},
	Nlm_Id = {100962782},
	Number = {7},
	Organization = {Transplantation Biology and the Department of Physiology, Mayo Clinic, Rochester, Minnesota 55905, USA.},
	Pages = {567-75},
	Pii = {nrm1678},
	Pubmed = {15957005},
	Title = {Biological implications of cell fusion},
	Uuid = {C7E0D578-A523-4852-83B9-15723F07EE35},
	Volume = {6},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrm1678}}

@article{Ogura:1995,
	Abstract = {Superfusion of guinea pig papillary muscles with Tyrode's solution that contained 0.3\%to 10\%dimethyl sulfoxide (DMSO) caused a small hyperpolarization, a prolongation of the action potential (e.g., 4\%, 15\%and 33\%prolongation with 1\%, 5\%and 10\%DMSO, respectively) and a reduction (<or = 14\%) in the maximal upstroke velocity (Vmax). Action potential prolongation was also induced by DMSO in muscles treated with the inorganic Ca++ channel blocker Co++ (5 mM) and in those depolarized with 24 mM K(+)-containing Tyrode's solution. In the latter case, there was no significant change in Vmax. In voltage-clamp experiments, superfusion of guinea pig ventricular myocytes with 0.1\%to 10\%DMSO solution had little effect on Ca++ and inward-rectifier K+ currents, moderately inhibited Cl- and Na+ currents, partially inhibited Na+ pump current and markedly depressed delayed-rectifier K+ current. The cell water shrinkages measured in muscles and myocytes superfused with DMSO solution appear to be only partially responsible for the solvent's effects. Other mechanisms that may be of greater importance in explaining the action of DMSO include direct block of channels by DMSO molecules and hindrance of channel hydration and opening related to osmotic stress. TY - JOUR M1 - 7540688},
	Author = {Ogura, T. and Shuba, L.M. and McDonald, T.F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Isbn = {0022-3565},
	Journal = {J Pharmacol Exp Ther},
	Keywords = {Dose-Response Relationship, Drug;Animals;In Vitro;Dimethyl Sulfoxide;Chlorides;Cell Membrane;Calcium;Ion Channels;Male;08 Aberrant cell cycle;Potassium;Action Potentials;Support, Non-U.S. Gov't;Heart Ventricles;Sodium;Body Water;Heart;EE abstr;Guinea Pigs},
	Number = {3},
	Organization = {Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada.},
	Pages = {1273-1286},
	Title = {Action potentials, ionic currents and cell water in guinea pig ventricular preparations exposed to dimethyl sulfoxide},
	Uuid = {02E1D7DC-C0C4-494C-BAF6-B4833B461128},
	Volume = {273},
	Year = {1995},
	Bdsk-Url-1 = {http://www.hubmed.org/display.cgi?issn=00223565&uids=7540688%20Polaris:Users:ackman:Desktop:query.fcgi}}

@article{Ohab:2006,
	Abstract = {Stroke causes cell death but also birth and migration of new neurons within sites of ischemic damage. The cellular environment that induces neuronal regeneration and migration after stroke has not been defined. We have used a model of long-distance migration of newly born neurons from the subventricular zone to cortex after stroke to define the cellular cues that induce neuronal regeneration after CNS injury. Mitotic, genetic, and viral labeling and chemokine/growth factor gain- and loss-of-function studies show that stroke induces neurogenesis from a GFAP-expressing progenitor cell in the subventricular zone and migration of newly born neurons into a unique neurovascular niche in peri-infarct cortex. Within this neurovascular niche, newly born, immature neurons closely associate with the remodeling vasculature. Neurogenesis and angiogenesis are causally linked through vascular production of stromal-derived factor 1 (SDF1) and angiopoietin 1 (Ang1). Furthermore, SDF1 and Ang1 promote post-stroke neuroblast migration and behavioral recovery. These experiments define a novel brain environment for neuronal regeneration after stroke and identify molecular mechanisms that are shared between angiogenesis and neurogenesis during functional recovery from brain injury.},
	Author = {Ohab, John J. and Fleming, Sheila and Blesch, Armin and Carmichael, S. Thomas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Recovery of Function;comparative study;Cell Communication;Mice, Transgenic;Cell Movement;Mice, Inbred C57BL;research support, non-u.s. gov't;Time Factors;Blood-Brain Barrier;Animals, Newborn;Neurons;Brain Ischemia;Cerebrovascular Accident;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Stem Cells;Endothelium, Vascular},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {50},
	Organization = {Department of Neurology, University of California, Los Angeles, Los Angeles, California 90095-1735, USA.},
	Pages = {13007-16},
	Pii = {26/50/13007},
	Pubmed = {17167090},
	Title = {A neurovascular niche for neurogenesis after stroke},
	Uuid = {63249198-C76F-4F0B-A01E-421942FC8C80},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4323-06.2006}}

@article{Ohagen:2003,
	Abstract = {The genetic evolution of human immunodeficiency virus type 1 (HIV-1) in the brain is distinct from that in lymphoid tissues, indicating tissue-specific compartmentalization of the virus. Few primary HIV-1 envelope glycoproteins (Envs) from uncultured brain tissues have been biologically well characterized. In this study, we analyzed 37 full-length env genes from uncultured brain biopsy and blood samples from four patients with AIDS. Phylogenetic analysis of intrapatient sequence sets showed distinct clustering of brain relative to blood env sequences. However, no brain-specific signature sequence was identified. Furthermore, there was no significant difference in the number or positions of N-linked glycosylation sites between brain and blood env sequences. The patterns of coreceptor usage were heterogeneous, with no clear distinction between brain and blood env clones. Nine Envs used CCR5 as a coreceptor, one used CXCR4, and two used both CCR5 and CXCR4 in cell-to-cell fusion assays. Eight Envs could also use CCR3, CCR8, GPR15, STRL33, Apj, and/or GPR1, but these coreceptors did not play a major role in virus entry into microglia. Recognition of epitopes by the 2F5, T30, AG10H9, F105, 17b, and C11 monoclonal antibodies varied among env clones, reflecting genetic and conformational heterogeneity. Envs from two patients contained 28 to 32 N-glycosylation sites in gp120, compared to around 25 in lab strains and well-characterized primary isolates. These results suggest that HIV-1 Envs in brain cannot be distinguished from those in blood on the basis of coreceptor usage or the number or positions of N-glycosylation sites, indicating that other properties underlie neurotropism. The study also demonstrates characteristics of primary HIV-1 Envs from uncultured tissues and implies that Env variants that are glycosylated more extensively than lab strains and well-characterized primary isolates should be considered during development of vaccines and neutralizing antibodies.},
	Author = {Ohagen, Asa and Devitt, Amy and Kunstman, Kevin J. and Gorry, Paul R. and Rose, Patrick P. and Korber, Bette and Taylor, Joann and Levy, Robert and Murphy, Robert L. and Wolinsky, Steven M. and Gabuzda, Dana},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Structure-Activity Relationship;HIV-1;Research Support, Non-U.S. Gov't;Receptors, CCR5;Molecular Sequence Data;Virus Replication;Phylogeny;Research Support, U.S. Gov't, P.H.S.;11 Glia;Amino Acid Sequence;Acquired Immunodeficiency Syndrome;Humans;Genes, env;Receptors, CXCR4;Brain;Viremia},
	Medline = {22942994},
	Month = {11},
	Nlm_Id = {0113724},
	Number = {22},
	Organization = {Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.},
	Pages = {12336-45},
	Pubmed = {14581570},
	Title = {Genetic and functional analysis of full-length human immunodeficiency virus type 1 env genes derived from brain and blood of patients with AIDS},
	Uuid = {0DAA3482-10A8-4CA0-BC83-8FC85497D379},
	Volume = {77},
	Year = {2003}}

@article{Ohnuma:2003,
	Abstract = {For a long time, it has been understood that neurogenesis is linked to proliferation and thus to the cell cycle. Recently, the gears that mediate this linkage have become accessible to molecular investigation. This review describes some of the progress that has been made in understanding how the molecular machinery of the cell cycle is used in the processes of size regulation in the brain, histogenesis, neuronal differentiation, and the maintenance of stem cells. 0896-6273 Journal Article Review Review, Tutorial},
	Author = {Ohnuma, S. and Harris, W. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Neuron},
	Keywords = {Neurons/*cytology/*physiology;10 Development;Human;Cell Cycle/*physiology;Cell Differentiation/physiology;Stem Cells/cytology/physiology;Support, Non-U.S. Gov't;Animals;F pdf},
	Number = {2},
	Organization = {Department of Oncology, The Hutchison/MRC Research Centre, University of Cambridge, Hills Road, Cambridge CB2 2XZ, United Kingdom. so218\@cam.ac.uk},
	Pages = {199-208},
	Pubmed = {14556704},
	Title = {Neurogenesis and the cell cycle},
	Uuid = {6E64FCE9-3254-43C7-B893-3C710B7F5A01},
	Volume = {40},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14556704}}

@article{Ohori:2006,
	Abstract = {Neurons and oligodendrocytes are highly vulnerable to various insults, and their spontaneous replacement occurs to only a limited extent after damage in the adult spinal cord. The environment of injured tissue is thus thought to restrict the regenerative capacity of endogenous neural stem/progenitor cells; strategies for overcoming such restrictions remain to be developed. Here, we combined growth factor treatment and genetic manipulation to stimulate neurogenesis and oligodendrogenesis by endogenous progenitors in vivo. The recombinant retrovirus pMXIG, which was designed to coexpress green fluorescent proteins (GFPs) and a neurogenic/gliogenic transcription factor, was directly injected into the injured spinal cord parenchyma to manipulate proliferative cells in situ. We found that cells expressing Olig2, Nkx2.2, and NG2 were enriched among virus-infected, GFP-positive (GFP+) cells. Moreover, a fraction of GFP+ cells formed neurospheres and differentiated into neurons, astrocytes, and oligodendrocytes in vitro, demonstrating that GFP retroviruses indeed infected endogenous neural progenitors in vivo. Neuronal differentiation of control virus-infected cells did not occur at a detectable level in the injured spinal cord. We found, however, that direct administration of fibroblast growth factor 2 and epidermal growth factor into lesioned tissue could induce a significant fraction of GFP-labeled cells to express immature neuronal markers. Moreover, retrovirus-mediated overexpression of the basic helix-loop-helix transcription factors Neurogenin2 and Mash1, together with growth factor treatment, enhanced the production and maturation of new neurons and oligodendrocytes, respectively. These results demonstrate that endogenous neural progenitors can be manipulated to replace neurons and oligodendrocytes lost to insults in the injured spinal cord.},
	Author = {Ohori, Yasuo and Yamamoto, Shin-ichi and Nagao, Motoshi and Sugimori, Michiya and Yamamoto, Naoya and Nakamura, Kozo and Nakafuku, Masato},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Transcription Factors;Cells, Cultured;Treatment Outcome;Rats;Proteoglycans;Basic Helix-Loop-Helix Transcription Factors;Oligodendroglia;Homeodomain Proteins;Rats, Sprague-Dawley;Retroviridae;Disease Models, Animal;Fibroblast Growth Factor 2;Genetic Vectors;research support, non-u.s. gov't;Green Fluorescent Proteins;Spinal Cord;Antigens;Gene Therapy;Intercellular Signaling Peptides and Proteins;Neurons;Epidermal Growth Factor;Spinal Cord Injuries;24 Pubmed search results 2008;Stem Cells;Nerve Tissue Proteins},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {46},
	Organization = {Division of Developmental Biology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio 45229-3039, USA.},
	Pages = {11948-60},
	Pii = {26/46/11948},
	Pubmed = {17108169},
	Title = {Growth factor treatment and genetic manipulation stimulate neurogenesis and oligodendrogenesis by endogenous neural progenitors in the injured adult spinal cord},
	Uuid = {26A84389-39E2-406B-85B4-14425E058AC8},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3127-06.2006}}

@article{Ohsawa:2004,
	Abstract = {Ionized calcium binding adaptor molecule 1 (Iba1) is a microglia/macrophage-specific calcium-binding protein. Iba1 has the actin-bundling activity and participates in membrane ruffling and phagocytosis in activated microglia. In order to understand the Iba1-related intracellular signalling pathway in greater detail, we employed a yeast two-hybrid screen to isolate an Iba1-interacting molecule and identified another actin-bundling protein, L-fimbrin. In response to stimulation, L-fimbrin accumulated and co-localized with Iba1 in membrane ruffles induced by M-CSF-stimulation and phagocytic cups formed by IgG-opsonized beads in microglial cell line MG5. L-fimbrin was shown to associate with Iba1 in cell lysate of COS-7 expressing L-fimbrin and Iba1. By using purified proteins, direct binding of Iba1 to L-fimbrin was demonstrated by immunoprecipitation, glutathione S-transferase pull-down assays and ligand overlay assays. The binding of Iba1 was also found to increase the actin-bundling activity of L-fimbrin. These results indicate that Iba1 forms complexes with L-fimbrin in membrane ruffles and phagocytic cups, and suggest that Iba1 co-operates with L-fimbrin in modulating actin reorganization to facilitate cell migration and phagocytosis by microglia.},
	Author = {Ohsawa, Keiko and Imai, Yoshinori and Sasaki, Yo and Kohsaka, Shinichi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Microinjections;Immunohistochemistry;Luminescent Proteins;Calcium-Binding Proteins;Brain;Cells, Cultured;Animals;Egtazic Acid;Proteins;Axotomy;Two-Hybrid System Techniques;11 Glia;Plasmids;Mutation;Not relevant;Membrane Glycoproteins;Comparative Study;Blotting, Western;Amino Acid Sequence;Facial Nerve;COS Cells;Calcium;Rats;Time Factors;Dose-Response Relationship, Drug;Microglia;Macrophage Colony-Stimulating Factor;Actins;Immunoglobulin G;Support, Non-U.S. Gov't;Recombinant Proteins;Rats, Wistar;Precipitin Tests;Cercopithecus aethiops},
	Month = {2},
	Nlm_Id = {2985190R},
	Number = {4},
	Organization = {Department of Neurochemistry, National Institute of Neuroscience, Tokyo, Japan. kohsaka\@ncnp.go.jp},
	Pages = {844-56},
	Pii = {2213},
	Pubmed = {14756805},
	Title = {Microglia/macrophage-specific protein Iba1 binds to fimbrin and enhances its actin-bundling activity},
	Uuid = {7E23523B-2635-4B90-BAFA-30376629DBFC},
	Volume = {88},
	Year = {2004}}

@article{Ohshima:1996,
	Abstract = {Although cyclin-dependent kinase 5 (Cdk5) is closely related to other cyclin-dependent kinases, its kinase activity is detected only in the postmitotic neurons. Cdk5 expression and kinase activity are correlated with the extent of differentiation of neuronal cells in developing brain. Cdk5 purified from nervous tissue phosphorylates neuronal cytoskeletal proteins including neurofilament proteins and microtubule-associated protein tau in vitro. These findings indicate that Cdk5 may have unique functions in neuronal cells, especially in the regulation of phosphorylation of cytoskeletal molecules. We report here generation of Cdk5(-/-) mice through gene targeting and their phenotypic analysis. Cdk5(-/-) mice exhibit unique lesions in the central nervous system associated with perinatal mortality. The brains of Cdk5(-/-) mice lack cortical laminar structure and cerebellar foliation. In addition, the large neurons in the brain stem and in the spinal cord show chromatolytic changes with accumulation of neurofilament immunoreactivity. These findings indicate that Cdk5 is an important molecule for brain development and neuronal differentiation and also suggest that Cdk5 may play critical roles in neuronal cytoskeleton structure and organization.},
	Author = {Ohshima, T. and Ward, J. M. and Huh, C. G. and Longenecker, G. and Veeranna and Pant, H. C. and Brady, R. O. and Martin, L. J. and Kulkarni, A. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Phosphorylation;24 Pubmed search results 2008;10 Development;Mice, Knockout;Cell Compartmentation;Genes, Lethal;Cyclin-Dependent Kinases;Neurofilament Proteins;Cyclins;Cerebellum;Protein-Serine-Threonine Kinases;10 genetics malformation;Animals;Cyclin-Dependent Kinase 5;Cerebral Cortex;Mice;Axons},
	Month = {10},
	Nlm_Id = {7505876},
	Number = {20},
	Organization = {National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892, USA.},
	Pages = {11173-8},
	Pubmed = {8855328},
	Title = {Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death},
	Uuid = {4ECB21B9-CA24-417C-916F-7721E7188D06},
	Volume = {93},
	Year = {1996}}

@article{Ojima:2004,
	Abstract = {Recent studies have shown that bone marrow (BM) cells, including the BM side population (BM-SP) cells that enrich hematopoietic stem cells (HSCs), are incorporated into skeletal muscle during regeneration, but it is not clear how and what kinds of BM cells contribute to muscle fiber regeneration. We found that a large number of SP cells migrated from BM to muscles following injury in BM-transplanted mice. These BM-derived SP cells in regenerating muscles expressed different surface markers from those of HSCs and could not reconstitute the mouse blood system. BM-derived SP/Mac-1(low) cells increased in number in regenerating muscles following injury. Importantly, our co-culture studies with activated satellite cells revealed that this fraction carried significant potential for myogenic differentiation. By contrast, mature inflammatory (Mac-1(high)) cells showed negligible myogenic activities. Further, these BM-derived SP/Mac-1(low) cells gave rise to mononucleate myocytes, indicating that their myogenesis was not caused by stochastic fusion with host myogenic cells, although they required cell-to-cell contact with myogenic cells for muscle differentiation. Taken together, our data suggest that neither HSCs nor mature inflammatory cells, but Mac-1(low) early myeloid cells in the BM-derived SP fraction, play an important role in regenerating skeletal muscles.},
	Author = {Ojima, Koichi and Uezumi, Akiyoshi and Miyoshi, Hiroyuki and Masuda, Satoru and Morita, Yohei and Fukase, Akiko and Hattori, Akihito and Nakauchi, Hiromitsu and Miyagoe-Suzuki, Yuko and Takeda, Shin'ichi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0006-291X},
	Journal = {Biochem Biophys Res Commun},
	Keywords = {Cell Differentiation;Animals;Models, Biological;Cell Movement;Mice, Transgenic;Myeloid Cells;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Bone Marrow Cells;Hematopoiesis;Macrophage-1 Antigen;Muscle, Skeletal;Mice;Muscle Fibers;Luminescent Proteins;Regeneration;Research Support, Non-U.S. Gov't},
	Month = {9},
	Nlm_Id = {0372516},
	Number = {4},
	Organization = {Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8502, Japan.},
	Pages = {1050-61},
	Pii = {S0006-291X(04)01564-5},
	Pubmed = {15358135},
	Title = {Mac-1(low) early myeloid cells in the bone marrow-derived SP fraction migrate into injured skeletal muscle and participate in muscle regeneration},
	Uuid = {44BE0FF7-9644-4C02-9ED9-6CCB7C9AE317},
	Volume = {321},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.bbrc.2004.07.069}}

@article{Okada:1999,
	Abstract = {To visualize the movements of cells and their processes in developing vertebrates, we constructed replication-incompetent retroviral vectors encoding green fluorescent protein (GFP) that can be detected as a single integrated copy per cell. To optimize GFP expression, the CMV enhancer and avian beta-actin promoter were incorporated within a retrovirus construct to drive transcription of redshifted (F64L, S65T) and codon-modified GFP (EGFP), EGFP tagged with GAP-43 sequences targeting the GFP to the cell membrane, or EGFP with additional mutations that increase its ability to fold properly at 37 degrees C (S147P or V163A, S175G). We have used these viruses to efficiently mark and follow the developmental progression of a large population of cells in rat neocortex and whole avian embryos. In the chick embryo, the migration and development of GFP-marked neural crest cells were monitored using time-lapse videomicroscopy. In the neocortex, GFP clearly delineates the morphology of a variety of neuronal and glial phenotypes. Cells expressing GFP display normal dendritic morphologies, and infected cells persist into adulthood. Cortical neurons appear to form normal local axonal and long-distance projections, suggesting that the presence of cytoplasmic or GAP-43-tagged GFP does not significantly interfere with normal development. 0014-4886 Journal Article},
	Author = {Okada, A. and Lansford, R. and Weimann, J. M. and Fraser, S. E. and McConnell, S. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Moloney murine leukemia virus;Terminal Repeat Sequences;Cerebral Cortex/cytology/*embryology;Genetic Vectors;Green Fluorescent Proteins;Cytomegalovirus;Vesicular stomatitis-Indiana virus;Luminescent Proteins;Cerebral Cortex;Animals;Neurons/cytology;Dendrites/ultrastructure;Cytomegalovirus/genetics;Axons/ultrastructure;Genes, Reporter;Research Support, U.S. Gov't, P.H.S.;Neural Crest;15 Retrovirus mechanism;Genetic Vectors/*genetics;Actins/genetics;Promoter Regions (Genetics);GAP-43 Protein;Membrane Proteins/analysis/genetics;Dendrites;*Genes, Reporter;Axons;Vesicular stomatitis-Indiana virus/*physiology;Support, U.S. Gov't, P.H.S.;Luminescent Proteins/*analysis/biosynthesis/genetics;Moloney murine leukemia virus/*genetics;Cell Lineage;Rats;Membrane Proteins;Actins;J;Enhancer Elements (Genetics);Microscopy, Video;Recombinant Fusion Proteins;Support, Non-U.S. Gov't;Neural Crest/*cytology;Neurons;GAP-43 Protein/genetics;Research Support, Non-U.S. Gov't;Recombinant Fusion Proteins/analysis/biosynthesis},
	Medline = {99263448},
	Month = {4},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Biological Sciences, Stanford University, Stanford, California, 94305, USA. amio\@leland.stanford.edu},
	Pages = {394-406},
	Pii = {S0014-4886(99)97033-4},
	Pubmed = {10328944},
	Title = {Imaging cells in the developing nervous system with retrovirus expressing modified green fluorescent protein},
	Uuid = {54C9EF70-D322-11DA-941C-000D9346EC2A},
	Volume = {156},
	Year = {1999},
	url = {papers/Okada_ExpNeurol1999},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.1999.7033}}

@article{Okano:1993,
	Abstract = {Expression of the cell cycle regulatory proteins RB and p34cdc2 was examined in the adult rat brain, with special emphasis on proliferation and neuronal differentiation in the hippocampal formation and olfactory bulb. RB-like immunoreactivity (RB-IR) was detected throughout the brain, with particularly intense staining observed in hippocampal pyramidal cells, pyriform cortex, and cerebellar Purkinje cells. Intense RB-IR and cdc2-IR were also detected in proliferating neuronal precursor cells in the subgranular region of the dentate gyrus and in the subependymal region extending from the anterior lateral ventricle into the olfactory bulb. Many of these cells developed into neurons as assessed by the expression of neuron-specific enolase (NSE) and, in the hippocampal formation, the expression of Fos-IR following pentylenetetrazol-induced seizure activity. A good correlation was observed between the number of proliferating cells expressing intense nuclear RB-IR staining and the number of thymidine-labeled cells that had differentiated into functional hippocampal neurons. A substantial decrease in RB-IR during differentiation was also observed and occurred prior to the expression of NSE. The possibility that the loss of RB may be necessary for neuronal differentiation to proceed is discussed. eng Journal Article},
	Author = {Okano, H. J. and Pfaff, D. W. and Gibbs, R. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Protein p34cdc2/*biosynthesis;Neurons/cytology/*metabolism;Rats;Brain/cytology/*metabolism;Cell Cycle;DNA/*biosynthesis;Animal;Rats, Sprague-Dawley;Kinetics;C abstr;Hippocampus/cytology/*metabolism;Time Factors;Olfactory Bulb/cytology/*metabolism;Male;Thymidine/*metabolism;Retinoblastoma Protein/*biosynthesis;Pyramidal Tracts/cytology/metabolism;Organ Specificity;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Tritium;Autoradiography},
	Number = {7},
	Organization = {Laboratory of Neurobiology and Behavior, Rockefeller University, New York, New York 10021.},
	Pages = {2930-8.},
	Title = {RB and Cdc2 expression in brain: correlations with 3H-thymidine incorporation and neurogenesis},
	Uuid = {3868963C-28D4-40EC-A6CA-23BA3AF4051F},
	Volume = {13},
	Year = {1993}}

@article{Olsen:2007,
	Abstract = {Each odorant receptor gene defines a unique type of olfactory receptor neuron (ORN) and a corresponding type of second-order neuron. Because each odor can activate multiple ORN types, information must ultimately be integrated across these processing channels to form a unified percept. Here, we show that, in Drosophila, integration begins at the level of second-order projection neurons (PNs). We genetically silence all the ORNs that normally express a particular odorant receptor and find that PNs postsynaptic to the silent glomerulus receive substantial lateral excitatory input from other glomeruli. Genetically confining odor-evoked ORN input to just one glomerulus reveals that most PNs postsynaptic to other glomeruli receive indirect excitatory input from the single ORN type that is active. Lateral connections between identified glomeruli vary in strength, and this pattern of connections is stereotyped across flies. Thus, a dense network of lateral connections distributes odor-evoked excitation between channels in the first brain region of the olfactory processing stream.},
	Author = {Olsen, Shawn R. and Bhandawat, Vikas and Wilson, Rachel I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {research support, non-u.s. gov't;21 Neurophysiology;research support, u.s. gov't, non-p.h.s.;research support, n.i.h., extramural;13 Olfactory bulb anatomy;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.},
	Pages = {89-103},
	Pii = {S0896-6273(07)00206-1},
	Pubmed = {17408580},
	Title = {Excitatory interactions between olfactory processing channels in the Drosophila antennal lobe},
	Uuid = {FFA98611-4CCB-4485-BD14-EF47C7629FB4},
	Volume = {54},
	Year = {2007},
	url = {papers/Olsen_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.03.010}}

@article{Olson:2006,
	Abstract = {Reelin and Disabled 1 (Dab1) are essential for positioning migrating neurons in the developing neocortex. Cell-autonomous RNA interference-mediated suppression of Dab1 in migrating neurons destined for layer 2/3 shifted the median position of these cells to deeper positions within the cortex. At the time of migration arrest [embryonic day 20 (E20) to E21], Dab1-suppressed cells were underrepresented in the upper approximately 40 microm of the cortex compared with controls, suggesting that Dab1 is essential for somal translocation through the cell-dense cortical plate. Closer examination of the morphology of Dab1-suppressed neurons at E20 revealed simplified leading processes that are less likely to contact the marginal zone (MZ), in which high levels of Reelin are expressed. Examination of Dab1-suppressed cells 3 d later (postnatal day 2) revealed simplified dendrites that are also less likely to contact the MZ. These data reveal a cell-autonomous role of Dab1 in dendritogenesis in the neocortex and suggest that remodeling of the leading process of a migrating neuron into a nascent dendrite by Reelin/Dab1 signaling plays an important role in cell positioning.},
	Author = {Olson, Eric C. and Kim, Seonhee and Walsh, Christopher A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {6},
	Organization = {Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, Department of Neurology, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {1767-75},
	Pii = {26/6/1767},
	Pubmed = {16467525},
	Title = {Impaired neuronal positioning and dendritogenesis in the neocortex after cell-autonomous Dab1 suppression},
	Uuid = {61680478-4675-4954-8031-242D49781043},
	Volume = {26},
	Year = {2006},
	url = {papers/Olson_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3000-05.2006}}

@article{Olveczky:2005,
	Abstract = {Songbirds learn their songs by trial-and-error experimentation, producing highly variable vocal output as juveniles. By comparing their own sounds to the song of a tutor, young songbirds gradually converge to a stable song that can be a remarkably good copy of the tutor song. Here we show that vocal variability in the learning songbird is induced by a basal-ganglia-related circuit, the output of which projects to the motor pathway via the lateral magnocellular nucleus of the nidopallium (LMAN). We found that pharmacological inactivation of LMAN dramatically reduced acoustic and sequence variability in the songs of juvenile zebra finches, doing so in a rapid and reversible manner. In addition, recordings from LMAN neurons projecting to the motor pathway revealed highly variable spiking activity across song renditions, showing that LMAN may act as a source of variability. Lastly, pharmacological blockade of synaptic inputs from LMAN to its target premotor area also reduced song variability. Our results establish that, in the juvenile songbird, the exploratory motor behavior required to learn a complex motor sequence is dependent on a dedicated neural circuit homologous to cortico-basal ganglia circuits in mammals.},
	Author = {Olveczky, Bence P. and Andalman, Aaron S. and Fee, Michale S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1545-7885},
	Journal = {PLoS Biol},
	Keywords = {21 Neurophysiology;Functional Laterality;Stereotaxic Techniques;Tetrodotoxin;Finches;Acoustic Stimulation;Animals;Muscle, Skeletal;24 Pubmed search results 2008;Basal Ganglia;Vocalization, Animal},
	Month = {5},
	Nlm_Id = {101183755},
	Number = {5},
	Organization = {McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.},
	Pages = {e153},
	Pii = {05-PLBI-RA-0094R1},
	Pubmed = {15826219},
	Title = {Vocal experimentation in the juvenile songbird requires a basal ganglia circuit},
	Uuid = {F002337E-5A3B-4248-9D23-F5335957180E},
	Volume = {3},
	Year = {2005},
	url = {papers/Olveczky_PLoSBiol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0030153}}

@article{Omi:2004,
	Abstract = {The effect of RNA interference (RNAi) induced by synthetic small interfering RNAs (siRNAs) on proliferating mammalian cells appears to last for approximately 3-7 days after its induction. Here we show that the RNAi activity induced by a synthetic 21-nucleotide siRNA duplex in postmitotic neurons, mouse primary hippocampal neurons and neurons that differentiated from mouse embryonal carcinoma P19 cells persists for at least 3 weeks, suggesting long-lasting RNAi activity in mammalian neurons. In addition, we also show that an apoptotic (or antiviral) pathway triggered by long dsRNAs is generated during neuronal differentiation of P19 cells, by which the sequence-specific RNAi activity involving long dsRNA appears to be masked.},
	Author = {Omi, Kazuya and Tokunaga, Katsushi and Hohjoh, Hirohiko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:55 -0400},
	Issn = {0014-5793},
	Journal = {FEBS Lett},
	Keywords = {Teratocarcinoma;Cell Differentiation;Animals;Cells, Cultured;Apoptosis;23 Technique;Hippocampus;Cell Line, Tumor;RNA, Small Interfering;Gene Expression Profiling;Time Factors;Mice, Inbred ICR;RNA, Double-Stranded;Support, Non-U.S. Gov't;Cytarabine;Neurons;23 RNAi;Mice;Cell Division;Tretinoin},
	Month = {1},
	Nlm_Id = {0155157},
	Number = {1-3},
	Organization = {Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.},
	Pages = {89-95},
	Pii = {S0014579304000171},
	Pubmed = {14759522},
	Title = {Long-lasting RNAi activity in mammalian neurons},
	Uuid = {6BE750E8-551C-4B19-8F4D-3DF5F98C0662},
	Volume = {558},
	Year = {2004},
	url = {papers/Omi_FEBSLett2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/S0014-5793(04)00017-1}}

@article{Omori:2004,
	Abstract = {The mechanism that regulates the plasticity of bone marrow cells (BMCs) into hepatocytes is poorly understood. We developed a green fluorescent protein/carbon tetrachloride model to find that BMC transplantation recovered liver damage. Serum albumin level and liver fibrosis were recovered by BMC transplantation. To understand the mechanism, we used DNA-chip technology to profile the change of transient gene expression before and after BMC transplantation. On the basis of gene expression with self-organizing map using specific equation, genes were classified into 153 clusters. The information is useful to understand the dramatic gene activation during the process of the plasticity of BMC.},
	Author = {Omori, Kaoru and Terai, Shuji and Ishikawa, Tsuyoshi and Aoyama, Kouji and Sakaida, Isao and Nishina, Hiroshi and Shinoda, Koh and Uchimura, Shunji and Hamamoto, Yoshihiko and Okita, Kiwamu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0014-5793},
	Journal = {FEBS Lett},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;Gene Expression Regulation;Bone Marrow Transplantation;Oligonucleotide Array Sequence Analysis;Female;Fibrosis;Liver;Mice, Inbred C57BL;11 Glia;Gene Expression Profiling;Green Fluorescent Proteins;Bone Marrow Cells;Multigene Family;Mice;Molecular Sequence Data;Hepatocytes;Carbon Tetrachloride},
	Month = {12},
	Nlm_Id = {0155157},
	Number = {1-2},
	Organization = {Department of Molecular Science and Applied Medicine (Gastroenterology and Hepatology), Yamaguchi University School of Medicine, Minami Kogushi 1-1-1, Ube, Yamaguchi 755 8505, Japan.},
	Pages = {10-20},
	Pii = {S0014579304013067},
	Pubmed = {15581608},
	Title = {Molecular signature associated with plasticity of bone marrow cell under persistent liver damage by self-organizing-map-based gene expression},
	Uuid = {9949C92A-E5B5-4042-BC19-B5572A27AD2B},
	Volume = {578},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.febslet.2004.09.090}}

@article{Ong:1995,
	Abstract = {Specimens of histologically normal human cerebral cortex and subcortical white matter were obtained during neurosurgical operations and studied by electron microscopy and immunocytochemistry using an antibody against HLA-DR. Greater numbers of labelled cells were present in the white matter than in the overlying cortex. The labelled cells consisted of ramified microglia and perivascular cells. Microglia were often found just outside the walls of small blood vessels, but perivascular cells were actually enclosed by two leaflets of basement membrane in the walls of capillaries, arterioles and venules up to 100 microns in luminal diameter. Labelled microglial processes were often seen enclosing neuronal processes in the cortex and myelinated and unmyelinated axons in the white matter. The enclosed processes appeared healthy, and without features of degenerating neurons. These observations are consistent with a previous suggestion that microglia continually modify the processes of central nervous system neurons by a process of phagocytosis. An intact blood-brain barrier is likely to be of great importance in preventing antigen presentation of the processed neuronal, and perhaps even oligodendrocytic, antigenic peptide fragments to circulating lymphocytes.},
	Author = {Ong, W. Y. and Leong, S. K. and Garey, L. J. and Tan, K. K. and Zhang, H. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0021-8359},
	Journal = {J Hirnforsch},
	Keywords = {Adult;Adolescent;Human;Microscopy, Electron;Tissue Fixation;HLA-DR Antigens;Immunohistochemistry;Female;11 Glia;Not relevant;Male;Brain;Cerebral Cortex;Support, Non-U.S. Gov't},
	Medline = {96128828},
	Nlm_Id = {0421521},
	Number = {4},
	Organization = {Department of Anatomy, National University of Singapore, Singapore.},
	Pages = {553-63},
	Pubmed = {8568227},
	Title = {A light and electron microscopic study of HLA-DR positive cells in the human cerebral cortex and subcortical white matter},
	Uuid = {895D6CDA-0A68-4C5C-8A98-69E8A2FAB3DF},
	Volume = {36},
	Year = {1995}}

@article{Onifer:1993,
	Abstract = {A clonal, neuronally-differentiating cell line, RN33B, was previously developed by retroviral infection of neural tissue derived from embryonic Sprague-Dawley raphe nuclei with a retrovirus encoding the temperature-sensitive allele of SV40 large T-antigen. In the present study, RN33B cells were transplanted into two target areas of the raphe nuclei, the spinal cord and hippocampal formation, of adult allogeneic hosts. Prior to transplantation, RN33B cells were infected in vitro with a retroviral vector carrying the Escherichia coli lacZ reporter gene and were visualized in vivo using a beta-galactosidase immunohistochemical technique. RN33B cells were seen throughout the spinal cord and hippocampal formation of the adult hosts at 15 days post-transplantation. T-antigen-immunoreactive nuclei were detected where RN33B cells were observed, but in much greater numbers than beta-galactosidase-immunoreactive cells. Bipolar RN33B cells were found in the spinal cord grey matter. RN33B cells with multipolar morphologies were visualized in the hippocampal and subicular pyramidal cell layers, and also in the dentate gyrus granule cell and polymorph layers, while bipolar RN33B cells were seen in the remainder of the hippocampal formation. The results suggest that immortalized neural cell lines of CNS origin can differentiate in the adult CNS with their ultimate morphology being determined by local tissue signals. We speculate that endogenous neutrophins may significantly influence RN33B cell differentiation in vivo. eng Journal Article},
	Author = {Onifer, S. M. and Whittemore, S. R. and Holets, V. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Journal = {Exp Neurol},
	Keywords = {Cell Differentiation;Rats, Sprague-Dawley;Rats, Inbred Lew;17 Transplant Regeneration;Lac Operon;Rats;L abstr;Cell Line;Escherichia coli/genetics;Raphe Nuclei/*cytology;Animal;Central Nervous System/*physiology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Neurons/*cytology/*transplantation},
	Number = {1},
	Organization = {Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami School of Medicine, Florida 33136.},
	Pages = {130-42.},
	Title = {Variable morphological differentiation of a raphe-derived neuronal cell line following transplantation into the adult rat CNS},
	Uuid = {1D42C629-673A-4304-8374-259FDFB128B7},
	Volume = {122},
	Year = {1993}}

@article{Ono:1999,
	Abstract = {Bone marrow transplantation with GFP-expressing cells from GFP-transgenic mice resulted in migration of GFP-positive cells into peripheral tissues and brain parenchyma. Most of these cells were observed as colony-like clusters. GFP-positive clusters in the brain were stained by antibody for ER-MP12, but those in the peripheral tissues were not. Since ER-MP12 antigen has been reported as a marker for murine early-stage myeloid precursor, this might suggest that some parts of phagocytic cells in the brain parenchyma such as microglia are derived from undifferentiated pluripotent hematopoietic cells.},
	Author = {Ono, K. and Takii, T. and Onozaki, K. and Ikawa, M. and Okabe, M. and Sawada, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0006-291X},
	Journal = {Biochem Biophys Res Commun},
	Keywords = {Lung;Animals;Bone Marrow Transplantation;Brain;Cell Movement;Mice, Transgenic;Liver;11 Glia;Green Fluorescent Proteins;Male;Reverse Transcriptase Polymerase Chain Reaction;Antigens, CD31;Transplantation Chimera;Mice, Inbred Strains;Mesencephalon;Flow Cytometry;Mice;Hematopoietic Stem Cells;Genes, Reporter;Biological Markers;Luminescent Proteins;Spleen;Research Support, Non-U.S. Gov't},
	Medline = {99400420},
	Month = {9},
	Nlm_Id = {0372516},
	Number = {3},
	Organization = {Faculty of Pharmaceutical Sciences, Nagoya City University, Mizuho, Nagoya, Aichi, 467-8603, Japan.},
	Pages = {610-4},
	Pii = {S0006291X99912238},
	Pubmed = {10471372},
	Title = {Migration of exogenous immature hematopoietic cells into adult mouse brain parenchyma under GFP-expressing bone marrow chimera},
	Uuid = {B95E346A-EEE9-49F1-900E-B050588553E7},
	Volume = {262},
	Year = {1999},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/bbrc.1999.1223}}

@article{Ono:1990,
	Abstract = {(E)-5-(2-Bromovinyl)-2'-deoxyuridine 5'-triphosphate (BrVdUTP) and (E)-5-(2-bromovinyl)-1-beta-D-arabinofuranosyluracil 5'-triphosphate (BrVarafUTP), which are known as specific inhibitors of herpes simplex viral (type 1 and 2) DNA polymerase, were found to be strong inhibitors of DNA polymerase gamma from human KB and murine myeloma cells. In fact BrVdUTP and BrVarafUTP were found to be stronger inhibitors of DNA polymerase gamma than of other DNA polymerases having viral (herpes simplex virus or retrovirus) origin or cellular (eukaryotic alpha and beta, or prokaryotic) origin. The mode of inhibition of DNA polymerase gamma by BrVdUTP and BrVarafUTP was competitive with respect to dTTP, the normal substrate. Whereas BrVdUTP was an efficient substrate for DNA polymerase gamma and other DNA polymerases that were examined, BrVarafUTP failed to serve as a substrate for DNA synthesis. Ki values for BrVdUTP (40 nM) and BrVarafUTP (7 nM) with DNA polymerase gamma, as determined with (rA)n.(dT) as the template.primer, were much smaller than the Km values for dTTP (0.16 microM and 0.71 microM for murine and human DNA polymerase gamma, respectively). Thus, the affinity of BrVdUTP or BrVarafUTP for DNA polymerase gamma was much stronger than that of dTTP.},
	Author = {Ono, K. and Nakane, H. and De Clercq, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0014-2956},
	Journal = {Eur J Biochem},
	Keywords = {DNA Polymerase I;24 Pubmed search results 2008;Arabinonucleotides;DNA Polymerase II;Kinetics;Simplexvirus;DNA Polymerase III;Cell Line;Antiviral Agents;DNA-Directed DNA Polymerase;DNA Replication;15 Retrovirus mechanism;Animals;Bromodeoxyuridine;Humans;Escherichia coli;KB Cells},
	Medline = {90322989},
	Month = {7},
	Nlm_Id = {0107600},
	Number = {3},
	Organization = {Laboratory of Viral Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.},
	Pages = {463-7},
	Pubmed = {2164928},
	Title = {Potent inhibitory effects of the 5'-triphosphates of (E)-5-(2-bromovinyl)-2'-deoxyuridine and (E)-5-(2-bromovinyl)-1-beta-D-arabinofuranosyluracil on DNA polymerase gamma},
	Uuid = {581808D6-ADCC-421D-B88A-E79D5F305E9A},
	Volume = {190},
	Year = {1990}}

@article{Orkin:2002,
	Abstract = {Hematopoietic stem cells (HSCs) provide for blood formation throughout the life of the individual. Studies of HSCs form a conceptual framework for the analysis of stem cells of other organ systems. We review here the origin of HSCs during embryological development, the relationship between hematopoiesis and vascular development and the potential plasticity of HSCs and other tissue stem cells. Recent experiments in the mouse have been widely interpreted as evidence for unprecedented transdifferentiation of tissue stem cells. The use of enriched, but impure, cell populations allows for alternative interpretation. In considering these findings, we draw a distinction here between the plasticity of adult stem cells and the heterogeneity of stem cell types that pre-exist within tissues.},
	Author = {Orkin, Stuart H. and Zon, Leonard I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2908},
	Journal = {Nat Immunol},
	Keywords = {Endothelium, Vascular;Cell Differentiation;Hematopoietic Stem Cells;Hematopoiesis;Research Support, U.S. Gov't, P.H.S.;review, tutorial;Mesoderm;Animals;Humans;review;Yolk Sac},
	Medline = {21918612},
	Month = {4},
	Nlm_Id = {100941354},
	Number = {4},
	Organization = {Division of Hematology and Oncology, Dana-Farber Cancer Institute and Children's Hospital, Department of Pediatrics, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115, USA. stuart\_orkin\@dfci.harvard.edu},
	Pages = {323-8},
	Pii = {ni0402-323},
	Pubmed = {11919568},
	Title = {Hematopoiesis and stem cells: plasticity versus developmental heterogeneity},
	Uuid = {BAA1C86B-C26D-11DA-969D-000D9346EC2A},
	Volume = {3},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ni0402-323}}

@article{Orlic:2001,
	Abstract = {Myocardial infarction leads to loss of tissue and impairment of cardiac performance. The remaining myocytes are unable to reconstitute the necrotic tissue, and the post-infarcted heart deteriorates with time. Injury to a target organ is sensed by distant stem cells, which migrate to the site of damage and undergo alternate stem cell differentiation; these events promote structural and functional repair. This high degree of stem cell plasticity prompted us to test whether dead myocardium could be restored by transplanting bone marrow cells in infarcted mice. We sorted lineage-negative (Lin-) bone marrow cells from transgenic mice expressing enhanced green fluorescent protein by fluorescence-activated cell sorting on the basis of c-kit expression. Shortly after coronary ligation, Lin- c-kitPOS cells were injected in the contracting wall bordering the infarct. Here we report that newly formed myocardium occupied 68\%of the infarcted portion of the ventricle 9 days after transplanting the bone marrow cells. The developing tissue comprised proliferating myocytes and vascular structures. Our studies indicate that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease.},
	Author = {Orlic, D. and Kajstura, J. and Chimenti, S. and Jakoniuk, I. and Anderson, S. M. and Li, B. and Pickel, J. and McKay, R. and Nadal-Ginard, B. and Bodine, D. M. and Leri, A. and Anversa, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Cell Differentiation;Proto-Oncogene Protein c-kit;Connexin 43;DNA-Binding Proteins;Animals;Transcription Factors;Bone Marrow Transplantation;Ki-67 Antigen;Female;Myocardium;Mice, Transgenic;Mice, Inbred C57BL;Green Fluorescent Proteins;Male;Research Support, U.S. Gov't, P.H.S.;Mice;Luminescent Proteins;Myocardial Infarction;Research Support, Non-U.S. Gov't},
	Medline = {21184879},
	Month = {4},
	Nlm_Id = {0410462},
	Number = {6829},
	Organization = {Hematopoiesis Section, Genetics and Molecular Biology Branch, NHGRI, NIH, Bethesda, MD 20892, USA.},
	Pages = {701-5},
	Pii = {35070587},
	Pubmed = {11287958},
	Title = {Bone marrow cells regenerate infarcted myocardium},
	Uuid = {BAA1C524-C26D-11DA-969D-000D9346EC2A},
	Volume = {410},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35070587}}

@article{Orlov:1988,
	Author = {Orlov, A. A. and Kurzina, N. P. and Shutov, A. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0097-0549},
	Journal = {Neurosci Behav Physiol},
	Keywords = {Conditioning (Psychology);Rats;Motor Activity;Animals;Male;24 Pubmed search results 2008;Neurons;Frontal Lobe},
	Medline = {88261667},
	Nlm_Id = {0330471},
	Number = {1},
	Organization = {Department of Physiology of Higher Nervous Activity, A. A. Zhdanov Leningrad State University.},
	Pages = {31-7},
	Pubmed = {3386793},
	Title = {Activity of medial wall neurons in frontal cortex of rat brain during delayed response reactions},
	Uuid = {EBF449DB-B4EA-4A35-9D60-7A126ADD1C25},
	Volume = {18},
	Year = {1988}}

@article{Ory:1996,
	Abstract = {We have generated a human 293-derived retroviral packaging cell line (293GPG) capable of producing high titers of recombinant Moloney murine leukemia virus particles that have incorporated the vesicular stomatitis virus G (VSV-G) protein. To achieve expression of the retroviral gag-pol polyprotein, the precise coding sequences for gag-pol were introduced into a vector which utilizes totally nonretroviral signals for gene expression. Because constitutive expression of the VSV-G protein is toxic in 293 cells, we used the tetR/VP 16 transactivator and teto minimal promoter system for inducible, tetracycline-regulatable expression of VSV-G. After stable transfection of the 293GPG packaging cell line with the MFG.SnlsLacZ retroviral vector construct, it was possible to readily isolate stable virus-producing cell lines with titers approaching 10(7) colony-forming units/ml. Transient transfection of 293GPG cells using a modified version of MFG.SnlsLacZ, in which the cytomegalovirus IE promoter was used to drive transcription of the proviral genome, led to titers of approximately 10(6) colony-forming units/ml. The retroviral/VSV-G pseudotypes generated using 293GPG cells were significantly more resistant to human complement than commonly used amphotropic vectors and could be highly concentrated (>1000-fold). This new packaging cell line may prove to be particularly useful for assessing the potential use of retroviral vectors for direct in vivo gene transfer. The design of the cell line also provides at least theoretical advantages over existing cell lines with regard to the possible release of replication-competent virus. 0027-8424 Journal Article},
	Author = {Ory, D. S. and Neugeboren, B. A. and Mulligan, R. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {RNA-Directed DNA Polymerase;Moloney murine leukemia virus;Blood;Cell Line;Vesicular stomatitis-Indiana virus;Animals;Kidney;3T3 Cells;Transfection/*methods;Base Sequence;Research Support, U.S. Gov't, P.H.S.;Culture Media;Promoter Regions (Genetics);Transfection;15 Retrovirus mechanism;beta-Galactosidase/biosynthesis;*Membrane Glycoproteins;Support, U.S. Gov't, P.H.S.;Viral Envelope Proteins;Viral Envelope Proteins/*biosynthesis/genetics;Moloney murine leukemia virus/*genetics;Membrane Glycoproteins;beta-Galactosidase;J;Recombinant Fusion Proteins;Mice;Vesicular stomatitis-Indiana virus/*genetics/metabolism;Polymerase Chain Reaction;Recombinant Fusion Proteins/*biosynthesis;Humans;DNA Primers;Human;RNA-Directed DNA Polymerase/biosynthesis},
	Medline = {97030206},
	Month = {10},
	Nlm_Id = {7505876},
	Number = {21},
	Organization = {Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142, USA.},
	Pages = {11400-6},
	Pubmed = {8876147},
	Title = {A stable human-derived packaging cell line for production of high titer retrovirus/vesicular stomatitis virus G pseudotypes},
	Uuid = {2D9429E6-AEE1-11DA-A7AA-000D9346EC2A},
	Volume = {93},
	Year = {1996},
	url = {papers/Ory_ProcNatlAcadSciUSA1996.pdf}}

@article{Osada:2005,
	Abstract = {Nuclei isolated from green fluorescent protein-marked neurons in the cerebral cortex of juvenile mice (14-21 d after birth) were injected into enucleated oocytes that were allowed to develop into blastocysts. Embryonic stem (ES) cell lines were established from the inner cell mass of 76 cloned blastocysts after injecting 2026 neuronal nuclei. Some ES cells were injected individually into enucleated oocytes (nuclear transfer). Other ES cells were transferred into the blastocoeles of tetraploid blastocysts (tetraploid complementation). Two-cell embryos after nuclear transfer were transferred to the oviducts of surrogate mothers. Four (1.5\%) of 272 nuclear-transferred two-cell embryos developed to term, and two (0.7\%) developed into fertile adults. Nineteen (1.9\%) of 992 tetraploid blastocysts receiving ES cells reached term, and 10 (1.0\%) developed into adults. These findings demonstrate that some of the nuclei of differentiated neurons in the cerebral cortex of juvenile mice maintain developmental pluripotency.},
	Author = {Osada, Tomoharu and Tamamaki, Nobuaki and Song, Si-Young Y. and Kakazu, Naoki and Yamazaki, Yukiko and Makino, Hatsune and Sasaki, Ayako and Hirayama, Teruyoshi and Hamada, Shun and Nave, Klaus-Armin A. and Yanagimachi, Ryuzo and Yagi, Takeshi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {08 Aberrant cell cycle;22 Stem cells;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {37},
	Organization = {Core Research for Evolutional Science and Technology Research Agency, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan. osada\@libra.ls.m-kagakia.co.jp},
	Pages = {8368-74},
	Pii = {25/37/8368},
	Pubmed = {16162918},
	Title = {Developmental pluripotency of the nuclei of neurons in the cerebral cortex of juvenile mice},
	Uuid = {DED7D68C-1038-45A6-AC11-7E23B2B9099F},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1591-05.2005}}

@article{Osuga:2000,
	Abstract = {Cyclin-dependent kinases (CDKs) are commonly known to regulate cell proliferation. However, previous reports suggest that in cultured postmitotic neurons, activation of CDKs is a signal for death rather than cell division. We determined whether CDK activation occurs in mature adult neurons during focal stroke in vivo and whether this signal was required for neuronal death after reperfusion injury. Cdk4/cyclin D1 levels and phosphorylation of its substrate retinoblastoma protein (pRb) increase after stroke. Deregulated levels of E2F1, a transcription factor regulated by pRb, are also observed. Administration of a CDK inhibitor blocks pRb phosphorylation and the increase in E2F1 levels and dramatically reduces neuronal death by 80\%. These results indicate that CDKs are an important therapeutic target for the treatment of reperfusion injury after ischemia. 0027-8424 Journal Article},
	Author = {Osuga, H. and Osuga, S. and Wang, F. and Fetni, R. and Hogan, M. J. and Slack, R. S. and Hakim, A. M. and Ikeda, J. E. and Park, D. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Animals;Rats;Enzyme Inhibitors/*pharmacology;Neurons/pathology/physiology;*Cell Cycle Proteins;Reperfusion Injury/*prevention &control;Cyclin-Dependent Kinases/*antagonists &inhibitors/metabolism;Apoptosis;EE pdf;Rats, Sprague-Dawley;Transcription Factors/metabolism;*Carrier Proteins;08 Aberrant cell cycle;Male;Support, Non-U.S. Gov't;Cerebrovascular Circulation/*drug effects/physiology;Brain/blood supply/pathology/physiopathology;Ischemic Attack, Transient/enzymology/*physiopathology;Piperidines/*pharmacology;Flavonoids/*pharmacology;Cyclin D1/metabolism},
	Number = {18},
	Organization = {Department of Molecular Neuroscience, Institute of Medical Sciences, Tokai University School of Medicine, Bohseidai, Isehara, Kanagawa, Japan 259-1193.},
	Pages = {10254-9},
	Pubmed = {10944192},
	Title = {Cyclin-dependent kinases as a therapeutic target for stroke},
	Uuid = {88EAA8AC-0384-4F50-952D-85599D95B8E5},
	Volume = {97},
	Year = {2000},
	url = {papers/Osuga_ProcNatlAcadSciUSA2000.pdf}}

@article{Otaki:1999,
	Abstract = {Neurestin is a putative transmembrane protein whose expression is developmentally regulated in neurons. Here we examined neurestin expression pattern in mitral/tufted cells in the developing rat olfactory bulb. In the main olfactory bulb, neurestin expression was segregated in the dorso-rostral area and in the ventro-caudal area, but not in between. In the accessory olfactory bulb, neurestin expression was found only in the far caudal area. This area did not completely correspond to a caudal half of the vomeronasal nerve and glomerular layers positive for a G-protein Go alpha. These spatio-temporal expression patterns suggest that neurestin functions as a target recognition molecule that specifies zonal projection patterns of olfactory and vomeronasal sensory neurons.},
	Author = {Otaki, J. M. and Firestein, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Neuroreport},
	Keywords = {In Situ Hybridization;*Brain Mapping;Membrane Proteins/*biosynthesis;Rats, Sprague-Dawley;Rats;Animal;Support, U.S. Gov't, P.H.S.;I abstr;Nerve Tissue Proteins/*biosynthesis;Fetal Development/physiology;13 Olfactory bulb anatomy;Olfactory Bulb/embryology/growth &development/*metabolism},
	Number = {12},
	Organization = {Department of Biological Sciences, Columbia University, New York, NY 10027, USA.},
	Pages = {2677-80.},
	Title = {Segregated expression of neurestin in the developing olfactory bulb},
	Uuid = {DFC21454-DFDA-48D1-9798-088B86EA236C},
	Volume = {10},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10574391}}

@article{Ourednik:2001,
	Abstract = {Many central nervous system regions at all stages of life contain neural stem cells (NSCs). We explored how these disparate NSC pools might emerge. A traceable clone of human NSCs was implanted intraventricularly to allow its integration into cerebral germinal zones of Old World monkey fetuses. The NSCs distributed into two subpopulations: One contributed to corticogenesis by migrating along radial glia to temporally appropriate layers of the cortical plate and differentiating into lamina-appropriate neurons or glia; the other remained undifferentiated and contributed to a secondary germinal zone (the subventricular zone) with occasional members interspersed throughout brain parenchyma. An early neurogenetic program allocates the progeny of NSCs either immediately for organogenesis or to undifferentiated pools for later use in the "postdevelopmental"brain. 0036-8075 Journal Article},
	Author = {Ourednik, V. and Ourednik, J. and Flax, J. D. and Zawada, W. M. and Hutt, C. and Yang, C. and Park, K. I. and Kim, S. U. and Sidman, R. L. and Freed, C. R. and Snyder, E. Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Science},
	Keywords = {10 Development;Cell Differentiation;Human;Animals;Stem Cell Transplantation;Brain Tissue Transplantation;Transplantation, Heterologous;Stem Cells/*cytology;*Cell Movement;Macaca radiata/embryology;Prosencephalon/*cytology/*embryology;Cell Lineage;Support, Non-U.S. Gov't;Clone Cells/cytology/transplantation;Neurons/*cytology/transplantation;Cell Transplantation;Neocortex/*cytology/*embryology;F},
	Number = {5536},
	Organization = {Department of Pediatrics, Children's Hospital, Harvard Medical School, 248 Enders Building, 300 Longwood Avenue, Boston, MA 02115, USA.},
	Pages = {1820-4},
	Pubmed = {11474066},
	Title = {Segregation of human neural stem cells in the developing primate forebrain},
	Uuid = {0196E2E7-7C2B-451B-BF39-F60F9A438750},
	Volume = {293},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11474066}}

@article{Overstreet:2004,
	Abstract = {Neurogenesis in the dentate gyrus continues into adulthood, yet little is known about the function of newly born neurons or how they integrate into an existing network of mature neurons. We made transgenic mice that selectively and transiently express enhanced green fluorescent protein (EGFP) in newly born granule cells of the dentate gyrus under the transcriptional control of proopiomelanocortin (POMC) genomic sequences. Analysis of transgenic pedigrees with truncation or deletion mutations indicated that EGFP expression in the dentate gyrus required cryptic POMC promoter regions dispensable for arcuate hypothalamic or pituitary expression. Unlike arcuate neurons, dentate granule cells did not express the endogenous POMC gene. EGFP-positive neurons had immature properties, including short spineless dendrites and small action potentials. Colocalization with bromodeoxyuridine indicated that EGFP-labeled granule cells were approximately 2 weeks postmitotic. EGFP-labeled cells expressed markers for immature granule cells but not the glial marker GFAP. The number of EGFP-labeled neurons declined with age and increased with exercise, paralleling neurogenesis. Our results indicate that POMC-EGFP marks immature granule cells and that adult-generated granule cells integrate quite slowly into the hippocampal circuitry.},
	Author = {Overstreet, Linda S. and Hentges, Shane T. and Bumaschny, Viviana F. and de Souza, Flavio S. J. and Smart, James L. and Santangelo, Andrea M. and Low, Malcolm J. and Westbrook, Gary L. and Rubinstein, Marcelo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Genes, Reporter;Exertion;Animals;Aging;Cell Count;Mice, Transgenic;Cell Movement;Mice, Inbred C57BL;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;Action Potentials;Sialic Acids;Pro-Opiomelanocortin;Dentate Gyrus;Neurons;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Luminescent Proteins;Biological Markers;Bromodeoxyuridine;Promoter Regions (Genetics);Neural Cell Adhesion Molecule L1;Transgenes},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {13},
	Organization = {Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA. overstre\@ohsu.edu},
	Pages = {3251-9},
	Pii = {24/13/3251},
	Pubmed = {15056704},
	Title = {A transgenic marker for newly born granule cells in dentate gyrus},
	Uuid = {D04106EE-E28D-4D50-92CC-A51B5E595DC4},
	Volume = {24},
	Year = {2004},
	url = {papers/Overstreet_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5173-03.2004}}

@article{Wadiche:2005,
	Abstract = {Neurogenesis in the dentate gyrus begins before birth, but then continues into adulthood. Consequently, many newborn granule cells must integrate into a pre-existing hippocampal network. Little is known about the timing of this process or the characteristics of the first established synapses. We used mice that transiently express EGFP in newborn granule cells to examine their synaptic input. Although newborn granule cells had functional glutamate receptors, evoked and spontaneous synaptic currents were exclusively GABAergic with immature characteristics including slow rise and decay phases and depolarized reversal potentials. Synaptic currents in newborn granule cells were relatively insensitive to the GABAA receptor modulator zolpidem compared to neighboring mature granule cells. Consistent with the kinetics and pharmacology, newborn granule cells isolated by fluorescent cell sorting lacked the alpha1 GABAA receptor subunit. Our results indicate that newborn granule cells initially receive only GABAergic synapses even in the adult.},
	Author = {Overstreet Wadiche, and Bromberg, and Bensen, and Westbrook,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {0375404},
	Organization = {Oregon Health & Science University, Vollum Institute, Portland, OR, USA.},
	Pii = {00633.2005},
	Pubmed = {16033936},
	Title = {GABAergic Signaling to Newborn Neurons in Dentate Gyrus},
	Uuid = {07003BB4-C456-4521-A63C-E38F2CBDB8F3},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1152/jn.00633.2005}}

@article{Overstreet-Wadiche:2006,
	Abstract = {A substantial fraction of adult-generated granule cells in the dentate gyrus survive and integrate into the existing neuronal network. These newborn neurons must navigate the environment of the adult brain, a setting that is presumably less optimized for neuronal maturation compared with that in the developing brain. We used EGFP (enhanced green fluorescent protein) expression in newborn granule cells to compare the maturation of adult-generated granule cells to those generated in neonates. Labeled newborn granule cells had indistinguishable physiological properties in adults and neonates, indicating they were at the same functional stage. However, the maturation of adult-generated granule cells was slower than neonatal-generated granule cells. Depolarizing GABAergic network activity and transcription factor activation were reduced in adults relative to neonates, suggesting a role for neural activity in the maturation of newborn granule cells. Consistent with this idea, maturation was altered in mice lacking the GABA synthetic enzyme GAD65 (glutamic acid decarboxylase 65). Together, these results provide evidence that activity-dependent processes in the local environment influence the maturation of newborn granule cells.},
	Author = {Overstreet-Wadiche, Linda S. and Bensen, Aesoon L. and Westbrook, Gary L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Aging;Neurons;24 Pubmed search results 2008;research support, n.i.h., extramural ;Nerve Regeneration;Cell Proliferation;Hippocampus;Mice, Inbred C57BL;Time Factors;Animals, Newborn;Animals;comparative study ;Cells, Cultured;Cerebellar Nuclei;Mice},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {8},
	Organization = {Vollum Institute, L474, Oregon Health & Science University, Portland, Oregon 97239, USA. overstre\@ohsu.edu},
	Pages = {2326-34},
	Pii = {26/8/2326},
	Pubmed = {16495460},
	Title = {Delayed development of adult-generated granule cells in dentate gyrus},
	Uuid = {5CDCFAD3-A40A-4B9D-BEC7-FC82634890BE},
	Volume = {26},
	Year = {2006},
	url = {papers/Overstreet-Wadiche_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4111-05.2006}}

@article{Overstreet-Wadiche:2006a,
	Abstract = {In humans and experimental animals, structural and functional changes in neural circuits can accompany the development of epilepsy. In the dentate gyrus, seizures enhance adult neurogenesis, but it is unclear to what extent newborn granule cells participate in seizure-induced synaptic reorganization. During the first weeks of their existence, mouse newborn granule cells labeled with enhanced green fluorescent protein have only short dendrites that lack excitatory input. We report that pilocarpine-induced seizures accelerated the morphological development of labeled granule cells, causing their dendrites to extend through the molecular layer. In whole-cell recordings 5-16 d after seizure induction, perforant-path stimulation now evoked glutamatergic input to newborn granule cells. These synaptic responses were mediated by monosynaptic as well as recurrent polysynaptic input. Thus, seizures facilitated functional integration of adult-generated granule cells. One month later, subsequent generations of newborn cells also showed alterations in dendrite morphology, suggesting persistent effects of seizures on granule cell maturation. The sensitivity of newborn granule cells to seizures could contribute to hyperexcitability during the latent period.},
	Author = {Overstreet-Wadiche, Linda S. and Bromberg, Daniel A. and Bensen, Aesoon L. and Westbrook, Gary L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {15},
	Organization = {Vollum Institute, L474, Oregon Health and Science University, Portland, Oregon 97239, USA. overstre\@ohsu.edu},
	Pages = {4095-103},
	Pii = {26/15/4095},
	Pubmed = {16611826},
	Title = {Seizures accelerate functional integration of adult-generated granule cells},
	Uuid = {A28CE264-D3F0-4579-ABB4-582CC192F03F},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5508-05.2006}}

@article{Packer:2003,
	Abstract = {Neural progenitor cells are widespread throughout the adult central nervous system but only give rise to neurons in specific loci. Negative regulators of neurogenesis have therefore been postulated, but none have yet been identified as subserving a significant role in the adult brain. Here we report that nitric oxide (NO) acts as an important negative regulator of cell proliferation in the adult mammalian brain. We used two independent approaches to examine the function of NO in adult neurogenesis. In a pharmacological approach, we suppressed NO production in the rat brain by intraventricular infusion of an NO synthase inhibitor. In a genetic approach, we generated a null mutant neuronal NO synthase knockout mouse line by targeting the exon encoding active center of the enzyme. In both models, the number of new cells generated in neurogenic areas of the adult brain, the olfactory subependyma and the dentate gyrus, was strongly augmented, which indicates that division of neural stem cells in the adult brain is controlled by NO and suggests a strategy for enhancing neurogenesis in the adult central nervous system. 0027-8424 Journal Article},
	Author = {Packer, M. A. and Stasiv, Y. and Benraiss, A. and Chmielnicki, E. and Grinberg, A. and Westphal, H. and Goldman, S. A. and Enikolopov, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {NG-Nitroarginine Methyl Ester/pharmacology;Central Nervous System/metabolism;Bromodeoxyuridine/pharmacology;Nitric-Oxide Synthase/metabolism;Rats;Animals;Microscopy, Confocal;Exons;Neurons/*metabolism/*physiology;Open Reading Frames;Models, Genetic;Nitric Oxide/*metabolism;Support, Non-U.S. Gov't;In Situ Nick-End Labeling;Mice, Knockout;Recombination, Genetic;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Molecular Sequence Data;C pdf;Brain/metabolism},
	Number = {16},
	Organization = {Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.},
	Pages = {9566-71},
	Title = {Nitric oxide negatively regulates mammalian adult neurogenesis},
	Uuid = {6B46DAFA-5804-4644-9FB6-87D6E306D47C},
	Volume = {100},
	Year = {2003},
	url = {papers/Packer_ProcNatlAcadSciUSA2003.pdf}}

@article{Pagano:2004,
	Abstract = {The family of cyclin-dependent kinases (Cdks) lies at the core of the machinery that drives the cell division cycle. Studies in cultured mammalian cells have provided insight into the cellular functions of many Cdks. Recent Cdk and cyclin knockouts in the mouse show that the functions of G1 cell cycle regulatory genes are often essential only in specific cell types, pointing to our limited understanding of tissue-specific expression, redundancy, and compensating mechanisms in the Cdk network.},
	Author = {Pagano, Michele and Jackson, Peter K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:55 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Embryo;Cell Differentiation;10 Development;Gene Expression Regulation, Developmental;G1 Phase;Cyclin-Dependent Kinases;Genes, cdc;Signal Transduction;Cyclins;review, tutorial;Mice;Animals;review;Organogenesis},
	Month = {9},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA. michele.pagano\@med.nyu.edu},
	Pages = {535-8},
	Pii = {S0092867404007949},
	Pubmed = {15339658},
	Title = {Wagging the dogma; tissue-specific cell cycle control in the mouse embryo},
	Uuid = {FE61C8B1-5636-4C20-91E6-C1825274BF9D},
	Volume = {118},
	Year = {2004},
	url = {papers/Pagano_Cell2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2004.08.013}}

@article{Pal:1988,
	Abstract = {We are using fluorescent endogenous phospholipids in virus membranes to study the factors that promote fusion on interaction with receptor membranes. To this end, vesicular stomatitis virus (VSV) grown in baby hamster kidney (BHK-21) cells was biologically labeled with fluorescent lipids, primarily phosphatidylcholine and phosphatidylethanolamine, derived from pyrene fatty acids. The pyrene lipids present in the virions showed a fluorescence spectrum typical of pyrene with an intense monomer and a broad excimer. Interaction of pyrene lipid labeled VSV with serum lipoproteins led to a spontaneous fast transfer of the small amount of pyrene fatty acids present in the envelope (t1/2 less than or equal to 7 min), followed by a considerably slower transfer of pyrene phospholipids from the membrane of the virions (t1/2 greater than or equal to 12 h). Incubation of pyrene phospholipid labeled VSV with phosphatidylserine small unilamellar vesicles resulted in fusion at low pH (pH 5.0) as measured by the change in the excimer/monomer fluorescence intensity ratio. Fusion kinetics was rapid, reaching a plateau after 4 min at pH 5.0 and 37 degrees C. Only negligible fusion was noted at neutral pH or at 4 degrees C. Fully infectious virions labeled biologically with fluorescent lipids provide a useful tool for studying mechanisms of cell-virus interactions and neutralization of viral infectivity by specific monoclonal antibodies reactive with viral membrane glycoprotein.},
	Author = {Pal, R. and Barenholz, Y. and Wagner, R. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0006-2960},
	Journal = {Biochemistry},
	Keywords = {Membrane Lipids;Phospholipids;Research Support, Non-U.S. Gov't;Kinetics;Liposomes;Research Support, U.S. Gov't, P.H.S.;Cell Line;Lipid Bilayers;Fluorescent Dyes;Receptors, Virus;Pyrenes;Vesicular stomatitis-Indiana virus;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Medline = {88163585},
	Month = {1},
	Nlm_Id = {0370623},
	Number = {1},
	Organization = {Department of Microbiology, University of Virginia School of Medicine, Charlottesville 22908.},
	Pages = {30-6},
	Pubmed = {2831956},
	Title = {Pyrene phospholipid as a biological fluorescent probe for studying fusion of virus membrane with liposomes},
	Uuid = {2BD2D776-EE2C-11DA-8605-000D9346EC2A},
	Volume = {27},
	Year = {1988}}

@article{Palma:2004,
	Abstract = {Stem cells are crucial for normal development and homeostasis, and their misbehavior may be related to the origin of cancer. Progress in these areas has been difficult because the mechanisms regulating stem cell lineages are not well understood. Here, we have investigated the role of the SHH-GLI pathway in the developing mouse neocortex. The results show that SHH signaling endogenously regulates the number of embryonic and postnatal mouse neocortical cells with stem cell properties, and controls precursor proliferation in a concentration-dependent manner in cooperation with EGF signaling. These findings identify a crucial mechanism for the regulation of the number of cells with stem cell properties that is unexpectedly conserved in different stem cell niches.},
	Author = {Palma, Veronica and Ruiz i Altaba, Ariel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {10 Development;Signal Transduction;Animals;Transcription Factors;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Trans-Activators;Mice, Mutant Strains;Phenotype;Neocortex;Mice, Inbred C57BL;Research Support, U.S. Gov't, P.H.S.;Mice, Knockout;Epidermal Growth Factor;Mice;Cell Division;22 Stem cells;Stem Cells;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Month = {1},
	Nlm_Id = {8701744},
	Number = {2},
	Organization = {The Skirball Institute and Department of Cell Biology, NYU School of Medicine, 540 First Avenue, New York, NY 10016, USA.},
	Pages = {337-45},
	Pii = {dev.00930},
	Pubmed = {14681189},
	Title = {Hedgehog-GLI signaling regulates the behavior of cells with stem cell properties in the developing neocortex},
	Uuid = {A80346D0-7B39-424C-996C-E5BE181816E6},
	Volume = {131},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.00930}}

@article{Palma:2005,
	Abstract = {Sonic hedgehog (Shh) signaling controls many aspects of ontogeny, orchestrating congruent growth and patterning. During brain development, Shh regulates early ventral patterning while later on it is critical for the regulation of precursor proliferation in the dorsal brain, namely in the neocortex, tectum and cerebellum. We have recently shown that Shh also controls the behavior of cells with stem cell properties in the mouse embryonic neocortex, and additional studies have implicated it in the control of cell proliferation in the adult ventral forebrain and in the hippocampus. However, it remains unclear whether it regulates adult stem cell lineages in an equivalent manner. Similarly, it is not known which cells respond to Shh signaling in stem cell niches. Here we demonstrate that Shh is required for cell proliferation in the mouse forebrain's subventricular zone (SVZ) stem cell niche and for the production of new olfactory interneurons in vivo. We identify two populations of Gli1(+) Shh signaling responding cells: GFAP(+) SVZ stem cells and GFAP(-) precursors. Consistently, we show that Shh regulates the self-renewal of neurosphere-forming stem cells and that it modulates proliferation of SVZ lineages by acting as a mitogen in cooperation with epidermal growth factor (EGF). Together, our data demonstrate a critical and conserved role of Shh signaling in the regulation of stem cell lineages in the adult mammalian brain, highlight the subventricular stem cell astrocytes and their more abundant derived precursors as in vivo targets of Shh signaling, and demonstrate the requirement for Shh signaling in postnatal and adult neurogenesis.},
	Author = {Palma, Ver{\'o}nica and Lim, Daniel A. and Dahmane, Nadia and S{\'a}nchez, Pilar and Brionne, Thomas C. and Herzberg, Claudia D. and Gitton, Yorick and Carleton, Alan and Alvarez-Buylla, Arturo and Altaba, Ariel Ruiz I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {04 Adult neurogenesis factors},
	Month = {1},
	Nlm_Id = {8701744},
	Number = {2},
	Organization = {The Skirball Institute, NYU School of Medicine, 540 First Avenue, New York, NY 10016, USA.},
	Pages = {335-44},
	Pii = {dev.01567},
	Pubmed = {15604099},
	Title = {Sonic hedgehog controls stem cell behavior in the postnatal and adult brain},
	Uuid = {1B9B5223-93BC-46C1-B2D2-0AA256B085BF},
	Volume = {132},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.01567}}

@article{Palmer:2006,
	Abstract = {ABSTRACT: BACKGROUND: Cell-based microarrays were first described by Ziauddin and Sabatini in 2001 as a powerful new approach for performing high throughput screens of gene function. An important application of cell-based microarrays is in screening for proteins that modulate gene networks. To this end, cells are grown over the surface of arrays of RNAi or expression reagents. Cells growing in the immediate vicinity of the arrayed reagents are transfected and the arrays can then be scanned for cells showing localised changes in function. Here we describe the construction of a large-scale microarray using expression plasmids containing human genes, its use in screening for genes that induce apoptosis when over-expressed and the characterisation of a number of these genes by following the transcriptional response of cell cultures during their induction of apoptosis. RESULTS: High-density cell-based arrays were successfully fabricated using 1,959 un-tagged open reading frames (ORFs) taken from the Mammalian Gene Collection (MGC) in mammalian expression vectors. The arrays were then used to screen for genes inducing apoptosis in Human Embryonic Kidney (HEK293T) cells. Using this approach, 10 genes were clearly identified and confirmed to induce apoptosis. Some of these genes have previously been linked to apoptosis, others not. The mechanism of action of three of the 10 genes were then characterised further by following the transcriptional events associated with apoptosis induction using expression profiling microarrays. This data demonstrates a clear pro-apoptotic transcriptional response in cells undergoing apoptosis and also suggests the use of common apoptotic pathways regardless of the nature of the over-expressed protein triggering cell death. CONCLUSIONS: This study reports the design and use of the first truly large-scale cell-based microarrays for over-expression studies. Ten genes were confirmed to induce apoptosis, some of which were not previously known to possess this activity. Transcriptome analysis on three of the 10 genes demonstrated their use of similar pathways to invoke apoptosis.},
	Author = {Palmer, and Miller, and Freeman,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {1471-2164},
	Journal = {BMC Genomics},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {100965258},
	Number = {1},
	Pages = {145},
	Pii = {1471-2164-7-145},
	Pubmed = {16768789},
	Title = {Identification and characterisation of human apoptosis inducing proteins using cell-based transfection microarrays and expression analysis},
	Uuid = {E872A026-0CBF-4C73-8158-B72D4E33C9B4},
	Volume = {7},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2164-7-145}}

@article{Palmer:2000,
	Abstract = {The thin lamina between the hippocampal hilus and granule cell layer, or subgranule zone (SGZ), is an area of active proliferation within the adult hippocampus known to generate new neurons throughout adult life. Although the neuronal fate of many dividing cells is well documented, little information is available about the phenotypes of cells in S- phase or how the dividing cells might interact with neighboring cells in the process of neurogenesis. Here, we make the unexpected observation that dividing cells are found in dense clusters associated with the vasculature and roughly 37\%of all dividing cells are immunoreactive for endothelial markers. Most of the newborn endothelial cells disappear over several weeks, suggesting that neurogenesis is intimately associated with a process of active vascular recruitment and subsequent remodeling. The present data provide the first evidence that adult neurogenesis occurs within an angiogenic niche. This environment may provide a novel interface where mesenchyme-derived cells and circulating factors influence plasticity in the adult central nervous system.},
	Author = {Palmer, T. D. and Willhoite, A. R. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Cell Survival;Rats/*physiology;BB;Neurons/*cytology/physiology;Aging/physiology;Female;Endothelium, Vascular/cytology;02 Adult neurogenesis migration;Animal;Capillaries/physiology;Stem Cells/cytology/metabolism;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;Rats, Inbred F344;Animals, Newborn;Neuroglia/physiology;Intermediate Filament Proteins/metabolism;Hippocampus/*blood supply/*cytology;Support, U.S. Gov't, P.H.S.;Cell Division;S Phase;Cell Aggregation/physiology;Bromodeoxyuridine;Blood Vessels/cytology/physiology;Neovascularization, Physiologic/physiology},
	Number = {4},
	Organization = {Stanford University, Department of Neurosurgery, Palo Alto, California 94305, USA. tpalmer\@stanford.edu},
	Pages = {479-94.},
	Title = {Vascular niche for adult hippocampal neurogenesis},
	Uuid = {C6417E5B-D2FA-4877-84CB-88CD177213F6},
	Volume = {425},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10975875}}

@article{Palmer:1999,
	Abstract = {During development of the mammalian brain, both neurons and glia are generated from multipotent neural stem cells. Although neurogenesis ceases in most areas at birth, stem cells continue to generate neurons within the subventricular zone and hippocampal dentate gyrus throughout adult life. In this work, we provide the first demonstration that precursors native to regions of the adult brain that generate only glia can also generate neurons after exposure to FGF-2 in vitro. When progenitors isolated from hippocampal tissue were directly compared with cells isolated from the neocortex, both populations were able to initiate a program of proliferative neurogenesis. Genetic marking and lineage analysis showed that a majority of the cells able to generate neurons were multipotent precursors; however, progeny from these precursors acquired the competence to differentiate into neurons only after exposure to FGF-2. The recruitment of similar FGF-2-responsive cells from the adult optic nerve, a structure well isolated from the neurogenic zones within the brain, confirmed that neuron-competent precursors naturally exist in widely divergent tissues of the adult brain.},
	Author = {Palmer, T. D. and Markakis, E. A. and Willhoite, A. R. and Safar, F. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Cells, Cultured;Rats;Female;Animal;Stem Cells/*cytology/drug effects;C abstr;Nerve Tissue Proteins/analysis;Male;Fibroblast Growth Factor, Basic/*pharmacology;Neuroglia/*cytology/drug effects;Rats, Inbred F344;Support, Non-U.S. Gov't;Organ Specificity;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Biological Markers/analysis;Hippocampus/*cytology;Neurons/*cytology/drug effects;Brain/*cytology/physiology},
	Number = {19},
	Organization = {The Salk Institute, Laboratory of Genetics, La Jolla, California 92037, USA.},
	Pages = {8487-97.},
	Title = {Fibroblast growth factor-2 activates a latent neurogenic program in neural stem cells from diverse regions of the adult CNS},
	Uuid = {EE62F486-9D54-466B-B51B-29DC7A6D8050},
	Volume = {19},
	Year = {1999},
	url = {papers/Palmer_JNeurosci1999.pdf}}

@article{Palmer:1995,
	Abstract = {Neurogenesis is restricted to discrete germinal zones within the developing and the adult central nervous systems. With few exceptions, cells that migrate away from these zones and into the parenchyma no longer participate in the generation of new neurons. In this work, we have found that basic fibroblast growth factor is able to stimulate the proliferation of neuronal and glial progenitors isolated from the septum and striatum of adult rats. These progenitors are indistinguishable from those isolated from the adult hippocampus and subventricular zone, two regions that generate neurons well into adult life. Although a variety of cell types are initially isolated from each brain region, the progenitor-like cells from all four regions are capable of considerable proliferation and, with limited serial passage, can be cultured as enriched populations of immature cells that are capable of differentiating into mature glia and neurons following density arrest and growth factor withdrawal. The fact that cells isolated from the septum and striatum proliferate and have the ability to differentiate into neurons once they are removed from their local environment indicates that neurogenesis may be restricted to discrete areas of the developing and the adult brain by regional differences in regulatory signals rather than from an absence of progenitors capable of responding to neurogenic cues.},
	Author = {Palmer, T. D. and Ray, J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Fibroblast Growth Factor, Basic/*pharmacology;Fluorescence;Rats, Inbred F344;Brain/*metabolism;Rats;Female;Immunohistochemistry;Time Factors;Animal;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Cells, Cultured;Neurons/*drug effects;Neuroglia/drug effects;C abstr;Support, Non-U.S. Gov't},
	Number = {5},
	Organization = {Laboratory of Genetics, Salk Institute, La Jolla, California 92037, USA, tpalmer\@salk.edu},
	Pages = {474-86.},
	Title = {FGF-2-responsive neuronal progenitors reside in proliferative and quiescent regions of the adult rodent brain},
	Uuid = {B16E1CCB-7A05-4001-8958-B4314A40FCD2},
	Volume = {6},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8581317}}

@article{Palmer:1997,
	Abstract = {Adult-derived hippocampal progenitors generate neurons, astrocytes, and oligodendrocytes in vitro and following grafting into the adult brain. Although these progenitors have a considerable capacity for in vitro self renewal, it is not known if each lineage is generated by separate committed precursors or by multipotent stem cells. By genetic marking, we have followed individual cells through the process of proliferative expansion, commitment, and differentiation. All three lineages are generated by single marked cells and the relative proportions of each lineage can be strongly influenced by environmental cues. Differentiation is accompanied by a characteristic progression of lineage-specific markers and can be potentiated by retinoic acid, elevated cyclic AMP, or neurotrophic factors. The ability to genetically mark and clone normal diploid hippocampal progenitors provides the first definitive evidence that multipotent neural stem cells exist outside of the adult striatal subventricular zone and supports the hypothesis that FGF-2-responsive neural stem cells may be broadly distributed in the adult brain. Using Smart Source Parsing},
	Author = {Palmer, T. D. and Takahashi, J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Hippocampus/*cytology/drug effects;Astrocytes/*cytology;Cell Survival/drug effects;Cells, Cultured;Rats;Neurons/*cytology/physiology;Nerve Growth Factors/pharmacology;Cyclic AMP/pharmacology;Female;Glucocorticoids, Synthetic/pharmacology;02 Adult neurogenesis migration;Animal;Oligodendroglia/*cytology;Stem Cells/*cytology;Dexamethasone/pharmacology;BB abstr;03 Adult neurogenesis progenitor source;Cell Line;Rats, Inbred F344;Support, Non-U.S. Gov't;Triiodothyronine/pharmacology;Support, U.S. Gov't, P.H.S.;Retinoids/pharmacology},
	Number = {6},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {389-404},
	Title = {The adult rat hippocampus contains primordial neural stem cells},
	Uuid = {F21C8354-6875-11DA-A4B6-000D9346EC2A},
	Volume = {8},
	Year = {1997},
	url = {papers/Palmer_MolCellNeurosci1997.pdf}}

@article{Palmer:2002,
	Abstract = {Adult neurogenesis is mediated by immature neural precursors that divide within the residual germinal matrices of the brain. In the paper by in this issue of Neuron, the "cause and effect"of adult neurogenesis takes a major step forward with the description of a vascular signaling network that influences neuronal precursor migration and fate. 0896-6273 Comment Journal Article},
	Author = {Palmer, T. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Central Nervous System/*blood supply/cytology/*growth &development;Endothelium, Vascular;02 Adult neurogenesis migration;Adult;Central Nervous System;03 Adult neurogenesis progenitor source;Human;Neovascularization, Physiologic;Neovascularization, Physiologic/*physiology;comment;Animals;Humans;Endothelium, Vascular/cytology/*growth &development/physiology;Male;BB abstr},
	Medline = {22082296},
	Month = {6},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Stanford University, Department of Neurosurgery, MSLS P309, Mail Code 5487, Stanford, CA 94305, USA.},
	Pages = {856-8},
	Pii = {S0896627302007389},
	Pubmed = {12086632},
	Title = {Adult neurogenesis and the vascular Nietzsche},
	Uuid = {FE916073-B73F-48F9-8BBE-00C43B757FF2},
	Volume = {34},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12086632}}

@article{Palmini:1995,
	Abstract = {Cortical dysplastic lesions (CDyLs) are often associated with severe partial epilepsies. We describe the electrographic counterpart of this high degree of epileptogenicity, manifested by continuous or frequent rhythmic epileptogenic discharges recorded directly from CDyLs during intraoperative electrocorticography (ECoG). These ictal or continuous epileptogenic discharges (I/CEDs) assumed one of the following three patterns: (1) repetitive electrographic seizures, (2) repetitive bursting discharges, or (3) continuous or quasicontinuous rhythmic spiking. One or more of these patterns were present in 23 of 34 patients (67\%) with intractable partial epilepsy associated with CDyLs, and in only 1 of 40 patients (2.5\%) with intractable partial epilepsy associated with other types of structural lesions. I/CEDs were usually spatially restricted, thus contrasting with the more widespread interictal ECoG epileptic activity, and tended to colocalize with the magnetic resonance imaging-defined lesion. Completeness of excision of cortical tissue displaying I/CEDs correlated positively with surgical outcome in patients with medically intractable seizures; i.e., three-fourths of the patients in whom it was entirely excised had favorable surgical outcome; in contrast, uniformly poor outcome was observed in those patients in whom areas containing I/CEDs remained in situ. We conclude that CDyLs are highly and intrinsically epileptogenic, and that intraoperative ECoG identification of this intrinsically epileptogenic dysplastic cortical tissue is crucial to decide the extent of excision for best seizure control.},
	Author = {Palmini, A. and Gambardella, A. and Andermann, F. and Dubeau, F. and da Costa, J. C. and Olivier, A. and Tampieri, D. and Gloor, P. and Quesney, F. and Andermann, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:29 -0400},
	Issn = {0364-5134},
	Journal = {Ann Neurol},
	Keywords = {Epilepsies, Partial;Electroencephalography;10 Development;Treatment Outcome;Adolescent;Adult;Female;Infant;Child, Preschool;10 genetics malformation;Child;Humans;Male;Cerebral Cortex;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {7707449},
	Number = {4},
	Organization = {Porto Alegre Epilepsy Surgery Program, Hospital Sao Lucas da PUCRS, Porto Alegre, Brazil.},
	Pages = {476-87},
	Pubmed = {7717684},
	Title = {Intrinsic epileptogenicity of human dysplastic cortex as suggested by corticography and surgical results},
	Uuid = {67D54861-47E5-41AE-B3C0-3D275F7B6C7A},
	Volume = {37},
	Year = {1995},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/ana.410370410}}

@article{Palop:2007,
	Abstract = {Neural network dysfunction may play an important role in Alzheimer's disease (AD). Neuronal circuits vulnerable to AD are also affected in human amyloid precursor protein (hAPP) transgenic mice. hAPP mice with high levels of amyloid-beta peptides in the brain develop AD-like abnormalities, including cognitive deficits and depletions of calcium-related proteins in the dentate gyrus, a region critically involved in learning and memory. Here, we report that hAPP mice have spontaneous nonconvulsive seizure activity in cortical and hippocampal networks, which is associated with GABAergic sprouting, enhanced synaptic inhibition, and synaptic plasticity deficits in the dentate gyrus. Many Abeta-induced neuronal alterations could be simulated in nontransgenic mice by excitotoxin challenge and prevented in hAPP mice by blocking overexcitation. Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD.},
	Author = {Palop, Jorge J. and Chin, Jeannie and Roberson, Erik D. and Wang, Jun and Thwin, Myo T. and Bien-Ly, Nga and Yoo, Jong and Ho, Kaitlyn O. and Yu, Gui-Qiu Q. and Kreitzer, Anatol and Finkbeiner, Steven and Noebels, Jeffrey L. and Mucke, Lennart},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {gamma-Aminobutyric Acid;Neurotoxins;Animals;Humans;Amyloid beta-Protein;Neural Pathways;Neuronal Plasticity;Synaptic Transmission;Neocortex;Epilepsy;Mice, Transgenic;research support, non-u.s. gov't;Amyloid beta-Protein Precursor;Disease Models, Animal;Alzheimer Disease;Mice, Knockout;21 Neurophysiology;Dentate Gyrus;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Neural Inhibition;Cognition Disorders},
	Month = {9},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA. jpalop\@gladstone.ucsf.edu},
	Pages = {697-711},
	Pii = {S0896-6273(07)00570-3},
	Pubmed = {17785178},
	Title = {Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease},
	Uuid = {86428C87-F894-454B-A2A0-23F6FFCD3D0B},
	Volume = {55},
	Year = {2007},
	url = {papers/Palop_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.07.025}}

@article{Paludan:2005,
	Abstract = {CD4+ T cells classically recognize antigens that are endocytosed and processed in lysosomes for presentation on major histocompatibility complex (MHC) class II molecules. Here, endogenous Epstein-Barr virus nuclear antigen 1 (EBNA1) was found to gain access to this pathway by autophagy. On inhibition of lysosomal acidification, EBNA1, the dominant CD4+ T cell antigen of latent Epstein-Barr virus infection, slowly accumulated in cytosolic autophagosomes. In addition, inhibition of autophagy decreased recognition by EBNA1-specific CD4+ T cell clones. Thus, lysosomal processing after autophagy may contribute to MHC class II-restricted surveillance of long-lived endogenous antigens including nuclear proteins relevant to disease.},
	Author = {Paludan, Casper and Schmid, Dorothee and Landthaler, Markus and Vockerodt, Martina and Kube, Dieter and Tuschl, Thomas and M{\"u}nz, Christian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Epstein-Barr Virus Nuclear Antigens;Lysosomes;Proteasome Endopeptidase Complex;Animals;Humans;Transfection;Cell Line, Transformed;15 Retrovirus mechanism;Cell Line, Tumor;B-Lymphocytes;11 Glia;14 Immune;Hydrogen-Ion Concentration;Chloroquine;Microsomes;Cell Line;Autophagy;Phagosomes;Antigen Presentation;CD4-Positive T-Lymphocytes;24 Pubmed search results 2008;Histocompatibility Antigens Class II;Research Support, Non-U.S. Gov't},
	Month = {1},
	Nlm_Id = {0404511},
	Number = {5709},
	Organization = {Laboratory of Viral Immunobiology, Rockefeller University, New York, NY 10021, USA.},
	Pages = {593-6},
	Pii = {1104904},
	Pubmed = {15591165},
	Title = {Endogenous MHC class II processing of a viral nuclear antigen after autophagy},
	Uuid = {03A6151C-2DB1-49FE-B1B2-1F721123AAA3},
	Volume = {307},
	Year = {2005},
	url = {papers/Paludan_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1104904}}

@article{Pang:2003,
	Abstract = {Studies using chronic in vivo BrdU exposure, isolating primitive stem cells, and determining BrdU labeling, indicate that stem cells cycle. BrdU is also incorporated into DNA during damage/repair. DNA, which has incorporated BrdU due to cycle transit is heavier than normal, while the density of DNA with damage/repair incorporation is intermediate. DNA density of purified lineage-rhodamine low (rho(low)) Hoechst low (Ho(low)) stem cells or FDC-P1 cell line cells-was assessed in vitro, after exposure to cytokines and BrdU (cycling model) or cytokines and BrdU with bleomycin to induce strand breaks and hydroxyurea to halt cycle progression (damage/repair model). We determined DNA density using cesium chloride (CsCl) gradients and either fluorometry or dot blot chemiluminesence. DNA from BrdU labeled cycling Lin-rho(lo)Ho(lo) or FDC-P1 cells was heavier than normal DNA, while damage repair DNA had an intermediate density. We then assessed BrdU labeling of Lin-rho(lo)Ho(lo) cells in vivo. We found that 70.9\%of lin-rho(lo)Ho(lo) cells labeled at 5 weeks. DNA density of these cells was low, in the damage/repair range, but similar results were obtained with stem cells, which had proliferated in vivo. Dilution of BrdU in in vitro culture of proliferating FDC-P1 cells also resulted in damage/repair density. We conclude that in vitro BrdU labeling models can distinguish between proliferation and damage/repair, but that we cannot obtain high enough in vivo levels to address this issue. All together, while we cannot absolutely exclude damage/repair as contributing to stem cell BrdU labeling, the data indicate that primitive bone marrow stem cells are probably a cycling population. 0021-9541 Journal Article},
	Author = {Pang, L. and Reddy, P. V. and McAuliffe, C. I. and Colvin, G. and Quesenberry, P. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {J Cell Physiol},
	Keywords = {Dose-Response Relationship, Drug;Animals;Chlorides/diagnostic use;Hydroxyurea/pharmacology;DNA Repair/drug effects/*genetics;Bleomycin/pharmacology;Hematopoietic Stem Cells/cytology/drug effects/*metabolism;Cesium/diagnostic use;Bromodeoxyuridine/diagnostic use/*metabolism;DNA Damage/drug effects/*genetics;Chromosomes/drug effects/genetics;EE;Cell Line;Cytokines/pharmacology;Cell Cycle/drug effects/*genetics;Support, U.S. Gov't, P.H.S.;Photic Stimulation/adverse effects;Mice;DNA/drug effects/*metabolism},
	Number = {2},
	Organization = {Cancer Center, University of Massachusetts, Worcester, Massachusetts, USA.},
	Pages = {251-60},
	Pubmed = {14502565},
	Title = {Studies on BrdU labeling of hematopoietic cells: stem cells and cell lines},
	Uuid = {F86584E2-CDF0-11D9-B244-000D9346EC2A},
	Volume = {197},
	Year = {2003},
	url = {papers/Pang_JCellPhysiol2003.pdf}}

@article{Pannasch:2006,
	Abstract = {Activation of microglia by LPS leads to an induction of cytokine and NO release, reduced proliferation and increased outward K(+) conductance, the latter involving the activation of Kv1.5 and Kv1.3 channels. We studied the role of these channels for microglial function using two strategies to interfere with channel expression, a Kv1.5 knockout (Kv1.5(-/-)) mouse and an antisense oligonucleotide (AO) approach. The LPS-induced NO release was reduced by AO Kv1.5 and completely absent in the Kv1.5(-/-) animal; the AO Kv1.3 had no effect. In contrast, proliferation was augmented with both, loss of Kv1.3 or Kv1.5 channel expression. After facial nerve lesion, proliferation rate was higher in Kv1.5(-/-) animals as compared to wild type. Patch clamp experiments confirmed the reduction of the LPS-induced outward current amplitude in Kv1.5(-/-) microglia as well as in Kv1.5- or Kv1.3 AO-treated cells. Our study indicates that induction of K(+) channel expression is a prerequisite for the full functional spectrum of microglial activation.},
	Author = {Pannasch, and F{\"a}rber, and Nolte, and Blonski, and Yan Chiu, and Messing, and Kettenmann,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {9100095},
	Number = {4},
	Organization = {Cellular Neuroscience, Max-Delbr{\"u}ck-Center for Molecular Medicine, Robert-R{\"o}ssle-Strae 10, 13125 Berlin, Germany.},
	Pages = {401-411},
	Pii = {S1044-7431(06)00190-4},
	Pubmed = {17055293},
	Title = {The potassium channels Kv1.5 and Kv1.3 modulate distinct functions of microglia},
	Uuid = {18439C4D-44A4-43E9-ABC9-2F2B6D68ACFD},
	Volume = {33},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2006.08.009}}

@article{Pardridge:2002,
	Abstract = {Brain drug development of either small molecule or large molecule (recombinant proteins, gene medicines) neurotherapeutics has been limited, owing to the restrictive transport properties of the brain microvasculature, which forms the blood-brain barrier (BBB) in vivo. Widespread drug delivery to the brain, while not feasible via craniotomy and intracerebral injection, is possible if the drug is delivered to brain via the transvascular route through the BBB. Novel brain drug delivery and drug targeting strategies can be developed from an understanding of the molecular and cellular biology of the brain microvascular and BBB transport processes. 0896-6273 Journal Article Review Review, Tutorial},
	Author = {Pardridge, W. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Neuron},
	Keywords = {Gene Therapy/*methods;Microcirculation/*drug effects/metabolism;Brain/*blood supply/*drug effects/metabolism;Human;Drug Administration Routes;Endothelium, Vascular/drug effects/metabolism;T;Blood-Brain Barrier/*drug effects/physiology;Carrier Proteins/drug effects/metabolism;Animals;Tight Junctions/drug effects/metabolism;23 Technique;Central Nervous System Diseases/*drug therapy},
	Number = {4},
	Organization = {Department of Medicine, School of Medicine, University of California, Los Angeles, Los Angeles, CA 90024, USA. wpardridge\@mednet.ucla.edu},
	Pages = {555-8},
	Title = {Drug and gene delivery to the brain: the vascular route},
	Uuid = {D8BFD5C3-DBC3-4BE6-8D50-4CF9803E63CD},
	Volume = {36},
	Year = {2002},
	url = {papers/Pardridge_Neuron2002.pdf}}

@article{Parent:2002,
	Abstract = {The persistence of neurogenesis in the forebrain subventricular zone (SVZ) of adult mammals suggests that the mature brain maintains the potential for neuronal replacement after injury. We examined whether focal ischemic injury in adult rat would increase SVZ neurogenesis and direct migration and neuronal differentiation of endogenous precursors in damaged regions. Focal stroke was induced in adult rats by 90-minute right middle cerebral artery occlusion (tMCAO). Cell proliferation and neurogenesis were assessed with bromodeoxyuridine (BrdU) labeling and immunostaining for cell type-specific markers. Brains examined 10-21 days after stroke showed markedly increased SVZ neurogenesis and chains of neuroblasts extending from the SVZ to the peri-infarct striatum. Many BrdU-labeled cells persisted in the striatum and cortex adjacent to infarcts, but at 35 days after tMCAO only BrdU-labeled cells in the neostriatum expressed neuronal markers. Newly generated cells in the injured neostriatum expressed markers of medium spiny neurons, which characterize most neostriatal neurons lost after tMCAO. These findings indicate that focal ischemic injury increases SVZ neurogenesis and directs neuroblast migration to sites of damage. Moreover, neuroblasts in the injured neostriatum appear to differentiate into a region-appropriate phenotype, which suggests that the mature brain is capable of replacing some neurons lost after ischemic injury. 0364-5134 Journal Article},
	Author = {Parent, J. M. and Vexler, Z. S. and Gong, C. and Derugin, N. and Ferriero, D. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Ann Neurol},
	Keywords = {Neurons/*cytology/pathology;Cell Division/physiology;Rats, Sprague-Dawley;Corpus Striatum/*cytology/pathology;Rats;Cerebrovascular Accident/*pathology;Support, U.S. Gov't, P.H.S.;D pdf;Animals;Male;Prosencephalon/*cytology/pathology},
	Number = {6},
	Organization = {Department of Neurology, University of Michigan Medical Center, 4412 Kresge III, 200 Zina Pitcher Place, Ann Arbor, MI 48109-0585, USA. parent\@umich.edu},
	Pages = {802-13},
	Title = {Rat forebrain neurogenesis and striatal neuron replacement after focal stroke},
	Uuid = {BAA15832-C26D-11DA-969D-000D9346EC2A},
	Volume = {52},
	Year = {2002},
	url = {papers/Parent_AnnNeurol2002.pdf}}

@article{Parent:2005,
	Abstract = {Neurogenesis in the hippocampal dentate gyrus persists throughout life and is increased by seizures. The dentate granule cell (DGC) layer is often abnormal in human and experimental temporal lobe epilepsy, with dispersion of the layer and the appearance of ectopic granule neurons in the hilus. We tested the hypothesis that these abnormalities result from aberrant DGC neurogenesis after seizure-induced injury. Bromodeoxyuridine labeling, in situ hybridization, and immunohistochemistry were used to identify proliferating progenitors and mature DGCs in the adult rat pilocarpine temporal lobe epilepsy model. We also examined dentate gyri from epileptic human hippocampal surgical specimens. Prox-1 immunohistochemistry and pulse-chase bromodeoxyuridine labeling showed that progenitors migrate aberrantly to the hilus and molecular layer after prolonged seizures and differentiate into ectopic DGCs in rat. Neuroblast marker expression indicated the delayed appearance of chainlike progenitor cell formations extending into the hilus and molecular layer, suggesting that seizures alter migratory behavior of DGC precursors. Ectopic putative DGCs also were found in the hilus and molecular layer of epileptic human dentate gyrus. These findings indicate that seizure-induced abnormalities of neuroblast migration lead to abnormal integration of newborn DGCs in the epileptic adult hippocampus, and implicate aberrant neurogenesis in the development or progression of recurrent seizures. Ann Neurol 2005.},
	Author = {Parent, and Elliott, and Pleasure, and Barbaro, and Lowenstein,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0364-5134},
	Journal = {Ann Neurol},
	Keywords = {10 Development;10 Hippocampus;06 Adult neurogenesis injury induced},
	Month = {10},
	Nlm_Id = {7707449},
	Organization = {Department of Neurology, University of Michigan Medical Center, Ann Arbor, MI.},
	Pubmed = {16261566},
	Title = {Aberrant seizure-induced neurogenesis in experimental temporal lobe epilepsy},
	Uuid = {93266F9B-E499-448A-9F8B-86C357DDFA20},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/ana.20699}}

@article{Parent:1997,
	Abstract = {The dentate granule cell layer of the rodent hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. In both human temporal lobe epilepsy and rodent models of limbic epilepsy, this same neuronal population undergoes extensive remodeling, including reorganization of mossy fibers, dispersion of the granule cell layer, and the appearance of granule cells in ectopic locations within the dentate gyrus. The mechanistic basis of these abnormalities, as well as their potential relationship to dentate granule cell neurogenesis, is unknown. We used a systemic chemoconvulsant model of temporal lobe epilepsy and bromodeoxyuridine (BrdU) labeling to investigate the effects of prolonged seizures on dentate granule cell neurogenesis in adult rats, and to examine the contribution of newly differentiated dentate granule cells to the network changes seen in this model. Pilocarpine-induced status epilepticus caused a dramatic and prolonged increase in cell proliferation in the dentate subgranular proliferative zone (SGZ), an area known to contain neuronal precursor cells. Colocalization of BrdU- immunolabeled cells with the neuron-specific markers turned on after division, 64 kDa, class III beta-tubulin, or microtubule-associated protein-2 showed that the vast majority of these mitotically active cells differentiated into neurons in the granule cell layer. Newly generated dentate granule cells also appeared in ectopic locations in the hilus and inner molecular layer of the dentate gyrus. Furthermore, developing granule cells projected axons aberrantly to both the CA3 pyramidal cell region and the dentate inner molecular layer. Induction of hippocampal seizure activity by perforant path stimulation resulted in an increase in SGZ mitotic activity similar to that seen with pilocarpine administration. These observations indicate that prolonged seizure discharges stimulate dentate granule cell neurogenesis, and that hippocampal network plasticity associated with epileptogenesis may arise from aberrant connections formed by newly born dentate granule cells.},
	Author = {Parent, J. M. and Yu, T. W. and Leibowitz, R. T. and Geschwind, D. H. and Sloviter, R. S. and Lowenstein, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {J Neurosci},
	Keywords = {Pilocarpine;Electric Stimulation;Rats;Neuronal Plasticity/physiology;Neurons/cytology/*physiology;Cell Movement/*physiology;Animal;Rats, Sprague-Dawley;Male;Status Epilepticus/chemically induced/*physiopathology;Support, Non-U.S. Gov't;Cell Division/physiology;Support, U.S. Gov't, P.H.S.;D;Dentate Gyrus/*cytology/physiopathology;Cell Differentiation/physiology;Parasympathomimetics;Bromodeoxyuridine},
	Number = {10},
	Organization = {Departments of Neurology and Anatomy, University of California, San Francisco, California 94143, USA.},
	Pages = {3727-38.},
	Title = {Dentate granule cell neurogenesis is increased by seizures and contributes to aberrant network reorganization in the adult rat hippocampus},
	Uuid = {A217B902-810F-11DA-9009-000D9346EC2A},
	Volume = {17},
	Year = {1997},
	url = {papers/Parent_JNeurosci1997.pdf}}

@article{Parent:2002a,
	Abstract = {Neuronal precursors in the adult rodent forebrain subventricular zone (SVZ) proliferate, migrate to the olfactory bulb in a restricted pathway known as the rostral migratory stream (RMS), and differentiate into neurons. The effects of injury on this neurogenic region of the mature brain are poorly understood. To determine whether seizure- induced injury modulates SVZ neurogenesis, we induced status epilepticus (SE) in adult rats by systemic chemoconvulsant administration and examined patterns of neuronal precursor proliferation and migration in the SVZ-olfactory bulb pathway. Within 1- 2 weeks after pilocarpine-induced SE, bromodeoxyuridine (BrdU) labeling and Nissl staining increased in the rostral forebrain SVZ. These changes were associated with an increase in cells expressing antigenic markers of SVZ neuroblasts 2-3 weeks after prolonged seizures. At these same time points the RMS expanded and contained more proliferating cells and immature neurons. BrdU labeling and stereotactic injections of retroviral reporters into the SVZ showed that prolonged seizures also increased neuroblast migration to the olfactory bulb and induced a portion of the neuronal precursors to exit the RMS prematurely. These findings indicate that SE expands the SVZ neuroblast population and alters neuronal precursor migration in the adult rat forebrain. Identification of the mechanisms underlying the response of neural progenitors to seizure-induced injury may help to advance brain regenerative therapies by using either transplanted or endogenous neural precursor cells.},
	Author = {Parent, J. M. and Valentin, V. V. and Lowenstein, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Pilocarpine;Animals;Rats;Neuronal Plasticity;D both;Cell Count;Rats, Sprague-Dawley;Cell Movement;Male;Status Epilepticus;Olfactory Bulb;Research Support, U.S. Gov't, P.H.S.;Prosencephalon;Cerebral Ventricles;Neurons;06 Adult neurogenesis injury induced;Cell Division;24 Pubmed search results 2008;Genes, Reporter;Immunohistochemistry;Stem Cells;Bromodeoxyuridine;Research Support, Non-U.S. Gov't},
	Medline = {21940964},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {8},
	Organization = {Department of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan 48104, USA. parent\@umich.edu},
	Pages = {3174-88.},
	Pii = {22/8/3174},
	Pubmed = {11943819},
	Title = {Prolonged seizures increase proliferating neuroblasts in the adult rat subventricular zone-olfactory bulb pathway},
	Uuid = {F4FD0D26-ECDB-11DA-8605-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/20026296},
	Bdsk-Url-2 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11943819%20http://www.jneurosci.org/cgi/content/full/22/8/3174%20http://www.jneurosci.org/cgi/content/abstract/22/8/3174}}

@article{Parent:2003,
	Abstract = {The persistence of neurogenesis in the adult mammalian forebrain suggests that endogenous precursors may be a potential source for neuronal replacement after injury or neurodegeneration. Limited knowledge exists, however, regarding the normal function of neurogenesis in the adult and its alteration by brain injury. Neural precursors generate neurons throughout life in the mammalian forebrain subventricular zone (SVZ)-olfactory bulb pathway and hippocampal dentate gyrus. Accumulating evidence indicates that various brain insults increase neurogenesis in these persistent germinative zones. Two brain injury models in particular, experimental epilepsy and stroke in the adult rodent, have provided significant insight into the consequences of injury-induced neurogenesis. Studies of dentate gyrus neurogenesis in adult rodent epilepsy models suggest that seizure-induced neurogenesis involves aberrant neuroblast migration and integration that may contribute to persistent hippocampal hyperexcitability. In contrast, adult rat forebrain SVZ neurogenesis induced by stroke may have reparative effects. SVZ neural precursors migrate to regions of focal or global ischemic injury and appear to form appropriate neuronal subtypes to replace damaged neurons. These findings underscore the need for a better understanding of injury-induced neurogenesis in the adult and suggest that the manipulation of endogenous neural precursors is a potential strategy for brain reparative therapies.},
	Author = {Parent, Jack M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {1073-8584},
	Journal = {Neuroscientist},
	Keywords = {Epilepsy;Cerebrovascular Accident;Cell Differentiation;Research Support, Non-U.S. Gov't;Brain Injuries;Models, Neurological;Stem Cells;Cell Division;Research Support, U.S. Gov't, P.H.S.;review, tutorial;Humans;Animals;24 Pubmed search results 2008;review;Neurons},
	Medline = {22815391},
	Month = {8},
	Nlm_Id = {9504819},
	Number = {4},
	Organization = {Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0585, USA. parent\@umich.edu},
	Pages = {261-72},
	Pubmed = {12934709},
	Title = {Injury-induced neurogenesis in the adult mammalian brain},
	Uuid = {C7FF7B6A-F4B5-499D-8789-2EA5B8468C05},
	Volume = {9},
	Year = {2003}}

@article{Park:2005,
	Abstract = {Prostate apoptosis response 4 (Par-4) is a leucine zipper containing protein that plays a role in apoptosis. Although Par-4 is expressed in neurons, its physiological role in the nervous system is unknown. Here we identify Par-4 as a regulatory component in dopamine signaling. Par-4 directly interacts with the dopamine D2 receptor (D2DR) via the calmodulin binding motif in the third cytoplasmic loop. Calmodulin can effectively compete with Par-4 binding in a Ca2+-dependent manner, providing a route for Ca2+-mediated downregulation of D2DR efficacy. To examine the importance of the Par-4/D2DR interaction in dopamine signaling in vivo, we used a mutant mouse lacking the D2DR interaction domain of Par-4, Par-4DeltaLZ. Primary neurons from Par-4DeltaLZ embryos exhibit an enhanced dopamine-cAMP-CREB signaling pathway, indicating an impairment in dopamine signaling in these cells. Remarkably, Par-4DeltaLZ mice display significantly increased depression-like behaviors. Collectively, these results provide evidence that Par-4 constitutes a molecular link between impaired dopamine signaling and depression.},
	Author = {Park, Sang Ki and Nguyen, Minh Dang and Fischer, Andr{\'e} and Luke, Margaret Po-Shan and Affar, El Bachir l. . B. and Dieffenbach, Paul Brian and Tseng, Huang-Chun C. and Shi, Yang and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {10 Development;Signal Transduction;Animals;Dopamine;Corpus Striatum;Up-Regulation;Mice, Mutant Strains;Cells, Cultured;Apoptosis Regulatory Proteins;Mutation;21 Neurodegenerative;Calcium;Cyclic AMP;Calmodulin;Depression;Cyclic AMP Response Element-Binding Protein;21 Neurophysiology;Neurons;Intracellular Signaling Peptides and Proteins;Receptors, Dopamine D2;Mice;Amino Acid Motifs;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {0413066},
	Number = {2},
	Organization = {Department of Pathology, Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.},
	Pages = {275-87},
	Pii = {S0092-8674(05)00555-6},
	Pubmed = {16051151},
	Title = {Par-4 links dopamine signaling and depression},
	Uuid = {CE5B6A65-4C5E-4FBA-A802-582D6D2101E8},
	Volume = {122},
	Year = {2005},
	url = {papers/Park_Cell2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.05.031}}

@article{Park:2002,
	Abstract = {Maternal separation in early life can increase vulnerability to neuropsychiatric disorders over the lifespan. To investigate the effect of acupuncture on cell proliferation in the dentate gyrus (DG), 5-bromo- 2prime prime or minute-deoxyuridine (BrdU)-immunohistochemistry was performed in maternally-separated rat pups. Maternal separation, for 7 days from postnatal day 14, induced a significant decrease of BrdU- immunoreactive cells in DG, while acupuncture treatment at acupoint Shenmen (HT7), at the end of the transverse crease of the ulnar wrist, resulted in the significant increase in the number of BrdU-positive cells in DG. However, acupuncture at acupoint ST36, near the knee joint, produced no increase in the number of BrdU-positive cells. These findings indicate that acupuncture at acupoint HT7 appears to stimulate cell proliferation, and we suggested that acupuncture may be useful in the treatment of diseases related to maternal separation.},
	Author = {Park, H. J. and Lim, S. and Lee, H. S. and Lee, H. J. and Yoo, Y. M. and Kim, S. A. and Yin, C. S. and Seo, J. C. and Chung, J. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Neurosci Lett},
	Keywords = {D abstr;06 Adult neurogenesis injury induced},
	Number = {3},
	Organization = {Department of Meridian and Acupuncture, College of Oriental Medicine, Kyung Hee University, 1 Hoegidong, Dongdaemoongu, Seoul, 130-701, South Korea},
	Pages = {153-156.},
	Title = {Acupuncture enhances cell proliferation in dentate gyrus of maternally- separated rats},
	Uuid = {D3ABD3BA-7C30-46BA-A73E-C9149CD22A9D},
	Volume = {319},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11834316}}

@article{Parras:2004,
	Abstract = {Progenitors in the telencephalic subventricular zone (SVZ) remain mitotically active throughout life, and produce different cell types at embryonic, postnatal and adult stages. Here we show that Mash1, an important proneural gene in the embryonic telencephalon, is broadly expressed in the postnatal SVZ, in progenitors for both neuronal and oligodendrocyte lineages. Moreover, Mash1 is required at birth for the generation of a large fraction of neuronal and oligodendrocyte precursors from the olfactory bulb. Clonal analysis in culture and transplantation experiments in postnatal brain demonstrate that this phenotype reflects a cell-autonomous function of Mash1 in specification of these two lineages. The conservation of Mash1 function in the postnatal SVZ suggests that the same transcription mechanisms operate throughout life to specify cell fates in this structure, and that the profound changes in the cell types produced reflect changes in the signalling environment of the SVZ.},
	Author = {Parras, Carlos M. and Galli, Rossella and Britz, Olivier and Soares, Sylvia and Galichet, Christophe and Battiste, James and Johnson, Jane E. and Nakafuku, Masato and Vescovi, Angelo and Guillemot, Fran\c{c}ois},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0261-4189},
	Journal = {EMBO J},
	Keywords = {01 Adult neurogenesis general},
	Month = {11},
	Nlm_Id = {8208664},
	Number = {22},
	Organization = {[1] Institut de G{\'e}n{\'e}tique et de Biologie Cellulaire et Mol{\'e}culaire, Illkirch, France [2] Division of Molecular Neurobiology, National Institute for Medical Research, The Ridgeway, Mill Hill, London, UK.},
	Pages = {4495-505},
	Pii = {7600447},
	Pubmed = {15496983},
	Title = {Mash1 specifies neurons and oligodendrocytes in the postnatal brain},
	Uuid = {E4459008-1729-4858-BC1F-FE4F5B26F8CB},
	Volume = {23},
	Year = {2004},
	url = {papers/Parras_EMBOJ2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.emboj.7600447}}

@article{Pastorino:2001,
	Abstract = {The goal of this project was to develop a novel gene transfer system based on macrophages (Mphi) as shuttles of recombinant retroviral vectors carrying therapeutic or marker genes. The murine Mphi cell line WGL5 was used as a source of Mphi for this study. We generated retrovirus-producing Mphi by transducing the WGL5 cells with a replication-defective retroviral vector carrying the enhanced green fluorescent protein (EGFP) reporter gene and the Moloney murine leukemia virus (MoMLV) as helper virus. We demonstrated stable integration of the recombinant retrovirus in the Mphi genome, efficient recombinant retrovirus production, and EGFP gene delivery to different cell lines in vitro. To evaluate Mphi-mediated EGFP gene transfer in vivo, allogeneic mice were injected s.c. with the retrovirus-producing WGL5 Mphi, that gave rise to solid tumor masses at the injection site, highly infiltrated with host leukocytes. We observed EGFP fluorescence in tumor-infiltrating CD4(+) and CD8(+) host T lymphocytes, providing direct evidence of the ability of engineered Mphi to mediate EGFP gene delivery to host cells in vivo. Moreover, we showed that retrovirus-producing Mphi could home to different organs in vivo following i.v. injection into mice. These data demonstrate that Mphi can be engineered as cellular vehicles for recombinant retroviruses carrying heterologous genes and suggest potential applications of this novel vector system for gene therapy.},
	Author = {Pastorino, S. and Massazza, S. and Cilli, M. and Varesio, L. and Bosco, M. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {T-Lymphocytes;Transduction, Genetic;Animals;Macrophages;Retroviridae;11 Glia;Microscopy, Fluorescence;Green Fluorescent Proteins;Genetic Vectors;Cell Line;CD8-Positive T-Lymphocytes;Injections, Subcutaneous;Gene Therapy;Mice;Injections, Intravenous;Luminescent Proteins;CD4-Positive T-Lymphocytes;Research Support, Non-U.S. Gov't},
	Medline = {21214791},
	Month = {3},
	Nlm_Id = {9421525},
	Number = {6},
	Organization = {Laboratory of Molecular Biology, G Gaslini Institute, Largo G Gaslini 5, 16147, Genova, Italy.},
	Pages = {431-41},
	Pubmed = {11313821},
	Title = {Generation of high-titer retroviral vector-producing macrophages as vehicles for in vivo gene transfer},
	Uuid = {6BA486A8-60B1-4D5C-977D-B713E351F911},
	Volume = {8},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301405}}

@article{Paton:1985,
	Abstract = {Thymidine autoradiography and retrograde transport of horseradish peroxidase (HRP) were combined to determine the connectivity of neurons born in adult canary forebrain. Adult male and female canaries were pretreated with [3H]thymidine to label cells undergoing DNA synthesis prior to mitosis. Thirty or 60 days later, neurons in a forebrain nucleus, hyperstriatium ventralis, pars caudalis (HVc), were labeled by retrograde transport of HRP injected into the only two nuclei known to receive a projection from HVc: robustus archistriatalis (RA) and area X of lobus parolfactorius. The birds were then killed and brain sections were treated to visualize cells containing HRP; these sections were processed for autoradiography to detect [3H]thymidine-labeled cells in the same tissue. More than 9\%of all neurons in HVc were thymidine labeled; but of the almost 20,000 HRP-labeled projection neurons examined, fewer than 20 (0.1\%) were labeled by the thymidine treatment. Furthermore, the median cell body size for area X-projecting cells was significantly larger than that of thymidine-labeled cells, and the median size of thymidine-labeled cells was significantly larger than that of RA-projecting cells. The simplest interpretation of these results is that the new neurons incorporated into nucleus HVc in adult canary brain are local interneurons, intermediate in size between neurons projecting to RA and area X.},
	Author = {Paton, J. A. and O'Loughlin, B. E. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neurosci},
	Keywords = {A;01 Adult neurogenesis general;Axonal Transport;Female;Microscopy, Electron;Autoradiography;Thymidine/metabolism;Horseradish Peroxidase/metabolism;Animal;Neurons/*cytology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;DNA Replication;Male;Birds/*anatomy &histology;Brain/*cytology},
	Number = {11},
	Pages = {3088-93.},
	Title = {Cells born in adult canary forebrain are local interneurons},
	Uuid = {8D5F85F2-13E7-4CA1-AC9A-6B88C62868E8},
	Volume = {5},
	Year = {1985},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=2414419}}

@article{Patrizio:2001,
	Abstract = {We have studied the modulation of cyclic AMP (cAMP) accumulation by the human immunodeficiency virus type 1 (HIV 1) protein Tat in microglia and astrocyte cultures obtained from neonatal rat brain. Pretreatment of microglia with recombinant Tat resulted in a dose- and time-dependent decrease of cAMP accumulation induced by subsequent exposure to isoproterenol (1 microM). The inhibitory action of 100 ng/mL Tat approached 50\%after 4 h of preincubation and reached a maximum of 70\%after 24 h. The Tat-induced time- and dose-dependent decrease of cAMP accumulation was observed also when microglial cultures were stimulated with the adenylyl cyclase activator forskolin (100 microM). In both cases, Tat inhibitory action was 70\%reverted by a specific monoclonal anti-Tat antibody, but was not prevented either by the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xantine (100 microM) or by a 16-h pretreatment of microglial cultures with the Gi protein inhibitor pertussis toxin (10 ng/mL). All these results suggested that the viral protein acts at a step of the cAMP transduction pathway other than receptors, G proteins and phosphodiesterases. The target of Tat appeared to be adenylyl cyclase, whose activity was markedly reduced (up to 60\%) in membranes prepared from Tat-treated microglial cells, both in basal conditions and after stimulation with isoproterenol and forskolin. The inability of the competitive inhibitor of nitric oxide synthase N(G)-monometyl- L-arginine (20 and 200 microM) to revert Tat action on forskolin-induced cAMP accumulation, and of two potent nitric oxide donors, PAPA and DETA (0.1-2 m M), to alter forskolin-induced cAMP accumulation, excluded an involvement of nitric oxide in Tat-induced adenylyl cyclase inhibition. On the contrary, two inhibitors of nuclear factor kappaB activation, N-tosyl-( L)-phenylalanine chloromethyl ketone (10 microM) and SN50 (25 microM), markedly prevented the reduction of forskolin-evoked cAMP accumulation by Tat, suggesting a possible role for this nuclear transcriptional factor in the regulation of adenylyl cyclase by Tat in microglia. This assumption was strengthened by the ability of lipopolysaccharide (100 ng/mL, 4 h) to mimic the inhibitory effect of the viral protein. Conversely, astrocyte cAMP accumulation was unaffected by the viral protein, as tested at various concentrations and time points. Finally, Tat inhibition of microglial adenylyl cyclase was not due to non-specific cytotoxicity. As cAMP has been reported to exert a neuroprotective role in several in vivo and in vitro models of brain pathologies, and microglia is believed to mediate Tat-induced neurotoxicity, these results suggest that the ability of Tat to inhibit cAMP synthesis in microglia may contribute to neuronal degeneration and cell death associated with HIV infection.},
	Author = {Patrizio, M. and Colucci, M. and Levi, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Tosylphenylalanyl Chloromethyl Ketone;Apoptosis;Energy Metabolism;Enzyme Activation;NF-kappa B;GTP-Binding Protein alpha Subunits, Gi-Go;Forskolin;Hydrazines;Antibodies, Monoclonal;Second Messenger Systems;Peptides;Nerve Degeneration;Lipopolysaccharides;Animals;Cyclic AMP;Pertussis Toxin;Cells, Cultured;Isoproterenol;Adenylate Cyclase Toxin;Nitric-Oxide Synthase;Adenylate Cyclase;Gene Products, tat;11 Glia;1-Methyl-3-isobutylxanthine;Virulence Factors, Bordetella;Cell Membrane;Nitric Oxide;Rats;HIV-1;Microglia;Recombinant Fusion Proteins;Arginine;Research Support, Non-U.S. Gov't;Rats, Wistar;Nitroso Compounds;Astrocytes;Nitric Oxide Donors},
	Medline = {21210796},
	Month = {4},
	Nlm_Id = {2985190R},
	Number = {2},
	Organization = {Neurobiology Section, Laboratory of Pathophysiology, Istituto Superiore di Sanit\`{a}, Rome, Italy. patrizio\@iss.it},
	Pages = {399-407},
	Pubmed = {11299302},
	Title = {Human immunodeficiency virus type 1 Tat protein decreases cyclic AMP synthesis in rat microglia cultures},
	Uuid = {8E7D330B-D254-4053-A2ED-CD06B1EC0A52},
	Volume = {77},
	Year = {2001},
	url = {papers/Patrizio_JNeurochem2001.pdf}}

@article{Patten:2006,
	Abstract = {Signaling by the Notch1 receptor is critical for the formation of radial glia in the developing nervous system. We have shown previously that Notch1 regulates the molecular and morphological differentiation of radial glia through the transcriptional activation of at least two genes, brain lipid binding protein (BLBP) and the erbB2 receptor tyrosine kinase. However, the mechanisms by which this occurs remained undefined. Here we demonstrate that Notch1 effects on radial glia gene expression are mediated by two downstream mechanisms, one that the depends on Suppressor of Hairless [Su(H)] and the other on Deltex1 (DTX1). These two Notch1-binding proteins contribute to the regulation of BLBP and erbB2 expression, respectively. Importantly, our results suggest that, although these events can occur simultaneously, a hierarchical relationship might exist between DTX1 and Su(H), because overexpression of DTX1 or a dominant-negative form of this protein inhibits Su(H)-mediated events but not vice versa. In contrast to the effects of DTX1 overexpression, interference RNA-mediated knock-down of DTX1 blocks Notch1-induced erbB2 promoter activation and radial glia formation selectively, without affecting Su(H)-dependent pathways, indicating that loss of DTX1 expression and expression of dominant-negative DTX1 result in different alterations in cell differentiation and gene expression. Together, these results show that Notch1 regulates radial glia formation through two distinct transcriptional mechanisms and that the outcomes of Notch1 signaling may depend on the relative expression levels of its coregulators.},
	Author = {Patten, Brooke A. and Sardi, S. Pablo and Koirala, Samir and Nakafuku, Masato and Corfas, Gabriel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Rats, Long-Evans;Signal Transduction;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Rats;Receptor, erbB-2;Up-Regulation;Animals;Transcription Factors;RNA Interference;Receptor, Notch1;Animals, Newborn;Neuroglia;Down-Regulation;Mice;Promoter Regions (Genetics);24 Pubmed search results 2008;Central Nervous System;Research Support, N.I.H., Extramural;Drosophila Proteins;Repressor Proteins;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {3102-8},
	Pii = {26/12/3102},
	Pubmed = {16554461},
	Title = {Notch1 signaling regulates radial glia differentiation through multiple transcriptional mechanisms},
	Uuid = {69AF85CE-326D-4C11-8858-A50542E9C448},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4829-05.2006}}

@article{Pautot:2008,
	Abstract = {A central challenge in neuroscience is to understand the formation and function of three-dimensional (3D) neuronal networks. In vitro studies have been mainly limited to measurements of small numbers of neurons connected in two dimensions. Here we demonstrate the use of colloids as moveable supports for neuronal growth, maturation, transfection and manipulation, where the colloids serve as guides for the assembly of controlled 3D, millimeter-sized neuronal networks. Process growth can be guided into layered connectivity with a density similar to what is found in vivo. The colloidal superstructures are optically transparent, enabling remote stimulation and recording of neuronal activity using layer-specific expression of light-activated channels and indicator dyes. The modular approach toward in vitro circuit construction provides a stepping stone for applications ranging from basic neuroscience to neuron-based screening of targeted drugs.},
	Author = {Pautot, Sophie and Wyart, Claire and Isacoff, Ehud Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1548-7105},
	Journal = {Nat Methods},
	Keywords = {Imaging, Three-Dimensional;research support, non-u.s. gov't;Lycopersicon esculentum;Rats;Tissue Engineering;research support, n.i.h., extramural;Nerve Net;Animals;Cells, Cultured;Colloids;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {101215604},
	Number = {8},
	Organization = {Department of Molecular and Cell Biology, Life Science Addition 271, Mail Code 3200, University of California, Berkeley, USA.},
	Pages = {735-40},
	Pii = {nmeth.1236},
	Pubmed = {18641658},
	Title = {Colloid-guided assembly of oriented 3D neuronal networks},
	Uuid = {6A0221BE-407C-46CB-828F-ACA7B32850FC},
	Volume = {5},
	Year = {2008},
	url = {papers/Pautot_NatMethods2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nmeth.1236}}

@article{Pawelek:2005,
	Abstract = {Malignant cells express molecular pathways that are also expressed by myeloid cells. Such behaviour is associated with loss of homotypic adhesion between cells, changes in the cellular matrix, induction of angiogenesis, motility, chemotaxis, and several immune-signalling pathways. The overlap between malignant cells and myeloid cells could be explained by one mechanism: fusion of myeloid cells and tumour cells, as noted in animal studies and in two patients with renal-cell carcinoma who underwent bone-marrow transplantation. An overlapping trait in these cells is their glycosylation patterns: hybrids have high expression of N-terminal glycosylation and beta1,6-branched oligosaccharides. In macrophages and cancer cells, these structures have a role in motility and systemic migration; in cancer, they are associated with metastasis and poor prognosis. In addition to myeloid traits, fusion might contribute to aneuploidy and plasticity in cancer. Understanding metastatic cells as myeloid-tumour hybrids suggests new strategies for diagnosis, treatment, and prevention of malignant disease.},
	Author = {Pawelek, John M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1470-2045},
	Journal = {Lancet Oncol},
	Keywords = {11 Glia;22 Stem cells;22 Cancer},
	Month = {12},
	Nlm_Id = {100957246},
	Number = {12},
	Organization = {Department of Dermatology and Yale Cancer Center, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8059, USA.},
	Pages = {988-93},
	Pii = {S1470-2045(05)70466-6},
	Pubmed = {16321767},
	Title = {Tumour-cell fusion as a source of myeloid traits in cancer},
	Uuid = {0E56B902-BF8F-11DA-969D-000D9346EC2A},
	Volume = {6},
	Year = {2005},
	url = {papers/Pawelek_LancetOncol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/S1470-2045(05)70466-6}}

@article{Payankaulam:2008,
	Abstract = {Quantitative measurements of the Hunchback transcription factor in Drosophila embryos show that its target genes can respond with a high degree of precision to the exact level of the protein, simulating a continuous, analog readout, while other target genes show a combinatorial effect, resembling a Boolean logic element.},
	Author = {Payankaulam, Sandhya and Arnosti, David N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {DNA-Binding Proteins;Embryonic Development;Gene Expression Regulation, Developmental;Trans-Activators;Embryo, Nonmammalian;Drosophila Proteins;Evolution, Molecular;Drosophila;Body Patterning;Models, Genetic;Animals;Homeodomain Proteins;24 Pubmed search results 2008;Transcription Factors},
	Month = {8},
	Nlm_Id = {9107782},
	Number = {15},
	Organization = {Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824-1319, USA.},
	Pages = {R653-R655},
	Pii = {S0960-9822(08)00797-5},
	Pubmed = {18682204},
	Title = {Gene regulation: boundaries within limits},
	Uuid = {A97BBE34-1055-424E-8A04-30719C009799},
	Volume = {18},
	Year = {2008},
	url = {papers/Payankaulam_CurrBiol2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2008.06.040}}

@article{Pearson:2003,
	Abstract = {Individual neural progenitors generate different cell types in a reproducible order in the retina, cerebral cortex and probably in the spinal cord. It is unknown how neural progenitors change over time to generate different cell types. It has been proposed that progenitors undergo progressive restriction or transit through distinct competence states; however, the underlying molecular mechanisms remain unclear. Here we investigate neural progenitor competence and temporal identity using an in vivo genetic system--Drosophila neuroblasts--where the Hunchback transcription factor is necessary and sufficient to specify early-born cell types. We show that neuroblasts gradually lose competence to generate early-born fates in response to Hunchback, similar to progressive restriction models, and that competence to acquire early-born fates is present in mitotic precursors but is lost in post-mitotic neurons. These results match those observed in vertebrate systems, and establish Drosophila neuroblasts as a model system for the molecular genetic analysis of neural progenitor competence and plasticity. 1476-4687 Journal Article},
	Author = {Pearson, B. J. and Doe, C. Q.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Nature},
	Keywords = {Stem Cells/*cytology;Drosophila Proteins/genetics/metabolism;Cell Differentiation;10 Development;F pdf;Phenotype;Neuronal Plasticity;Time Factors;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Drosophila melanogaster/*cytology/embryology/genetics/metabolism;Mitosis;Animals;Support, Non-U.S. Gov't;Transcription Factors/genetics/metabolism;DNA-Binding Proteins/genetics/metabolism;Cell Lineage},
	Number = {6958},
	Organization = {Institutes of Neuroscience and Molecular Biology, Howard Hughes Medical Institute, University of Oregon 1254, Eugene, Oregon 97403, USA.},
	Pages = {624-8},
	Pubmed = {14534589},
	Title = {Regulation of neuroblast competence in Drosophila},
	Uuid = {87218A21-B7AD-4087-ADF5-F63BB64D4EB6},
	Volume = {425},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14534589}}

@article{Pekcec:2006,
	Abstract = {Multipotent neural precursors have been suggested to exist in many parts of the adult mammalian brain. In the present study, we characterized the neurogenic potential in the piriform cortex of adult rats. Proliferation rates as detected by 5'-bromodeoxyuridine-labeling proved to be low when compared with the major neurogenic brain regions (i.e. the hippocampus and the subventricular zone). 5'-Bromodeoxyuridine/NeuN-labeling in accordance with doublecortin, polysialylated neural cell adhesion molecule, and TUC-4-labeling indicated that neuronal differentiation of newborn cells occurs predominantly in layer II of the piriform cortex. Many of the cells exhibited a pyramidal cell morphology. The lack of 5'-bromodeoxyuridine/NeuN-labeled cells 12 weeks after 5'-bromodeoxyuridine administration argued against long-term survival of newborn neurons in the piriform cortex.},
	Author = {Pekcec, Anton and L{\"o}scher, Wolfgang and Potschka, Heidrun},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0959-4965},
	Journal = {Neuroreport},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {9100935},
	Number = {6},
	Organization = {aDepartment of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine and bCenter for Systems Neuroscience, Hannover, Germany.},
	Pages = {571-4},
	Pii = {00001756-200604240-00003},
	Pubmed = {16603913},
	Title = {Neurogenesis in the adult rat piriform cortex},
	Uuid = {6FA19224-E333-4D7F-933E-776EA1F7C2BE},
	Volume = {17},
	Year = {2006}}

@article{Pellier:1994,
	Abstract = {Immunocytochemical and histochemical methods have been used to describe the neuronal population migrating from the rat olfactory placode and to analyze the spatio-temporal evolution of this neuronal migration during development. Several neuronal markers, such as binding to the lectin Ulex europaeus (UEA I) and the presence of neuron-specific enolase (NSE), olfactory marker protein (OMP), and luteinizing hormone-releasing hormone (LHRH), have been tested in order to determine whether migrating neurons originate from both the medial and the lateral parts of the placode and whether they all express LHRH. Our data show that a large population of differentiated migrating neurons can be identified with an antibody against NSE from the 14th day of gestation and with UEA I one day later. Migrating neurons are closely associated with both the vomeronasal axon fascicles emerging from the medial pit and the olfactory axons originating from the lateral pit. However, the neuron migration from the lateral pit appears to be more discrete than that from the medial pit. No LHRH immunoreactivity has been detected among neurons migrating from the lateral pit. Some neurons accompanying the olfactory axon fascicles exhibit a high level of maturation as shown by their OMP-positivity. Numerous neurons positive for both NSE and UEA I have also been observed within the presumptive olfactory nerve layer in early embryonic stages. eng Journal Article},
	Author = {Pellier, V. and Astic, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Journal = {Cell Tissue Res},
	Keywords = {I abstr;Pregnancy;13 Olfactory bulb anatomy;Neurons/chemistry/*physiology;Rats;Glycoconjugates/analysis;Immunoenzyme Techniques;Female;Cell Movement;Animal;Nasal Cavity/chemistry/cytology/*innervation;Antibodies;Epithelium/chemistry/cytology;Support, Non-U.S. Gov't;Animals, Newborn;Rats, Wistar/embryology;Phosphopyruvate Hydratase/analysis;Gonadorelin/analysis;Lectins;Olfactory Bulb/*chemistry/cytology;Fetal Development},
	Number = {3},
	Organization = {Laboratoire de Physiologie Neurosensorielle, UCB/Lyon I, Villeurbanne, France.},
	Pages = {587-98.},
	Title = {Histochemical and immunocytochemical study of the migration of neurons from the rat olfactory placode},
	Uuid = {325FF868-8385-409F-9CE5-B760B6446427},
	Volume = {275},
	Year = {1994}}

@article{Peluffo:2003,
	Abstract = {Successful introduction of therapeutic genes into the central nervous system (CNS) requires the further development of efficient transfer vehicles that avoid viral vector-dependent adverse reactions while maintaining high transfection efficiency. The multifunctional protein 249AL was recently constructed for in vitro gene delivery. Here, we explore the capability of this vector for in vivo gene delivery to the postnatal rat CNS. Significant transgene expression was observed both in the excitotoxically injured and noninjured brain after intracortical injection of the DNA-contaning-249AL vector. In the injured brain, a widespread expression occurred in the entire lesioned area and retrograde transport of the vector toward distant thalamic nuclei and transgene expression were observed. Neurons, astrocytes, microglia, and endothelial cells expressed the transgene. No recruitment of leukocytes, demyelination, interleukin-1beta expression, or increase in astrocyte/microglial activation was observed at 6 days postinjection. In conclusion, the 249AL vector shows promising properties for gene therapy intervention in the CNS, including the targeting of different cell populations.},
	Author = {Peluffo, H. and Ar{\'\i}s, A. and Acarin, L. and Gonz{\'a}lez, B. and Villaverde, A. and Castellano, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1043-0342},
	Journal = {Hum Gene Ther},
	Keywords = {Research Support, Non-U.S. Gov't;beta-Galactosidase;Animals;Densitometry;Rats;Transfection;Comparative Study;11 Glia;Green Fluorescent Proteins;Genetic Vectors;Gene Therapy;Blotting, Western;Escherichia coli;Luminescent Proteins;Central Nervous System;Immunohistochemistry;Gene Expression;Transgenes},
	Medline = {22833556},
	Month = {9},
	Nlm_Id = {9008950},
	Number = {13},
	Organization = {Unitat d'Histologia, Departament de Biologia Cellular, Fisiologia i Immunologia, Universitat Aut\`{o}noma de Barcelona, 08193 Barcelona, Spain. hugo.peluffo\@uab.es},
	Pages = {1215-23},
	Pubmed = {12952593},
	Title = {Nonviral gene delivery to the central nervous system based on a novel integrin-targeting multifunctional protein},
	Uuid = {A2B02FE1-F129-4C40-AEAA-7049B089ED6D},
	Volume = {14},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/104303403767740759}}

@article{Pencea:2001,
	Abstract = {Throughout life, the anterior part of the postnatal rodent subventricular zone (SVZa), surrounding the lateral ventricles, contains a prolific source of neuronal progenitor cells that retain their capacity to concurrently generate neurons and migrate along the rostral migratory stream (RMS) to the olfactory bulb, where they differentiate into interneurons. This study was designed to determine whether the SVZ and RMS of the postnatal primate also harbor a specialized population of neuronal progenitors with the capacity to divide while they migrate. In order to reveal the spatial-temporal changes in the distribution and composition of the neuronal progenitor cells in the primate SVZ and RMS, seven rhesus monkeys, ranging in age from 2 days to 8 years, were given a single injection of the cell proliferation marker bromodeoxyuridine (BrdU) 3 h before they were perfused. The phenotypic identity of the BrdU(+) cells was revealed by double labeling sagittal sections with cell type-specific markers. From birth onward the distribution of BrdU(+) cells with a neuronal phenotype is extensive and largely overlapping with that of the rodent. Similar to the rodent brain the neuronal progenitors are most numerous in neonates. The BrdU(+) neurons in the primate forebrain extend lateral and ventral to the lateral ventricle and all along the RMS. The cytoarchitectonic arrangement and appearance of the neuronal progenitor cells is quite varied in the primate compared to the rodent; in some locations the cells are aligned in parallel arrays resembling the neuronal chains of the adult rodent RMS, whereas in other positions the cells have a homogeneous "honeycomb"arrangement. The chains are progressively more pervasive in older primates. Akin to the RMS of adult rodents, in the primate SVZ and RMS the astrocytes often form long tubes enveloping the chains of neuronal progenitors. Our study demonstrates that the primate forebrain, similar to the rodent forebrain, harbors a specialized population of mitotically active neuronal progenitor cells that undergo extensive rearrangements while continuing to proliferate throughout life. Copyright 2001 Academic Press.},
	Author = {Pencea, V. and Bingaman, K. D. and Freedman, L. J. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Rodentia;Cell Differentiation;Animals;Aging;Rats;Comparative Study;Phenotype;Cell Count;02 Adult neurogenesis migration;Cell Movement;Olfactory Bulb;Prosencephalon;Macaca mulatta;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;B;Neurons;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Stem Cells;Bromodeoxyuridine;Lateral Ventricles;Research Support, Non-U.S. Gov't},
	Medline = {21538599},
	Month = {11},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia, 30322},
	Pages = {1-16.},
	Pii = {S0014488601977684},
	Pubmed = {11681836},
	Title = {Neurogenesis in the subventricular zone and rostral migratory stream of the neonatal and adult primate forebrain},
	Uuid = {366B65DE-0FFE-4530-AA64-93D9181BD7E4},
	Volume = {172},
	Year = {2001},
	url = {papers/Pencea_ExpNeurol2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.2001.7768}}

@article{Pencea:2003,
	Abstract = {The aim of this study was to elucidate the embryological origins of the unique neuronal progenitor cells that form the rostral migratory stream (RMS), the path traversed by cells from the anterior part of the forebrain subventricular zone (SVZa) en route to the olfactory bulb. To determine when and where cells constituting the RMS initially exhibit their characteristic neuronal phenotype and high mitotic capacity, we analyzed the cells of the rat forebrain between embryonic day 14 (E14) and postnatal day 2 (P2). At E14, cells with a neuronal phenotype were observed within the ventricular zone in close proximity to the mantle layer of the future olfactory bulb. By E15, cells expressing neuronal markers are also PSA-NCAM immunoreactive and become aligned in chains of similarly oriented cells, a hallmark of the postnatal RMS. The cells that form chains organize into a patch that enlarges in the anterior-posterior and medial-lateral dimensions from E16 to E22 (birth). In comparing the forebrain cytoarchitecture to the pattern of cell type-specific staining, the patch constitutes only the central part of the proximal RMS. Early during development, the region of the RMS surrounding the patch expresses low levels of PSA-NCAM and neuron-specific markers. The proliferative activity of cells forming the patch vs. nonpatch regions of the RMS was analyzed following a short bromodeoxyuridine (BrdU) exposure. Between E15 and E22, the patch can be recognized by the mitotic activity of its cells; the cells of the patch incorporate less BrdU than the nonpatch portion of the RMS. The time course of appearance of cells forming the RMS indicates that the RMS arises in advance and independently of the cortical SVZ. Although the patch and the nonpatch regions of the embryonic RMS appear to merge postnatally, the two regions may originate separately under the influence of distinct intrinsic and extrinsic factors.},
	Author = {Pencea, Viorica and Luskin, Marla B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Cell Movement;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Immunohistochemistry;Rats;Research Support, U.S. Gov't, P.H.S.;Neural Cell Adhesion Molecule L1;Cell Division;Stem Cells;Animals, Newborn;Olfactory Bulb;Prosencephalon;Cerebral Ventricles;Bromodeoxyuridine;Sialic Acids;Neurons;Animals},
	Medline = {22719500},
	Month = {9},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {402-18},
	Pubmed = {12836176},
	Title = {Prenatal development of the rodent rostral migratory stream},
	Uuid = {C388116B-2C66-435E-B422-6C2311CB4C8D},
	Volume = {463},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10746}}

@article{Pencea:2001a,
	Abstract = {The findings that brain-derived neurotrophic factor (BDNF) promotes in vitro the survival and/or differentiation of postnatal subventricular zone (SVZ) progenitor cells and increases in vivo the number of the newly generated neurons in the adult rostral migratory stream and olfactory bulb prompted us to investigate whether the infusion of BDNF influences the proliferation and/or differentiation of cells in other regions of the adult forebrain. We examined the distribution and phenotype of newly generated cells in the adult rat forebrain 16 d after intraventricular administration of BDNF in conjunction with the cell proliferation marker bromodeoxyuridine (BrdU) for 12 d. BDNF infusion resulted in numerous BrdU(+) cells, not only in the SVZ lining the infused lateral ventricle, but moreover, in specific parenchymal structures lining the lateral and third ventricles, including the striatum and septum, as well as the thalamus and hypothalamus, in which neurogenesis had never been demonstrated previously during adulthood. In each region, newly generated cells expressed the neuronal marker microtubule-associated protein-2, or neuron-specific tubulin, identified by the antibody TuJ1. The percentage of the newly generated cells expressing TuJ1 ranged from 27 to 42\%, suggesting that the adult forebrain has a more profound capacity to produce neurons than recognized previously. The extent of cell proliferation after BDNF infusion was correlated with the level of expression of full-length TrkB, the high-affinity receptor for BDNF, despite the fact that the BrdU(+) cells were not themselves TrkB(+). Collectively, our results demonstrate that the adult brain parenchyma may recruit and/or generate new neurons, which could replace those lost as a result of injury or disease.},
	Author = {Pencea, V. and Bingaman, K. D. and Wiegand, S. J. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Microtubule-Associated Proteins;Tissue Distribution;Animals;Corpus Striatum;Rats;C both;Phenotype;Brain-Derived Neurotrophic Factor;Antigens, Differentiation;Septum of Brain;Cell Count;Rats, Sprague-Dawley;Injections, Intraventricular;Prosencephalon;Research Support, U.S. Gov't, P.H.S.;Hypothalamus;Thalamus;Neurons;Receptor, trkB;04 Adult neurogenesis factors;Cell Division;24 Pubmed search results 2008;Bromodeoxyuridine;Lateral Ventricles;Research Support, Non-U.S. Gov't},
	Medline = {21408167},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Departments of Cell Biology and Neurosurgery, Emory University School of Medicine, Atlanta, Georgia 30322, and Regeneron Pharmaceuticals Inc., Tarrytown, New York 10591.},
	Pages = {6706-17.},
	Pii = {21/17/6706},
	Pubmed = {11517260},
	Title = {Infusion of Brain-Derived Neurotrophic Factor into the Lateral Ventricle of the Adult Rat Leads to New Neurons in the Parenchyma of the Striatum, Septum, Thalamus, and Hypothalamus},
	Uuid = {9F1B91C2-BC72-47EB-9CB1-34D00B4551EF},
	Volume = {21},
	Year = {2001},
	url = {papers/Pencea_JNeurosci2001}}

@article{Pennartz:2004,
	Abstract = {The progeny of neural stem cells in the subventricular zone (SVZ) of the adult mammalian brain consists in polysialylated NCAM-expressing immature neurons (PSA(+) cells), which migrate to the olfactory bulb (OB) to differentiate into GABAergic interneurons. We purified murine PSA(+) cells directly from the adult brain by FACS and analyzed their gene expression profile by SAGE. Comparative analyses led to the identification of precursor-enriched genes, including Survivin, Sox-4, Meis2, Dishevelled-2, C3aR1 and Riken 3110003A17, and many so far uncharacterized transcripts. Cluster analysis showed that groups of genes involved in axon guidance and gene clusters implicated in chemotaxis are strongly upregulated, indicating a role of both cues in the control of cell migration in the adult brain. Furthermore, genes involved in apoptosis and cell proliferation are co-expressed, suggesting that the amount of precursors that is present in the adult brain is a result of an equilibrium of these processes.},
	Author = {Pennartz, Sandra and Belvindrah, Richard and Tomiuk, Stefan and Zimmer, C{\'e}line and Hofmann, Kay and Conradt, Marcus and Bosio, Andreas and Cremer, Harold},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;Cell Differentiation;Cell Culture Techniques;Animals;Cells, Cultured;Gene Expression Regulation, Developmental;Cell Separation;Oligonucleotide Array Sequence Analysis;Brain;Apoptosis;Chemotaxis;Cell Movement;Homeostasis;Mice, Inbred C57BL;Gene Expression Profiling;Male;Sialic Acids;Neurons;Multigene Family;Flow Cytometry;Mice;Cell Division;24 Pubmed search results 2008;Neural Cell Adhesion Molecule L1;Stem Cells;Cues;Interneurons;Nerve Tissue Proteins},
	Month = {4},
	Nlm_Id = {9100095},
	Number = {4},
	Organization = {Memorec Biotec GmbH, a Miltenyi Biotec Company, 50829 Cologne, Germany.},
	Pages = {692-706},
	Pii = {S1044743103003993},
	Pubmed = {15080897},
	Title = {Purification of neuronal precursors from the adult mouse brain: comprehensive gene expression analysis provides new insights into the control of cell migration, differentiation, and homeostasis},
	Uuid = {DA575BEE-B4B0-4D2D-A979-EE67EFD267D6},
	Volume = {25},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2003.12.011}}

@article{Pennell:1997,
	Abstract = {In order to illuminate functional roles of microglial cells within neural allografts, we have transplanted both whole and microglial and endothelial cell-depleted E14 neural cell suspensions into the intact striatum of Sprague-Dawley rats. Following posttransplantation times of up to 30 days, the intrastrial allografts were analyzed histochemically using the Griffonia simplicifolia B4 isolectin, a marker for both microglia and blood vessels. Our results indicate that both whole and depleted suspension grafts develop identically in terms of neovascularization and microglial colonization. In both types of transplants microglial cells appeared before any blood vessels were apparent. The main phase of graft vascularization occurred between days 7 and 10 posttransplantation and neovascularization was complete by day 21, as revealed by quantitative image analysis. Microglial cells, which were present as ameboid cells during early posttransplantation times, underwent continuing cell differentiation with time that paralleled graft vascular development. By 30 days posttransplantation microglia within the grafts had assumed the fully ramified phenotype characteristic of resting adult microglia. During graft development and vascularization, microglia were often seen in close proximity to ingrowing blood vessels and vascular sprouts. In conclusion, our study has shown that microglial colonization of grafts and graft vascularization occurs independent of donor-derived microglial and endothelial cells, and suggests that the great majority of microglia and vessels within the graft are host derived. We hypothesize that the host microglia invading the allografts play an active role in promoting graft neovascularization.},
	Author = {Pennell, N. A. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0963-6897},
	Journal = {Cell Transplant},
	Keywords = {Pregnancy;Endothelium;Animals;Cell Separation;Corpus Striatum;Brain Tissue Transplantation;Rats;Microglia;Female;Rats, Sprague-Dawley;Not relevant;11 Glia;Neovascularization, Physiologic;Spinal Cord;Male;Fetal Tissue Transplantation;Support, Non-U.S. Gov't;Cerebral Cortex;Support, U.S. Gov't, Non-P.H.S.;Graft Survival;Brain Stem},
	Medline = {97314981},
	Nlm_Id = {9208854},
	Number = {3},
	Organization = {Department of Neuroscience, University of Florida Brain Institute, Gainesville 32610, USA.},
	Pages = {221-30},
	Pii = {S0963689797000304},
	Pubmed = {9171155},
	Title = {Colonization of neural allografts by host microglial cells: relationship to graft neovascularization},
	Uuid = {ED6E9EE5-71A2-4761-BD48-07204E1F4E35},
	Volume = {6},
	Year = {1997}}

@article{Pennell:1998,
	Abstract = {In light of a recent interest in the transplantation of cultured microglial cells, we have examined the use of the fluorescent dye Fluoro-Gold (FG) as a tracer for these cells. Following injection into the adult rat brain, FG prelabeled microglial cells were readily traceable for up to 2 weeks with minimal labeling of endogenous cell populations. Some of the injected cells differentiated into ramified microglial cells as a result of exposure to the adult CNS environment. Injection of free FG into the adult rat brain resulted in the widespread labeling of neurons and perivascular cells, but not endogenous microglial cells, indicating that perivascular cells, but not resting microglia, are actively pinocytotic cells of the CNS. Our results show that FG is an effective label for the tracing of transplanted microglial cells.},
	Author = {Pennell, N. A. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Neurons;Brain Tissue Transplantation;Cell Differentiation;Rats;Not relevant;Time Factors;Fluorescent Dyes;11 Glia;Microglia;Animals, Newborn;Rats, Wistar;Cells, Cultured;Stilbamidines;Animals;Brain;Cell Movement},
	Medline = {98220656},
	Month = {5},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida Brain Institute, Gainesville 32610, USA.},
	Pages = {84-8},
	Pii = {10.1002/(SICI)1098-1136(199805)23:1<84::AID-GLIA8>3.0.CO;2-4},
	Pubmed = {9562187},
	Title = {Tracing of fluoro-gold prelabeled microglia injected into the adult rat brain},
	Uuid = {BA8B047B-10F8-4EB3-B940-E9A82890FF75},
	Volume = {23},
	Year = {1998},
	url = {papers/Pennell_Glia1998.pdf}}

@article{Pennell:1994,
	Abstract = {The B4-isolectin from Griffonia simplicifolia is known to stain microglial cells in a variety of species. The present report describes a lectin staining method that has been modified to facilitate staining of resting microglia, as well as perivascular cells, in vibratome sections of normal sheep brain. This modified method employs tissue fixed in formaldehyde or paraformaldehyde and requires incubating sections with Triton X-100 prior to staining.},
	Author = {Pennell, N. A. and Hurley, S. D. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0301-5564},
	Journal = {Histochemistry},
	Keywords = {Staining and Labeling;Microtomy;Neuroglia;Lectins;Not relevant;11 Glia;Sheep;Fixatives;Animals},
	Medline = {95213184},
	Month = {12},
	Nlm_Id = {0411300},
	Number = {6},
	Organization = {Department of Neuroscience, JHMHC, University of Florida, Gainesville 32610.},
	Pages = {483-6},
	Pubmed = {7535300},
	Title = {Lectin staining of sheep microglia},
	Uuid = {21648FD2-7CC1-43F6-9012-07514FF8744C},
	Volume = {102},
	Year = {1994}}

@article{Pennisi:2006,
	Author = {Pennisi, Elizabeth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Signal Transduction;Synaptic Membranes;Animals;Humans;Invertebrates;Multiprotein Complexes;Synaptic Transmission;Brain;news;Evolution, Molecular;Gene Expression Profiling;19 Neocortical evolution;Evolution;Brain Chemistry;Cognition;Receptors, Neurotransmitter;Organ Size;24 Pubmed search results 2008;Membrane Proteins;Nerve Tissue Proteins;Vertebrates},
	Month = {10},
	Nlm_Id = {0404511},
	Number = {5797},
	Pages = {244-5},
	Pii = {314/5797/244},
	Pubmed = {17038601},
	Title = {Neuroscience. Brain evolution on the far side},
	Uuid = {DE5CB4C2-49D5-478F-99A0-408916094F4B},
	Volume = {314},
	Year = {2006},
	url = {papers/Pennisi_Science2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.314.5797.244}}

@article{Pentney:2002,
	Abstract = {Neuronal migration disorders (NMDs) can be associated with neurological dysfunction such as mental retardation, and clusters of disorganized cells (heterotopias) often act as seizure foci in medically intractable partial epilepsies. Methylazoxymethanol (MAM) treatment of pregnant rats results in neuronal heterotopias in offspring, especially in hippocampal area CA1. Although the neurons in dysplastic areas in this model are frequently hyperexcitable, the precise mechanisms controlling excitability remain unclear. Here, we used IR-DIC videomicroscopy and whole cell voltage-clamp techniques to test whether the potent anti-excitatory actions of neuropeptide Y (NPY) affected synaptic excitation of heterotopic neurons. We also compared several synaptic and intrinsic properties of heterotopic, layer 2-3 cortical, and CA1 pyramidal neurons, to further characterize heterotopic cells. NPY powerfully inhibited synaptic excitation onto normal and normotopic CA1 cells but was nearly ineffective on responses evoked in heterotopic cells from stimulation sites within the heterotopia. Glutamatergic synaptic responses on heterotopic cells exhibited a comparatively small, D-2-amino-5-phosphopentanoic acid-sensitive, N-methyl-D-aspartate component. Heterotopic neurons also differed from normal CA1 cells in postsynaptic membrane currents, possessing a prominent inwardly rectifying K(+) current sensitive to Cs(+) and Ba(2+), similar to neocortical layer 2-3 pyramidal cells. CA1 cells instead had a prominent Cs(+)- and 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyrimidinium chloride-sensitive I(h) and negligible inward rectification, unlike heterotopic cells. Thus heterotopic CA1 cells appear to share numerous physiological similarities with neocortical neurons. The lack of NPY's effects on intra-heterotopic inputs, the small contribution of I(h), and abnormal glutamate receptor function, may all contribute to the lowered threshold for epileptiform activity observed in hippocampal heterotopias and could be important factors in epilepsies associated with NMDs.},
	Author = {Pentney, A. R. and Baraban, S. C. and Colmers, W. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {Research Support, Non-U.S. Gov't;Pregnancy;Synaptic Membranes;Electrophysiology;Animals;Rats;21 Epilepsy;Neocortex;Female;Epilepsy;Rats, Sprague-Dawley;Hippocampus;Pyramidal Cells;Abnormalities, Drug-Induced;Teratogens;Neuropeptide Y;Research Support, U.S. Gov't, P.H.S.;Histocytochemistry;Potassium Channels;21 Neurophysiology;Methylazoxymethanol Acetate;Potassium Channel Blockers;Membrane Potentials;24 Pubmed search results 2008;Receptors, N-Methyl-D-Aspartate;Excitatory Postsynaptic Potentials},
	Medline = {22311398},
	Month = {11},
	Nlm_Id = {0375404},
	Number = {5},
	Organization = {Department of Pharmacology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada.},
	Pages = {2745-54},
	Pubmed = {12424309},
	Title = {NPY sensitivity and postsynaptic properties of heterotopic neurons in the MAM model of malformation-associated epilepsy},
	Uuid = {4C5247FA-16D3-406C-A6E8-E07E44060733},
	Volume = {88},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1152/jn.00500.2002}}

@article{Pena:2007,
	Abstract = {The use of arynes and related species as substrates in metal-catalyzed cycloaddition reactions leads to structurally interesting products. Palladium-catalyzed cyclotrimerization of arynes provides a new method for the synthesis of polycyclic aromatic hydrocarbons. For instance, the chemoselective formal [2 + 2 + 2] cocycloaddition of 2,3-triphenylynes with alkynes affords extended triphenylenes, which are good candidates to behave as liquid crystals. Cotrimerization of benzyne and electron-deficient alkenes selectively affords dihydrophenanthrenes or ortho-olefinated biaryls depending on the catalytic system employed. The use of 2,2'-bis(diphenylphosphino)-1,1'-binophythyl (BINAP)-based palladium(0) catalysts in the cocyclotrimerization of 7-methoxynaphthalyne and dimethyl acetylenedicarboxylate affords an enantiomerically enriched tetrasubstituted pentahelicene, the first example of a metal-catalyzed enantioselective reaction involving arynes. Strained cyclic alkynes can also participate in the palladium-catalyzed cyclotrimerization reactions, which again lead to structurally interesting products. (c) 2007 The Japan Chemical Journal Forum and Wiley Periodicals, Inc. Chem Rec 7: 326-333; 2007: Published online in Wiley InterScience (www.interscience.wiley.com) DOI 10.1002/tcr.20132.},
	Author = {Pe\~{n}a, and P{\'e}rez, and Guiti{\'a}n,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1527-8999},
	Journal = {Chem Rec},
	Keywords = {24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {101085550},
	Number = {6},
	Organization = {Departamento de Qu{\'\i}mica Org{\'a}nica, Facultad de Qu{\'\i}mica, Universidad de Santiago de Compostela, 15782 Santiago de Compostela, Spain.},
	Pages = {326-333},
	Pubmed = {18050279},
	Title = {Cyclotrimerization reactions of arynes and strained cycloalkynes},
	Uuid = {B61C3A8A-4CDF-4215-BA20-32A7D48779AF},
	Volume = {7},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/tcr.20132}}

@article{Peretto:1999,
	Abstract = {The persistence of neurogenesis and structural plasticity was believed until recently to be restricted to lower vertebrates and songbirds. Nevertheless, it has now been ascertained that these phenomena can occur in the adult mammalian nervous system, at least in three distinct sites: the olfactory neuroepithelium of the nasal mucosa and two brain regions, namely, the hippocampal dentate gyrus and the olfactory bulb. The newly generated cells of the olfactory bulb originate from the subependymal layer, a remnant of the primitive subventricular zone persisting in the adult forebrain. Besides being characterized by high rates of cell proliferation, the subependymal layer is a site of long- distance tangential cell migration, wherein migrating cells form chains enwrapped by a particular type of astrocytes. These glial cells give rise to channels (glial tubes) that separate single chains from the surrounding mature tissue. The cellular composition and the pattern of cell migration in the mammalian subependymal layer appear to be quite different in neonatal and adult animals, changing strikingly in the postnatal period. Other features of uniqueness involve the capability of neuronal precursors to divide while undergoing migration and the presence of multipotent stem cells. Thus, the subependymal layer is an area of the adult mammalian brain endowed with a cohort of phenomena proper of neural development, persisting into (and adapted to) the fully mature nervous tissue. Such features make this system an optimal model to unravel mechanisms permitting highly dynamic structural plasticity during adulthood, in the perspective of providing strategies for possible brain repair.},
	Author = {Peretto, P. and Merighi, A. and Fasolo, A. and Bonfanti, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Brain Res Bull},
	Keywords = {*Cell Movement;Cell Adhesion Molecules/analysis;Cell Differentiation;02 Adult neurogenesis migration;B;Prosencephalon/chemistry/*cytology;Neurons/chemistry/cytology/*physiology;Rats;*Neuronal Plasticity;Immunohistochemistry;Cell Division;Animal;Support, Non-U.S. Gov't;Mice;Neuroglia/chemistry/*cytology},
	Number = {4},
	Organization = {Department of Veterinary Morphophysiology, University of Turin, Italy.},
	Pages = {221-43.},
	Title = {The subependymal layer in rodents: a site of structural plasticity and cell migration in the adult mammalian brain},
	Uuid = {75FAA72B-50D0-4F51-B094-99F755B10F44},
	Volume = {49},
	Year = {1999},
	url = {../../Volumes/Vega/Users/ackman/James/Endnotelibraries/OMEGAData/2449757952perettoreview}}

@article{Peri:2008,
	Abstract = {A significant proportion of neurons in the brain undergo programmed cell death. In order to prevent the diffusion of damaging degradation products, dying neurons are quickly digested by microglia. Despite the importance of microglia in several neuronal pathologies, the mechanism underlying their degradation of neurons remains elusive. Here, we exploit a microglial population in the zebrafish to study this process in intact living brains. In vivo imaging reveals that digestion of neurons occurs in compartments arising from the progressive fusion of vesicles. We demonstrate that this fusion is mediated by the v0-ATPase a1 subunit. By applying live pH indicators, we show that the a1 subunit mediates fusion between phagosomes and lysosomes during phagocytosis, a function that is independent of its proton pump activity. As a real-time description of microglial phagocytosis in vivo, this work advances our understanding of microglial-mediated neuronal degeneration, a hallmark of many neuronal diseases.},
	Author = {Peri, Francesca and N{\"u}sslein-Volhard, Christiane},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {Zebrafish;research support, non-u.s. gov't;Embryo, Nonmammalian;Animals, Genetically Modified;Apoptosis;Zebrafish Proteins;Vacuolar Proton-Translocating ATPases;Microglia;Phagosomes;Animals;Brain;Phagocytosis;Neurons;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Max Planck Institute for Developmental Biology, Spemannstr. 35, 72076 T{\"u}bingen, Germany. peri\@embl.de},
	Pages = {916-27},
	Pii = {S0092-8674(08)00611-9},
	Pubmed = {18510934},
	Title = {Live imaging of neuronal degradation by microglia reveals a role for v0-ATPase a1 in phagosomal fusion in vivo},
	Uuid = {A9AB465A-93F2-4948-B200-515C71032D57},
	Volume = {133},
	Year = {2008},
	url = {papers/Peri_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.04.037}}

@article{Perron:2005,
	Abstract = {Antigen expression of a human endogenous retrovirus family, HERV-W, in normal human brain and multiple sclerosis lesions was studied by immunohistochemistry by three independent groups. The HERV-W multicopy family was identified in human DNA from the previously characterized multiple sclerosis-associated retroviral element (MSRV). A panel of antibodies against envelope (ENV) and capsid (GAG) antigens was tested. A physiological expression of GAG proteins in neuronal cells was observed in normal brain, whereas there was a striking accumulation of GAG antigen in axonal structures in demyelinated white matter from patients with MS. Prominent HERV-W GAG expression was also detected in endothelial cells of MS lesions from acute or actively demyelinating cases, a pattern not found in any control. A physiological expression of ENV proteins was detected in microglia in normal brain; however,a specific expression in macrophages was apparently restricted to early MS lesions. Thus, converging results from three groups confirm that GAG and ENV proteins encoded by the HERV-W multicopy gene family are expressed in cells of the central nervous system under normal conditions. Similar to HERV-W7q ENV (Syncitin), which is expressed in placenta and has been shown to have a physiological function in syncytio-trophoblast fusion, HERV-W GAG may thus also have a physiological function in human brain. This expression differs in MS lesions, which may either reflect differential regulation of inherited HERV-W copies, or expression of "infectious" MSRV copies. This is compatible with a pathophysiological role in MS, but also illustrates the ambivalence of such HERV antigens, which can be expressed in cell-specific patterns, under physiological or pathological conditions.},
	Author = {Perron, Herv{\'e} and Lazarini, Fran\c{c}oise and Ruprecht, Klemens and P{\'e}choux-Longin, Christine and Seilhean, Danielle and Sazdovitch, V{\'e}ronique and Cr{\'e}ange, Alain and Battail-Poirot, Nicole and Siba{\"\i}, Genevi\`{e}ve and Santoro, Lyse and Jolivet, Michel and Darlix, Jean-Luc L. and Rieckmann, Peter and Arzberger, Thomas and Hauw, Jean-Jacques J. and Lassmann, Hans},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1355-0284},
	Journal = {J Neurovirol},
	Keywords = {Endogenous Retroviruses;Multiple Sclerosis;Adult;Aged;Immunohistochemistry;Female;Gene Products, env;multicenter study;Middle Aged;Microglia;11 Glia;Humans;Brain;Gene Products, gag;Neurons;Male},
	Month = {2},
	Nlm_Id = {9508123},
	Number = {1},
	Organization = {bioM{\'e}rieux, R&D, Chemin de l'Orme, 69280 Marcy L'Etoile, France. herve\_perron\@eu.biomerieux.com},
	Pages = {23-33},
	Pii = {LXQWW2G05118N6M1},
	Pubmed = {15804956},
	Title = {Human endogenous retrovirus (HERV)-W ENV and GAG proteins: physiological expression in human brain and pathophysiological modulation in multiple sclerosis lesions},
	Uuid = {79EC0B8C-EE5A-11DA-8605-000D9346EC2A},
	Volume = {11},
	Year = {2005},
	url = {papers/Perron_JNeurovirol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1080/13550280590901741}}

@article{Persons:1997,
	Abstract = {We have investigated the utility of the green fluorescent protein (GFP) to serve as a marker to assess retroviral gene transfer into hematopoietic cells and as a tool to identify and enrich for cells expressing high levels of the vector-encoded transcript. GFP, by virtue of a naturally occurring chromophore encoded in its primary sequence, displays autonomous fluorescence, thus eliminating the need for antibody or cytochemical staining to detect its expression. A bicistronic murine stem cell virus (MSCV)-based retroviral vector was constructed containing the GFP cDNA and a mutant, human dihydrofolate reductase gene. High-titer, ecotropic retroviral producer cells free of replication competent virus were generated and used to transduce murine bone marrow cells by cocultivation. Within 24 hours after completion of the transduction procedure, a high proportion (40\%to 70\%) of the marrow cells were intensely fluorescent compared to mock-transduced cells or cells transduced with a control retrovirus. Erythroid and myeloid hematopoietic colonies derived from GFP-transduced marrow were easily scored for retroviral gene transfer by direct in situ fluorescence microscopy. Clonogenic progenitors expressing increased levels of antifolate drug resistance could be enriched from the GFP-transduced marrow population by fluorescence activated cell sorting of cells expressing high levels of GFP. In vivo, splenic hematopoietic colonies and peripheral blood cells from animals transplanted with GFP-transduced marrow displayed intense fluorescence. These results show that GFP is an excellent marker for scoring and tracking gene-modified hematopoietic cells and for allowing rapid selection and enrichment of transduced cells expressing high levels of the transgene.},
	Author = {Persons, D. A. and Allay, J. A. and Allay, E. R. and Smeyne, R. J. and Ashmun, R. A. and Sorrentino, B. P. and Nienhuis, A. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Gene Transfer Techniques;Luminescent Proteins;Research Support, Non-U.S. Gov't;Bone Marrow Cells;Hematopoiesis;Research Support, U.S. Gov't, P.H.S.;Retroviridae;Genetic Markers;Gene Expression;11 Glia;Green Fluorescent Proteins;Animals;Humans;Mice;Genetic Vectors},
	Medline = {97436537},
	Month = {9},
	Nlm_Id = {7603509},
	Number = {5},
	Organization = {Department of Hematology/Oncology, St Jude Children's Research Hospital, Memphis, TN 38105-2794, USA.},
	Pages = {1777-86},
	Pubmed = {9292510},
	Title = {Retroviral-mediated transfer of the green fluorescent protein gene into murine hematopoietic cells facilitates scoring and selection of transduced progenitors in vitro and identification of genetically modified cells in vivo},
	Uuid = {235CD182-647C-4D86-AF05-382D1D3D14B8},
	Volume = {90},
	Year = {1997}}

@article{Pertz:2006,
	Abstract = {Rho family GTPases regulate the actin and adhesion dynamics that control cell migration. Current models postulate that Rac promotes membrane protrusion at the leading edge and that RhoA regulates contractility in the cell body. However, there is evidence that RhoA also regulates membrane protrusion. Here we use a fluorescent biosensor, based on a novel design preserving reversible membrane interactions, to visualize the spatiotemporal dynamics of RhoA activity during cell migration. In randomly migrating cells, RhoA activity is concentrated in a sharp band directly at the edge of protrusions. It is observed sporadically in retracting tails, and is low in the cell body. RhoA activity is also associated with peripheral ruffles and pinocytic vesicles, but not with dorsal ruffles induced by platelet-derived growth factor (PDGF). In contrast to randomly migrating cells, PDGF-induced membrane protrusions have low RhoA activity, potentially because PDGF strongly activates Rac, which has previously been shown to antagonize RhoA activity. Our data therefore show that different extracellular cues induce distinct patterns of RhoA signalling during membrane protrusion.},
	Author = {Pertz, Olivier and Hodgson, Louis and Klemke, Richard L. and Hahn, Klaus M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {0410462},
	Number = {7087},
	Organization = {University of North Carolina at Chapel Hill, Department of Pharmacology and Lineberger Cancer Center, Chapel Hill, North Carolina 27599, USA. khahn\@med.unc.edu},
	Pages = {1069-72},
	Pii = {nature04665},
	Pubmed = {16547516},
	Title = {Spatiotemporal dynamics of RhoA activity in migrating cells},
	Uuid = {2D00F86D-884D-4409-AD7F-D7529089F755},
	Volume = {440},
	Year = {2006},
	url = {papers/Pertz_Nature2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature04665}}

@article{Peters:2004a,
	Abstract = {Complete envelope genes were amplified from autopsy brain tissue of five individuals who had died of AIDS and had neurological complications. Lymph node samples were included for two of the patients. Nineteen different envelope clones from the five patients had distinct V1V2 sequences. Thirteen of the envelopes were functional and conferred fusigenicity and infectivity for CD4(+) CCR5(+) cells. Infectivity and cell-cell fusion assays showed that most envelopes used both CCR5 and CCR3. One brain-derived envelope used a broad range of coreceptors, while three other brain envelopes from one individual were restricted to CCR5. However, there was no correlation between tissue of origin and coreceptor use. Envelopes showed two very distinct phenotypes depending on their capacity to infect macrophages and to exploit low levels of CD4 and/or CCR5 for infection. Envelopes that were highly fusigenic and tropic for macrophages were identified in brain tissue from four of the five patients. The enhanced macrophage tropism correlated with reduced sensitivity to inhibition by Q4120, a CD4-specific antibody, but not with sensitivity to the CCR5 inhibitor, TAK779. The highly macrophage-tropic envelopes were able to infect cells expressing low levels of CD4 and/or CCR5. Comparison with several well-characterized macrophage-tropic envelopes showed that the four identified patient envelopes were at the top limit of macrophage tropism. In contrast, all four lymph node-derived envelopes exhibited a non-macrophage-tropic phenotype and required high levels of CD4 for infection. Our data support the presence of envelopes that are highly fusigenic and tropic for macrophages in the brains of patients with neurological complications. These envelopes are able to infect cells that express low levels of CD4 and/or CCR5 and may have adapted for replication in brain macrophages and microglia, which are known to express limited amounts of CD4.},
	Author = {Peters, Paul J. and Bhattacharya, Jayanta and Hibbitts, Samantha and Dittmar, Matthias T. and Simmons, Graham and Bell, Jeanne and Simmonds, Peter and Clapham, Paul R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Gene Products, env;HIV-1;Humans;Macrophages;Cells, Cultured;Phenotype;Brain;Cell Fusion;Antigens, CD4;Lymph Nodes;11 Glia;HIV Infections;Peptide Fragments;Research Support, U.S. Gov't, P.H.S.;Receptors, CCR5;Polymerase Chain Reaction;Amino Acid Sequence;Molecular Sequence Data;HIV Envelope Protein gp120;AIDS Dementia Complex},
	Month = {7},
	Nlm_Id = {0113724},
	Number = {13},
	Organization = {Program in Molecular Medicine and Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester MA 01605, USA.},
	Pages = {6915-26},
	Pii = {78/13/6915},
	Pubmed = {15194768},
	Title = {Biological analysis of human immunodeficiency virus type 1 R5 envelopes amplified from brain and lymph node tissues of AIDS patients with neuropathology reveals two distinct tropism phenotypes and identifies envelopes in the brain that confer an enhanced tropism and fusigenicity for macrophages},
	Uuid = {6BA60E90-4892-41A1-811A-371BC898A9E2},
	Volume = {78},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.78.13.6915-6926.2004}}

@article{Petersen:2004a,
	Abstract = {We used two-channel three-dimensional time-lapse fluorescence confocal imaging in live rat hippocampal slice cultures (1-7 days in vitro) to determine the motility behaviors of activated microglia as they engage dead and dying cells following traumatic brain tissue injury. Live microglia were labeled with a fluorescently conjugated lectin (IB(4)), and dead neurons were labeled with a membrane-impermeant fluorescent DNA-binding dye (Sytox Orange or To-Pro-3). Tissue injury during the slicing procedure induced neuronal death and microglial activation, but the density of dead cells diminished approximately 10-fold by 7 days in vitro as resident microglia cleared dead cells. In time-lapse movies (4-20 h long), activated microglia exhibited varying levels of motile and locomotory activity. The motility of microglia could change abruptly following contact by other microglia or death of nearby cells. When neighboring cells died, some microglia rapidly moved toward or extended a process to engulf the dead cell, consistent with a chemotactic signaling response. Dead cell nuclei usually were engulfed and carried along by highly motile and locomoting microglia. The mean time to engulfment was approximately 5 times faster for newly deceased cells (33 min) than for extant dead cells (160 min), suggesting that the efficacy of microglial phagocytosis in situ might vary with time after cell death or mode of cell death. These observations demonstrate that activated microglia are heterogeneous with respect to motile activity following traumatic tissue injury and further indicate that cell motility in situ is temporally regulated at the single cell level, possibly by direct cell-cell contact and by diffusible substances emanating from nearby dead cells.},
	Author = {Petersen, Mark A. and Dailey, Michael E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Phagocytosis;Animals;In Vitro;Rats;Microscopy, Confocal;Microglia;Cell Communication;Rats, Sprague-Dawley;Hippocampus;Cell Movement;Not relevant;11 Glia;Alpha;Support, Non-U.S. Gov't;Neurons;Cell Nucleus;Support, U.S. Gov't, P.H.S.;Cell Death},
	Month = {4},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Biological Sciences, University of Iowa, Iowa City, Iowa, USA.},
	Pages = {195-206},
	Pubmed = {15042586},
	Title = {Diverse microglial motility behaviors during clearance of dead cells in hippocampal slices},
	Uuid = {EBCF3C42-7CBD-4B88-B9B0-9E4F09B7FCED},
	Volume = {46},
	Year = {2004},
	url = {papers/Petersen_Glia2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10362}}

@article{Peterson:2004,
	Abstract = {Estrogens have neurotrophic and neuroprotective properties. The synthesis of estrogen occurs via the expression of aromatase. Previous studies have shown that injury to the vertebrate brain results in a rapid and dramatic up-regulation of aromatase expression in astrocytes around the lesion. As part of experiments examining injury-induced glial aromatization, we identified aromatase in radial glia of the zebra finch brain. Adult female zebra finches received a penetrating injury to the right hippocampus. Twenty-four hours after lesioning, birds were administered bromodeoxyuridine (BrdU) and sacrificed 2 hours, 1 day, or 7 days later. We determined the distribution of aromatase and BrdU labeling by using immunocytochemistry. Radial aromatase was localized to cells lining the lateral ventricle adjacent to the lesioned hippocampus. Injury also induced a dramatic accumulation of newly generated cells labeled with BrdU around the lesion. BrdU labeling was strongly associated with aromatase-positive radial fibers, suggesting the migration of newly generated cells along these fibers. In the songbird brain, estrogen supports neuronal recruitment and promotes the survival and addition of new neurons. The presence of aromatase in radial glia provides a mechanism of estrogen delivery to postmitotic cells. Radial aromatization may be a key feature in the repair of the vertebrate brain following neural injury.},
	Author = {Peterson, Richard S. and Lee, Diane W. and Fernando, Gowry and Schlinger, Barney A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Cell Differentiation;Animals;Songbirds;Up-Regulation;Neuronal Plasticity;Neuroprotective Agents;Female;Antigens, Differentiation;Aromatase;Hippocampus;Wounds, Penetrating;Vimentin;Disease Models, Animal;Cell Movement;Nerve Regeneration;Brain Injuries;Research Support, U.S. Gov't, P.H.S.;Neuroglia;Neurons;Cell Division;24 Pubmed search results 2008;Stem Cells},
	Month = {7},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Department of Physiological Science, University of California, Los Angeles, California 90095, USA. rsp\@ucla.edu},
	Pages = {261-9},
	Pubmed = {15211466},
	Title = {Radial glia express aromatase in the injured zebra finch brain},
	Uuid = {C8D1B639-E436-4C0D-8BB6-ED74834AA3CD},
	Volume = {475},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20157}}

@article{Petitto:2003,
	Abstract = {Following facial nerve axotomy in mice, T cells cross the intact blood-brain barrier (BBB), home to nerve cell bodies in the facial motor nucleus (FMN), and augment neuroregenerative processes. The pivotal T cell immunoregulatory cytokine, IL-2, appears to have bidirectional effects on neuronal and microglial cell function, suggesting rival hypotheses that IL-2 could either enhance or disrupt processes associated with regeneration of axotomized facial motor neurons. We tested these competing hypotheses by comparing the effect of facial nerve axotomy on C57BL/6-IL-2(-/-) knockout and C57BL/6-IL-2(+/+) wild-type littermates. Since IL-2 may also be produced endogenously in the brain, we also sought to determine whether differences between the knockout and wild-type mice were attributable to loss of IL-2 gene expression in the CNS, loss of peripheral sources of IL-2 and the associated effects on T cell function, or a combination of these factors. To address this question, we bred novel congenic mice with the SCID mutation (mice lacking T cell derived IL-2) that were homozygous for either the IL-2 knockout or wild-type gene alleles (C57BL/6scid-IL-2(-/-) and C57BL/6scid-IL-2(+/+) littermates, respectively). Groups were assessed for differences in (1) T lymphocytes entering the axotomized FMN; (2) perineuronal CD11b(+) microglial phagocytic clusters, a measure of motor neuron death; and (3) activated microglial cells as measured by MHC-II positivity. C57BL/6-IL-2(-/-) knockout mice had significantly higher numbers of T cells and lower numbers of activated MHC-II-positive microglial cells in the regenerating FMN than wild-type littermates, although the number of CD11b(+) phagocytic microglia clusters did not differ. Thus, despite the significant impairment of T cell function known to be associated with loss of peripheral IL-2, the increased number of T cells entering the axotomized FMN appears to have sufficient activity to support neuroregenerative processes. Congenic C57BL/6scid-IL-2(-/-) knockout mice had lower numbers of CD11b(+) microglial phagocytic clusters than congenic C57BL/6scid-IL-2(+/+) wild-type littermates, suggesting that loss of the IL-2 gene in the CNS (and possibly the loss of other unknown sources of the gene) enhanced neuronal regeneration. Further study of IL-2's complex actions in neuronal injury may provide greater understanding of key variables that determine whether or not immunological processes in the brain are proregenerative.},
	Author = {Petitto, John M. and Huang, Zhi and Lo, Jeannette and Streit, Wolfgang J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {T-Lymphocytes;Lymphocyte Count;Animals;Microglia;Female;Mutation;Mice, SCID;Not relevant;Chemotaxis, Leukocyte;11 Glia;Male;Nerve Regeneration;Facial Nerve Injuries;Interleukin-2;Mice, Knockout;Support, U.S. Gov't, P.H.S.;Gliosis;Mice;Motor Neurons;Immunohistochemistry;Retrograde Degeneration;Facial Nerve;Histocompatibility Antigens Class II},
	Medline = {22396249},
	Month = {1},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Psychiatry, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL 32610-0256, USA. jpetitto\@ufl.edu},
	Pages = {95-103},
	Pii = {S0165572802004228},
	Pubmed = {12507776},
	Title = {IL-2 gene knockout affects T lymphocyte trafficking and the microglial response to regenerating facial motor neurons},
	Uuid = {7A4103B8-FCA2-4576-B3AC-9B1842C5C060},
	Volume = {134},
	Year = {2003}}

@article{Petreanu:2002,
	Abstract = {Young neurons born in the subventricular zone (SVZ) of adult mice migrate to the olfactory bulb (OB) where they differentiate into granule cells (GCs) and periglomerular interneurons. Using retroviral labeling of precursors in the SVZ, we describe five stages and the timing for the maturation of newly formed GCs: (1) tangentially migrating neuroblasts (days 2-7); (2) radially migrating young neurons (days 5-7); (3) GCs with a simple unbranched dendrite that does not extend beyond the mitral cell layer (days 9-13); (4) GCs with a nonspiny branched dendrite in the external plexiform layer (days 11-22); and (5) mature GCs (days 15-30). Using [3H]thymidine, we show that the maximum number of labeled GCs is observed around day 15 after injection. Interestingly, between days 15 and 45 after birth, soon after the cells developed spines, the number of [3H]thymidine-labeled GCs declined by 50\%. Using anosmic mice, we found that sensory input was critical for the survival of GCs from day 15 to 45 after labeling. However, the number and morphology of 15-d-old cells in the granule cell layer was similar in anosmic and wild-type mice. We infer that the lack of activity did not have an effect on the generation, migration, and early differentiation of granule cells. Soon after young GCs matured, and presumably became synaptically connected, their survival depended on the level of activity that they received. This selection mechanism might allow the construction of specific OB circuits based on olfactory experience and suggests possible functions of OB cell replacement. 1529-2401 Journal Article},
	Author = {Petreanu, L. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Smell;Cell Survival;Cell Death/*physiology;Aging/physiology;Male;Lateral Ventricles/cytology;Animals;B pdf;Smell/*physiology;Research Support, U.S. Gov't, P.H.S.;Cell Movement;Bromodeoxyuridine;Stem Cells/cytology;Cell Division;Mice, Inbred C57BL;Cell Differentiation/physiology;Lateral Ventricles;Olfactory Bulb;Dendrites;Neurons/classification/*cytology/*physiology;Support, U.S. Gov't, P.H.S.;Dendrites/physiology/ultrastructure;Aging;02 Adult neurogenesis migration;Cell Death;Cell Movement/physiology;Stem Cells;Mice, Knockout;Olfaction Disorders;Mice;Olfactory Bulb/*cytology/*physiology;Neurons;Olfaction Disorders/physiopathology},
	Medline = {22117915},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {The Rockefeller University, New York, New York 10021, USA.},
	Pages = {6106-13},
	Pii = {22/14/6106},
	Pubmed = {12122071},
	Title = {Maturation and death of adult-born olfactory bulb granule neurons: role of olfaction},
	Uuid = {33D7490E-5DF8-4FE9-A103-50F695FA7B80},
	Volume = {22},
	Year = {2002},
	url = {papers/Petreanu_JNeurosci2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/20026588}}

@article{Petridis:2004,
	Abstract = {Expression of polysialic acid (PSA) promotes migration of progenitor cells from the subventricular zone (SVZ) to the olfactory bulb, where they differentiate into interneurons. This differentiation has been found to coincide with a loss of PSA. Moreover, specific removal of PSA from the mouse SVZ by endoneuraminidase-N was found to cause premature differentiation, as evidenced by neurite outgrowth and tyrosine hydroxylase synthesis in vivo and by expression of neurofilament-L and betaIII-tubulin in SVZ explant cultures. This differentiation involved activation of mitogen-activated protein kinase through p59fyn and was blocked by its inhibition. The effects of PSA removal were found to be cell contact-dependent and to be reduced by anti-neural cell adhesion molecule antibodies. These findings indicate that PSA expression regulates the fate of SVZ precursors by two contact-dependent mechanisms, the previously reported reduction in cell-cell adhesion that allows cell translocation, and the postponement of cell differentiation that otherwise would be induced by signals generated through surface molecule-mediated cell-cell interactions. Developmental Dynamics 230:675-684, 2004. 1058-8388 Journal Article},
	Author = {Petridis, A. K. and El Maarouf, A. and Rutishauser, U.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Dev Dyn},
	Keywords = {02 Adult neurogenesis migration;B, C pdf},
	Number = {4},
	Organization = {Cellular and Developmental Neuroscience, Program in Cell Biology, Memorial Sloan-Kettering Cancer Center, New York, New York.},
	Pages = {675-84},
	Title = {Polysialic acid regulates cell contact-dependent neuronal differentiation of progenitor cells from the subventricular zone},
	Uuid = {9753D88D-9E6F-4031-BFF4-84714B5DE81A},
	Volume = {230},
	Year = {2004},
	url = {papers/Petridis_DevDyn2004.pdf}}

@article{Petritsch:2003,
	Abstract = {Asymmetric cell divisions generate cellular diversity. In Drosophila, embryonic neuroblasts target cell fate determinants basally, rotate their spindles by 90 degrees to align with the apical-basal axis, and divide asymmetrically in a stem cell-like fashion. In this process, apically localized Bazooka recruits Inscuteable and other proteins to form an apical complex, which then specifies spindle orientation and basal localization of the cell fate determinants and their adapter proteins such as Miranda. Here we report that Miranda localization requires the unconventional myosin VI Jaguar (Jar). In jar null mutant embryos, Miranda is delocalized and the spindle is misoriented, but the Inscuteable crescent remains apical. Miranda directly binds to Jar, raising the possibility that Miranda and its associated proteins are translocated basally by this actin-based motor. Our studies demonstrate that a class VI myosin is necessary for basal protein targeting and spindle orientation in neuroblasts. 1534-5807 Journal Article},
	Author = {Petritsch, C. and Tavosanis, G. and Turck, C. W. and Jan, L. Y. and Jan, Y. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Dev Cell},
	Keywords = {Cell Cycle Proteins/metabolism;Neurons/*physiology;Myosin Heavy Chains/*physiology;Animals;10 Development;Immunoenzyme Techniques;Drosophila Proteins/*physiology;Biological Transport;Mitotic Spindle Apparatus/*physiology;Drosophila melanogaster/*embryology/genetics;Cell Movement;Cell Polarity;RNA Interference;Immunoblotting;Support, Non-U.S. Gov't;Cytoskeletal Proteins/metabolism;Carrier Proteins/metabolism;Cell Division/physiology;Embryo, Nonmammalian/cytology;Support, U.S. Gov't, Non-P.H.S.;Cell Differentiation/physiology;F},
	Number = {2},
	Organization = {Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, San Francisco, CA 94143, USA.},
	Pages = {273-81},
	Pubmed = {12586070},
	Title = {The Drosophila myosin VI Jaguar is required for basal protein targeting and correct spindle orientation in mitotic neuroblasts},
	Uuid = {C93A147F-4731-46EA-B42B-65412832A4A7},
	Volume = {4},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12586070}}

@article{Petruska:1997,
	Abstract = {The alpha-D-galactose specific isolectin I-B4 from Griffonia simplicifolia (GS-I-B4) labels CNS microglia and certain peripheral neurons, including a subpopulation of small dark, type B dorsal root ganglion cells, some post-ganglionic sympathetic axons, and nearly all peripheral gustatory axons. The innervation patterns of GS-I-B4 reactive sensory ganglion cells are unknown for many peripheral target tissues, including their probable primary target, the skin. The present study describes the distribution of GS-I-B4 reactive axons in hairy and glabrous hindpaw skin and in the glans penis of rats, using both single and double-labelling histochemical techniques. Neuronal processes were identified using (1) histochemistry with horseradish peroxidase conjugated GS-I-B4 or (2) immunohistochemistry against PGP 9.5 to identify all axons, and biotinylated lectin histochemistry with avidin-FITC to identify the subpopulation of GS-I-B4 reactive axons. GS-I-B4 strongly labelled unmyelinated cutaneous sensory afferents, as well as some sympathetic efferents and visceral afferents. lectin reactive axons were seen to innervate the upper hair shaft epidermis in hairy skin, and were abundant in the shallow dermis in hairy and glabrous skin and glans penis. Lectin reactive axons were also abundant in the lamina propria and distal urethral epithelium of the penis. These results provide new evidence for the cutaneous sensory role of GS-I-B4 reactive primary afferents, as well as evidence to support the contention that the lectin is a specific marker for a subpopulation of unmyelinated axons and not simply a marker for the myelination state of an axon.},
	Author = {Petruska, J. C. and Streit, W. J. and Johnson, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0899-0220},
	Journal = {Somatosens Mot Res},
	Keywords = {Animals;Rats;Immunoenzyme Techniques;Penis;Female;Neurons, Afferent;Rats, Sprague-Dawley;Axons;Not relevant;11 Glia;Mechanoreceptors;Skin;Male;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Nerve Fibers;Lectins;Peripheral Nerves},
	Medline = {97385711},
	Nlm_Id = {8904127},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida, Gainesville 32610, USA.},
	Pages = {17-26},
	Pubmed = {9241725},
	Title = {Localization of unmyelinated axons in rat skin and mucocutaneous tissue utilizing the isolectin GS-I-B4},
	Uuid = {3B4C9BDA-B456-4DE6-8569-FD055513A3B9},
	Volume = {14},
	Year = {1997}}

@article{Philippe:2006,
	Abstract = {Lentivirus-derived vectors are among the most promising viral vectors for gene therapy currently available, but their use in clinical practice is limited by the associated risk of insertional mutagenesis. We have overcome this problem by developing a nonintegrative lentiviral vector derived from HIV type 1 with a class 1 integrase (IN) mutation (replacement of the 262RRK motif by AAH). We generated and characterized HIV type 1 vectors carrying this deficient enzyme and expressing the GFP or neomycin phosphotransferase transgene (NEO) under control of the immediate early promoter of human CMV. These mutant vectors efficiently transduced dividing cell lines and nondividing neural primary cultures in vitro. After transduction, transient GFP fluorescence was observed in dividing cells, whereas long-term GFP fluorescence was observed in nondividing cells, consistent with the viral genome remaining episomal. Moreover, G418 selection of cells transduced with vectors expressing the NEO gene showed that residual integration activity was lower than that of the intact IN by a factor of 500-1,250. These nonintegrative vectors were also efficient in vivo, allowing GFP expression in mouse brain cells after the stereotactic injection of IN-deficient vector particles. Thus, we have developed a generation of lentiviral vectors with a nonintegrative phenotype of great potential value for secure viral gene transfer in clinical applications.},
	Author = {Philippe, St{\'e}phanie and Sarkis, Chamsy and Barkats, Martine and Mammeri, Hamid and Ladroue, Charline and Petit, Caroline and Mallet, Jacques and Serguera, Che},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {research support, non-u.s. gov't;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {7505876},
	Number = {47},
	Organization = {Laboratoire de G{\'e}n{\'e}tique Mol{\'e}culaire de la Neurotransmission et des Processus Neurod{\'e}g{\'e}n{\'e}ratifs, Universit{\'e} Pierre et Marie Curie Paris 6, Centre National de la Recherche Scientifique, Unit{\'e} Mixte de Recherche 7091, 83 bd de l'H\^{o}pital, 75013 Paris, France.},
	Pages = {17684-9},
	Pii = {0606197103},
	Pubmed = {17095605},
	Title = {Lentiviral vectors with a defective integrase allow efficient and sustained transgene expression in vitro and in vivo},
	Uuid = {4723949C-1085-44F9-9E3D-6992CF26548F},
	Volume = {103},
	Year = {2006},
	url = {papers/Philippe_ProcNatlAcadSciUSA2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0606197103}}

@article{Piacibello:2002,
	Abstract = {The ability of advanced-generation lentiviral vectors to transfer the green fluorescent protein (GFP) gene into human hematopoietic stem cells (HSCs) was studied in culture conditions that allowed expansion of transplantable human HSCs. Following 96 hours' exposure to flt3/flk2 ligand (FL), thrombopoietin (TPO), stem cell factor (SCF), and interleukin-6 (IL-6) and overnight incubation with vector particles, cord blood (CB) CD34(+) cells were further cultured for up to 4 weeks. CD34(+) cell expansion was similar for both transduced and control cells. Transduction efficiency of nonobese diabetic/severe combined immunodeficient (NOD/SCID) repopulating cells (SRCs) was assessed by transplants into NOD/SCID mice. Mice that received transplants of transduced week 1 and week 4 expanded cells showed higher levels of human engraftment than mice receiving transplants of transduced nonexpanded cells (with transplants of 1 x 10(5) CD34(+) cells, the percentages of CD45(+) cells were 20.5 +/- 4.5 [week 1, expanded] and 27.2 +/- 8.2 [week 4, expanded] vs 11.7 +/- 2.5 [nonexpanded]; n = 5). The GFP(+)/CD45(+) cell fraction was similar in all cases (12.5\%+/- 2.9\%and 12.2\%+/- 2.7\%vs 12.7\%+/- 2.1\%). Engraftment was multilineage, with GFP(+)/lineage(+) cells. Clonality analysis performed on the bone marrow of mice receiving transduced and week 4 expanded cells suggested that more than one integrant likely contributed to the engraftment of GFP-expressing cells. Serial transplantations were performed with transduced week 4 expanded CB cells. Secondary engraftment levels were 10.7\%+/- 4.3\%(n = 12); 19.7\%+/- 6.2\%of human cells were GFP(+). In tertiary transplants the percentage of CD45(+) cells was lower (4.3\%+/- 1.7\%; n = 10); 14.8\%+/- 5.9\%of human cells were GFP(+), and human engraftment was multilineage. These results show that lentiviral vectors efficiently transduce HSCs, which can undergo expansion and maintain proliferation and self-renewal ability.},
	Author = {Piacibello, Wanda and Bruno, Stefania and Sanavio, Fiorella and Droetto, Sara and Gunetti, Monica and Ailles, Laurie and Santoni de Sio, Francesca and Viale, Andrea and Gammaitoni, Loretta and Lombardo, Angelo and Naldini, Luigi and Aglietta, Massimo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Antigens, CD45;Mice, Inbred NOD;HIV-1;Hematopoietic Cell Growth Factors;Colony-Forming Units Assay;Animals;Transfection;Transplantation, Heterologous;Humans;Recombinant Proteins;Cells, Cultured;Mice, SCID;11 Glia;Immunophenotyping;Time Factors;Green Fluorescent Proteins;Genetic Vectors;Cell Lineage;Gene Therapy;Cord Blood Stem Cell Transplantation;Mice;Hematopoietic Stem Cells;Luminescent Proteins;Genes, Reporter;Cell Division;Graft Survival;Clone Cells;Research Support, Non-U.S. Gov't},
	Medline = {22340756},
	Month = {12},
	Nlm_Id = {7603509},
	Number = {13},
	Organization = {Department of Oncological Sciences, University of Torino Medical School, Torino, Italy. wanda.piacibello\@ircc.it},
	Pages = {4391-400},
	Pii = {100/13/4391},
	Pubmed = {12453876},
	Title = {Lentiviral gene transfer and ex vivo expansion of human primitive stem cells capable of primary, secondary, and tertiary multilineage repopulation in NOD/SCID mice. Nonobese diabetic/severe combined immunodeficient},
	Uuid = {9E580E96-D147-4565-B0C3-B2D64AC0D4F1},
	Volume = {100},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood.V100.13.4391}}

@article{Picard-Riera:2004,
	Abstract = {Mitotic activity persists in various regions of the adult mammal CNS. While evidences of neurogenesis appeared, many studies focused on the features of the adult stem cells from germinative areas such as the subventricular zone of the lateral ventricles, the dentate gyrus of the hippocampus, the cortex, the fourth ventricle and the central canal of the spinal cord. In the present paper, we review the potentialities of the adult germinative areas in terms of proliferation, migration and differentiation in non pathological situation and in response to different type of CNS injury. Adult endogenous stem cells are activated in response to various injuries but their capacities to migrate and to undergo either neurogenesis or gliogenesis differ according to the lesion-type and the germinative zone from which they arise. Different works demonstrated that epigenic factors such as growth factors can enhance the repair potential of the adult stem cells. Reactivation and mobilization of endogenous stem cells as well as demonstration of their long-term survival and functionality appear to be interesting strategies to investigate in order to promote endogenous repair of the adult CNS.},
	Author = {Picard-Riera, Nathalie and Nait-Oumesmar, Brahim and Baron-Van Evercooren, Anne},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Stem Cell Transplantation;Research Support, Non-U.S. Gov't;Central Nervous System;Wound Healing;Nerve Regeneration;Stem Cells;Growth Substances;22 Stem cells;review, tutorial;Tissue Therapy;Humans;Animals;review;Brain Injuries},
	Month = {4},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale, U546, Laboratoire des Affections de la My{\'e}line et des Canaux Ioniques Musculaires, Institut F{\'e}d{\'e}ratif des Neurosciences, CHU Piti{\'e}-Salp\^{e}tri\`{e}re, Paris, France.},
	Pages = {223-31},
	Pubmed = {15048920},
	Title = {Endogenous adult neural stem cells: limits and potential to repair the injured central nervous system},
	Uuid = {71C377B0-9C8A-4897-8FC2-D9EC2745E6B0},
	Volume = {76},
	Year = {2004},
	url = {papers/Picard-Riera_JNeurosciRes2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20040}}

@article{Pickard:2002,
	Abstract = {Intravitreal injection of the attenuated strain of pseudorabies virus (PRV Bartha) results in transneuronal spread of virus to a restricted set of central nuclei in the rat and mouse. We examined the pattern of central infection in the golden hamster after intravitreal inoculation with a recombinant strain of PRV Bartha constructed to express enhanced green fluorescent protein (PRV 152). Neurons in a subset of retinorecipient nuclei [i.e., suprachiasmatic nucleus (SCN), intergeniculate leaflet, olivary pretectal nucleus (OPN), and lateral terminal nucleus] and autonomic nuclei [i.e., paraventricular hypothalamic nucleus and Edinger-Westphal nucleus (EW)] are labeled by late stages of infection. Infection of the EW precedes infection in retinorecipient structures, raising the possibility that the SCN becomes infected by retrograde transsynaptic infection via autonomic (i.e., EW) circuits. We tested this hypothesis in two ways: (1) by removing the infected eye 24 hr after PRV 152 inoculation, well before viral infection first appears in the SCN; and (2) by examining central infection after intravitreal PRV 152 injection in animals with ablation of the EW. The pattern and time course of central infection were unchanged after enucleation, whereas EW ablation before intravitreal inoculation eliminated viral infection in the SCN. The results of EW lesions along with known connections between EW, OPN, and SCN indicate that intravitreal injection of PRV Bartha produces a retrograde infection of the autonomic innervation of the eye, which subsequently labels a restricted set of retinorecipient nuclei via retrograde trans-synaptic infection. These results, taken together with other genetic data, indicate that the mutations in PRV Bartha render the virus incapable of anterograde transport. PRV Bartha is thus a retrograde transsynaptic marker in the CNS. 1529-2401 Journal Article},
	Author = {Pickard, G. E. and Smeraski, C. A. and Tomlinson, C. C. and Banfield, B. W. and Kaufman, J. and Wilcox, C. L. and Enquist, L. W. and Sollars, P. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neurosci},
	Keywords = {Hamsters;Animals;Suprachiasmatic Nucleus/pathology/*virology;Disease Progression;Synapses/pathology/virology;J abstr;Biological Transport;Herpesvirus 1, Suid/genetics/*growth &development;15 Retrovirus mechanism;Pseudorabies/pathology/*virology;Neurons/pathology/virology;Vitreous Body/*virology;Mesocricetus;Eye Enucleation;Visual Pathways/pathology/virology;Autonomic Nervous System/pathology/*virology;Support, U.S. Gov't, P.H.S.;*Axonal Transport/physiology;Genes, Reporter;Retinal Ganglion Cells/pathology/virology;Luminescent Proteins/genetics},
	Number = {7},
	Organization = {Department of Anatomy, Colorado State University, Fort Collins, Colorado 80523, USA. gpickard\@lamar.colostate.edu},
	Pages = {2701-10},
	Pubmed = {11923435},
	Title = {Intravitreal injection of the attenuated pseudorabies virus PRV Bartha results in infection of the hamster suprachiasmatic nucleus only by retrograde transsynaptic transport via autonomic circuits},
	Uuid = {1E3D6FB0-3360-44B2-8694-D69A59896EEE},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11923435}}

@article{Pielak:2004,
	Abstract = {Initial studies suggested that spatial organization of the putative polar body contractile ring was determined by the peripheral aster in Spisula [Biol. Bull. 205 (2003) 192]. Here we report detailed supporting observations, including testing of aster and ring function with inhibitors. The metaphase peripheral aster was confirmed to spread cortically in an umbrella-like pattern, with microtubule-poor center. The aster disassembled during anaphase, leaving the spindle docked at the F-actin-poor center of a newly generated cortical F-actin ring that closely approximated the aster in location, measured diameter range, and pattern. Cytochalasin D and latrunculin-B permitted all events except ring and polar body formation. Nocodazole disassembly or taxol stabilization of the peripheral aster produced poorly defined rings or bulging anaphase asters within the ring center, respectively, inhibiting polar body formation. Polar body extrusion occurred at the ring center, the diameter of which diminished. Ring contractility-previously assumed-was verified using blebbistatin, a myosin-II ATPase inhibitor that permitted ring assembly but blocked polar body extrusion. The data support the hypothesis that peripheral aster spreading, perhaps dynein-driven, is causally related to polar body contractile ring formation, with anaphase entry and aster disassembly also required for polar body biogenesis. Previously reported astral spreading during embryonic micromere formation suggests that related mechanisms are involved in asymmetric somatic cytokinesis. 0012-1606 Journal Article},
	Author = {Pielak, R. M. and Gaysinskaya, V. A. and Cohen, W. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Dev Biol},
	Keywords = {EE pdf;Actins/chemistry;08 Aberrant cell cycle;Cytoskeleton/chemistry;Cell Division;Support, U.S. Gov't, Non-P.H.S.;Microtubules/chemistry;Centrosome/physiology;Animals;Support, Non-U.S. Gov't;Clams/*embryology;Myosin Type II/metabolism},
	Number = {2},
	Organization = {Department of Biological Sciences, Hunter College, New York, NY 10021, USA.},
	Pages = {421-32},
	Title = {Formation and function of the polar body contractile ring in Spisula},
	Uuid = {804B1380-C789-42DA-AA21-71436098A258},
	Volume = {269},
	Year = {2004},
	url = {papers/Pielak_DevBiol2004.pdf}}

@article{Pinching:1971,
	Author = {Pinching, A. J. and Powell, T. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0021-9533},
	Journal = {J Cell Sci},
	Keywords = {Synapses;Glycogen;Cell Membrane;Neuroglia;Dendrites;13 Olfactory bulb anatomy;Limbic System;Microscopy, Electron;Rats;Nerve Endings;Ribosomes;Animals;Cytoplasmic Granules;Cytoplasm;Axons},
	Medline = {72053370},
	Month = {9},
	Nlm_Id = {0052457},
	Number = {2},
	Pages = {379-409},
	Pubmed = {5124504},
	Title = {The neuropil of the periglomerular region of the olfactory bulb},
	Uuid = {FBEC1778-D067-11DA-8A8C-000D9346EC2A},
	Volume = {9},
	Year = {1971}}

@article{Pixley:1998,
	Abstract = {The rate of neurogenesis in the peripheral olfactory neuroepithelium is regulated by unknown mechanisms. The members of the insulin-like growth factor (IGF) family can influence neuronal generation, survival and/or differentiation. Several members of this family, in particular IGF-1, are expressed at high levels in the olfactory bulb and epithelium, where they could influence the generation and/or survival of olfactory receptor neurons (ORNs). To explore the role of IGF-1 in the olfactory epithelium (OE), we asked which cells expressed IGF-1 receptors (IGF- 1Rs), using olfactory cell cultures and cryostat-cut tissue sections of neonatal (postnatal day four) and adult rat OE. An antibody specific for the alpha subunit of the IGF-1R densely labeled a subset of ORNs but not other cell types in sections and cultures. These ORNs were primarily immature, as determined by double labeling with neuronal markers. The number of IGF-1R-labeled cells as well as the levels of IGF-1R protein (determined by immunoprecipitation and Western blotting) decreased with age, which is consistent with normal developmental changes. To study IGF-1 effects in the intact animal, we infused IGF-1 and related growth factors into the noses of newborn Sprague-Dawley rats, i.e., when the epithelium is still developing. Growth factors or carrier solution (0.9\%NaCl with 0.25\%bovine serum albumin to prevent nonspecific binding) were applied (10 microliters) to the left nostril once per day starting shortly after birth on postnatal day 1 (P1), P2 and P3, and the animals were sacrificed on P4 by decapitation. After paraformaldehyde immersion fixation, cryostat sections of the olfactory area of the nose were immunostained for the proliferating cell nuclear antigen (PCNA). Sections were position-matched by turbinate structure and then epithelial height and area of PCNA staining at the base of the epithelium (which represents division of primarily neuronal precursors) were measured by image analysis. Both were significantly increased by rat IGF-1 (20 ng/ml, 2.6 nM), but not insulin (20 ng/ml, 2.6 nM) or an IGF-1 derivative, LongR3 IGF-1 (200 ng/ml, 22 nM), that does not bind to the IGF-1 binding proteins (IGFBPs). Thus IGF-1 appears to influence the rate of olfactory neurogenesis, and its actions are not modified by the IGFBPs. These data suggest an important role for IGF-1 in the OE.},
	Author = {Pixley, S. K. and Dangoria, N. S. and Odoms, K. K. and Hastings, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {Rats, Sprague-Dawley;C;Rats;Hypoglycemic Agents/pharmacology;Animal;Cattle;Insulin-Like Growth Factor I/*pharmacology;Olfactory Receptor Neurons/*cytology;Cells, Cultured;04 Adult neurogenesis factors;Insulin/pharmacology;Support, U.S. Gov't, P.H.S.;Cell Differentiation/drug effects},
	Organization = {Department of Cell Biology, University of Cincinnati College of Medicine, Ohio 45267, USA. sarah.pixley\@uc.edu},
	Pages = {244-7.},
	Title = {Effects of insulin-like growth factor 1 on olfactory neurogenesis in vivo and in vitro},
	Uuid = {43577B85-7A37-4437-B445-EC0F34A8C75E},
	Volume = {855},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9929614}}

@article{Pixley:1984,
	Abstract = {A monoclonal antibody to vimentin (RBA1) and a polyclonal antiserum to glial fibrillary acidic protein (GFAP) were used in double labeling experiments to examine astrocyte intermediate filaments in development and wounding. RBA1 bound to radial glia in newborn rat parietal cortex that are predominantly anti-GFAP-negative. The RBA1-positive radial fibers disappeared by postnatal day 20 with the greatest rate of disappearance occurring between day 8 and day 15. Between birth and day 20, the anti-GFAP staining increased to the adult pattern in mature shaped astrocytes. Some overlay was observed between the binding patterns of the two antibodies. Stab wounds to cortical areas were made at a developmental time when there were normally no RBA1-positive astrocytes. RBA1-positivity was present in some astrocytes but only at the edges of the wounds. The distribution patterns of RBA1-positive cells led to hypotheses concerning the possible function of vimentin in astrocytes and its regulation during development and wounding.},
	Author = {Pixley, S. K. and de Vellis, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {10 Development;Glial Fibrillary Acidic Protein;Research Support, Non-U.S. Gov't;Rats;10 Hippocampus;Antibodies, Monoclonal;Research Support, U.S. Gov't, P.H.S.;Astrocytes;Cerebellum;Research Support, U.S. Gov't, Non-P.H.S.;Fluorescent Antibody Technique;Animals;Cerebral Cortex;Vimentin},
	Medline = {85001403},
	Month = {8},
	Nlm_Id = {0045503},
	Number = {2},
	Pages = {201-9},
	Pubmed = {6383523},
	Title = {Transition between immature radial glia and mature astrocytes studied with a monoclonal antibody to vimentin},
	Uuid = {64F46DA3-69C2-4CB3-AAAE-A0F52E774130},
	Volume = {317},
	Year = {1984}}

@article{Pixley:1984a,
	Abstract = {A monoclonal antibody was developed using rat astrocytes purified in vitro as the starting antigenic material. Selection of the monoclonal was on the basis of astrocyte binding specificity in brain sections using indirect immunofluorescence techniques. The antibody (RBA2) that was chosen was specific for astrocytes in that it did not stain neurons or oligodendrocytes in frozen brain sections. It did, however, show binding to vascular smooth muscle and meningeal cells. The antigenic determinant(s) was determined to be on filaments of the intermediate-size class in cultured astrocytes and fibroblasts. From analysis of binding patterns in various tissues and in immunoblots, it was found that RBA2 cross-reacted strongly with glial fibrillary acidic protein (GFAP) and desmin. There was a weaker cross-reactivity to a vimentin-associated component. It is proposed that this antibody can be used as an astrocyte and blood vessel marker in brain sections, a vimentin marker in cultures and as a probe of intermediate filament composition and distribution.},
	Author = {Pixley, S. K. and Kobayashi, Y. and de Vellis, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Glial Fibrillary Acidic Protein;10 Development;10 Hippocampus;Animals;Astrocytes;Cells, Cultured;Mice, Inbred BALB C;Rats;Fluorescent Antibody Technique;Comparative Study;Research Support, U.S. Gov't, Non-P.H.S.;Cross Reactions;Cell Line;Research Support, U.S. Gov't, P.H.S.;Antibody Specificity;Antibodies, Monoclonal;Intermediate Filament Proteins;Epitopes;Mice;Research Support, Non-U.S. Gov't},
	Medline = {85083150},
	Nlm_Id = {7600111},
	Number = {4},
	Pages = {525-41},
	Pubmed = {6210375},
	Title = {Monoclonal antibody to intermediate filament proteins in astrocytes},
	Uuid = {B4E79C49-367A-409C-9220-4F414864F9C7},
	Volume = {12},
	Year = {1984},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.490120402}}

@article{Pixley:1992,
	Abstract = {Olfactory receptor neurons (ORNs) are replaced and differentiate in adult animals, but differentiation in dissociated cell culture has not been demonstrated. To test whether contact with the CNS regulates maturation, neonatal rat olfactory cells were grown on a culture substrate or on CNS astrocytes. Mature ORNs, immunopositive for olfactory marker protein (OMP), disappeared rapidly from both systems. Neurons positive for neuron-specific tubulin (immature and mature) disappeared from substrate-only cultures, but remained abundant in the cocultures. OMP-positive neurons reappeared after 10 days in vitro. Pulse labeling with [3H]thymidine showed extensive neurogenesis of both immature and mature olfactory neurons. This demonstrates, in vitro, both division and differentiation of olfactory progenitor cells. eng Journal Article},
	Author = {Pixley, S. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Journal = {Neuron},
	Keywords = {Cell Differentiation;Stem Cells/cytology/*physiology;Neuroglia/cytology/*physiology;G abstr;Cytological Techniques;Cell Aging;Neurons/cytology/*physiology;Cell Survival;Cell Division;11 Glia;Animal;Support, U.S. Gov't, P.H.S.;Olfactory Bulb/*cytology;Cells, Cultured;Nasal Cavity/cytology;Support, Non-U.S. Gov't;Brain/*cytology},
	Number = {6},
	Organization = {Department of Anatomy and Cell Biology, University of Cincinnati College of Medicine, Ohio 45267-0521.},
	Pages = {1191-204.},
	Title = {CNS glial cells support in vitro survival, division, and differentiation of dissociated olfactory neuronal progenitor cells},
	Uuid = {6AEC5568-F1D1-416C-92AE-E71A3822D17D},
	Volume = {8},
	Year = {1992}}

@article{Pixley:1994,
	Abstract = {Production and differentiation of olfactory neurons occur in spherical, multi-neuronal aggregates that form in cultures where dissociated newborn rat nasal cells are plated on to CNS glial cells. We show here that neuronal cell bodies were primarily located in the peripheral layers of the spheres, and almost every neuronal sphere contained one or several non-cellular central cavities. The dendrite-like processes of the olfactory neurons, immunostained for neuron-specific tubulin or the olfactory marker protein, were aligned and directed towards the central cavities. Olfactory neurons in the intact animal show a similar relationship with the nasal lumen. Non-neuronal cells formed multiple layers centrally, bordering the cavities. This degree of phenotypic re-creation is unusual in a dissociated monolayer culture system. eng Journal Article},
	Author = {Pixley, S. K. and Bage, M. and Miller, D. and Miller, M. L. and Shi, M. and Hastings, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Journal = {Neuroreport},
	Keywords = {13 Olfactory bulb anatomy;Cell Differentiation;Cell Separation;Cells, Cultured;Epithelium/cytology;Rats;Neurons/*ultrastructure;Phenotype;Animal;Cell Movement;Astrocytes/physiology;Cell Communication;Cell Polarity;Rats, Sprague-Dawley;Nerve Tissue Proteins/analysis;Animals, Newborn;Brain/cytology;Support, U.S. Gov't, P.H.S.;Nasal Mucosa/*cytology;Biological Markers/analysis;I abstr},
	Number = {5},
	Organization = {Department of Anatomy and Cell Biology, University of Cincinnati Medical College, OH 45267-0521.},
	Pages = {543-8.},
	Title = {Olfactory neurons in vitro show phenotypic orientation in epithelial spheres},
	Uuid = {7648665C-EF2A-49AF-B097-A675C8F0C563},
	Volume = {5},
	Year = {1994}}

@article{Pizzorusso:2002,
	Abstract = {In young animals, monocular deprivation leads to an ocular dominance shift, whereas in adults after the critical period there is no such shift. Chondroitin sulphate proteoglycans (CSPGs) are components of the extracellular matrix (ECM) inhibitory for axonal sprouting. We tested whether the developmental maturation of the ECM is inhibitory for experience-dependent plasticity in the visual cortex. The organization of CSPGs into perineuronal nets coincided with the end of the critical period and was delayed by dark rearing. After CSPG degradation with chondroitinase-ABC in adult rats, monocular deprivation caused an ocular dominance shift toward the nondeprived eye. The mature ECM is thus inhibitory for experience-dependent plasticity, and degradation of CSPGs reactivates cortical plasticity. 1095-9203 Journal Article},
	Author = {Pizzorusso, T. and Medini, P. and Berardi, N. and Chierzi, S. and Fawcett, J. W. and Maffei, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Science},
	Keywords = {Extracellular Matrix/*metabolism;Animals;Axons/physiology;*Neuronal Plasticity;Rats;Proteochondroitin Sulfates/*metabolism;*Dominance, Ocular;Visual Cortex/*physiology;Darkness;Synapses/physiology;11 Glia;Time Factors;Support, Non-U.S. Gov't;Extracellular Matrix Proteins/metabolism;Chondroitin ABC Lyase/*metabolism;Light;Nerve Tissue Proteins/metabolism;G pdf;Visual Acuity;Neurons/physiology;Glycosaminoglycans/metabolism},
	Number = {5596},
	Organization = {Scuola Normale Superiore, 56100 Pisa, Italy. tommaso\@in.pi.cnr.it},
	Pages = {1248-51},
	Title = {Reactivation of ocular dominance plasticity in the adult visual cortex},
	Uuid = {7BF008FC-F6AC-4F07-A18F-087722765B26},
	Volume = {298},
	Year = {2002},
	url = {papers/Pizzorusso_Science2002.pdf}}

@article{Pleasure:2000,
	Abstract = {The dentate gyrus of the hippocampus is uniquely organized with a displaced proliferative zone that continues to generate dentate granule cells throughout life. We have analyzed the expression of Notch receptors, Notch ligands, and basic helix-loop-helix (bHLH) genes during dentate gyrus development to determine whether the need to maintain a pool of undifferentiated precursors is reflected in the patterns of expression of these genes. Many of these genes are expressed diffusely throughout the cortical neuroepithelium at embryonic days 16 and 17 in the rat, just preceding the migration of newly born granule cells and dentate precursor cells into the dentate anlage. However, at this time, Mash1, Math3, and Id3 expression are all concentrated in the area that specifically gives rise to granule cells and dentate precursor cells. Two days later, at the time of migration of the first granule cells and dentate precursor cells, cells expressing Mash1 are seen in the migratory route from the subventricular zone to the developing dentate gyrus. Newly born granule cells expressing NeuroD are also present in this migratory pathway. In the first postnatal week, precursor cells expressing Mash1 reside in the dentate hilus, and by the third postnatal week they have largely taken up their final position in the subgranular zone along the hilar side of the dentate granule cell layer. After terminal differentiation, granule cells born in the hilus or the subgranular zone begin to express NeuroD followed by NeuroD2. This study establishes that the expression patterns of bHLH mRNAs evolve during the formation of the dentate gyrus, and the precursor cells resident in the mature dentate gyrus share features with precursor cells found in development. Thus, many of the same mechanisms that are known to regulate cell fate and precursor pool size in other brain regions are likely to be operative in the dentate gyrus at all stages of development.},
	Author = {Pleasure, S. J. and Collins, A. E. and Lowenstein, D. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Pregnancy;Cell Differentiation;Animals;Transcription Factors;DNA-Binding Proteins;Gene Expression Regulation, Developmental;Rats;Female;Cell Movement;Rats, Sprague-Dawley;Embryo;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Neurons;Dentate Gyrus;Membrane Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {20394094},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {16},
	Organization = {Department of Neurology, Epilepsy Research Laboratory, University of California, San Francisco, California 94143, USA.},
	Pages = {6095-105},
	Pii = {20/16/6095},
	Pubmed = {10934259},
	Title = {Unique expression patterns of cell fate molecules delineate sequential stages of dentate gyrus development},
	Uuid = {AD8B0A18-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {20},
	Year = {2000},
	url = {papers/Pleasure_JNeurosci2000.pdf}}

@article{Pluchino:2003,
	Abstract = {Widespread demyelination and axonal loss are the pathological hallmarks of multiple sclerosis. The multifocal nature of this chronic inflammatory disease of the central nervous system complicates cellular therapy and puts emphasis on both the donor cell origin and the route of cell transplantation. We established syngenic adult neural stem cell cultures and injected them into an animal model of multiple sclerosis--experimental autoimmune encephalomyelitis (EAE) in the mouse--either intravenously or intracerebroventricularly. In both cases, significant numbers of donor cells entered into demyelinating areas of the central nervous system and differentiated into mature brain cells. Within these areas, oligodendrocyte progenitors markedly increased, with many of them being of donor origin and actively remyelinating axons. Furthermore, a significant reduction of astrogliosis and a marked decrease in the extent of demyelination and axonal loss were observed in transplanted animals. The functional impairment caused by EAE was almost abolished in transplanted mice, both clinically and neurophysiologically. Thus, adult neural precursor cells promote multifocal remyelination and functional recovery after intravenous or intrathecal injection in a chronic model of multiple sclerosis. 0028-0836 Journal Article},
	Author = {Pluchino, S. and Quattrini, A. and Brambilla, E. and Gritti, A. and Salani, G. and Dina, G. and Galli, R. and Del Carro, U. and Amadio, S. and Bergami, A. and Furlan, R. and Comi, G. and Vescovi, A. L. and Martino, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:56 -0400},
	Journal = {Nature},
	Keywords = {Cell Differentiation;Animals;Disease Progression;Encephalomyelitis, Experimental;Brain Tissue Transplantation;*Stem Cell Transplantation;L pdf;Cell Movement;Cell Count;Stem Cells/cytology;Aging/*physiology;Chronic Disease;17 Transplant Regeneration;Injections, Intraventricular;Oligodendroglia/cytology/pathology;Support, Non-U.S. Gov't;Autoimmune/metabolism/pathology/physiopathology/therapy;Nerve Fibers, Myelinated/metabolism/pathology;RNA, Messenger/genetics/metabolism;Mice;Injections, Intravenous;Neurons/*cytology/metabolism/pathology/*transplantation;*Tissue Therapy;Axons/metabolism/pathology;Multiple Sclerosis/metabolism/*pathology/physiopathology/*therapy;Growth Substances/genetics},
	Number = {6933},
	Organization = {Neuroimmunology Unit-DIBIT, San Raffaele Hospital, via Olgettina 58, 20132 Milano, Italy.},
	Pages = {688-94},
	Title = {Injection of adult neurospheres induces recovery in a chronic model of multiple sclerosis},
	Uuid = {8A098DB8-2922-4919-8B5A-60035F7C5770},
	Volume = {422},
	Year = {2003},
	url = {papers/Pluchino_Nature2003.pdf}}

@article{Pluchino:2005,
	Abstract = {In degenerative disorders of the central nervous system (CNS), transplantation of neural multipotent (stem) precursor cells (NPCs) is aimed at replacing damaged neural cells. Here we show that in CNS inflammation, NPCs are able to promote neuroprotection by maintaining undifferentiated features and exerting unexpected immune-like functions. In a mouse model of chronic CNS inflammation, systemically injected adult syngeneic NPCs use constitutively activated integrins and functional chemokine receptors to selectively enter the inflamed CNS. These undifferentiated cells survive repeated episodes of CNS inflammation by accumulating within perivascular areas where reactive astrocytes, inflamed endothelial cells and encephalitogenic T cells produce neurogenic and gliogenic regulators. In perivascular CNS areas, surviving adult NPCs induce apoptosis of blood-borne CNS-infiltrating encephalitogenic T cells, thus protecting against chronic neural tissue loss as well as disease-related disability. These results indicate that undifferentiated adult NPCs have relevant therapeutic potential in chronic inflammatory CNS disorders because they display immune-like functions that promote long-lasting neuroprotection.},
	Author = {Pluchino, Stefano and Zanotti, Lucia and Rossi, Barbara and Brambilla, Elena and Ottoboni, Linda and Salani, Giuliana and Martinello, Marianna and Cattalini, Alessandro and Bergami, Alessandra and Furlan, Roberto and Comi, Giancarlo and Constantin, Gabriela and Martino, Gianvito},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {T-Lymphocytes;Cell Differentiation;Animals;Stem Cell Transplantation;Brain Tissue Transplantation;Multipotent Stem Cells;Chemotaxis;Neuroprotective Agents;Apoptosis;11 Glia;Chronic Disease;17 Transplant Regeneration;Disease Models, Animal;Microspheres;Cell Adhesion;Encephalomyelitis, Autoimmune, Experimental;Receptors, Chemokine;Integrin alpha4beta1;Mice;24 Pubmed search results 2008;Central Nervous System;Inflammation;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {0410462},
	Number = {7048},
	Organization = {Neuroimmunology Unit-DIBIT, Vita-Salute University, San Raffaele Hospital, via Olgettina 58, 20132 Milan, Italy.},
	Pages = {266-71},
	Pii = {nature03889},
	Pubmed = {16015332},
	Title = {Neurosphere-derived multipotent precursors promote neuroprotection by an immunomodulatory mechanism},
	Uuid = {93B44DD9-F510-4A37-9A7E-5460339A2031},
	Volume = {436},
	Year = {2005},
	url = {papers/Pluchino_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03889}}

@article{Plumpe:2006,
	Abstract = {BACKGROUND: In the course of adult hippocampal neurogenesis most regulation takes place during the phase of doublecortin (DCX) expression, either as pro-proliferative effect on precursor cells or as survival-promoting effect on postmitotic cells. We here obtained quantitative data about the proliferative population and the dynamics of postmitotic dendrite development during the period of DCX expression. The question was, whether any indication could be obtained that the initiation of dendrite development is timely bound to the exit from the cell cycle. Alternatively, the temporal course of morphological maturation might be subject to additional regulatory events. RESULTS: We found that (1) 20\%of the DCX population were precursor cells in cell cycle, whereas more than 70\%were postmitotic, (2) the time span until newborn cells had reached the most mature stage associated with DCX expression varied between 3 days and several weeks, (3) positive or negative regulation of precursor cell proliferation did not alter the pattern and dynamics of dendrite development. Dendrite maturation was largely independent of close contacts to astrocytes. CONCLUSION: These data imply that dendrite maturation of immature neurons is initiated at varying times after cell cycle exit, is variable in duration, and is controlled independently of the regulation of precursor cell proliferation. We conclude that in addition to the major regulatory events in cell proliferation and selective survival, additional micro-regulatory events influence the course of adult hippocampal neurogenesis.},
	Author = {Pl{\"u}mpe, Tobias and Ehninger, Dan and Steiner, Barbara and Klempin, Friederike and Jessberger, Sebastian and Brandt, Moritz and R{\"o}mer, Benedikt and Rodriguez, Gerardo Ramirez and Kronenberg, Golo and Kempermann, Gerd},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1471-2202},
	Journal = {BMC Neurosci},
	Keywords = {Cell Survival;Microtubule-Associated Proteins;Animals;Astrocytes;Seizures;comparative study;Physical Conditioning, Animal;Female;Cell Count;Mice, Transgenic;Hippocampus;Mice, Inbred C57BL;Kainic Acid;research support, non-u.s. gov't;Behavior, Animal;Cell Proliferation;Dendrites;Neuropeptides;In Situ Nick-End Labeling;Blotting, Western;Neurons;Organogenesis;Age Factors;Maze Learning;Mice;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine},
	Nlm_Id = {100966986},
	Organization = {Max Delbr{\"u}ck Center for Molecular Medicine (MDC) Berlin-Buch, Germany. biotobi\@gmx.net <biotobi\@gmx.net>},
	Pages = {77},
	Pii = {1471-2202-7-77},
	Pubmed = {17105671},
	Title = {Variability of doublecortin-associated dendrite maturation in adult hippocampal neurogenesis is independent of the regulation of precursor cell proliferation},
	Uuid = {C272549E-5DD7-4AED-A5CD-9EC43D453504},
	Volume = {7},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2202-7-77}}

@article{Pogosian:1971,
	Author = {Pogosian, V. I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0004-1947},
	Journal = {Arkh Anat Gistol Embriol},
	Keywords = {Axons;Dendrites;Dogs;Animals;24 Pubmed search results 2008;Neurons;Frontal Lobe},
	Medline = {72167811},
	Month = {9},
	Nlm_Id = {0370603},
	Number = {9},
	Pages = {32-9},
	Pubmed = {5147139},
	Title = {[Neuronal thorns in the frontal cortex of the dog]},
	Uuid = {C896C208-A421-4334-805F-880AADC1760A},
	Volume = {61},
	Year = {1971}}

@article{Poleshchuk:1988,
	Abstract = {Ultrastructural changes, various by their character and the degree of expression, have been found in axons of the spinal cord of guinea-pigs with amyotrophic leukospongiosis (AL) (a slow infection of the CNS). The dependence of the degree of degenerative changes on the disease duration is shown. Absorption of cellular debris by oligodendrocytes and astrocytes is noted. It seems that microglia does not participate in phagocytosis. The conclusion has been made that experimental AL is a convenient model for studying the mechanisms of death of the central axons and analysis of the glia cell function under the conditions of keeping the blood-brain barrier intact.},
	Author = {Poleshchuk, N. N. and Votiakov, V. I. and Shalapenok, L. S. and Kolomiets, N. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0365-9615},
	Journal = {Biull Eksp Biol Med},
	Keywords = {Spinal Cord Diseases;Nerve Degeneration;Blood-Brain Barrier;Comparative Study;Microscopy, Electron;Guinea Pigs;English Abstract;Not relevant;Time Factors;11 Glia;Spinal Cord;Animals;Slow Virus Diseases;Axons},
	Medline = {89088498},
	Month = {12},
	Nlm_Id = {0370627},
	Number = {12},
	Pages = {734-7},
	Pubmed = {3207884},
	Title = {[Ultrastructural changes in the axons of the central nervous system in experimental amyotrophic leukospongiosis]},
	Uuid = {FC30437D-F5B2-4CED-AD28-87EA000D2C9B},
	Volume = {106},
	Year = {1988}}

@article{Polleux:2002,
	Abstract = {During telencephalic development, cells from the medial ganglionic eminence (MGE) are thought to migrate to the neocortex to give rise to a majority of cortical GABAergic interneurons. By combining time-lapse video-microscopy, immunofluorescence and pharmacological perturbations in a new in vitro migration assay, we find that MGE-derived cells migrate through the entire extent of the cortex and into the CA fields of the hippocampus, but avoid the dentate gyrus. Migrating neurons initially travel within the marginal zone and intermediate zone, and can enter the cortical plate from either location. Tangential migration is strongly stimulated by BDNF and NT4 and attenuated by the Trk-family inhibitor, K252a, suggesting that migration is regulated by TrkB signaling. Furthermore, TrkB-null mice show a significant decrease in the number of calbindin-positive neurons migrating tangentially in the embryonic cortex. BDNF and NT4 cause rapid activation of PI3-kinase in MGE cells, and inhibition of PI3-kinase (but not of MAP kinase or PLCgamma) dramatically attenuates tangential migration. These observations suggest that TrkB signaling, via PI3-kinase activation, plays an important role in controlling interneuron migration in the developing cerebral cortex.},
	Author = {Polleux, Franck and Whitford, Kristin L. and Dijkhuizen, Paul A. and Vitalis, Tania and Ghosh, Anirvan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Research Support, Non-U.S. Gov't;Signal Transduction;Animals;Cells, Cultured;Coculture Techniques;Mice, Mutant Strains;Enzyme Inhibitors;Brain-Derived Neurotrophic Factor;Female;Cell Movement;Chromones;Phospholipase C;Green Fluorescent Proteins;Ganglia, Sensory;Morpholines;1-Phosphatidylinositol 3-Kinase;Nerve Growth Factors;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Neurons;Receptor, trkB;Cell Transplantation;Mice;Carbazoles;24 Pubmed search results 2008;Luminescent Proteins;Isoenzymes;Phospholipase C gamma},
	Medline = {22065264},
	Month = {7},
	Nlm_Id = {8701744},
	Number = {13},
	Organization = {INSERM U.371, 18 avenue Doyen L{\'e}pine, 69675 Bron, France.},
	Pages = {3147-60},
	Pubmed = {12070090},
	Title = {Control of cortical interneuron migration by neurotrophins and PI3-kinase signaling},
	Uuid = {1EE8D059-D248-42B1-A584-787BBD6EFBC0},
	Volume = {129},
	Year = {2002}}

@article{Polo:2006,
	Abstract = {Endocytosis is used by eukaryotic cells to regulate nutrient internalization, signal transduction, and the composition of the plasma membrane. However, a more complex picture is emerging, in which endocytic pathways integrate diverse signals, thereby contributing to a higher level of cellular and organismal organization. In this way, endocytosis and cell signaling are intertwined in many biological processes, such as cell motility and cell fate determination.},
	Author = {Polo, Simona and Di Fiore, Pier Paolo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {IFOM, Istituto FIRC di Oncologia Molecolare, Via Adamello 16, 20134 Milan, Italy. simona.polo\@ifom-ieo-campus.it},
	Pages = {897-900},
	Pii = {S0092-8674(06)00242-X},
	Pubmed = {16530038},
	Title = {Endocytosis conducts the cell signaling orchestra},
	Uuid = {62D36A7A-1789-4F29-AD83-97EBE141F30E},
	Volume = {124},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.02.025}}

@article{Polo-Parada:2001,
	Abstract = {Although functional neuromuscular junctions (NMJs) form in NCAM-deficient mice, they exhibit multiple alterations in presynaptic organization and function. Profound depression and unusual periodic total transmission failures with repetitive stimulation point to a defect in vesicle mobilization/cycling, and these defects were mimicked in (+/+) NMJs by inhibitors of myosin light chain kinase, known to affect vesicle mobilization. Two separate release mechanisms, utilizing different endocytic machinery and Ca(2+) channels, were shown to coexist in (-/-) terminals, with the mature process targeted to presynaptic membrane opposed to muscle, and an abnormally retained immature process targeted to the remainder of the presynaptic terminal and axon. Thus, NCAM plays a critical and heretofore unsuspected role in the molecular organization of the presynaptic NMJ.},
	Author = {Polo-Parada, L. and Bose, C. M. and Landmesser, L. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Electric Stimulation;Synaptic Vesicles;Research Support, Non-U.S. Gov't;Mice, Knockout;Neural Cell Adhesion Molecules;Presynaptic Terminals;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred C57BL;Neuromuscular Junction;Neurotransmitter Agents;Calcium Channels;Synaptic Transmission;Animals;Mice;24 Pubmed search results 2008},
	Medline = {21603129},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA.},
	Pages = {815-28},
	Pii = {S0896-6273(01)00521-9},
	Pubmed = {11738028},
	Title = {Alterations in transmission, vesicle dynamics, and transmitter release machinery at NCAM-deficient neuromuscular junctions},
	Uuid = {921257D0-9222-42F6-9190-781A8665EFCC},
	Volume = {32},
	Year = {2001}}

@article{Poluch:2007,
	Abstract = {During cerebral cortical development, gamma-aminobutyric acidergic (GABAergic) interneurons arise from a different site than projection neurons. GABAergic cells are generated in the subpallial ganglionic eminence (GE), while excitatory projection neurons arise from the neocortical ventricular zone. Our laboratory studies a model of cortical dysplasia that displays specific disruption of GABAergic mechanisms and an alteration in the overall balance of excitation in the neocortex. To produce this model, the birth of neurons on a specific gestational day in ferrets (embryonic day 33 [E33]) is interrupted by injection of the antimitotic methylazoxymethanol (MAM). We hypothesized that migration of interneurons might be disrupted in this cortical dysplasia paradigm. We observed that although interneurons migrate into the neocortex in both normal and dysplastic cortex, the migrating cells become disoriented over time after E33 MAM treatment. Coculture experiments using normal GE and MAM-treated cortex (and vice versa) demonstrate that cues dictating proper orientation of migrating interneurons arise from the cortex and are not intrinsic to the migrating cells. As a consequence, interneurons in mature brains of MAM-treated animals are abnormally distributed. We report that GABA(A) receptor activation is crucial to the proper positioning of interneurons migrating into the cortex from the GE in normal and MAM-treated animals.},
	Author = {Poluch, and Jablonska, and Juliano,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008;21 Epilepsy},
	Month = {4},
	Nlm_Id = {9110718},
	Organization = {Department of Anatomy, Physiology and Genetics, USUHS, Bethesda, MD 20814, USA.},
	Pii = {bhm032},
	Pubmed = {17443019},
	Title = {Alteration of Interneuron Migration in a Ferret Model of Cortical Dysplasia},
	Uuid = {4EBB882C-E90C-4DB7-A752-A2A2F5D0545F},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhm032}}

@article{Poluektova:2005,
	Abstract = {Cognitive, behavioral, and motor impairments, during progressive human immunodeficiency virus type 1 (HIV-1) infection, are linked to activation of brain mononuclear phagocytes (MP; perivascular macrophages and microglia). Activated MPs effect a giant cell encephalitis and neuroinflammatory responses that are mirrored in severe combined immunodeficient (SCID) mice injected with human monocyte-derived macrophages (MDM). Whether activated human MDMs positioned in the basal ganglia affect hippocampal neuronal plasticity, the brain subregion involved in learning and memory, is unknown. Thus, immunohistochemical techniques were used for detection of newborn neurons (polysialylated neuronal cell adhesion molecule [PSA-NCAM]) and cell proliferation (Ki-67) to assay MDM effects on neuronal development in mouse models of HIV-1 encephalitis. Immunodeficient (C.B.-17/SCID and nonobese diabetic/SCID, NOD/SCID) and immune competent (C.B.-17) mice were injected with uninfected or HIV-1-infected MDM. Sham-operated or unmanipulated mice served as controls. Neuronal plasticity was evaluated in the hippocampal dentate gyrus (DG) at days 7 and 28. By day 7, increased numbers of Ki-67(+) cells, PSA-NCAM(+) cells and dendrites in DG were observed in sham-operated animals. In contrast, significant reductions in neuronal precursors and altered neuronal morphology paralleled increased microglial activation in both HIV-1-infected and uninfected MDM-injected animals. DG cellular composition was restored at day 28. We posit that activated MDM induce inflammation and diminish DG neuronal plasticity. These data provide novel explanations for the cognitive impairments manifested during advanced HIV-1 infection. (c) 2005 Wiley-Liss, Inc.},
	Author = {Poluektova, and Meyer, and Walters, and Paez, and Gendelman,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {11 Glia},
	Month = {8},
	Nlm_Id = {8806785},
	Organization = {Laboratory of Neuroregeneration, Department of Pharmacology and Experimental Neuroscience, Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska.},
	Pubmed = {16078235},
	Title = {Macrophage-induced inflammation affects hippocampal plasticity and neuronal development in a murine model of HIV-1 encephalitis},
	Uuid = {074C8CB9-92B2-4E18-925D-102778127A21},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20253}}

@article{Pomerantz:2004,
	Abstract = {The goal of regenerative medicine is to restore form and function to damaged tissues. One potential therapeutic approach involves the use of autologous cells derived from the bone marrow (bone marrow-derived cells, BMDCs). Advances in nuclear transplantation, experimental heterokaryon formation and the observed plasticity of gene expression and phenotype reported in multiple phyla provide evidence for nuclear plasticity. Recent observations have extended these findings to show that endogenous cells within the bone marrow have the capacity to incorporate into defective tissues and be reprogrammed. Irrespective of the mechanism, the potential for new gene expression patterns by BMDCs in recipient tissues holds promise for developing cellular therapies for both proliferative and post-mitotic tissues.},
	Author = {Pomerantz, Jason and Blau, Helen M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {review;Research Support, Non-U.S. Gov't;Totipotent Stem Cells;Bone Marrow Cells;08 Aberrant cell cycle;Regeneration;Stem Cells;Research Support, U.S. Gov't, P.H.S.;Gene Expression Regulation;22 Stem cells;Humans;Animals;24 Pubmed search results 2008;Cell Nucleus;Cytoplasm},
	Month = {9},
	Nlm_Id = {100890575},
	Number = {9},
	Organization = {Baxter Laboratory in Genetic Pharmacology and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.},
	Pages = {810-6},
	Pii = {ncb0904-810},
	Pubmed = {15340448},
	Title = {Nuclear reprogramming: a key to stem cell function in regenerative medicine},
	Uuid = {0A74CD49-1B4B-11DB-87EC-000D9346EC2A},
	Volume = {6},
	Year = {2004},
	url = {papers/Pomerantz_NatCellBiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb0904-810}}

@article{Ponomarev:2006,
	Abstract = {Microglial cells are monocytic lineage cells that reside in the CNS and have the capacity to become activated during various pathological conditions. Although it was demonstrated that activation of microglial cells could be achieved in vitro by the engagement of CD40-CD40L interactions in combination with proinflammatory cytokines, the exact factors that mediate activation of microglial cells in vivo during CNS autoimmunity are ill-defined. To investigate the role of CD40 in microglial cell activation during experimental autoimmune encephalomyelitis (EAE), we used bone marrow chimera mice that allowed us to distinguish microglial cells from peripheral macrophages and render microglial cells deficient in CD40. We found that the first step of microglial cell activation was CD40-independent and occurred during EAE onset. The first step of activation consisted of microglial cell proliferation and up-regulation of the activation markers MHC class II, CD40, and CD86. At the peak of disease, microglial cells underwent a second step of activation, which was characterized by a further enhancement in activation marker expression along with a reduction in proliferation. The second step of microglial cell activation was CD40-dependent and the failure of CD40-deficient microglial cells to achieve a full level of activation during EAE was correlated with reduced expansion of encephalitogenic T cells and leukocyte infiltration in the CNS, and amelioration of clinical symptoms. Thus, our findings demonstrate that CD40 expression on microglial cells is necessary to complete their activation process during EAE, which is important for disease progression.},
	Author = {Ponomarev, Eugene D. and Shriver, Leah P. and Dittel, Bonnie N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:38 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {11 Glia},
	Month = {2},
	Nlm_Id = {2985117R},
	Number = {3},
	Organization = {Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI 53201.},
	Pages = {1402-10},
	Pii = {176/3/1402},
	Pubmed = {16424167},
	Title = {CD40 Expression by Microglial Cells Is Required for Their Completion of a Two-Step Activation Process during Central Nervous System Autoimmune Inflammation},
	Uuid = {BA43445B-EFA5-4681-A51C-4AA58224687F},
	Volume = {176},
	Year = {2006}}

@article{Ponti:2006,
	Abstract = {Protracted neurogenesis occurs at different postnatal stages in different brain locations, whereby leading to site-specific adult neurogenesis in some cases. No spontaneous genesis of neurons occurs in the cerebellum after the postnatal genesis of granule cells from the external germinal layer (EGL), a transitory actively proliferating zone which is thought to be exhausted before puberty. Here, we show the protracted genesis of newly generated neuronal precursors in the cerebellar cortex of young rabbits, persisting beyond puberty. Neuroblasts generated within an actively proliferating subpial layer thus extending the postnatal EGL are arranged to form thousands of tangential chains reminiscent of those responsible for cell migration in the forebrain subventricular zone. These subpial chains cover the whole cerebellar surface from the 2nd to the 5th month of life, then disappearing after puberty. In addition, we describe the appearance of similar groups of cells at the end of granule cell genesis in the mouse cerebellum, here limited to the short period of EGL exhaustion (4-5 days). These results show common features do exist in the postnatal reorganization of secondary germinal layers of brain and cerebellum at specific stages, parallel to differences in the slowing down of cerebellar neurogenesis among mammalian species.},
	Author = {Ponti, and Peretto, and Bonfanti,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {0372762},
	Organization = {Department of Veterinary Morphophysiology, University of Turin, Via Leonardo da Vinci 44, 10095 Grugliasco, Italy.},
	Pii = {S0012-1606(06)00134-5},
	Pubmed = {16581058},
	Title = {A subpial, transitory germinal zone forms chains of neuronal precursors in the rabbit cerebellum},
	Uuid = {2FEAADE6-43E4-4960-9242-EB9A831BD7E3},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2006.02.037}}

@article{Popesco:2006,
	Abstract = {Extreme gene duplication is a major source of evolutionary novelty. A genome-wide survey of gene copy number variation among human and great ape lineages revealed that the most striking human lineage-specific amplification was due to an unknown gene, MGC8902, which is predicted to encode multiple copies of a protein domain of unknown function (DUF1220). Sequences encoding these domains are virtually all primate-specific, show signs of positive selection, and are increasingly amplified generally as a function of a species' evolutionary proximity to humans, where the greatest number of copies (212) is found. DUF1220 domains are highly expressed in brain regions associated with higher cognitive function, and in brain show neuron-specific expression preferentially in cell bodies and dendrites.},
	Author = {Popesco, Magdalena C. and Maclaren, Erik J. and Hopkins, Janet and Dumas, Laura and Cox, Michael and Meltesen, Lynne and McGavran, Loris and Wyckoff, Gerald J. and Sikela, James M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {24 Pubmed search results 2008;19 Neocortical evolution},
	Month = {9},
	Nlm_Id = {0404511},
	Number = {5791},
	Organization = {Human Medical Genetics, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA.},
	Pages = {1304-7},
	Pii = {313/5791/1304},
	Pubmed = {16946073},
	Title = {Human lineage-specific amplification, selection, and neuronal expression of DUF1220 domains},
	Uuid = {7FBF4C30-9C18-49CA-A80A-D74A563A02BA},
	Volume = {313},
	Year = {2006},
	url = {papers/Popesco_Science2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1127980}}

@article{Popovich:2001,
	Abstract = {Brain and spinal cord inflammation that develops after traumatic injury is believed to differentially influence the structural and/or physiological integrity of surviving neurons and glia. It is possible that the functional dichotomy of CNS inflammation results from the activity of a heterogeneous macrophage population elicited by trauma. Indeed, unique functions have been attributed to macrophages derived from resident microglia versus those originating from infiltrating monocytes. Thus, whether progressive tissue injury or repair is favored could be explained by the disproportionate contributions of one macrophage subset relative to the other. Descriptive neuroanatomical studies are a reasonable first approach to revealing a relationship between microglia, recruited blood monocytes/macrophages, and regions of tissue degeneration and/or repair. Unfortunately, it is not possible to differentiate between CNS macrophage subsets using conventional immunohistochemical approaches. In the present study, we have used radiation bone marrow chimeric rats to definitively characterize the macrophage reaction elicited by experimental spinal contusion injury. In chimeric animals, antibodies raised against unique cell surface molecules expressed on bone marrow-derived cells (BMCs) were used to distinguish infiltrating BMCs from resident microglial-derived macrophages. Our findings indicate that the onset and plateau of macrophage activation (previously shown to be 3 and 7 days postinjury, respectively) is dominated initially by microglial-derived macrophages and then is supplanted by hematogenous cells. While resident macrophages are ubiquitously distributed throughout the injury site, leukocyte-derived monocytes exclusively infiltrate the gray matter and to a lesser extent subpial white matter. Generally, monocyte foci in white matter remain associated with the lumen or abluminal surface of blood vessels, i.e. few cells actually infiltrate the parenchyma. If functional differences exist between CNS macrophage subsets, differences in the time-dependent accumulation and distribution of these cell types could differentially influence the survival of surrounding neurons and glia.},
	Author = {Popovich, P. G. and Hickey, W. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Rats, Inbred Lew;Animals;Monocytes;Macrophages;Image Processing, Computer-Assisted;Rats;Bone Marrow Transplantation;Rats, Inbred BN;Microglia;Cell Count;11 Glia;Disease Models, Animal;Crosses, Genetic;Male;Radiation Chimera;Spinal Cord Injuries;Research Support, U.S. Gov't, P.H.S.;Wounds, Nonpenetrating;Wallerian Degeneration;Immunohistochemistry;Retrograde Degeneration},
	Medline = {21337698},
	Month = {7},
	Nlm_Id = {2985192R},
	Number = {7},
	Organization = {Department of Molecular Virology, Immunology &Medica Genetics, The Ohio State University College of Medicine and Public Health, Columbus, USA.},
	Pages = {676-85},
	Pubmed = {11444796},
	Title = {Bone marrow chimeric rats reveal the unique distribution of resident and recruited macrophages in the contused rat spinal cord},
	Uuid = {22352207-F735-43EE-8A05-E53FA2309F85},
	Volume = {60},
	Year = {2001}}

@article{Popovich:1993,
	Abstract = {Following contusion injury to the dorsal surface of thoracic rat spinal cord, major histocompatibility complex (MHC) class II (Ia) antigen expression by microglia was evaluated throughout the developing lesion. Past investigations of various central nervous system (CNS) lesions have examined short-term or acute sequelae of post-traumatic Ia expression. This report demonstrates that in animals allowed to recover for 18 (sub-chronic) and 45 (chronic) days post-injury, MHC class II antigen is expressed differently at rostral and caudal extents of the lesion as compared with the lesion's epicenter. Following contusion injury to the thoracic spinal cord, sub-chronically injured animals demonstrated Ia-positive microglial staining throughout the white matter rostral and caudal to the epicenter of the lesion, whereas Ia-positive microglia and/or perivascular cells are localized within the gray matter adjacent to it. MHC class II immunoreactivity is down-regulated on microglia at chronic survival times but clusters of Ia-positive macrophages are prominent in regions of maximal degeneration at the epicenter of the lesion. Our findings support the theory that two distinct populations of macrophages participate in resolving traumatic injury. One population is the parenchymal CNS microglia and the other is presumably exudate macrophages derived from the blood. Furthermore, the immunocompetence of these cells as measured by MHC expression may be differentially regulated. This hypothesis is based on differences in Ia-positive staining observed between microglia and macrophages over time concomitant with differences in the spatial distribution of these cell types.},
	Author = {Popovich, P. G. and Streit, W. J. and Stokes, B. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0897-7151},
	Journal = {J Neurotrauma},
	Keywords = {Down-Regulation;Indicators and Reagents;Neuroglia;Rats, Sprague-Dawley;Spinal Cord Injuries;Rats;Female;Histocompatibility Antigens Class II;Not relevant;Immunohistochemistry;T-Lymphocytes;11 Glia;Contusions;Support, U.S. Gov't, P.H.S.;Animals},
	Medline = {93308731},
	Nlm_Id = {8811626},
	Number = {1},
	Organization = {Department of Physiology, Ohio State University, College of Medicine, Columbus.},
	Pages = {37-46},
	Pubmed = {8320731},
	Title = {Differential expression of MHC class II antigen in the contused rat spinal cord},
	Uuid = {A94ADCD3-8128-4CFB-A6E9-AC992CB18B7F},
	Volume = {10},
	Year = {1993}}

@article{Porter:2005,
	Abstract = {The gamma-amino-butyric acid type A receptors (GABAAR) are a heteropentameric receptor complex, composed of 16 possible subunits in various combinations, forming a ligand-gated ion channel. Subunit composition is the primary determinant of GABAAR physiology and pharmacology. Here we have measured mRNA levels for 16 GABAAR subunits in isolated dentate granule neurons (DGN) from eight pediatric patients undergoing resective surgery for intractable epilepsy. We found tightly correlated expression of a subset of GABAAR subunit mRNAs within a single DGN (alpha1, gamma1, and gamma2; alpha4, alpha5, and beta2; alpha4 and beta3). Analysis of inter-patient variability (ANOVA) of eleven highly expressed GABAAR subunit mRNAs found seven of the subunits varied between patients, as did whole cell GABAAR currents. Due to inter-patient differences, there is heterogeneity in DGN GABAAR subunit mRNA and physiology within pediatric epilepsy patients. Patient-specific GABAAR expression might contribute to variability in anti-epileptic drug efficacy, side-effect profiles, and seizure susceptibility.},
	Author = {Porter, Brenda E. and Zhang, Guojun and Celix, Juanita and Hsu, Fu-chun C. and Raol, YogendraSinh H. and Telfeian, Albert and Gallagher, Paul R. and Coulter, Douglas A. and Brooks-Kayal, Amy R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0969-9961},
	Journal = {Neurobiol Dis},
	Keywords = {Epilepsy;Adolescent;21 Neurophysiology;Hippocampus;Comparative Study;Research Support, U.S. Gov't, P.H.S.;Gene Expression Regulation;Protein Subunits;Child, Preschool;Child;RNA, Messenger;Humans;24 Pubmed search results 2008;21 Epilepsy;Receptors, GABA-A},
	Month = {4},
	Nlm_Id = {9500169},
	Number = {3},
	Organization = {Division of Neurology, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. porterb\@email.chop.edu},
	Pages = {484-91},
	Pii = {S0969-9961(04)00321-3},
	Pubmed = {15755675},
	Title = {Heterogeneous GABAA receptor subunit expression in pediatric epilepsy patients},
	Uuid = {7A6B3822-6DE5-42CA-9B8F-B89A70562A79},
	Volume = {18},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.nbd.2004.12.010}}

@article{Porter:2003,
	Abstract = {BACKGROUND: Risk factors for temporal lobe epilepsy (TLE) include history of CNS infection, family history of epilepsy, and history of febrile convulsions (FC). Pre-existing cortical dysplasia (CD) may also predispose to refractory TLE, independent of other risk factors for epilepsy. METHODS: The authors reviewed the neuropathologic features of surgical tissue from temporal lobectomies of 33 pediatric patients with refractory TLE, with and without a history of epilepsy risk factors. RESULTS: CD was found in 64\%(21/33) of all patients with refractory TLE, including 73\%(11/15) patients with a history of FC, 66\%(2/3) patients with CNS infections, and 83\%(5/6) patients with a family history of epilepsy. Disrupted cortical lamination, dystrophic and maloriented neurons, and balloon cells characterized the CD found in the temporal neocortex. CONCLUSION: CD was seen in 21 of 33 surgical specimens from children with refractory TLE, including those with and without other epilepsy risk factors.},
	Author = {Porter, B. E. and Judkins, A. R. and Clancy, R. R. and Duhaime, A. and Dlugos, D. J. and Golden, J. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {1526-632X},
	Journal = {Neurology},
	Keywords = {Causality;10 Development;Follow-Up Studies;Humans;Treatment Outcome;Risk Factors;Neocortex;Female;Child;Hippocampus;21 Dysplasia-heterotopia;research support, non-u.s. gov't;Brain Diseases;Male;Epilepsy, Temporal Lobe;21 Neurophysiology;10 genetics malformation;research support, u.s. gov't, p.h.s.;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {0401060},
	Number = {3},
	Organization = {Pediatric Regional Epilepsy Program, Children's Hospital of Philadelphia, and Department of Pediatrics and Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA. Porterb\@email.chop.edu},
	Pages = {365-8},
	Pubmed = {12913199},
	Title = {Dysplasia: a common finding in intractable pediatric temporal lobe epilepsy},
	Uuid = {858F019B-21F2-4D9F-A885-8FF635DCE547},
	Volume = {61},
	Year = {2003}}

@article{Posnett:2001,
	Abstract = {We usually think of superantigens (SAg) as dangerous toxins that may cause toxic shock syndrome and death. Now, based on two papers in this issue of Immunity, it seems that we all have SAg genes within us, lying dormant and waiting to be activated under special circumstances.},
	Author = {Posnett, D. N. and Yarilina, A. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {1074-7613},
	Journal = {Immunity},
	Keywords = {15 ERVs retroelements;Endogenous Retroviruses;Virus Diseases;24 Pubmed search results 2008;T-Lymphocytes;Mammary Tumor Virus, Mouse;comment;15 Retrovirus mechanism;Humans;Superantigens;Lymphocyte Activation;review;Antigens, Viral},
	Medline = {21527022},
	Month = {10},
	Nlm_Id = {9432918},
	Number = {4},
	Organization = {Department of Medicine, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA. dposnett\@med.cornell.edu},
	Pages = {503-6},
	Pii = {S1074761301002114},
	Pubmed = {11672533},
	Title = {Sleeping with the enemy--endogenous superantigens in humans},
	Uuid = {1F9D3C38-F424-481F-B659-086D9B200AF2},
	Volume = {15},
	Year = {2001}}

@article{Poulsen:1999,
	Abstract = {Following intraperitoneal (IP) inoculation of neonatal mice, the polytropic recombinant murine leukemia virus (MuLV), Fr98, induces a severe brain disease characterized by ataxia, seizures and death. In contrast, no apparent clinical neurological disease is seen after IP infection with Fr54, a polytropic MuLV differing from Fr98 in its envelope gene sequences. In the brain both Fr98 and Fr54 infect primarily capillary endothelial cells and microglia. However, the level of microglial infection by Fr98 is twofold higher than by Fr54, which might account for the difference in neurovirulence. In the present study, in order to test directly whether an increase in the number of microglia infected by Fr54 would be sufficient to induce clinical disease, we attempted to increase the level of Fr54 in the brain by changing the route of infection. After intraventricular inoculation with Fr54-infected neural stem cells (clone C17.2), a well-established vehicle for delivery of viruses and genes to the brain, mice became ataxic and died 4 weeks postinfection. In these mice induction of brain disease was correlated with a higher level of viral antigen in the cerebrum and an increase in the number of infected microglial cells in all brain regions examined compared with mice inoculated IP. In contrast, mice inoculated with neural stem cells infected with an ecotropic nonneurovirulent murine leukemia virus, FB29, developed no clinical disease in spite of evidence for widespread infection of microglia in brain. Since the main differences between Fr54 and FB29 are in the SU (gp70) region of the envelope gene, this region is most likely to account for the differences in induction of CNS disease seen in the current experiments.},
	Author = {Poulsen, D. J. and Favara, C. and Snyder, E. Y. and Portis, J. and Chesebro, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {Animals;Tumor Virus Infections;Recombinant Proteins;Microglia;Capsid;Brain;Not relevant;11 Glia;Brain Diseases;Leukemia Virus, Murine;Viral Envelope Proteins;Retroviridae Infections;Mice, Inbred Strains;Neurons;Viral Load;Mice;Virulence;Stem Cells},
	Medline = {20013306},
	Month = {10},
	Nlm_Id = {0110674},
	Number = {1},
	Organization = {Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, Hamilton, Montana 59840, USA.},
	Pages = {23-9},
	Pii = {S0042682299999178},
	Pubmed = {10544079},
	Title = {Increased neurovirulence of polytropic mouse retroviruses delivered by inoculation of brain with infected neural stem cells},
	Uuid = {62B7BE58-83D3-4122-9D75-2729C5B20E08},
	Volume = {263},
	Year = {1999},
	url = {papers/Poulsen_Virology1999.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/viro.1999.9917}}

@article{Poulter:1992,
	Abstract = {The expression of mRNAs coding for alpha 1, alpha 2, alpha 3, alpha 5, and alpha 6 subunits of the GABAA neurotransmitter receptor was followed during the development of the rat CNS by in situ hybridization histochemistry. Expression of these subunit mRNAs in tissue sections of embryonic day 15 and 17 (E15, E17) whole rat and in brain at ages greater than E17 to adult were varied, transient, and region specific. Subunit mRNAs first detected at E15 were those coding for the alpha 2 and alpha 3 subunits. At E17, alpha 2, alpha 3, and alpha 5 mRNAs were present in abundance in numerous areas in the CNS, with lower but significant amounts of alpha 6 being present in the cortical neuroepithelial layers. However, alpha 6 subunit mRNA expression in the cortex declined until little or no alpha 6 mRNA was detected at E19. alpha 1 subunit mRNA first appeared at E19 in the cortex, followed by expression in the hippocampus by postnatal 5 (PN5). Particularly high expression of alpha 2 and alpha 5 subunit mRNAs was detected throughout the developing CNS, but they were most abundant in the olfactory bulb neurons. The high levels of alpha 2 and alpha 5 subunit mRNAs began to decline around PN5 to the amounts observed in adult. These results demonstrate that numerous GABAA receptor alpha-subunits are expressed before birth in a region- and age-specific manner. This complex and varied expression supports the hypothesis that GABA may play a role in cellular and synaptic differentiation.},
	Author = {Poulter, M. O. and Barker, J. L. and O'Carroll, A. M. and Lolait, S. J. and Mahan, L. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neurosci},
	Keywords = {Base Sequence;Tissue Distribution;Molecular Sequence Data;Rats;Oligonucleotide Probes/genetics;Time Factors;Receptors, GABA-A/*genetics;*Fetal Development;Animal;Fetus/*metabolism;RNA, Messenger/*metabolism;Animals, Newborn;I-1;Brain/embryology/growth &development/*metabolism;13 Olfactory bulb anatomy},
	Number = {8},
	Organization = {Laboratories of Neurophysiology, NINDS, NIH, Bethesda, Maryland 20892.},
	Pages = {2888-900.},
	Title = {Differential and transient expression of GABAA receptor alpha-subunit mRNAs in the developing rat CNS},
	Uuid = {FB3D447F-9C22-44B4-AB26-D95933014DB4},
	Volume = {12},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1322978}}

@article{Powell:1999,
	Abstract = {Transgenic mice overexpressing cytokines facilitate analysis of the effects of these immunomodulators on indigenous cells of the central nervous system. This study examines morphological aspects of demyelination and permeability changes, in a recently described transgenic model (termed GFAP-IL3). GFAP-IL3 mice develop progressive motor disease at approximately 5 months. Lesions identified after disease onset, showed activation of microglia, astroglial proliferation with phagocytosis of lipids, and immigration of macrophages and mast cells into neural parenchyma. Lymphocytes failed to appear until the later stages of the disease. Later, cerebellar and brain stem white matter contained focal demyelinating lesions with intense macrophage infiltration and a proliferative astrocytosis. Dystrophic axonal changes were noted, in addition to demyelination in heavily infiltrated lesions. Mast cells, variably present in the thalamus and meninges of wild type mice, were greatly increased at these sites in GFAP-IL3 mice. Blood-brain barrier (BBB) defects were documented with leakage of intravenously injected horseradish peroxidase. Mast cell infiltration into the CNS and their degranulation at the site of injury, may represent initial events in a spontaneous process of macrophage mediated demyelination in which glial cells and macrophages are both involved in the phagocytic process.},
	Author = {Powell, H. C. and Garrett, R. S. and Brett, F. M. and Chiang, C. S. and Chen, E. and Masliah, E. and Campbell, I. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {1015-6305},
	Journal = {Brain Pathol},
	Keywords = {Phagocytosis;Animals;Astrocytes;Brain;Axons;Interleukin-3;Mice, Transgenic;Not relevant;11 Glia;Blood-Brain Barrier;Axonal Transport;Organ Specificity;Neuroglia;Horseradish Peroxidase;Support, U.S. Gov't, P.H.S.;Support, U.S. Gov't, Non-P.H.S.;Cerebellum;Mice;Cell Division;Demyelinating Diseases;Mast Cells;Glial Fibrillary Acidic Protein},
	Medline = {99235145},
	Month = {4},
	Nlm_Id = {9216781},
	Number = {2},
	Organization = {Veterans Administration Research Service, VAMC San Diego, La Jolla, CA, USA. hpowell\@ucsd.edu},
	Pages = {219-35},
	Pubmed = {10219739},
	Title = {Response of glia, mast cells and the blood brain barrier, in transgenic mice expressing interleukin-3 in astrocytes, an experimental model for CNS demyelination},
	Uuid = {35637761-95B3-4940-9E59-965B5F10BCC2},
	Volume = {9},
	Year = {1999}}

@article{Pozniak:2006,
	Abstract = {ABSTRACT : Adult neurogenesis in the hippocampus is under complex genetic control. A recent comparative study of two inbred mouse strains using quantitative trait locus analysis has revealed that cell survival is most highly correlated with neurogenesis and identified candidate genes for further investigation.},
	Author = {Pozniak, and Pleasure,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1465-6914},
	Journal = {Genome Biol},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {100960660},
	Number = {3},
	Organization = {Department of Neurology, Programs in Neuroscience and Developmental Biology, University of California, San Francisco, CA 94143, USA,. sam.pleasure\@ucsf.edu.},
	Pages = {207},
	Pii = {gb-2006-7-3-207},
	Pubmed = {16584531},
	Title = {Genetic control of hippocampal neurogenesis},
	Uuid = {E1EC7D9A-2906-44BE-AACB-F802A01FD705},
	Volume = {7},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/gb-2006-7-3-207}}

@article{Prasanth:2002,
	Abstract = {Origin recognition complex (ORC) proteins serve as a landing pad for the assembly of a multiprotein prereplicative complex, which is required to initiate DNA replication. During mitosis, the smallest subunit of human ORC, Orc6, localizes to kinetochores and to a reticular-like structure around the cell periphery. As chromosomes segregate during anaphase, the reticular structures align along the plane of cell division and some Orc6 localizes to the midbody before cells separate. Silencing of Orc6 expression by small interfering RNA (siRNA) resulted in cells with multipolar spindles, aberrant mitosis, formation of multinucleated cells, and decreased DNA replication. Prolonged periods of Orc6 depletion caused a decrease in cell proliferation and increased cell death. These results implicate Orc6 as an essential gene that coordinates chromosome replication and segregation with cytokinesis. 1095-9203 Journal Article},
	Author = {Prasanth, S. G. and Prasanth, K. V. and Stillman, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Science},
	Keywords = {Human;EE both;Animals;Centromere/metabolism;Cells, Cultured;Recombinant Fusion Proteins/analysis;Fluorescent Antibody Technique;Transfection;Mitosis;Phenotype;*Chromosome Segregation;Kinetochores/metabolism;RNA, Small Interfering;08 Aberrant cell cycle;Cell Line;Bromodeoxyuridine/metabolism;DNA-Binding Proteins/genetics/metabolism/*physiology;Tumor Cells, Cultured;Gene Silencing;Support, U.S. Gov't, P.H.S.;Mitotic Spindle Apparatus/ultrastructure;Polyploidy;RNA, Untranslated/metabolism/pharmacology;*DNA Replication;Cell Nucleus/metabolism;Cell Death;Chromosomes, Human/*metabolism;*Cell Division},
	Number = {5583},
	Organization = {Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.},
	Pages = {1026-31},
	Title = {Orc6 involved in DNA replication, chromosome segregation, and cytokinesis},
	Uuid = {93811CEF-EDC6-4877-9DA7-1B707C4692AB},
	Volume = {297},
	Year = {2002},
	url = {papers/Prasanth_Science2002.pdf}}

@article{Prat:2005,
	Abstract = {PURPOSE OF REVIEW: The aim of this article is to describe recent observations regarding the basis for the initiation and disease evolution of multiple sclerosis. RECENT FINDINGS: A current debate is where and what initiates the neuroinflammatory reaction that characterizes the acute multiple sclerosis lesion. Immune sensitization to neural antigens could develop within the systemic compartment consequent to exposure to cross-reacting, possibly viral derived, peptides (molecular mimicry). Although CD4 T cells are considered central to initiating central nervous system inflammation, the actual extent and specificity of tissue injury reflects the array of adaptive (CD8 T cells and antibody) and innate (microglia/macrophages) immune constituents present in the lesions. Neuropathologic studies indicate that lethal changes in neural cells (oligodendrocytes) could also be the initiating event, reflecting as yet unidentified acquired insults (e.g. exogenous virus or reactivated endogenous retrovirus) or intrinsic abnormalities ('neurodegenerative' hypothesis). Recurrence or persistence of the disease process can reflect events occurring at multiple sites including expansion of the immune repertoire in response to neural antigens transported to regional lymph nodes (determinant spreading), especially if immune regulatory mechanisms are defective; alterations in blood-brain barrier properties consequent to initial cellular transmigration; and participation of endogenous (microglia, astrocytes) or long lived infiltrating cells (macrophages, B cells in ectopic germinal centers) in regulating and effecting immune functions within the central nervous system. Accumulating neurologic deficit reflects the balance between injury and repair; the latter also being negatively or positively (trophic support and clearance of tissue debris) impacted by inflammatory processes. SUMMARY: Understanding the full spectrum of multiple sclerosis presents a continuing challenge for both immunology and neurobiology.},
	Author = {Prat, Alexandre and Antel, Jack},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {1350-7540},
	Journal = {Curr Opin Neurol},
	Keywords = {15 ERVs retroelements;Multiple Sclerosis;Blood-Brain Barrier;T-Lymphocytes;Encephalomyelitis, Autoimmune, Experimental;15 Retrovirus mechanism;Animals;Disease Progression;Humans;review;24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {9319162},
	Number = {3},
	Organization = {Neuroimmunology Laboratory and Multiple Sclerosis Clinic, CHUM Notre-Dame Hospital, Montreal, Quebec, Canada.},
	Pages = {225-30},
	Pii = {00019052-200506000-00004},
	Pubmed = {15891404},
	Title = {Pathogenesis of multiple sclerosis},
	Uuid = {AC0D9B35-ED30-42B2-8CFE-D433C52B6EAC},
	Volume = {18},
	Year = {2005}}

@article{Prem-veer-Reddy:1980,
	Abstract = {In the DNA-synthesizing phase (S phase) of CHEF/18 Chinese hamster embryo fibroblast cells, six enzymes associated with DNA metabolism, including DNA polymerase (deoxynucleoside triphosphate:DNA deoxynucleotidyl-transferase, EC 2.7.7.7), were largely localized in the nuclear region (karyoplasts). By contrast, in quiescent and G1 phase cells these enzymatic activites were mainly absent from the nucleus and were recovered in the cytoplasmic portion (cytoplasts). These nuclear (but not cytoplasmic) enzymatic activities cosedimented rapidly on sucrose density gradients. Further, the rapidly sedimenting enzyme activities were unique to cells in S phase. An organized supramolecular structure that allows channeling of metabolites into DNA was demonstrated by kinetics of nucleotide incorporation. "Permeabilized" cells selectively channeled incorporation of ribonucleoside diphosphates into DNA in preference to deoxyribonucleoside triphosphates. Deoxyribonucleoside triphosphate incorporation occurred when ribonucleoside-diphosphate reductase (2'-deoxyribonucleoside-diphosphate: oxidized-thioredoxin 2'-oxidoreductase, EC 1.17.4.1) activity was abolished by hydroxyurea. Our interpretation is that during DNA replication, the nucleus contains a complex of DNA precursor-synthesizing enzymes juxtaposed with the "replication apparatus" comprising DNA polymerase, other enzymes, and structural proteins. Functional integrity of this structure is impaired when one of its essential components is inactivated. We propose the name "replitase" for this multienzyme complex for DNA replication and suggest that it incorporates precursors rapidly and efficiently. Possibly its assembly signals the initiation of the S phase of the cell cycle.},
	Author = {Prem veer Reddy, G. and Pardee, A. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Hamsters;Ribonucleoside Diphosphate Reductase;Nucleoside-Diphosphate Kinase;Animals;Cells, Cultured;Thymidine Kinase;Cell Cycle;Fibroblasts;Cytoplasm;15 Retrovirus mechanism;Ribonucleosides;DNA Replication;Tetrahydrofolate Dehydrogenase;Multienzyme Complexes;Cricetulus;DNA Polymerase II;DNA-Directed DNA Polymerase;Research Support, U.S. Gov't, P.H.S.;Thymidylate Synthase;Cell Compartmentation;Nucleoside-Phosphate Kinase;Cell Nucleus;24 Pubmed search results 2008;Cytidine Monophosphate;Deoxyribonucleosides},
	Medline = {81013874},
	Month = {6},
	Nlm_Id = {7505876},
	Number = {6},
	Pages = {3312-16},
	Pubmed = {6251456},
	Title = {Multienzyme complex for metabolic channeling in mammalian DNA replication},
	Uuid = {6D29909F-B4E4-48B2-891C-D048357AF3A6},
	Volume = {77},
	Year = {1980}}

@article{Price:1987,
	Abstract = {We describe a cell-lineage marking system applicable to the vertebrate nervous system. The basis of the technique is gene transfer using the retroviral vector system. We used Escherichia coli beta-galactosidase as a marker gene and demonstrate a high level of expression of this marker from the viral long terminal repeat promoter, with simultaneous expression of the Tn5 neo gene from the simian virus 40 early promoter. This expression has allowed us to detect individual infected cells histochemically. We applied this marking technique to the study of lineage relationships in the developing vertebrate nervous system, both in vivo and in culture. In the rat retina, we injected virus in vivo and histochemically identified clones of marked neural cells. In addition, we used this virus to infect cultures of rat cerebral cortex and have analyzed the clonal relationships of morphologically different neural cell types. The host range of the marking system extends to avian as well as mammalian species. Thus, this system should have broad applicability as a means of gene transfer and expression in the nervous system.},
	Author = {Price, J. and Turner, D. and Cepko, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Retina;10 Development;Rats, Inbred F344;Research Support, Non-U.S. Gov't;Rats;Cell Line;Retroviridae;Research Support, U.S. Gov't, P.H.S.;Astrocytes;Genes;Nervous System;beta-Galactosidase;Animals;Culture Techniques;24 Pubmed search results 2008;Cerebral Cortex;Cloning, Molecular},
	Medline = {87092353},
	Month = {1},
	Nlm_Id = {7505876},
	Number = {1},
	Pages = {156-60},
	Pubmed = {3099292},
	Title = {Lineage analysis in the vertebrate nervous system by retrovirus-mediated gene transfer},
	Uuid = {B207B4E6-EE2B-11DA-8605-000D9346EC2A},
	Volume = {84},
	Year = {1987},
	url = {papers/Price_ProcNatlAcadSciUSA1987.pdf}}

@article{Priller:2003,
	Abstract = {While the brain has traditionally been considered a rather secluded site, recent studies suggest that adult bone marrow (BM)-derived stem cells can generate glia and neurons in rodents and humans. Macrophages and microglia are the first to appear in the murine brain after transplantation of genetically marked BM cells. Within weeks after transplantation, some authors have found astrocytes and cells expressing neuronal antigens. We detected cerebellar Purkinje neurons and interneurons, such as basket cells, expressing the green fluorescent protein (GFP) 10-15 months after transplantation of GFP-labeled BM cells. The results push the boundaries of our classic view of lineage restriction.},
	Author = {Priller, Josef},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0948-6143},
	Journal = {Histochem Cell Biol},
	Keywords = {Cell Differentiation;Purkinje Cells;Astrocytes;Animals;Humans;Stem Cell Transplantation;Neuronal Plasticity;lectures;Bone Marrow Transplantation;Brain;Microglia;11 Glia;Green Fluorescent Proteins;Histocytochemistry;Adult;Transplantation Tolerance;Mice;Luminescent Proteins},
	Medline = {22800872},
	Month = {8},
	Nlm_Id = {9506663},
	Number = {2},
	Organization = {Department of Neurology, Charit{\'e}, Humboldt-University, Schumannstrasse 20/21, 10117 Berlin, Germany. josef.priller\@charite.de},
	Pages = {85-91},
	Pubmed = {12898276},
	Title = {Robert Feulgen Prize Lecture. Grenzg{\"a}nger: adult bone marrow cells populate the brain},
	Uuid = {BBBD75FA-04FF-4C87-A032-089E16E8FBDE},
	Volume = {120},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00418-003-0559-7}}

@article{Priller:2001,
	Abstract = {The versatility of stem cells has only recently been fully recognized. There is evidence that upon adoptive bone marrow (BM) transplantation (BMT), donor-derived cells can give rise to neuronal phenotypes in the brains of recipient mice. Yet only few cells with the characteristic shape of neurons were detected 1-6 mo post-BMT using transgenic or newborn mutant mice. To evaluate the potential of BM to generate mature neurons in adult C57BL/6 mice, we transferred the enhanced green fluorescent protein (GFP) gene into BM cells using a murine stem cell virus-based retroviral vector. Stable and high level long-term GFP expression was observed in mice transplanted with the transduced BM. Engraftment of GFP-expressing cells in the brain was monitored by intravital microscopy. In a long-term follow up of 15 mo post-BMT, fully developed Purkinje neurons were found to express GFP in both cerebellar hemispheres and in all chimeric mice. GFP-positive Purkinje cells were also detected in BM chimeras from transgenic mice that ubiquitously express GFP. Based on morphologic criteria and the expression of glutamic acid decarboxylase, the newly generated Purkinje cells were functional.},
	Author = {Priller, J. and Persons, D. A. and Klett, F. F. and Kempermann, G. and Kreutzberg, G. W. and Dirnagl, U.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {Purkinje Cells;Transduction, Genetic;Microscopy, Immunoelectron;Animals;Stem Cell Transplantation;Bone Marrow Transplantation;Microscopy, Confocal;Mice, Inbred C57BL;Recombinant Fusion Proteins;Retroviridae;Male;Hematopoietic Stem Cell Transplantation;Green Fluorescent Proteins;Transplantation Chimera;Bone Marrow Cells;Transplantation, Isogeneic;Cell Transplantation;Flow Cytometry;Cerebellum;Mice;Luminescent Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {21581896},
	Month = {11},
	Nlm_Id = {0375356},
	Number = {5},
	Organization = {Department of Neurology, Charit{\'e}, Humboldt-University, 10117 Berlin, Germany. josef.priller\@charite.de},
	Pages = {733-8},
	Pii = {jcb.200105103},
	Pubmed = {11724815},
	Title = {Neogenesis of cerebellar Purkinje neurons from gene-marked bone marrow cells in vivo},
	Uuid = {F5C87A00-D3AF-11D9-A0E9-000D9346EC2A},
	Volume = {155},
	Year = {2001},
	url = {papers/Priller_JCellBiol2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200105103}}

@article{Priller:2006,
	Abstract = {Prion neuroinvasion is accompanied by maximal activation of microglia, the significance of which for pathogenesis is unknown. Here, we used bone marrow (BM) cells expressing GFP (green fluorescent protein) to study the turnover of microglia in mouse scrapie. We found that >or=50\%of all brain microglia were replaced by BM-derived cells before clinical disease onset. In terminally sick mice, microglia density increased threefold to fourfold. Hence BM-derived microglia rapidly and efficaciously colonize the brain in scrapie. Whereas reconstitution of wild-type mice with prion protein-deficient (Prnp(o/o)) BM did not alter scrapie pathogenesis, Prnp(o/o) mice transplanted with wild-type BM cells were resistant to peripherally administered prions despite high levels of infectivity in the spleen. Cerebellar homogenates from prion-inoculated Prnp(o/o) mice reconstituted with >10\%of wild-type microglia failed to infect transgenic mice overexpressing the cellular prion protein. Hence, in contrast to previous reports, microglia are not competent for efficient prion transport and replication in vivo.},
	Author = {Priller, Josef and Prinz, Marco and Heikenwalder, Mathias and Zeller, Nicolas and Schwarz, Petra and Heppner, Frank L. and Aguzzi, Adriano},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Animals;RNA;Cells, Cultured;comparative study;Bone Marrow Transplantation;Microglia;Cell Count;Mice, Inbred C57BL;Green Fluorescent Proteins;research support, non-u.s. gov't;Reverse Transcriptase Polymerase Chain Reaction;Infection;Bone Marrow Cells;Animals, Newborn;Mice, Knockout;Blotting, Western;Flow Cytometry;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Immunohistochemistry;Prions;Gene Expression;Scrapie;Cytokines},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {45},
	Organization = {Institute of Neuropathology, Department of Pathology, University of Zurich, 8091 Zurich, Switzerland. josef.priller\@charite.de},
	Pages = {11753-62},
	Pii = {26/45/11753},
	Pubmed = {17093096},
	Title = {Early and rapid engraftment of bone marrow-derived microglia in scrapie},
	Uuid = {2CD045DC-D693-4240-9E0F-C0CAA1DF3BC1},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2275-06.2006}}

@article{Priller:2001a,
	Abstract = {Gene therapy in the central nervous system (CNS) is hindered by the presence of the blood-brain barrier, which restricts access of serum constituents and peripheral cells to the brain parenchyma. Expression of exogenously administered genes in the CNS has been achieved in vivo using highly invasive routes, or ex vivo relying on the direct implantation of genetically modified cells into the brain. Here we provide evidence for a novel, noninvasive approach for targeting potential therapeutic factors to the CNS. Genetically-modified hematopoietic cells enter the CNS and differentiate into microglia after bone-marrow transplantation. Up to a quarter of the regional microglial population is donor-derived by four months after transplantation. Microglial engraftment is enhanced by neuropathology, and gene-modified myeloid cells are specifically attracted to the sites of neuronal damage. Thus, microglia may serve as vehicles for gene delivery to the nervous system.},
	Author = {Priller, J. and Fl{\"u}gel, A. and Wehner, T. and Boentert, M. and Haas, C. A. and Prinz, M. and Fern{\'a}ndez-Klett, F. and Prass, K. and Bechmann, I. and de Boer, B. A. and Frotscher, M. and Kreutzberg, G. W. and Persons, D. A. and Dirnagl, U.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1078-8956},
	Journal = {Nat Med},
	Keywords = {Cell Differentiation;Animals;Gene Targeting;Bone Marrow Transplantation;Recombinant Proteins;Microglia;Mice, Inbred C57BL;11 Glia;Retroviridae;Green Fluorescent Proteins;Blood-Brain Barrier;Male;Genetic Vectors;Bone Marrow Cells;Gene Therapy;Brain Ischemia;Mice;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {21583810},
	Month = {12},
	Nlm_Id = {9502015},
	Number = {12},
	Organization = {Department of Neurology, Charit{\'e}, Humboldt-University, Berlin, Germany. josef.priller\@charite.de},
	Pages = {1356-61},
	Pii = {nm1201-1356},
	Pubmed = {11726978},
	Title = {Targeting gene-modified hematopoietic cells to the central nervous system: use of green fluorescent protein uncovers microglial engraftment},
	Uuid = {558E1B51-A8C6-41C9-B9C1-9442F577B0B9},
	Volume = {7},
	Year = {2001},
	url = {papers/Priller_NatMed2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nm1201-1356}}

@article{Prince:1997,
	Abstract = {Several lines of evidence have suggested that decreases in postsynaptic inhibition may have a role in epileptogenesis in cortical structures. However, other studies have suggested that GABAergic inhibition is spared, or even augmented in some forms of post-lesional epilepsy. In the studies described here, inhibitory events were recorded in two models of post-lesional chronic epileptogenesis. (i) As previously reported (D.A. Prince and G.-F. Tseng. J. Neurophysiol. 69: 1276-1291. 1993), epileptiform activity develops in slices from partially isolated rat neocortical islands 2-3 weeks after the initial in vivo lesion. In this model of post-traumatic epilepsy, large amplitude polyphasic inhibitory postsynaptic currents (IPSCs) in layer V pyramidal neurons are associated with each interictal epileptiform field potential. The frequency of spontaneous IPSCs as well as miniature IPSCs was significantly increased in neocortical slices from the epileptogenic chronically injured cortex versus controls. Immunocytochemical reactions for parvalbumin and calbindin, calcium binding proteins present in subgroups of GABAergic neurons, showed an increased staining of both neuropil and somata within the epileptogenic tissue. Immunoreactivity for glutamic acid decarboxylase (GAD) and GABA also appeared to be increased in the neuropil. (ii) Cortical microgyri resembling human malformations were produced by freeze lesions made transcranially in P0 rat cortex (K.M. Jacobs, M.J. Gutnick, and D.A. Prince. Cereb. Cortex, 6: 514-523. 1996). The boundary between the four-layered microgyrus and surrounding cortex become epileptogenic within about 2 weeks, as judged by evoked extracellular field potentials and cellular activities. Epileptogenesis in the surrounding cortex is not altered when the microgyrus itself is isolated by transcortical cuts. Patch-clamp recordings from layer V neurons in the epileptogenic zone showed that spontaneous IPSCs are larger and more dependent on glutamatergic synapses than in control neurons. The amplitudes of polysynaptic IPSCs evoked by threshold stimulation were also larger than in control cells. Although evaluation of inhibitory events in these models is still incomplete, results to date suggest that GABAergic inhibition may be enhanced in epileptogenic areas associated with chronic cortical injury. Sprouting of axonal arborizations of pyramidal cells onto interneurons, upregulation of GABAergic neurons, and perhaps sprouting of inhibitory axons that make increased numbers of contacts onto pyramidal cells may all contribute to the increased inhibitory drive. Results in these models do not support the disinhibitory hypothesis of chronic epileptogenesis.},
	Author = {Prince, D. A. and Jacobs, K. M. and Salin, P. A. and Hoffman, S. and Parada, I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0008-4212},
	Journal = {Can J Physiol Pharmacol},
	Keywords = {21 Epilepsy;Epilepsies, Partial;Research Support, Non-U.S. Gov't;21 Neurophysiology;Rats;Pyramidal Cells;Research Support, U.S. Gov't, P.H.S.;Neural Inhibition;gamma-Aminobutyric Acid;Animals;Humans;Cerebral Cortex;Epilepsy, Post-Traumatic;24 Pubmed search results 2008},
	Medline = {97393960},
	Month = {5},
	Nlm_Id = {0372712},
	Number = {5},
	Organization = {Stanford University School of Medicine, Department of Neurology and Neurological Sciences, CA 94305-5300, USA.},
	Pages = {500-7},
	Pubmed = {9250384},
	Title = {Chronic focal neocortical epileptogenesis: does disinhibition play a role?},
	Uuid = {77C29702-A916-4A10-B942-A552B4176500},
	Volume = {75},
	Year = {1997}}

@article{Probst:2001,
	Abstract = {A number of pathological changes have been reported in relation to CA1 pyramidal cells in Alzheimer's disease (AD), among them hyperphosphorylation of tau protein followed by the formation of filamentous tau lesions, granulovacuolar degeneration (GVD), Hirano bodies and spindle-shaped dilatations of distal apical dendrites. Juxtacellular clusters of glutamate receptor (GluR)-positive granules around pyramidal cells of the CA1 sector have been recently reported under the term "non-plaque dystrophic dendrites". We independently found that CA1 pyramidal cells in AD patients are regularly surrounded by ubiquitin-positive granules measuring 1-4 microns in diameter, which we have termed perisomatic granules (PSG). Using confocal microscopy, ubiquitin- and GluR-reactive granules were found to largely coincide and to correspond to the same structure. By immunoelectron microscopy PSG were found to consist of GluR1-2-reactive enlarged synaptic boutons containing tubulo-filamentous or floccular material. PSG were found to be consistently associated with pyramidal (principal) cells but not with interneurons of the CA1 sector. Dual-labeling experiments have shown that PSG are preferentially associated with tau-immunoreactive "pretangle" neurons but not with cells containing filamentous tau inclusions or with tau-negative nerve cell bodies. The number of PSG was found to increase with the severity of AD changes with almost no PSG found in Braak stages I and II and few in stage III. Furthermore, PSG were not AD specific, as shown by their presence around CA1 pyramidal cells in Pick's disease. The reasons for GluR reactivity and ubiquitin complex formation in enlarged perisomatic boutons are unclear. Marked changes in GluR subunits have been observed in association with even moderate AD pathology in hippocampal pyramidal cells in AD and our findings suggest a pathogenic link between PSG and early tau pathology in CA1 neurons. PSG might represent residual and abnormally clustered GluR subunits in degenerating perisomatic neurites. Our work confirms and extend previous study on perisomatic "non-plaque dystrophic dendrites" in AD and establish PSG as a pathological entity distinct from GVD. In addition PSG should be acknowledged among main histological changes associated with hippocampal neurons in AD and Pick's disease.},
	Author = {Probst, A. and Herzig, M. C. and Mistl, C. and Ipsen, S. and Tolnay, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Human;Receptors, Glutamate;Vacuoles;Cytoplasm;Female;Cytoplasmic Granules;Extracellular Space;Hippocampus;Pick Disease of the Brain;Not relevant;11 Glia;Ubiquitin;Male;Dendrites;Aged;Neuropil;Alzheimer Disease;Aged, 80 and over;Immunohistochemistry;Microscopy, Electron;Cell Death},
	Medline = {21604277},
	Month = {12},
	Nlm_Id = {0412041},
	Number = {6},
	Organization = {Institute of Pathology, Division of Neuropathology, University of Basel, Sch{\"o}nbeinstrasse 40, CH-4003 Basel, Switzerland. aprobst\@uhbs.ch},
	Pages = {636-44},
	Pubmed = {11761725},
	Title = {Perisomatic granules (non-plaque dystrophic dendrites) of hippocampal CA1 neurons in Alzheimer's disease and Pick's disease: a lesion distinct from granulovacuolar degeneration},
	Uuid = {B48B34B5-E2C3-4B4F-B6A2-620E8CBCACB4},
	Volume = {102},
	Year = {2001}}

@article{Proctor:2005,
	Abstract = {We showed previously that loss of the integrin beta8 subunit, which forms alphavbeta8 heterodimers, results in abnormal vascular development in the yolk sac, placenta, and brain. Animals lacking the integrin beta8 (itgbeta8) gene die either at midgestation, because of insufficient vascularization of the placenta and yolk sac, or shortly after birth with severe intracerebral hemorrhage. To specifically focus on the role of integrins containing the beta8 subunit in the brain, and to avoid early lethalities, we used a targeted deletion strategy to delete itgbeta8 only from cell types within the brain. Ablating itgbeta8 from vascular endothelial cells or from migrating neurons did not result in cerebral hemorrhage. Targeted deletion of itgbeta8 from the neuroepithelium, however, resulted in bilateral hemorrhage at postnatal day 0, although the phenotype was less severe than in itgbeta8-null animals. Newborn mice lacking itgbeta8 from the neuroepithelium had hemorrhages in the cortex, ganglionic eminence, and thalamus, as well as abnormal vascular morphogenesis, and disorganized glia. Interestingly, adult mice lacking itgbeta8 from cells derived from the neuroepithelium did not show signs of hemorrhage. We propose that defective association between vascular endothelial cells and glia lacking itgbeta8 is responsible for the leaky vasculature seen during development but that an unidentified compensatory mechanism repairs the vasculature after birth.},
	Author = {Proctor, John M. and Zang, Keling and Wang, Denan and Wang, Rong and Reichardt, Louis F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {43},
	Organization = {Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, California 94143, USA.},
	Pages = {9940-8},
	Pii = {25/43/9940},
	Pubmed = {16251442},
	Title = {Vascular development of the brain requires beta8 integrin expression in the neuroepithelium},
	Uuid = {20614251-EE89-40AC-9F98-569B90B9E7E2},
	Volume = {25},
	Year = {2005},
	url = {papers/Proctor_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3467-05.2005}}

@article{Puig:2002,
	Abstract = {To investigate to what extent myeloablation, graft size, and ex vivo manipulation influence the engraftment and long-term survival of transduced murine hematopoietic cells, groups of C57BL/6J (CD45.2) mice receiving total body irradiation (TBI) (1-9 Gy) or no irradiation were transplanted with either transduced bone marrow (BM) cells, at two cell doses, or with fresh BM cells from B6/SJL (CD45.1) congenic mice. Short (40 days) and long-term (5 months) engraftment and transgene expression were measured by FACS analysis. No donor cells were detected in the hematopoietic tissues of non-myeloablated mice, whereas in the irradiated animals, levels of engraftment correlated well with the dose of TBI administered. Similar percentages of transgene-expressing cells were found in the grafted hematopoietic cells of all groups of mice, regardless of the dose of TBI administered or the level of engraftment achieved. This suggests that the engrafted animals could become tolerant to the transgene product (enhanced green fluorescent protein, EGFP). Our results indicate that TBI facilitates the engraftment of manipulated hematopoietic cells in a dose-dependent manner, that mice engrafted with EGFP(+) hematopoietic cells probably acquire tolerance to EGFP, and that increasing the graft size and reducing the ex vivo manipulation required for retroviral gene transfer of hematopoietic cells also enhances their engrafting potential.},
	Author = {Puig, T. and K{\'a}d{\'a}r, E. and Lim{\'o}n, A. and Cancelas, J. A. and Eixarch, H. and Luqu{\'\i}n, L. and Garc{\'\i}a, M. and Barquinero, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;Animals;Regression Analysis;Female;Mice, Inbred C57BL;Retroviridae;11 Glia;Time Factors;Hematopoietic Stem Cell Transplantation;Green Fluorescent Proteins;Genetic Vectors;Gene Therapy;Flow Cytometry;Mice;Transplantation Conditioning;Luminescent Proteins;Stem Cells;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {22265327},
	Month = {11},
	Nlm_Id = {9421525},
	Number = {21},
	Organization = {Facultat de Biologia, Universitat de Girona, Spain.},
	Pages = {1472-9},
	Pubmed = {12378410},
	Title = {Myeloablation enhances engraftment of transduced murine hematopoietic cells, but does not influence long-term expression of the transgene},
	Uuid = {F1476AC4-2406-405F-90BD-8B94311CE37F},
	Volume = {9},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3301826}}

@article{Pukrop:2006,
	Abstract = {Interactions between neoplastic and stromal cells contribute to tumor progression. Wnt genes, involved in cell migration and often deregulated in cancers, are attractive candidates to regulate these effects. We have recently shown that coculture of breast cancer cells with macrophages enhances invasiveness via matrix metalloproteases and TNF-alpha. Here we demonstrate that coculture of MCF-7 cells and macrophages leads to up-regulation of Wnt 5a in the latter. This was accompanied by activation of AP-1/c-Jun in MCF-7. Recombinant Wnt 5a mimicked the coculture effect. Wnt 5a was also detectable in tumor-associated macrophages in primary breast cancers. Experiments with agonists and antagonists of Wnt signaling revealed that a functional canonical pathway in the tumor cells was a necessary prerequisite; however, noncanonical signaling via Wnt 5a and the Jun-N-terminal kinase pathway was critical for invasiveness. It was also responsible for induction of matrix metalloprotease-7, known to release TNF-alpha. All these effects could be antagonized by dickkopf-1. Our results indicate that Wnt 5a is essential for macrophage-induced invasiveness, because it regulates tumor cell migration as well as proteolytic activity of the macrophages. The function of Wnt 5a as either a suppressor or promoter of malignant progression seems to be modulated by intercellular interactions. Wnt 5a detection in tumor-associated macrophages in breast cancer biopsies supports the assumption that similar events play a role in vivo.},
	Author = {Pukrop, T. and Klemm, F. and Hagemann, Th and Gradl, D. and Schulz, M. and Siemes, S. and Tr{\"u}mper, L. and Binder, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {7505876},
	Number = {14},
	Organization = {*Department of Haematology/Oncology, Georg-August University, 37099 G{\"o}ttingen, Germany.},
	Pages = {5454-9},
	Pii = {0509703103},
	Pubmed = {16569699},
	Title = {Wnt 5a signaling is critical for macrophage-induced invasion of breast cancer cell lines},
	Uuid = {FC3CBFB7-8CAC-48FA-BD35-D3BFDE59347A},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0509703103}}

@article{Pumiglia:2006,
	Author = {Pumiglia, Kevin and Temple, Sally},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Humans;24 Pubmed search results 2008;Cell Differentiation;Serpins;Eye Proteins;Neuronal Plasticity;Stem Cells;Angiogenesis Inhibitors;comment;Blood Vessels;Animals;Brain;Brain Neoplasms;Nerve Growth Factors;news},
	Month = {3},
	Nlm_Id = {9809671},
	Number = {3},
	Pages = {299-300},
	Pii = {nn0306-299},
	Pubmed = {16498420},
	Title = {PEDF: bridging neurovascular interactions in the stem cell niche},
	Uuid = {30803BB7-A690-4ED4-96A7-71875107155D},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn0306-299}}

@article{Puri:1988,
	Abstract = {Fusion of vesicular stomatitis virus (VSV) with Vero cells was measured after exposure of the virus to low pH under a variety of experimental conditions. The method of relief of fluorescence self-quenching of the probe octadecylrhodamine was used to monitor fusion. Incubation of the virus at pH 5.5 prior to binding to cells led to significant enhancement of fusion at the plasma membrane, whereas fusion via the endocytic pathway was inhibited. Fusion of pH 5.5-pretreated VSV showed a similar pH threshold for fusion as nontreated virus, and it was blocked by antibody to VSV G protein. Activation of VSV by pretreatment at low pH was only slightly dependent on temperature. In contrast, when VSV was first bound to target cells and subsequently exposed at 4 degrees C to the low pH, activation of the fusion process did not occur. The pH 5.5-mediated activation of VSV could be reversed by returning the pH to neutral in the absence of target membranes. The low pH pretreatment also led to aggregation of virus; large aggregates could be pelleted by low speed centrifugation and only the effects of the supernatant, which consist of single virions and/or microaggregates, were considered. The data were analyzed in the framework of an allosteric model according to which viral spike glycoproteins undergo a pH-dependent conformational transition to an active (fusion-competent) state. Based on that analysis we conclude that the conformational transition to the active state is rate-limiting for fusion and that the viral spike glycoproteins are fusion-competent only in their protonated form.},
	Author = {Puri, A. and Winick, J. and Lowy, R. J. and Covell, D. and Eidelman, O. and Walter, A. and Blumenthal, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {Vero Cells;Allosteric Regulation;Kinetics;Cell Line;Receptors, Virus;Thermodynamics;Models, Theoretical;Vesicular stomatitis-Indiana virus;delete_this;Animals;Hydrogen-Ion Concentration;Virus Activation;15 Retrovirus mechanism},
	Medline = {88169591},
	Month = {4},
	Nlm_Id = {2985121R},
	Number = {10},
	Organization = {Section on Membrane Structure and Function, National Cancer Institute, Bethesda, Maryland 20892.},
	Pages = {4749-53},
	Pubmed = {2832405},
	Title = {Activation of vesicular stomatitis virus fusion with cells by pretreatment at low pH},
	Uuid = {7D65DAC8-EE2C-11DA-8605-000D9346EC2A},
	Volume = {263},
	Year = {1988},
	url = {papers/Puri_JBiolChem1988.pdf}}

@article{Purpura:1982,
	Abstract = {Cortical biopsies obtained from 5 young children with severe neurobehavioral retardation of unknown etiology have been analyzed using Golgi and EM techniques. The normally cylindrical geometry of individual dendritic processes of pyramidal and non-pyramidal neurons is interrupted by the formation of distinct varicosities. While over 90\%of observed cells are affected, the extent of varicosity formation varies from cell to cell and is most prominent in medium and small pyramidal cells. Varicosities may occur in the periphery only, or they may extend proximally to primary dendritic trunks. Accompanying changes include thin and irregular proximal processes, loss of dendritic spines, and predominance of long, thin tortuous spines. Ultrastructural analysis reveals characteristic changes in the cytoskeleton of these processes. Microtubules, within the larger proximal processes, twist and turn, relative to one another and relative to the long axis of the process. In varicose regions, microtubules course in roughly parallel array through constricted segments, only to splay away from one another on entering an expansion. Synapses are evident on constricted and expanded segments, as well as on spines. Alterations in dendritic structure of both pyramidal and non-pyramidal neurons may represent a primary target in the pathobiological process underlying neurobehavioral failure.},
	Author = {Purpura, D. P. and Bodick, N. and Suzuki, K. and Rapin, I. and Wurzelmann, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Staining and Labeling;10 Development;Dendrites;Golgi Apparatus;Infant;Microscopy, Electron;Microtubules;Get paper from library;Research Support, U.S. Gov't, P.H.S.;Developmental Disabilities;Female;10 Structural plasticity;Male;Humans;24 Pubmed search results 2008;Cerebral Cortex;case reports},
	Medline = {83102362},
	Month = {11},
	Nlm_Id = {0045503},
	Number = {3},
	Pages = {287-97},
	Pubmed = {6185182},
	Title = {Microtubule disarray in cortical dendrites and neurobehavioral failure. I. Golgi and electron microscopic studies},
	Uuid = {EBA9C056-89F2-4FA8-AB54-E31B65EE61D7},
	Volume = {281},
	Year = {1982}}

@article{Putz:2005,
	Abstract = {The balance between proliferation and apoptosis is critical for proper development of the nervous system. Yet, little is known about molecules that regulate apoptosis of proliferative neurons. Here we identify a soluble, secreted form of CPG15 expressed in embryonic rat brain regions undergoing rapid proliferation and apoptosis, and show that it protects cultured cortical neurons from apoptosis by preventing activation of caspase 3. Using a lentivirus-delivered small hairpin RNA, we demonstrate that endogenous CPG15 is essential for the survival of undifferentiated cortical progenitors in vitro and in vivo. We further show that CPG15 overexpression in vivo expands the progenitor pool by preventing apoptosis, resulting in an enlarged, indented cortical plate and cellular heterotopias within the ventricular zone, similar to the phenotypes of mutant mice with supernumerary forebrain progenitors. CPG15 expressed during mammalian forebrain morphogenesis may help balance neuronal number by countering apoptosis in specific neuroblasts subpopulations, thus influencing final brain size and shape.},
	Author = {Putz, and Harwell, and Nedivi,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Membrane Proteins;Mice;Embryonic Development;Animals, Newborn;Blotting, Northern;Age Factors;Cell Cycle;Stem Cells;Mice, Transgenic;In Situ Nick-End Labeling;research support, u.s. gov't, p.h.s. ;Apoptosis;Cells, Cultured;Phospholipase C;Cell Membrane;Proto-Oncogene Proteins c-akt;Cell Fractionation;Green Fluorescent Proteins;comparative study ;Bromodeoxyuridine;Rats, Sprague-Dawley;24 Pubmed search results 2008;Cerebral Cortex;21 Neurophysiology;Intermediate Filament Proteins;Male;Proto-Oncogene Proteins;Cloning, Molecular;Food Deprivation;Receptors, Transferrin;Embryo;Histones;Humans;Neurons;Pregnancy;In Situ Hybridization;Neurofilament Proteins;Time Factors;Female;Fluorescent Antibody Technique;RNA, Messenger;RNA, Catalytic;research support, non-u.s. gov't ;Transfection;Gene Expression Regulation, Developmental;Ki-67 Antigen;Analysis of Variance;Animals;Protein-Serine-Threonine Kinases;Cell Count;Blotting, Western;Lentivirus;in vitro ;Nerve Tissue Proteins;Rats},
	Month = {2},
	Nlm_Id = {9809671},
	Number = {3},
	Organization = {[1] The Picower Center for Learning and Memory, Departments of Brain and Cognitive Sciences and Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. [2] These authors contributed equally to this work.},
	Pages = {322-31},
	Pii = {nn1407},
	Pubmed = {15711540},
	Title = {Soluble CPG15 expressed during early development rescues cortical progenitors from apoptosis},
	Uuid = {591AD97E-3F0A-4CEE-9A47-F58CA8E5601E},
	Volume = {8},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1407}}

@article{Qian:1997,
	Abstract = {The embryonic cerebral cortex contains a population of stem-like founder cells capable of generating large, mixed clones of neurons and glia in vitro. We report that the default state of early cortical stem cells is neuronal, and that stem cells are heterogeneous in the number of neurons that they generate. In low fibroblast growth factor (FGF2) concentrations, most maintain this specification, generating solely neuronal progeny. Oligodendroglial production within these clones is stimulated by a higher, threshold level of FGF2, and astrocyte production requires additional environmental factors. Because most cortical neurons are born before glia in vivo, these data support a model in which the scheduled production of cortical cells involves an intrinsic neuronal program in the early stem cells and exposure to environmental, glia-inducing signals. 0896-6273 Journal Article},
	Author = {Qian, X. and Davis, A. A. and Goderie, S. K. and Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Journal = {Neuron},
	Keywords = {Cell Differentiation/drug effects;Pregnancy;Animals;Cells, Cultured;Embryo and Fetal Development;Cerebral Cortex/cytology/*embryology;Stem Cells/*cytology/drug effects/physiology;Oligodendroglia/cytology/drug effects;Female;Glial Fibrillary Acidic Protein/analysis;Neuroglia/*cytology/drug effects;DNA Primers;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Receptors, Fibroblast Growth Factor/biosynthesis;Mice;Polymerase Chain Reaction;Fibroblast Growth Factor 2/*pharmacology;Clone Cells;Neurons/*cytology/drug effects;C pdf},
	Number = {1},
	Organization = {Department of Pharmacology and Neuroscience, Albany Medical College, NY 12208, USA.},
	Pages = {81-93},
	Title = {FGF2 concentration regulates the generation of neurons and glia from multipotent cortical stem cells},
	Uuid = {79893BE1-80C7-469E-99E8-EEDE2927FC11},
	Volume = {18},
	Year = {1997},
	url = {papers/Qian_Neuron1997.pdf}}

@article{Qiao:2005,
	Abstract = {BACKGROUND: Excessive production of interleukin (IL)-4, IL-13 and interferon (IFN)-gamma is thought to be important in the development of allergic disease and atopy. Several investigators have linked the IL-4 and IL-4R genes to allergic disease and atopy. The aim of this study is to further explore the mechanism of penicillins allergy and evaluate the possible role of the IL-4 C-589T and IL-4RalphaQ576R polymorphisms in modulating the allergic responses to penicillins. METHODS: Radioallergosorbent test (RAST) was used to detect eight kinds of specific immunoglobulin E (IgE) to penicillins in serum. Serum levels of IL-4, IL-13 and IFN-gamma were measured by using enzyme-linked immunosorbent assay (ELISA). The IL-4 C-589T and IL-4RalphaQ576R polymorphisms were genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). RESULTS: Compared with control subjects, there were significantly higher levels of IL-4, IL-13 and IFN-gamma in allergic patients with positive specific IgE (P < 0.01), and the lower levels of IL-4 and IFN-gamma were observed in allergic patients with negative specific IgE (P < 0.05). We found a growing trend of IL-4 and IL-13 levels with the kind increasing of positive specific IgE, and even there were significant correlations between the three kinds of cytokines and many kinds of specific IgE (P < 0.05). The IL-4Ralpha*Q576 allele was significantly increased in patients with penicillins allergy compared with control subjects (P < 0.01). Furthermore, the allele was strongly associated with increased serum-specific benzylpenicilloyl (BPO)-, phenoxomethylpenicillanyl (PVA)- or ampicillanyl (APA)-IgE levels in patients with positive specific IgE (P < 0.05). CONCLUSIONS: These data suggest that IL-4, IL-13 and IFN-gamma play an important roles in penicillins allergy. The IL-4RalphaQ576R polymorphism may involve in the development of penicillins allergy, and through modulating specific serum IgE levels.},
	Author = {Qiao, H-L L. and Yang, J. and Zhang, Y-W W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0105-4538},
	Journal = {Allergy},
	Keywords = {Arginine;Cytokines;Research Support, Non-U.S. Gov't;Humans;Middle Aged;Interleukin-4;Receptors, Cell Surface;Penicillins;Drug Hypersensitivity;Female;Immunoglobulin E;Interferon Type II;Child;14 Immune;Male;Glutamine;Aged;Interleukin-13;Adult;Protein Isoforms;24 Pubmed search results 2008;Adolescent},
	Month = {8},
	Nlm_Id = {7804028},
	Number = {8},
	Organization = {Department of Clinical Pharmacology, School of Medicine, Zhengzhou University, Zhengzhou, China.},
	Pages = {1053-9},
	Pii = {ALL816},
	Pubmed = {15969687},
	Title = {Relationships between specific serum IgE, cytokines and polymorphisms in the IL-4, IL-4Ralpha in patients with penicillins allergy},
	Uuid = {3579DD33-E1BF-4345-A1C3-BFD9096A1961},
	Volume = {60},
	Year = {2005},
	url = {papers/Qiao_Allergy2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1398-9995.2005.00816.x}}

@article{Qin:2006,
	Abstract = {The transcription factor E2F1 is known to regulate cell proliferation and has been thought to modulate tumorigenesis via this mechanism alone. Here we show that mice deficient in E2F1 exhibit enhanced angiogenesis. The proangiogenic phenotype in E2F1 deficiency is the result of overproduction of vascular endothelial growth factor (VEGF) and is prevented by VEGF blockade. Under hypoxic conditions, E2F1 down-regulates the expression of VEGF promoter activity by associating with p53 and specifically down-regulating expression of VEGF but not other hypoxia-inducible genes, suggesting a promoter structure context-dependent regulation mechanism. We found that the minimum VEGF promoter mediating transcriptional repression by E2F1 features an E2F1- binding site with four Sp-1 sites in close proximity. These data disclose an unexpected function of endogenous E2F1: regulation of angiogenic activity via p53-dependent transcriptional control of VEGF expression.},
	Author = {Qin, and Kishore, and Dolan, and Silver, and Wecker, and Luedemann, and Thorne, and Hanley, and Curry, and Heyd, and Dinesh, and Kearney, and Martelli, and Murayama, and Goukassian, and Zhu, and Losordo,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {7505876},
	Number = {29},
	Organization = {*Division of Cardiovascular Research, Tufts University School of Medicine, Caritas St. Elizabeths Medical Center, Boston, MA 02135.},
	Pages = {11015-11020},
	Pii = {0509533103},
	Pubmed = {16835303},
	Title = {Cell cycle regulator E2F1 modulates angiogenesis via p53-dependent transcriptional control of VEGF},
	Uuid = {0FEAF92A-B1D2-4834-A825-4009AA7D639F},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0509533103}}

@article{Quesenberry:2005,
	Author = {Quesenberry, Peter J. and Dooner, Gerri and Dooner, Mark and Abedi, Mehrdad},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {17 Transplant Regeneration;08 Aberrant cell cycle;22 Stem cells},
	Month = {5},
	Nlm_Id = {0404511},
	Number = {5725},
	Organization = {Department of Research, The Center for Stem Cell Biology, Providence, RI 02908-4735, USA. pquesenberry\@rwmc.org},
	Pages = {1121-2},
	Pii = {308/5725/1121},
	Pubmed = {15905387},
	Title = {Developmental biology: Ignoratio elenchi: red herrings in stem cell research},
	Uuid = {4CE79725-0EF4-45D8-9A03-D290E60A307D},
	Volume = {308},
	Year = {2005},
	url = {papers/Quesenberry_Science2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1104432}}

@article{Quinn:1995,
	Abstract = {Fluorescent neuroanatomic techniques, such as immunofluorescence and retrograde and anterograde tracing studies, derive great utility from their specificity. However, the specificity can be a drawback as well, in that it may be difficult to assess labeled neurons or neural processes in their cytoarchitectonic context. We report the characteristics of a newly synthesized fluorescent counterstain, Fluoro Nissl Green (3,8-diamino-10H-quindoline) with spectral characteristics similar to fluorescein. This Nissl-like counterstain can be used as a green neuronal counterstain for red-emitting markers such as rhodamine and Di-I. 0304-3940 Journal Article},
	Author = {Quinn, B. and Toga, A. W. and Motamed, S. and Merlic, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:56 -0400},
	Journal = {Neurosci Lett},
	Keywords = {*Quinolines;Rats;T pdf;*Alkaloids;Neurons/*cytology;*Fluorescent Dyes;*Indoles;Support, Non-U.S. Gov't;Animals;Male;23 Technique},
	Number = {3},
	Organization = {Department of Neurology, University of California, Los Angeles 90024, USA.},
	Pages = {169-72},
	Title = {Fluoro nissl green: a novel fluorescent counterstain for neuroanatomy},
	Uuid = {95B1ED7A-FC6A-48B7-A297-7F521C957188},
	Volume = {184},
	Year = {1995},
	url = {papers/Quinn_NeurosciLett1995.pdf}}

@article{Quintana:2006,
	Abstract = {Transient anoxia/hypoglycaemia in organotypic hippocampal slice cultures, a model of transient brain ischaemia, ultimately results in delayed cell death. Although the mechanisms underlying this delayed death remain unknown, an increase in excitatory drive has been postulated. We report here that transient anoxia/hypoglycaemia in rat hippocampal slice cultures resulted in a 70-80\%enhancement of evoked, alpha-amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid (AMPA) receptor-mediated, excitatory responses lasting over 60 min. This effect was prevented by blockade of N-methyl-d-aspartate (NMDA) receptors, did not involve changes of paired-pulse facilitation ratio, but was associated with a 50\%increase in amplitude, but not frequency, of spontaneous miniature excitatory postsynaptic currents (mEPSCs). Consistent with this, paired recordings revealed the appearance of AMPA receptor-mediated EPSCs at previously silent synapses and occlusion by prior induction of long-term potentiation (LTP). Transient anoxia/hypoglycaemia further resulted in a 63\%potentiation of evoked NMDA receptor-dependent synaptic responses, accounting for the 20\%increase in ratio of AMPA to NMDA responses. No change in rectification properties of AMPA receptor-mediated currents could be detected within the first hour following anoxia/hypoglycaemia-induced potentiation. Western blot analyses of slice cultures exposed to either control conditions or a short anoxia/hypoglycaemia revealed a marked, 50-70\%increase of GluR1, GluR2/3 and NR1 subunits 1 h, but not 15 min, after the anoxic/hypoglycaemic episode. This increase was blocked by an inhibitor of protein synthesis. Together these results indicate that a transient anoxia/hypoglycaemia is associated with a marked enhancement of excitatory transmission sharing similarities with the mechanisms underlying LTP, and is correlated with an increased synthesis of excitatory receptor subunits.},
	Author = {Quintana, Patrice and Alberi, Stefano and Hakkoum, David and Muller, Dominique},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Receptors, Glutamate;Electric Stimulation;Animals;Hypoglycemia;Gene Expression Regulation;Rats;alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;Patch-Clamp Techniques;Excitatory Amino Acid Agonists;in vitro ;Hippocampus;comparative study ;Anoxia;Time Factors;research support, non-u.s. gov't ;Animals, Newborn;Blotting, Western;21 Neurophysiology;N-Methylaspartate;24 Pubmed search results 2008;Dose-Response Relationship, Radiation;Excitatory Postsynaptic Potentials},
	Month = {2},
	Nlm_Id = {8918110},
	Number = {4},
	Organization = {Department of Basic Neurosciences, University of Geneva, 1211 Geneva 4, Switzerland.},
	Pages = {975-83},
	Pii = {EJN4617},
	Pubmed = {16519662},
	Title = {Glutamate receptor changes associated with transient anoxia/hypoglycaemia in hippocampal slice cultures},
	Uuid = {B803B4DF-A797-4A11-840B-A4A24E91AA69},
	Volume = {23},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2006.04617.x}}

@article{Raballo:2000,
	Abstract = {Little is known about regionally specific signals that control the number of neuronal progenitor cells in vivo. We have previously shown that the germline mutation of the basic fibroblast growth factor (Fgf2) gene results in a reduction in the number of cortical neurons in the adult. We show here that Fgf2 is expressed in the pseudostratified ventricular epithelium (PVE) in a dorsoventral gradient and that Fgf2 and its receptor, Fgfr-1, are downregulated by mid to late stages of neurogenesis. In Fgf2 knockout mice, the volume and cell number of the dorsal PVE (the cerebral cortical anlage) are substantially smaller, whereas the volume of the basal PVE is unchanged. The dorsal PVE of Fgf2 knockout mice has a 50\%decrease in founder cells and a reduced expansion of the progenitor pool over the first portion of neurogenesis. Despite this reduction, the degree of apoptosis within the PVE is not changed in the Fgf2 knockouts. Cortical neuron number was decreased by 45\%in Fgf2 knockout mice by the end of neurogenesis, whereas the number of neurons in the basal ganglia was unaffected. Microscopically, the frontal cerebral cortex of neonatal Fgf2 null mutant mice lacked large neurons in deep cortical layers. We suggest that Fgf2 is required for the generation of a specific class of cortical neurons arising from the dorsal PVE.},
	Author = {Raballo, R. and Rhee, J. and Lyn-Cook, R. and Leckman, J. F. and Schwartz, M. L. and Vaccarino, F. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {J Neurosci},
	Keywords = {C-16;*Gene Expression Regulation, Developmental;Apoptosis;Animal;Telencephalon/*embryology;Choroid Plexus/embryology;Receptors, Fibroblast Growth Factor/genetics/*physiology;Prosencephalon/embryology;Receptor Protein-Tyrosine Kinases/genetics/*physiology;Mice, Knockout;04 Adult neurogenesis factors;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Germ-Line Mutation;Gestational Age;Cerebral Cortex/*embryology;Fibroblast Growth Factor, Basic/deficiency/genetics/*physiology;Fetal Development},
	Number = {13},
	Organization = {Child Study Center and Section of Neurobiology, Yale University, New Haven, Connecticut 06520, USA.},
	Pages = {5012-23.},
	Title = {Basic fibroblast growth factor (Fgf2) is necessary for cell proliferation and neurogenesis in the developing cerebral cortex},
	Uuid = {862E996C-1FD9-4AFE-999F-B319BAFCE050},
	Volume = {20},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10864959}}

@article{Rabchevsky:2000,
	Abstract = {We have recently demonstrated that following a moderate contusion spinal cord injury (SCI) to rats, subsequent administration of basic fibroblast growth factor (bFGF) significantly enhances functional recovery and tissue sparing. To further characterize the effects of bFGF, we evaluated its efficacy after a more severe contusion injury at T(10) using the NYU impactor. Immediately after SCI, osmotic minipumps were implanted into the lateral ventricle and lumbar thecal sac to deliver bFGF at 3 or 6 microg per day versus control vehicle for 1 week. Animals were behaviorally tested for 6 weeks before histological assessment of tissue sparing through the injured segment and glial reactivity distal to the lesion. Compared to moderate SCI, all rats had more prolonged and sustained functional deficits 6 weeks after severe contusion. Subjects treated with bFGF had pronounced recovery of hindlimb movements from 2 to 6 weeks compared to controls, manifested in significantly higher behavioral scores. Only marginal tissue sparing was seen rostral to the injury in bFGF-treated spinal cords versus controls. Optical density measurements of astrocyte and microglial cell immunoreactivity in bFGF-treated spinal cords showed that after 6 weeks they approximated controls, although astrocyte immunoreactivity remained higher in controls rostrally. In summary, intrathecal infusion of bFGF following severe SCI significantly restores gross hindlimb motor function that is not correlated with significant tissue sparing. In light of previous evidence that pharmacological intervention with bFGF after moderate SCI enhances tissue preservation, the current findings indicate that yet undefined mechanisms contribute to the enhanced functional recovery following bFGF treatment. 0014-4886 Journal Article},
	Author = {Rabchevsky, A. G. and Fugaccia, I. and Turner, A. F. and Blades, D. A. and Mattson, M. P. and Scheff, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:58 -0400},
	Journal = {Exp Neurol},
	Keywords = {Spinal Cord Injuries/*drug therapy/pathology/surgery;Dose-Response Relationship, Drug;Glial Fibrillary Acidic Protein/metabolism;Animals;Rats;Fibroblast Growth Factor 2/*administration &dosage;Lumbosacral Region;Movement/drug effects;Female;Thoracic Vertebrae/surgery;Hindlimb/innervation;Rats, Sprague-Dawley;Injections, Intraventricular;Analysis of Variance;Support, Non-U.S. Gov't;Wounds, Nonpenetrating;Gliosis/metabolism/pathology;Recovery of Function/*drug effects;Injections, Spinal;Laminectomy;04 Adult neurogenesis factors;Membrane Glycoproteins/metabolism;Behavior, Animal/drug effects/physiology;C pdf;Infusion Pumps, Implantable},
	Number = {2},
	Organization = {Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536-0230, USA.},
	Pages = {280-91},
	Pubmed = {10915567},
	Title = {Basic fibroblast growth factor (bFGF) enhances functional recovery following severe spinal cord injury to the rat},
	Uuid = {0E66C9F8-92F0-4F61-A7A9-01C7637E24E3},
	Volume = {164},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10915567}}

@article{Rabchevsky:1997,
	Abstract = {There is contrasting in vitro and in vivo evidence regarding glial cell involvement in central nervous system (CNS) regeneration. This study has investigated the histological events that follow implantation of either microglia, mixed microglia/astrocytes, or astrocytes into the injured adult rat spinal cord. We have conducted an immunohistochemical characterization of the cellular profiles within and neuritic extension into various grafts consisting of gelfoam (GF) matrices impregnated with cultured microglia and/or astrocytes. After 2-5 weeks, prominent neuritic growth was observed into OX-42-immunoreactive (IR) microglial implants. These grafts were infiltrated by numerous host cellular elements including microvasculature and Schwann cells, and they demonstrated conspicuous laminin IR. Often, the patterns for laminin and OX-42 IR in microglial grafts were overlapping, suggesting partial expression of laminin on transplanted microglial cells. Mixed grafts of microglia and astrocytes demonstrated presence of neurites and laminin-IR elements with similar intensity as microglial grafts, while astroglial implants showed the least amount of neurite ingrowth. Some control implants consisting of cell-free GF showed marginal in-growth of neurites in areas of infiltrating OX-42-IR host cells. Collectively, our findings support a neurite growth-promoting role of activated microglia and suggest that microglia may counteract mechanisms that inhibit CNS regeneration. It remains to be determined whether the observed neurite growth-promoting effects are mediated directly by grafted and/or endogenous microglia, or whether this occurs via the recruitment of host Schwann cells.},
	Author = {Rabchevsky, A. G. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Animals;Astrocytes;Cells, Cultured;Rats;Fluorescent Antibody Technique;Microglia;Lipopolysaccharides;Cell Communication;Rats, Sprague-Dawley;Neurites;Not relevant;Gelatin Sponge, Absorbable;11 Glia;Laminin;Nerve Regeneration;Spinal Cord Injuries;Support, Non-U.S. Gov't;Animals, Newborn;Neurons;Host vs Graft Reaction;Support, U.S. Gov't, P.H.S.;Microcirculation;Cell Division;Biological Markers;Data Interpretation, Statistical},
	Medline = {97135699},
	Month = {1},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610, USA.},
	Pages = {34-48},
	Pii = {10.1002/(SICI)1097-4547(19970101)47:1<34::AID-JNR4>3.0.CO;2-G},
	Pubmed = {8981236},
	Title = {Grafting of cultured microglial cells into the lesioned spinal cord of adult rats enhances neurite outgrowth},
	Uuid = {7020DB5E-3EA4-493B-B255-863BA286B46B},
	Volume = {47},
	Year = {1997}}

@article{Rafols:1995,
	Abstract = {The neocortex and the hippocampus were examined for lipid peroxidation products and ultrastructural alterations by fluorescence and electron microscopy, respectively, in rats subjected to 10 min of cardiac arrest or 10 min cardiac arrest and either 90 or 360 min reperfusion. Lipid peroxidation products were observed after 90 min reperfusion in the perikarya and proximal dendrites of neocortical pyramidal neurons and in the hippocampal hilar cells and CA1, region; the fluorescence was most intense at the base of the apical dendrite, the region of the Golgi apparatus. After 90 min of reperfusion, the CA1, showed considerable stretches of rough endoplasmic reticulum devoid of ribosomes and the Golgi cisternae were shorter and widely dilated. The neocortex showed similar endoplasmic reticulum changes, but no significant alterations to the Golgi were noted. In addition there were areas where strings of ribosomes appear to be detaching from the endoplasmic reticulum. After 360 min reperfusion in both the neocortex and the hippocampus, the damage appeared more severe. The Golgi was fragmented into vacuoles, membranous whorls had appeared, and dense aggregates of smooth vesicles were seen coalescing with each other and the vacuoles. These observations suggest that early Golgi involvement is a more important marker of lethal injury than ribosome release from the endoplasmic reticulum. The areas of disturbed Golgi ultrastructure correspond to those areas that show evidence of lipid peroxidation and imply that lipid peroxidation may be causally related to the disturbance in Golgi ultrastructure.},
	Author = {Rafols, J. A. and Daya, A. M. and O'Neil, B. J. and Krause, G. S. and Neumar, R. W. and White, B. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Brain Ischemia;Golgi Apparatus;Rats;Microscopy, Electron;Lipid Peroxidation;Hippocampus;Not relevant;Heart Arrest;11 Glia;Cell Death;Support, U.S. Gov't, P.H.S.;Reperfusion;Animals;Support, Non-U.S. Gov't;Rats, Inbred Strains;Fluorescence;Neurons},
	Medline = {96057170},
	Nlm_Id = {0412041},
	Number = {1},
	Organization = {Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI 48201, USA.},
	Pages = {17-30},
	Pubmed = {7572075},
	Title = {Global brain ischemia and reperfusion: Golgi apparatus ultrastructure in neurons selectively vulnerable to death},
	Uuid = {13B0D8A3-FCA3-49C0-B9C6-38CC9A8AD504},
	Volume = {90},
	Year = {1995}}

@article{Raibon:2002,
	Abstract = {Intravitreal injection of the microglia inhibitor tuftsin 1-3 leads to an increase in retinal ganglion cell axonal regeneration into peripheral nerve grafts and a decrease in phagocytic cells in the retina. However, the relation of phagocytic cells and particularly microglia towards axonal regeneration remains unclear. Initially, to assess this, tuftsin 1-3's effect on axonal regeneration was reexamined by doing a dose-response study. Optimal doses were found to be 2.5 microg/ml and 250 microg/ml in rats and hamsters respectively. We then studied retinal phagocytic cells in rats. Microglial cells were classified as resting or activated based on their morphology following OX42 immunolabelling. In controls, most microglial cells were in the resting state. Optic nerve cut led to an increase in the total number of microglia and a ten-fold elevation in the proportion of activated cells; changes were more pronounced at the optic nerve stump. Anastomosis of an autologous segment of sciatic nerve to the stump of the freshly cut optic nerve minimized the overall increase in microglia, and combined with 2.5 microg/ml tuftsin 1-3, lead to a marked blunting of activation. Preservation within the retina of a higher proportion of resting over active form of microglia, and not the prevention of microglial proliferation per se, may be a crucial factor in allowing additional retinal ganglion cell axons to regenerate into peripheral nerve grafts.},
	Author = {Raibon, E. and Sauv{\'e}, Y. and Carter, D. A. and Gaillard, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Peripheral Nerves;Research Support, Non-U.S. Gov't;Hamsters;Animals;Rats, Inbred BN;Blood Proteins;Rats;Microglia;Female;Antigens, CD;Antigens, Neoplasm;Rats, Sprague-Dawley;Avian Proteins;Cell Count;Antigens, Surface;11 Glia;Axons;Nerve Regeneration;Membrane Glycoproteins;Mesocricetus;Transplants;24 Pubmed search results 2008;Retinal Ganglion Cells},
	Medline = {22538728},
	Month = {1},
	Nlm_Id = {0364620},
	Number = {1},
	Organization = {UMR 6558 CNRS, Facult{\'e} des Sciences, Poitiers, France.},
	Pages = {57-71},
	Pii = {5115502},
	Pubmed = {12652088},
	Title = {Microglial changes accompanying the promotion of retinal ganglion cell axonal regeneration into peripheral nerve grafts},
	Uuid = {63220C22-95E1-4509-B0AF-DEA393452581},
	Volume = {31},
	Year = {2002}}

@article{Raivich:2003,
	Abstract = {Studies using mouse axotomised facial motoneuron model show a strong and highly selective entry of CD3+ lymphocytes into the affected nucleus, with a maximum at Day 14, which coincides with the peak of neuronal cell death, microglial phagocytosis, and increased synthesis of interleukin-1 beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and interferon-gamma (IFNgamma). We explored the possible involvement of these cytokines during the main phase of lymphocyte recruitment into the axotomised facial motor nucleus 7-21 days after nerve cut using mice homozygously deficient for IL1 receptor type 1 (IL1R1-/-), TNF receptor type 1 (TNFR1-/-), type 2 (TNFR2-/-) and type 1 and 2 (TNFR1&2-/-), IFNgamma receptor type 1 (IFNgammaR1-/-), and the appropriate controls for the genetic background. Transgenic deletion of IL1R1 led to a 54\%decrease and that of TNFR2 to a 44\%reduction in the number of CD3+ T-cells in the axotomised facial motor nucleus, with a similar relative decrease at Day 7, 14, and 21. Deletion of TNFR1 or IFNgammaR1 had no significant effect. Deletion of both TNFR1 and 2 (TNFR1&2-/-) caused a somewhat stronger, 63\%decrease than did TNFR2 deletion alone, but this could be due to an almost complete inhibition of neuronal cell death. No mutations seemed to inhibit aggregation of CD3+ T-cells around glial nodules consisting of Ca-ion binding adaptor protein-1 (IBA1)+ phagocytotic microglia and neuronal debris. Altogether, the current data show the importance of IL1R1 and TNFR2 as the key players during the main phase of lymphocyte recruitment to the damaged part of the central nervous system.},
	Author = {Raivich, Gennadij and Bohatschek, Marion and Werner, Alexander and Jones, Leonard L. and Galiano, Matthias and Kloss, Christian U. A. and Zhu, Xing-Zu Z. and Pfeffer, Klaus and Liu, Zhi Qiang},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Receptors, Cytokine;Phagocytosis;Animals;Comparative Study;Lymphocytes;Microglia;Cell Communication;Cell Movement;Mice, Inbred C57BL;Not relevant;11 Glia;Support, Non-U.S. Gov't;Mice, Knockout;Axotomy;Mice;Inflammation;Brain Stem;Facial Nerve;Cytokines},
	Medline = {22658411},
	Month = {6},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {Department of Neuromorphology, Max-Planck Institute for Neurobiology, Martinsried, Germany. g.raivich\@ucl.ac.uk},
	Pages = {726-33},
	Pubmed = {12774313},
	Title = {Lymphocyte infiltration in the injured brain: role of proinflammatory cytokines},
	Uuid = {99B4BD00-5843-4FFC-9A73-BCD4CAB088CB},
	Volume = {72},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10621}}

@article{Raivich:2004,
	Abstract = {Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is highly expressed in response to neuronal trauma. Here we have investigated the role of c-jun during axonal regeneration using mice lacking c-jun in the central nervous system. After transection of the facial nerve, the absence of c-Jun caused severe defects in several aspects of the axonal response, including perineuronal sprouting, lymphocyte recruitment, and microglial activation. c-Jun-deficient motorneurons were atrophic, resistant to axotomy-induced cell death, and showed reduced target muscle reinnervation. Expression of CD44, galanin, and alpha7beta1 integrin, molecules known to be involved in regeneration, was greatly impaired, suggesting a mechanism for c-Jun-mediated axonal growth. Taken together, our results identify c-Jun as an important regulator of axonal regeneration in the injured central nervous system.},
	Author = {Raivich, Gennadij and Bohatschek, Marion and Da Costa, Clive and Iwata, Osuke and Galiano, Matthias and Hristova, Maria and Nateri, Abdolrahman S. and Makwana, Milan and Riera-Sans, Llu{\'\i}s and Wolfer, David P. and Lipp, Hans-Peter P. and Aguzzi, Adriano and Wagner, Erwin F. and Behrens, Axel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:30 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Animals;Galanin;Recovery of Function;Neuronal Plasticity;Transcription Factor AP-1;Integrins;Microglia;Lymphocyte Activation;Mice, Transgenic;Antigens, CD44;Atrophy;Not relevant;11 Glia;Proto-Oncogene Proteins c-jun;Nerve Regeneration;Facial Nerve Injuries;Support, Non-U.S. Gov't;Axotomy;Muscle, Skeletal;Down-Regulation;Gliosis;Motor Neurons;Mice;Growth Cones;Cell Death;Facial Nerve},
	Month = {7},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Perinatal Brain Repair Group, Department of Obstetrics and Gynaecology, University College London, 86-96 Chenies Mews, London WC1E 6HX, United Kingdom.},
	Pages = {57-67},
	Pii = {S0896627304003575},
	Pubmed = {15233917},
	Title = {The AP-1 transcription factor c-Jun is required for efficient axonal regeneration},
	Uuid = {0921FE53-70BE-42A9-9A35-9C3022739C93},
	Volume = {43},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2004.06.005}}

@article{Rakic:1985,
	Abstract = {Autoradiographic analysis of juvenile and adult monkeys that received single or multiple injection of the specific DNA precursor, [3H]thymidine, demonstrates slight turnover of glial cells, but failed to provide any evidence of either neuronal addition or replacement. Therefore, while the brains of nonmammalian vertebrates and possibly some nonprimate mammals may display variable degrees of postembryonic neurogenesis, all neurons of the primate central nervous system are generated during restricted developmental periods, mostly before birth and not after infancy. It is not surprising that a stable population of neurons in mature primates, including man, may be essential for the retention of memory and learned behavior. Using Smart Source Parsing},
	Author = {Rakic, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Ann N Y Acad Sci},
	Keywords = {Human;Oligodendroglia/cytology;Neurons/*cytology/metabolism;Thymidine/metabolism;Comparative Study;Mitosis;Brain/*cytology/embryology/metabolism;Female;DNA/*biosynthesis;*Aging;Animal;Glial Fibrillary Acidic Protein/analysis;Species Specificity;Male;01 Adult neurogenesis general;Support, Non-U.S. Gov't;Histocytochemistry;Macaca mulatta;Support, U.S. Gov't, P.H.S.;Cell Division;Microscopy, Electron;Autoradiography;A-3;Neuroglia/cytology},
	Pages = {193-211},
	Title = {DNA synthesis and cell division in the adult primate brain},
	Uuid = {6B7E198B-65AD-4AA4-839C-487115867E2D},
	Volume = {457},
	Year = {1985},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=3913364}}

@article{Rami:1987,
	Abstract = {An immunocytochemical study of cholecalcin (28-kDa calcium-binding protein, CaBP, calbindin) was carried out during the development of the rat hippocampus. In normal animals, the protein appeared from Postnatal Day 3 in the granule cells of the dentate gyrus and from Day 5 in the CA1-CA2 pyramidal cells of Ammon's horn. The cells of both regions thus showed positive cholecalcin labeling about 1 week after their formation. The sequence of labeling of the granule cells was a reflection of the major sequences of neurogenesis. Cholecalcin could not be detected in hippocampal cells until dendritic arborization and axon growth had occurred. There was a good correlation between the appearance of cholecalcin and the onset of synaptogenesis. In animals with an experimentally altered thyroid state, in which hippocampal development is retarded or accelerated due to abnormal cell maturation, cholecalcin appearance was similarly retarded or accelerated. Cholecalcin seems to be synthesized at the same time as the hippocampal cells become functional.},
	Author = {Rami, A. and Br{\'e}hier, A. and Thomasset, M. and Rabi{\'e}, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {10 Development;10 Hippocampus;Tissue Distribution;Animals;Synapses;Aging;Rats;Comparative Study;Immunoenzyme Techniques;Thyroxine;Hippocampus;Rats, Inbred Strains;Calcium-Binding Protein, Vitamin D-Dependent;Animals, Newborn;Hypothyroidism;Histocytochemistry;Hyperthyroidism;Research Support, Non-U.S. Gov't},
	Medline = {88030416},
	Month = {11},
	Nlm_Id = {0372762},
	Number = {1},
	Organization = {CNRS UA 1197, Universit{\'e} des Sciences et Techniques du Languedoc, Montpellier, France.},
	Pages = {228-38},
	Pubmed = {3311850},
	Title = {Cholecalcin (28-kDa calcium-binding protein) in the rat hippocampus: development in normal animals and in altered thyroid states. An immunocytochemical study},
	Uuid = {A6B90A8B-B0C5-4439-BE5E-9CA5A840F3B4},
	Volume = {124},
	Year = {1987}}

@article{Ramirez-Amaya:2006,
	Abstract = {Although it is established that new granule cells can be born and can survive in the adult mammalian hippocampus, there remains some question concerning the functional integration of these neurons into behaviorally relevant neural networks. By using high-resolution confocal microscopy, we have applied a new strategy to address the question of functional integration of newborn neurons into networks that mediate spatial information processing and memory formation. Exploration-induced expression of the immediate-early gene Arc in hippocampal cells has been linked to cellular activity observed in electrophysiological recordings under the same behavioral conditions. We investigated whether mature (5-month-old), newborn granule cells express Arc in response to a discrete spatial experience by detecting the expression of Arc in combination with NeuN (neuron-specific nuclear protein)-positive and bromodeoxyuridine-positive cells. We found that mature new granule cells do indeed express Arc in response to an exploration experience, supporting the idea that these cells are well integrated into hippocampal circuits. The proportion of mature newborn neurons that expressed Arc in response to exploration, however, was significantly higher (approximately 2.8\%) than the proportion of cells that expressed Arc in the already existing population of granule cells (approximately 1.6\%; p < 0.01). This finding extends previous data suggesting that the cellular physiology of newborn granule neurons differs from that of the existing population by indicating that these properties are retained in mature adult-generated neurons. Thus, these data have interesting implications for network models of spatial information processing and the role of hippocampal circuits in memory, indicating that mature new neurons are selectively recruited into hippocampal cell assemblies in higher proportions than older cells.},
	Author = {Ramirez-Amaya, Victor and Marrone, Diano F. and Gage, Fred H. and Worley, Paul F. and Barnes, Carol A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {in vitro;Animals;Gene Expression Regulation;Rats;Neuronal Plasticity;Microscopy, Confocal;comparative study;Exploratory Behavior;Phosphopyruvate Hydratase;Cell Count;Hippocampus;research support, non-u.s. gov't;Behavior, Animal;01 Adult neurogenesis general;Rats, Inbred F344;Analysis of Variance;Nerve Net;Neurons;research support, n.i.h., extramural;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine;Nerve Tissue Proteins;Cytoskeletal Proteins},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {47},
	Organization = {Arizona Research Laboratories Division of Neural Systems, Memory, and Aging, University of Arizona, Tucson, Arizona 85724, USA.},
	Pages = {12237-41},
	Pii = {26/47/12237},
	Pubmed = {17122048},
	Title = {Integration of new neurons into functional neural networks},
	Uuid = {E64B3B4F-8A51-4031-8EC6-5693942DEA32},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2195-06.2006}}

@article{Ramirez-Castillejo:2002,
	Abstract = {The lizard medial cortex, a region homologous to the mammalian dentate gyrus, shows postnatal neurogenesis and the surprising ability to replace its neurons after being lesioned specifically with the neurotoxin 3-acetylpyridine. As the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) is expressed during neuronal migration and differentiation, we have studied its distribution in adult lizards and also during the lesion-regeneration process. In the medial cortex of control animals, many labeled fusiform somata, presumably corresponding to migratory neuroblasts, appeared in the inner plexiform layer. There were also scattered immunoreactive granule neurons in the cell layer. Double immunocytochemistry with 5'-bromodeoxyuridine revealed that some of the PSA-NCAM-expressing cells in the inner plexiform and cell layers were generated recently. PSA-NCAM immunoreactivity was also present in the dorsomedial, dorsal, and lateral cortices, as well as in the dorsal ventricular ridge, the nucleus accumbens, and the nucleus sphericus. Twelve hours after the injection of 3-acetylpyridine, some medial cortex granule neurons appeared degenerated, although some of them still expressed PSA-NCAM. One to 2 days after the injection, most granule neurons appeared degenerated and no PSA-NCAM immunoreactivity was detected in the medial cortex cell layer. Four to 7 days after treatment, abundant labeled fusiform cells populated the inner plexiform layer and some immunoreactive somata were seen in the cell layer. Fifteen to 30 days after the neurotoxin injection, the number of PSA-NCAM expressing granule neurons augmented considerably and the level was still above control levels in lizards that survived 42 days. Our results show for the first time the expression of PSA-NCAM in a reptile brain, where it appears to participate in the migration and differentiation of granule neurons during adult neurogenesis and regeneration.},
	Author = {Ramirez-Castillejo, Carmen and Nacher, Juan and Molowny, Asuncion and Ponsoda, Xavier and Lopez-Garcia, Carlos},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Neurons;Animals;Nerve Fibers;Research Support, Non-U.S. Gov't;Nerve Regeneration;Immunohistochemistry;Neural Cell Adhesion Molecule L1;Hippocampus;Antibodies, Monoclonal;Biological Markers;Cell Division;Lizards;Age Factors;Bromodeoxyuridine;24 Pubmed search results 2008;Sialic Acids;Cerebral Cortex},
	Medline = {22260352},
	Month = {11},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Neurobiologia, Biologia Celular, Facultad de Ciencias Biologicas, Universidad de Valencia, 46100 Burjassot, Spain.},
	Pages = {145-56},
	Pubmed = {12373780},
	Title = {PSA-NCAM immunocytochemistry in the cerebral cortex and other telencephalic areas of the lizard Podarcis hispanica: differential expression during medial cortex neuronal regeneration},
	Uuid = {DBCD6088-B4CB-4505-B590-AE0EB0D93E9E},
	Volume = {453},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10390}}

@article{Ramirez-Castillejo:2006,
	Abstract = {Adult stem cells are characterized by self-renewal and multilineage differentiation, and these properties seem to be regulated by signals from adjacent differentiated cell types and by extracellular matrix molecules, which collectively define the stem cell "niche." Self-renewal is essential for the lifelong persistence of stem cells, but its regulation is poorly understood. In the mammalian brain, neurogenesis persists in two germinal areas, the subventricular zone (SVZ) and the hippocampus, where continuous postnatal neuronal production seems to be supported by neural stem cells (NSCs). Here we show that pigment epithelium-derived factor (PEDF) is secreted by components of the murine SVZ and promotes self-renewal of adult NSCs in vitro. In addition, intraventricular PEDF infusion activated slowly dividing stem cells, whereas a blockade of endogenous PEDF decreased their cycling. These data demonstrate that PEDF is a niche-derived regulator of adult NSCs and provide evidence for a role for PEDF protein in NSC maintenance.},
	Author = {Ram{\'\i}rez-Castillejo, Carmen and S{\'a}nchez-S{\'a}nchez, Francisco and Andreu-Agull{\'o}, Celia and Ferr{\'o}n, Sacri R. and Aroca-Aguilar, J. Daniel and S{\'a}nchez, Pilar and Mira, Helena and Escribano, Julio and Fari\~{n}as, Isabel},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Serpins;Research Support, Non-U.S. Gov't;Cell Differentiation;Signal Transduction;Animals;Cells, Cultured;Humans;Neuronal Plasticity;Cell Cycle;Cercopithecus aethiops;Telencephalon;Hippocampus;Eye Proteins;COS Cells;Cell Proliferation;Nerve Growth Factors;Injections, Intraventricular;Neurons;Ependyma;Mice;Cell Division;24 Pubmed search results 2008;Stem Cells;Lateral Ventricles;Endothelium, Vascular},
	Month = {3},
	Nlm_Id = {9809671},
	Number = {3},
	Organization = {Departamento de Biolog{\'\i}a Celular, Universidad de Valencia, Burjassot 46100, Spain.},
	Pages = {331-9},
	Pii = {nn1657},
	Pubmed = {16491078},
	Title = {Pigment epithelium-derived factor is a niche signal for neural stem cell renewal},
	Uuid = {F859D6C5-03BC-41FA-A4BB-8DF9EB7EC11C},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1657}}

@article{Raponi:2007,
	Abstract = {During the postnatal development, astrocytic cells in the neocortex progressively lose their neural stem cell (NSC) potential, whereas this peculiar attribute is preserved in the adult subventricular zone (SVZ). To understand this fundamental difference, many reports suggest that adult subventricular GFAP-expressing cells might be maintained in immature developmental stage. Here, we show that S100B, a marker of glial cells, is absent from GFAP-expressing cells of the SVZ and that its onset of expression characterizes a terminal maturation stage of cortical astrocytic cells. Nevertheless, when cultured in vitro, SVZ astrocytic cells developed as S100B expressing cells, as do cortical astrocytic cells, suggesting that SVZ microenvironment represses S100B expression. Using transgenic s100b-EGFP cells, we then demonstrated that S100B expression coincides with the loss of neurosphere forming abilities of GFAP expressing cells. By doing grafting experiments with cells derived from beta-actin-GFP mice, we next found that S100B expression in astrocytic cells is repressed in the SVZ, but not in the striatal parenchyma. Furthermore, we showed that treatment with epidermal growth factor represses S100B expression in GFAP-expressing cells in vitro as well as in vivo. Altogether, our results indicate that the S100B expression defines a late developmental stage after which GFAP-expressing cells lose their NSC potential and suggest that S100B expression is repressed by adult SVZ microenvironment.},
	Author = {Raponi, Eric and Agenes, Fabien and Delphin, Christian and Assard, Nicole and Baudier, Jacques and Legraverend, Catherine and Deloulme, Jean-Christophe C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {INSERM, EMI 01-04, Grenoble, France.},
	Pages = {165-77},
	Pubmed = {17078026},
	Title = {S100B expression defines a state in which GFAP-expressing cells lose their neural stem cell potential and acquire a more mature developmental stage},
	Uuid = {B9EC7A24-A1C9-4A12-B33F-B6120B28B2DA},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20445}}

@article{Rappert:2004,
	Abstract = {Microglia are the resident macrophage population of the CNS and are considered its major immunocompetent elements. They are activated by any type of brain pathology and can migrate to the lesion site. The chemokine CXCL10 is expressed in neurons in response to brain injury and is a signaling candidate for activating microglia and directing them to the lesion site. We recently identified CXCR3, the corresponding receptor for CXCL10, in microglia and demonstrated that this receptor system controls microglial migration. We have now tested the impact of CXCR3 signaling on cellular responses after entorhinal cortex lesion. In wild-type mice, microglia migrate within the first 3 d after lesion into the zone of axonal degeneration, where 8 d after lesion denervated dendrites of interneurons are subsequently lost. In contrast, the recruitment of microglia was impaired in CXCR3 knock-out mice, and, strikingly, denervated distal dendrites were maintained in zones of axonal degeneration. No differences between wild-type and knock-out mice were observed after facial nerve axotomy, as a lesion model for assessing microglial proliferation. This shows that CXCR3 signaling is crucial in microglia recruitment but not proliferation, and this recruitment is an essential element for neuronal reorganization.},
	Author = {Rappert, Angelika and Bechmann, Ingo and Pivneva, Tatyana and Mahlo, Jacqueline and Biber, Knut and Nolte, Christiane and Kovac, Adam D. and Gerard, Craig and Boddeke, Hendrikus W. G. M. and Nitsch, Robert and Kettenmann, Helmut},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {39},
	Organization = {Department of Cellular Neuroscience, Max Delbr{\"u}ck Center for Molecular Medicine, 13092 Berlin, Germany.},
	Pages = {8500-9},
	Pii = {24/39/8500},
	Pubmed = {15456824},
	Title = {CXCR3-dependent microglial recruitment is essential for dendrite loss after brain lesion},
	Uuid = {3463ECDC-EE15-11DA-8605-000D9346EC2A},
	Volume = {24},
	Year = {2004},
	url = {papers/Rappert_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2451-04.2004}}

@article{Rasika:1999,
	Abstract = {New neurons are incorporated into the high vocal center (HVC), a nucleus of the adult canary (Serinus canaria) brain that plays a critical role in the acquisition and production of learned song. Recruitment of new neurons in the HVC is seasonally regulated and depends upon testosterone levels. We show here that brain-derived neurotrophic factor (BDNF) is present in the HVC of adult males but is not detectable in that of females, though the HVC of both sexes has BDNF receptors (TrkB). Testosterone treatment increases the levels of BDNF protein in the female HVC, and BDNF infused into the HVC of adult females triples the number of new neurons. Infusion of a neutralizing antibody to BDNF blocks the testosterone-induced increase in new neurons. Our results demonstrate that BDNF is involved in the regulation of neuronal replacement in the adult canary brain and suggest that the effects of testosterone are mediated through BDNF.},
	Author = {Rasika, S. and Alvarez-Buylla, A. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Neuron},
	Keywords = {C-8;Receptor, Ciliary Neurotrophic Factor;Testosterone/antagonists &inhibitors/*pharmacology;Cell Survival/drug effects;Female;Recruitment (Neurology)/physiology;Animal;Receptor Protein-Tyrosine Kinases/metabolism;Male;Vocalization, Animal/physiology;Canaries;Brain/cytology/metabolism/*physiology;Brain-Derived Neurotrophic Factor/immunology/metabolism/*pharmacology;Sex Characteristics;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Antibodies/pharmacology;Receptors, Nerve Growth Factor/metabolism;Neurons/*drug effects/physiology},
	Number = {1},
	Organization = {The Rockefeller University, New York, New York 10021, USA.},
	Pages = {53-62.},
	Title = {BDNF mediates the effects of testosterone on the survival of new neurons in an adult brain},
	Uuid = {07CC7E48-D8CA-4BD5-A36F-6B0B57687E1F},
	Volume = {22},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10027289}}

@article{Rasika:1994,
	Abstract = {New neurons are added to the high vocal center (HVC) of adult male and female canaries. Exogenous testosterone induces a marked increase in HVC size in adult female canaries, though the mechanisms responsible for this increase remain unknown. To understand the mechanisms, we analyzed the effects of testosterone on neuronal recruitment in the female HVC. Intact adult female canaries received Silastic implants that were empty or filled with testosterone. Birds in the short- survival group received the Silastic implant, followed by a single injection of [3H]thymidine 2 days later, and were killed on the following day. Birds in the long-survival group were injected once a day for 5 days with [3H]thymidine and received the Silastic implant 20 and 40 days later. These birds were killed 60 days after the first injection of [3H]thymidine. The number of 3H-labeled ventricular zone cells above, rostral, or caudal to HVC was not affected by the hormone treatment in the short-survival birds, suggesting that testosterone did not affect neuronal production. However, the number of 3H-labeled HVC neurons that projected to robust nucleus of the archistriatum (RA) in the long-survival birds was three times greater in the hormone-treated than in the control group, though the total number of RA-projecting cells did not change significantly. Testosterone also induced an increase in the size of the HVC cells that project to RA. Thus, these experiments suggest that testosterone affects the recruitment and/or survival of newly generated RA-projecting HVC neurons but does not affect their production.},
	Author = {Rasika, S. and Nottebohm, F. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {*Brain Mapping;Support, U.S. Gov't, P.H.S.;Female;Autoradiography;Thymidine/metabolism;Testosterone/*pharmacology;Animal;04 Adult neurogenesis factors;Canaries/*physiology;Tritium;Vocalization, Animal/*physiology;Cell Survival/drug effects;Neurons/cytology/drug effects/*physiology;Brain/cytology/drug effects/*physiology;C abstr},
	Number = {17},
	Organization = {Laboratory of Animal Behavior, Rockefeller University, New York, NY 10021.},
	Pages = {7854-8.},
	Title = {Testosterone increases the recruitment and/or survival of new high vocal center neurons in adult female canaries},
	Uuid = {E2061B67-D7C3-40FC-A7DB-136D24FD39E9},
	Volume = {91},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8058723}}

@article{Rasin:2007,
	Abstract = {The polarity and adhesion of radial glial cells (RGCs), which function as progenitors and migrational guides for neurons, are critical for morphogenesis of the cerebral cortex. These characteristics largely depend on cadherin-based adherens junctions, which anchor apical end-feet of adjacent RGCs to each other at the ventricular surface. Here, we show that mouse numb and numb-like are required for maintaining radial glial adherens junctions. Numb accumulates in the apical end-feet, where it localizes to adherens junction-associated vesicles and interacts with cadherins. Numb and Numbl inactivation in RGCs decreases proper basolateral insertion of cadherins and disrupts adherens junctions and polarity, leading to progenitor dispersion and disorganized cortical lamination. Conversely, overexpression of Numb prolongs RGC polarization, in a cadherin-dependent manner, beyond the normal neurogenic period. Thus, by regulating RGC adhesion and polarity, Numb and Numbl are required for the tissue architecture of neurogenic niches and the cerebral cortex.},
	Author = {Rasin, Mladen-Roko R. and Gazula, Valeswara-Rao R. and Breunig, Joshua J. and Kwan, Kenneth Y. and Johnson, Matthew B. and Liu-Chen, Susan and Li, Hua-Shun S. and Jan, Lily Yeh and Jan, Yuh-Nung N. and Rakic, Pasko and Sestan, Nenad},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Animals;RNA;Cells, Cultured;Humans;Electroporation;Cell Polarity;research support, non-u.s. gov't;In Situ Hybridization;Cadherins;Cell Adhesion;Endosomes;Mice, Knockout;Neurons;Neuroglia;Cerebral Ventricles;Blotting, Western;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Immunohistochemistry;Membrane Proteins;Microscopy, Electron;Nerve Tissue Proteins;Stem Cells},
	Month = {7},
	Nlm_Id = {9809671},
	Number = {7},
	Organization = {Department of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510, USA.},
	Pages = {819-27},
	Pii = {nn1924},
	Pubmed = {17589506},
	Title = {Numb and Numbl are required for maintenance of cadherin-based adhesion and polarity of neural progenitors},
	Uuid = {949DA7F0-26F5-4FD4-B9E7-08ED9B708A66},
	Volume = {10},
	Year = {2007},
	url = {papers/Rasin_NatNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1924}}

@article{Ravizza:2005,
	Abstract = {PURPOSE: We investigated the activation of microglia and astrocytes, induction of cytokines, and hippocampal neuronal damage, 4 and 24 h after kainic acid-induced status epilepticus (SE) in postnatal day (PN) 9, 15, and 21 rats. METHODS: Limbic seizures were induced by systemic injection of kainic acid. Glia activation and neuronal cell loss were studied by using immunocytochemistry and Western blot. Cytokine expression was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) followed by Southern blot quantification. RESULTS: After SE onset, hippocampal glia activation, cytokine expression, and neuronal damage are all age-dependent phenomena. In the hippocampus, neuronal injury occurs only when cytokines are induced in glia, and cytokine synthesis precedes the appearance of degenerating neurons. Neuronal injury is more pronounced when interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) are produced in addition to IL-1beta. CONCLUSIONS: This study shows that cytokine induction in rat brain after sustained seizures is age dependent, and it is associated with the appearance of cell injury.},
	Author = {Ravizza, Teresa and Rizzi, Massimo and Perego, Carlo and Richichi, Cristina and Vel{\'\i}skov{\'a}, Jana and Mosh{\'e}, Solomon L. and De Simoni, M. Grazia and Vezzani, Annamaria},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Cytokines;Nerve Degeneration;Astrocytes;Animals;Rats;Tumor Necrosis Factor-alpha;Rats, Sprague-Dawley;Hippocampus;Kainic Acid;11 Glia;Disease Models, Animal;Male;Reverse Transcriptase Polymerase Chain Reaction;Status Epilepticus;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Blotting, Western;Neuroglia;Inflammation Mediators;Gliosis;Interleukin-6;Research Support, N.I.H., Extramural;Immunohistochemistry;Inflammation;Research Support, Non-U.S. Gov't},
	Nlm_Id = {2983306R},
	Organization = {Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milan, Italy. ravizza\@marionegri.it},
	Pages = {113-7},
	Pii = {EPI01006},
	Pubmed = {15987264},
	Title = {Inflammatory response and glia activation in developing rat hippocampus after status epilepticus},
	Uuid = {0AE85ABD-BC2A-4DF4-A0DA-301F14D97956},
	Volume = {46 Suppl 5},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1528-1167.2005.01006.x}}

@article{Raymond:1995,
	Abstract = {Cerebral cortical dysgenesis (CD) is a heterogeneous disorder of cortical development and organization commonly associated with epilepsy, with a variety of subtypes. We reviewed the clinical, EEG and neuroimaging features in 100 adult patients with CD. There were 39 men and 61 women with a median age of 27 years (range 15-63 years). All patients were referred because of medically refractory epilepsy. Median age at seizure onset was 10 years (range 3 weeks to 39 years); in 30 patients, onset was in adulthood. The epilepsy was classified as generalized in 16 patients and localization-related in 84. Of the latter, the epileptic syndromes in decreasing frequency were frontal (32\%), temporal (31\%), parietal (14\%) and occipital (7\%). Only 15\%of patients had a history of status epilepticus. Prenatal/perinatal problems were reported in 32 patients but these were severe in only four: exposure to drugs (three) and infection (one) during the first trimester. Delayed developmental milestones were seen in 10\%, mental retardation in 9\%, additional congenital abnormalities in 4\%and neurological deficits in 14\%of patients. Diagnosis of CD was based on neuroimaging in 70, pathology in four and both methods in the remaining 26. The following subcategories were identified: agyria/diffuse macrogyria (four patients), focal macrogyria (16), focal polymicrogyria (one), focal macrogyria/polymicrogyria associated with a cleft (11), minor gyral abnormalities (seven), subependymal grey matter heterotopia (20), bilateral subcortical laminar grey matter heterotopia (eight), tuberous sclerosis (five), focal cortical dysplasia/microdysgenesis (seven) and dysembryoplastic neuroepithelial tumours (DNT) (21). Sixty-eight percent of patients had normal CT and 19 out of 36 patients had normal previous conventional MRI. MRI-based hippocampal volume measurements in 47 patients revealed ratios (smaller: larger hippocampus) of < 0.90 in 16, 0.90-0.94 in 14 and > or = 0.95 in 17 patients. EEGs were normal in only five patients. Alpha rhythm was preserved in 78 patients, including one patient with bilateral posterior macrogyria. Localized polymorphic slow activity was present in 43 patients. Five of 68 patients with focal/unilateral CD had only bilateral independent/synchronous spiking and 14 out of 32 with diffuse/bilateral CD only focal/unilateral spiking. In 60 patients with nondiffuse CD or with abnormal gyration or DNT, the epileptiform abnormalities were less extensive than coextensive with the lesion in 28, more extensive than and overlapped the lesion in 18 and remote from the lesion in five; nine patients did not have epileptiform abnormalities. There was poor correlation between the epileptic syndromes and EEG abnormalities and the location/extent of CD as defined by MRI and pathology.(ABSTRACT TRUNCATED AT 400 WORDS)},
	Author = {Raymond, A. A. and Fish, D. R. and Sisodiya, S. M. and Alsanjari, N. and Stevens, J. M. and Shorvon, S. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0006-8950},
	Journal = {Brain},
	Keywords = {Glioma;10 Development;Magnetic Resonance Imaging;Child, Preschool;Humans;Treatment Outcome;Middle Aged;Tuberous Sclerosis;Diagnosis, Differential;Congenital Abnormalities;London;Female;Epilepsy;Infant;Child;Mental Retardation;Tomography, X-Ray Computed;review;Male;10 genetics malformation;Cerebral Cortex;Retrospective Studies;Ependyma;Adult;Infant, Newborn;24 Pubmed search results 2008;Choristoma;Electroencephalography;Adolescent},
	Month = {6},
	Nlm_Id = {0372537},
	Organization = {Epilepsy Research Group, National Hospital for Neurology and Neurosurgery, London, UK.},
	Pages = {629-60},
	Pubmed = {7600083},
	Title = {Abnormalities of gyration, heterotopias, tuberous sclerosis, focal cortical dysplasia, microdysgenesis, dysembryoplastic neuroepithelial tumour and dysgenesis of the archicortex in epilepsy. Clinical, EEG and neuroimaging features in 100 adult patients},
	Uuid = {50136D41-4FE5-41AF-940E-DF1D120535A4},
	Volume = {118 ( Pt 3)},
	Year = {1995},
	url = {papers/Raymond_Brain1995.pdf}}

@article{Recchi:2006,
	Author = {Recchi, Chiara and Chavrier, Philippe},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {Animals;comment;ADP-Ribosylation Factors;Proteins;Models, Biological;Protein Transport;Vacuolar Proton-Translocating ATPases;Hydrogen-Ion Concentration;15 Retrovirus mechanism;11 Glia;23 Technique;news;GTPase-Activating Proteins;Endosomes;Endocytosis;Transport Vesicles;Mice;24 Pubmed search results 2008;15 PS VSVG receptor},
	Month = {2},
	Nlm_Id = {100890575},
	Number = {2},
	Pages = {107-9},
	Pii = {ncb0206-107},
	Pubmed = {16450005},
	Title = {V-ATPase: a potential pH sensor},
	Uuid = {4FA8EDA2-AA6E-4E7C-B75D-7C4BFB8E4A2F},
	Volume = {8},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb0206-107}}

@article{Redmond:1996,
	Abstract = {In the mammalian brain, an important phase of neurogenesis occurs postnatally in the subventricular zone (SVZ). This region consists of a heterogeneous population of cells, some mitotically active, others postmitotic. A subset of mitotically active SVZ precursor cells gives rise to a population of neurons that migrates over a long distance to their final destination, the olfactory bulb. Other SVZ precursor cells continue to proliferate or undergo cell death. The combination of genes that regulates proliferation and cell fate determination of SVZ precursor cells remains to be identified. We have used the rat homolog of the human homeobox gene PBX1 in Northern analysis and in situ hybridization studies to determine the temporal and regional localization of PBX1 expression during embryonic and postnatal rat brain development. PBX1 is expressed embryonically in the telencephalon. In addition, it is expressed at high levels postnatally in the SVZ, in the migratory pathway to the olfactory bulb, and in the layers of the olfactory bulb that are the targets of these migratory neurons. Combining in situ hybridization for PBX1 with immunostaining for markers of cell proliferation (PCNA), postmitotic neurons (class III beta-tubulin), and glia (GFAP), we show that SVZ proliferating cells and their neuronal progeny express rat PBX1 mRNA, whereas glial cells do not express detectable levels of PBX1. The expression of PBX1 in SVZ precursor cells and postmitotic neurons suggests a role for PBX1 in the generation of olfactory bulb interneurons and in mammalian neurogenesis.},
	Author = {Redmond, L. and Hockfield, S. and Morabito, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci},
	Keywords = {Tubulin/metabolism;Cerebral Ventricles/*physiology;Gene Expression Regulation;Base Sequence;Oligonucleotides, Antisense/genetics;Rats;Oligonucleotide Probes/genetics;Stem Cells/physiology;*Gene Expression;Aging/physiology;Animal;C abstr;Neural Pathways/physiology;Olfactory Bulb/cytology/*physiology;Animals, Newborn/*physiology;*Genes, Homeobox;04 Adult neurogenesis factors;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;RNA, Messenger/metabolism;Molecular Sequence Data;Interneurons/*physiology},
	Number = {9},
	Organization = {Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8066, USA.},
	Pages = {2972-82.},
	Title = {The divergent homeobox gene PBX1 is expressed in the postnatal subventricular zone and interneurons of the olfactory bulb},
	Uuid = {B9624345-5EC5-4BC7-A883-BE0AEAD8C198},
	Volume = {16},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8622127}}

@article{Rehen:2005,
	Abstract = {The mouse brain contains genetically distinct cells that differ with respect to chromosome number manifested as aneuploidy (Rehen et al., 2001); however, the relevance to humans is not known. Here, using double-label fluorescence in situ hybridization for the autosome chromosome 21 (chromosome 21 point probes combined with chromosome 21 "paint" probes), along with immunocytochemistry and cell sorting, we present evidence for chromosome gain and loss in the human brain. Chromosome 21 aneuploid cells constitute approximately 4\%of the estimated one trillion cells in the human brain and include non-neuronal cells and postmitotic neurons identified by the neuronspecific nuclear protein marker. In comparison, human interphase lymphocytes present chromosome 21 aneuploidy rates of 0.6\%. Together, these data demonstrate that human brain cells (both neurons and non-neuronal cells) can be aneuploid and that the resulting genetic mosaicism is a normal feature of the human CNS.},
	Author = {Rehen, Stevens K. and Yung, Yun C. and McCreight, Matthew P. and Kaushal, Dhruv and Yang, Amy H. and Almeida, Beatriz S. V. and Kingsbury, Marcy A. and Cabral, K{\'a}tia M. S. and McConnell, Michael J. and Anliker, Brigitte and Fontanoz, Marisa and Chun, Jerold},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {08 Aberrant cell cycle},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {9},
	Organization = {Helen L. Dorris Child and Adolescent Neuropsychiatric Disorder Institute, The Scripps Research Institute, La Jolla, California 92037, USA.},
	Pages = {2176-80},
	Pii = {25/9/2176},
	Pubmed = {15745943},
	Title = {Constitutional aneuploidy in the normal human brain},
	Uuid = {2707D202-1248-4214-A33E-7120D240FA04},
	Volume = {25},
	Year = {2005},
	url = {papers/Rehen_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4560-04.2005}}

@article{Rehen:2001,
	Abstract = {A basic assumption about the normal nervous system is that its neurons possess identical genomes. Here we present direct evidence for genomic variability, manifested as chromosomal aneuploidy, among developing and mature neurons. Analysis of mouse embryonic cerebral cortical neuroblasts in situ detected lagging chromosomes during mitosis, suggesting the normal generation of aneuploidy in these somatic cells. Spectral karyotype analysis identified approximately 33\%of neuroblasts as aneuploid. Most cells lacked one chromosome, whereas others showed hyperploidy, monosomy, and/or trisomy. The prevalence of aneuploidy was reduced by culturing cortical explants in medium containing fibroblast growth factor 2. Interphase fluorescence in situ hybridization on embryonic cortical cells supported the rate of aneuploidy observed by spectral karyotyping and detected aneuploidy in adult neurons. Our results demonstrate that genomes of developing and adult neurons can be different at the level of whole chromosomes. 0027-8424 Journal Article},
	Author = {Rehen, S. K. and McConnell, M. J. and Kaushal, D. and Kingsbury, M. A. and Yang, A. H. and Chun, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Mice, Inbred BALB C;In Situ Hybridization, Fluorescence;Interphase;Animals;*Variation (Genetics);Neurons/*ultrastructure;Female;EE pdf;*Chromosomes;08 Aberrant cell cycle;Male;Aneuploidy;Support, Non-U.S. Gov't;Cerebral Cortex/*ultrastructure;Karyotyping;Flow Cytometry;Support, U.S. Gov't, P.H.S.;Mice;Immunohistochemistry},
	Number = {23},
	Organization = {Department of Pharmacology, School of Medicine, University of California, San Diego, CA 92093-0636, USA.},
	Pages = {13361-6},
	Title = {Chromosomal variation in neurons of the developing and adult mammalian nervous system},
	Uuid = {03BA246E-ABCF-4510-B214-2D424CBE6101},
	Volume = {98},
	Year = {2001},
	url = {papers/Rehen_ProcNatlAcadSciUSA2001.pdf}}

@article{Reichert:2001,
	Abstract = {The removal of damaged myelin is central to repair after injury to axons and in autoimmune demyelinating diseases. Complement receptor 3 (CR3/MAC-1) plays a major role in mediating the phagocytosis of damaged myelin by macrophages and microglia. We studied the modulation (inhibition and augmentation) of CR3/MAC-1 mediated myelin phagocytosis by mAbs that bind to distinct epitopes of subunits alphaM and beta2 of CR3/MAC-1. mAb M1/70 anti-alpha(M) and mAb 5C6 anti-alpha(M) inhibited, whereas mAb M18/2 anti-beta2 augmented myelin phagocytosis. This mAb-induced modulation of myelin phagocytosis occurred in the presence and absence of active complement. Inhibition induced by M1/70 or 5C6 did not add when the two were combined. Combining M1/70 or 5C6 with M18/2 reduced the augmentation induced by M18/2 alone. CR3/MAC-1-mediated myelin phagocytosis may thus be subjected to modulation between efficient and inefficient functional/activation states. These observations and conclusions may offer an explanation for the observed discrepancy between efficient myelin phagocytosis in experimental allergic encephalomyelitis and inefficient myelin phagocytosis after injury to CNS axons, although in both instances macrophages/microglia express CR3/MAC-1.},
	Author = {Reichert, F. and Slobodov, U. and Makranz, C. and Rotshenker, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0969-9961},
	Journal = {Neurobiol Dis},
	Keywords = {Nerve Regeneration;Antibodies, Monoclonal;Macrophage-1 Antigen;Mice, Inbred C57BL;Myelin Sheath;Not relevant;Epitopes;11 Glia;Macrophages;Mice;Support, Non-U.S. Gov't;Phagocytosis;Male;Animals},
	Medline = {21337051},
	Month = {6},
	Nlm_Id = {9500169},
	Number = {3},
	Organization = {Department of Anatomy &Cell Biology, Hebrew University-Hadassah Medical School, Jerusalem, 91120, Israel.},
	Pages = {504-12},
	Pii = {S0969996101903833},
	Pubmed = {11442357},
	Title = {Modulation (inhibition and augmentation) of complement receptor-3-mediated myelin phagocytosis},
	Uuid = {467899AE-146E-42C7-B759-9DD7DA16AD47},
	Volume = {8},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/nbdi.2001.0383}}

@article{Reid:1997,
	Abstract = {Cell lineage analysis with retroviral libraries suggests that clonal progeny disperse widely in rodent cortex. To determine whether widespread dispersion is a general mammalian plan and to investigate phylogenetic differences in cortical development, we analyzed cell lineage in the ferret, a carnivore and near relative of the cat. The ferret possesses a highly developed, folded cerebral cortex, characteristic of higher mammalian species. Progenitor cells of the ferret cerebral cortex were tagged with an amphotropic retroviral library encoding alkaline phosphatase, and sibling relationships were determined using the polymerase chain reaction. Neuronal clones were single neurons (52\%) or large clones (48\%; average, 7 neurons) containing neurons and glia in widespread cortical locations. Neuronal clones in the ferret labeled at middle to late neurogenesis (embryonic day 33-35) contained large numbers of neurons and showed little tendency to cluster. The large proportion of single neuron clones, contrasted with the large size of multicell clones, suggests that some progenitors divide asymmetrically, producing a postmitotic neuron and regenerating a multipotential cell.},
	Author = {Reid, C. B. and Tavazoie, S. F. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {10 Development;Cell Differentiation;Embryonic Induction;Animals;Ferrets;Pregnancy;Phenotype;research support, u.s. gov't, p.h.s. ;Models, Biological;Female;Staining and Labeling;Retroviridae;Alkaline Phosphatase;research support, non-u.s. gov't ;Cerebral Cortex;Neurons;Polymerase Chain Reaction;Cell Division;24 Pubmed search results 2008;Stem Cells;Clone Cells;Gestational Age},
	Month = {6},
	Nlm_Id = {8701744},
	Number = {12},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115, USA.},
	Pages = {2441-50},
	Pubmed = {9199370},
	Title = {Clonal dispersion and evidence for asymmetric cell division in ferret cortex},
	Uuid = {4D2D807A-FABD-4C76-B2A1-4C78DE06034B},
	Volume = {124},
	Year = {1997},
	url = {papers/Reid_Development1997.pdf}}

@article{Reid:1999,
	Abstract = {To understand the clonal relationship of various olfactory bulb (OB) cell types, OB progenitor cells were infected at embryonic day (E) 14, E15, and E17 with retroviral libraries encoding alkaline phosphatase or beta-galactosidase. After survival to postnatal day 10-15, sibling relationships were identified by polymerase chain reaction DNA amplification of distinct sequences in the retroviral constructs. Within the OB, clonal progeny dispersed widely in all directions. In sharp contrast, however, clonal dispersion between the OB and neocortex was not observed, although occasional clonal dispersion between the OB and pyriform and hippocampal regions could not be excluded. Most clones (84\%) contained a single cell type, especially after E17 injections, suggesting the existence of either restricted precursors, or multipotential progenitors instructed by a restricted cellular environment. Mixed OB clones (16\%) contained multiple cell types in the OB, or occasionally glial or neuronal cells outside the OB, demonstrating the existence of multipotential OB progenitors, likely at a stage before formation of the olfactory rostral migratory stream. Surprisingly, OB glial cells were not labeled, suggesting distinct lineages or perhaps distinct migratory paths for glia and neurons into the OB. A hierarchical cell lineage is proposed that involves a multipotential progenitor that gives rise to potentially more limited progenitors.},
	Author = {Reid, C. B. and Liang, I. and Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Fetal Development/physiology;Neuroglia/cytology/physiology;Neurons/cytology/physiology;13 Olfactory bulb anatomy;Rats, Long-Evans;Rats;Cell Line;Prosencephalon/embryology;I pdf;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Olfactory Bulb/*embryology;Polymerase Chain Reaction;Embryo/cytology/physiology;Cell Movement/physiology},
	Number = {1},
	Organization = {Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {106-18.},
	Title = {Clonal mixing, clonal restriction, and specification of cell types in the developing rat olfactory bulb},
	Uuid = {C434B816-DC7A-4E08-8324-E03DC4E04626},
	Volume = {403},
	Year = {1999},
	url = {papers/Reid_JCompNeurol1999}}

@article{Reisman:1989,
	Abstract = {Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells. 0270-7306 Journal Article},
	Author = {Reisman, D. and Rotter, V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Mol Cell Biol},
	Keywords = {Cell Differentiation;RNA/analysis;Human;EE, DMSO, abstr;Cell Line;Gene Expression Regulation;Promoter Regions (Genetics);08 Aberrant cell cycle;Chloramphenicol O-Acetyltransferase/genetics;Moloney murine leukemia virus/*genetics;Dimethyl Sulfoxide/pharmacology;*Enhancer Elements (Genetics);Simian virus 40/genetics;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Granulocytes/*metabolism;Genetic Vectors},
	Number = {8},
	Organization = {Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.},
	Pages = {3571-5},
	Pubmed = {2477690},
	Title = {Induced expression from the Moloney murine leukemia virus long terminal repeat during differentiation of human myeloid cells is mediated through its transcriptional enhancer},
	Uuid = {60822156-EF26-4B76-AF5A-57815EEB760F},
	Volume = {9},
	Year = {1989},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2477690}}

@article{Reiss:2007,
	Abstract = {It has been hypothesized that phenotypic variation in mammals could in part be due to incomplete and variable silencing of retrotransposons in somatic cells. This theory is based on the fact that some recent endogenous retroviral (ERV) insertions in the mouse exert variable effects on genes in isogenic animals, depending on the variable state of ERV methylation. In this article, we review the evidence for this and related phenomena and suggest that such stochastic epigenetic silencing is restricted to very recent insertions. We also present a model to explain the acquisition of a more stable epigenetic state for transposable element insertions through time.},
	Author = {Reiss, Daphne and Mager, Dixie L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0378-1119},
	Journal = {Gene},
	Keywords = {DNA Methylation;Endogenous Retroviruses;Epigenesis, Genetic;research support, non-u.s. gov't;Retroelements;24 Pubmed search results 2008;Selection (Genetics);Stochastic Processes;Gene Silencing;Evolution, Molecular;Time Factors;Models, Genetic;Animals;Genomic Instability;Humans;review;Mice},
	Month = {4},
	Nlm_Id = {7706761},
	Number = {1-2},
	Organization = {Terry Fox Laboratory, BC Cancer Agency, 675 West 10th Avenue, Vancouver, British Columbia, Canada V5Z1L3.},
	Pages = {130-5},
	Pii = {S0378-1119(06)00504-X},
	Pubmed = {16987613},
	Title = {Stochastic epigenetic silencing of retrotransposons: does stability come with age?},
	Uuid = {9D089468-C51F-4CE8-A891-50E575AF7512},
	Volume = {390},
	Year = {2007},
	url = {papers/Reiss_Gene2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.gene.2006.07.032}}

@article{Reya:2001,
	Abstract = {Stem cell biology has come of age. Unequivocal proof that stem cells exist in the haematopoietic system has given way to the prospective isolation of several tissue-specific stem and progenitor cells, the initial delineation of their properties and expressed genetic programmes, and the beginnings of their utility in regenerative medicine. Perhaps the most important and useful property of stem cells is that of self-renewal. Through this property, striking parallels can be found between stem cells and cancer cells: tumours may often originate from the transformation of normal stem cells, similar signalling pathways may regulate self-renewal in stem cells and cancer cells, and cancer cells may include 'cancer stem cells'- rare cells with indefinite potential for self-renewal that drive tumorigenesis. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Reya, T. and Morrison, S. J. and Clarke, M. F. and Weissman, I. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Nature},
	Keywords = {Mutation;F abstr;10 Development;Cell Transformation, Neoplastic;Hematopoietic Stem Cells;Human;Leukemia/pathology;Signal Transduction;Cell Division;Regeneration;*Stem Cells;Neoplasms/*pathology;Animals},
	Number = {6859},
	Organization = {Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Palo Alto, California 94305, USA. irv\@stanford.edu},
	Pages = {105-11},
	Pubmed = {11689955},
	Title = {Stem cells, cancer, and cancer stem cells},
	Uuid = {8ECE38A0-C9CC-4CB3-830E-A47656F71300},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689955}}

@article{Reynolds:1992,
	Abstract = {Neurogenesis in the mammalian central nervous system is believed to end in the period just after birth; in the mouse striatum no new neurons are produced after the first few days after birth. In this study, cells isolated from the striatum of the adult mouse brain were induced to proliferate in vitro by epidermal growth factor. The proliferating cells initially expressed nestin, an intermediate filament found in neuroepithelial stem cells, and subsequently developed the morphology and antigenic properties of neurons and astrocytes. Newly generated cells with neuronal morphology were immunoreactive for gamma-aminobutyric acid and substance P, two neurotransmitters of the adult striatum in vivo. Thus, cells of the adult mouse striatum have the capacity to divide and differentiate into neurons and astrocytes. 92205351 0036-8075 Journal Article},
	Author = {Reynolds, B. A. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {Science},
	Keywords = {Glial Fibrillary Acidic Protein/metabolism;Culture Media, Serum-Free;In Vitro;Astrocytes/*cytology;Fluorescent Antibody Technique;B-2;Neurons/*cytology;Cell Survival/drug effects;Cells, Cultured;Intermediate Filaments/metabolism;Animal;02 Adult neurogenesis migration;Corpus Striatum/*cytology;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Intermediate Filament Proteins/metabolism;Mice;Phosphopyruvate Hydratase/metabolism;Cell Division/drug effects},
	Number = {5052},
	Organization = {Department of Pathology, University of Calgary Faculty of Medicine, Alberta, Canada.},
	Pages = {1707-10},
	Title = {Generation of neurons and astrocytes from isolated cells of the adult mammalian central nervous system},
	Uuid = {9B592C38-0B59-4B73-8852-43C4B205E3C3},
	Volume = {255},
	Year = {1992},
	url = {papers/Reynolds_Science1992.pdf}}

@article{Rezaie:1997,
	Author = {Rezaie, P. and Male, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0300-5127},
	Journal = {Biochem Soc Trans},
	Keywords = {Gestational Age;Intercellular Adhesion Molecule-1;Research Support, Non-U.S. Gov't;Fetus;Cell Adhesion Molecules;Vascular Cell Adhesion Molecule-1;Antigens, CD31;P-Selectin;Antigens, CD;11 Glia;Microglia;Macrophages;Cerebrovascular Circulation;Humans;Cerebral Cortex;Corpus Callosum},
	Medline = {97334547},
	Month = {5},
	Nlm_Id = {7506897},
	Number = {2},
	Organization = {Department of Neuropathology, Institute of Psychiatry, London.},
	Pages = {170S},
	Pubmed = {9191214},
	Title = {Expression of adhesion molecules on human foetal cerebral vessels: relationship to colonisation by microglial precursors},
	Uuid = {7C8DABEF-19CE-4217-9413-A373EEFB89E0},
	Volume = {25},
	Year = {1997}}

@article{Rezaie:2001,
	Abstract = {Alterations in the phenotype and function of microglia, the resident mononuclear phagocytes of the central nervous system, are among the earliest indications of pathology within the brain and spinal cord. The prion diseases, also known as spongiform encephalopathies, are fatal neurodegenerative disorders with sporadic, genetic or acquired infectious manifestations. A hallmark of all prion diseases is the aberrant metabolism and resulting accumulation of the prion protein. Conversion of the normal cellular protein [PrP(c)] into the abnormal pathogenic (or disease-causing) isoform [PrP(Sc)] involves a conformational alteration whereby the alpha-helical content is transformed into beta-sheet. The histological characteristics of these disorders are spongiform change, astrocytosis, neuronal loss and progressive accumulation of the protease-resistant prion isoform. An additional upregulation in microglial response has been reported in Kuru, Creutzfeldt-Jakob disease (CJD), Gerstmann-Str{\"a}ussler-Scheinker syndrome (GSS), scrapie, in transgenic murine models and in culture, where microglial activation often accompanies prion protein deposition and neuronal loss. This article will review the roles of microglia in spongiform encephalopathies.},
	Author = {Rezaie, P. and Lantos, P. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0165-0173},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {Research Support, Non-U.S. Gov't;Encephalitis;11 Glia;Microglia;review, tutorial;Animals;Humans;review;Prion Diseases},
	Medline = {21142106},
	Month = {3},
	Nlm_Id = {8908638},
	Number = {1},
	Organization = {Department of Neuropathology, Institute of Psychiatry, King's College London, DeCrespigny Park, SE5 8AF, London, UK. p.rezaie\@iop.kcl..ac.uk},
	Pages = {55-72},
	Pii = {S016501730100042X},
	Pubmed = {11245886},
	Title = {Microglia and the pathogenesis of spongiform encephalopathies},
	Uuid = {CCA46AF7-BFE3-445B-BB1F-ACA4D5976F29},
	Volume = {35},
	Year = {2001}}

@article{Rezaie:1997a,
	Abstract = {Microglia represent the primary immune effector cells of the adult central nervous system (CNS). The origin of these cells has been a subject of intense debate over the last century. However, immunohistochemical and chimera developmental studies in rodents support the hypothesis that microglia are monocytic in origin. There have been relatively few studies to date on microglia in human fetal development, and the mechanisms by which microglial precursors enter the developing CNS are as yet unknown. It is possible that microglial precursors use combinations of adhesion molecules on cerebral endothelium to gain entry into the developing CNS. In the present study, we have shown the distribution of microglia within human fetal cerebral cortex between 16 and 22 weeks of gestation using RCA-1 lectin histochemistry. We have also demonstrated dual anti-macrophage antibody labelling of these cells in conjunction with adhesion molecules ICAM-1, ICAM-2 and PECAM on cerebral endothelium throughout this period. We conclude that fetal microglia usually occur at highly vascularised sites within the developing human fetal brain and are more specifically associated with the expression of ICAM-2 on cerebral endothelium.},
	Author = {Rezaie, P. and Cairns, N. J. and Male, D. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0165-3806},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Endothelium, Vascular;Gestational Age;Research Support, Non-U.S. Gov't;Embryonic and Fetal Development;Comparative Study;Lectins;Immunohistochemistry;Biological Markers;11 Glia;Microglia;Macrophages;Histocytochemistry;Humans;Brain;Cell Adhesion Molecules, Neuronal},
	Medline = {98126196},
	Month = {12},
	Nlm_Id = {8908639},
	Number = {1-2},
	Organization = {Department of Neuropathology, Institute of Psychiatry, London, UK. spkadkm\@iop.bpmf.ac.uk},
	Pages = {175-89},
	Pubmed = {9466720},
	Title = {Expression of adhesion molecules on human fetal cerebral vessels: relationship to microglial colonisation during development},
	Uuid = {9D160946-E20F-41F3-85A0-ECDC4F5E872F},
	Volume = {104},
	Year = {1997}}

@article{Rezaie:1999,
	Abstract = {Microglia, the intrinsic macrophages of the nervous system, colonise the cerebrum around the second trimester in man. In order to determine the extent of microglial influx into the nervous system, we have examined their distribution within the human fetal spinal cord in relation to astrocytic and vascular development between 9 and 16 weeks of gestation, using conventional immunohistochemistry [CD11b; CD45; CD64; CD68; ICAM-1; ICAM-2; VCAM-1; PECAM; GFAP; vimentin] and lectin histochemistry [RCA-1]. Microglia are identifiable by 9 weeks, within the ventricular/sub-ventricular zones. Human fetal microglia display heterogeneity in phenotype and are more readily identified by CD68 in the spinal cord. There is a marked influx of cells dorsal and ventral to the neural cavity, from the marginal layer [meninges/connective tissue] with advancing gestational age, with greatest cell densities towards the end of the time period in this study. This inward migration is associated with progressive vascularisation, ICAM-2 expression and co-localises with GFAP and vimentin positive radial glia. The patterns of microglial migration in human fetal cord differ from that within the cerebrum, but generally conform to a route following white to gray matter.},
	Author = {Rezaie, P. and Patel, K. and Male, D. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0165-3806},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Gestational Age;Research Support, Non-U.S. Gov't;Fetus;Immunohistochemistry;Phenotype;11 Glia;Microglia;Spinal Cord;Humans},
	Medline = {99296479},
	Month = {6},
	Nlm_Id = {8908639},
	Number = {1},
	Organization = {Department of Neuropathology, Institute of Psychiatry, De Crespigny Park, London SE5 8JN, UK. p.rezaie\@iop.kcl.ac.uk},
	Pages = {71-81},
	Pii = {S0165380699000437},
	Pubmed = {10366704},
	Title = {Microglia in the human fetal spinal cord--patterns of distribution, morphology and phenotype},
	Uuid = {1509467B-ADDB-416C-9512-C8040B46C062},
	Volume = {115},
	Year = {1999}}

@article{Rezaie:2004,
	Abstract = {We have recently begun to gain a clearer understanding of the phasing and patterns of colonization of the developing human brain by microglia. In this study we investigated the distribution, morphology and phenotype of microglia specifically within the wall of the human telencephalon from 12 to 24 gestational weeks (gw), a period that corresponds to the development of thalamocortical fibres passing through the transient subplate region of the developing cerebral wall. Sections from a total of 45 human fetal brains were immunoreacted to detect CD68 and MHC class II antigens and histochemically reacted with RCA-1 and tomato lectins. These markers were differentially expressed by anatomically discrete populations of microglia in the cerebral wall: two cell populations were noted during the initial phase of colonization (12-14 gw): (i) CD68++ RCA-1+ MHC II- amoeboid cells aligned within the subplate, and (ii) RCA-1++ CD68- MHC II- progenitors in the marginal layer and lower cortical plate that progressively ramified within the subplate, without seemingly passing through an 'amoeboid' state. At this stage microglia were largely absent from the germinal layers and the intermediate zone. From 14 to 15 gw, however, MHC class II positive cells were also detected within germinal layers and in the corpus callosum, and these cells, which coexpressed CD68 antigen (a marker associated with phagocytosis), further populated the lower half of the telencephalon from 18 to 24 gw. These findings are discussed in relation to developmental events that take place during the second trimester within the wall of the telencephalon.},
	Author = {Rezaie, and Dean, and Male, and Ulfig,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {11 Glia},
	Nlm_Id = {9110718},
	Organization = {Department of Biological Sciences, Faculty of Science, The Open University, Walton Hall, Milton Keynes, MK7 6AA, UK; Department of Neuropathology, Institute of Psychiatry, King's College London, DeCrespigny Park, London SE5 8AF, UK.},
	Pii = {bhh194},
	Pubmed = {15483047},
	Title = {Microglia in the Cerebral Wall of the Human Telencephalon at Second Trimester},
	Uuid = {E4FA846C-D0FE-4933-966D-F24F3BBC692D},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhh194}}

@article{Rezaie:2002,
	Abstract = {Microglia are mononuclear phagocytes of the central nervous system and are considered to derive from circulating bone marrow progenitors that colonize the developing human nervous system in the second trimester. They first appear as ameboid forms and progressively differentiate to process-bearing "ramified" forms with maturation. Signals driving this transformation are known to be partly derived from astrocytes. In this investigation we have used cocultures of astrocytes and microglia to demonstrate the relationship between motility and morphology of microglia associated with signals derived from astrocytes. Analysis of progressive cultures using time-lapse video microscopy clearly demonstrates the dynamic nature of microglia. We observe that ameboid microglial cells progressively ramify when cocultured with astrocytes, mirroring the "differentiation" of microglia in situ during development. We further demonstrate that individual cells undergo morphological transformations from "ramified" to "bipolar" to "tripolar" and "ameboid" states in accordance with local environmental cues associated with astrocytes in subconfluent cultures. Remarkably, cells are still capable of migration at velocities of 20-35 microm/h in a fully ramified state overlying confluent astrocytes, as determined by image analysis of motility. This is in keeping with the capacity of microglia for a rapid response to inflammatory cues in the CNS. We also demonstrate selective expression of the chemokines MIP-1alpha and MCP-1 by confluent human fetal astrocytes in cocultures and propose a role for these chemotactic cytokines as regulators of microglial motility and differentiation. The interchangeable morphological continuum of microglia supports the view that these cells represent a single heterogeneous population of resident mononuclear phagocytes capable of marked plasticity.},
	Author = {Rezaie, P. and Trillo-Pazos, G. and Greenwood, J. and Everall, I. P. and Male, D. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0014-4827},
	Journal = {Exp Cell Res},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;Image Processing, Computer-Assisted;Fetus;Cell Communication;Macrophage Inflammatory Protein-1;Astrocytes;Stem Cells;Coculture Techniques;Microscopy, Video;11 Glia;Microglia;Chemokines;Humans;Monocyte Chemoattractant Protein-1;Cell Movement;Brain},
	Medline = {21846026},
	Month = {3},
	Nlm_Id = {0373226},
	Number = {1},
	Organization = {Department of Neuropathology, Institute of Psychiatry, King's College London, DeCrespigny Park, London, SE5 8AF, United Kingdom. p.rezaie\@iop.kcl.ac.uk},
	Pages = {68-82},
	Pii = {S001448270195431X},
	Pubmed = {11855858},
	Title = {Motility and ramification of human fetal microglia in culture: an investigation using time-lapse video microscopy and image analysis},
	Uuid = {A15F1383-C756-42F8-8289-1E95910FC703},
	Volume = {274},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/excr.2001.5431}}

@article{Rezaie:2002a,
	Abstract = {Chemokines play specific roles in directing the recruitment of leukocyte subsets into inflammatory foci within the central nervous system (CNS). The involvement of these cytokines as mediators of inflammation is widely accepted. Recently, it has become evident that cells of the CNS (astrocytes, microglia, and neurons) not only synthesize, but also respond functionally or chemotactically to chemokines. We previously reported developmental events associated with colonization of the human fetal CNS by mononuclear phagocytes (microglial precursors), which essentially takes place within the first two trimesters of life. As part of the array of signals driving colonization, we noted specific anatomical distribution of chemokines and chemokine receptors expressed during this period. In order to further characterize expression of these molecules, we have isolated and cultured material from human fetal CNS. We demonstrate that unstimulated subconfluent human fetal glial cultures express high levels of CCR2 and CXCR4 receptors in cytoplasmic vesicles. Type I astrocytes, and associated ameboid microglia in particular, express high levels of surface and cytoplasmic CXCR4. Of the chemokines tested (MIP-1alpha, MIP-1beta, MCP-1, MCP-3, RANTES, SDF-1, IL-8, IP-10), only MIP-1alpha, detected specifically on microglia, was expressed both constitutively and consistently. Low variable levels of MCP-1, MIP-1alpha, and RANTES were also noted in unstimulated glial cultures. Recombinant human chemokines rhMCP-1 and rhMIP-1alpha also displayed proliferative effects on glial cultures at [10 ng/ml], but displayed variable effects on CCR2 levels on these cells. rhMCP-1 specifically upregulated CCR2 expression on cultured glia at [50 ng/ml]. It is gradually becoming evident that chemokines are important in embryonic development. The observation that human fetal glial cells and their progenitors express specific receptors for chemokines and can be stimulated to produce MCP-1, as well as proliferate in response to chemokines, supports a role for these cytokines as regulatory factors during development.},
	Author = {Rezaie, P. and Trillo-Pazos, G. and Everall, I. P. and Male, D. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Fetus;Receptors, CXCR4;Astrocytes;Cells, Cultured;Humans;Recombinant Proteins;Microglia;Lipopolysaccharides;Cell Movement;11 Glia;Chemokines, CC;Receptors, Chemokine;Macrophage Inflammatory Protein-1;Cell Division;Central Nervous System;Monocyte Chemoattractant Protein-1;Immunohistochemistry;Colony-Stimulating Factors;Research Support, Non-U.S. Gov't},
	Medline = {21610744},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Department of Neuropathology, Institute of Psychiatry, King's College London, London, UK. p.rezaie\@iop.kcl.ac.uk},
	Pages = {64-75},
	Pii = {10.1002/glia.1128},
	Pubmed = {11746784},
	Title = {Expression of beta-chemokines and chemokine receptors in human fetal astrocyte and microglial co-cultures: potential role of chemokines in the developing CNS},
	Uuid = {7AD40F64-0799-4088-B9B7-DC9284F03023},
	Volume = {37},
	Year = {2002}}

@article{Rezaie:2002b,
	Abstract = {More than a century and a half has elapsed since the first accounts of mesodermal phagocytic elements were proposed within the central nervous system. Over the intervening decades, body and substance were added to this concept through the advancement of histological techniques at the disposal of the researcher and the acute and keen-minded skills of the pathologist. Notable among these pioneering efforts were the contributions of W. Ford Robertson, Santiago Ramon y Cajal, Pio del Rio-Hortega and Wilder Penfield amongst an entire cavalcade of other noteworthy figures. The term 'mesoglia' and 'third element of the nervous system' was bestowed upon these cells towards the beginning of the twentieth century to account for their separate origins from neurons and macroglia. It was later amended by del Rio-Hortega in 1919, to 'microglia' in order to further discriminate between true mesodermal elements and oligodendrocytes, previously regarded as a component of 'mesoglia'. This particular contention sparked much controversy among del Rio-Hortega's peers and resulted in an escalation of fruitful research throughout Europe that eventually declined up to the outbreak of the Second World War. The post-war years were a period of the 'dark ages' that cast doubt on the very existence and nature of microglia, until the 'renaissance' of research was once again rejuvenated in the 1960s, by a new cohort of intrigued minds: Cammermeyer, Blinzinger, Kreutzberg and others who saw in the 'third element' the potential that is now commonly ascribed to microglia: the intrinsic immune effector cells of the CNS. It is now universally accepted that microglia are involved as the first line of rapid defence in any pathology of the nervous system, and as such, present a diagnostic tool for the neuropathologist. Although our knowledge of microglia stems from an extensive body of work conducted over the last two decades, much of the earlier work (pre-1960s) has remained somewhat obscure. This is partly accountable due to the limited availability of translated works, and additionally to the lack of a compendium of these articles. This paper will present a comprehensive overview of the pioneering research on mononuclear phagocytes within the central nervous system, which has direct bearing on our present-day understanding of the concept of microglia.},
	Author = {Rezaie, Payam and Male, David},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0964-704X},
	Journal = {J Hist Neurosci},
	Keywords = {History, 19th Century;Monocytes;Ectoderm;Neuroglia;Central Nervous System;History, 20th Century;Neurosciences;historical article;11 Glia;Microglia;Mesoderm;Animals;Humans;Phagocytosis},
	Medline = {22445846},
	Month = {12},
	Nlm_Id = {9441330},
	Number = {4},
	Organization = {Department of Neuropathology, Institute of Psychiatry, SE5 8AF, UK. p.rezaie\@iop.kc1.ac.uk},
	Pages = {325-74},
	Pubmed = {12557654},
	Title = {Mesoglia &microglia--a historical review of the concept of mononuclear phagocytes within the central nervous system},
	Uuid = {01EA53A6-3A0D-437E-A69F-A3FBB626BCEB},
	Volume = {11},
	Year = {2002}}

@article{Rezaie:1999a,
	Abstract = {Microglia are the immune effector cells of the nervous system. The prevailing view is that microglia are derived from circulating precursors in the blood, which originate from the bone-marrow. Colonisation of the central nervous system (CNS) by microglia is an orchestrated response during human fetal development related to the maturation of the nervous system. It coincides with vascularisation, formation of radial glia, neuronal migration and myelination primarily in the 4th-5th months and beyond. Microglial influx generally conforms to a route following white matter tracts to gray areas. We have observed that colonisation of the spinal cord begins around 9 weeks, with the major influx and distribution of microglia commencing around 16 weeks. In the cerebrum, colonisation is in progress during the second trimester, and ramified microglial forms are widely distributed within the intermediate zone by the first half of intra-uterine life (20-22 weeks). A distinct pattern of migration occurs along radial glia, white matter tracts and vasculature. The distribution of these cells is likely to be co-ordinated by spatially and temporally regulated, anatomical expression of chemokines including RANTES and MCP-1 in the cortex; by ICAM-2 and PECAM on radiating cerebral vessels and on capillaries within the germinal layer, and apoptotic cell death overlying this region. The phenotype and functional characteristics of fetal microglia are also outlined in this review. The need for specific cellular interactions and targeting is greater within the central nervous system than in other tissues. In this respect, microglia may additionally contribute towards CNS histogenesis.},
	Author = {Rezaie, P. and Male, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {1059-910X},
	Journal = {Microsc Res Tech},
	Keywords = {Research Support, Non-U.S. Gov't;Embryonic and Fetal Development;Cytokines;Phenotype;Colony-Forming Units Assay;Microglia;Spinal Cord;11 Glia;Humans;Brain;Cell Movement;review},
	Medline = {99330517},
	Month = {6},
	Nlm_Id = {9203012},
	Number = {6},
	Organization = {Department of Neuropathology, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, United Kingdom. p.rezaie\@iop.kcl.ac.uk},
	Pages = {359-82},
	Pii = {10.1002/(SICI)1097-0029(19990615)45:6<359::AID-JEMT4>3.0.CO;2-D},
	Pubmed = {10402264},
	Title = {Colonisation of the developing human brain and spinal cord by microglia: a review},
	Uuid = {3695183E-35AB-4F0D-9A94-BDEF23E65DA5},
	Volume = {45},
	Year = {1999}}

@article{Rezaie:2002c,
	Abstract = {Periventricular leukomalacia (PVL) occurring in premature infants, represents a major precursor for neurological and intellectual impairment, and cerebral palsy in later life. The disorder is characterized by multifocal areas of necrosis found deep in the cortical white matter, which are often symmetrical and occur adjacent to the lateral ventricles. There is no known cure for PVL. Factors predisposing to PVL include birth trauma, asphyxia and respiratory failure, cardiopulmonary defects, premature birth/low birthweight, associated immature cerebrovascular development and lack of appropriate autoregulation of cerebral blood flow in response to hypoxic-ischemic insults. The intrinsic vulnerability of oligodendrocyte precursors is considered as central to the pathogenesis of PVL. These cells are susceptible to a variety of injurious stimuli including free radicals and excitotoxicity induced by hypoxic-ischemic injury (resulting from cerebral hypoperfusion), lack of trophic stimuli, as well as secondary associated events involving microglial and astrocytic activation and the release of pro-inflammatory cytokines TNF-alpha and IL-6. It is yet unclear whether activated astrocytes and microglia act as principal participants in the development of PVL lesions, or whether they are representatives of an incidental pathological response directed towards repair of tissue injury in PVL. Nevertheless, the accumulated evidence points to a pathological contribution of microglia towards damage. The topography of lesions in PVL most likely reflects a combination of the relatively immature cerebrovasculature together with a failure in perfusion and/or hypoxia during the greatest period of vulnerability occurring around mid-to-late gestation. Mechanisms underlying the pathogenesis of PVL have so far been related to prenatal ischemic injury to the brain initiated within the third trimester, which result in global cognitive and developmental delay and motor disturbances. Over the past few years, several epidemiological and experimental studies have implicated intrauterine infection and chorioamnionitis as causative in the pathogenesis of PVL. In particular, recent investigations have shown that inflammatory responses in the fetus and neonate can contribute towards neonatal brain injury and development-related disabilities including cerebral palsy. This review presents current concepts on the pathogenesis of PVL and emphasizes the increasing evidence for an inflammatory pathogenic component to this disorder, either resulting from hypoxic-ischemic injury or from infection. These findings provide the basis for clinical approaches targeted at protecting the premature brain from inflammatory damage, which may prove beneficial for treating PVL, if identified early in pathogenesis.},
	Author = {Rezaie, Payam and Dean, Andrew},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0919-6544},
	Journal = {Neuropathology},
	Keywords = {Leukomalacia, Periventricular;11 Glia;review, tutorial;Humans;Brain;Infant, Newborn;review},
	Medline = {22303200},
	Month = {9},
	Nlm_Id = {9606526},
	Number = {3},
	Organization = {Department of Neuropathology, Institute of Psychiatry, King's College London, UK. p.rezaie\@iop.kcl.ac.uk},
	Pages = {106-32},
	Pubmed = {12416551},
	Title = {Periventricular leukomalacia, inflammation and white matter lesions within the developing nervous system},
	Uuid = {07489C42-5780-4070-8BF0-3CF4893825E5},
	Volume = {22},
	Year = {2002}}

@article{Ricard:2001,
	Abstract = {The Unc-33-like phosphoprotein/collapsin response mediator protein (Ulip/CRMP) family consists of four homologous phosphoproteins considered crucial for brain development. Autoantibodies produced against member(s) of this family by patients with paraneoplastic neurological diseases have made it possible to clone a fifth human Ulip/CRMP and characterize its cellular and anatomical distribution in developing brain. This protein, referred to as Ulip6/CRMP5, is highly expressed during rat brain development in postmitotic neural precursors and in the fasciculi of fibers, suggesting its involvement in neuronal migration/differentiation and axonal growth. In the adult, Ulip6/CRMP5 is still expressed in some neurons, namely in areas that retain neurogenesis and in oligodendrocytes in the midbrain, hindbrain, and spinal cord. Ulip2/CRMP2 and Ulip6/CRMP5 are coexpressed in postmitotic neural precursors at certain times during development and in oligodendrocytes in the adult. Because Ulip2/CRMP2 has been reported to mediate semaphorin-3A (Sema3A) signal in developing neurons, in studies to understand the function of Ulip6/CRMP5 and Ulip2/CRMP2 in the adult, purified adult rat brain oligodendrocytes were cultured in a Sema3A- conditioned medium. Oligodendrocytes were found to have Sema3A binding sites and to express neuropilin-1, the major Sema3A receptor component. In the presence of Sema3A, these oligodendrocytes displayed a dramatic reduction in process extension, which was reversed by removal of Sema3A and prevented by anti-neuropilin-1, anti-Ulip6/CRMP5, anti-Ulip2/CRMP2 antibodies, or VEGF-165, another neuropilin-1 ligand. These results indicate the existence in the adult brain of a Sema3A signaling pathway that modulates oligodendrocyte process extension mediated by neuropilin- 1, Ulip6/CRMP5, and Ulip2/CRMP2, and they open new fields of investigation of neuron/oligodendrocyte interactions in the normal and pathological brain.},
	Author = {Ricard, D. and Rogemond, V. and Charrier, E. and Aguera, M. and Bagnard, D. and Belin, M. F. and Thomasset, N. and Honnorat, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {18},
	Organization = {Institut National de la Sante et de la Recherche Medicale U 433, Institut Federatif des Neurosciences de Lyon, Hopital Neurologique, 69003 Lyon, France.},
	Pages = {7203-14.},
	Title = {Isolation and expression pattern of human unc-33-like phosphoprotein 6/collapsin response mediator protein 5 (ulip6/crmp5): coexistence with ulip2/crmp2 in sema3a- sensitive oligodendrocytes},
	Uuid = {B7DE1AE7-BF49-4784-93D6-2E67481900AC},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11549731%20http://www.jneurosci.org/cgi/content/full/21/18/7203%20http://www.jneurosci.org/cgi/content/abstract/21/18/7203}}

@article{Rickmann:1987,
	Abstract = {The temporal and spatial patterns of development of radial glial processes in the rat dentate gyrus have been studied in immunohistochemical preparations stained for the presence of either the glial fibrillary acidic protein (GFAP) or the vimentin-associated antigen R4. Additional electron microscopic (EM) observations were made from material prepared either immunohistochemically or by the Golgi method. R4 immunoreactive radial fibers were observed in the incipient dentate gyrus as early as E13 and by E14 the density of stained fibers was clearly higher in the anlage of the dentate gyrus than in the adjacent hippocampus. By E15 it was possible to identify in the EM the endfeet of radial glial cells that contained numerous glycogen particles. GFAP-positive radial processes were first observed on E17; these processes tended to be of larger diameter than those stained with the R4 antibody, suggesting that they were among the more mature processes. The orientation of both the R4- and GFAP-positive glial processes changed throughout the last week of embryonic life and by the end of the first postnatal week they formed a complex meshwork of intertwined processes. The distribution of their cell bodies also changed with time; initially their perikarya were located in the neuroepithelium at the lateral margin of the hippocampal primordium; later they were found mainly beneath the granule cell layer. Dividing cells that contained GFAP were observed along the trajectory of the migrating granule cell precursors and in the hilus of the dentate gyrus; at later stages some GFAP-positive mitotic figures were seen within and immediately below the granule cell layer. On the basis of these observations, we have attempted to reconstruct the role that radial glial processes play in the morphogenesis of the dentate gyrus. First, radial processes extend from the neuroepithelium to the pial surface prior to the migration of neurons that will form the dentate gyrus. These early generated glia appear to form the boundaries of the developing dentate gyrus and provide an internal lattice that may guide the initial wave of migrating progenitor cells. As the dentate gyrus enlarges, these early formed processes maintain their contacts along the hippocampal fissure and along the pial surface of the dentate anlage. Thus, with time they become increasingly distorted and are ultimately compressed into two bundles; one lies deep to the hippocampal fissure parallel to the granule cell layer and the other is located at the fimbriodentate juncture.(ABSTRACT TRUNCATED AT 400 WORDS)},
	Author = {Rickmann, M. and Amaral, D. G. and Cowan, W. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Embryo;Neuroglia;Research Support, Non-U.S. Gov't;Hippocampus;Rats;Research Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Cell Division;Animals, Newborn;Animals;Rats, Inbred Strains},
	Medline = {88059849},
	Month = {10},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {Developmental Neurobiology Laboratory, Salk Institute for Biological Studies, San Diego, California 92138.},
	Pages = {449-79},
	Pubmed = {3680638},
	Title = {Organization of radial glial cells during the development of the rat dentate gyrus},
	Uuid = {2C5E7838-690C-11DA-A4B6-000D9346EC2A},
	Volume = {264},
	Year = {1987},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.902640403}}

@article{Riederer:1990,
	Abstract = {MAP5, a microtubule-associated protein characteristic of differentiating neurons, was studied in the developing visual cortex and corpus callosum of the cat. In juvenile cortical tissue, during the first month after birth, MAP5 is present as a protein doublet of molecular weights of 320 and 300 kDa, defined as MAP5a and MAP5b, respectively. MAP5a is the phosphorylated form. MAP5a decreases two weeks after birth and is no longer detectable at the beginning of the second postnatal month; MAP5b also decreases after the second postnatal week but more slowly and it is still present in the adult. In the corpus callosum only MAP5a is present between birth and the end of the first postnatal month. Afterwards only MAP5b is present but decreases in concentration more than 3-fold towards adulthood. Our immunocytochemical studies show MAP5 in somata, dendrites and axonal processes of cortical neurons. In adult tissue it is very prominent in pyramidal cells of layer V. In the corpus callosum MAP5 is present in axons at all ages. There is strong evidence that MAP5a is located in axons while MAP5b seems restricted to somata and dendrites until P28, but is found in callosal axons from P39 onwards. Biochemical experiments indicate that the state of phosphorylation of MAP5 influences its association with structural components. After high speed centrifugation of early postnatal brain tissue, MAP5a remains with pellet fractions while most MAP5b is soluble. In conclusion, phosphorylation of MAP5 may regulate (1) its intracellular distribution within axons and dendrites, and (2) its ability to interact with other subcellular components.},
	Author = {Riederer, B. M. and Guadano-Ferraz, A. and Innocenti, G. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0165-3806},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Aging;Cerebral Cortex;Phosphorylation;Organ Specificity;Cats;Immunohistochemistry;Not relevant;11 Glia;Subcellular Fractions;Animals, Newborn;Support, Non-U.S. Gov't;Microtubule-Associated Proteins;Molecular Weight;Animals;Corpus Callosum},
	Medline = {91084995},
	Month = {11},
	Nlm_Id = {8908639},
	Number = {2},
	Organization = {Institute of Anatomy, University of Lausanne, Switzerland.},
	Pages = {235-43},
	Pubmed = {2261685},
	Title = {Difference in distribution of microtubule-associated proteins 5a and 5b during the development of cerebral cortex and corpus callosum in cats: dependence on phosphorylation},
	Uuid = {FFEAD651-B423-4663-B573-8136D9BBED37},
	Volume = {56},
	Year = {1990}}

@article{Rieske:1989,
	Abstract = {In order to study microglial cells and microglia-derived brain macrophages in vitro, a method has been developed which allows the transfer of mitotic microglial cells from adult rat brain into tissue culture. The studies were performed on facial motor nuclei which were explanted after axotomy of the facial nerve. Outgrowing cells were identified and characterized by (i) morphological criteria using light and electron microscopy, (ii) in vivo [3H]thymidine labeling combined with subsequent in vitro autoradiography, (iii) immunocytochemistry for vimentin, GFAP, Fc and complement receptors, MHC antigens, laminin, fibronectin, factor VIII related- and 04 antigen as well as lectin histochemistry, and (iv) functional in vitro tests. In addition, a microglial cell line was established from proliferating cells. The results indicate that perineuronal microglia rather than astrocytes, perivascular cells, oligodendrocytes or endothelial cells may become phagocytic after having been activated by axotomy in situ.},
	Author = {Rieske, E. and Graeber, M. B. and Tetzlaff, W. and Czlonkowska, A. and Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Thymidine;Neuroglia;Facial Nerve;Rats;Get paper from library;Time Factors;Not relevant;11 Glia;Cell Division;Macrophages;Male;Animals;Rats, Inbred Strains;Cells, Cultured;Phagocytosis},
	Medline = {89323793},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, F.R.G.},
	Pages = {1-14},
	Pubmed = {2752292},
	Title = {Microglia and microglia-derived brain macrophages in culture: generation from axotomized rat facial nuclei, identification and characterization in vitro},
	Uuid = {12ADF646-750D-4424-8710-603508706DC9},
	Volume = {492},
	Year = {1989}}

@article{Rietze:2000,
	Abstract = {Previous studies of the adult hippocampus of rodents and primates have reported neuro- and gliogenesis restricted to the region of the dentate gyrus. In the present study, by employing a prolonged bromodeoxyuridine (BrdU) labeling protocol that attempts to account for cytokinetic changes as an animal ages, we have identified mitotically active cells in multiple regions of the hippocampus, especially in Ammon's horn, of the adult mouse. Immediately following the labeling period, the BrdU- labeled cells did not express known markers for neurons and astrocytes. Subsequent analysis at 3-24 weeks after labeling demonstrated BrdU- labeled neurons and glia in these regions of the hippocampus. Although neuro- and gliogenesis in the adult mammalian hippocampus have been reported previously, these results demonstrate that the phenomenon is not limited to the region of the dentate gyrus, but rather extends into Ammon's horn. Furthermore, it suggests that ongoing cell production, albeit discrete and limited in nature, may be widespread in the adult mammalian central nervous system.},
	Author = {Rietze, R. and Poulin, P. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Hippocampus/cytology/*growth &development/metabolism;BB both;Neurons/cytology/*metabolism;Thymidine;Cell Count;02 Adult neurogenesis migration;Animal;Time Factors;Male;Astrocytes/cytology/*metabolism;03 Adult neurogenesis progenitor source;Stem Cells/cytology/*metabolism;Mice, Inbred Strains;Support, Non-U.S. Gov't;Tritium/diagnostic use;Mitosis/*physiology;Age Factors;Cell Differentiation/physiology;Mice/anatomy &histology/*growth &development/metabolism;Bromodeoxyuridine},
	Number = {3},
	Organization = {Genes &Development Research Group, Department of Cell Biology and Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta T2N 4N1, Canada.},
	Pages = {397-408.},
	Title = {Mitotically active cells that generate neurons and astrocytes are present in multiple regions of the adult mouse hippocampus},
	Uuid = {40B78F7E-FF83-46D2-A871-8FDB53BCEFFB},
	Volume = {424},
	Year = {2000},
	url = {papers/Rietze_JCompNeurol2000}}

@article{Rietze:2001,
	Abstract = {The adult mammalian central nervous system (CNS) contains a population of neural stem cells (NSCs) with properties said to include the generation of non-neural progeny. However, the precise identity, location and potential of the NSC in situ remain unclear. We purified NSCs from the adult mouse brain by flow cytometry, and directly examined the cells'properties. Here we show that one type of NSC, which expresses the protein nestin but only low levels of PNA-binding and HSA proteins, is found in both ependymal and subventricular zones and accounts for about 63\%of the total NSC activity. Furthermore, the selective depletion of the population of this stem cell in querkopf mutant mice (which are deficient in production of olfactory neurons) suggests that it acts as a major functional stem cell in vivo. Most freshly isolated NSCs, when co-cultured with a muscle cell line, rapidly differentiated in vitro into myocytes that contain myosin heavy chain (MyHC). This demonstrates that a predominant, functional type of stem cell exists in the periventricular region of the adult brain with the intrinsic ability to generate neural and non-neural cells.},
	Author = {Rietze, R. L. and Valcanis, H. and Brooker, G. F. and Thomas, T. and Voss, A. K. and Bartlett, P. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Nature},
	Keywords = {02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;BB},
	Number = {6848},
	Organization = {The Walter and Eliza Hall Institute of Medical Research, Royal Parade, Parkville, Victoria 3050, Australia.},
	Pages = {736-9.},
	Title = {Purification of a pluripotent neural stem cell from the adult mouse brain},
	Uuid = {38CFF028-17BF-4841-A6E6-CFAE0B1D38A6},
	Volume = {412},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11507641}}

@article{Rinaman:1991,
	Abstract = {When the neural tracer Fluoro-Gold is used to retrogradely label a population of axotomized neurons, cellular labeling can persist in the axotomized nucleus even when Nissl staining indicates that the injured neurons have degenerated. In order to determine the identity of the labeled cells that remain, this study combines retrograde transport of Fluoro-Gold with immunocytochemical methods for identification of specific non-neuronal cell types following peripheral axotomy and Fluoro-Gold labeling of motoneurons in the dorsal motor nucleus of the vagus in neonatal and adult rats. Fourteen days following cervical vagotomy in neonatal rats, Nissl staining revealed a virtually complete loss of vagal motoneurons. Fourteen days after cervical vagotomy in adult rats, vagal motoneuronal loss was not yet extensive but chromatolysis had clearly begun. Injection of Fluoro-Gold into the vagus nerve just prior to the vagotomy led to Fluoro-Gold labeling of remaining vagal motoneurons. In addition, many other small, brightly labeled cells were present in the lesioned vagal nuclei of all rats. Immunofluorescent identification of astrocytes with anti-glial fibrillary acidic protein and microglia and macrophages with OX42 (anti-C3bi complement receptor) and ED1 (anti-monocyte/macrophage cytoplasmic antigen) demonstrated that the small, bright Fluoro-Gold-labeled cells were non-neuronal, non-astrocytic phagocytes, including microglia. These results indicate that phagocytic microglia and other macrophages sequester Fluoro-Gold in the axotomized dorsal motor nucleus of the vagus of neonatal and adult rats, leading to persistence of fluorescent cellular labeling following the loss of retrogradely labeled axotomized neurons.},
	Author = {Rinaman, L. and Milligan, C. E. and Levitt, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Fluorescent Dyes;Phagocytosis;Nerve Degeneration;Vagotomy;Animals;Macrophages;Rats;Comparative Study;Female;Vagus Nerve;Rats, Inbred Strains;Not relevant;11 Glia;Stilbamidines;Axonal Transport;Animals, Newborn;Neuroglia;Age Factors;Motor Neurons;Support, U.S. Gov't, P.H.S.;Biological Markers},
	Medline = {92093168},
	Nlm_Id = {7605074},
	Number = {3},
	Organization = {Medical College of Pennsylvania, Department of Anatomy and Neurobiology, Philadelphia 19129.},
	Pages = {765-76},
	Pubmed = {1721690},
	Title = {Persistence of fluoro-gold following degeneration of labeled motoneurons is due to phagocytosis by microglia and macrophages},
	Uuid = {D78E67C7-5B66-424E-B6A7-E26B97F3F70B},
	Volume = {44},
	Year = {1991}}

@article{Ringheim:1995,
	Abstract = {Interleukin-3 (IL-3), interleukin-5 (IL-5), and granulocyte macrophage-colony stimulating factor (GM-CSF) are cytokines that bind to receptor complexes comprised of unique alpha-receptor subunits specific for each ligand and a commonly shared beta-receptor subunit. Previous studies have shown that IL-3 and GM-CSF induce mitosis in microglia and macrophage cells, indicating the functional presence of their cognate receptors. In this study, it is shown that the third member of this cytokine group, IL-5, also serves as a microglia mitogen. Proliferative effects were seen in culture on both murine microglia and a murine macrophage cell line, RAW 264.7. Since IL-5 is known to be secreted by both microglia and astrocytes in response to inflammatory stimuli, these results indicate that IL-5 may be involved in the cytokine-immune cascades leading to microglia proliferation in areas affected by disease and tissue damage.},
	Author = {Ringheim, G. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Tumor Necrosis Factor;Interleukins;Interleukin-5;Mitogens;Granulocyte-Macrophage Colony-Stimulating Factor;Cell Division;11 Glia;Microglia;Animals, Newborn;Mice;Animals;Cerebral Cortex;Bromodeoxyuridine;Endotoxins},
	Medline = {96274817},
	Month = {12},
	Nlm_Id = {7600130},
	Number = {2},
	Organization = {Neuroscience Therapeutic Domain, Hoechst-Roussel Pharmaceuticals, Inc., Somerville, NJ 08876, USA.},
	Pages = {131-4},
	Pii = {0304394095121536},
	Pubmed = {8848235},
	Title = {Mitogenic effects of interleukin-5 on microglia},
	Uuid = {DF39CAAC-E779-4BCE-B61B-3BA7BEB63732},
	Volume = {201},
	Year = {1995}}

@article{Riolobos:2001,
	Abstract = {The long-term effect of transplanting embryonic frontal cortex into a unilateral frontal cortex lesion has been studied in adult rats. Before surgery, activity in an open field, muscular strength of both forelimbs, and performance in a paw-reaching-for-food task were scored in 26 rats. In 21 animals a unilateral cortex lesion was then made in the forelimb motor area of the hemisphere contralateral to the preferred paw in the paw-reaching-for-food task, while the other 5 animals were sham-operated. On retesting, the lesion animals changed the preferred paw. A solid homotopic transplant of embryonic tissue (embryonic day 17) was then placed in the lesion cavity in 11 of the lesion rats. Three months later neither lesion alone nor lesion plus transplantation affected open field behavior and muscular strength, but the lesion permanently affected performance in the paw-reaching-for-food task, as shown by a change of preferred paw and a functional deficit in the paw contralateral to the lesion. Transplantation ameliorated the deficits caused by the lesion, but this was only evident when animals were forced to reach with the paw contralateral to the lesion plus transplant. The behavioral results were independent of the size of the lesion and graft. Connections between graft and host tissue were studied by means of the fluorescent tracer 1,1'-dioctadecyl-3,3,3'3'-tetramethylindocarbocyanine perchlorate (DiI). A dense array of labeled fibers was found in the host cortex adjacent to the transplant. The results suggest that functional recovery depends on grafting but is only evident when the animal is obliged to use the affected limb.},
	Author = {Riolobos, A. S. and Heredia, M. and de la Fuente, J. A. and Criado, J. M. and Yajeya, J. and Campos, J. and Santacana, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1074-7427},
	Journal = {Neurobiol Learn Mem},
	Keywords = {Movement Disorders;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Behavior, Animal;Motor Cortex;Rats;Rats, Wistar;Transplantation, Homologous;Recovery of Function;Forelimb;Muscle, Skeletal;Animals;Male;Fetal Tissue Transplantation;Frontal Lobe},
	Medline = {21198233},
	Month = {5},
	Nlm_Id = {9508166},
	Number = {3},
	Organization = {Departamento de Fisiolog{\'\i}a y Farmacolog{\'\i}a, Universidad de Salamanca, Madrid, Spain.},
	Pages = {274-92},
	Pii = {S1074742700939790},
	Pubmed = {11300734},
	Title = {Functional recovery of skilled forelimb use in rats obliged to use the impaired limb after grafting of the frontal cortex lesion with homotopic fetal cortex},
	Uuid = {0100E08D-B20C-4A2D-AB23-57A6ECC39DBE},
	Volume = {75},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/nlme.2000.3979}}

@article{Rispeter:1997,
	Abstract = {The synthesis of long cDNA molecules encoding the complete genome of RNA viruses has recently been demonstrated; this major improvement has numerous practical applications such as construction of infectious cDNA clones or study of sequence variability at the level of a single RNA molecule. Using hepatitis C virus (HCV) as a model, we established an RT-PCR technique for amplification of cDNA fragments with a length of about 5 kb. The RT reaction was carried out with a Moloney murine leukaemia virus reverse transcriptase lacking detectable RNase H activity. For PCR reactions an enzyme mix containing Taq and Pwo DNA polymerases was used. Hot start and addition of 5\%DMSO were also important to efficiently achieve long PCR products. About 10(6) HCV genome equivalents/ml in serum were needed in order to amplify the HCV genome in only two cDNA fragments covering about 98\%of the complete genome. Analysis of the HCV quasi-species is also possible by this method as shown by sequencing of the hypervariable region 1 (HVR1) after cloning of cDNAs. The integrity of the long cDNA clones was proven by (1) restriction analyses, (2) partial sequencing and (3) expression of respective gene products. In vitro transcribed cDNAs were translated in rabbit reticulocyte lysate. Structural and nonstructural HCV proteins were identified by immunoprecipitation using patient serum. These results suggest that the two cDNA clones encode a complete and functional open reading frame of HCV. 0022-1317 Journal Article},
	Author = {Rispeter, K. and Lu, M. and Lechner, S. and Zibert, A. and Roggendorf, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Gen Virol},
	Keywords = {Hepacivirus/*genetics;*Genome, Viral;Molecular Sequence Data;Human;EE, DMSO, abstr;08 Aberrant cell cycle;Amino Acid Sequence;Rabbits;DNA, Complementary/*genetics;Support, Non-U.S. Gov't;Animals;Cloning, Molecular;Open Reading Frames/*genetics;Polymerase Chain Reaction},
	Organization = {Institut fur Virologie, Universitatsklinikum Essen, Germany.},
	Pages = {2751-9},
	Pubmed = {9367360},
	Title = {Cloning and characterization of a complete open reading frame of the hepatitis C virus genome in only two cDNA fragments},
	Uuid = {8E2807D6-96BB-46C3-928D-E570178CE1A4},
	Volume = {78 ( Pt 11)},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9367360}}

@article{Rivest:2006,
	Abstract = {Microglia are the resident immune cells of the brain, and they are under permanent activity to patrol the cerebral microenvironment. A proper inhibitory feedback onto these cells is critical during both intact and injury conditions. In this issue of Neuron, Eljaschewitsch and colleagues report that such feedback is provided by the endogenous cannabinoid anandamine and CB(1/2) receptor signaling, which ultimately leads to mitogen-activated protein kinase phosphatase-1 (MKP-1) induction. MKP-1 interferes with lipopolysaccharide-induced toll-like receptor 4 signaling and limits brain damage due to exaggerated microglial reactivity following acute NMDA injury.},
	Author = {Rivest, Serge},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {24 Pubmed search results 2008;Feedback, Biochemical;Microglia;11 Glia;Cannabinoids;comment;Animals;Brain;Humans;Cytoprotection;Immune System},
	Month = {1},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Laboratory of Molecular Endocrinology, CHUL Research Center and Department of Anatomy and Physiology, Laval University, 2705, boul. Laurier, Qu{\'e}bec , Canada G1V-4G2.},
	Pages = {4-8},
	Pii = {S0896-6273(05)01050-0},
	Pubmed = {16387633},
	Title = {Cannabinoids in microglia: a new trick for immune surveillance and neuroprotection},
	Uuid = {2AB98EA6-BBF3-49ED-BDEE-F1C933473734},
	Volume = {49},
	Year = {2006},
	url = {papers/Rivest_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.12.004}}

@article{Rizvi:2006,
	Abstract = {Transplanted adult bone marrow-derived cells (BMDCs) have been shown to adopt the phenotype and function of several nonhematopoietic cell lineages and promote tumorigenesis. Beyond its cancer enhancing potential, cell fusion has recently emerged as an explanation of how BMDCs regenerate diseased heptocytes, contribute to Purkinje neurons and skeletal and cardiac muscle cells, and participate in skin and heart regeneration. Although bone marrow-derived epithelial cells also have been observed in the intestine, fusion as a mechanism has not been investigated. Here, we show that transplanted BMDCs fuse with both normal and neoplastic intestinal epithelium. Long-term repopulation by donor-derived cells was detected in all principal intestinal epithelial lineages including enterocytes, goblet cells, Paneth cells, and enteroendocrine cells, suggesting that the fusion partners of the BMDCs are long-lived intestinal progenitors or stem cells. Fusion of BMDCs with neoplastic epithelium did not result in tumor initiation. Our findings suggest an unexpected role for BMDCs in both regeneration and tumorigenesis of the intestine.},
	Author = {Rizvi, and Swain, and Davies, and Bailey, and Decker, and Willenbring, and Grompe, and Fleming, and Wong,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {7505876},
	Organization = {Departments of Surgery, Dermatology, Cell and Developmental Biology, and Molecular and Medical Genetics, Center for Hematologic Malignancies, Division of Hematology and Medical Oncology, and Oregon Cancer Institute, Oregon Stem Cell Center, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239.},
	Pii = {0508593103},
	Pubmed = {16606845},
	Title = {Bone marrow-derived cells fuse with normal and transformed intestinal stem cells},
	Uuid = {2AFA34E2-01FB-4B7B-89B8-7AA2D38ADC6E},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0508593103}}

@article{Roberts:1987,
	Abstract = {We have previously observed that lysosomes redistribute from their normal location in neuronal cell bodies to the dendrites following an intracerebroventricular injection of an antimitotic such as colchicine, vinblastine or vincristine. In the present study, we have followed the developmental distribution of lysosomes in the brains of untreated rats, using a lysosomal marker enzyme, dipeptidylaminopeptidase II. A relatively high concentration of neuronal lysosomes was found in the dendrites of olfactory bulb mitral cell neurons and in hippocampal granule and pyramidal cell neurons from postnatal day 1 (P1) to P8. As the animals matured, the pattern of lysosomal enzyme distribution was reversed. Lysosomes became progressively less concentrated in the dendrites and more concentrated in neuronal cell bodies. In cerebellar Purkinje cells, lysosomes were only found in the cell bodies during the first week after birth. Between P9 and P19, lysosomes appeared in the dendrites of these neurons and, with maturity, progressively disappeared from the dendrites and were concentrated mainly in cell bodies. The presence of lysosomes in the dendrites of developing animals suggests that the transport of lysosomes to the dendrites, induced by microtubule poisons, mimics a physiological process which is normally present during development. eng Journal Article},
	Author = {Roberts, V. J. and Gorenstein, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Journal = {Dev Neurosci},
	Keywords = {F abstr;10 Development;Purkinje Cells/ultrastructure;Rats, Inbred F344;Rats;Lysosomes/*ultrastructure;Hippocampus/cytology/ultrastructure;Time Factors;Olfactory Bulb/cytology/ultrastructure;Brain/cytology/growth &development/*ultrastructure;Animal;Neurons/*ultrastructure;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't},
	Number = {4},
	Organization = {Department of Pharmacology, University of California, Irvine.},
	Pages = {255-64.},
	Title = {Examination of the transient distribution of lysosomes in neurons of developing rat brains},
	Uuid = {A693B572-36D9-4DBC-91F9-C1ADB0B568F2},
	Volume = {9},
	Year = {1987}}

@article{Roberts:2006,
	Abstract = {CNS abnormalities can be detected during chronic human immunodeficiency virus (HIV) infection, before the development of opportunistic infections or other sequelae of immunodeficiency. However, although end-stage dementia caused by HIV has been linked to the presence of infected and activated macrophages and microglia in the brain, the nature of the changes resulting in the motor and cognitive disorders in the chronic stage is unknown. Using simian immunodeficiency virus-infected rhesus monkeys, we sought the molecular basis for CNS dysfunction. In the chronic stable stage, nearly 2 years after infection, all animals had verified CNS functional abnormalities. Both virus and infiltrating lymphocytes (CD8+ T-cells) were found in the brain. Molecular analysis revealed that the expression of several immune response genes was increased, including CCL5, which has pleiotropic effects on neurons as well as immune cells. CCL5 was significantly upregulated throughout the course of infection, and in the chronic phase was present in the infiltrating lymphocytes. We have identified an altered state of the CNS at an important stage of the viral-host interaction, likely arising to protect against the virus but in the long term leading to damaging processes.},
	Author = {Roberts, Eleanor S. and Huitron-Resendiz, Salvador and Taffe, Michael A. and Marcondes, Maria Cecilia G. and Flynn, Claudia T. and Lanigan, Caroline M. and Hammond, Jennifer A. and Head, Steven R. and Henriksen, Steven J. and Fox, Howard S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California, 92037, USA.},
	Pages = {4577-85},
	Pii = {26/17/4577},
	Pubmed = {16641237},
	Title = {Host response and dysfunction in the CNS during chronic simian immunodeficiency virus infection},
	Uuid = {C70D5895-A396-4391-A041-985F1FB8FC14},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4504-05.2006}}

@article{Roche:2006,
	Abstract = {The vesicular stomatitis virus has an atypical membrane fusion glycoprotein (G) exhibiting a pH-dependent equilibrium between two forms at the virus surface. Membrane fusion is triggered during the transition from the high- to low-pH form. The structure of G in its low-pH form shows the classic hairpin conformation observed in all other fusion proteins in their postfusion conformation, in spite of a novel fold combining features of fusion proteins from classes I and II. The structure provides a framework for understanding the reversibility of the G conformational change. Unexpectedly, G is homologous to gB of herpesviruses, which raises important questions on viral evolution.},
	Author = {Roche, St{\'e}phane and Bressanelli, St{\'e}phane and Rey, F{\'e}lix A. and Gaudin, Yves},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Viral Fusion Proteins;Protein Subunits;Models, Molecular;Protein Folding;Vesicular stomatitis-Indiana virus;Crystallography, X-Ray;Mutation;Evolution, Molecular;15 Retrovirus mechanism;Hydrogen-Ion Concentration;Protein Structure, Secondary;Viral Envelope Proteins;Protein Conformation;Membrane Glycoproteins;Protein Structure, Tertiary;Protein Structure, Quaternary;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;15 PS VSVG receptor;Crystallization;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {0404511},
	Number = {5784},
	Organization = {CNRS, Unit{\'e} Mixte de Recherche (UMR) 2472, Institut F{\'e}d{\'e}ratif de Recherche (IFR) 115, Virologie Mol{\'e}culaire et Structurale, 91198, Gif sur Yvette, France.},
	Pages = {187-91},
	Pii = {313/5784/187},
	Pubmed = {16840692},
	Title = {Crystal structure of the low-pH form of the vesicular stomatitis virus glycoprotein G},
	Uuid = {88AE12A5-4333-11DB-A5D2-000D9346EC2A},
	Volume = {313},
	Year = {2006},
	url = {papers/Roche_Science2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1127683}}

@article{Rochefort:2002,
	Abstract = {In the mammalian forebrain, most neurons originate from proliferating cells in the ventricular zone lining the lateral ventricles, including a discrete area of the subventricular zone (SVZ). In this region, neurogenesis continues into adulthood. Most of the cells generated in the SVZ are neuronal precursors with progeny that migrate rostrally along a pathway known as the rostral migratory stream before they reach the main olfactory bulb (MOB) where they differentiate into local interneurons. The olfactory system thus provides an attractive model to investigate neuronal production and survival, processes involving interplay between genetic and epigenetic influences. The present study was conducted to investigate whether exposure to an odor-enriched environment affects neurogenesis and learning in adult mice. Animals housed in either a standard or an odor-enriched environment for 40 d were injected intraperitoneally with bromodeoxyuridine (BrdU) to detect proliferation among progenitor cells and to follow their survival in the MOB. The number of BrdU-labeled neurons was not altered 4 hr after a single BrdU injection. In contrast, the number of surviving progenitors 3 weeks after BrdU injection was markedly increased in animals housed in an enriched environment. This effect was specific because enriched odor exposure did not influence hippocampal neurogenesis. Finally, we showed that adult mice housed in odor- enriched cages display improved olfactory memory without a change in spatial learning performance. By maintaining a constitutive turnover of granule cells subjected to modulation by environmental cues, ongoing bulbar neurogenesis could be associated with improved olfactory memory.},
	Author = {Rochefort, C. and Gheusi, G. and Vincent, J. D. and Lledo, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:57 -0400},
	Journal = {J Neurosci},
	Keywords = {B pdf},
	Number = {7},
	Organization = {Perception and Memory Laboratory, Centre National de la Recherche Scientifique Unite de Recherche Associee 2182, Institut Pasteur, 75 724 Paris Cedex 15, France.},
	Pages = {2679-89.},
	Title = {Enriched odor exposure increases the number of newborn neurons in the adult olfactory bulb and improves odor memory},
	Uuid = {56191CD2-CDEF-11D9-B244-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	url = {papers/Rochefort_JNeurosci2002.pdf}}

@article{Roe:1993,
	Abstract = {In synchronized rat or mouse cells infected with Moloney murine leukemia virus (MLV), integration of viral DNA and production of viral proteins occur only after the cells traverse mitosis. Integration is blocked when cells are prevented from progressing through mitosis. Viral nucleoprotein complexes isolated from arrested cells contain full-length viral DNA and can integrate this viral DNA in vitro, showing that the block to integration in arrested cells is not due to a lack of mature integration machinery. When infected cells traverse mitosis, there is a sharp increase in nuclear accumulation of viral DNA. The dependence of integration on mitosis may therefore be due to a requirement for mitosis and nuclear envelope breakdown for entry of the viral integration complex into the nucleus. 0261-4189 Journal Article},
	Author = {Roe, T. and Reynolds, T. C. and Yu, G. and Brown, P. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {Embo J},
	Keywords = {Animals;Cells, Cultured;Rats;J abstr;*Mitosis;Metaphase;*Virus Integration;15 Retrovirus mechanism;G2 Phase;Viral Proteins/biosynthesis;Support, Non-U.S. Gov't;Genome, Viral;DNA, Viral/*metabolism;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Moloney murine leukemia virus/genetics/*physiology;Mice;Cell Nucleus/metabolism;Nucleoproteins/metabolism},
	Number = {5},
	Organization = {Department of Biochemistry, Stanford University, CA 94305.},
	Pages = {2099-108},
	Pubmed = {8491198},
	Title = {Integration of murine leukemia virus DNA depends on mitosis},
	Uuid = {892E779B-EA2C-11DA-920C-000D9346EC2A},
	Volume = {12},
	Year = {1993},
	url = {papers/Roe_EmboJ1993.pdf}}

@article{Roelink:2000,
	Abstract = {Recent genetic studies have shown that the signalling factor Wnt3a is required for formation of the hippocampus; the developmental consequences of Wnt signalling in the hippocampus are mediated by multiple HMG-box transcription factors, with LEF-1 being required just for formation of the dentate gyrus.},
	Author = {Roelink, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {DNA-Binding Proteins;10 Development;Hippocampus;10 Hippocampus;Embryonic Induction;Mice, Mutant Strains;review, tutorial;High Mobility Group Proteins;Animals;Mice;Proteins;review;Transcription Factors},
	Medline = {20219677},
	Month = {4},
	Nlm_Id = {9107782},
	Number = {7},
	Organization = {Department of Biological Structure, Center for Developmental Biology, University of Washington, Box 357420, Seattle, 98117-7420, USA. roelink\@u.washington.edu},
	Pages = {R279-81},
	Pii = {S0960-9822(00)00407-3},
	Pubmed = {10753739},
	Title = {Hippocampus formation: an intriguing collaboration},
	Uuid = {8EBD90A3-D863-4504-8195-41AD1561A067},
	Volume = {10},
	Year = {2000},
	url = {papers/Roelink_CurrBiol2000.pdf}}

@article{Roelofs:2005,
	Abstract = {Human glial fibrillary acidic protein-delta (GFAP-delta) is a GFAP protein isoform that is encoded by an alternative splice variant of the GFAP-gene. As a result, GFAP-delta protein differs from the predominant splice form, GFAP-alpha, by its C-terminal protein sequence. In this study, we show that GFAP-delta protein is not expressed by all GFAP-expressing astrocytes but specifically by a subpopulation located in the subpial zone of the cerebral cortex, the subgranular zone of the hippocampus, and, most intensely, by a ribbon of astrocytes following the ependymal layer of the cerebral ventricles. Therefore, at least in the sub ventricular zone (SVZ), GFAP-delta specifically marks the population of astrocytes that contain the neural stem cells in the adult human brain. Interestingly, the SVZ astrocytes actively splice GFAP-delta transcripts, in contrast to astrocytes adjacent to this layer. Furthermore, we show that GFAP-delta protein, unlike GFAP-alpha, is not upregulated in astrogliosis. Our data therefore indicate a different functional role for GFAP-delta in astrocyte physiology. Finally, transfection studies showed that GFAP-delta protein expression has a negative effect on GFAP filament formation, and therefore could be important for modulating intermediate filament cytoskeletal properties, possibly facilitating astrocyte motility. Further studies on GFAP-delta and the cells that express it are important for gaining insights into its function during differentiation, migration and during health and disease. (c) 2005 Wiley-Liss, Inc.},
	Author = {Roelofs, and Fischer, and Houtman, and Sluijs, and Van Haren, and Van Leeuwen, and Hol,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {8806785},
	Organization = {Netherlands Institute for Brain Research, Graduate School Neurosciences, Amsterdam, the Netherlands.},
	Pubmed = {16001427},
	Title = {Adult human subventricular, subgranular, and subpial zones contain astrocytes with a specialized intermediate filament cytoskeleton},
	Uuid = {1F144850-F432-4BF3-96EB-58C567FCD672},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20243}}

@article{Rogers:1992,
	Abstract = {Many dopaminergic cells of the substantia nigra are known to contain the calcium-binding proteins calretinin and calbindin-D28k. Catecholaminergic cell groups throughout the rat brain were therefore examined by two-colour immunofluorescence to determine whether they too contained these calcium-binding proteins as well as tyrosine hydroxylase (TH). Some TH+ cell groups are mostly positive for both calretinin and calbindin, notably in the ventral tegmental area, the interfascicular nucleus, and parts of the substantia nigra. Other TH+ cell groups in the midbrain, hindbrain and hypothalamus are very diverse; different cell groups are positive for calretinin, or calbindin, or both, or neither. In the olfactory bulb, entirely separate sets of periglomerular cells are positive for TH, calretinin and calbindin. However, there is considerable heterogeneity in calcium- binding protein expression within most cell groups, even in the substantia nigra. This could be a sign that calcium-binding proteins are regulated according to aspects of neuronal activity.},
	Author = {Rogers, J. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Brain Res},
	Keywords = {I;Brain/*metabolism;Rats;Immunohistochemistry;Calcium-Binding Protein, Vitamin D-Dependent/immunology/*metabolism;Biological Markers;Tyrosine 3-Monooxygenase/immunology/*metabolism;In Vitro;Antibodies, Monoclonal/immunology;Brain Mapping;Animal;Support, Non-U.S. Gov't;Catecholamines/metabolism;13 Olfactory bulb anatomy},
	Number = {2},
	Organization = {Department of Physiology, University of Cambridge, UK.},
	Pages = {203-10.},
	Title = {Immunohistochemical markers in rat brain: colocalization of calretinin and calbindin-D28k with tyrosine hydroxylase},
	Uuid = {49DA0CF2-47F3-44E2-A30C-033991A275C0},
	Volume = {587},
	Year = {1992},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=1356063}}

@article{Rogers:1997,
	Abstract = {For an understanding of the aberrant biology seen in mouse mutations and identification of more subtle phenotype variation, there is a need for a full clinical and pathological characterization of the animals. Although there has been some use of sophisticated techniques, the majority of behavioral and functional analyses in mice have been qualitative rather than quantitative in nature. There is, however, no comprehensive routine screening and testing protocol designed to identify and characterize phenotype variation or disorders associated with the mouse genome. We have developed the SHIRPA procedure to characterize the phenotype of mice in three stages. The primary screen utilizes standard methods to provide a behavioral and functional profile by observational assessment. The secondary screen involves a comprehensive behavioral assessment battery and pathological analysis. These protocols provide the framework for a general phenotype assessment that is suitable for a wide range of applications, including the characterization of spontaneous and induced mutants, the analysis of transgenic and gene-targeted phenotypes, and the definition of variation between strains. The tertiary screening stage described is tailored to the assessment of existing or potential models of neurological disease, as well as the assessment of phenotypic variability that may be the result of unknown genetic influences. SHIRPA utilizes standardized protocols for behavioral and functional assessment that provide a sensitive measure for quantifying phenotype expression in the mouse. These paradigms can be refined to test the function of specific neural pathways, which will, in turn, contribute to a greater understanding of neurological disorders.},
	Author = {Rogers, D. C. and Fisher, E. M. and Brown, S. D. and Peters, J. and Hunter, A. J. and Martin, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0938-8990},
	Journal = {Mamm Genome},
	Keywords = {Variation (Genetics);24 Pubmed search results 2008;23 Technique;Behavior, Animal;Phenotype;Neural Pathways;Genome;Animals;Genetics, Behavioral;Mice;Nervous System Diseases;Research Design},
	Month = {10},
	Nlm_Id = {9100916},
	Number = {10},
	Organization = {SmithKline Beecham Pharmaceuticals, New Frontiers Science Park, Harlow, UK.},
	Pages = {711-3},
	Pubmed = {9321461},
	Title = {Behavioral and functional analysis of mouse phenotype: SHIRPA, a proposed protocol for comprehensive phenotype assessment},
	Uuid = {D007B8FB-DBAA-4A24-ACA8-EF10B16CE24D},
	Volume = {8},
	Year = {1997}}

@article{Rolls:2007,
	Abstract = {Neurogenesis - the formation of new neurons in the adult brain - is considered to be one of the mechanisms by which the brain maintains its lifelong plasticity in response to extrinsic and intrinsic changes. The mechanisms underlying the regulation of neurogenesis are largely unknown. Here, we show that Toll-like receptors (TLRs), a family of highly conserved pattern-recognizing receptors involved in neural system development in Drosophila and innate immune activity in mammals, regulate adult hippocampal neurogenesis. We show that TLR2 and TLR4 are found on adult neural stem/progenitor cells (NPCs) and have distinct and opposing functions in NPC proliferation and differentiation both in vitro and in vivo. TLR2 deficiency in mice impaired hippocampal neurogenesis, whereas the absence of TLR4 resulted in enhanced proliferation and neuronal differentiation. In vitro studies further indicated that TLR2 and TLR4 directly modulated self-renewal and the cell-fate decision of NPCs. The activation of TLRs on the NPCs was mediated via MyD88 and induced PKCalpha/beta-dependent activation of the NF-kappaB signalling pathway. Thus, our study identified TLRs as players in adult neurogenesis and emphasizes their specified and diverse role in cell renewal.},
	Author = {Rolls, Asya and Shechter, Ravid and London, Anat and Ziv, Yaniv and Ronen, Ayal and Levy, Rinat and Schwartz, Michal},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {100890575},
	Number = {9},
	Organization = {Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel.},
	Pages = {1081-8},
	Pii = {ncb1629},
	Pubmed = {17704767},
	Title = {Toll-like receptors modulate adult hippocampal neurogenesis},
	Uuid = {C80F8CFC-0C25-4742-A433-EC0EBA995E2B},
	Volume = {9},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb1629}}

@article{Romanko:2004,
	Abstract = {Perinatal hypoxic-ischemic (H/I) brain injury remains a major cause of neurologic disability. Because we have previously demonstrated that this insult depletes cells from the subventricular zone (SVZ), the goal of the present investigation was to compare the relative vulnerability to H/I of neural stem cells versus progenitors. The dorsolateral SVZs of P6 rats were examined at 2 to 48 hours of recovery from H/I using hematoxylin and eosin, in situ end labeling (ISEL), terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling (TUNEL), electron microscopy, and immunofluorescence. Pyknotic nuclei and ISEL cells were observed by 4 hours of recovery, peaked at 12 hours, and persisted for at least 48 hours. Many active-caspase-3 cells were observed at 12 hours and they comprised one third of the total TUNEL population. Electron microscopy revealed that hybrid cell deaths predominated at 12 hours of recovery. Importantly, few dying cells were observed in the medial SVZ, where putative stem cells reside, and no nestin medial SVZ cells showed caspase-3 activation. By contrast, active-caspase-3/PSA-NCAM progenitors were prominent in the lateral SVZ. These data demonstrate that early progenitors are vulnerable to H/I, whereas neural stem cells are resilient. The demise of these early progenitors may lead to the depletion of neuronal and late oligodendrocyte progenitors, contributing to cerebral dysgenesis after perinatal insults. 0271-678x Journal Article},
	Author = {Romanko, M. J. and Rothstein, R. P. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {C, D abstr;04 Adult neurogenesis factors},
	Number = {7},
	Organization = {Department of Neural and Behavioral Sciences, Pennsylvania State University, College of Medicine, Hershey, Pennsylvania 17033, USA.},
	Pages = {814-25},
	Pubmed = {15241190},
	Title = {Neural stem cells in the subventricular zone are resilient to hypoxia/ischemia whereas progenitors are vulnerable},
	Uuid = {E1FE6A7C-6FF7-42AC-B789-C95BF40A084D},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15241190}}

@article{Romijn:1994,
	Abstract = {The aim of this study was to investigate whether the rat cerebral cortex, damaged by hypoxia-ischemia in early postnatal life, would show an increased seizure susceptibility and/or spontaneous epileptic discharges in adulthood. To that end 12-13-day-old Wistar rat pups were unilaterally exposed to hypoxic-ischemic conditions. After a recovery period of about 2.5 months, recording and stimulation electrodes were permanently implanted over the left and right fronto-parietal neocortex. Long-term recording of baseline electrocortical activity showed that only those animals that had incurred severe brain damage, as was reflected by the presence of a cortical infarction, ran a high risk of developing permanent epileptic activity. With the aid of the stimulation electrodes the initial threshold for localized seizure activity was found to be the same for the experimental and non-treated groups. However, when the kindling-like decline of this threshold was assessed by repeated testing over a 2-week period, the infarcted animals tended to a more rapid decline but a higher stabilization level than the non-infarcted and control animals.},
	Author = {Romijn, H. J. and Voskuyl, R. A. and Coenen, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0920-1211},
	Journal = {Epilepsy Res},
	Keywords = {Electric Stimulation;Animals;Rats;Seizures;Brain;21 Epilepsy;Female;Epilepsy;Rats, Wistar;Male;Animals, Newborn;Hypoxia, Brain;Cerebral Cortex;21 Neurophysiology;Brain Ischemia;24 Pubmed search results 2008;Electroencephalography;Research Support, Non-U.S. Gov't},
	Medline = {94229038},
	Month = {1},
	Nlm_Id = {8703089},
	Number = {1},
	Organization = {Netherlands Institute for Brain Research, Amsterdam.},
	Pages = {31-42},
	Pubmed = {8174523},
	Title = {Hypoxic-ischemic encephalopathy sustained in early postnatal life may result in permanent epileptic activity and an altered cortical convulsive threshold in rat},
	Uuid = {3B114799-E770-449D-83EF-13D97B049247},
	Volume = {17},
	Year = {1994}}

@article{Root:1983,
	Abstract = {Weanling albino rats were fed semisynthetic diets deficient or sufficient in vitamin B6 or copper, or both, for 2 or 3 months. Brains were examined by light and electron microscopy after Golgi impregnation or conventional tissue processing for electron microscopy. Golgi impregnation revealed that some pyramidal cells of the cerebral cortex, particularly in layers III and V, showed partial to nearly complete dendritic loss. This occurred in all deficient groups but was most typical of deficiency of vitamin B6. Swelling in dendrites or perikarya was more typical of copper deficiency. Ultrastructural observation revealed large vacuoles in cellular processes of the cerebral cortex in deficient groups. The hippocampus of copper-deficient rats contained dark, apparently degenerating processes while axonal swellings were seen in vitamin B6 deficiency. These abnormalities are discussed as evidence for accelerated aging of neurons related to poor nutritional status.},
	Author = {Root, E. J. and Longenecker, J. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0002-9165},
	Journal = {Am J Clin Nutr},
	Keywords = {Pyridoxine;Copper;Aging;10 Development;Research Support, Non-U.S. Gov't;Dendrites;Neuroglia;Golgi Apparatus;Rats;Hippocampus;Vitamin B 6 Deficiency;10 Structural plasticity;Animals;Brain;Male;Cerebral Cortex;24 Pubmed search results 2008},
	Medline = {83175466},
	Month = {4},
	Nlm_Id = {0376027},
	Number = {4},
	Pages = {540-52},
	Pubmed = {6837489},
	Title = {Brain cell alterations suggesting premature aging induced by dietary deficiency of vitamin B6 and/or copper},
	Uuid = {C301DC44-DEF8-4679-A06E-1D85CA52922F},
	Volume = {37},
	Year = {1983}}

@article{Rosen:1996,
	Abstract = {Freezing injury to the cortical plate of the newborn rat results in the formation of a focal region of cerebrocortical microdysgenesis resembling, in many ways, human 4-layered microgyria. Previous research has shown that neurons born during embryonic day (E) 20 migrate through the initial damage and take their place in the cell-dense layer of the microgyric lesion. The current study was conducted to determine: (1) whether neurons generated earlier in development would be found in microgyric cortex; and (2) whether the freezing injury would stimulate production of neurons postnatally. Rat pups from mothers who were injected with S-phase markers on E15, E17, E19, and E21 were subjected to freezing injury of the cortex to induce microgyria on postnatal day (P) 1. Other pups received a freezing lesion and then pulse or cumulative injections of S-phase markers for the next 72 h. Neurons born on E17 and E19 were found scattered throughout the cell-dense layer of the microgyric cortex. Early (E15) generated neurons were nearly absent in the microgyric cortex, and there was no evidence of postnatal induction of cortical neurogenesis. These results are considered in light of recent work demonstrating postnatal neocortical neurogenesis in response to early neocortical injury.},
	Author = {Rosen, G. D. and Sherman, G. F. and Galaburda, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Animals;Humans;Aging;Rats;Brain;21 Epilepsy;Rats, Wistar;Disease Models, Animal;Embryonic and Fetal Development;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Cerebral Cortex;Neurons;Freezing;21 Neurophysiology;Cell Division;24 Pubmed search results 2008;S Phase},
	Medline = {96440073},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Dyslexia Research Laboratory, Beth Israel Hospital, Boston, MA 02215, USA. glenn\_rosen\@bih.harvard.edu},
	Pages = {71-8},
	Pii = {0006-8993(96)00351-4},
	Pubmed = {8842384},
	Title = {Birthdates of neurons in induced microgyria},
	Uuid = {10F5FA39-45AA-4B0B-988E-E81A3C3A8DB0},
	Volume = {727},
	Year = {1996}}

@article{Roskams:2005,
	Author = {Roskams, A. Jane and Tetzlaff, Wolfram},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cell Differentiation;17 Transplant Regeneration;Spinal Cord Injuries;Stem Cells;comment;Animals;Humans;24 Pubmed search results 2008;Stem Cell Transplantation;review},
	Month = {6},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Zoology and ICORD (International Collaboration on Repair Discoveries), University of British Columbia, 6270 University Boulevard, Vancouver, BC, Canada V6T 1Z4.},
	Pages = {267-72},
	Pii = {S0014-4886(05)00047-6},
	Pubmed = {15869930},
	Title = {Directing stem cells and progenitor cells on the stage of spinal cord injury},
	Uuid = {A2207411-142F-48C5-B0D8-8135492C7E13},
	Volume = {193},
	Year = {2005},
	url = {papers/Roskams_ExpNeurol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.expneurol.2005.01.023}}

@article{Ross:2003,
	Abstract = {Transcription factors with bHLH motifs modulate critical events in the development of the mammalian neocortex. Multipotent cortical progenitors are maintained in a proliferative state by bHLH factors from the Id and Hes families. The transition from proliferation to neurogenesis involves a coordinate increase in the activity of proneural bHLH factors (Mash1, Neurogenin1, and Neurogenin2) and a decrease in the activity of Hes and Id factors. As development proceeds, inhibition of proneural bHLH factors in cortical progenitors promotes the formation of astrocytes. Finally, the formation of oligodendrocytes is triggered by an increase in the activity of bHLH factors Olig1 and Olig2 that may be coupled with a decrease in Id activity. Thus, bHLH factors have key roles in corticogenesis, affecting the timing of differentiation and the specification of cell fate. 0896-6273 Journal Article Review Review, Tutorial},
	Author = {Ross, S. E. and Greenberg, M. E. and Stiles, C. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Neuron},
	Keywords = {Astrocytes/cytology;Cell Differentiation/*physiology;10 Development;Neurons/cytology;Multipotent Stem Cells/physiology;Cell Lineage/*physiology;Human;F both;Neocortex/*cytology/*embryology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Animals;Oligodendroglia/cytology;Helix-Loop-Helix Motifs/*physiology;Transcription Factors/chemistry/physiology},
	Number = {1},
	Organization = {Division of Neuroscience, Children's Hospital, Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {13-25},
	Pubmed = {12848929},
	Title = {Basic helix-loop-helix factors in cortical development},
	Uuid = {36BF42F3-BEB0-4C96-925A-8A8B26C0C946},
	Volume = {39},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12848929}}

@article{Rossi:2002,
	Abstract = {There is a pressing need for treatments for neurodegenerative diseases. Hopes have been raised by the prospect of neural stem cell therapy; however, despite intense research activities and media attention, stem cell therapy for neurological disorders is still a distant goal. Effective strategies must be developed to isolate, enrich and propagate homogeneous populations of neural stem cells, and to identify the molecules and mechanisms that are required for their proper integration into the injured brain. This article examines these requirements, discusses the results obtained so far, and considers the steps that need to be taken to provide instruction to donor cells and to elucidate the neurogenic potential of the adult central nervous system environment. 1471-003x Journal Article Review Review, Tutorial},
	Author = {Rossi, F. and Cattaneo, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:57 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {*Stem Cell Transplantation;17 Transplant Regeneration;Human;Nervous System Diseases/pathology/*therapy;Cell Differentiation/physiology;Neurons/physiology/*transplantation;Stem Cells/physiology;L pdf;Animals;Support, Non-U.S. Gov't},
	Number = {5},
	Organization = {Rita Levi Montalcini Center for Brain Repair, Department of Neuroscience, Section of Physiology, University of Turin, Corso Raffaello 30, 10125 Turin, Italy. ferdinando.rossi\@unito.it},
	Pages = {401-9},
	Title = {Opinion: neural stem cell therapy for neurological diseases: dreams and reality},
	Uuid = {0D076052-DD04-4EE6-8D26-7B5F9DBBE14B},
	Volume = {3},
	Year = {2002},
	url = {papers/Rossi_NatRevNeurosci2002.pdf}}

@article{Rossner:2004,
	Author = {Rossner, Mike and Yamada, Kenneth M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {Image Processing, Computer-Assisted;Software;Research;Ethics;Publishing;24 Pubmed search results 2008;news},
	Month = {7},
	Nlm_Id = {0375356},
	Number = {1},
	Pages = {11-5},
	Pii = {jcb.200406019},
	Pubmed = {15240566},
	Title = {What's in a picture? The temptation of image manipulation},
	Uuid = {B7DD0EFD-F85C-498F-A8CD-3D29B9849D51},
	Volume = {166},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200406019}}

@article{Rothkamm:2003,
	Abstract = {Little is known about the quantitative contributions of nonhomologous end joining (NHEJ) and homologous recombination (HR) to DNA double-strand break (DSB) repair in different cell cycle phases after physiologically relevant doses of ionizing radiation. Using immunofluorescence detection of gamma-H2AX nuclear foci as a novel approach for monitoring the repair of DSBs, we show here that NHEJ-defective hamster cells (CHO mutant V3 cells) have strongly reduced repair in all cell cycle phases after 1 Gy of irradiation. In contrast, HR-defective CHO irs1SF cells have a minor repair defect in G(1), greater impairment in S, and a substantial defect in late S/G(2). Furthermore, the radiosensitivity of irs1SF cells is slight in G(1) but dramatically higher in late S/G(2), while V3 cells show high sensitivity throughout the cell cycle. These findings show that NHEJ is important in all cell cycle phases, while HR is particularly important in late S/G(2), where both pathways contribute to repair and radioresistance. In contrast to DSBs produced by ionizing radiation, DSBs produced by the replication inhibitor aphidicolin are repaired entirely by HR. irs1SF, but not V3, cells show hypersensitivity to aphidicolin treatment. These data provide the first evaluation of the cell cycle-specific contributions of NHEJ and HR to the repair of radiation-induced versus replication-associated DSBs. 0270-7306 Journal Article},
	Author = {Rothkamm, K. and Kruger, I. and Thompson, L. H. and Lobrich, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Mol Cell Biol},
	Keywords = {Hamsters;Animals;Bromodeoxyuridine/pharmacology;Phenotype;Cell Cycle;CHO Cells;08 Aberrant cell cycle;Microscopy, Fluorescence;EE;Time Factors;Cell Line;*Recombination, Genetic;G2 Phase;Support, Non-U.S. Gov't;Flow Cytometry;Support, U.S. Gov't, Non-P.H.S.;*DNA Damage;Antimetabolites, Antineoplastic/pharmacology;G1 Phase;S Phase;Cell Nucleus/metabolism;Dose-Response Relationship, Radiation;*DNA Repair},
	Number = {16},
	Organization = {Fachrichtung Biophysik, Universitat des Saarlandes, D-66421 Homburg/Saar, Germany.},
	Pages = {5706-15},
	Pubmed = {12897142},
	Title = {Pathways of DNA double-strand break repair during the mammalian cell cycle},
	Uuid = {A9330763-EE5C-4DBB-AC1A-EB58A888A159},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12897142}}

@article{Rothstein:2004,
	Abstract = {1087-0156 Comment News},
	Author = {Rothstein, J. D. and Snyder, E. Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Nat Biotechnol},
	Keywords = {T abstr;23 Technique},
	Number = {3},
	Pages = {283-5},
	Pubmed = {14990948},
	Title = {Reality and immortality--neural stem cells for therapies},
	Uuid = {88085D72-580F-4AD2-9EC7-982D570F1C66},
	Volume = {22},
	Year = {2004},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14990948}}

@article{Rotshenker:2003,
	Abstract = {Microglia and macrophages play critical roles in the response of the central and peripheral nervous systems (CNS and PNS, respectively) to injury and disease, one of which is the removal of degenerated myelin by phagocytosis. Myelin removal is efficient during Wallerian degeneration, which follows injury to PNS axons, and in CNS autoimmune demyelinating diseases (e.g., multiple sclerosis) but is inefficient after injury to CNS axons. We suggest that inefficient myelin removal results from deficient microglia activation, reflected by the failure to up-regulate Galectin-3/MAC-2 expression, which marks a state of activation correlated with efficient myelin phagocytosis. Surprisingly, whether or not executing myelin phagocytosis, CNS microglia express the alphaM/beta2 integrin complement receptor-3 (CR3/MAC-1), which has the potential of mediating efficient myelin phagocytosis. We hypothesize that CR3/MAC-1 might be present in distinct inactive and active states that determine, respectively, efficient and inefficient CR3/MAC-1-mediated myelin phagocytosis. We present evidence that CR3/MAC-1-mediated myelin phagocytosis is regulated in microglia and macrophages. First, CR3/MAC-1- mediated myelin phagocytosis has complement-dependent and -independent components. Second, an active complement system augments CR3/MAC-1-mediated myelin phagocytosis. Third, anti-alphaM monoclonal antibodies (MAbs) inhibit and anti-beta2 MAbs augment CR3/MAC-1-mediated myelin phagocytosis in the presence and absence of an active complement system. Fourth, an active complement system modulates MAb-induced regulation of CR3/MAC-1-mediated myelin phagocytosis. Overall, MAb-induced phagocytosis regulation might range three- to sevenfold from inefficient to efficient. We suggest that one of the mechanisms underlying MAb-induced phagocytosis regulation is the induction/stabilization of inactive and active conformational changes. Monoclonal antibody-induced phagocytosis regulation must reveal a mechanism by which native extracellular molecules bind to and regulate CR3/MAC-1-mediated myelin phagocytosis in microglia and macrophages.},
	Author = {Rotshenker, Shlomo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0895-8696},
	Journal = {J Mol Neurosci},
	Keywords = {Not relevant;11 Glia},
	Medline = {22863582},
	Nlm_Id = {9002991},
	Number = {1},
	Organization = {Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School and the Eric Roland Center for Neurodegenerative Diseases, POB 12272, Jerusalem 91120, Israel. ROTSH\@md.huji.ac.il},
	Pages = {65-72},
	Pii = {JMN-21-1-65},
	Pubmed = {14500997},
	Title = {Microglia and macrophage activation and the regulation of complement-receptor-3 (CR3/MAC-1)-mediated myelin phagocytosis in injury and disease},
	Uuid = {B377DFC1-08BC-459B-94B9-EAAD9ADAE423},
	Volume = {21},
	Year = {2003}}

@article{Rousselot:1995,
	Abstract = {In the brain of adult mice, cell division persists in the subventricular zone (SVZ) of the lateral ventricles. These SVZ cells migrate rostrally 3-5 mm to the olfactory bulb, where they differentiate into neurons. We have investigated the distribution of PSA-N-CAM in the adult mouse forebrain. Immunoreactivity for PSA-N-CAM precisely reveals the migratory pathway of SVZ cells. This pathway of PSA-N-CAM positive cells starts in the lateral wall of the lateral ventricle, where immunopositive cells form weblike patterns. The PSA-N-CAM positive pathway extends rostrally between the corpus callosum and the striatum into the anterior ventral telencephalon, and then into the core of the olfactory bulb. Experiments in which [3H]-thymidine was injected systemically indicated that the majority of the dividing cells on the SVZ of the lateral ventricle and along the migratory pathway are positive to PSA-N-CAM or closely associated with PSA-N-CAM. Microinjection of [3H]-thymidine into the SVZ of the lateral ventricle to label a small patch of dividing SVZ cells shows that neuroblasts that migrated away from the injection site are positive or are closely associated with other cells that are positive for PSA-N-CAM. Migrating cells are tethered together, forming long chains of immunopositive cells. The migratory pathway is formed by 30-40 of these immunopositive chains. Radially oriented individual PSA-N-CAM positive cells were observed in the olfactory bulb. These cells seem to have broken away from chains of immunopositive cells in the core of the olfactory bulb and to be migrating to more superficial layers. Little is known about the mechanisms of tangential migration during development and in adulthood. The cell-cell arrangement revealed by PSA-N-CAM staining suggests new models for this form of neuronal migration. PSA-N-CAM localization along the migratory pathway to the olfactory bulb suggests that in the adult brain this molecule plays a role in migration of neuronal precursors. eng Journal Article},
	Author = {Rousselot, P. and Lois, C. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Journal = {J Comp Neurol},
	Keywords = {02 Adult neurogenesis migration;Cell Adhesion Molecules, Neuronal/*metabolism;Immunohistochemistry;Female;Models, Neurological;Thymidine/metabolism;Animal;Antibodies, Monoclonal/immunology;Cerebral Ventricles/*cytology;Pregnancy;B abstr;Olfactory Bulb/*cytology;Support, Non-U.S. Gov't;Mice;Neural Pathways/cytology;Male;Support, U.S. Gov't, P.H.S.},
	Number = {1},
	Organization = {Rockefeller University, New York, New York 10021.},
	Pages = {51-61.},
	Title = {Embryonic (PSA) N-CAM reveals chains of migrating neuroblasts between the lateral ventricle and the olfactory bulb of adult mice},
	Uuid = {D6D89552-340A-4676-BBD5-3212FE00A70A},
	Volume = {351},
	Year = {1995}}

@article{Rowland:1993,
	Abstract = {The frontal cortices of rats which received either D,L- or D-fenfluramine (DFEN) for 4 days were examined 18 h to 2 weeks following treatment for changes in synaptosomal uptake of serotonin (5HT), paroxetine binding, 5HT-immunoreactivity (5HT-IR), and both astrocytic (GFAP) and microglial markers. Additional rats received intracerebroventricular injections of the neurotoxin 5,7-dihydroxytryptamine (DHT). Consistent with previous reports, D,L- and DFEN produced dose-dependent losses of both 5HT uptake and paroxetine binding, and loss of 5HT-IR which coincided with an abnormal or 'swollen' appearance of immunoreactive axon processes. Recovery of these serotonergic indices was greatest following the lowest doses of DFEN, but was absent after 5,7-DHT treatment. No evidence for an increase in GFAP synthesis or microglial activation was observed in frontal cortices of rats treated with either DFEN or 5,7-DHT. We conclude that the presence of swollen 5HT-IR axons in the cortices of both the 5,7-DHT and DFEN groups is insufficient to trigger the glial responses often associated with neuronal degeneration. Thus, it remains to be determined if swollen 5HT-IR axons are a prelude to neurodegeneration, or whether they represent reversible changes in axonal immunochemistry associated with decreases in 5HT levels. The implications of the data for the clinical safety of DFEN are briefly discussed.},
	Author = {Rowland, N. E. and Kalehua, A. N. and Li, B. H. and Semple-Rowland, S. L. and Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Dose-Response Relationship, Drug;Binding Sites;Animals;Rats;Microglia;Fenfluramine;Rats, Sprague-Dawley;Not relevant;11 Glia;Male;Support, Non-U.S. Gov't;Injections, Subcutaneous;Cerebral Cortex;Blotting, Western;Immunohistochemistry;Stereoisomerism;Administration, Oral;Serotonin},
	Medline = {94073730},
	Month = {10},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Department of Psychology, University of Florida, Gainesville 32611-2065.},
	Pages = {35-43},
	Pubmed = {8252414},
	Title = {Loss of serotonin uptake sites and immunoreactivity in rat cortex after dexfenfluramine occur without parallel glial cell reactions},
	Uuid = {E6841A16-0760-4309-BD09-17799DF1F6D3},
	Volume = {624},
	Year = {1993}}

@article{Roy:2000,
	Abstract = {Neurogenesis persists in the adult mammalian hippocampus. To identify and isolate neuronal progenitor cells of the adult human hippocampus, we transfected ventricular zone-free dissociates of surgically-excised dentate gyrus with DNA encoding humanized green fluorescent protein (hGFP), placed under the control of either the nestin enhancer (E/nestin) or the Talpha1 tubulin promoter (P/Talpha1), two regulatory regions that direct transcription in neural progenitor cells. The resultant P/Talpha1:hGFP+ and E/nestin:enhanced (E)GFP+ cells expressed betaIII-tubulin or microtubule-associated protein-2; many incorporated bromodeoxyuridine, indicating their genesis in vitro. Using fluorescence-activated cell sorting, the E/nestin:EGFP+ and P/Talpha1:hGFP+ cells were isolated to near purity, and matured antigenically and physiologically as neurons. Thus, the adult human hippocampus contains mitotically competent neuronal progenitors that can be selectively extracted. The isolation of these cells may provide a cellular substrate for re-populating the damaged or degenerated adult hippocampus.},
	Author = {Roy, N. S. and Wang, S. and Jiang, L. and Kang, J. and Benraiss, A. and Harrison-Restelli, C. and Fraser, R. A. and Couldwell, W. T. and Kawaguchi, A. and Okano, H. and Nedergaard, M. and Goldman, S. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Nat Med},
	Keywords = {Human;Cells, Cultured;Neurons/*cytology/physiology;Transfection;Tubulin/*genetics;A-11;Dentate Gyrus/*cytology;01 Adult neurogenesis general;Luminescent Proteins/analysis/genetics;*Transcription, Genetic;Intermediate Filament Proteins/genetics;Support, Non-U.S. Gov't;Adult;Flow Cytometry;Support, U.S. Gov't, P.H.S.;Stem Cells/*cytology/physiology;Promoter Regions (Genetics);Hippocampus/*cytology},
	Number = {3},
	Organization = {Departments of Neurology and Neuroscience, Cornell University Medical College, 1300 York Ave. Room E607, New York, New York 10021, USA.},
	Pages = {271-7.},
	Title = {In vitro neurogenesis by progenitor cells isolated from the adult human hippocampus},
	Uuid = {8A2EA8D8-1021-4FAD-940A-52C96AF49BDF},
	Volume = {6},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10700228%20http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v3/n3/full/nm0300_271.html%20http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v3/n3/full//nm0300_271.html}}

@article{Rozovsky:1998,
	Abstract = {Astrocytes and microglia from cerebral cortex of 3-, 6-, 12-, and 24-month-old F344 male rat donors showed progressively greater proliferation during primary culture. Microglia from aging donor brains exhibited an amoeboid-like morphology and express antigens characteristic of an activated state (e.g., major histocompatibility complex class II). Moreover, microglia from aging donors were less sensitive to several types of regulators. Granulocyte-macrophage colony stimulating factor stimulated proliferation in microglia from young, but not aging brains. Transforming growth factor (TGF)-beta1 inhibited astrocytic and microglial proliferation in cultures from young, but not aging donors. Similarly, the inhibition of lipopolysaccharide-induced NO production by TGF-beta1 in microglia was impaired in cultures from 12-month (middle-age) brains. Another aging change detected by middle age, increased glial fibrillary acidic protein (GFAP) expression, also persisted in astrocytes from 12- to 24-month-old brains, as evaluated by increased activity of a 5'-upstream GFAP promoter construct. Thus, both microglia and astrocytes originated from aging cerebral cortex maintain in vitro at least some of the activated phenotypes of aging glia that are observed in vivo. This new in vitro cell model may allow efficient analysis of glial age changes.},
	Author = {Rozovsky, I. and Finch, C. E. and Morgan, T. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0197-4580},
	Journal = {Neurobiol Aging},
	Keywords = {Animals;Astrocytes;Cells, Cultured;Aging;Rats;Transforming Growth Factor beta;Phenotype;Microglia;Thymidine;11 Glia;Male;Rats, Inbred F344;Support, Non-U.S. Gov't;Down-Regulation;Nitrogen;Support, U.S. Gov't, P.H.S.;Cell Division;Immunohistochemistry;Glial Fibrillary Acidic Protein},
	Medline = {98221002},
	Nlm_Id = {8100437},
	Number = {1},
	Organization = {Andrus Gerontology Center and Department of Biological Sciences University of Southern California, Los Angeles 90080-0191, USA.},
	Pages = {97-103},
	Pii = {S0197458097001693},
	Pubmed = {9562510},
	Title = {Age-related activation of microglia and astrocytes: in vitro studies show persistent phenotypes of aging, increased proliferation, and resistance to down-regulation},
	Uuid = {E21496B7-4E6A-47EB-B2AD-EE116EAE1D01},
	Volume = {19},
	Year = {1998}}

@article{Ryder:1990,
	Abstract = {Neural cell lines were produced by retroviral vector-mediated transduction of the avian myc oncogene. Target cells were mitotic progenitor cells of postnatal mouse olfactory bulb and cerebellum, and postnatal rat cerebral cortex. Infection of the first two areas, where neurogenesis and gliogenesis occur postnatally, produced multipotent clonal lines that exhibited phenotypes of both neuronal and glial cells, and one line with a stable neuronal phenotype. Infection of cerebral cortex, where gliogenesis, but not neurogenesis, occurs postnatally, generated mortal clones that exhibited cells of glial phenotype. These lines should prove valuable for both in vitro and in vivo studies aimed at understanding the control of cell fate and differentiation of neural progenitors. eng Journal Article},
	Author = {Ryder, E. F. and Snyder, E. Y. and Cepko, C. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Journal = {J Neurobiol},
	Keywords = {Cell Differentiation;*Transduction, Genetic;Rats;Neurons/*cytology;Cell Line, Transformed;Cerebellum/cytology;Animal;Stem Cells/cytology;23 Technique;*Cell Transformation, Viral;Genetic Vectors;Support, Non-U.S. Gov't;Retroviridae/genetics;Olfactory Bulb/cytology;T abstr;Support, U.S. Gov't, P.H.S.;Cerebral Cortex/cytology;Mice;Neuroglia/*cytology;*Oncogenes;Clone Cells},
	Number = {2},
	Organization = {Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115.},
	Pages = {356-75.},
	Title = {Establishment and characterization of multipotent neural cell lines using retrovirus vector-mediated oncogene transfer},
	Uuid = {866BDA71-71B9-4CA1-916E-EA9330F390F8},
	Volume = {21},
	Year = {1990}}

@article{Rytting:1999,
	Abstract = {The development of a colorimetric capture assay for HIV-1 reverse transcriptase (RT) activity is described. This assay consisted of three basic steps: enzyme purification, RT reaction and product detection, which were all performed in the same microtitre plate. Mouse monoclonal anti-RT antibodies of subclass G2a were bound by polyclonal goat anti-(mouse IgG2a) immobilized in the wells of a microtitre plate. The monoclonal antibodies (mAbs) were selected for their ability to bind HIV-1 RT without hampering the polymerase activity. The assay system first involved the RT's adherence to the immobilized mAbs. Non-specific enzymes and other impurities were removed by a simple wash, after which an RT reaction mixture containing BrdUTP as nucleotide substrate was added. After the RT reaction substrate and product had been separated by washing of the plate, the amount of BrdUMP-DNA in the wells was finally detected with alkaline-phosphatase-conjugated mouse anti-BrdU antibodies of subclass IgG1. The background signal in this system was similar to the signals obtained with control wells coated with BSA only. A detection limit of 1.2 micro-units of RT activity, corresponding to 0.3 pg of RT protein, was obtained for the capture assay when applying colorimetric product detection. The assay detected RTs from HIV-1 subtypes A and B and one of the two D type isolates tested. None of the five non-HIV-1 RTs tested was found positive. At least 50 microl of human serum or plasma per sample could be included in the capture assay without adverse effects on the recovery of the RT activity.},
	Author = {Rytting, A. S. and Akerblom, L. and Gronowitz, J. S. and K{\"a}llander, C. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0885-4513},
	Journal = {Biotechnol Appl Biochem},
	Keywords = {Colorimetry;Enzyme-Linked Immunosorbent Assay;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Antibodies, Monoclonal;Deoxyuracil Nucleotides;HIV-1 Reverse Transcriptase;15 Retrovirus mechanism;Animals;Enzymes, Immobilized;Bromodeoxyuridine;Isoenzymes;Mice},
	Medline = {99268838},
	Month = {6},
	Nlm_Id = {8609465},
	Organization = {Department of Genetics and Pathology, Section of Medical Genetics, Uppsala University, BMC, Box 578, SE-751 23 Uppsala, Sweden.},
	Pages = {241-50},
	Pubmed = {10334955},
	Title = {Colorimetric capture assay for human-immunodeficiency-virus-I reverse transcriptase activity},
	Uuid = {AEC61CA8-3169-4B5B-9069-12C795B5EBFF},
	Volume = {29 ( Pt 3)},
	Year = {1999}}

@article{Ryzhova:2002,
	Abstract = {Simian immunodeficiency virus (SIV)-infected macaques develop an encephalitis (SIVE) that is pathologically virtually indistinguishable from that associated with HIV infection, with multinucleated giant cells (MNGCs) being the principal histopathological manifestation. To dissect SIV variants responsible for MNGC development, we examined the relationships between env sequences transcribed in individual MNGCs and those from genomic DNA of brain and spleen tissues. The brain-specific variant found in all brain clones was dominant among the clones from MNGCs, suggesting a role in the formation of giant cells. Furthermore, two additional minor groups of sequences were present in MNGCs. One group consisted of sequences closely related to those from spleen, indicating recent and probably multiple episodes of neuroinvasion. The second group represented clones similar or identical to the initial inoculum. The survival of archival sequences and their activation presumably by the fusion of productively and quiescently infected macrophages/microglia identify the central nervous system as a possible anatomical reservoir for latent infection.},
	Author = {Ryzhova, Elena V. and Crino, Peter and Shawver, Linda and Westmoreland, Susan V. and Lackner, Andrew A. and Gonz{\'a}lez-Scarano, Francisco},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {RNA, Viral;Encephalitis, Viral;Animals;Virus Latency;Comparative Study;SIV;Brain;Sequence Alignment;Phylogeny;Female;Genes, env;11 Glia;Giant Cells;Male;Disease Models, Animal;Support, Non-U.S. Gov't;Macaca mulatta;Research Support, U.S. Gov't, P.H.S.;Simian Acquired Immunodeficiency Syndrome;Support, U.S. Gov't, P.H.S.;DNA, Viral;Amino Acid Sequence;Molecular Sequence Data;Spleen;Research Support, Non-U.S. Gov't},
	Medline = {22080395},
	Month = {5},
	Nlm_Id = {0110674},
	Number = {1},
	Organization = {Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.},
	Pages = {57-67},
	Pii = {S0042682202913954},
	Pubmed = {12083836},
	Title = {Simian immunodeficiency virus encephalitis: analysis of envelope sequences from individual brain multinucleated giant cells and tissue samples},
	Uuid = {807AA3FF-B780-4B8B-86F4-6F539A783522},
	Volume = {297},
	Year = {2002}}

@article{Saenz:2004,
	Abstract = {The circumstances under which unintegrated lentivirus DNA can persist and be a functional template for transcription and protein expression are not clear. We constructed and validated the first class I (nonpleiotropic) integrase (IN) mutants for a non-human lentivirus (feline immunodeficiency virus [FIV]) and analyzed both these and known class I human immunodeficiency virus type 1 IN mutants. The FIV IN mutants (D66V and D66V/D118A) had class I properties: Gag/Pol precursor expression, proteolytic processing, particle formation, and reverse transcriptase (RT) production were normal, while the transduction of dividing fibroblasts was prevented and integration was blocked. When injected into rat retinas, the wild-type (WT) vector produced extensive, persistent transgene expression, compared with only rare positive neuronal cells for the IN mutant vector. In contrast, both WT and mutant vectors produced entirely equivalent, effective transduction levels of primary rat neurons (retinal ganglion cells). By testing the hypothesis that the unexpected retinal neuron transduction was related to cell cycle status, we found that when fibroblasts were growth arrested, transduction and internally promoted transgene expression were not inhibited at all by the class I FIV or HIV-1 IN mutations. Cells were then transduced under aphidicolin arrest and were released from the block 48 h later. Vector expression was stable and durable during repeated passaging in WT vector-transduced cells, while the release of cells transduced with equivalent RT units of class I IN mutant FIV or HIV vector resulted in a steady decline of expression, from 97 to 0\%of cells by day 10. Southern blot and PCR analyses showed a lack of integration, irrespective of cell cycle, for the class I mutants and an increase in one- and two-long terminal repeat circular and linear unintegrated DNAs in growth-arrested cells. We conclude that if cell division is prevented, unintegrated FIV and HIV-1 vector DNAs can produce high-level internally promoted transgene expression equivalent to WT vectors. The expression correlates with the unintegrated DNA levels. These observations may facilitate the study of the roles of IN and other preintegration complex components in preintegration phases of infection by (i) providing an alternative way to monitor unintegrated nuclear cDNA forms, (ii) restricting ascertainment to the transcriptionally functional subset of unintegrated DNA, (iii) enabling analysis in individual, nondividing cells, and (iv) uncoupling other potential functions of IN from integration.},
	Author = {Saenz, Dyana T. and Loewen, Nils and Peretz, Mary and Whitwam, Todd and Barraza, Rom{\'a}n and Howell, Kyle G. and Holmes, Jonathan M. and Good, Margaret and Poeschla, Eric M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Research Support, Non-U.S. Gov't;Transduction, Genetic;Animals;Humans;Rats;Immunodeficiency Virus, Feline;Lentivirus;Sequence Alignment;Mutation;Rats, Sprague-Dawley;Integrases;15 Retrovirus mechanism;Hela Cells;Cell Line;Research Support, U.S. Gov't, P.H.S.;HIV Integrase;DNA, Viral;Virus Integration;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;Cats;Retinal Ganglion Cells},
	Month = {3},
	Nlm_Id = {0113724},
	Number = {6},
	Organization = {Molecular Medicine Program, Departments of Immunology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.},
	Pages = {2906-20},
	Pubmed = {14990709},
	Title = {Unintegrated lentivirus DNA persistence and accessibility to expression in nondividing cells: analysis with class I integrase mutants},
	Uuid = {28D1163B-C204-4C7F-9A6B-3E1796D5A04C},
	Volume = {78},
	Year = {2004}}

@article{Saghatelyan:2003,
	Abstract = {Over the past few decades, research exploring how the brain perceives, discriminates, and recognizes odorant molecules has received a growing interest. Today, olfaction is no longer considered a matter of poetry. Chemical senses entered the biological era when an increasing number of scientists started to elucidate the early stages of the olfactory pathway. A combination of genetic, biochemical, cellular, electrophysiological and behavioral methods has provided a picture of how odor information is processed in the olfactory system as it moves from the periphery to higher areas of the brain. Our group is exploring the physiology of the main olfactory bulb, the first processing relay in the mammalian brain. From different electrophysiological approaches, we are attempting to understand the cellular rules that contribute to the synaptic transmission and plasticity at this central relay. How olfactory sensory inputs, originating from the olfactory epithelium located in the nasal cavity, are encoded in the main olfactory bulb remains a crucial question for understanding odor processing. More importantly, the persistence of a high level of neurogenesis continuously supplying the adult olfactory bulb with newborn local neurons provides an attractive model to investigate how basic olfactory functions are maintained when a large proportion of local neurons are continuously renewed. For this purpose, we summarize the current ideas concerning the molecular mechanisms and organizational strategies used by the olfactory system to encode and process information in the main olfactory bulb. We discuss the degree of sensitivity of the bulbar neuronal network activity to the persistence of this high level of neurogenesis that is modulated by sensory experience. Finally, it is worth mentioning that analyzing the molecular mechanisms and organizational strategies used by the olfactory system to transduce, encode, and process odorant information in the olfactory bulb should aid in understanding the general neural mechanisms involved in both sensory perception and memory. Due to space constraints, this review focuses exclusively on the olfactory systems of vertebrates and primarily those of mammals. 0928-4257 Journal Article},
	Author = {Saghatelyan, A. and Carleton, A. and Lagier, S. and de Chevigny, A. and Lledo, P. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {J Physiol Paris},
	Keywords = {01 Adult neurogenesis general;A, I, M pdf},
	Number = {4-6},
	Organization = {Laboratory of Perception and Memory, Centre National de la Recherche Scientifique, Unite de Recherche Associee 2182, Institut Pasteur, 25 rue du Dr Roux, 75724 Paris, France.},
	Pages = {517-28},
	Title = {Local neurons play key roles in the mammalian olfactory bulb},
	Uuid = {DF85165C-DEAE-4FF8-9775-6950D0DA8F5F},
	Volume = {97},
	Year = {2003},
	url = {papers/Saghatelyan_JPhysiolParis2003.pdf}}

@article{Sahara:2001,
	Abstract = {The cellular localization of metabotropic glutamate receptors (mGluRs) (mGluR1alpha, 2/3, 5a and 7) in the main and accessory olfactory bulb (MOB and AOB) of adult rats was compared by using affinity purified polyclonal antibodies directed to their C-termini. mGluR1alpha and mGluR5a immunoreactivities were located in comparable structures of the MOB and AOB with different levels of intensity. mGluR5a reactivity was high in the AOB. mGluR2/3 showed a different pattern of expression in the MOB compared to that observed in the AOB; the periglomerular region of the MOB was strongly stained, but in the AOB it was the mitral/tufted cell layer that was intense. The mitral cell bodies in the MOB were strongly immunoreactive for mGluR7. These differences in the distribution of mGluRs in the MOB and AOB may reflect differences in synaptic transmission and sensitivity to neuromodulation in the two systems.},
	Author = {Sahara, Y. and Kubota, T. and Ichikawa, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {Neurosci Lett},
	Keywords = {I pdf;13 Olfactory bulb anatomy},
	Number = {2},
	Organization = {Department of Maxillofacial Biology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, 113-8549, Tokyo, Japan},
	Pages = {59-62.},
	Title = {Cellular localization of metabotropic glutamate receptors mGluR1, 2/3, 5 and 7 in the main and accessory olfactory bulb of the rat},
	Uuid = {86F7F8E8-181D-4C25-BA6C-6E94B0320216},
	Volume = {312},
	Year = {2001},
	url = {papers/Sahara_NeurosciLett2001}}

@article{Sahay:2007,
	Abstract = {The development of new treatments for depression is predicated upon identification of neural substrates and mechanisms that underlie its etiology and pathophysiology. The heterogeneity of depression indicates that its origin may lie in dysfunction of multiple brain regions. Here we evaluate adult hippocampal neurogenesis as a candidate mechanism for the etiology of depression and as a substrate for antidepressant action. Current evidence indicates that adult hippocampal neurogenesis may not be a major contributor to the development of depression, but may be required for some of the behavioral effects of antidepressants. We next revisit the functional differentiation of the hippocampus along the septo-temporal axis within the context of adult hippocampal neurogenesis and suggest that neurogenesis in the ventral dentate gyrus may be preferentially involved in regulation of emotion. Finally, we speculate on how increased adult hippocampal neurogenesis may modulate dentate gyrus function to confer the behavioral effects of antidepressants.},
	Author = {Sahay, Amar and Hen, Rene},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {9809671},
	Number = {9},
	Organization = {Department of Neuroscience, Division of Integrative Neuroscience, Columbia University, 1051 Riverside Drive, Box 87, PI Annex, Room 767B, New York, New York 10032, USA. as2619\@columbia.edu},
	Pages = {1110-5},
	Pii = {nn1969},
	Pubmed = {17726477},
	Title = {Adult hippocampal neurogenesis in depression},
	Uuid = {A8EAB088-BC16-46D4-9731-AA120262C797},
	Volume = {10},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1969}}

@article{Sailer:1997,
	Abstract = {Ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole) is a green fluorescent plant alkaloid that inhibits DNA topoisomerase II activity and possesses pharmacologic activity toward both murine and human leukemias in vivo. In this flow cytometric study, the uptake of ellipticine was monitored as a function of cell volume and cell cycle phase in viable human promyelocytic (HL-60) cells costained with the DNA fluorochrome Hoechst 33342. Uptake of ellipticine was time and dose dependent; however, drug content was quantitatively similar in all phases of the cell cycle when normalized for DNA content or similar to cell size when correlated with cell volume. The fluorescence lifetime values of ellipticine in HL-60 cells, as analyzed by novel flow cytometric analysis, reached a plateau when the intra-cellular ellipticine intensity was still rising with increasing drug concentration. Since the free drug and the different subcellular ellipticine complexes, including DNA and RNA, had different lifetime values, the changes in the lifetime values appear to reflect differing proportions of unbound drug to that bound to different cellular constituents in the cells. Further development of phase-sensitive flow cytometry will provide for multiple lifetime determinations so that quantitation of drugs bound to the different cellular components can be performed along with the simultaneous determination of total drug uptake and cell cycle position. Such analyses should provide useful information for the design of drugs with greater affinity for cytotoxic targets.},
	Author = {Sailer, B. L. and Valdez, J. G. and Steinkamp, J. A. and Darzynkiewicz, Z. and Crissman, H. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0014-4827},
	Journal = {Exp Cell Res},
	Keywords = {Flow Cytometry;Cell Size;RNA, Neoplasm;Cell Compartmentation;Research Support, U.S. Gov't, P.H.S.;Time Factors;Dose-Response Relationship, Drug;Cell Survival;Fluorescent Dyes;Cell Cycle;Research Support, U.S. Gov't, Non-P.H.S.;HL-60 Cells;DNA, Neoplasm;Humans;Antineoplastic Agents;24 Pubmed search results 2008;Ellipticines},
	Medline = {98005057},
	Month = {10},
	Nlm_Id = {0373226},
	Number = {1},
	Organization = {Life Sciences Division, Los Alamos National Laboratory, New Mexico 87545, USA.},
	Pages = {259-67},
	Pii = {S0014482797937174},
	Pubmed = {9344606},
	Title = {Monitoring uptake of ellipticine and its fluorescence lifetime in relation to the cell cycle phase by flow cytometry},
	Uuid = {B61A9903-45D4-452D-85BF-FC084FD54C43},
	Volume = {236},
	Year = {1997}}

@article{Sairanen:2005,
	Abstract = {Antidepressants increase proliferation of neuronal progenitor cells and expression of brain-derived neurotrophic factor (BDNF) in the hippocampus. We investigated the role of BDNF signaling in antidepressant-induced neurogenesis by using transgenic mice with either reduced BDNF levels (BDNF+/-) or impaired trkB activation (trkB.T1-overexpressing mice). In both transgenic strains, chronic (21 d) imipramine treatment increased the number of bromodeoxyuridine (BrdU)-positive cells to degree similar to that seen in wild-type mice 24 h after BrdU administration, although the basal proliferation rate was increased in both transgenic strains. Three weeks after BrdU administration and the last antidepressant injection, the amount of newborn (BrdU- or TUC-4-positive) cells was significantly reduced in both BDNF+/- and trkB.T1-overexpressing mice, which suggests that normal BDNF signaling is required for the long-term survival of newborn hippocampal neurons. Moreover, the antidepressant-induced increase in the surviving BrdU-positive neurons seen in wild-type mice 3 weeks after treatment was essentially lost in mice with reduced BDNF signaling. Furthermore, we observed that chronic treatment with imipramine or fluoxetine produced a temporally similar increase in both BrdU-positive and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end-labeled neurons in the dentate gyrus, indicating that these drugs simultaneously increase both neurogenesis and neuronal elimination. These data suggest that antidepressants increase turnover of hippocampal neurons rather than neurogenesis per se and that BDNF signaling is required for the long-term survival of newborn neurons in mouse hippocampus.},
	Author = {Sairanen, Mikko and Lucas, Guilherme and Ernfors, Patrik and Castr{\'e}n, Maija and Castr{\'e}n, Eero},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {04 Adult neurogenesis factors},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {5},
	Organization = {Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland.},
	Pages = {1089-94},
	Pii = {25/5/1089},
	Pubmed = {15689544},
	Title = {Brain-derived neurotrophic factor and antidepressant drugs have different but coordinated effects on neuronal turnover, proliferation, and survival in the adult dentate gyrus},
	Uuid = {EDFD38EC-D360-436D-9DE3-8C29EC397416},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3741-04.2005}}

@article{Sakaguchi:2006,
	Abstract = {In the subventricular zone of the adult mammalian forebrain, neural stem cells (NSCs) reside and proliferate to generate young neurons. We screened factors that promoted the proliferation of NSCs in vitro by a recently developed proteomics technique, the ProteinChip system. In this screen, we identified a soluble carbohydrate-binding protein, Galectin-1, as a candidate. We show herein that Galectin-1 is expressed in a subset of slowly dividing subventricular zone astrocytes, which includes the NSCs. Based on results from intraventricular infusion experiments and phenotypic analyses of knockout mice, we demonstrate that Galectin-1 is an endogenous factor that promotes the proliferation of NSCs in the adult brain.},
	Author = {Sakaguchi, Masanori and Shingo, Tetsuro and Shimazaki, Takuya and Okano, Hirotaka James and Shiwa, Mieko and Ishibashi, Satoru and Oguro, Hideyuki and Ninomiya, Mikiko and Kadoya, Toshihiko and Horie, Hidenori and Shibuya, Akira and Mizusawa, Hidehiro and Poirier, Fran\c{c}oise and Nakauchi, Hiromitsu and Sawamoto, Kazunobu and Okano, Hideyuki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {7505876},
	Number = {18},
	Organization = {Department of Physiology and Bridgestone Laboratory of Developmental and Regenerative Neurobiology, Keio University School of Medicine, Tokyo 160-8582, Japan.},
	Pages = {7112-7},
	Pii = {0508793103},
	Pubmed = {16636291},
	Title = {A carbohydrate-binding protein, Galectin-1, promotes proliferation of adult neural stem cells},
	Uuid = {A1DA9C54-8B3E-4D72-A052-D2C03B503153},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0508793103}}

@article{Sakurai:2004,
	Abstract = {Current therapies for lysosomal storage diseases (LSDs), enzyme replacement therapy and bone marrow transplantation are effective for visceral organ pathology of LSD, but their effectiveness for brain involvement in LSDs is still a subject of controversy. As an alternative approach, we transplanted genetically modified bone marrow stromal (BMS) cells to lateral ventricle of newborn mucopolysaccharidosis VII (MPS VII) mice. MPS VII is one of LSDs and caused by deficiency of beta-glucuronidase (GUSB), resulting in accumulation of glycosaminoglycans (GAGs) in brain. At 2 weeks after transplantation, the GUSB enzyme-positive cells were identified in olfactory bulb, striatum and cerebral cortex, and the enzymatic activities in various brain areas increased. The GAGs contents in brain were reduced to near normal level at 4 weeks after transplantation. Although GUSB activity declined to homozygous level after 8 weeks, the reduction of GAGs persisted for 16 weeks. Microscopic examination indicated that the lysosomal distention was not found in treated animal brain. Cognitive function in MPS VII animals as evaluated by Morris Water Maze test in treated mice showed a marked improvement over nontreated animals. Brain transplantation of genetically modified BMS cells appears to be a promising approach to treat diffuse CNS involvement of LSDs.},
	Author = {Sakurai, K. and Iizuka, S. and Shen, J-S S. and Meng, X-L L. and Mori, T. and Umezawa, A. and Ohashi, T. and Eto, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Transduction, Genetic;Behavior, Animal;Research Support, Non-U.S. Gov't;Mucopolysaccharidosis VII;Bone Marrow Cells;Retroviridae;Bone Marrow Transplantation;Gene Expression;Mice, Mutant Strains;Injections, Intraventricular;Gene Therapy;11 Glia;Glucuronidase;Brain;Mice;Animals;Genetic Vectors},
	Month = {10},
	Nlm_Id = {9421525},
	Number = {19},
	Organization = {Department of Gene Therapy, Institute of DNA Medicine, The Jikei University School of Medicine, Tokyo, Japan.},
	Pages = {1475-81},
	Pii = {3302338},
	Pubmed = {15295619},
	Title = {Brain transplantation of genetically modified bone marrow stromal cells corrects CNS pathology and cognitive function in MPS VII mice},
	Uuid = {005BBEB1-3E84-4B35-ACE7-C647C48E6B5A},
	Volume = {11},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3302338}}

@article{Sakurai:2001,
	Abstract = {The structurally related cell adhesion molecules L1 and Nr-CAM have overlapping expression patterns in cerebellar granule cells. Here we analyzed their involvement in granule cell development using mutant mice. Nr-CAM-deficient cerebellar granule cells failed to extend neurites in vitro on contactin, a known ligand for Nr-CAM expressed in the cerebellum, confirming that these mice are functionally null for Nr-CAM. In vivo, Nr-CAM-null cerebella did not exhibit obvious histological defects, although a mild size reduction of several lobes was observed, most notably lobes IV and V in the vermis. Mice deficient for both L1 and Nr-CAM exhibited severe cerebellar folial defects and a reduction in the thickness of the inner granule cell layer. Additionally, anti-L1 antibodies specifically disrupted survival and maintenance of Nr-CAM-deficient granule cells in cerebellar cultures treated with antibodies. The combined results indicate that Nr-CAM and L1 play a role in cerebellar granule cell development, and suggest that closely related molecules in the L1 family have overlapping functions.},
	Author = {Sakurai, T. and Lustig, M. and Babiarz, J. and Furley, A. J. and Tait, S. and Brophy, P. J. and Brown, S. A. and Brown, L. Y. and Mason, C. A. and Grumet, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {Leukocyte L1 Antigen Complex;Purkinje Cells;Animals;Brain;Female;Neurites;Cell Adhesion Molecules, Neuronal;Male;Cerebellar Cortex;Research Support, U.S. Gov't, P.H.S.;Membrane Glycoproteins;Mice, Knockout;Protein-Tyrosine-Phosphatase;Mice;24 Pubmed search results 2008;Cell Adhesion Molecules;Nerve Tissue Proteins;Neural Cell Adhesion Molecules},
	Medline = {21448627},
	Month = {9},
	Nlm_Id = {0375356},
	Number = {6},
	Organization = {W.M. Keck Center for Collaborative Neuroscience, Rutgers University, Piscataway, NJ 08854, USA.},
	Pages = {1259-73},
	Pii = {154/6/1259},
	Pubmed = {11564762},
	Title = {Overlapping functions of the cell adhesion molecules Nr-CAM and L1 in cerebellar granule cell development},
	Uuid = {2A9946AD-52AC-4ABA-9EB5-0CFD6F0EAA85},
	Volume = {154},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200104122}}

@article{Samanta:2007,
	Abstract = {Progenitor cells that express the transcription factor olig1 generate several neural cell types including oligodendrocytes and GABAergic interneurons in the dorsal cortex. The fate of these progenitor cells is regulated by a number of signals including bone morphogenetic proteins (BMPs) secreted in the dorsal forebrain. BMPs signal by binding to heteromeric serine-threonine kinase receptors formed by type I (BMPR1a, BMPR1b, Alk2) and type II (BMPRII) subunits. To determine the specific role of the BMPR1a subunit in lineage commitment by olig1-expressing cells, we used a cre/loxP genetic approach to ablate BMPR1a in these cells while leaving signaling from other subunits intact. There was a reduction in numbers of immature oligodendrocytes in the BMPR1a-null mutant brains at birth. However, by postnatal day 20, the BMPR1a-null mice had a significant increase in the number of mature and immature oligodendrocytes compared with wild-type littermates. There was also an increase in the proportion of calbindin-positive interneurons in the dorsomedial cortex of BMPR1a-null mice at birth without any change in the number of parvalbumin- or calretinin-positive cells. These effects were attributable, at least in part, to a decrease in the length of the cell cycle in subventricular zone progenitor cells. Thus, our findings indicate that BMPR1a mediates the suppressive effects of BMP signaling on oligodendrocyte lineage commitment and on the specification of calbindin-positive interneurons in the dorsomedial cortex.},
	Author = {Samanta, Jayshree and Burke, Gordon M. and McGuire, Tammy and Pisarek, Anna J. and Mukhopadhyay, Abhishek and Mishina, Yuji and Kessler, John A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Aging;gamma-Aminobutyric Acid;Signal Transduction;Animals;Astrocytes;Aging;Cell Cycle;Basic Helix-Loop-Helix Transcription Factors;Oligodendroglia;Mutation;Cell Count;Bone Morphogenetic Proteins;Mice, Inbred C57BL;Calcium-Binding Protein, Vitamin D-Dependent;Bone Morphogenetic Protein Receptors, Type I;Smad Proteins;Animals, Newborn;Cell Lineage;Cerebral Cortex;Neurons;Mice;Interneurons;24 Pubmed search results 2008;Death;Stem Cells},
	Month = {7},
	Nlm_Id = {8102140},
	Number = {28},
	Organization = {Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.},
	Pages = {7397-407},
	Pii = {27/28/7397},
	Pubmed = {17626200},
	Title = {BMPR1a signaling determines numbers of oligodendrocytes and calbindin-expressing interneurons in the cortex},
	Uuid = {67103AAA-9C19-402E-AA8E-A994A6E7AFB0},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1434-07.2007}}

@article{Sanada:2005,
	Abstract = {Neurons in the developing mammalian brain are generated from progenitor cells in the proliferative ventricular zone, and control of progenitor division is essential to produce the correct number of neurons during neurogenesis. Here we establish that Gbetagamma subunits of heterotrimeric G proteins are required for proper mitotic-spindle orientation of neural progenitors in the developing neocortex. Interfering with Gbetagamma function in progenitors causes a shift in spindle orientation from apical-basal divisions to planar divisions. This results in hyperdifferentiation of progenitors into neurons as a consequence of both daughter cells adopting a neural fate instead of the normal asymmetric cell fates. Silencing AGS3, a nonreceptor activator of Gbetagamma, results in defects similar to the impairment of Gbetagamma, providing evidence that AGS3-Gbetagamma signaling in progenitors regulates apical-basal division and asymmetric cell-fate decisions. Furthermore, our observations indicate that the cell-fate decision of daughter cells is coupled to mitotic-spindle orientation in progenitors.},
	Author = {Sanada, Kamon and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {10 Development;Cell Differentiation;Signal Transduction;Animals;Gene Expression Regulation;Carrier Proteins;Rats;GTP-Binding Protein beta Subunits;Mitotic Spindle Apparatus;GTP-Binding Protein gamma Subunits;Cell Polarity;RNA Interference;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Neurons;Gene Silencing;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {7},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.},
	Pages = {119-31},
	Pii = {S0092-8674(05)00454-X},
	Pubmed = {16009138},
	Title = {G protein betagamma subunits and AGS3 control spindle orientation and asymmetric cell fate of cerebral cortical progenitors},
	Uuid = {45428CCD-AB5F-41A4-BA9C-8603576CE6BB},
	Volume = {122},
	Year = {2005},
	url = {papers/Sanada_Cell2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.05.009}}

@article{Sanada:2004,
	Abstract = {Disabled-1 regulates laminar organization in the developing mammalian brain. Although mutation of the disabled-1 gene in scrambler mice results in abnormalities in neuronal positioning, migratory behavior linked to Disabled-1 signaling is not completely understood. Here we show that newborn neurons in the scrambler cortex remain attached to the process of their parental radial glia during the entire course of radial migration, whereas wild-type neurons detach from the glial fiber in the later stage of migration. This abnormal neuronal-glial adhesion is highly linked to the positional abnormality of scrambler neurons and depends intrinsically on Disabled-1 Tyr220 and Tyr232, potential phosphorylation sites during corticogenesis. Importantly, phosphorylation at those sites regulates alpha3 integrin levels, which is critical for the timely detachment of migrating neurons from radial glia. Altogether, these results outline the molecular mechanism by which Disabled-1 signaling controls the adhesive property of neurons to radial glia, thereby maintaining proper neuronal positioning during corticogenesis.},
	Author = {Sanada, Kamon and Gupta, Amitabh and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Animals;10 Development;Neuroglia;Cell Adhesion;Comparative Study;Nerve Tissue Proteins;Signal Transduction;Mice, Transgenic;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Cell Movement;Cerebral Cortex;Neurons;Mice},
	Month = {4},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.},
	Pages = {197-211},
	Pii = {S0896627304002223},
	Pubmed = {15091337},
	Title = {Disabled-1-regulated adhesion of migrating neurons to radial glial fiber contributes to neuronal positioning during early corticogenesis},
	Uuid = {0263B7B6-0BF9-4249-9D8B-E677CB0A8700},
	Volume = {42},
	Year = {2004},
	url = {papers/Sanada_Neuron2004.pdf}}

@article{Sanai:2004,
	Abstract = {The subventricular zone (SVZ) is a principal source of adult neural stem cells in the rodent brain, generating thousands of olfactory bulb neurons every day. If the adult human brain contains a comparable germinal region, this could have considerable implications for future neuroregenerative therapy. Stem cells have been isolated from the human brain, but the identity, organization and function of adult neural stem cells in the human SVZ are unknown. Here we describe a ribbon of SVZ astrocytes lining the lateral ventricles of the adult human brain that proliferate in vivo and behave as multipotent progenitor cells in vitro. This astrocytic ribbon has not been observed in other vertebrates studied. Unexpectedly, we find no evidence of chains of migrating neuroblasts in the SVZ or in the pathway to the olfactory bulb. Our work identifies SVZ astrocytes as neural stem cells in a niche of unique organization in the adult human brain. 1476-4687 Journal Article},
	Author = {Sanai, N. and Tramontin, A. D. and Quinones-Hinojosa, A. and Barbaro, N. M. and Gupta, N. and Kunwar, S. and Lawton, M. T. and McDermott, M. W. and Parsa, A. T. and Manuel-Garcia Verdugo, J. and Berger, M. S. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Journal = {Nature},
	Keywords = {*Cell Movement;01 Adult neurogenesis general;Cell Differentiation;Brain/*cytology/ultrastructure;Adult;Human;Olfactory Bulb/cytology/ultrastructure;Cell Division;Autopsy;Support, U.S. Gov't, P.H.S.;Astrocytes/*cytology/ultrastructure;Multipotent Stem Cells/*cytology/ultrastructure;Cells, Cultured;Support, Non-U.S. Gov't;Neurons/*cytology/ultrastructure;A pdf;Biopsy},
	Number = {6976},
	Organization = {Department of Neurological Surgery and Brain Tumor Research Center, University of California San Francisco, San Francisco, California 94143, USA. nsanai\@itsa.ucsf.edu},
	Pages = {740-4},
	Title = {Unique astrocyte ribbon in adult human brain contains neural stem cells but lacks chain migration},
	Uuid = {4C112649-21D4-4EF7-A286-18BB953F54FF},
	Volume = {427},
	Year = {2004},
	url = {papers/Sanai_Nature2004.pdf}}

@article{Sanchez-Ramos:2000,
	Abstract = {Bone marrow stromal cells (BMSC) normally give rise to bone, cartilage, and mesenchymal cells. Recently, bone marrow cells have been shown to have the capacity to differentiate into myocytes, hepatocytes, and glial cells. We now demonstrate that human and mouse BMSC can be induced to differentiate into neural cells under experimental cell culture conditions. BMSC cultured in the presence of EGF or BDNF expressed the protein and mRNA for nestin, a marker of neural precursors. These cultures also expressed glial fibrillary acidic protein (GFAP) and neuron-specific nuclear protein (NeuN). When labeled human or mouse BMSC were cultured with rat fetal mesencephalic or striatal cells, a small proportion of BMSC-derived cells differentiated into neuron-like cells expressing NeuN and glial cells expressing GFAP. 0014-4886 Journal Article},
	Author = {Sanchez-Ramos, J. and Song, S. and Cardozo-Pelaez, F. and Hazzi, C. and Stedeford, T. and Willing, A. and Freeman, T. B. and Saporta, S. and Janssen, W. and Patel, N. and Cooper, D. R. and Sanberg, P. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Exp Neurol},
	Keywords = {*Interleukin-6;Human;RNA, Messenger/biosynthesis;Neurons/*cytology/metabolism;Corpus Striatum/cytology;Cells, Cultured;Animals;Rats;10 Development;Tretinoin/pharmacology;Rats, Sprague-Dawley;Mice, Transgenic;Mice, Inbred C57BL;Mesencephalon/cytology;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Stromal Cells/*cytology/drug effects;Coculture;*Cell Differentiation/drug effects;Support, U.S. Gov't, Non-P.H.S.;Growth Inhibitors/pharmacology;Mice;Fibronectins/metabolism;Antigens, Differentiation/biosynthesis;Brain-Derived Neurotrophic Factor/pharmacology;Lymphokines/pharmacology;F;Bone Marrow Cells/*cytology/drug effects;Neuroglia/cytology/metabolism},
	Number = {2},
	Organization = {Department of Neurology, University of South Florida, Tampa, USA.},
	Pages = {247-56},
	Pubmed = {10915564},
	Title = {Adult bone marrow stromal cells differentiate into neural cells in vitro},
	Uuid = {BE67843C-33BC-4A77-BE3E-5840E160D7EA},
	Volume = {164},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10915564}}

@article{Sancini:2001,
	Abstract = {Knockout Otx1 mice present a microcephalic phenotype mainly due to reduced deep neocortical layers and spontaneous recurrent seizures. We investigated the excitable properties of layer V pyramidal neurons in neocortical slices prepared from Otx1-/- mice and age-matched controls. The qualitative firing properties of the neurons of Otx1-/- mice were identical to those found in wild-type controls, but the proportion of intrinsically bursting (IB) neurons was significantly smaller. This is in line with the lack of the Otx1 gene contribution to the generation and differentiation of neurons destined for the deep neocortical layers, in which IB neurons are located selectively in wild-type rodents. The pyramidal neurons recorded in Otx1-/- mice responded to near-threshold electrical stimulation of the underlying white matter, with aberrant polysynaptic excitatory potentials often leading to late action potential generation. When the strength of the stimulus was increased, the great majority of the Otx1-/- neurons (78\%) responded with a prominent biphasic inhibitory postsynaptic potential that was significantly larger than that observed in the wild-type mice, and was often followed by complex postinhibitory depolarizing events. Both late excitatory postsynaptic potentials and postinhibitory excitation were selectively suppressed by NMDA receptor antagonists, but not by AMPA antagonists. We conclude that the cortical abnormalities of Otx1-/- neocortex due to a selective loss of large projecting neurons lead to a complex rearrangement of local circuitry, which is characterized by an excess of N-methyl-d-aspartate-mediated polysynaptic excitation that is counteracted by GABA-mediated inhibition in only a limited range of stimulus intensity. Prominent postsynaptic inhibitory potentials may also act as a further pro-epileptogenic event by synchronizing abnormal excitatory potentials.},
	Author = {Sancini, G. and Franceschetti, S. and Lavazza, T. and Panzica, F. and Cipelletti, B. and Frassoni, C. and Spreafico, R. and Acampora, D. and Avanzini, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {gamma-Aminobutyric Acid;Excitatory Amino Acid Antagonists;Transcription Factors;Electric Stimulation;Animals;Gene Expression Regulation, Developmental;Rats;Otx Transcription Factors;Synaptic Transmission;21 Epilepsy;Homeodomain Proteins;Epilepsy;2-Amino-5-phosphonovalerate;Pyramidal Cells;Receptors, AMPA;Action Potentials;Nervous System Malformations;Mice, Knockout;21 Neurophysiology;Cerebral Cortex;Cell Size;Mice;6-Cyano-7-nitroquinoxaline-2,3-dione;24 Pubmed search results 2008;Receptors, N-Methyl-D-Aspartate;Nerve Tissue Proteins;Neural Inhibition;Research Support, Non-U.S. Gov't},
	Medline = {21541151},
	Month = {10},
	Nlm_Id = {8918110},
	Number = {7},
	Organization = {Istituto Nazionale Neurologico C. Besta, Via Celoria 11, 20133 Milan, Italy.},
	Pages = {1065-74},
	Pii = {1723},
	Pubmed = {11683898},
	Title = {Potentially epileptogenic dysfunction of cortical NMDA- and GABA-mediated neurotransmission in Otx1-/- mice},
	Uuid = {3B0C8880-E17F-496F-9E3C-E1ABDE17F769},
	Volume = {14},
	Year = {2001}}

@article{Sanes:1989,
	Abstract = {Analysis of neural cell lineage in vertebrates has been limited by a lack of methods for introducing stable tracers into individual cells at relatively late stages of development. Recent progress in the design of recombinant retroviral vectors provides a novel approach to this problem. When a retrovirus infects a dividing cell, its genome integrates into a chromosome of the infected cell and is inherited by that cell's progeny. For lineage tracing, viral structural genes are replaced by a bacterial beta-galactosidase gene; infected cells are therefore unable to produce new virions, but can produce galactosidase, which is detectable histochemically. By infecting cells and identifying their progeny at appropriate stages, it has been possible to obtain new data on cell lineage in retina, cerebral cortex, optic tectum, and peripheral nerve.},
	Author = {Sanes, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {Retroviridae;Cell Division;Histocytochemistry;Nervous System;Animals;15 Retrovirus mechanism;Galactosidases;review},
	Medline = {89267944},
	Month = {1},
	Nlm_Id = {7808616},
	Number = {1},
	Pages = {21-8},
	Pubmed = {2471334},
	Title = {Analysing cell lineage with a recombinant retrovirus},
	Uuid = {FBEC10D5-D067-11DA-8A8C-000D9346EC2A},
	Volume = {12},
	Year = {1989}}

@article{Santos:2000,
	Abstract = {PURPOSE: Animal models are useful for the study of status epilepticus (SE)-induced epileptogenesis and neurological sequelae, especially during early brain development. Here, we show several permanent abnormalities in animals subjected to multiple SE during early development. METHODS: Wistar pup rats (7 to 9 days old) were subjected to three consecutive episodes of SE induced by systemic pilocarpine injections. To study the long-lasting consequences of early-induced SE. chronic electroencephalographic recordings were made from the hippocampus and cortex and several behavioral tests (inhibitory step-down avoidance, rota-rod, open field, elevated plus-maze, and Skinner box) were performed at postnatal days 30 to 90. We also investigated in vitro electrophysiological responses of the CA1 area using extracellular recordings in hippocampal slices. A histological analysis was done using cresyl violet staining 24 hours and several months after SE induction. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL staining) 24 hours after the last SE episode. RESULTS: Electroencephalographic recordings from 30- to 90-day-old rats that had been subjected to multiple SE episodes in early life showed marked changes compared with those from nontreated controls. These included frequent episodes of continuous complex spiking activity and high-voltage ictal discharges, with a small percentage of these rats presenting spontaneous behavioral seizures. These animals also presented evidence of severe cognitive deficit in adulthood. In vitro, a persistent hyperexcitability of the CA1 area was detected in experimental animals. Histological analysis of the brains did not reveal any major long-term pathological changes. Nevertheless, an increased number of TUNEL-positive nuclei were present in some animals in both the hippocampus and the thalamus. CONCLUSIONS: These data show persistent abnormalities in animals subjected to multiple SE episodes during early postnatal development. SE may result in important plastic changes in critical periods of brain maturation leading to long-lasting epileptogenesis, as manifested by electrographic epileptiform discharges, behavioral deficits, and in vitro hyperexcitability of hippocampal networks.},
	Author = {Santos, N. F. and Marques, R. H. and Correia, L. and Sinigaglia-Coimbra, R. and Calderazzo, L. and Sanabria, E. R. and Cavalheiro, E. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Pilocarpine;Animals;Rats;Neuronal Plasticity;Brain;Apoptosis;21 Epilepsy;Hippocampus;Rats, Wistar;Disease Models, Animal;Behavior, Animal;Male;Status Epilepticus;In Situ Nick-End Labeling;Cerebral Cortex;21 Neurophysiology;Age Factors;24 Pubmed search results 2008;Electroencephalography;Research Support, Non-U.S. Gov't},
	Medline = {20452150},
	Nlm_Id = {2983306R},
	Organization = {Laborat{\'o}rio de Neurologia Experimental, Universidade Federal de S\~{a}o Paulo-Escola Paulista de Medicina, Brazil.},
	Pages = {S57-63},
	Pubmed = {10999521},
	Title = {Multiple pilocarpine-induced status epilepticus in developing rats: a long-term behavioral and electrophysiological study},
	Uuid = {2954266D-BC5E-45B3-B04C-1A1AFE25DEEB},
	Volume = {41 Suppl 6},
	Year = {2000}}

@article{Santra:2006,
	Abstract = {Doublecortin (DCX) is one of the three genes found from Affymetrix gene chip analysis related to glioma patient survival. Two other genes (e.g., osteonectin and semaphorin 3B) are well characterized as antioncogenic and tumor suppressor genes. However, there is no report about the involvement of DCX in cancer. Here, we show that gene transfer technology into DCX-deficient glioblastoma cell lines, such as A172, U87, U251N, RG2, and 9L, with DCX cDNA significantly suppressed growth of these glioma cells. U87 cells with ectopic expression of DCX exhibit a marked suppression of the transformed phenotype as growth arrested in the G(2) phase of the cell cycle progression, small colony formation in soft agar, and no tumor formation in nude rats. This transformed phenotype can be restored by knocking down DCX expression with DCX small interfering RNA. DCX was highly phosphorylated in glioma cells. Phosphorylation in the glioma cells was greater than in noncancer cells such as mouse NIH 3T3 and human embryonic kidney 293T cells. Coimmunoprecipitation of the phosphorylated DCX and spinophilin/neurabin II from DCX-synthesizing glioma cells indicated their interaction. This interaction would lead to a block of anchorage-independent growth as neurabin II is a synergistic inhibitor of anchorage-independent growth with p14ARF (ARF). Interaction between phosphorylated DCX and neurabin II may induce the association of the protein phosphatase 1 catalytic subunit (PP1) with neurabin II and inactivate PP1 and block mitosis during G(2) and M phases of the cell cycle progression. Thus, DCX seems to be a tumor suppressor of glioma.},
	Author = {Santra, Manoranjan and Zhang, Xuepeng and Santra, Sutapa and Jiang, Feng and Chopp, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0008-5472},
	Journal = {Cancer Res},
	Keywords = {Gene Expression Regulation, Neoplastic;Microtubule-Associated Proteins;Animals;Humans;Rats;Phosphorylation;Cell Cycle;Mitosis;Lentivirus;Cell Line, Tumor;RNA, Messenger;Brain Neoplasms;RNA, Small Interfering;Genetic Vectors;Neuropeptides;Glioblastoma;3T3 Cells;research support, n.i.h., extramural;Mice;Protein Biosynthesis;22 Stem cells;24 Pubmed search results 2008;Survival;22 Cancer;Transcription, Genetic},
	Month = {12},
	Nlm_Id = {2984705R},
	Number = {24},
	Organization = {Department of Neurology, Henry Ford Health Sciences Center, Detroit, Michigan 48202, USA.},
	Pages = {11726-35},
	Pii = {66/24/11726},
	Pubmed = {17178868},
	Title = {Ectopic doublecortin gene expression suppresses the malignant phenotype in glioblastoma cells},
	Uuid = {0A37EB51-63A7-4A00-80A9-2FAC77FA88C6},
	Volume = {66},
	Year = {2006},
	url = {papers/Santra_CancerRes2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1158/0008-5472.CAN-06-1978}}

@article{Sapir:2008,
	Abstract = {Membrane fusion is a fundamental requirement in numerous developmental, physiological, and pathological processes in eukaryotes. So far, only a limited number of viral and cellular fusogens, proteins that fuse membranes, have been isolated and characterized. Despite the diversity in structures and functions of known fusogens, some common principles of action apply to all fusion reactions. These can serve as guidelines in the search for new fusogens, and may allow the formulation of a cross-species, unified theory to explain divergent and convergent evolutionary principles of membrane fusion.},
	Author = {Sapir, Amir and Avinoam, Ori and Podbilewicz, Benjamin and Chernomordik, Leonid V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1534-5807},
	Journal = {Dev Cell},
	Keywords = {15 ERVs retroelements;research support, non-u.s. gov't;08 Aberrant cell cycle;research support, n.i.h., intramural;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {101120028},
	Number = {1},
	Organization = {Department of Biology, The Technion, Israel Institute of Technology, Haifa 32000, Israel.},
	Pages = {11-21},
	Pii = {S1534-5807(07)00485-6},
	Pubmed = {18194649},
	Title = {Viral and developmental cell fusion mechanisms: conservation and divergence},
	Uuid = {FCA61FE0-0367-4B8A-90E0-87CC19150FCF},
	Volume = {14},
	Year = {2008},
	url = {papers/Sapir_DevCell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.devcel.2007.12.008}}

@article{Sarkisian:1999a,
	Abstract = {PURPOSE: Disorders in normal central nervous system (CNS) development are often associated with epilepsy. This report characterizes seizures in a novel genetic model of developmental epilepsy, the Flathead (FH) rat. METHODS: Animals (n = 76) ages P0-22 were monitored for clinical and electrographic seizure activity. The effects of various AEDs on seizure frequency and duration also were assessed: phenobarbital (PB; 40 mg/kg), valproate (VPA; 400 mg/kg), or ethosuximide (ESM; 600 mg/kg). RESULTS: FHs display episodes of behavior characterized by whole-body tremor, strub tail, alternating forelimb clonus, and complete tonus. EEG recordings from neocortex reveal that FH seizures are bilateral and begin around P7. Seizures occur at a frequency of approximately six per hour from P7 to P18 and the average duration of seizures increases through development. PB, VPA, and ESM failed to prevent seizures; however, PB significantly increased the interval of seizures but had no effects on the duration of seizures, whereas VPA decreased the duration of seizures and not the interval. CONCLUSIONS: Seizures in FH rats occur at a constant and high frequency through a defined period in early postnatal development, and these seizures are not completely blocked by high doses of PB, VPA, or ESM. Because FH is a single-locus mutant displaying a highly regular pattern of seizure activity, it is an ideal model for examining the process of epileptogenesis in the developing brain, evaluating new AED therapies, and determining the identity of a gene essential to the normal development of cortical excitability.},
	Author = {Sarkisian, M.R. and Rattan, S. and D'Mello, S.R. and LoTurco, J.J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Journal = {Epilepsia},
	Keywords = {CK},
	Pages = {394-400},
	Title = {Characterization of seizures in the flathead rat: a new genetic model of epilepsy in early postnatal development},
	Uuid = {D7AD22C8-69B0-11DA-A4B6-000D9346EC2A},
	Volume = {40},
	Year = {1999}}

@article{Sarkisian:1999,
	Abstract = {PURPOSE: Disorders in normal central nervous system (CNS) development are often associated with epilepsy. This report characterizes seizures in a novel genetic model of developmental epilepsy, the Flathead (FH) rat. METHODS: Animals (n = 76) ages P0-22 were monitored for clinical and electrographic seizure activity. The effects of various AEDs on seizure frequency and duration also were assessed: phenobarbital (PB; 40 mg/kg), valproate (VPA; 400 mg/kg), or ethosuximide (ESM; 600 mg/kg). RESULTS: FHs display episodes of behavior characterized by whole-body tremor, strub tail, alternating forelimb clonus, and complete tonus. EEG recordings from neocortex reveal that FH seizures are bilateral and begin around P7. Seizures occur at a frequency of approximately six per hour from P7 to P18 and the average duration of seizures increases through development. PB, VPA, and ESM failed to prevent seizures; however, PB significantly increased the interval of seizures but had no effects on the duration of seizures, whereas VPA decreased the duration of seizures and not the interval. CONCLUSIONS: Seizures in FH rats occur at a constant and high frequency through a defined period in early postnatal development, and these seizures are not completely blocked by high doses of PB, VPA, or ESM. Because FH is a single-locus mutant displaying a highly regular pattern of seizure activity, it is an ideal model for examining the process of epileptogenesis in the developing brain, evaluating new AED therapies, and determining the identity of a gene essential to the normal development of cortical excitability.},
	Author = {Sarkisian, M. R. and Rattan, S. and D'Mello, S. R. and LoTurco, J. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Rats, Mutant Strains;Animals;Rats;Seizures;Phenobarbital;Brain;Valproic Acid;Female;Epilepsy;Mutation;21 Dysplasia-heterotopia;Rats, Wistar;research support, non-u.s. gov't;Behavior, Animal;Models, Genetic;Disease Models, Animal;Ethosuximide;Male;research support, u.s. gov't, p.h.s.;21 Neurophysiology;Cerebral Cortex;24 Pubmed search results 2008;Electroencephalography;Anticonvulsants},
	Month = {4},
	Nlm_Id = {2983306R},
	Number = {4},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, Storrs 06269, USA.},
	Pages = {394-400},
	Pubmed = {10219263},
	Title = {Characterization of seizures in the flathead rat: a new genetic model of epilepsy in early postnatal development},
	Uuid = {E06D81CF-2705-4AF9-BFF9-B626418A72E8},
	Volume = {40},
	Year = {1999}}

@article{Sarkisian:2006,
	Abstract = {Periventricular heterotopia (PVH) is a congenital malformation of human cerebral cortex frequently associated with Filamin-A (FLN-A) mutations but the pathogenetic mechanisms remain unclear. Here, we show that the MEKK4 (MAP3K4) pathway is involved in Fln-A regulation and PVH formation. MEKK4(-/-) mice developed PVH associated with breaches in the neuroependymal lining which were largely comprised of neurons that failed to reach the cortical plate. RNA interference (RNAi) targeting MEKK4 also impaired neuronal migration. Expression of Fln was elevated in MEKK4(-/-) forebrain, most notably near sites of failed neuronal migration. Importantly, recombinant MKK4 protein precipitated a complex containing MEKK4 and Fln-A, and MKK4 mediated signaling between MEKK4 and Fln-A, suggesting that MKK4 may bridge these molecules during development. Finally, we showed that wild-type FLN-A overexpression inhibited neuronal migration. Collectively, our results demonstrate a link between MEKK4 and Fln-A that impacts neuronal migration initiation and provides insight into the pathogenesis of human PVH.},
	Author = {Sarkisian, Matthew R. and Bartley, Christopher M. and Chi, Hongbo and Nakamura, Fumihiko and Hashimoto-Torii, Kazue and Torii, Masaaki and Flavell, Richard A. and Rakic, Pasko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:45:56 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {research support, non-u.s. gov't;research support, u.s. gov't, p.h.s.;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Department of Neurobiology and Kavli Institute of Neuroscience, Yale University School of Medicine, New Haven, Connecticut 06520, USA.},
	Pages = {789-801},
	Pii = {S0896-6273(06)00823-3},
	Pubmed = {17145501},
	Title = {MEKK4 signaling regulates filamin expression and neuronal migration},
	Uuid = {05E99490-3D5C-48ED-BA8A-42754CE3BB29},
	Volume = {52},
	Year = {2006},
	url = {papers/Sarkisian_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.10.024}}

@article{Sasaki:1989,
	Abstract = {We isolated two subclasses of astrocytes, oligodendrocytes and ameboid microglia from Lewis rat cerebral cortex and analyzed Ia antigen expression on each glial cell type by immunofluorescent microscopy and cytofluorometry. All of these expressed little or no Ia without interferon-gamma (IFN-gamma) treatment. Following IFN-gamma treatment, Ia expression was observed on a majority (approximately 80\%) of ameboid microglia, on half (approximately 55\%) of the type 1 astrocytes, on a small number (approximately 7\%) of type 2 astrocytes, but not on oligodendrocytes. These findings suggest that the type 1 astrocyte and microglia may play more predominant roles in Ia-related, immune-mediated intracerebral lesions although the type 2 astrocytes may also be involved. 90062513 0165-5728 Journal Article},
	Author = {Sasaki, A. and Levison, S. W. and Ting, J. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neuroimmunol},
	Keywords = {Histocompatibility Antigens Class II/*immunology;Flow Cytometry;Rats, Inbred Lew;G abstr;Rats;Comparative Study;Oligodendroglia/immunology;Animal;11 Glia;Cerebral Cortex/cytology/*immunology;Microscopy, Fluorescence;Neuroglia/*immunology/ultrastructure;Cells, Cultured;Support, Non-U.S. Gov't;Astrocytes/immunology},
	Number = {1},
	Organization = {Lineberger Cancer Center, University of North Carolina, Chapel Hill 27599.},
	Pages = {63-74},
	Pubmed = {2584392},
	Title = {Comparison and quantitation of Ia antigen expression on cultured macroglia and ameboid microglia from Lewis rat cerebral cortex: analyses and implications},
	Uuid = {0D6CABE3-3E12-4B35-BBE1-93D0FE585CE9},
	Volume = {25},
	Year = {1989},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2584392}}

@article{Sasaki:1990,
	Abstract = {The roles of intracellular second messengers in interferon-gamma (IFN-gamma)-induced Ia antigen (Ag) expression by astroglia and microglia were examined. Ia Ag on both glia types was induced by IFN-gamma. Reagents known to increase intracellular cAMP or activate intracellular protein kinase C (PKC) reduced IFN-gamma-induced Ia Ag expression by astroglia. In contrast, increasing intracellular cAMP had no suppressive effect on Ia Ag expression by microglia. These results indicate (1) cAMP and PKC negatively regulate IFN-gamma-induced Ia expression on astroglia, and (2) Ia expression is regulated differentially in astroglia vs. microglia. These findings may explain the frequent observation of Ia+ microglia (or macrophages) but not astroglia in various neurodegenerative diseases. 91009783 0165-5728 Journal Article},
	Author = {Sasaki, A. and Levison, S. W. and Ting, J. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neuroimmunol},
	Keywords = {Neuroglia/*immunology;Enzyme Activation;Second Messenger Systems/*physiology;Protein Kinase C/*physiology;G abstr;Rats;Tetradecanoylphorbol Acetate/pharmacology;Animal;11 Glia;Histocompatibility Antigens Class II/*analysis;Cells, Cultured;Support, Non-U.S. Gov't;Rats, Inbred Strains;Interferon Type II/*pharmacology;Cyclic AMP/*physiology},
	Number = {1-3},
	Organization = {Lineberger Cancer Center, University of North Carolina, Chapel Hill 27599.},
	Pages = {213-22},
	Pubmed = {2170439},
	Title = {Differential suppression of interferon-gamma-induced Ia antigen expression on cultured rat astroglia and microglia by second messengers},
	Uuid = {8EDC6C49-6025-410C-9192-A2141BB9C8BC},
	Volume = {29},
	Year = {1990},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2170439}}

@article{Sasaki:1996,
	Abstract = {The immunophenotype of perivascular cells (PC) in temporal lobe tissues obtained at autopsy in 48 patients (aged 41-88 years) was characterized using light and electron microscopic immunocytochemistry with a variety of antibodies. In all cases studied, PC bearing CD11c (Ki-M1P) and CD68 (KP1) were distributed throughout the temporal cortex. In addition to Ki-M1P and KP1, the monoclonal antibodies against major histocompatibility complex (MHC) class II antigen (Ag) (LN-3, CR3.43), anti-leucocyte common antigen (LCA), LN-5, Mac 387 were all found in PC with variable immunoreactivity. In contrast, LN-1 and OPD4 were not found in PC, although the former showed nearly constant staining of resting microglia. Semiquantitative analysis disclosed differences in the numbers of cells labeled with the markers in the 21 normal brains (Ki-M1P >KP1 >>LCA, LN-3, LN-5 >>Mac 387). Ultrastructurally, immunoreactivity for Ki-M1P, KP1, and LN-3 was observed in PC with cytoplasm containing dense lysosomal bodies. In brains from patients with Alzheimer's type dementia, PC were seen in the wall of beta-amyloid protein-positive small vessels. However, there was no definite alteration of antigenicity in PC from AD brains compared with those from normal brains. The immunophenotype of PC was similar to that of macrophages, which were observed in the perivascular spaces and the leptomeninges in some normal and diseased brains. In contrast with PC, however, macrophages showed high incidence of labeling for some macrophage markers LN-5 and Mac 387. These findings demonstrate that PC may be a normal constituent of the adult human brain with a variable expression of monocyte/macrophages markers and MHC class II Ag and that PC could be distinguished from resting microglia by their morphology and by their immunophenotype.},
	Author = {Sasaki, A. and Nakazato, Y. and Ogawa, A. and Sugihara, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {1320-5463},
	Journal = {Pathol Int},
	Keywords = {Humans;Amyloid beta-Protein;Middle Aged;Pericytes;Macrophages;Immunoenzyme Techniques;Female;Antigens, CD;Cell Count;11 Glia;Immunophenotyping;Male;Aged;Alzheimer Disease;Aged, 80 and over;Adult;Temporal Lobe;Biological Markers;Histocompatibility Antigens Class II;Blood Vessels},
	Medline = {20305900},
	Month = {1},
	Nlm_Id = {9431380},
	Number = {1},
	Organization = {Department of Pathology, Gunma University School of Medicine, Maebashi, Japan.},
	Pages = {15-23},
	Pubmed = {10846545},
	Title = {The immunophenotype of perivascular cells in the human brain},
	Uuid = {30B580C2-62A5-4E51-A897-C0011E046F8E},
	Volume = {46},
	Year = {1996}}

@article{Sato:2007a,
	Abstract = {Wiskott-Aldrich syndrome protein (WASP) plays important roles in TCR signaling, but its roles in signal transduction in innate immune cells have not been well characterized. As microglia are the primary immune effector cells in the brain, WASP may possibly have important roles in microglial activation, such as production of inflammatory and anti-inflammatory cytokines and neurotoxic factors. Here, we established a microglial cell line from WASP dominant-negative transgenic (Tg) mice overexpressing the N-terminal enabled/vasodilator-stimulated phosphoprotein homology 1 (EVH1) domain. WASP Tg microglia were impaired in production of inflammatory cytokines such as tumor necrosis factor-alpha, IL-6 and IL-1beta upon LPS stimulation, whereas anti-inflammatory IL-10 production was significantly enhanced. Also, LPS-induced phosphorylation of nuclear factor kappaB was reduced in WASP Tg microglia. Furthermore, WASP Tg microglia exhibited less cytotoxicity against co-cultured neurons after stimulation by LPS and IFN-gamma, with a concordant decrease in nitric oxide production. These results strongly suggest that WASP may have pivotal roles through the EVH1 domain in the LPS signaling cascade, either directly or indirectly, and modulates inflammatory immune responses in microglia.},
	Author = {Sato, Mitsuru and Ogihara, Kazumasa and Sawahata, Ryoko and Sekikawa, Kenji and Kitani, Hiroshi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0953-8178},
	Journal = {Int Immunol},
	Keywords = {research support, non-u.s. gov't;11 Glia;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {8916182},
	Number = {8},
	Organization = {Transgenic Animal Research Center, National Institute of Agrobiological Sciences, 1-2 Ohwashi, Tsukuba, Ibaraki 305-8634, Japan. sato\_mitsuru\@affrc.go.jp},
	Pages = {901-11},
	Pii = {dxm074},
	Pubmed = {17698982},
	Title = {Impaired LPS-induced signaling in microglia overexpressing the Wiskott-Aldrich syndrome protein N-terminal domain},
	Uuid = {44646809-B493-4A56-9891-C96EC8387952},
	Volume = {19},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/intimm/dxm074}}

@article{Satoh:2000,
	Abstract = {The effects of activin A were investigated on the development of a multipotent neural stem cell line (MEB5) and an astrocyte progenitor cell line (AP-16) that were established from murine central nervous system (CNS). Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis demonstrated that each cell line expresses both type I and type II activin receptors and signaling molecules for activin, Smad2, Smad3, and Smad4. Activin A did not affect the proliferation of MEB5 and AP-16 cells. When each cell line was treated alone with activin A, glial fibrillary acidic protein (GFAP), a marker for astrocytes, was induced in AP-16 cells, but not in MEB5 cells. However, activin A accelerated the leukemia inhibitory factor (LIF)-induced astroglial differentiation of MEB5 cells. These results suggest that activin promotes astrocyte differentiation of CNS neural progenitors, and the competence to activin is different between multipotent stem cells and unipotent astrocyte progenitor cells.},
	Author = {Satoh, M. and Sugino, H. and Yoshida, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Neurosci Lett},
	Keywords = {Activin Receptors, Type II;Glial Fibrillary Acidic Protein/metabolism;Cell Differentiation/*drug effects;DNA-Binding Proteins/genetics;RNA, Messenger/analysis/genetics;Stem Cells/cytology/*drug effects;Neurons/cytology/*drug effects;Receptors, Growth Factor/genetics;Astrocytes/cytology/*drug effects;Animal;C abstr;Mice, Inbred C3H;Activin Receptors, Type I;Activins;Cell Line;Support, Non-U.S. Gov't;Central Nervous System/*cytology/drug effects;Inhibins/*pharmacology;04 Adult neurogenesis factors;Growth Inhibitors/pharmacology;Mice;Lymphokines/pharmacology;Trans-Activators/genetics;Cell Division/drug effects},
	Number = {3},
	Organization = {Animal Cell Bank, Institute for Fermentation, Osaka (IFO), 2-17-85 Juso- honmachi, Yodogawa-ku, Osaka, Japan. satoh-motonobu\@ifo.or.jp},
	Pages = {143-6.},
	Title = {Activin promotes astrocytic differentiation of a multipotent neural stem cell line and an astrocyte progenitor cell line from murine central nervous system},
	Uuid = {1D167BE4-4B96-4880-9011-5133CC956DAB},
	Volume = {284},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10773419}}

@article{Saura:2003,
	Abstract = {Microglia can be isolated with high purity but low yield by shaking off loosely adherent cells from mixed glial cultures. Here we describe a new technique for isolating microglia with an average yield close to 2,000,000 microglial cells/mouse pup, more than five times higher than that of the shaking method. Confluent mixed glial cultures are subjected to mild trypsinization (0.05-0.12\%) in the presence of 0.2-0.5 mM EDTA and 0.5-0.8 mM Ca2+. This results in the detachment of an intact layer of cells containing virtually all the astrocytes, leaving undisturbed a population of firmly attached cells identified as >98\%microglia. These almost pure microglial preparations can be kept in culture for weeks and show proliferation and phagocytosis. Treatment with macrophage colony-stimulating factor and lipopolysaccharide, alone or in the presence of interferon gamma, induces typical microglial responses in terms of proliferation, morphological changes, nuclear factor-kappaB translocation, NO, and tumor necrosis alpha release and phagocytosis. This method allows for the preparation of highly enriched mouse or rat microglial cultures with ease and reproducibility. Because of its high yield, it can be especially convenient when high amounts of microglial protein/mRNA are required or in cases in which the starting material is limited, such as microglial cultures from transgenic animals.},
	Author = {Saura, Josep and Tusell, Josep Maria and Serratosa, Joan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Trypsin;Cells, Cultured;Cell Separation;Tumor Necrosis Factor;NF-kappa B;Mice, Inbred C57BL;Cell Division;Cell Count;11 Glia;Microglia;Not relevant;Nitric Oxide;Mice;Support, Non-U.S. Gov't;Phagocytosis;Animals;Brain},
	Medline = {22964698},
	Month = {12},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Pharmacology and Toxicology, Institut d'Investigacions Biom\`{e}diques de Barcelona, IIBB-CSIC, Barcelona, Spain. jsafat\@iibb.csic.es},
	Pages = {183-9},
	Pubmed = {14603460},
	Title = {High-yield isolation of murine microglia by mild trypsinization},
	Uuid = {522AE522-755E-4747-82AD-9975FCAA6AD8},
	Volume = {44},
	Year = {2003},
	url = {papers/Saura_Glia2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10274}}

@article{Sawamoto:2001,
	Abstract = {Mesencephalic precursor cells may one day provide dopaminergic neurons for the treatment of Parkinson's disease. However, the generation of dopaminergic neurons from mesencephalic precursors has been difficult to follow, partly because an appropriate means for recognizing mesencephalic ventricular zone precursors has not been available. To visualize and isolate mesencephalic precursor cells from a mixed population, we used transgenic mice and rats carrying green fluorescent protein (GFP) cDNA under the control of the nestin enhancer. nestin- driven GFP was detected in the mesencephalic ventricular zone, and it colocalized with specific markers for neural precursor cells. In addition, data from flow-cytometry indicated that Prominin/CD133, a cell-surface marker for ventricular zone cells, was expressed specifically in these GFP-positive (GFP(+)) cells. After sorting by fluorescence-activated cell sorting, the GFP(+) cells proliferated in vitro and expressed precursor cell markers but not neuronal markers. Using clonogenic sphere formation assays, we showed that this sorted population was enriched in multipotent precursor cells that could differentiate into both neurons and glia. Importantly, many neurons generated from nestin-GFP-sorted mesencephalic precursors developed a dopaminergic phenotype in vitro. Finally, nestin-GFP(+) cells were transplanted into the striatum of a rat model of Parkinson's disease. Bromodeoxyuridine-tyrosine hydroxylase double-labeling revealed that the transplanted cells generated new dopaminergic neurons within the host striatum. The implanted cells were able to restore dopaminergic function in the host striatum, as assessed by a behavioral measure: recovery from amphetamine-induced rotation. Together, these findings indicate that precursor cells harvested from the embryonic ventral mesencephalon can generate dopaminergic neurons able to restore function to the chemically denervated adult striatum.},
	Author = {Sawamoto, K. and Nakao, N. and Kakishita, K. and Ogawa, Y. and Toyama, Y. and Yamamoto, A. and Yamaguchi, M. and Mori, K. and Goldman, S. A. and Itakura, T. and Okano, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci},
	Keywords = {Mesencephalon/cytology/embryology/*transplantation;Intermediate Filament Proteins/genetics/*metabolism;Disease Models, Animal;Male;Cells, Cultured;Flow Cytometry;03 Adult neurogenesis progenitor source;Recombinant Fusion Proteins/genetics/*metabolism;Transgenes;Brain Tissue Transplantation;Cell Differentiation/physiology;Oxidopamine;Support, U.S. Gov't, P.H.S.;Luminescent Proteins/genetics;Animal;Rats, Sprague-Dawley;Brain/pathology/surgery;Fetal Tissue Transplantation;Graft Survival;Colony-Forming Units Assay;02 Adult neurogenesis migration;Rats;BB;Neurons/cytology/*metabolism;Female;Membrane Glycoproteins/biosynthesis;Mice;Treatment Outcome;Stem Cells/cytology/metabolism/*transplantation;Dopamine/biosynthesis;Support, Non-U.S. Gov't;Animals, Transgenic;Parkinsonian Disorders/chemically induced/*therapy},
	Number = {11},
	Organization = {Division of Neuroanatomy, Department of Neuroscience, Biomedical Research Center, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.},
	Pages = {3895-903.},
	Title = {Generation of dopaminergic neurons in the adult brain from mesencephalic precursor cells labeled with a nestin-GFP transgene},
	Uuid = {42270861-99A5-4A32-9619-8D8B202438B0},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11356877%20http://www.jneurosci.org/cgi/content/full/21/11/3895%20http://www.jneurosci.org/cgi/content/abstract/21/11/3895}}

@article{Saxe:2006,
	Abstract = {Although hippocampal neurogenesis has been described in many adult mammals, the functional impact of this process on physiology and behavior remains unclear. In the present study, we used two independent methods to ablate hippocampal neurogenesis and found that each procedure caused a limited behavioral deficit and a loss of synaptic plasticity within the dentate gyrus. Specifically, focal X irradiation of the hippocampus or genetic ablation of glial fibrillary acidic protein-positive neural progenitor cells impaired contextual fear conditioning but not cued conditioning. Hippocampal-dependent spatial learning tasks such as the Morris water maze and Y maze were unaffected. These findings show that adult-born neurons make a distinct contribution to some but not all hippocampal functions. In a parallel set of experiments, we show that long-term potentiation elicited in the dentate gyrus in the absence of GABA blockers requires the presence of new neurons, as it is eliminated by each of our ablation procedures. These data show that new hippocampal neurons can be preferentially recruited over mature granule cells in vitro and may provide a framework for how this small cell population can influence behavior.},
	Author = {Saxe, Michael D. and Battaglia, Fortunato and Wang, Jing-Wen W. and Malleret, Gael and David, Denis J. and Monckton, James E. and Garcia, A. Denise R. and Sofroniew, Michael V. and Kandel, Eric R. and Santarelli, Luca and Hen, Ren{\'e} and Drew, Michael R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Conditioning (Psychology);Glial Fibrillary Acidic Protein;Hippocampus;Neuronal Plasticity;Fear;Memory;Mice, Transgenic;Electrophysiology;Thymidine Kinase;Animals;Male;Mice;Neurons;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {7505876},
	Number = {46},
	Organization = {Center For Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.},
	Pages = {17501-6},
	Pii = {0607207103},
	Pubmed = {17088541},
	Title = {Ablation of hippocampal neurogenesis impairs contextual fear conditioning and synaptic plasticity in the dentate gyrus},
	Uuid = {8CF6207C-8B1C-4DD2-B137-9A77C7E239D5},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0607207103}}

@article{Saxe:2007,
	Abstract = {To explore the function of adult hippocampal neurogenesis, we ablated cell proliferation by using two independent and complementary methods: (i) a focal hippocampal irradiation and (ii) an inducible and reversible genetic elimination of neural progenitor cells. Previous studies using these methods found a weakening of contextual fear conditioning but no change in spatial reference memory, suggesting a supportive role for neurogenesis in some, but not all, hippocampal-dependent memory tasks. In the present study, we examined hippocampal-dependent and -independent working memory using different radial maze tasks. Surprisingly, ablating neurogenesis caused an improvement of hippocampal-dependent working memory when repetitive information was presented in a single day. These findings suggest that adult-born cells in the dentate gyrus have different, and in some cases, opposite roles in distinct types of memory.},
	Author = {Saxe, Michael D. and Malleret, Ga{\"e}l and Vronskaya, Svetlana and Mendez, Indira and Garcia, A. Denise and Sofroniew, Michael V. and Kandel, Eric R. and Hen, Ren{\'e}},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {01 Adult neurogenesis general;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7505876},
	Number = {11},
	Organization = {*Center for Neurobiology and Behavior and Howard Hughes Medical Institute, Columbia University, 722 West 168th Street, New York, NY 10032.},
	Pages = {4642-6},
	Pii = {0611718104},
	Pubmed = {17360577},
	Title = {Paradoxical influence of hippocampal neurogenesis on working memory},
	Uuid = {41943302-B19A-4EFA-8239-847B22D68AC5},
	Volume = {104},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0611718104}}

@article{Scaradavou:1997,
	Abstract = {The purposes of the research reported here were first to explore a murine model for human placental and umbilical cord blood transplantation and second to evaluate the engraftment ability of ex vivo cultured hematopoietic cells. Murine near-term fetal and neonatal peripheral blood (FNPB) cells, genetically marked with the human multiple drug resistance transgene (MDR1) were used for syngeneic transplants into sublethally irradiated adult mice. Donor cells were transplanted either fresh and untreated, or after ex vivo culture in the presence of the hematopoietic growth factors recombinant murine stem cell factor, recombinant human interleukin-3 (rHu IL-3), and rHu IL-6, in a liquid culture system. To evaluate, count, and characterize FNPB progenitor cell-derived colonies, neonatal mouse mononuclear cells were cultured directly in methylcellulose with growth factors. To assess their ex vivo expansion ability, FNPB mononuclear cells were first cultured in liquid medium for 3 to 8 days and then transferred to semisolid assay plates. Evaluation of the cell counts after liquid culture showed a 1.4- to 11.6-fold increase, and the numbers of colonies observed in methylcellulose were similar to those produced by fresh FNPB cells. Donor-type engraftment was demonstrated by polymerase chain reaction (PCR) amplification of the human MDR1 transgene in the peripheral blood of all surviving animals (5 of 7 recipients of the fresh, and 3 of 8 recipients of the ex vivo-cultured cells) 2 to 4 months after transplantation. The proportion of donor leukocytes in the peripheral blood of the recipients (chimerism) was evaluated using fluorescence in situ hybridization (FISH) analysis 4 to 6 months after transplantation and ranged from 2\%to 26\%. In addition, bone marrow cultures were obtained from two recipient animals: one had received fresh-untreated cells and was evaluated 8 months after transplant, the other had received ex vivo cultured cells and was tested 14 months after grafting. The derived hematopoietic colonies were tested by PCR and the transgene was detected, conclusively proving long-term engraftment of donor cells. These results indicate that FNPB transplants can be successfully performed in sublethally irradiated mice with and without ex vivo culture. Long-term donor-type engraftment with sustained chimerism has been demonstrated. Thus, murine neonatal blood grafts can be used as an animal model for cord blood transplantation for gene therapy studies where complete myeloablation is not desirable and partial replacement of defective marrow may be sufficient. Furthermore, the possibility of numerically expanding hematopoietic progenitor cells contained in neonatal blood without affecting their engraftment ability could facilitate use of cord blood grafts in adult recipients.},
	Author = {Scaradavou, A. and Isola, L. and Rubinstein, P. and Galperin, Y. and Najfeld, V. and Berlin, D. and Gordon, J. and Weinberg, R. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Animals;Colony-Forming Units Assay;Humans;Cells, Cultured;Bone Marrow Transplantation;Models, Biological;Female;Mice, Transgenic;11 Glia;Methylcellulose;Male;Hematopoietic Stem Cell Transplantation;Leukocyte Count;Radiation Chimera;Mice, Inbred Strains;Research Support, U.S. Gov't, P.H.S.;Leukocyte Transfusion;Survival Analysis;Animals, Newborn;Fetal Blood;Mice;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {97180166},
	Month = {2},
	Nlm_Id = {7603509},
	Number = {3},
	Organization = {Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, USA.},
	Pages = {1089-99},
	Pubmed = {9028342},
	Title = {A murine model for human cord blood transplantation: near-term fetal and neonatal peripheral blood cells can achieve long-term bone marrow engraftment in sublethally irradiated adult recipients},
	Uuid = {13CF6F38-8477-48AE-9028-0C3BD851E5C2},
	Volume = {89},
	Year = {1997}}

@article{Scerri:2005,
	Abstract = {RATIONALE: Nicotine is reported to improve learning and memory in experimental animals. Improved learning and memory has also been related to increased neurogenesis in the dentate gyrus (DG) of the hippocampal formation. Surprisingly, recent studies suggest that self-administered nicotine depresses cell proliferation in the DG. OBJECTIVE: To test the hypothesis that the effects of nicotine on cell proliferation in the DG and learning and memory depend upon the nicotine dose administered. METHODS: Rats were chronically infused from subcutaneous osmotic mini pumps with nicotine (0.25 or 4 mg kg(-1) day(-1)) or the saline vehicle for 10 days. Half the rats in each treatment group were trained to locate a hidden platform in a water maze task on days 4-7; a probe trial was performed on day 8. The remaining rats remained in their home cages. The effects of nicotine and of training in the water maze task on cell genesis in the DG were determined by measuring 5-bromo-2'-deoxyuridine (BrDU) uptake using fluorescence immunohistochemistry. RESULTS: Training in the water maze task increased cell proliferation in the DG. Infusions of nicotine at 4 mg kg(-1) day(-1), but not 0.25 mg kg(-1) day(-1), decreased cell proliferation in both untrained animals and animals trained in the maze and impaired spatial learning. CONCLUSIONS: The data suggest that learning in the water maze task is impaired by higher doses of nicotine tested, and that this response may be related to reduced cell genesis in the DG.},
	Author = {Scerri, and Stewart, and Breen, and Balfour,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0033-3158},
	Journal = {Psychopharmacology (Berl)},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {7608025},
	Organization = {Section of Psychiatry and Behavioural Sciences, Division of Pathology and Neuroscience, Ninewells Hospital and Medical School, University of Dundee, Dundee, Scotland, DD1 9SY, UK, d.j.k.balfour\@dundee.ac.uk.},
	Pages = {1-7},
	Pubmed = {16025316},
	Title = {The effects of chronic nicotine on spatial learning and bromodeoxyuridine incorporation into the dentate gyrus of the rat},
	Uuid = {ADFD5F91-E269-49F5-8B84-3E636ADB8639},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00213-005-0086-4}}

@article{Scharff:2000,
	Abstract = {In the high vocal center (HVC) of adult songbirds, increases in spontaneous neuronal replacement correlate with song changes and with cell death. We experimentally induced death of specific HVC neuron types in adult male zebra finches using targeted photolysis. Induced death of a projection neuron type that normally turns over resulted in compensatory replacement of the same type. Induced death of the normally nonreplaced type did not stimulate their replacement. In juveniles, death of the latter type increased recruitment of the replaceable kind. We infer that neuronal death regulates the recruitment of replaceable neurons. Song deteriorated in some birds only after elimination of replaceable neurons. Behavioral deficits were transient and followed by variable degrees of recovery. This raises the possibility that induced neuronal replacement can restore a learned behavior.},
	Author = {Scharff, C. and Kirn, J. R. and Grossman, M. and Macklis, J. D. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Neuron},
	Keywords = {Brain/cytology/physiology;Porphyrins;Cell Division/physiology;Songbirds/*physiology;Neurons/*cytology/physiology;06 Adult neurogenesis injury induced;Cell Death/physiology;Animal;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Nerve Degeneration/chemically induced/physiopathology;D-11;Support, Non-U.S. Gov't;Vocalization, Animal/*physiology;Age Factors;Learning/physiology;Male},
	Number = {2},
	Organization = {Department of Animal Behavior, The Rockefeller University, New York, New York 10021, USA. scharfc\@rockvax.rockefeller.edu},
	Pages = {481-92.},
	Title = {Targeted neuronal death affects neuronal replacement and vocal behavior in adult songbirds},
	Uuid = {0A1A36FA-0EA4-40FC-8EB1-935DF4EC78B8},
	Volume = {25},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10719901}}

@article{Scheiffele:2000,
	Abstract = {Most neurons form synapses exclusively with other neurons, but little is known about the molecular mechanisms mediating synaptogenesis in the central nervous system. Using an in vitro system, we demonstrate that neuroligin-1 and -2, postsynaptically localized proteins, can trigger the de novo formation of presynaptic structure. Nonneuronal cells engineered to express neuroligins induce morphological and functional presynaptic differentiation in contacting axons. This activity can be inhibited by addition of a soluble version of beta-neurexin, a receptor for neuroligin. Furthermore, addition of soluble beta-neurexin to a coculture of defined pre- and postsynaptic CNS neurons inhibits synaptic vesicle clustering in axons contacting target neurons. Our results suggest that neuroligins are part of the machinery employed during the formation and remodeling of CNS synapses.},
	Author = {Scheiffele, P. and Fan, J. and Choih, J. and Fetter, R. and Serafini, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Synapses;Cell Differentiation;10 Development;research support, non-u.s. gov't;Membrane Proteins;Nerve Tissue Proteins;Gene Expression Regulation;10 circuit formation;Coculture Techniques;COS Cells;Animals;Humans;24 Pubmed search results 2008;Neurons},
	Month = {6},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA. scheiffe\@uclink4.berkeley.edu},
	Pages = {657-69},
	Pii = {S0092-8674(00)80877-6},
	Pubmed = {10892652},
	Title = {Neuroligin expressed in nonneuronal cells triggers presynaptic development in contacting axons},
	Uuid = {6BAFB064-D8D4-4BA6-AD85-432452A3222A},
	Volume = {101},
	Year = {2000},
	url = {papers/Scheiffele_Cell2000.pdf}}

@article{Schermer:2002,
	Abstract = {Cytokines play an important role in the regulation of proliferation and migration in the central nervous system. The aim of this study was to determine if granulocyte macrophage-colony stimulating factor (GM-CSF) activates cells in the cortex of organotypic brain slice cultures. Our data show that murine GM-CSF markedly stimulated the proliferation and migration of small round microglia from a cortex slice. These round cells were strongly positive for integrin CD11b (OX-42), isolectin B4-lectin-binding, the monocytic marker ED1 and partly expressed major histocompatibility complex (MHC) class II antigen (OX-6). Only some differentiated microglia were visible which expressed the integrin CD11c and MHCII. GM-CSF enhanced the proliferation as analyzed by bromodeoxyuridine incorporation. The number of migrated cells decreased during culturing and enhanced terminal dUTP nick-end labelling positive nuclei were found. Taken together, our data conclude that GM-CSF is an important cytokine, which regulates the proliferation and migration of cortical microglia.},
	Author = {Schermer, Christine and Humpel, Christian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Cell Differentiation;Signal Transduction;Animals;Rats;Microglia;Immunologic Surveillance;Cell Movement;11 Glia;Granulocyte-Macrophage Colony-Stimulating Factor;Animals, Newborn;Support, Non-U.S. Gov't;Membrane Glycoproteins;Cerebral Cortex;Cell Division;Immunohistochemistry;Membrane Proteins;Organ Culture;Lectins;Histocompatibility Antigens Class II},
	Medline = {22129465},
	Month = {8},
	Nlm_Id = {7600130},
	Number = {2},
	Organization = {Laboratory of Psychiatry, Department of Psychiatry, University Innsbruck, Anichstrasse 35, 6020, Innsbruck, Austria.},
	Pages = {180-4},
	Pii = {S0304394002004962},
	Pubmed = {12133583},
	Title = {Granulocyte macrophage-colony stimulating factor activates microglia in rat cortex organotypic brain slices},
	Uuid = {F31A27E2-C3EC-458C-AC2E-5D944B0EB8A9},
	Volume = {328},
	Year = {2002},
	url = {papers/Schermer_NeurosciLett2002.pdf}}

@article{Schiefer:1999,
	Abstract = {Microglial motility was studied in living mammalian brain tissue using infrared gradient contrast microscopy in combination with video contrast enhancement and time lapse video recording. The infrared gradient contrast allows the visualization of living cells up to a depth of 60 microm in brain slices, in regions where cell bodies remain largely uninjured by the tissue preparation and are visible in their natural environment. In contrast to other techniques, including confocal microscopy, this procedure does not require any staining or labeling of cell membranes and thus guarantees the investigation of tissue which has not been altered, apart from during preparation. Microglial cells are activated and increase in number in the facial nucleus following peripheral axotomy. Thus we established the preparation of longitudinal rat brainstem slices containing the axotomized facial nucleus as a source of activated microglial cells. During prolonged video time lapse recordings, two different types of microglial cell motility could be observed. Microglial cells which had accumulated at the surface of the slice remained stationary but showed activity of the cell soma, developing pseudopods of different shape and size which undulated and which were used for phagocytosis of cell debris. Microglial phagocytosis of bacteria could be documented for the first time in situ. In contrast, ameboid microglia which did not display pseudopods but showed migratory capacity, could be observed exclusively in the depth of the tissue. Some of these cells maintained a close contact to neurons and appeared to move along their dendrites, a finding that may be relevant to the role of microglia in "synaptic stripping", the displacement of synapses following axotomy. This approach provides a valuable opportunity to investigate the interactions between activated microglial cells and the surrounding cellular and extracellular structures in the absence of staining or labeling, thus opening a wide field for the analysis of the cellular mechanisms involved in numerous pathologies of the CNS.},
	Author = {Schiefer, J. and Kampe, K. and Dodt, H. U. and Zieglg{\"a}nsberger, W. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Solitary Nucleus;Brain Stem;Image Processing, Computer-Assisted;Facial Nerve;Motor Neurons;Rats;Not relevant;Rats, Wistar;Microscopy, Video;11 Glia;Microglia;In Vitro;Axotomy;Animals;Cell Movement;Male},
	Medline = {20229902},
	Month = {6},
	Nlm_Id = {0364620},
	Number = {6},
	Organization = {Department of Neurology, Technical University Aachen, Pauwelsstr. 30, D-52057 Aachen, Germany.},
	Pages = {439-53},
	Pubmed = {10767097},
	Title = {Microglial motility in the rat facial nucleus following peripheral axotomy},
	Uuid = {B1B72030-38A8-456D-BBDC-455265FD995E},
	Volume = {28},
	Year = {1999}}

@article{Schiffer:2006,
	Abstract = {Nestin is a marker of early stages of neurocytogenesis. It has been studied in 50 neuroepithelial tumors, mostly gliomas of different malignancy grades, by immunohistochemistry, immunofluorescence, immunoblotting, and confocal microscopy and compared with GFAP and Vimentin. As an early marker of differentiation, Nestin is almost not expressed in diffuse astrocytomas, variably expressed in anaplastic astrocytomas and strongly and irregularly expressed in glioblastomas. Negative in oligodendrogliomas, it stains ependymomas and shows a gradient of expression in pilocytic astrocytomas. In glioblastomas, Nestin distribution does not completely correspond to that of GFAP and Vimentin with which its expression varies in tumor cells in a complementary way, as confirmed by confocal microscopy. Tumor cells can thus either derive from or differentiate toward the neurocytogenetic stages. Hypothetically, they could be put in relation with radial glia where during embriogenesis the three antigens are successively expressed. Completely negative cells of invasive or recurrent glioblastomas may represent malignant selected clones after accumulation of mutations or early stem cells not expressing antigens.},
	Author = {Schiffer, and Manazza, and Tamagno,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7600130},
	Organization = {Foundation Policlinico di Monza, Neuro-bio-oncology Center (Vercelli)/University of Turin, Italy.},
	Pii = {S0304-3940(06)00138-8},
	Pubmed = {16529857},
	Title = {Nestin expression in neuroepithelial tumors},
	Uuid = {BD31C835-285A-4746-9456-009BA3B4A707},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neulet.2006.02.034}}

@article{Schiller:2004,
	Abstract = {Epileptic seizures are composed of recurrent bursts of intense firing separated by periods of electrical quiescence. The mechanisms responsible for sustaining seizures and generating recurrent bursts are yet unclear. Using whole cell voltage recordings combined with intracellular calcium fluorescence imaging from bicuculline (BCC)-treated neocortical brain slices, I showed isolated paroxysmal depolarization shift (PDS) discharges were followed by a sustained afterdepolarization waveform (SADW) with an average peak amplitude of 3.3 +/- 0.9 mV and average half-width of 6.2 +/- 0.6 s. The SADW was mediated by the calcium-activated nonspecific cation current (I(can)) as it had a reversal potential of -33.1 +/- 6.8 mV, was unaffected by changing the intracellular chloride concentrations, was markedly diminished by buffering [Ca(2+)](i) with intracellular bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA), and was reversibly abolished by the I(can) blocker flufenamic acid (FFA). The Ca(2+) influx responsible for activation of I(can) was mediated by both N-methyl-d-aspartate-receptor channels, voltage-gated calcium channels and, to a lesser extent, internal calcium stores. In addition to isolated PDS discharges, BCC-treated brain slices also produced seizure-like events, which were accompanied by a prolonged depolarizing waveform underlying individual ictal bursts. The similarities between the initial part of this waveform and the SADW and the fact it was markedly reduced by buffering [Ca(2+)](i) with BAPTA strongly suggested it was mediated, at least in part, by I(can). Addition of FFA reversibly eliminated recurrent bursting, and transformed seizure-like events into isolated PDS responses. These results indicated I(can) was activated during epileptiform discharges and probably participated in sustaining seizure-like events.},
	Author = {Schiller, Yitzhak},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {Epilepsy;Electric Conductivity;Research Support, Non-U.S. Gov't;Ion Channels;21 Neurophysiology;Rats;Time Factors;Calcium;Cations;In Vitro;21 Calcium imaging;Neocortex;Electrophysiology;Rats, Wistar;Animals;24 Pubmed search results 2008;Flufenamic Acid},
	Month = {8},
	Nlm_Id = {0375404},
	Number = {2},
	Organization = {Department of Technology, Rambam Medical Center, 1 Efron St., P.O.B 9602 Haifa, Israel 31096. y\_schiller\@yahoo.com},
	Pages = {862-72},
	Pii = {92/2/862},
	Pubmed = {15277598},
	Title = {Activation of a calcium-activated cation current during epileptiform discharges and its possible role in sustaining seizure-like events in neocortical slices},
	Uuid = {B31FFC1F-3ABF-4E4F-A372-64353385D073},
	Volume = {92},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1152/jn.00972.2003}}

@article{Schilling:2003,
	Abstract = {Resident microglia and hematogenous macrophages play crucial roles in the pathogenetic cascade following cerebral ischemia but may functionally differ regarding neuroprotective and cytotoxic properties. Distinction between these cells has not been possible due to a lack of discriminating cellular markers. We generated bone marrow chimeric mice by transplanting bone marrow from green fluorescent protein (GFP) transgenic mice into irradiated wild-type recipients. Transient focal cerebral ischemia was induced by transient middle cerebral artery occlusion (MCAO) for 30 min. Resident microglia and infiltrating macrophages were identified by immunohistochemistry and GFP fluorescence after 1-28 days. The first blood-derived cells infiltrating the infarct area were seen on Day 1 and identified as granulocytes. Hematogenous GFP(+) macrophages were rarely observed on Day 2, reached peak numbers on Day 7, and decreased thereafter. In contrast, resident GFP(-) microglial cells rapidly became activated already on Day 1 after MCAO. Even on Days 4 and 7, most macrophage-like cells remained GFP(-), indicating their derivation from resident microglia. Hematogenous macrophages were able to acquire a ramified morphology indistinguishable from resident microglia while microglial cells could develop into a phagocytic phenotype indistinguishable from infiltrating macrophages. The vast majority of macrophages in the infarct area are derived from local microglia, revealing a remarkable predominance of local defense mechanisms over immune cells arriving from the blood. GFP bone marrow chimeric mice are a powerful tool to further differentiate the function of resident microglia and hematogenous macrophages following cerebral ischemia.},
	Author = {Schilling, Matthias and Besselmann, Michael and Leonhard, Christine and Mueller, Marcus and Ringelstein, E. Bernd and Kiefer, Reinhard},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Animals;Astrocytes;Disease Progression;Macrophages;Bone Marrow Transplantation;Brain;Microglia;Cell Movement;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Male;Radiation Chimera;Disease Models, Animal;Mice;Luminescent Proteins;Immunohistochemistry;Ischemic Attack, Transient;Research Support, Non-U.S. Gov't},
	Medline = {22838167},
	Month = {9},
	Nlm_Id = {0370712},
	Number = {1},
	Organization = {Department of Neurology, Universit{\"a}tsklinikum M{\"u}nster, M{\"u}nster, Germany.},
	Pages = {25-33},
	Pii = {S0014488603000827},
	Pubmed = {12957485},
	Title = {Microglial activation precedes and predominates over macrophage infiltration in transient focal cerebral ischemia: a study in green fluorescent protein transgenic bone marrow chimeric mice},
	Uuid = {597432AA-BF69-11DA-969D-000D9346EC2A},
	Volume = {183},
	Year = {2003},
	url = {papers/Schilling_ExpNeurol2003.pdf}}

@article{Schipke:2002,
	Abstract = {Pathologic impacts in the brain lead to a widespread activation of microglial cells far beyond the site of injury. Here, we demonstrate that glial Ca2+ waves can trigger responses in microglial cells. We elicited Ca2+ waves in corpus callosum glial cells by electrical stimulation or local adenosine triphosphate (ATP) ejection in acute brain slices. Macroglial cells, but not microglia, were bulk-loaded with Ca2+-sensitive dyes. Using a transgenic animal in which astrocytes were labeled by the enhanced green fluorescence protein (EGFP) allowed us to identify the reacting cell populations: the wave activated a Ca2+ response in both astrocytes and non-astrocytic glial cells and spread over hundreds of micrometers even into the adjacent cortical and ventricular cell layers. Regenerative ATP release and subsequent activation of metabotropic purinergic receptors caused the propagation of the glial Ca2+ wave: the wave was blocked by the purinergic receptor antagonist Reactive Blue 2 and was not affected by the gap junction blocker octanol, but enhanced in Ca2+ free saline. To test whether microglial cells respond to the wave, microglial cells were labeled with a dye-coupled lectin and membrane currents were recorded with the patch-clamp technique. When the wave passed by, a current with the characteristics of a purinergic response was activated. Thus, Ca2+ waves in situ are not restricted to astrocytic cells, but broadly activate different glial cell types.},
	Author = {Schipke, Carola G. and Boucsein, Clemens and Ohlemeyer, Carsten and Kirchhoff, Frank and Kettenmann, Helmut},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {Electric Stimulation;Adenosine Triphosphate;Astrocytes;Calcium;In Vitro;11 Glia;Microglia;Calcium Signaling;Animals;Brain;Membrane Potentials;Mice},
	Medline = {21676357},
	Month = {2},
	Nlm_Id = {8804484},
	Number = {2},
	Organization = {Max-Delbr{\"u}ck Center for Molecular Medicine, Cellular Neuroscience, D-13092 Berlin, Germany.},
	Pages = {255-7},
	Pii = {01-0514fje},
	Pubmed = {11772946},
	Title = {Astrocyte Ca2+ waves trigger responses in microglial cells in brain slices},
	Uuid = {D01CF6DE-1B03-4AB4-A7AB-B8A1BD51EC96},
	Volume = {16},
	Year = {2002},
	url = {papers/Schipke_FASEBJ2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.01-0514fje}}

@article{Schlief:2007,
	Abstract = {In both the vertebrate nose and the insect antenna, most olfactory receptor neurons (ORNs) respond to multiple odors. However, some ORNs respond to just a single odor, or at most to a few highly related odors. It has been hypothesized that narrowly tuned ORNs project to narrowly tuned neurons in the brain, and that these dedicated circuits mediate innate behavioral responses to a particular ligand. Here we have investigated neural activity and behavior downstream from two narrowly tuned ORN types in Drosophila melanogaster. We found that genetically ablating either of these ORN types impairs innate behavioral attraction to their cognate ligand. Neurons in the antennal lobe postsynaptic to one of these ORN types are, like their presynaptic ORNs, narrowly tuned to a pheromone. However, neurons postsynaptic to the second ORN type are broadly tuned. These results demonstrate that some narrowly tuned ORNs project to dedicated central circuits, ensuring a tight connection between stimulus and behavior, whereas others project to central neurons that participate in the ensemble representations of many odors.},
	Author = {Schlief, Michelle L. and Wilson, Rachel I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {21 Neurophysiology;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {9809671},
	Number = {5},
	Organization = {Department of Neurobiology, Harvard Medical School, 220 Longwood Ave., Boston, Massachusetts 02115, USA.},
	Pages = {623-30},
	Pii = {nn1881},
	Pubmed = {17417635},
	Title = {Olfactory processing and behavior downstream from highly selective receptor neurons},
	Uuid = {98FC3D69-784F-42B2-89D0-20F1986CAFDE},
	Volume = {10},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1881}}

@article{Schmid:2005,
	Abstract = {Extracellular matrix-like molecule reelin and cell surface adhesion receptors such as alpha3beta1 integrin can regulate neuronal migration and position in the developing cerebral cortex. Here we show that alpha3beta1 integrin binds to the N-terminal region of reelin, a site distinct from the region of reelin shown to associate with other reelin receptors such as VLDLR/ApoER2. Furthermore, Dab1, a member of the reelin signaling pathway, can complex with the cytoplasmic region of beta1 integrin in a reelin-dependent manner. Thus, alpha3beta1 integrin-reelin interactions may contribute to appropriate neuronal placement in the developing cerebral cortex.},
	Author = {Schmid, and Jo, and Shelton, and Kreidberg, and Anton,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {10 Development},
	Month = {2},
	Nlm_Id = {9110718},
	Organization = {UNC Neuroscience Center and the Department of Cell and Molecular Physiology, The University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.},
	Pii = {bhi041},
	Pubmed = {15703255},
	Title = {Reelin, Integrin and Dab1 Interactions during Embryonic Cerebral Cortical Development},
	Uuid = {A1AFA11D-9BF3-40E6-A976-6C8B9BD4DE89},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhi041}}

@article{Schmid:2004,
	Abstract = {We show that alpha3 integrin mutation disrupts distinct aspects of neuronal migration and placement in the cerebral cortex. The preplate develops normally in alpha3 integrin mutant mice. However, time lapse imaging of migrating neurons in embryonic cortical slices indicates retarded radial and tangential migration of neurons, but not ventricular zone-directed migration. Examination of the actin cytoskeleton of alpha3 integrin mutant cortical cells reveals aberrant actin cytoskeletal dynamics at the leading edges. Deficits are also evident in the ability of developing neurons to probe their cellular environment with filopodial and lamellipodial activity. Calbindin or calretinin positive upper layer neurons as well as the deep layer neurons of alpha3 integrin mutant mice expressing EGFP were misplaced. These results suggest that alpha3beta1 integrin deficiency impairs distinct patterns of neuronal migration and placement through dysregulated actin dynamics and defective ability to search and respond to migration modulating cues in the developing cortex.},
	Author = {Schmid, and Shelton, and Stanco, and Yokota, and Kreidberg, and Anton,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {10 Development},
	Nlm_Id = {8701744},
	Number = {24},
	Organization = {UNC Neuroscience Center and the Department of Cell and Molecular Physiology, The University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.},
	Pages = {6023-6031},
	Pii = {dev.01532},
	Pubmed = {15537685},
	Title = {\{alpha\}3\{beta\}1 integrin modulates neuronal migration and placement during early stages of cerebral cortical development},
	Uuid = {E32BA570-4229-477E-A249-6639D0F7A3F6},
	Volume = {131},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.01532}}

@article{Schmidt-Hieber:2004,
	Abstract = {Neural stem cells in various regions of the vertebrate brain continuously generate neurons throughout life. In the mammalian hippocampus, a region important for spatial and episodic memory, thousands of new granule cells are produced per day, with the exact number depending on environmental conditions and physical exercise. The survival of these neurons is improved by learning and conversely learning may be promoted by neurogenesis. Although it has been suggested that newly generated neurons may have specific properties to facilitate learning, the cellular and synaptic mechanisms of plasticity in these neurons are largely unknown. Here we show that young granule cells in the adult hippocampus differ substantially from mature granule cells in both active and passive membrane properties. In young neurons, T-type Ca2+ channels can generate isolated Ca2+ spikes and boost fast Na+ action potentials, contributing to the induction of synaptic plasticity. Associative long-term potentiation can be induced more easily in young neurons than in mature neurons under identical conditions. Thus, newly generated neurons express unique mechanisms to facilitate synaptic plasticity, which may be important for the formation of new memories.},
	Author = {Schmidt-Hieber, Christoph and Jonas, Peter and Bischofberger, Josef},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Cell Aging;Long-Term Potentiation;Cell Differentiation;Animals;Synapses;In Vitro;Rats;Neuronal Plasticity;Memory;Calcium Channels, T-Type;Hippocampus;Rats, Wistar;Calcium;Male;Dendrites;01 Adult neurogenesis general;Support, Non-U.S. Gov't;Action Potentials;Sodium},
	Month = {5},
	Nlm_Id = {0410462},
	Number = {6988},
	Organization = {Physiologisches Institut der Universit{\"a}t Freiburg, D-79104 Freiburg, Germany.},
	Pages = {184-7},
	Pii = {nature02553},
	Pubmed = {15107864},
	Title = {Enhanced synaptic plasticity in newly generated granule cells of the adult hippocampus},
	Uuid = {B4E3C892-1537-4FE4-AD2C-23FFB9B3B4BF},
	Volume = {429},
	Year = {2004},
	url = {papers/Schmidt-Hieber_Nature2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature02553}}

@article{Schmitt:1998,
	Abstract = {Microglial reactivity associated with induction of MHC class II (HLA-DR) antigen is a sensitive indicator for pathological events in the CNS. To assess the response of glial cells after lesions of supraspinal descending tracts, HLA-DR, CD68 and GFAP were studied immunohistochemically on spinal cord tissue of 5 patients who died after unilateral infarction of the middle cerebral artery territory, and 5 control cases. In patients who died shortly after a stroke (4-14 days) increased HLA-DR-immunoreactivity (HLA-DR-IR) could be observed in the intermediate grey matter and in the ventral horn. The CD68-IR was much less intense. After longer survival times (5 weeks to 4 months). HLA-DR-IR in the grey matter was clearly lower than that observed in the spinal cord of short survival times, but very abundant in the dorsolateral funiculus, specifically within the corticospinal tract. In white matter areas, CD68-IR was almost identical to the HLA-DR-IR. Within the grey matter, CD68-IR was similar to the control tissue. A moderate increase of GFAP-positive astrocytes could be seen only in the grey matter after longer survival times. It seems probable, that the dynamics of HLA-DR-positive microglia reflect the early phagocytosis of presynaptic terminals by microglia in target regions of descending fibre tracts. In the white matter, the removal of degenerating axons by phagocytosing microglia expressing HLA-DR and CD68 antigens is a slower process which occurs over a period of months.},
	Author = {Schmitt, A. B. and Brook, G. A. and Buss, A. and Nacimiento, W. and Noth, J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Human;Antigens, Differentiation, Myelomonocytic;Middle Aged;Microglia;Female;Antigens, CD;Cerebral Infarction;Not relevant;11 Glia;Time Factors;Cerebrovascular Disorders;Aged;Male;Spinal Cord;Support, Non-U.S. Gov't;HLA-DR Antigens;Survival Analysis;Aged, 80 and over;Adult;Histocompatibility Antigens Class II;Glial Fibrillary Acidic Protein},
	Medline = {98382909},
	Month = {6},
	Nlm_Id = {7609829},
	Number = {3},
	Organization = {Department of Neurology, Technical University, School of Medicine, Aachen, Germany.},
	Pages = {167-76},
	Pubmed = {9717181},
	Title = {Dynamics of microglial activation in the spinal cord after cerebral infarction are revealed by expression of MHC class II antigen},
	Uuid = {FF3A72A7-8166-4BE6-92FA-9273568CD365},
	Volume = {24},
	Year = {1998}}

@article{Schneider:2005,
	Abstract = {G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong antiapoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neuronal differentiation in vitro. G-CSF markedly improved long-term behavioral outcome after cortical ischemia, while stimulating neural progenitor response in vivo, providing a link to functional recovery. Thus, G-CSF is an endogenous ligand in the CNS that has a dual activity beneficial both in counteracting acute neuronal degeneration and contributing to long-term plasticity after cerebral ischemia. We therefore propose G-CSF as a potential new drug for stroke and neurodegenerative diseases.},
	Author = {Schneider, and Kr{\"u}ger, and Steigleder, and Weber, and Pitzer, and Laage, and Aronowski, and Maurer, and Gassler, and Mier, and Hasselblatt, and Kollmar, and Schwab, and Sommer, and Bach, and Kuhn, and Sch{\"a}bitz,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:31 -0400},
	Issn = {0021-9738},
	Journal = {J Clin Invest},
	Keywords = {24 Pubmed search results 2008},
	Month = {7},
	Nlm_Id = {7802877},
	Organization = {Axaron Bioscience AG, Heidelberg, Germany.},
	Pubmed = {16007267},
	Title = {The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis},
	Uuid = {AD55CC30-8B48-4419-8DDF-15077B378705},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1172/JCI23559}}

@article{Schoen:1992,
	Abstract = {The ecto-enzyme 5'-nucleotidase was localized immunocytochemically in the axotomized rat facial nucleus. As revealed by the monoclonal antibody 5N4-2,5'-nucleotidase immunoreactivity markedly increased on perineuronal microglia during the first week following axotomy, and gradually disappeared from these cells by the end of the third post-operative week. Interestingly, parenchymal microglia were not or only weakly stained. These findings indicate that 5'-nucleotidase 5N4-2-immunoreactivity may serve as a marker for perineuronal microglia, a population of satellite glial cells that appear to be actively engaged in lesion-induced synaptic changes during regeneration.},
	Author = {Schoen, S. W. and Graeber, M. B. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Tissue Distribution;Neuroglia;Facial Nerve;Rats;Immunohistochemistry;Time Factors;Denervation;Rats, Wistar;11 Glia;5'-Nucleotidase;Animals;Axons},
	Medline = {93100085},
	Nlm_Id = {8806785},
	Number = {4},
	Organization = {Department of Neuromorphology, Max-Planck-Institute of Psychiatry, Martinsried, Germany.},
	Pages = {314-7},
	Pubmed = {1464463},
	Title = {5'-Nucleotidase immunoreactivity of perineuronal microglia responding to rat facial nerve axotomy},
	Uuid = {FE4A258C-BB28-4B3F-939C-0B990038BEA1},
	Volume = {6},
	Year = {1992}}

@article{Schools:2003,
	Abstract = {We have recently described a subgroup of isolated glial fibrillary acidic protein-positive (GFAP+) hippocampal astrocytes that predominantly express outwardly rectifying currents (which we term "ORAs"for outwardly rectifying astrocytes), which are similar to the currents already described for hippocampal GFAP- "complex glia."We now report that post-recording staining of cells that were first selected as "complex"by morphology and then confirmed by their electrophysiological characteristics were NG2+ approximately 90\%of the time. Also, the morphology of freshly isolated NG2+ cells differs from that of isolated GFAP+ ORAs in having a smaller and round cell body with thinner processes, which usually are collapsed back onto the soma. Upon detailed examination, NG2+ cells were found to differ quantitatively in some electrophysiological characteristics from GFAP+ ORAs. The outward, transient K+ currents (IKa) in the NG2+ cells showed a slower decay than the IKa in ORAs, and their density decreased in NG2+ cells from older animals. The other two major cation currents, the voltage-activated Na+ and outwardly delayed rectifier K+ currents, were similar in NG2+ cells and ORAs. To further distinguish isolated complex cells from outwardly rectifying GFAP+ astrocytes, we performed immunocytochemistry for glial markers in fixed, freshly isolated rat hippocampal glia. NG2+ cells were negative for GFAP and also for the astrocytic glutamate transporters GLT-1 and GLAST. Thus the isolated hippocampal NG2+ glial cells, though having an electrophysiological phenotype similar to that of ORAs, are an immunologically and morphologically distinct glial cell population and most likely represent NG2+ cells in situ. 0360-4012 Journal Article},
	Author = {Schools, G. P. and Zhou, M. and Kimelberg, H. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Animals;Electric Conductivity;Cells, Cultured;Rats;Comparative Study;Immunohistochemistry/methods;Cell Count;Patch-Clamp Techniques/*methods;11 Glia;Time Factors;Antigens/*analysis/immunology;Proteoglycans/*analysis/immunology;Animals, Newborn;Glial Fibrillary Acidic Protein/immunology;Amino Acid Transport System X-AG/metabolism;Anesthetics, Local/pharmacology;Tetrodotoxin/pharmacology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;G pdf;Hippocampus/*cytology/metabolism;Neuroglia/classification/drug effects/*metabolism/physiology},
	Number = {6},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, New York 12208, USA.},
	Pages = {765-77},
	Pubmed = {12949902},
	Title = {Electrophysiologically "complex"glial cells freshly isolated from the hippocampus are immunopositive for the chondroitin sulfate proteoglycan NG2},
	Uuid = {63CF07C2-5187-4BC2-A060-DD58BAFCD2E5},
	Volume = {73},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12949902}}

@article{Schottler:1998,
	Abstract = {Orthograde and retrograde tracers were used to examine subcortical connections of neurons in the neurological mutant tish rat. This animal exhibits bilateral heterotopia similar to those observed in epileptic humans with subcortical band heterotopia. Terminal varicosities were labeled in the striatum, thalamus, brainstem, and spinal cord following injections of the anterograde tracer biotinylated dextran amine (BDA) into the heterotopic cortex. The general topography of corticothalamic projections was evaluated by injecting the retrograde tracer Fluoro-Gold (FG) into ventral thalamic nuclei. Retrograde labeling of small-to-medium sized neurons was observed in layer VI of topographically restricted portions of the normotopic cortex. Similar appearing cells were labeled in the neighboring portions of the underlying heterotopia; however, these neurons did not display characteristic lamination or radial orientation. Thalamocortical terminals labeled by injecting BDA into the ventroposterolateral nucleus (VPL) were observed primarily in layer IV of the medial aspect of the normotopic somatosensory cortex. In contrast, a radial column of terminals was present in the underlying heterotopia. Typical barrel labeling was found in the lateral aspect of the normotopic somatosensory cortex after injecting the ventroposteromedial nucleus (VPM), whereas more diffuse patches of labeling were observed in the underlying heterotopia. Heterotopic neurons in the tish cortex, thus, exhibit characteristic features of subcortical connectivity. Both normotopic and heterotopic neurons in the tish brain project to appropriate subcortical sites and establish bidirectional topographic connections with the thalamus. These results suggest that primary sensory-motor information is represented in a parallel manner in the normotopic and heterotopic cortices of the tish rat.},
	Author = {Schottler, F. and Couture, D. and Rao, A. and Kahn, H. and Lee, K. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {24 Pubmed search results 2008;Motor Cortex;Rats;Dextrans;Research Support, U.S. Gov't, P.H.S.;Efferent Pathways;Fluorescent Dyes;Rats, Mutant Strains;Neural Pathways;Biotin;Brain Mapping;Somatosensory Cortex;Thalamus;Afferent Pathways;Animals;Neurons;Microinjections},
	Medline = {98250426},
	Month = {5},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Neurological Surgery, Health Sciences Center, University of Virginia, Charlottesville 22908, USA.},
	Pages = {29-42},
	Pii = {10.1002/(SICI)1096-9861(19980525)395:1<29::AID-CNE3>3.0.CO;2-J},
	Pubmed = {9590544},
	Title = {Subcortical connections of normotopic and heterotopic neurons in sensory and motor cortices of the tish mutant rat},
	Uuid = {D15C3349-5695-45E1-B7E9-C1DCF3F96AD8},
	Volume = {395},
	Year = {1998},
	url = {papers/Schottler_JCompNeurol1998.pdf}}

@article{Schottler:2001,
	Abstract = {The tish rat is a neurological mutant exhibiting bilateral cortical heterotopia similar to those found in certain epileptic patients. Previous work has shown that thalamocortical fibers originating in the ventroposteromedial nucleus, which in normal animals segregate as 'barrel' representations for individual whiskers, terminate in both normotopic and heterotopic areas of the tish cortex (Schottler et al., 1998). Thalamocortical innervation terminates as barrels in layer IV and diffusely in layer VI of the normotopic area. Discrete patches of terminals are also observed in the underlying heterotopic area suggesting that representations of individual vibrissa may be present in the heterotopic somatosensory areas. The present study examines this issue by investigating the organization of the vibrissal somatosensory system in the tish cortex. Staining for cytochrome oxidase or Nissl substance reveals a normal complement of vibrissal barrels in the normotopic area of the tish cortex. Dense patches of cytochrome oxidase staining are also found in the underlying lateral portions of the heterotopic area (i.e. the same area that is innervated by the ventroposteromedial nucleus). Injections of retrograde tracers into vibrissal areas of either the normotopic or heterotopic area produce topographically organized labeling of neurons restricted to one or a small number of barreloids within the ventroposteromedial nucleus of the thalamus. Physical stimulation of a single whisker (D3 or E3) elicits enhanced uptake of [(14)C]2-deoxyglucose in restricted zones of both the normotopic and heterotopic areas, demonstrating that single whisker stimulation can increase functional activity in both normotopic and heterotopic neurons. These findings indicate that the barrels are intact in the normotopic area and are most consistent with the hypothesis that at least some of the individual vibrissae are 'dually' represented in normotopic and heterotopic positions in the primary somatosensory areas of the tish cortex.},
	Author = {Schottler, F. and Fabiato, H. and Leland, J. M. and Chang, L. Y. and Lotfi, P. and Getachew, F. and Lee, K. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Animals;Gene Expression Regulation, Developmental;Rats;Ventral Thalamic Nuclei;Neural Pathways;Epilepsy;Rats, Sprague-Dawley;Vibrissae;21 Dysplasia-heterotopia;Organ Culture Techniques;Deoxyglucose;Research Support, U.S. Gov't, P.H.S.;Nervous System Malformations;Evoked Potentials, Somatosensory;21 Neurophysiology;Neurons;Electron Transport Complex IV;Somatosensory Cortex;Body Patterning;24 Pubmed search results 2008;Choristoma;Rats, Mutant Strains},
	Medline = {21592848},
	Nlm_Id = {7605074},
	Number = {2},
	Organization = {Department of Neuroscience, University of Virginia, Box 801392, MR4 Annex, Charlottesville, VA 22098, USA.},
	Pages = {217-35},
	Pii = {S0306-4522(01)00395-5},
	Pubmed = {11734356},
	Title = {Normotopic and heterotopic cortical representations of mystacial vibrissae in rats with subcortical band heterotopia},
	Uuid = {F13F6998-638B-4249-B147-D6F61ADF4802},
	Volume = {108},
	Year = {2001},
	url = {papers/Schottler_Neuroscience2001.pdf}}

@article{Schroeter:2001,
	Abstract = {We have recently described a novel population of CD8+ phagocytes that are strongly recruited to focal ischemic lesions of the rat brain but absent from axotomized central fiber tracts. To assess the relative contribution of infiltrating macrophages and resident microglia to the CD8+ phagocyte response, we selectively depleted peripheral macrophages by systemic administration of dichloromethylene diphosphonate-filled liposomes prior to the induction of permanent ischemia by photothrombosis of cortical microvessels. Macrophage depletion led to a dramatic reduction but not complete abolishment of CD8+ cells in the ensuing infarcts. Systemic administration of monoclonal antibody Ox-8 eliminated CD8+ cells from peripheral lymphoid organs but had no effect on CD8+ phagocytes in the ischemic brain lesions. To further characterize the lesion conditions inducing the recruitment of CD8+ phagocytes, we induced mild focal ischemia by transient occlusion of the middle cerebral artery that leads to a core infarction with ischemic pannecrosis surrounded by areas with selective neuronal cell death. Recruitment of CD8+ phagocytes was restricted to areas of ischemic pannecrosis. In areas undergoing selective neuronal loss microglia up-regulated complement receptor-3, exhibited ED1 immunoreactivity (indicating phagocytic activity), and to some extent expressed CD4, but not CD8 antigens. In conclusion our present study shows that CD8+ phagocytes in focal brain ischemia are predominantly derived from hematogenous macrophages and selectively target to areas of ischemic pannecrosis.},
	Author = {Schroeter, M. and Jander, S. and Huitinga, I. and Stoll, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0001-6322},
	Journal = {Acta Neuropathol (Berl)},
	Keywords = {Phagocytosis;Animals;Macrophages;Rats;Infarction, Middle Cerebral Artery;Lymphocytes;Microglia;Antigens, CD4;Macrophage Activation;Not relevant;Phagocytes;Rats, Wistar;11 Glia;Support, Non-U.S. Gov't;Membrane Glycoproteins;Antigens, CD8;Brain Ischemia;Immunohistochemistry;Membrane Proteins;Necrosis;Clodronic Acid;Glial Fibrillary Acidic Protein},
	Medline = {21377043},
	Month = {5},
	Nlm_Id = {0412041},
	Number = {5},
	Organization = {Department of Neurology and Center for Biological and Medical Research, Heinrich-Heine-University, D{\"u}sseldorf, Germany.},
	Pages = {440-8},
	Pubmed = {11484815},
	Title = {CD8+ phagocytes in focal ischemia of the rat brain: predominant origin from hematogenous macrophages and targeting to areas of pannecrosis},
	Uuid = {4DC17467-5FBA-483D-8494-CDB7DEEFAD99},
	Volume = {101},
	Year = {2001}}

@article{Schuetz:2004,
	Abstract = {Retinal ganglion cells (RGCs) regenerating through peripheral nerve grafts show enhanced survival after further axonal injury for at least 4 weeks [Restor. Neurol. Neurosci. 21 (2003) 11]. Here, we examined the survival of the neurons and their microglial phagocytosis in dependence of the site of reaxotomy. Therefore, the optic nerve in adult rats was transected at different distances from the eye cup and replaced with an autologous piece of sciatic nerve. After 14 days of axonal growth, the regenerated neurites were reaxotomized either within the remaining optic stump or within the graft and their cell bodies were retrogradely labeled. Reaxotomy of regenerated ganglion cells within the remaining optic nerve resulted in reduced (but not significant) ganglion cell survival and significant microglial phagocytosis in contrast to reaxotomy within the peripheral nerve graft. Furthermore, phagocytosis-dependent labeling using two different fluorescent tracers revealed that the same microglial cell can phagocytose further dying ganglion cells within 14 days after the first activation. The results suggest that the intrasciatic segments of axons receive some trophic support that is retrogradely transported and required to limit the microglial activation. The microglial capability to phagocytose dying neurons several fold emphasizes their function in permanent scavenging within the retina.},
	Author = {Schuetz, Erik and Thanos, Solon},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0361-9230},
	Journal = {Brain Res Bull},
	Keywords = {Retina;Sciatic Nerve;Rats, Sprague-Dawley;Nerve Regeneration;Cell Communication;Female;Rats;Not relevant;11 Glia;Microglia;Retinal Ganglion Cells;Optic Nerve;Axotomy;Animals;Support, Non-U.S. Gov't;Male;Phagocytosis},
	Medline = {23341186},
	Month = {2},
	Nlm_Id = {7605818},
	Number = {5},
	Organization = {Department of Experimental Ophthalmology, University Eye Hospital M{\"u}nster, Domagkstrasse 15, 48149 M{\"u}nster, Germany.},
	Pages = {391-6},
	Pii = {S0361923003002995},
	Pubmed = {15168904},
	Title = {Neuro-glial interactions in the adult rat retina after reaxotomy of ganglion cells: examination of neuron survival and phagocytic microglia using fluorescent tracers},
	Uuid = {FA7FA605-F5D4-4E5C-90E6-AE000FE6F122},
	Volume = {62},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainresbull.2003.10.008}}

@article{Schulz:1995,
	Abstract = {Recent evidence has linked excitotoxicity with the generation of free radicals. We examined whether free radical spin traps can attenuate excitotoxic lesions in vivo. Pretreatment with N-tert-butyl-alpha-(2- sulfophenyl)-nitrone (S-PBN) significantly attenuated striatal excitotoxic lesions in rats produced by N-methyl-D-aspartate (NMDA), kainic acid, and alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA). In a similar manner, striatal lesions produced by 1-methyl- 4-phenylpyridinium (MPP+), malonate, and 3-acetylpyridine were significantly attenuated by either S-PBN or alpha-phenyl-N-tert- butylnitrone (PBN) treatment. Administration of S-PBN in combination with the NMDA antagonist MK-801 produced additive effects against malonate and 3-acetylpyridine toxicity. Malonate injections resulted in increased production of hydroxyl free radicals (.OH) as assessed by the conversion of salicylate to 2,3- and 2,5-dihydroxybenzoic acid (DHBA). This increase was significantly attenuated by S-PBN, consistent with a free radical scavenging effect. S-PBN had no effects on malonate- induced ATP depletions and had no significant effect on spontaneous striatal electrophysiologic activity. These results provide the first direct in vivo evidence for the involvement of free radicals in excitotoxicity and suggest that antioxidants may be useful in treating neurologic illnesses in which excitotoxic mechanisms have been implicated.},
	Author = {Schulz, J. B. and Henshaw, D. R. and Siwek, D. and Jenkins, B. G. and Ferrante, R. J. and Cipolloni, P. B. and Kowall, N. W. and Rosen, B. R. and Beal, M. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurochem},
	Keywords = {N-Methylaspartate/*pharmacology;E-3;Dizocilpine Maleate/pharmacology;Electrophysiology;Kainic Acid/pharmacology;Rats;Cells, Cultured;07 Excitotoxicity Apoptosis;Animal;Free Radicals;Rats, Sprague-Dawley;Male;Support, Non-U.S. Gov't;Brain/*drug effects/physiology;Receptors, Glutamate/drug effects/*physiology;Support, U.S. Gov't, P.H.S.;Cell Death/drug effects;Hydroxyl Radical/metabolism;alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology;Nitrogen Oxides/pharmacology;Neurons/*drug effects/physiology;Free Radical Scavengers/*pharmacology},
	Number = {5},
	Organization = {Neurochemistry Laboratory, Massachusetts General Hospital 02114, USA.},
	Pages = {2239-47.},
	Title = {Involvement of free radicals in excitotoxicity in vivo},
	Uuid = {C75B07A9-9154-4186-A9C1-A0F124785D9E},
	Volume = {64},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7536809}}

@article{Schumann:1979,
	Author = {Schumann, G. and Gisler, R. H. and Brownbill, A. F. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0065-2598},
	Journal = {Adv Exp Med Biol},
	Keywords = {15 ERVs retroelements;Spleen;Mice;Mice, Inbred BALB C;Cytotoxicity, Immunologic;B-Lymphocytes;24 Pubmed search results 2008;Retroviridae;T-Lymphocytes;Immunosuppression;Macrophages;15 Retrovirus mechanism;Animals;Lymphocyte Culture Test, Mixed;Hemolytic Plaque Technique;Antibodies, Viral;Immune Sera},
	Medline = {79228515},
	Nlm_Id = {0121103},
	Pages = {233-7},
	Pubmed = {223415},
	Title = {Are endogenous C-type viruses physiologically required for the regulation of the humoral immune response?},
	Uuid = {2CC70E17-A78C-425D-BE8F-9A5A4ABEDBB4},
	Volume = {114},
	Year = {1979}}

@article{Schumann:1976,
	Abstract = {We reported previously in vitro induction of endogenous C-type viruses from normal mouse spleen cells by lipopolysaccharide (LPS) as well as by combination treatment with concanabalin A and 5-bromo-2'-deoxyuridine (Con A/BrdU). To identify the cell types sensitive to virus induction and to study the relationship of mitogenicity to virus induction we have compared T cell populations (BALB/c thymus cells and cortisone-resistant thymus cells), B cell populations (nu/nu spleen cells and lymph node cells), adherent BALB/c peritoneal cells and mixed populations (BALB/c spleen cells, macrophage-depleted BALB/c spleen cells, and lymph node cells). LPS-induction occurred only in B cell-containing populations. In contrast, induction by Con A/BrdU depended on the presence of both T and B cells. In both instances, neither macrophages nor hemopoietic cells appeared to be a major source of virus. Treatment with anti-Ig serum and complement reduced virus induction by LPS/BrdU but not by Con A/BrdU suggesting that different cell populations produce virus after stimulation with these two different mitogens.},
	Author = {Schumann, G. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Complement System Proteins;T-Lymphocytes;Mice, Inbred BALB C;Animals;Macrophages;Antibodies, Anti-Idiotypic;Lipopolysaccharides;15 Retrovirus mechanism;Lymph Nodes;B-Lymphocytes;Retroviridae;Mitogens;Concanavalin A;Mice, Nude;Mice;24 Pubmed search results 2008;15 ERVs retroelements;Spleen},
	Medline = {76144682},
	Month = {4},
	Nlm_Id = {2985117R},
	Number = {4},
	Pages = {1145-50},
	Pubmed = {176274},
	Title = {Mitogen induction of murine C-type viruses. I. Analysis of lymphoid cell subpopulations},
	Uuid = {A5CB72FF-F4B7-45C0-81EE-919AE94C342A},
	Volume = {116},
	Year = {1976}}

@article{Schumann:1978,
	Abstract = {We have analyzed the effects of an antiserum prepared against BALB/c endogenous xenotropic C-type virus on the humoral immune response of mice. Both in vivo and in vitro, this serum suppresses the response to sheep red blood cells, an effect that can be absorbed out by purified BALB/c xenotropic C-type virus or Friend leukemia virus, but not by Rous sarcoma virus. The serum produces its maximum effect when administered together with or before the antigen, but not 24 hr later. This suggests that it acts on an early event of the immune response. Evidence is presented to show that the critical viral antigen is expressed before the spleen cells are experimentally stimulated by antigen. The same immunosuppressive effect was observed in a variety of mouse strains, including the high-leukemia incidence AKR strain and virus-free 129/J mice, indicating that it is independent of the expression of endogenous virus. The finding that a viral antigen is involved in the transition from a resting to a dividing lymphocyte is discussed with respect to viral involvement in leukemia.},
	Author = {Schumann, G. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {15 ERVs retroelements;Immune Sera;Mice, Inbred AKR;Mice, Inbred BALB C;Mice, Inbred DBA;Retroviridae;Mice, Inbred C57BL;Time Factors;Immunosuppression;15 Retrovirus mechanism;Animals;Mice;24 Pubmed search results 2008;Hemolytic Plaque Technique;Antigen-Antibody Reactions},
	Medline = {78195399},
	Month = {6},
	Nlm_Id = {2985117R},
	Number = {6},
	Pages = {1913-6},
	Pubmed = {207777},
	Title = {Immunosuppressive activity of antibody directed against endogenous C-type virus interferes with early events of the immune response},
	Uuid = {5E401B2F-D516-418C-AFA6-B7C5151447E0},
	Volume = {120},
	Year = {1978}}

@article{Schumann:1977,
	Author = {Schumann, G. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {Dose-Response Relationship, Drug;Drug Synergism;Animals;Gammaretrovirus;DNA;Lipopolysaccharides;Culture Techniques;15 Retrovirus mechanism;Polysaccharides;Lymph Nodes;Retroviridae;Mitogens;Mice, Inbred Strains;Escherichia coli;Age Factors;Genotype;Mice;24 Pubmed search results 2008;Virus Replication;Bromodeoxyuridine;15 ERVs retroelements;Spleen},
	Medline = {77197290},
	Month = {6},
	Nlm_Id = {0110674},
	Number = {1},
	Pages = {81-7},
	Pubmed = {194404},
	Title = {Mitogen induction of murine C-type viruses. III. Effect of culture conditions, age, and genotype},
	Uuid = {9528DBF0-BC35-415E-800E-D93ED736E9AA},
	Volume = {79},
	Year = {1977}}

@article{Schwab:1998,
	Abstract = {Basic helix-loop-helix (bHLH) genes have emerged as important regulators of neuronal determination and differentiation in vertebrates. Three putative neuronal differentiation factors [NEX for neuronal helix-loop-helix protein-1 (mammalian atonal homolog-2), neuroD (beta-2), and NDRF for neuroD-related factor (neuroD2)] are highly homologous to each other in the bHLH region and comprise a new bHLH subfamily. To study the role of NEX, the first bHLH protein identified in this group, we have disrupted the NEX gene by homologous recombination. NEX-deficient mice have no obvious developmental defect, and CNS neurons appear fully differentiated. To investigate further whether the absence of NEX is compensated for by neuroD and NDRF, we compared the spatiotemporal expression of all three genes. We demonstrate, by in situ hybridization, that the transcription patterns of NEX, neuroD, and NDRF genes are highly overlapping in the developing CNS of normal rats between embryonic day 12 and adult stages but are not strictly identical. The most prominent transcription of each gene marks the dorsal neuroepithelium of the telencephalon in early development and is sustained in the adult neocortex, hippocampus, and cerebellum. In general, neuroD provides the earliest marker of neuronal differentiation in any given region compared with NDRF or NEX. Whereas a few CNS regions are specific for neuroD, no region was detected in which solely NEX or NDRF is expressed. This suggests that the function of the mutant NEX gene in neuronal differentiation is compensated for by neuroD and NDRF and that, in analogy with myogenic bHLH proteins, neuronal differentiation factors are at least in part equivalent in function.},
	Author = {Schwab, M. H. and Druffel-Augustin, S. and Gass, P. and Jung, M. and Klugmann, M. and Bartholomae, A. and Rossner, M. J. and Nave, K. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Aging;Cell Differentiation;Rats, Sprague-Dawley;Research Support, Non-U.S. Gov't;Embryonic and Fetal Development;Helix-Loop-Helix Motifs;Rats;Nerve Tissue Proteins;Neuropeptides;Gene Expression;Mice, Transgenic;Animals, Newborn;Mice;Brain;Animals;Neurons},
	Medline = {98122897},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {4},
	Organization = {Zentrum f{\"u}r Molekulare Biologie (ZMBH), University of Heidelberg, D-69120 Heidelberg, Germany.},
	Pages = {1408-18},
	Pubmed = {9454850},
	Title = {Neuronal basic helix-loop-helix proteins (NEX, neuroD, NDRF): spatiotemporal expression and targeted disruption of the NEX gene in transgenic mice},
	Uuid = {AD8B2456-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {18},
	Year = {1998},
	url = {papers/Schwab_JNeurosci1998.pdf}}

@article{Schwab:2000,
	Abstract = {The transcription factors neuronal helix-loop-helix protein (NEX)/mammalian atonal homolog 2 (Math-2), BETA2/neuronal determination factor (NeuroD), and NeuroD-related factor (NDRF)/NeuroD2 comprise a family of Drosophila atonal-related basic helix-loop-helix (bHLH) proteins with highly overlapping expression in the developing forebrain. The ability of BETA2/NeuroD and NDRF to convert ectodermal cells into neurons after mRNA injection into Xenopus oocytes suggested a role in specifying neuronal cell fate. However, neuronal bHLH genes are largely transcribed in CNS neurons, which are fully committed. Here we analyze a defect in mice lacking BETA2/NeuroD, and in NEX*BETA2/NeuroD double mutants, demonstrating that bHLH proteins are required in vivo for terminal neuronal differentiation. Most strikingly, presumptive granule cells of the dentate gyrus are generated but fail to mature, lack normal sodium currents, and show little dendritic arborization. Long-term hippocampal slice cultures demonstrate secondary alterations of entorhinal and commissural/associational projections. The primary developmental arrest appears to be restricted to granule cells in which an autoregulatory system involving all three neuronal bHLH genes has failed.},
	Author = {Schwab, M. H. and Bartholomae, A. and Heimrich, B. and Feldmeyer, D. and Druffel-Augustin, S. and Goebbels, S. and Naya, F. J. and Zhao, S. and Frotscher, M. and Tsai, M. J. and Nave, K. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Trans-Activation (Genetics);Viral Proteins;Cell Differentiation;Animals;Gene Expression Regulation, Developmental;Helix-Loop-Helix Motifs;Apoptosis;Ki-67 Antigen;Integrases;Patch-Clamp Techniques;Cell Adhesion Molecules, Neuronal;Mice, Inbred C57BL;Extracellular Matrix Proteins;Action Potentials;Research Support, U.S. Gov't, P.H.S.;Mice, Knockout;Animals, Newborn;Dentate Gyrus;Neurons;In Situ Nick-End Labeling;Mice;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {20266180},
	Month = {5},
	Nlm_Id = {8102140},
	Number = {10},
	Organization = {Zentrum f{\"u}r Molekulare Biologie, University of Heidelberg, D-69120 Heidelberg, Germany.},
	Pages = {3714-24},
	Pii = {20/10/3714},
	Pubmed = {10804213},
	Title = {Neuronal basic helix-loop-helix proteins (NEX and BETA2/Neuro D) regulate terminal granule cell differentiation in the hippocampus},
	Uuid = {08B5407B-716F-11DA-A383-000D9346EC2A},
	Volume = {20},
	Year = {2000},
	url = {papers/Schwab_JNeurosci2000.pdf}}

@article{Schwartz:2005,
	Abstract = {The failure of the spinal cord to recover after injury has been associated with the immune privilege mechanism that suppresses immune activity throughout the central nervous system. Primed macrophages and dendritic cells were shown to promote neurological recovery in preclinical models of spinal cord injury. A cell therapy consisting of autologous incubated macrophages is now being tested on spinal cord injury patients in clinical trials.},
	Author = {Schwartz, M. and Yoles, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0065-1419},
	Journal = {Acta Neurochir Suppl},
	Keywords = {Treatment Outcome;Spinal Cord Injuries;Nerve Regeneration;Rats;Recovery of Function;11 Glia;Research;review, tutorial;Macrophages;Dendritic Cells;Humans;Clinical Trials;Pilot Projects;review;Animals},
	Medline = {102323079},
	Nlm_Id = {100962752},
	Organization = {Department Neurophysiology, Weizmann Institute of Science, Rehovot, Israel.},
	Pages = {147-50},
	Pubmed = {15986745},
	Title = {Macrophages and dendritic cells treatment of spinal cord injury: from the bench to the clinic},
	Uuid = {B0A23399-4FBF-4CBD-B1C0-30619DB343CD},
	Volume = {93},
	Year = {2005}}

@article{Schwartz:1974,
	Author = {Schwartz, S. A. and Panem, S. and Stefanski, E. and Kirsten, W. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0008-5472},
	Journal = {Cancer Res},
	Keywords = {Tritium;Antigens, Viral;Animals;Cells, Cultured;Rats;Fluorescent Antibody Technique;Centrifugation, Density Gradient;15 Retrovirus mechanism;Uridine;Retroviridae;Time Factors;Rats, Inbred WF;Embryo;Animals, Newborn;DNA Nucleotidyltransferases;Mice;24 Pubmed search results 2008;Microscopy, Electron;Bromodeoxyuridine;15 ERVs retroelements;Neoplasms, Experimental;Cell Transformation, Neoplastic},
	Medline = {74278198},
	Month = {9},
	Nlm_Id = {2984705R},
	Number = {9},
	Pages = {2255-9},
	Pubmed = {4367286},
	Title = {Endogenous type C particles from rat embryo cells treated with 5-bromodeoxyuridine},
	Uuid = {8DFFB0F6-4328-11DB-A5D2-000D9346EC2A},
	Volume = {34},
	Year = {1974}}

@article{Schwartz:2006,
	Abstract = {Microglia, the standby cells for immune defense in the CNS, have a reputation for exacerbating the neural damage that occurs in neurodegenerative diseases. However, research over the past few years has established that microglia do not constitute a single, uniform cell population, but rather comprise a family of cells with diverse phenotypes - some that are beneficial and others that the CNS can barely tolerate and that are therefore destructive. This finding raised several questions. What instructs microglia to acquire a particular phenotype, and how do these phenotypes differ? How committed are microglia to a specific phenotype? Can destructive microglia become protective, and can protective microglia retain their beneficial phenotype even when they encounter a destructive environment? Here, we address these questions, and the background of research that elicited them.},
	Author = {Schwartz, and Butovsky, and Br{\"u}ck, and Hanisch,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {7808616},
	Organization = {The Weizmann Institute of Science, POB 26, Rehovot, 76100, Israel.},
	Pii = {S0166-2236(05)00323-1},
	Pubmed = {16406093},
	Title = {Microglial phenotype: is the commitment reversible?},
	Uuid = {0A94FD2F-1436-4B30-858C-A09C34FE35AD},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tins.2005.12.005}}

@article{Schwarz:2000,
	Abstract = {PURPOSE: Neuronal migration disorders (NMD) are often associated with therapy-resistant epilepsy. In human cerebral cortex, this hyperexcitability has been correlated with a loss of inhibitory interneurons. We used a rat model of focal cortical NMD (microgyria) to determine whether the expression of epileptiform activity in this model coincides with a decrease in inhibitory interneurons. METHODS: In 2-to 4-month-old rats, the density of interneurons immunoreactive for gamma-aminobutyric acid (GABA), calbindin, and parvalbumin was determined in fronto-parietal cortex in nine 200-microm-wide sectors located up to 2.5 mm lateral and 2.0 mm medial from the lesion center in primary parietal cortex (Par1). Quantitative measurements in homotopic areas of age-matched sham-operated rats served as controls. RESULTS: The freeze lesion performed in newborn rat cortex resulted in adult rats with a microgyrus extending in a rostro-caudal direction from frontal to occipital cortex. The density of GABA-and parvalbumin-positive neurons in fronto-parietal cortex was not significantly different between lesioned and control animals. Only the density of calbindin-immunoreactive neurons located 1.0 mm lateral and 0.5 mm medial from the lesion was significantly (Student t test, p < 0.05) larger in freeze-lesioned rats (5,817 +/- 562 and 6,400 +/- 795 cells per mm3, respectively; n = 12) compared with measurements in homotopic regions in Par1 cortex of controls (4,507 +/- 281 and 4, 061 +/- 319 cells per mm3, respectively; n = 5). CONCLUSIONS: The previously reported widespread functional changes in this model of cortical NMD are not related to a general loss of inhibitory interneurons. Other factors, such as a decrease in GABA receptor density, modifications in GABAA receptor subunit composition, or alterations in the excitatory network, e.g., an increase in the density of calbindin-immunoreactive pyramidal cells, more likely contribute to the global disinhibition and widespread expression of pathophysiological activity in this model of cortical NMD.},
	Author = {Schwarz, P. and Stichel, C. C. and Luhmann, H. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {gamma-Aminobutyric Acid;Animals;Humans;Frontal Lobe;Rats;Parietal Lobe;Neocortex;21 Epilepsy;Epilepsy;Cell Count;Pyramidal Cells;Rats, Wistar;Calcium-Binding Protein, Vitamin D-Dependent;Disease Models, Animal;Animals, Newborn;Freezing;21 Neurophysiology;Parvalbumins;Receptors, GABA;Adult;Neural Tube Defects;Interneurons;24 Pubmed search results 2008;Immunohistochemistry;Neural Inhibition;Research Support, Non-U.S. Gov't},
	Medline = {20357668},
	Month = {7},
	Nlm_Id = {2983306R},
	Number = {7},
	Organization = {Institute of Neurophysiology, University of D{\"u}sseldorf, D{\"u}sseldorf, Germany.},
	Pages = {781-7},
	Pubmed = {10897147},
	Title = {Characterization of neuronal migration disorders in neocortical structures: loss or preservation of inhibitory interneurons?},
	Uuid = {87F1BD6E-66F0-4A45-B058-E690C0DA2BFF},
	Volume = {41},
	Year = {2000}}

@article{Schwarz:2006,
	Abstract = {Small interfering RNAs (siRNAs), the guides that direct RNA interference (RNAi), provide a powerful tool to reduce the expression of a single gene in human cells. Ideally, dominant, gain-of-function human diseases could be treated using siRNAs that specifically silence the mutant disease allele, while leaving expression of the wild-type allele unperturbed. Previous reports suggest that siRNAs can be designed with single nucleotide specificity, but no rational basis for the design of siRNAs with single nucleotide discrimination has been proposed. We systematically identified siRNAs that discriminate between the wild-type and mutant alleles of two disease genes: the human Cu, Zn superoxide dismutase (SOD1) gene, which contributes to the progression of hereditary amyotrophic lateral sclerosis through the gain of a toxic property, and the huntingtin (HTT) gene, which causes Huntington disease when its CAG-repeat region expands beyond approximately 35 repeats. Using cell-free RNAi reactions in Drosophila embryo lysate and reporter assays and microarray analysis of off-target effects in cultured human cells, we identified positions within an siRNA that are most sensitive to mismatches. We also show that purine:purine mismatches imbue an siRNA with greater discriminatory power than other types of base mismatches. siRNAs in which either a G:U wobble or a mismatch is located in the "seed" sequence, the specialized siRNA guide region responsible for target binding, displayed lower levels of selectivity than those in which the mismatch was located 3' to the seed; this region of an siRNA is critical for target cleavage but not siRNA binding. Our data suggest that siRNAs can be designed to discriminate between the wild-type and mutant alleles of many genes that differ by just a single nucleotide.},
	Author = {Schwarz, and Ding, and Kennington, and Moore, and Schelter, and Burchard, and Linsley, and Aronin, and Xu, and Zamore,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1553-7404},
	Journal = {PLoS Genet},
	Keywords = {23 RNAi;23 Technique},
	Month = {9},
	Nlm_Id = {101239074},
	Number = {9},
	Pii = {06-PLGE-RA-0180R2},
	Pubmed = {16965178},
	Title = {Designing siRNA That Distinguish between Genes That Differ by a Single Nucleotide},
	Uuid = {FEC9B7C4-48A4-11DB-A317-000D9346EC2A},
	Volume = {2},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pgen.0020140}}

@article{Schwob:1994,
	Abstract = {Replication-incompetent retroviral vectors that encode the heritable marker enzyme, beta-galactosidase, were used to study the lineage relationships of cells in the olfactory epithelium of unmanipulated animals and in the olfactory epithelium as it reconstitutes after lesion. Virally-marked cells are categorized as to type based on their position in the epithelium and on expression of NCAM (limited to neurons) and the carbohydrate moiety recognized by Griffonia lectin (limited to the dark/horizontal basal cells and the microvillar class of supporting cells). Direct injections of the vectors into the olfactory epithelium of otherwise intact animals produce clusters of beta-galactosidase-labeled cells when assessed 6-10 days after infection; these clusters are composed of neurons and NCAM-negative/lectin-negative light/globose basal cells exclusively. In contrast, clusters of virally-marked cells after MeBr-induced lesion of the epithelium frequently contain both neurons and supporting cells, as well as both types of basal cells. Other clusters contain supporting cells and/or Bowman's gland/duct cells. It is likely that the clusters of marked cells are derived from a single founder cell, i.e. the cells are clonal and lineally related, since the clusters are widely dispersed. Furthermore, infusion of mixtures of viruses that can be distinguished on the basis of the type and subcellular localization of the marker enzyme that is expressed produce clusters that are homogenous with respect to enzyme type, providing strong evidence in favor of the notion that the clusters are clonal in nature. Thus, the founders of the clones that contain neurons, supporting cells and basal cells are pluripotent in their capacity for differentiation. It is unlikely that the pluripotent cells are found in Bowman's gland/duct, since we have yet to observe a clone that contains neurons and cells in Bowman's gland/duct. Hence, the pluripotent stem cells are to be found in the basal cell compartment of the epithelium. However, the exact nature of these stem cells remains unknown and a subject for future investigation. eng Journal Article},
	Author = {Schwob, J. E. and Huard, J. M. and Luskin, M. B. and Youngentob, S. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0379-864X},
	Journal = {Chem Senses},
	Keywords = {Cell Adhesion Molecules, Neuronal/biosynthesis;Genetic Vectors;Mitosis/physiology;Cell Line;Immunohistochemistry;Male;Retroviridae/*genetics;Mitosis;beta-Galactosidase/genetics;Genetic Vectors/*physiology;Animals;I abstr;Plant Lectins;Research Support, U.S. Gov't, P.H.S.;Hydrocarbons, Brominated;Olfactory Mucosa/cytology/metabolism/*physiology;Olfactory Mucosa;Support, U.S. Gov't, P.H.S.;Lectins;Animal;Neurons/enzymology/metabolism/physiology;Rats, Sprague-Dawley;Hydrocarbons, Brominated/toxicity;13 Olfactory bulb anatomy;Retroviridae;beta-Galactosidase;02 Adult neurogenesis migration;Rats;Cell Adhesion Molecules, Neuronal;Neurons},
	Medline = {95253830},
	Month = {12},
	Nlm_Id = {8217190},
	Number = {6},
	Organization = {Department of Anatomy and Cell Biology, SUNY Health Science Center, Syracuse 13210, USA.},
	Pages = {671-82.},
	Pubmed = {7735846},
	Title = {Retroviral lineage studies of the rat olfactory epithelium},
	Uuid = {C82592C1-79B5-4427-B0EE-702B75FD7376},
	Volume = {19},
	Year = {1994}}

@article{Schwob:2001,
	Abstract = {Viral upper respiratory infections are the most common cause of clinical olfactory dysfunction, but the pathogenesis of dysosmia after viral infection is poorly understood. Biopsies of the olfactory mucosa in patients that complain of dysosmia after viral infection fall into two categories: one in which no olfactory epithelium is seen and another in which the epithelium is disordered and populated mainly by immature neurons. We have used intranasal inoculation with an olfactory bulb line variant of MHV to study the consequences of viral infection on peripheral olfactory structures. MHV OBLV has little direct effect on the olfactory epithelium, but causes extensive spongiotic degeneration and destruction of mitral cells and interneurons in the olfactory bulb such that the axonal projection from the bulb via the lateral olfactory tract is markedly reduced. Moreover, surviving mitral cells apparently remain disconnected from the sensory neuron input to the glomerular layer, judging from retrograde labeling studies using Dil. The damage to the bulb indirectly causes a persistent, long-term increase in the turnover of sensory neurons in the epithelium, i.e. the relative proportion of immature to mature sensory neurons and the rate of basal cell proliferation both increase. The changes that develop after inoculation with MHV OBLV closely resemble the disordering of the olfactory epithelium in some patient biopsies. Thus, damage to the olfactory nerve or bulb may contribute to a form of post-viral olfactory dysfunction and MHV OBLV is a useful model for studying the pathogenesis of this form of dysosmia.},
	Author = {Schwob, J. E. and Saha, S. and Youngentob, S. L. and Jubelt, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Chem Senses},
	Keywords = {I pdf;13 Olfactory bulb anatomy},
	Number = {8},
	Organization = {Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, MA 02111, USA. jim.schwob\@tufts.edu},
	Pages = {937-52.},
	Title = {Intranasal inoculation with the olfactory bulb line variant of mouse hepatitis virus causes extensive destruction of the olfactory bulb and accelerated turnover of neurons in the olfactory epithelium of mice},
	Uuid = {364E6366-D4EA-4ECE-B27B-8C89546CB5E4},
	Volume = {26},
	Year = {2001},
	url = {papers/Schwob_ChemSenses2001}}

@article{Sciamanna:2005,
	Abstract = {Undifferentiated cells and embryos express high levels of endogenous non-telomerase reverse transcriptase (RT) of retroposon/retroviral origin. We previously found that RT inhibitors modulate cell growth and differentiation in several cell lines. We have now sought to establish whether high levels of RT activity are directly linked to cell transformation. To address this possibility, we have employed two different approaches to inhibit RT activity in melanoma and prostate carcinoma cell lines: pharmacological inhibition by two characterized RT inhibitors, nevirapine and efavirenz, and downregulation of expression of RT-encoding LINE-1 elements by RNA interference (RNAi). Both treatments reduced proliferation, induced morphological differentiation and reprogrammed gene expression. These features are reversible upon discontinuation of the anti-RT treatment, suggesting that RT contributes to an epigenetic level of control. Most importantly, inhibition of RT activity in vivo antagonized tumor growth in animal experiments. Moreover, pretreatment with RT inhibitors attenuated the tumorigenic phenotype of prostate carcinoma cells inoculated in nude mice. Based on these data, the endogenous RT can be regarded as an epigenetic regulator of cell differentiation and proliferation and may represent a novel target in cancer therapy.},
	Author = {Sciamanna, Ilaria and Landriscina, Matteo and Pittoggi, Carmine and Quirino, Michela and Mearelli, Cristina and Beraldi, Rosanna and Mattei, Elisabetta and Serafino, Annalucia and Cassano, Alessandra and Sinibaldi-Vallebona, Paola and Garaci, Enrico and Barone, Carlo and Spadafora, Corrado},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0950-9232},
	Journal = {Oncogene},
	Keywords = {Microscopy, Confocal;Research Support, Non-U.S. Gov't;Enzyme Inhibitors;RNA-Directed DNA Polymerase;Reverse Transcriptase Polymerase Chain Reaction;Cell Line, Tumor;Melanoma;Cell Division;Cell Cycle;22 Stem cells;15 Retrovirus mechanism;22 Cancer;Humans;RNA, Small Interfering;24 Pubmed search results 2008;Bromodeoxyuridine},
	Month = {6},
	Nlm_Id = {8711562},
	Number = {24},
	Organization = {Istituto Superiore di Sanit\`{a}, Viale Regina Elena 299, Via del Castro Laurenziano 25, 00161 Rome, Italy.},
	Pages = {3923-31},
	Pii = {1208562},
	Pubmed = {15806170},
	Title = {Inhibition of endogenous reverse transcriptase antagonizes human tumor growth},
	Uuid = {2463D447-EE54-11DA-8605-000D9346EC2A},
	Volume = {24},
	Year = {2005},
	url = {papers/Sciamanna_Oncogene2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.onc.1208562}}

@article{Seaberg:2002,
	Abstract = {Neurogenesis persists in two adult brain regions: the ventricular subependyma and the subgranular cell layer in the hippocampal dentate gyrus (DG). Previous work in many laboratories has shown explicitly that multipotential, self-renewing stem cells in the subependyma are the source of newly generated migrating neurons that traverse the rostral migratory stream and incorporate into the olfactory bulb as interneurons. These stem cells have been specifically isolated from the subependyma, and their properties of self-renewal and multipotentiality have been demonstrated in vitro. In contrast, it is a widely held assumption that the "hippocampal"stem cells that can be isolated in vitro from adult hippocampus reside in the neurogenic subgranular layer and represent the source of new granule cell neurons, but this has never been tested directly. Primary cell isolates derived from the precise microdissection of adult rodent neurogenic regions were compared using two very different commonly used culture methods: a clonal colony-forming (neurosphere) assay and a monolayer culture system. Importantly, both of these culture methods generated the same conclusion: stem cells can be isolated from hippocampus-adjacent regions of subependyma, but the adult DG proper does not contain a population of resident neural stem cells. Indeed, although the lateral ventricle and other ventricular subependymal regions directly adjacent to the hippocampus contain neural stem cells that exhibit long-term self-renewal and multipotentiality, separate neuronal and glial progenitors with limited self-renewal capacity are present in the adult DG, suggesting that neuron-specific progenitors and not multipotential stem cells are the source of newly generated DG neurons throughout adulthood. 21871798 1529-2401 Journal Article},
	Author = {Seaberg, R. M. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {J Neurosci},
	Keywords = {B-24;Cerebral Ventricles/*cytology;Colony-Forming Units Assay;Cells, Cultured;Neurons/*cytology;Aging;Rats;Proteoglycans;Animal;Cell Count;Drug Combinations;Ependyma/*cytology;Laminin;Stem Cells/*cytology;Dentate Gyrus/*cytology;Male;Rats, Wistar;Animals, Newborn;Support, Non-U.S. Gov't;Spheroids/cytology;Mice;Cell Differentiation/physiology;Immunohistochemistry;Artifacts;Collagen;Neuroglia/cytology;Clone Cells/cytology},
	Number = {5},
	Organization = {Department of Anatomy and Cell Biology, University of Toronto, Toronto M5S 1A8, Canada. raewyn.seaberg\@utoronto.ca},
	Pages = {1784-93},
	Pubmed = {11880507},
	Title = {Adult rodent neurogenic regions: the ventricular subependyma contains neural stem cells, but the dentate gyrus contains restricted progenitors},
	Uuid = {AD8AFEE2-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	url = {papers/Seaberg_JNeurosci2002.pdf}}

@article{Seamon:2002,
	Abstract = {The effects of inserting reported nuclear localization signals (NLSs) into the Moloney murine leukemia virus (Mo-MuLV) integrase (IN) protein, within a replication-competent viral construct, were studied. In contrast to the virus harboring IN fused to the simian virus 40 (SV40) large T antigen NLS (SV40 NLS) (J. A. Seamon, M. Adams, S. Sengupta, and M. J. Roth, Virology 274:412-419, 2000), a codon-modified SV40 NLS was stably expressed during viral propagation. Incorporation of the codon-modified SV40 NLS into IN, however, altered the packaging of the Gag-Pol precursor in the virus; viral particles contained decreased levels of reverse transcriptase (RT) and IN. In addition, the virus showed delayed kinetics of viral DNA synthesis upon infection. A panel of infectious MuLVs containing alternative IN-NLS fusions was generated and assayed for cell cycle-independent infection. Viral infection with the NLS-tagged proteins, however, remained dependent on passage of the cells through mitosis. This finding has direct implications for engineering murine-based retroviral vectors for gene therapy.},
	Author = {Seamon, Jennifer A. and Jones, Kathryn S. and Miller, Christina and Roth, Monica J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Animals;Base Sequence;Antigens, Polyomavirus Transforming;Transfection;Cell Cycle;Integrases;15 Retrovirus mechanism;DNA Replication;Genetic Vectors;Nuclear Localization Signal;Cell Line;Moloney murine leukemia virus;Gene Therapy;Support, U.S. Gov't, P.H.S.;DNA, Viral;Virus Integration;Amino Acid Sequence;Mice;Dogs;Virus Replication;Molecular Sequence Data},
	Medline = {22129266},
	Month = {8},
	Nlm_Id = {0113724},
	Number = {16},
	Organization = {Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854, USA.},
	Pages = {8475-84},
	Pubmed = {12134052},
	Title = {Inserting a nuclear targeting signal into a replication-competent Moloney murine leukemia virus affects viral export and is not sufficient for cell cycle-independent infection},
	Uuid = {A1B3B732-6459-409E-BB37-94D722225305},
	Volume = {76},
	Year = {2002},
	url = {papers/Seamon_JVirol2002.pdf}}

@article{Sears:2003,
	Abstract = {Cell death plays an essential role in development, and the removal of cell corpses presents an important challenge for the developing organism. Macrophages are largely responsible for the clearance of cell corpses in Drosophila melanogaster and mammalian systems. We have examined the developmental requirement for macrophages in Drosophila and find that macrophage function is essential for central nervous system (CNS) morphogenesis. We generate and analyze mutations in the Pvr locus, which encodes a receptor tyrosine kinase of the PDGF/VEGF family that is required for hemocyte migration. We find that loss of Pvr function causes the mispositioning of glia within the CNS and the disruption of the CNS axon scaffold. We further find that inhibition of hemocyte development or of Croquemort, a receptor required for macrophage-mediated corpse engulfment, causes similar CNS defects. These data indicate that macrophage-mediated clearance of cell corpses is required for proper morphogenesis of the Drosophila CNS.},
	Author = {Sears, Heather C. and Kennedy, Caleb J. and Garrity, Paul A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Research Support, Non-U.S. Gov't;Central Nervous System;Neuroglia;Research Support, U.S. Gov't, P.H.S.;Drosophila;Macrophages;Animals;24 Pubmed search results 2008;Axons},
	Medline = {22694524},
	Month = {8},
	Nlm_Id = {8701744},
	Number = {15},
	Organization = {Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue 68-230B, Cambridge, MA 02139, USA.},
	Pages = {3557-65},
	Pubmed = {12810602},
	Title = {Macrophage-mediated corpse engulfment is required for normal Drosophila CNS morphogenesis},
	Uuid = {81EEEB1B-C24C-49F0-9A4D-790A3F89950A},
	Volume = {130},
	Year = {2003}}

@article{Seidenfaden:2006,
	Abstract = {In the adult mouse forebrain, large numbers of neuronal precursors, destined to become GABA- and dopamine-producing interneurons of the olfactory bulb (OB), are generated in the subventricular zone (SVZ). Although this neurogenic system represents a potential reservoir of stem and progenitor cells for brain repair approaches, information about the survival and differentiation of SVZ-derived cells in ectopic brain regions is still fragmentary. We show here that ectopic grafting of SVZ tissue gave rise to two morphologically distinguishable cell types displaying oligodendrocytic or astrocytic characteristics. Since SVZ tissue contains neuronal and glial progenitors, we used magnetic cell sorting to deplete A2B5+ glial progenitors from the dissociated SVZ and to positively select cells that express PSA-NCAM. This procedure allowed the purification of neuronal precursors expressing TUJ1, DCX and GAD65/67. Transplantation of these cells led again to the generation of the same two glial cell types, showing that committed interneuron precursors undergo glial differentiation outside their normal environment.},
	Author = {Seidenfaden, Ralph and Desoeuvre, Ang{\'e}lique and Bosio, Andreas and Virard, Isabelle and Cremer, Harold},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Nlm_Id = {9100095},
	Number = {1-2},
	Organization = {Institut de Biologie du D{\'e}veloppement de Marseille, CNRS, Universit{\'e} de la M{\'e}diteran{\'e}e, Campus de Luminy-case 907, 13288 Marseille cedex 9, France. seidenfa\@ibdm.univ-mrs.fr},
	Pages = {187-98},
	Pii = {S1044-7431(06)00075-3},
	Pubmed = {16730456},
	Title = {Glial conversion of SVZ-derived committed neuronal precursors after ectopic grafting into the adult brain},
	Uuid = {43F3DEBD-4423-11DB-A5D2-000D9346EC2A},
	Volume = {32},
	Year = {2006},
	url = {papers/Seidenfaden_MolCellNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.mcn.2006.04.003}}

@article{Seipp:1997,
	Abstract = {Hepatitis C virus (HCV) is a major cause of chronic viral hepatitis. Development of anti-viral strategies has been hampered by the lack of efficient cell systems to propagate HCV in vitro. To establish a long-term culture system, we tested human hepatoma (HuH7, HepG2) and porcine non-hepatoma (PK15, STE) cell lines, as well as several culture and infection conditions. As a marker for virus replication, minus-strand HCV RNA in infected cells was detected by an enhanced detection system using nested RT-PCR followed by hybridization analysis. Short-term efficiency of HCV infection (10 days) was slightly increased by addition of polyethylene glycol (PEG) and/or dimethyl sulfoxide (DMSO) to culture media during inoculation of HuH7, PK15 and STE cells, but no augmentation in long-term culture was achieved, suggesting enhanced attachment of HCV to cells rather than more efficient infection. A stabilizing effect on HCV propagation was observed for 50 days in a serum-free medium with stimulation of the low-density lipoprotein (LDL) receptor expression by lovastatin. Using partially serum-free culture conditions, long-term persistence of HCV in cells and release of virions into supernatant was achieved for up to 130 days. Infectivity of released virions in supernatants after long-term culturing (day 30-80) was shown by successful infection of fresh cells. In conclusion, supplementation with PEG, DMSO and lovastatin during inoculation did not enhance virus replication substantially, but continued stimulation of LDL-receptor expression resulted in infections which persisted for over 4 months. These data support the hypothesis of an LDL-receptor mediated uptake of HCV into cells in vitro. Journal Article},
	Author = {Seipp, S. and Mueller, H. M. and Pfaff, E. and Stremmel, W. and Theilmann, L. and Goeser, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Journal = {J Gen Virol},
	Keywords = {Aged;Hepacivirus/genetics/ growth &development;Human;Female;08 Aberrant cell cycle;Time Factors;EE abstr;Hepatitis C/ virology;Swine;Support, Non-U.S. Gov't;Cells, Cultured;Animals;RNA, Viral/ analysis/biosynthesis;Polymerase Chain Reaction/methods},
	Organization = {Department of Internal Medicine, University of Heidelberg, Germany. Stefanie\_Seipp\@krzmail.krz.uni-heidelberg.de},
	Pages = {2467-76},
	Title = {Establishment of persistent hepatitis C virus infection and replication in vitro},
	Uuid = {65B39FF7-9289-49C2-872A-678BAE575E1D},
	Volume = {78 ( Pt 10)},
	Year = {1997}}

@article{Sekerkova:2004,
	Abstract = {Bromodeoxyuridine (BrdU) is broadly used in neuroscience to study embryonic development and adult neurogenesis. The potential toxicity of this halogenated pyrimidine analogue is frequently neglected. In this study, we administered BrdU in small doses by the progressively delayed cumulative labeling method to immunocytochemically tag different cerebellar cell types with antibodies to specific markers and BrdU in the same section. The well-known structure of the cerebellum made it possible to ascertain several toxic effects of the treatment. Time-pregnant rats were given five or six injections of 5 or 6 mg of BrdU ( approximately 12-20 mg/kg) at 8-hour intervals over 2 successive days between day 11 and 21 of pregnancy (E11-E12 to E20-E21), and the adult progeny was processed by immunocytochemistry. We demonstrate that this treatment effectively labeled distinct cerebellar cell populations but produced striking defects in the proliferation, migration, and settling of the Purkinje cells; reduced the size of the cerebellar cortex and nuclei; produced defects in the patterning of foliation; and also affected litter size, body weight, and mortality of the offspring. The observed toxic effects were consistent within individual treatment groups but varied between different treatment groups. Treatment with BrdU at the peak of neurogenesis of cerebellar projection neurons (E14) produced the most severe malformations. We observed no overt effects on the timing of neurogenesis for cerebellar neurons and glia across experimental groups. In conclusion, BrdU is a useful tool to study neural development, but its cytotoxicity represents a serious pitfall particularly when multiple doses are used to label cells. 0021-9967 Journal Article},
	Author = {Sekerkova, G. and Ilijic, E. and Mugnaini, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {J Comp Neurol},
	Keywords = {EE, T pdf;08 Aberrant cell cycle},
	Number = {3},
	Organization = {Northwestern University Institute for Neuroscience, Chicago, Illinois 60611, USA.},
	Pages = {221-39},
	Title = {Bromodeoxyuridine administered during neurogenesis of the projection neurons causes cerebellar defects in rat},
	Uuid = {3DCF5ED6-EC97-41F8-A64A-58394DE48BCA},
	Volume = {470},
	Year = {2004},
	url = {papers/Sekerkova_JCompNeurol2004.pdf}}

@article{Seki:1996,
	Abstract = {We observed the enhancing effect of dimethylsulfoxide (DMSO) on infection of human T cells with human immunodeficiency virus type 1 (HIV-1). Similar enhancing effects were also found in related polar chemicals such as dimethylformamide, hexamethylenebisacetamide, sodium butyrate and retinoic acid. In acute infection of the human MT-4 T cell line, DMSO at a concentration of 1\%reduced the amounts of HIV-1 required to establish similar infection by one log. Furthermore, infection of peripheral blood lymphocytes with HIV-1 was also augmented several times by DMSO. HIV-1 production from persistently infected human T cell lines, but not monocytic cell lines, was enhanced by DMSO and related polar chemicals. DMSO enhanced transcription of HIV-1 RNA in persistently infected T cell lines, and the enhancing effect of DMSO on HIV-1 production was inhibited by staurosporine, a protein kinase inhibitor. These findings suggested that DMSO enhanced HIV-1 infection of T cells mainly at the step of transcription of viral RNA. 0006-291x Journal Article},
	Author = {Seki, J. and Ikeda, R. and Hoshino, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Biochem Biophys Res Commun},
	Keywords = {Tretinoin/pharmacology;Virus Replication/*drug effects;T-Lymphocytes/*drug effects/virology;EE, DMSO pdf;Human;Butyric Acid;Cell Line;HIV-1/genetics/*physiology;08 Aberrant cell cycle;Butyric Acids/pharmacology;Dimethyl Sulfoxide/*pharmacology;Support, Non-U.S. Gov't;Acetamides/pharmacology;Dimethylformamide/pharmacology},
	Number = {3},
	Organization = {Department of Hygiene and Virology, Gunma University School of Medicine, Japan.},
	Pages = {724-9},
	Title = {Dimethyl sulfoxide and related polar compounds enhance infection of human T cells with HIV-1 in vitro},
	Uuid = {89CBE17D-6B28-49DA-A8BF-31D5745D0786},
	Volume = {227},
	Year = {1996},
	url = {papers/Seki_BiochemBiophysResCommun1996.pdf}}

@article{Seki:1993,
	Abstract = {The expression of a highly polysialylated neural cell adhesion molecule (NCAM-H) appeared in motor neurons, presumptive commissural neurons and floor plate at embryonic day 12, and then spread throughout the spinal cord during late embryonic and early postnatal stages. In the adult stage, the expression almost disappeared, but remained in the superficial laminae of the dorsal horn, the lateral spinal nucleus and the area around the central canal. These results suggest that the NCAM- H expression of the spinal cord is involved in the developmental events and possibly in the processing system of somatic and/or visceral information during the adult stage.},
	Author = {Seki, T. and Arai, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Staining and Labeling;02 Adult neurogenesis migration;Tissue Distribution;Cell Adhesion Molecules, Neuronal/*metabolism;Rats;Rats, Wistar;Animal;B abstr;Aging/*metabolism;Support, Non-U.S. Gov't;Spinal Cord/embryology/growth &development/*metabolism;Immunologic Techniques},
	Number = {1},
	Pages = {141-5.},
	Title = {Highly polysialylated NCAM expression in the developing and adult rat spinal cord},
	Uuid = {A099F432-58D7-4BAA-86C0-D90D68042679},
	Volume = {73},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7685664}}

@article{Seki:1999,
	Abstract = {The granule cell layer of the adult dentate gyrus possesses two characteristics of an immature nervous system. The first is that granule cells continue to be generated in the innermost region of the granule cell layer, and newly generated and developing granule cells in the adult express highly polysialylated neural cell adhesion molecule (PSA-NCAM). PSA-NCAM-expressing apical dendrites have dynamically unstable processes such as irregular shafts and many stick-like or fan-shaped fine processes. The second is that radial glia-like cells expressing glial fibrillary acidic protein (GFAP) remain in a similar region of the granular layer. The numbers of PSA-NCAM-expressing granule cells and GFAP-expressing radial glia-like cells show a parallel age-dependent decrease during aging. Moreover, by using confocal laser scanning microscopy and immunoelectron microscopy, we demonstrated that PSA-NCAM-expressing dendrites and GFAP-expressing radial processes are partly in contact with each other, and occasionally the radial glial processes envelop the PSA-NCAM-positive dendritic processes. The temporal and spatial relationship between the two immature elements suggests that the processes of the radial glia-like cells are closely associated with the dendritic growth of the newly generated granule cells in the adult dentate gyrus and that these two immature features of neurons and glia in the dentate gyrus diminish with age.},
	Author = {Seki, T. and Arai, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Glial Fibrillary Acidic Protein;10 Development;10 Hippocampus;Animals;Microscopy, Immunoelectron;Neural Cell Adhesion Molecules;Gene Expression Regulation, Developmental;Aging;Rats;Microscopy, Confocal;Rats, Wistar;Male;Dendrites;Sialic Acids;Neuroglia;Dentate Gyrus;Neurons;Neural Cell Adhesion Molecule L1;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {99332494},
	Month = {8},
	Nlm_Id = {0406041},
	Number = {3},
	Organization = {Department of Anatomy, Juntendo University School of Medicine, Tokyo, Japan. tseki\@med.juntendo.ac.jp},
	Pages = {503-13},
	Pii = {10.1002/(SICI)1096-9861(19990802)410:3<503::AID-CNE11>3.0.CO;2-H},
	Pubmed = {10404415},
	Title = {Temporal and spacial relationships between PSA-NCAM-expressing, newly generated granule cells, and radial glia-like cells in the adult dentate gyrus},
	Uuid = {EC36A228-5E74-4E18-9AB5-2E6D221419DB},
	Volume = {410},
	Year = {1999},
	url = {papers/Seki_JCompNeurol1999.pdf}}

@article{Seki:2007,
	Abstract = {Adult neurogenesis occurs in the subgranular zone and innermost part of the dentate granule cell layer. To examine how neural precursor cells proliferate, migrate, and extend their neurites, we performed BrdU- and improved retrovirus-green fluorescence protein (GFP)-labeling analyses. Soon after labeling the majority of BrdU+ cells and GFP+ cells expressed Ki67, a cell cycle marker, and formed clusters together with PSA+ neuroblasts. Most of the Ki67+ proliferating cells expressed Hu, an immature and mature neuronal marker, and the subpopulation expressed both Hu+ and GFAP+. In the clusters, Ki67+ and PSA+ cells strongly expressed beta-catenin and N-cadherin, but PSA+ cells outside the clusters did not. Therefore, it was mainly Hu+ neuronal precursor cells that proliferated within clusters in which the cluster cells are closely associated via cell adhesion molecules, such as N-cadherin/beta-cateninIn and PSA. The newly generated cells appeared to stay in the clusters for a few days and then disperse around the clusters. The findings of this in vivo analysis and in vitro time-lapse imaging of early postnatal hippocampal slices support the notion that most postmitotic neuroblasts migrate tangentially from clusters, extending tangentially oriented processes, one of which often retains close contact with the clusters, and finally extend radial processes, or prospective apical dendrites. These results suggest that the clustering cells and tangentially migrating cells have a systematic cellular arrangement and intercellular interaction. J. Comp. Neurol. 502:275-290, 2007. (c) 2007 Wiley-Liss, Inc.},
	Author = {Seki, Tatsunori and Namba, Takashi and Mochizuki, Hideki and Onodera, Masafumi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {02 Adult neurogenesis migration;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Department of Anatomy, Juntendo University School of Medicine, Tokyo, Japan.},
	Pages = {275-90},
	Pubmed = {17348003},
	Title = {Clustering, migration, and neurite formation of neural precursor cells in the adult rat hippocampus},
	Uuid = {423C77D8-798F-4758-A8B0-FBC6C2452C93},
	Volume = {502},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.21301}}

@article{Seki:1993a,
	Abstract = {We have found in the adult rat that the persistent expression of a highly polysialylated neural cell adhesion molecule (NCAM-H) that is generally specific to developing tissues, remains restrictively in the cells of the deepest portion of the dentate granular layer. Since the granule cells are known to continue to be generated in this region during the adult period, we have tried to determine whether NCAM-H is expressed by newly generated granule cells. Immunoelectron microscopic observation revealed that about half of the NCAM-H-expressing cells had the features of dentate granule cells, and that the rest of these cells appeared to be immature cells. Double immunostaining for NCAM-H and glial fibrillary acidic protein (GFAP) revealed that the NCAM-H- expressing cells differed from GFAP-positive glial cells. In rats injected with 5-bromo-2'-deoxyuridine (BrdU) at post-natal day 35, double immunostaining for NCAM-H and BrdU demonstrated that the BrdU- labeled cells expressed NCAM-H at 12 d after the injection but not at 80 d. These results provide the first direct evidence that NCAM-H is expressed transiently by newly generated granule cells that may add new neuronal circuits to the adult hippocampal formation.},
	Author = {Seki, T. and Arai, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci},
	Keywords = {Staining and Labeling;Granulocytes/*metabolism/ultrastructure;02 Adult neurogenesis migration;Glial Fibrillary Acidic Protein/metabolism;Cell Adhesion Molecules, Neuronal/*metabolism;Rats;Rats, Wistar;Animal;Hippocampus/cytology/*metabolism/ultrastructure;B abstr;Microscopy, Immunoelectron;Support, Non-U.S. Gov't;Bromodeoxyuridine;Male;Immunologic Techniques},
	Number = {6},
	Organization = {Department of Anatomy, Juntendo University School of Medicine, Tokyo, Japan.},
	Pages = {2351-8.},
	Title = {Highly polysialylated neural cell adhesion molecule (NCAM-H) is expressed by newly generated granule cells in the dentate gyrus of the adult rat},
	Uuid = {7B9EC824-1BBB-454D-B43D-63EC9ADA8085},
	Volume = {13},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7684771}}

@article{Seki:2002,
	Abstract = {Neurogenesis is known to continue in the adult hippocampus of mammals, including humans. The present experiments were undertaken to examine the nature of developing neurons generated in the dentate gyrus of young and older rodents using immature neuronal markers such as highly polysialylated neural cell adhesion molecules (PSA-NCAM), collapsin response-mediated protein-4 (CRMP-4) and NeuroD. Most PSA-expressing cells are simultaneously positive for CRMP-4 and NeuroD in young rats. More than half of the PSA-positive cells were also positive for mature neuronal markers such as NeuN and MAP2, although the intensity of the immunoreactivities was relatively weak. BrdU analysis revealed that CRMP-4 is expressed for a longer period than PSA in BrdU-labeled neurons. The number of immature neurons expressing PSA, NeuroD or CRMP-4 decreased in older rodents, but no qualitative difference was found in the expression patterns of these molecular markers between young and older rodents. These results suggest not only that immunohistochemistry, using a combination of these immature and mature neuronal markers, is helpful for clarifying the developmental state of newly generated neurons, but also that newly generated neurons in young adult and older rodents have similar properties.},
	Author = {Seki, Tatsunori},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {10 Development;Cell Differentiation;Animals;10 Hippocampus;Microtubule-Associated Proteins;Gene Expression Regulation, Developmental;Aging;Rats;Basic Helix-Loop-Helix Transcription Factors;Axons;Hippocampus;Mice, Inbred C57BL;Rats, Wistar;Male;Dendrites;Nerve Regeneration;Sialic Acids;Neurons;Dentate Gyrus;Mice;Neural Cell Adhesion Molecule L1;Immunohistochemistry;Cell Division;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22278738},
	Month = {11},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Department of Anatomy, Juntendo University School of Medicine, Tokyo, Japan. tseki\@med.juntendo.ac.jp},
	Pages = {327-34},
	Pubmed = {12391592},
	Title = {Expression patterns of immature neuronal markers PSA-NCAM, CRMP-4 and NeuroD in the hippocampus of young adult and aged rodents},
	Uuid = {9EDC6004-EDE9-4D66-9A05-00F33E53CCE0},
	Volume = {70},
	Year = {2002},
	url = {papers/Seki_JNeurosciRes2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10387}}

@article{Seki:1993b,
	Abstract = {The neural cell adhesion molecule (NCAM) is a cell surface glycoprotein which is thought to mediate cell adhesion and recognition. During developmental stages, NCAM is highly polysialylated (NCAM-H) by a unique alpha-2,8-linked polysialic acid chain (PSA), and this PSA portion of NCAM-H has been found to be closely associated with various developmental processes of the nervous system. Further, recent immunohistochemical investigations have revealed that even in the adult nervous system, a persistent PSA expression has been found confined to several regions: the olfactory bulb, the piriform cortex, the hippocampal dentate gyrus, the hypothalamus, some nuclei of the medulla and the dorsal horn of the spinal cord, which are related directly or indirectly to sensory systems. Moreover, in the dentate gyrus and olfactory bulb the expression is connected with adult neurogenesis that may add new neuronal circuits to the adult neural tissue. Therefore, the possible role of NCAM-H in the central nervous system may be associated not only with neural development, but also with adult functions, such as the processing system of sensory information and neuronal plasticity.},
	Author = {Seki, T. and Arai, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Neurosci Res},
	Keywords = {Cell Adhesion Molecules,;Sialic Acids/biosynthesis/chemistry/metabolism/*physiology;Central Nervous System/growth &development/*metabolism/physiology;Human;Neuronal/biosynthesis/chemistry/metabolism/*physiology;Animal;04 Adult neurogenesis factors;Support, Non-U.S. Gov't;C abstr},
	Number = {4},
	Organization = {Department of Anatomy, Juntendo University School of Medicine, Tokyo, Japan.},
	Pages = {265-90.},
	Title = {Distribution and possible roles of the highly polysialylated neural cell adhesion molecule (NCAM-H) in the developing and adult central nervous system},
	Uuid = {15454CAB-1BE1-478A-AC7E-DFDB20F6A244},
	Volume = {17},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8264989}}

@article{Selkirk:2002,
	Abstract = {Advances in the development of highly infectious, replication-deficient recombinant retroviruses provide an efficient means of stable transfer of gene expression. Coupled with ex vivo transduction, surrogate cell populations can be readily implanted into the brain, thus serving as vehicles for delivering selected gene products into the central nervous system (CNS). Here we report that rat astrocytes can be routinely and safely isolated from brain tissue of a living donor by use of short-term gelatin sponge implants. The mature, nontransformed astrocytes were easily expanded, maintained in long-term tissue cultures and were efficiently transduced with an amphotropic retrovirus harboring a heterologous, fused transgene. In vitro retroviral infection rendered the nontransformed cells essentially 100\%viable after exposure. The level of efficiency of infection (30-50\%effective genome integration of provirus and expression of transgene in target cell populations) and minimal cell toxicity obviated the need to harvest large numbers of target cells. Cultured transduced astrocytes were resilient and exhibited select peptide expression for up to 1 year. Subsequently, transduced astrocytes were used in a series of experiments in which cells were transplanted intracerebrally in syngeneic animals. Post-implantation, astrocytes seeded locally and either insinuated into the surrounding parenchyma in situ or exhibited a variable degree of migration, depending on the anatomic source of astrocytes and the targeted brain implantation site. Transduced astrocytes remained viable in excess of 8 months post-transplantation and exhibited sustained transgenic peptide expression of green fluorescent protein/neomycin phosphotransferase in vivo. The sequential isolation and culture of nontransformed, mature, adult astrocytes and recombinant retrovirus-mediated transduction in vitro followed by brain reimplantation represents a safe and effective means for transferring genetic expression to the CNS. This study lays the foundation for exploring the utility of using a human autologous transplantation system as a potential gene delivery approach to treat neurological disorders. Prepared and utilized in this manner, autologous astrocytes may serve as a vehicle to deliver gene therapy to the CNS.},
	Author = {Selkirk, S. M. and Greenberg, S. J. and Plunkett, R. J. and Barone, T. A. and Lis, A. and Spence, P. O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Cell Culture Techniques;Transduction, Genetic;Astrocytes;Animals;Central Nervous System Diseases;Rats;Cell Separation;Brain;Kanamycin Kinase;Retroviridae;11 Glia;Green Fluorescent Proteins;Genetic Vectors;Rats, Inbred F344;Gene Therapy;Transplantation, Autologous;Luminescent Proteins;Models, Animal;Research Support, Non-U.S. Gov't},
	Medline = {21935227},
	Month = {4},
	Nlm_Id = {9421525},
	Number = {7},
	Organization = {Laboratory of Neuroimmunology and Neurovirology, Department of Neurology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.},
	Pages = {432-43},
	Pubmed = {11938458},
	Title = {Syngeneic central nervous system transplantation of genetically transduced mature, adult astrocytes},
	Uuid = {3CCBDDCF-AF95-4094-98E5-5AF9926A30E0},
	Volume = {9},
	Year = {2002},
	url = {papers/Selkirk_GeneTher2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301643}}

@article{Semkova:1999,
	Abstract = {Neurotrophins and other neurotrophic factors have been shown to support the survival and differentiation of many neuronal populations of the central and peripheral nervous system. Therefore, administering neurotrophic factors could represent an alternative strategy for the treatment of acute and chronic brain disorders. However, the delivery of neurotrophic factors to the brain is one of the largest obstacles in the development of effective therapy for neurodegenerative disorders, because these proteins are not able to cross the blood-brain barrier. The induction of growth factor synthesis in the brain tissue by systemically administered lipophilic drugs, such as beta-adrenoceptor agonists, shown to increase endogenous nerve growth factor (NGF) synthesis in the brain, would be an elegant way to overcome these problems of application. Stimulation of beta-adrenoceptors with clenbuterol led to increased NGF synthesis in cultured central nervous system (CNS) cells and rat brain tissue. Clenbuterol-induced NGF expression was reduced to the control levels by coadministration of beta-adrenoceptor antagonist propranolol. Furthermore, clenbuterol protected rat hippocampal neurons subjected to excitotoxic damage. The neuroprotective effect of clenbuterol in vitro depended on increased NGF synthesis, since the neuroprotection was abolished by NGF antisense oligonucleotide as well as by antibodies directed against NGF itself. In vivo, clenbuterol protected rat hippocampus in a model of transient forebrain ischemia and reduced the infarct volume in a rat model of permanent middle cerebral artery occlusion (MCAo). The neuroprotective effect of clenbuterol in vivo was accompanied by enhanced NGF synthesis in brain tissue. These findings support our hypothesis that orally active NGF inducers may have a potential as therapeutic agents for the treatment of neurodegenerative disorders and stroke.},
	Author = {Semkova, I. and Krieglstein, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {Cell Differentiation;Brain/*physiology;Neuroprotective Agents;Neurons/cytology/pathology/*physiology;Rats;Human;Cell Survival;Brain Diseases/*physiopathology/therapy;Animal;04 Adult neurogenesis factors;C-10;Neurodegenerative Diseases/*physiopathology/therapy;Nerve Growth Factors/genetics/*physiology/therapeutic use},
	Number = {2},
	Organization = {Hannover Medical School, Center of Anatomy, OE 4140, Carl-Neuberg Str. 1, D-30623, Hannover, Germany. semkova.irina\@mh-hannover.de},
	Pages = {176-88.},
	Title = {Neuroprotection mediated via neurotrophic factors and induction of neurotrophic factors},
	Uuid = {B01A2B79-4A47-4875-8C6C-757BD9FE5872},
	Volume = {30},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10525174%20http://www.elsevier.com:80/cgi-bin/cas/tree/store/bresr/cas_sub/browse/browse.cgi?year=1999&volume=30&issue=2&aid=90260}}

@article{Sengupta:2003,
	Abstract = {PURPOSE: Age-related macular degeneration (ARMD) is the primary cause of blindness in people aged of 50 years or more. The wet form leads to severe loss of central vision. Recent evidence supports that adult hematopoietic stem cells (HSCs) contribute to preretinal neovascularization. In the current study, it was determined whether HSCs, by producing both blood and blood vessels, provide functional hemangioblast activity during choroidal neovascularization (CNV) in mice. METHODS: Gfp chimeric mice were developed by bone marrow ablation of C57BL/6J mice and reconstitution with donor tissue from gfp(+/+) transgenic mice. Gfp chimeric mice underwent laser rupture of Bruch's membrane and were killed and eyes enucleated at 1, 2, 3, and 4 weeks after laser injury. CNV was examined by confocal microscopy of retinal flatmounts. Because endothelial progenitor cells (EPCs) derive from HSCs, immunocytochemistry was used to quantify relative the EPC contribution to CNV. RESULTS: Laser injury alone was sufficient to induce stem cell recruitment and subsequent CNV. Gfp+ cells formed part of the functional vasculature in the choroid as early as 1 week after injury and were present for the duration of the study. The relative EPC contribution to CNV remained fairly constant throughout the study and constituted almost 50\%of the total vasculature. CONCLUSIONS: Adult stem cells are recruited to the choroid in a model of CNV, where they contribute to forming aberrant new vessels. This observation suggests that targeting stem cell recruitment to the eye may offer a novel therapeutic strategy for ARMD.},
	Author = {Sengupta, Nilanjana and Caballero, Sergio and Mames, Robert N. and Butler, Jason M. and Scott, Edward W. and Grant, Maria B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0146-0404},
	Journal = {Invest Ophthalmol Vis Sci},
	Keywords = {Blood Vessels;Fluorescent Antibody Technique, Indirect;Animals;Blood Cells;Microscopy, Confocal;Indicators and Reagents;Mice, Transgenic;Choroidal Neovascularization;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Bruch Membrane;Antigens, CD31;Hematopoietic Stem Cell Transplantation;Bone Marrow;Research Support, U.S. Gov't, P.H.S.;Flow Cytometry;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Laser Coagulation;Research Support, Non-U.S. Gov't},
	Medline = {22939977},
	Month = {11},
	Nlm_Id = {7703701},
	Number = {11},
	Organization = {Program in Stem Cell Biology, University of Florida, Florida, USA.},
	Pages = {4908-13},
	Pubmed = {14578416},
	Title = {The role of adult bone marrow-derived stem cells in choroidal neovascularization},
	Uuid = {194777C5-E0B5-43BA-899B-93CC2901C2D4},
	Volume = {44},
	Year = {2003}}

@article{Sensenbrenner:1997,
	Abstract = {Recent studies have revealed that proteins such as growth-associated protein 43 (GAP-43) and neuron-specific enolase (NSE), believed for many years to be expressed exclusively in neurons, are also present in glial cells under some circumstances. Here we present an overview of these observations. GAP-43 is expressed both in vitro and in vivo transiently in immature rat oligodendroglial cells of the central nervous system, in Schwann cell precursors, and in non-myelin-forming Schwann cells of the peripheral nervous system. GAP-43 mRNA is also present in oligodendroglial cells and Schwann cells, indicating that GAP-43 is synthesized in these cells. GAP-43 is also expressed in type 2 astrocytes (stellate-shaped astrocytes) and in some reactive astrocytes but not in type 1 astrocytes (flat protoplasmic astrocytes). These results suggest that GAP-43 plays a more general role in neural plasticity during development of the central and peripheral nervous systems. NSE enzymatic activity and protein and mRNA have been detected in rat cultured oligodendrocytes at levels comparable to those of cultured neurons. NSE expression increases during the differentiation of oligodendrocyte precursors into oligodendrocytes. In vivo, NSE protein is expressed in differentiating oligodendrocytes and is repressed in fully mature adult cells. The upregulation of NSE in differentiating oligodendrocytes coincides with the formation of large amounts of membrane structures and of protoplasmic processes. Similarly, NSE becomes detectable in glial neoplasms and reactive glial cells at the time when these cells undergo morphological changes. The expression of the glycolytic isozyme NSE in these cells, which do not normally contain it, could reflect a response to higher energy demands. This expression may also be related to the neurotrophic and neuroprotective properties demonstrated for this enolase isoform. NSE activity and protein and mRNA have also been found in cultured rat type 1-like astrocytes but at much lower levels than in neurons and oligodendrocytes. Thus GAP-43 and NSE should be used with caution as neuron-specific markers in studies of normal and pathological neural development.},
	Author = {Sensenbrenner, M. and Lucas, M. and Deloulme, J. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0946-2716},
	Journal = {J Mol Med},
	Keywords = {01 Adult neurogenesis general;Neuroglia;Central Nervous System;Research Support, Non-U.S. Gov't;Rats;Schwann Cells;Astrocytes;Phosphopyruvate Hydratase;GAP-43 Protein;Cells, Cultured;Animals;24 Pubmed search results 2008;review},
	Medline = {98012069},
	Month = {9},
	Nlm_Id = {9504370},
	Number = {9},
	Organization = {Laboratoire de Neurobiologie Ontog{\'e}nique, CNRS ERS 110, Centre de Neurochimie, Strasbourg, France.},
	Pages = {653-63},
	Pubmed = {9351704},
	Title = {Expression of two neuronal markers, growth-associated protein 43 and neuron-specific enolase, in rat glial cells},
	Uuid = {E65819E3-2902-4148-AD25-36419D418E0B},
	Volume = {75},
	Year = {1997}}

@article{Seress:1991,
	Abstract = {Calcium-binding proteins calbindin D28k (CaBP) and parvalbumin (PV) were localized in neurons of the monkey hippocampal formation. CaBP immunoreactivity is present in all granule cells and in a large proportion of CA1 and CA2 pyramidal neurons, as well as in a distinct population of local circuit neurons. In the dentate gyrus, CaBP-immunoreactive nongranule cells are present in the molecular layer and in the hilar region, but they do not include the pyramidal basket cells at the hilar border. In the Ammon's horn, CaBP-positive, nonpyramidal neurons are more frequent in the CA3 area than in any other parts of the hippocampal formation. They are concentrated in the strata oriens and pyramidale of areas CA1-3, whereas only a few small neurons were found in the strata lucidum and radiatum of CA3 and in the stratum moleculare of the CA1 area. PV is exclusively present in local circuit neurons both in the dentate gyrus and in Ammon's horn. In the dentate gyrus the presumed basket cells at the hilar border exhibit PV immunoreactivity. In the hilar region and molecular layer only a relatively small number of cells are immunoreactive for PV. Most of these PV-positive cell bodies are located in the inner half of the molecular layer, with occasional horizontal cells at the hippocampal fissure. In Ammon's horn, strata oriens and pyramidale of areas CA1-3 contain a large number of PV-positive cells. There are no PV-immunoreactive cells in the strata lucidum, radiatum, or lacunosum moleculare. The CaBP- and PV-containing neurons form different subpopulations of cells in the monkey hippocampal formation. With the exception of a basket cell type in the monkey dentate gyrus, the CaBP- and PV-positive cell types were found to be remarkably similar in rodents and primates.},
	Author = {Seress, L. and Guly{\'a}s, A. I. and Freund, T. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {10 Development;Research Support, Non-U.S. Gov't;Calcium-Binding Protein, Vitamin D-Dependent;Macaca mulatta;Female;10 Hippocampus;Immunohistochemistry;Parvalbumins;Hippocampus;Pyramidal Tracts;Interneurons;Animals;Neurons},
	Medline = {92105482},
	Month = {11},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Department of Physiology, University Medical School P{\'e}cs, Hungary.},
	Pages = {162-77},
	Pubmed = {1761752},
	Title = {Parvalbumin- and calbindin D28k-immunoreactive neurons in the hippocampal formation of the macaque monkey},
	Uuid = {111B4FE6-CC41-41B5-990E-FEF3C8856464},
	Volume = {313},
	Year = {1991},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.903130112}}

@article{Seri:2004,
	Abstract = {New neurons continue to be born in the subgranular zone (SGZ) of the dentate gyrus in the hippocampus of adult mammals, including humans. Previous work has shown that astrocytes function as the progenitors of these new neurons through immature intermediate D cells. In the first part of the present study, we determined the structure of each of these progenitors and how they are organized in three dimensions. Serial-section reconstructions of the SGZ, using confocal and electron microscopy demonstrate that SGZ astrocytes form baskets that hold clusters of D cells, largely insulating them from the hilus. Two types of glial fibrillary acidic protein-expressing astrocytes (radial and horizontal) and three classes of doublecortin and PSA-NCAM-positive D cells (D1, D2, D3) were observed. Radial astrocytes appear to interact closely with clusters of D cells forming radial proliferative units. In the second part of this study, we show that retrovirally labeled radial astrocytes give rise to granule neurons. We also used bromodeoxyuridine and [3H]thymidine labeling to study the sequence of appearance of the different D cells after a 7-day treatment with anti-mitotics. This analysis, together with retroviral labeling data, suggest that radial astrocytes divide to generate D1 cells, which in turn divide once to form postmitotic D2 cells. D2 cells mature through a D3 stage to form new granule neurons. These observations provide a model of how the germinal zone of the adult hippocampus is organized and suggest a sequence of cellular stages in the generation of new granule neurons.},
	Author = {Seri, Bettina and Garc{\'\i}a-Verdugo, Jos{\'e} Manuel and Collado-Morente, Lucia and McEwen, Bruce S. and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Cell Differentiation;10 Development;03 Adult neurogenesis progenitor source;Comparative Study;10 Hippocampus;Dentate Gyrus;Germ Layers;Research Support, U.S. Gov't, P.H.S.;Animals;Mice;Cell Lineage},
	Month = {10},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {University of California, San Francisco, Department of Neurological Surgery and Program in Developmental and Stem Cell Research, San Francisco, California 94143, USA.},
	Pages = {359-78},
	Pubmed = {15384070},
	Title = {Cell types, lineage, and architecture of the germinal zone in the adult dentate gyrus},
	Uuid = {4380B721-7FED-11DA-9A2D-000D9346EC2A},
	Volume = {478},
	Year = {2004},
	url = {papers/Seri_JCompNeurol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.20288}}

@article{Seri:2001,
	Abstract = {Neurogenesis in the dentate gyrus of the hippocampus persists throughout life in many vertebrates, including humans. The progenitors of these new neurons reside in the subgranular layer (SGL) of the dentate gyrus. Although stem cells that can self-renew and generate new neurons and glia have been cultured from the adult mammalian hippocampus, the in vivo primary precursors for the formation of new neurons have not been identified. Here we show that SGL cells, which express glial fibrillary acidic protein and have the characteristics of astrocytes, divide and generate new neurons under normal conditions or after the chemical removal of actively dividing cells. We also describe a population of small electron-dense SGL cells, which we call type D cells and are derived from the astrocytes and probably function as a transient precursor in the formation of new neurons. These results reveal the origins of new neurons in the adult hippocampus.},
	Author = {Seri, B. and Garcia-Verdugo, J. M. and McEwen, B. S. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {J Neurosci},
	Keywords = {02 Adult neurogenesis migration;10 Development;03 Adult neurogenesis progenitor source;10 Hippocampus;BB},
	Number = {18},
	Organization = {The Rockefeller University, New York, New York 10021, USA.},
	Pages = {7153-60.},
	Title = {Astrocytes give rise to new neurons in the adult mammalian hippocampus},
	Uuid = {F21C94AB-6875-11DA-A4B6-000D9346EC2A},
	Volume = {21},
	Year = {2001},
	url = {papers/Seri_JNeurosci2001}}

@article{Serizawa:2006,
	Abstract = {In the mouse, olfactory sensory neurons (OSNs) expressing the same odorant receptor (OR) converge their axons to a specific set of glomeruli in the olfactory bulb. To study how OR-instructed axonal fasciculation is controlled, we searched for genes whose expression profiles are correlated with the expressed ORs. Using the transgenic mouse in which the majority of OSNs express a particular OR, we identified such genes coding for the homophilic adhesive molecules Kirrel2/Kirrel3 and repulsive molecules ephrin-A5/EphA5. In the CNGA2 knockout mouse, where the odor-evoked cation influx is disrupted, Kirrel2 and EphA5 were downregulated, while Kirrel3 and ephrin-A5 were upregulated, indicating that these genes are transcribed in an activity-dependent manner. Mosaic analysis demonstrated that gain of function of these genes generates duplicated glomeruli. We propose that a specific set of adhesive/repulsive molecules, whose expression levels are determined by OR molecules, regulate the axonal fasciculation of OSNs during the process of glomerular map formation.},
	Author = {Serizawa, Shou and Miyamichi, Kazunari and Takeuchi, Haruki and Yamagishi, Yuya and Suzuki, Misao and Sakano, Hitoshi},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Models, Biological;Protein Binding;24 Pubmed search results 2008;research support, non-u.s. gov't;Carrier Proteins;Cell Adhesion Molecules;Membrane Proteins;Ephrin-A5;Receptor, EphA5;Mice, Transgenic;Olfactory Bulb;Neurons, Afferent;Animals;Mice;Receptors, Odorant;13 Olfactory bulb anatomy;Axons},
	Month = {12},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Department of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Tokyo 113-0032, Japan.},
	Pages = {1057-69},
	Pii = {S0092-8674(06)01404-8},
	Pubmed = {17129788},
	Title = {A neuronal identity code for the odorant receptor-specific and activity-dependent axon sorting},
	Uuid = {F298058E-76BB-4682-952F-84E34DE87F9C},
	Volume = {127},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.10.031}}

@article{Shalizi:2006,
	Abstract = {Postsynaptic differentiation of dendrites is an essential step in synapse formation. We report here a requirement for the transcription factor myocyte enhancer factor 2A (MEF2A) in the morphogenesis of postsynaptic granule neuron dendritic claws in the cerebellar cortex. A transcriptional repressor form of MEF2A that is sumoylated at lysine-403 promoted dendritic claw differentiation. Activity-dependent calcium signaling induced a calcineurin-mediated dephosphorylation of MEF2A at serine-408 and, thereby, promoted a switch from sumoylation to acetylation at lysine-403, which led to inhibition of dendritic claw differentiation. Our findings define a mechanism underlying postsynaptic differentiation that may modulate activity-dependent synapse development and plasticity in the brain.},
	Author = {Shalizi, Aryaman and Gaudilli\`{e}re, Brice and Yuan, Zengqiang and Stegm{\"u}ller, Judith and Shirogane, Takahiro and Ge, Qingyuan and Tan, Yi and Schulman, Brenda and Harper, J. Wade and Bonni, Azad},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Transcription, Genetic;10 Development;Cell Differentiation;Calcium Signaling;Animals;Synapses;In Vitro;Rats;Transfection;Acetylation;Humans;Phosphorylation;Electroporation;RNA Interference;Recombinant Fusion Proteins;Calcium;Small Ubiquitin-Related Modifier Proteins;Dendrites;Cerebellar Cortex;Myogenic Regulatory Factors;Cell Line;Morphogenesis;Neurons;Calcineurin;24 Pubmed search results 2008;Research Support, N.I.H., Extramural;Research Support, Non-U.S. Gov't},
	Month = {2},
	Nlm_Id = {0404511},
	Number = {5763},
	Organization = {Department of Pathology, Harvard Medical School, 77 Louis Pasteur Avenue, Boston, MA 02115, USA.},
	Pages = {1012-7},
	Pii = {311/5763/1012},
	Pubmed = {16484498},
	Title = {A calcium-regulated MEF2 sumoylation switch controls postsynaptic differentiation},
	Uuid = {82661870-3CDA-4C9F-BF00-0FECD0C8384B},
	Volume = {311},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1122513}}

@article{Shaner:2004,
	Abstract = {Fluorescent proteins are genetically encoded, easily imaged reporters crucial in biology and biotechnology. When a protein is tagged by fusion to a fluorescent protein, interactions between fluorescent proteins can undesirably disturb targeting or function. Unfortunately, all wild-type yellow-to-red fluorescent proteins reported so far are obligately tetrameric and often toxic or disruptive. The first true monomer was mRFP1, derived from the Discosoma sp. fluorescent protein "DsRed" by directed evolution first to increase the speed of maturation, then to break each subunit interface while restoring fluorescence, which cumulatively required 33 substitutions. Although mRFP1 has already proven widely useful, several properties could bear improvement and more colors would be welcome. We report the next generation of monomers. The latest red version matures more completely, is more tolerant of N-terminal fusions and is over tenfold more photostable than mRFP1. Three monomers with distinguishable hues from yellow-orange to red-orange have higher quantum efficiencies.},
	Author = {Shaner, Nathan C. and Campbell, Robert E. and Steinbach, Paul A. and Giepmans, Ben N. G. and Palmer, Amy E. and Tsien, Roger Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {letter;23 Technique},
	Month = {12},
	Nlm_Id = {9604648},
	Number = {12},
	Pages = {1567-72},
	Pii = {nbt1037},
	Pubmed = {15558047},
	Title = {Improved monomeric red, orange and yellow fluorescent proteins derived from Discosoma sp. red fluorescent protein},
	Uuid = {E1B32A1E-9E5A-4F00-A239-D8E16748B002},
	Volume = {22},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt1037}}

@article{Shankle:1998,
	Abstract = {The generalization of the finding of no postnatal neurogenesis in non-human primates to humans may be incorrect because: (1) rhesus macaques belong to a superfamily that diverged more than 25 million years ago from the superfamily including the genus Homo; (2) the pulse thymidine labeling method, which demonstrates DNA synthesis rather than mitosis per se, is less reliable than some have assumed. This study examines changes in the number of neurons in a column underneath a cortical surface area of 1 mm2, extending through all cortical layers (mm2-column) for 35 gyri (representing about 73\%of the human cerebral cortex) based on the data of J.L. Conel (1939 to 1967). We corrected these data, derived from his measures of cortical neuronal packing density, somal breadth and height, and cortical layer thickness at postnatal ages 0, 1, 3, 6, 15, 24, 48, and 72 months, for shrinkage and stereological errors. In all 35 gyri, neuron number/mm2-column: (1) initially declines (mu = 46\%decline, sigma = 8\%), 95\%of which is due to surface area expansion (mean age of nadir value = 15.8 months); (2) then increases to age 72 months by 70\%(mu = 1.7-fold increase, (mu rate = 1.1\%per month). Because of a a concomitant 1.3-fold increase in cortical surface from 15 to 72 months, total cortical neuron number increases 2.2-fold. The close agreement between neuron number/mm2-column for Conel's age 72-month data to the corresponding values reported by others for adult human and primate cortex using more modern methods suggests the finding is not an artifact. Neuronal proliferative fate-determining factors provide at least four mechanisms for increasing cortical neuron number postnatally, with or without DNA synthesis.},
	Author = {Shankle, W. R. and Landing, B. H. and Rafii, M. S. and Schiano, A. and Chen, J. M. and Hara, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0022-5193},
	Journal = {J Theor Biol},
	Keywords = {Cell Survival;Cell Differentiation;Animals;Child, Preschool;Humans;Aging;Databases, Factual;Macaca;Female;Phylogeny;Infant;Cell Count;Computational Biology;Macaca fascicularis;Child;Cell Movement;Male;Statistics;Cerebral Cortex;Neurons;Infant, Newborn;Cell Division;Brain Mapping},
	Medline = {98295040},
	Month = {3},
	Nlm_Id = {0376342},
	Number = {2},
	Organization = {Department of Cognitive Sciences, University of California, Irvine 92697-5100, USA. rshankle\@uci.edu},
	Pages = {115-40},
	Pii = {S0022519397905701},
	Pubmed = {9631564},
	Title = {Evidence for a postnatal doubling of neuron number in the developing human cerebral cortex between 15 months and 6 years},
	Uuid = {BAA15396-C26D-11DA-969D-000D9346EC2A},
	Volume = {191},
	Year = {1998},
	url = {papers/Shankle_JTheorBiol1998.pdf}}

@article{Shariful-Islam:1998,
	Abstract = {To investigate the possible role of nitric oxide (NO) in adult neurogenesis and neuron-glial migration in the rostral migratory stream (RMS), we used a double-labeled immunofluorescence technique together with confocal laser scanning microscopy, and examined the localization of nitric oxide synthase (NOS), the highly polysialylated isoform of neural cell adhesion molecule (PSA-N-CAM), and the astroglial marker in brain, S100 protein (S100), throughout the length of the subependymal layer (SEL) to olfactory bulb (OB) pathway of the adult guinea pig forebrain. Blast-like, beaded, clustered immature cellular elements stained for PSA-N-CAM and those having a typical astrocytic phenotypes positive for S100 protein were densely interlaced throughout the entire length of the SEL. Some S100 positive ependymoglial cells (tanycytes) gave off their basal projections into the closely packed PSA-N-CAM immunopositive clusters in the rostral extension of the subependymal zone (SEZre). The SEL was devoid of NOS immunoreactivity. A dense network of punctate, fenestrated and radially oriented immature cellular elements positive both for NOS and PSA-N-CAM intermingled and overlapped in the inner part of the internal granular layer (IGr), whereas in the outer part, PSA-N-CAM expression gradually diminished and the cells shifted to mature bipolar, spherical or spindle-shaped granule cells with uniform cellular contours, which were exclusively immunopositive for NOS. Radially oriented astroglial phenotypes were intertwined with PSA-N-CAM neuronal clusters in the SEL, and were closely apposed to NOS neuronal elements in the IGr. In summary, these results showed a distinct separation of neurons and glia as revealed by PSA-N-CAM and S100 protein immunostaining, and an inverse spatio- temporal correlation of expression between PSA-N-CAM (immature neuroblasts) and NOS (mature neurons) in the adult guinea pig RMS.},
	Author = {Shariful Islam, A. T. and Nakamura, K. and Seki, T. and Kuraoka, A. and Hirata, K. and Emson, P. C. and Kawabuchi, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Brain Res Dev Brain Res},
	Keywords = {Microscopy, Confocal;Nitric-Oxide Synthase/*biosynthesis;C;Female;Immunohistochemistry;Neural Cell Adhesion Molecules/*biosynthesis;Guinea Pigs;Electrophoresis, Polyacrylamide Gel;Animal;Prosencephalon/*cytology/growth &development/*metabolism;Sialic Acids/*metabolism;04 Adult neurogenesis factors;Blotting, Western;Support, Non-U.S. Gov't;Nerve Tissue Protein S 100/*biosynthesis;Male;Cell Movement/physiology},
	Number = {2},
	Organization = {Department of Anatomy, Faculty of Medicine, Kyushu University, Fukuoka 812-82, Japan. sharif\@anatl.med.kyushu-u.ac.jp},
	Pages = {191-205.},
	Title = {Expression of NOS, PSA-N-CAM and S100 protein in the granule cell migration pathway of the adult guinea pig forebrain},
	Uuid = {0C4F9ECA-ADF5-4052-9D7B-18FE9EB06B6B},
	Volume = {107},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9593889%20http://www.elsevier.com:80/cgi-bin/cas/tree/store/bresd/cas_sub/browse/browse.cgi?year=1998&volume=107&issue=2&aid=52483}}

@article{Sharma:1999,
	Abstract = {Cortical epileptic focus was produced by an intracortical injection of FeCl3 in rat cerebral cortex using standard techniques. How after its onset in the cortical focus, the epileptiform activity evolved with time in the thalamus and substantia nigra has been determined. To study the propagation of the epileptiform activity, the local EEG and multiple unit action potentials were recorded from these structures simultaneously with the cortical epileptiform EEG. The results showed that in thalamus and substantia nigra epileptiform activity appeared simultaneously with that in the cortical focus. Intensity of epileptic activity in thalamus and substantia nigra on the whole increased in parallel with that in the cortical focus. The results suggest that the thalamic and nigral epileptiform activity may reinforce the cortical epileptiform activity.},
	Author = {Sharma, V. and Singh, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0019-5189},
	Journal = {Indian J Exp Biol},
	Keywords = {Epilepsy;24 Pubmed search results 2008;Electroencephalography;Research Support, Non-U.S. Gov't;21 Epilepsy;21 Neurophysiology;Rats;Rats, Wistar;Electrophysiology;Male;Thalamus;Animals;Ferric Compounds;Substantia Nigra},
	Medline = {99422286},
	Month = {5},
	Nlm_Id = {0233411},
	Number = {5},
	Organization = {Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.},
	Pages = {461-7},
	Pubmed = {10492618},
	Title = {Electroencephalographic study of iron-induced chronic focal cortical epilepsy in rat: propagation of cortical epileptic activity to substantia nigra and thalamus},
	Uuid = {EEE98AAD-E426-40DC-8D8D-D86B07589064},
	Volume = {37},
	Year = {1999}}

@article{Sharp:1986,
	Author = {Sharp, F. R. and Gonzalez, M. F. and Ferriero, D. M. and Sagar, S. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Research Support, Non-U.S. Gov't;Nerve Regeneration;Motor Cortex;Rats;Research Support, U.S. Gov't, P.H.S.;Research Support, U.S. Gov't, Non-P.H.S.;Dihydrolipoamide Dehydrogenase;Animals;24 Pubmed search results 2008;Neurons;Frontal Lobe},
	Medline = {86231562},
	Month = {4},
	Nlm_Id = {7600130},
	Number = {2},
	Pages = {204-8},
	Pubmed = {3754939},
	Title = {Injured adult neocortical neurons sprout fibers into surviving fetal frontal cortex transplants: evidence using NADPH-diaphorase staining},
	Uuid = {9730F299-840F-4F29-A9D7-6278A9D88E1C},
	Volume = {65},
	Year = {1986}}

@article{Sharpless:1992,
	Abstract = {Human immunodeficiency virus type 1 (HIV-1), the agent of AIDS, frequently infects the central nervous system. We inoculated adult human brain cultures with chimeric viruses containing parts of the env gene of a cloned primary isolate from brain tissue, HIV-1 JRFl, inserted into the cloned DNA of a T-cell-tropic strain. A chimeric virus containing the carboxy-terminal portion of HIV-1 JRFl env did not replicate in these brain tissue cultures, while a chimera expressing an env-encoded protein containing 158 amino acids of HIV-1 JRFl gp120, including the V3 loop, replicated well in brain microglial cells, as it does in blood macrophages. Infection of brain microglial cells with such a chimera was blocked by an antibody to the V3 loop of gp 120. Thus, env determinants in the region of gp120, outside the CD4-binding site and comprising the V3 loop, are critical for efficient viral binding to and/or entry into human brain microglia.},
	Author = {Sharpless, N. E. and O'Brien, W. A. and Verdin, E. and Kufta, C. V. and Chen, I. S. and Dubois-Dalcq, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Gene Products, env;HIV-1;Humans;Base Sequence;Cells, Cultured;Brain;Antigens, CD4;Kinetics;Recombinant Fusion Proteins;11 Glia;Proviruses;Research Support, U.S. Gov't, P.H.S.;Peptide Fragments;Neuroglia;DNA, Viral;Virus Replication;Molecular Sequence Data;HIV Envelope Protein gp120},
	Medline = {92194506},
	Month = {4},
	Nlm_Id = {0113724},
	Number = {4},
	Organization = {Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892.},
	Pages = {2588-93},
	Pubmed = {1548785},
	Title = {Human immunodeficiency virus type 1 tropism for brain microglial cells is determined by a region of the env glycoprotein that also controls macrophage tropism},
	Uuid = {9DE4B33C-1A3B-4646-A5E1-A15618C69C86},
	Volume = {66},
	Year = {1992}}

@article{Shatry:2004,
	Abstract = {These studies investigate the involvement of the spleen in progenitor (PC) cell numbers and "cross-talk" with the marrow compartment following syngeneic or allogeneic bone marrow transplantation (BMT) in sham or fully splenectomized mice. Intact recipient B6 mice were lethally irradiated prior to transplant with T cell-depleted bone marrow (BM-TCD).The kinetics of PC reconstitution following i.v. transplant consistently revealed a dramatic increase in splenic colony-forming unit interleukin-3 (CFU IL-3) and CFU (high proliferative potential-(HPP) levels between days 5 and 12 post-BMT. Direct injection of TCD-BM into the recipient marrow cavity did not alter this pattern of reconstitution in the splenic compartment. In contrast to spleens from normal adult B6 mice containing 0.9\%and 0.6\%of the total combined splenic and marrow committed (CFU IL-3) and primitive (CFU-HPP) progenitors, respectively, spleens of syngeneic BMT recipients at day 12 contained a 10-fold increase (p <0.001) over the progenitor levels in normal spleens. These splenic numbers decreased to normal, homeostatic levels by day 28 post-BMT. In contrast, the level of marrow CFU IL-3 progenitors continued to increase post-transplant, reaching near homeostatic levels by day 28 post-BMT. Interestingly, early seeding of 5- (and -6)carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled or green fluorescent protein (GFP) donor bone marrow cells (BMC) to the marrow compartment was not different in sham splenectomies or recipients splenectomized 14 days earlier. However, recipient splenectomy consistently resulted in significantly higher numbers of CFU IL-3 in the bone marrow during the first 2 weeks post-transplant compared to sham controls. These elevated levels exceeded the combined progenitor numbers of the splenic and marrow compartments of intact recipients. Notably, this increase in marrow progenitor activity in splenectomized recipients was observed after syngeneic as well as allogeneic BMT. Allogeneic transplants across major, or those limited to minor, histocompatibility antigen differences exhibited this increased marrow progenitor activity. Splenectomy performed 2 h post-transplant to assure "normal" marrow seeding also resulted in higher marrow progenitor activity. Thus, this "marrow response" to splenectomy is not induced by early "shunting" of infused BM cells to the marrow compartment. These results suggest that communication between the splenic and marrow compartments following syngeneic and allogeneic BMT exists during early hematopoietic reconstitution, one effect of which is to impact the compartmental distribution of donor progenitor cells. The role of the spleen on engraftment, chimerism, and tolerance in allogeneic BMT models are now under investigation.},
	Author = {Shatry, Alwi M. and Jones, Monica and Levy, Robert B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1547-3287},
	Journal = {Stem Cells Dev},
	Keywords = {Mice, Inbred BALB C;T-Lymphocytes;Animals;Colony-Forming Units Assay;Bone Marrow Transplantation;Female;Interleukin-3;Kinetics;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Time Factors;Male;Bone Marrow;Hematopoiesis;Research Support, U.S. Gov't, P.H.S.;Transplantation, Homologous;Flow Cytometry;Mice;Luminescent Proteins;Stem Cells;Spleen;Research Support, Non-U.S. Gov't},
	Month = {2},
	Nlm_Id = {101197107},
	Number = {1},
	Organization = {Department of Microbiology, University of Miami School of Medicine, Miami, FL 33101, USA. Alwi\_shatry\@yahoo.com},
	Pages = {51-62},
	Pubmed = {15068693},
	Title = {The effect of the spleen on compartmental levels and distribution of donor progenitor cells after syngeneic and allogeneic bone marrow transplants},
	Uuid = {957BFC8A-90FC-4FB5-8220-174C7D3EF2C7},
	Volume = {13},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1089/154732804773099254}}

@article{Shaw:2004,
	Abstract = {Early theories of tumor angiogenesis suggested that preexisting vessels surrounding the tumor were the principal source of the tumor vasculature but recent evidence suggests that endothelial progenitor cells (EPC) migrate from the marrow play an important role in developing the tumor blood supply. In a mouse model, in which the vascularization of a transplantable tumor was studied after bone marrow (BM) transplantation, we show that cells that express Tie-2, Sca-1, CD31 and CD45 function as both BM EPC and primitive hematopoietic stem cells. BM cells from transgenic mice expressing green fluorescent protein (GFP) under the control of the endothelial lineage-specific Tie-2 promoter (Tie-2 /GFP) were used to reconstitute irradiated (12 Gy) wild-type mice. Five donor BM cell populations were studied: (1) whole BM; (2) Sca-1-enriched BMC; (3) GFP/Tie-2+, Sca-1+ BMC; (4) GFP/Tie-2-, Sca-1+ BMC and (5) Sca-1-depleted BMC. After 4 weeks, the mice were injected with Tg.AC tumor cells. Three weeks later, sections from the tumors were stained for CD31 and examined for Tie-2-driven GFP expression. BM-derived endothelial cells were found only in mice transplanted with bone marrow containing populations of Tie-2+, Sca-1+ cells. As few as 3500 of these cells were sufficient to radioprotect lethally irradiated mice. Thus, we conclude that a rare subset of BMC (approximately 4 x 10(-3)\%) with the putative properties of hemangioblasts have an active Tie-2 promoter. Selection of Tie-2+Sca-1+ BMC enriches for marrow-derived EPCs that participate in tumor angiogenesis and cells that can provide hematopoietic reconstitution of marrow-ablated mice.},
	Author = {Shaw, J. P. and Basch, R. and Shamamian, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {1079-9796},
	Journal = {Blood Cells Mol Dis},
	Keywords = {Research Support, Non-U.S. Gov't;Antigens, CD45;Animals;Cell Separation;Bone Marrow Transplantation;Endothelial Cells;Receptor, TIE-2;11 Glia;Green Fluorescent Proteins;Male;Antigens, CD31;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred Strains;Mice;Hematopoietic Stem Cells;Luminescent Proteins;Stem Cells;Neoplasms, Experimental;Promoter Regions (Genetics);Endothelium, Vascular},
	Nlm_Id = {9509932},
	Number = {1},
	Organization = {Department of Surgery, S.A. Localio Laboratory for Surgical Research, New York University School of Medicine, New York, NY 10016, USA.},
	Pages = {168-75},
	Pii = {S107997960300247X},
	Pubmed = {14757432},
	Title = {Hematopoietic stem cells and endothelial cell precursors express Tie-2, CD31 and CD45},
	Uuid = {E1426B26-DC83-4FE3-AE2A-288B984B8EAF},
	Volume = {32},
	Year = {2004}}

@article{Shearer:2003,
	Abstract = {Invading meningeal cells form a barrier to axon regeneration after damage to the spinal cord and other parts of the CNS, axons stopping at the interface between meningeal cells and astrocytes. Axon behavior was examined using an in vitro model of astrocyte/meningeal cell interfaces, created by plating aggregates of astrocytes and meningeal cells onto coverslips. At these interfaces growth of dorsal root ganglion axons attempting to grow from astrocytes to meningeal cells was blocked, but axons grew rapidly from meningeal cells onto astrocytes. Meningeal cells were examined for expression of axon growth inhibitory molecules, and found to express NG2, versican, and semaphorins 3A and 3C. Astrocytes express growth promoting molecules, including N-Cadherin, laminin, fibronectin, and tenascin-C. We treated cultures in various ways to attempt to promote axon growth across the inhibitory boundaries. Blockade of NG2 with antibody and blockade of neuropilin 2 but not neuropilin 1 both promoted axon growth from astrocytes to meningeal cells. Blockade of permissive molecules on astrocytes with N-Cadherin blocking peptide or anti beta-1 integrin had no effect. Manipulation of axonal signalling pathways also increased axon growth from astrocytes to meningeal cells. Increasing cAMP levels and inactivation of rho were both effective when the cultures were fixed in paraformaldehyde, demonstrating that their effect is on axons and not via effects on the glial cells. 1044-7431 Journal Article},
	Author = {Shearer, M. C. and Niclou, S. P. and Brown, D. and Asher, R. A. and Holtmaat, A. J. and Levine, J. M. and Verhaagen, J. and Fawcett, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {G abstr;11 Glia},
	Number = {4},
	Organization = {Department of Physiology and Cambridge Centre for Brain Repair, University of Cambridge, Cambridge CB2 3EG, England, UK.},
	Pages = {913-25},
	Pubmed = {14697658},
	Title = {The astrocyte/meningeal cell interface is a barrier to neurite outgrowth which can be overcome by manipulation of inhibitory molecules or axonal signalling pathways},
	Uuid = {B476C549-12B5-4D57-A519-8D2A6654BC3C},
	Volume = {24},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14697658}}

@article{Shechter:2007,
	Abstract = {Neural stem/progenitor cells are known to exist in the intact spinal cord, but the presence of newly formed neurons during adulthood has not been documented there to date. Here, we report the appearance of newly formed neurons under normal physiological conditions. These neurons are immature, express a GABAergic phenotype, and are primarily located in the dorsal part of the spinal cord. This localization appeared to be mediated by stromal-derived factor-1/CXC-chemokine receptor-4 signaling in the dorsal region. The extent of spinal cord neurogenesis was found to be greatly influenced by immune system integrity and in particular by myelin-specific T cells. These observations provide evidence for in vivo spinal cord neurogenesis under nonpathological conditions and introduce novel mechanisms regulating adult spinal cord plasticity.},
	Author = {Shechter, Ravid and Ziv, Yaniv and Schwartz, Michal},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1549-4918},
	Journal = {Stem Cells},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {9304532},
	Number = {9},
	Organization = {Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel.},
	Pages = {2277-82},
	Pii = {2006-0705},
	Pubmed = {17540856},
	Title = {New GABAergic interneurons supported by myelin-specific T cells are formed in intact adult spinal cord},
	Uuid = {8BAF58DB-200B-4031-9DA0-E4B956E3918B},
	Volume = {25},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1634/stemcells.2006-0705}}

@article{Sheen:1999,

@article{Sheen:2002,
	Abstract = {Mutations in the X-linked gene Filamin A (FLNA) lead to the human neurological disorder, periventricular heterotopia (PH). Although PH is characterized by a failure in neuronal migration into the cerebral cortex with consequent formation of nodules in the ventricular and subventricular zones, many neurons appear to migrate normally, even in males, suggesting compensatory mechanisms. Here we characterize expression patterns for FlnA and a highly homologous protein Filamin B (FlnB) within the nervous system, in order to better understand their potential roles in cortical development. FlnA mRNA was widely expressed in all cortical layers while FlnB mRNA was most highly expressed in the ventricular and subventricular zones during development. In adulthood, widespread but reduced expression of FlnA and FlnB persisted throughout the cerebral cortex. FlnA and FlnB proteins were highly expressed in both the leading processes and somata of migratory neurons during corticogenesis. Postnatally, FlnA immunoreactivity was largely localized to the cell body with FlnB in the soma and neuropil during neuronal differentiation. In adulthood, diminished expression of both proteins localized to the cell soma and nucleus. Moreover, the putative FLNB homodimerization domain strongly interacted with itself or the corresponding homologous region of FLNA by yeast two-hybrid interaction, the two proteins co-localized within neuronal precursors by immunocytochemistry and the existence of FLNA-FLNB heterodimers could be detected by co-immunoprecipitation. These results suggest that FLNA and FLNB may form both homodimers and heterodimers and that their interaction could potentially compensate for the loss of FLNA function during cortical development within PH individuals.},
	Author = {Sheen, Volney L. and Feng, Yuanyi and Graham, Donna and Takafuta, Toshiro and Shapiro, Sandor S. and Walsh, Christopher A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0964-6906},
	Journal = {Hum Mol Genet},
	Keywords = {Animals;Humans;Gene Expression Regulation, Developmental;Rats;Microfilament Proteins;Immunoenzyme Techniques;21 Epilepsy;Cell Movement;Rats, Sprague-Dawley;Mice, Inbred C57BL;RNA, Messenger;Dimerization;In Situ Hybridization;Research Support, U.S. Gov't, P.H.S.;Saccharomyces cerevisiae;Blotting, Western;21 Neurophysiology;Neurons;Cerebral Cortex;Mice;24 Pubmed search results 2008;Contractile Proteins;Two-Hybrid System Techniques;Precipitin Tests;Research Support, Non-U.S. Gov't},
	Medline = {22281257},
	Month = {11},
	Nlm_Id = {9208958},
	Number = {23},
	Organization = {Division of Neurogenetics, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA.},
	Pages = {2845-54},
	Pubmed = {12393796},
	Title = {Filamin A and Filamin B are co-expressed within neurons during periods of neuronal migration and can physically interact},
	Uuid = {0164F618-8369-477F-9786-067F73F8F18D},
	Volume = {11},
	Year = {2002}}

@article{Shen:2002,
	Abstract = {Stem cells and neuroblasts derived from mouse embryos undergo repeated asymmetric cell divisions, generating neural lineage trees similar to those of invertebrates. In Drosophila, unequal distribution of Numb protein during mitosis produces asymmetric cell divisions and consequently diverse neural cell fates. We investigated whether a mouse homologue m-numb had a similar role during mouse cortical development. Progenitor cells isolated from the embryonic mouse cortex were followed as they underwent their next cell division in vitro. Numb distribution was predominantly asymmetric during asymmetric cell divisions yielding a beta-tubulin III(-) progenitor and a beta-tubulin III(+) neuronal cell (P/N divisions) and predominantly symmetric during divisions producing two neurons (N/N divisions). Cells from the numb knockout mouse underwent significantly fewer asymmetric P/N divisions compared to wild type, indicating a causal role for Numb. When progenitor cells derived from early (E10) cortex undergo P/N divisions, both daughters express the progenitor marker Nestin, indicating their immature state, and Numb segregates into the P or N daughter with similar frequency. In contrast, when progenitor cells derived from later E13 cortex (during active neurogenesis in vivo) undergo P/N divisions they produce a Nestin(+) progenitor and a Nestin(-) neuronal daughter, and Numb segregates preferentially into the neuronal daughter. Thus during mouse cortical neurogenesis, as in Drosophila neurogenesis, asymmetric segregation of Numb could inhibit Notch activity in one daughter to induce neuronal differentiation. At terminal divisions generating two neurons, Numb was symmetrically distributed in approximately 80\%of pairs and asymmetrically in 20\%. We found a significant association between Numb distribution and morphology: most sisters of neuron pairs with symmetric Numb were similar and most with asymmetric Numb were different. Developing cortical neurons with Numb had longer processes than those without. Numb is expressed by neuroblasts and stem cells and can be asymmetrically segregated by both. These data indicate Numb has an important role in generating asymmetric cell divisions and diverse cell fates during mouse cortical development. 0950-1991 Journal Article},
	Author = {Shen, Q. and Zhong, W. and Jan, Y. N. and Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Development},
	Keywords = {Support, U.S. Gov't, P.H.S.;10 Development;Neurons/*metabolism;Mice, Knockout;Female;Embryonic Induction;Cell Division;Membrane Proteins/genetics/*metabolism;F;Cerebral Cortex/*cytology/*embryology;Multipotent Stem Cells/*physiology;Cells, Cultured;Animals;Nerve Tissue Proteins/genetics/*metabolism;Mice;Tubulin/metabolism},
	Number = {20},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA.},
	Pages = {4843-53},
	Pubmed = {12361975},
	Title = {Asymmetric Numb distribution is critical for asymmetric cell division of mouse cerebral cortical stem cells and neuroblasts},
	Uuid = {1E264FD2-BAAC-410D-A123-BC0780331AD4},
	Volume = {129},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12361975}}

@article{Shen:1998,
	Abstract = {The cytoarchitectural simplicity of the cerebral cortex makes it an attractive system to study central nervous system (CNS) histogenesis--the process whereby diverse cells are generated in the right numbers at the appropriate place and time. Recently, multipotent stem cells have been implicated in this process, as progenitor cells for diverse types of cortical neurons and glia. Continuous analysis of stem cell clone development reveals stereotyped division patterns within their lineage trees, highly reminiscent of neural lineage trees in arthropods and Caenorhabditis elegans. Given that these division patterns play a critical part in generating diverse neural types in invertebrates, we speculate that they play a similar role in the cortex. Because stereotyped lineage trees can be observed from cells growing at clonal density, cell-intrinsic factors are likely to have a key role in stem cell behavior. Cortical stem cells also respond to environmental signals to alter the types of cells they generate, providing the means for feedback regulation on the germinal zone. Evidence is accumulating that cortical stem cells, influenced by intrinsic programs and environmental signals, actually change with development-for example, by reducing the number and types of neurons they produce. Age-related changes in the stem cell population may have a critical role in orchestrating development; whether these cells truly self-renew is a point of discussion. In summary, we propose that cortical stem cells are the focus of regulatory mechanisms central to the development of the cortical cytoarchitecture.},
	Author = {Shen, Q. and Qian, X. and Capela, A. and Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Embryo;Cell Line;Stem Cells;Research Support, U.S. Gov't, P.H.S.;22 Stem cells;review, tutorial;Animals;Cerebral Cortex;Neurons;review},
	Medline = {98376147},
	Month = {8},
	Nlm_Id = {0213640},
	Number = {2},
	Organization = {Albany Medical College, New York 12208-3479, USA.},
	Pages = {162-74},
	Pii = {10.1002/(SICI)1097-4695(199808)36:2<162::AID-NEU5>3.0.CO;2-#},
	Pubmed = {9712302},
	Title = {Stem cells in the embryonic cerebral cortex: their role in histogenesis and patterning},
	Uuid = {9D439A13-55CE-4681-989D-845052DC54B3},
	Volume = {36},
	Year = {1998},
	url = {papers/Shen_JNeurobiol1998.pdf}}

@article{Shen:2006,
	Abstract = {In the developing cerebral cortex, neurons are born on a predictable schedule. Here we show in mice that the essential timing mechanism is programmed within individual progenitor cells, and its expression depends solely on cell-intrinsic and environmental factors generated within the clonal lineage. Multipotent progenitor cells undergo repeated asymmetric divisions, sequentially generating neurons in their normal in vivo order: first preplate cells, including Cajal-Retzius neurons, then deep and finally superficial cortical plate neurons. As each cortical layer arises, stem cells and neuroblasts become restricted from generating earlier-born neuron types. Growth as neurospheres or in co-culture with younger cells did not restore their plasticity. Using short-hairpin RNA (shRNA) to reduce Foxg1 expression reset the timing of mid- but not late-gestation progenitors, allowing them to remake preplate neurons and then cortical-plate neurons. Our data demonstrate that neural stem cells change neuropotency during development and have a window of plasticity when restrictions can be reversed.},
	Author = {Shen, Qin and Wang, Yue and Dimos, John T. and Fasano, Christopher A. and Phoenix, Timothy N. and Lemischka, Ihor R. and Ivanova, Natalia B. and Stifani, Stefano and Morrisey, Edward E. and Temple, Sally},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, New York 12208, USA.},
	Pages = {743-51},
	Pii = {nn1694},
	Pubmed = {16680166},
	Title = {The timing of cortical neurogenesis is encoded within lineages of individual progenitor cells},
	Uuid = {A73408F1-7BDC-4A94-A5D6-BAB27BABAE09},
	Volume = {9},
	Year = {2006},
	url = {papers/Shen_NatNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1694}}

@article{Shen:1984,
	Abstract = {The neurological reactions in Wallerian degeneration have been studied by electron microscopy in the optic nerve of adult albino rats from 7 to 120 days after unilateral enucleation. Reactive astrocytes contained abundant dense bodies, numerous microtubules and hyperplastic glial filaments. These astrocytes also assisted phagocytosis of degenerated myelin sheaths and in glial scar formation. Oligodendrocytes disconnected their cytoplasmic extensions, which were phagocytosed by microglial cells and astrocytes, by increased production of lysosomes. Microglial cells consisted of crinkled, long, rough endoplasmic reticula, several highly-active Golgi complexes, laminar inclusions and globoid lipid droplets. Microglia engulfed and lysed the disintegrated axons and myelin sheaths.},
	Author = {Shen, C. L. and Liu, K. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:40 -0400},
	Issn = {0255-6596},
	Journal = {Proc Natl Sci Counc Repub China B},
	Keywords = {Neuroglia;Wallerian Degeneration;Nerve Degeneration;Rats;Microscopy, Electron;Astrocytes;Postoperative Complications;Ophthalmologic Surgical Procedures;Not relevant;11 Glia;Optic Nerve;Animals;Oligodendroglia;Support, Non-U.S. Gov't;Phagocytosis},
	Medline = {87261528},
	Month = {10},
	Nlm_Id = {8502426},
	Number = {4},
	Pages = {324-34},
	Pubmed = {6571594},
	Title = {Neuroglia of the adult rat optic nerve in the course of wallerian degeneration},
	Uuid = {62AFA50A-D1E1-45DB-929E-E54585032A44},
	Volume = {8},
	Year = {1984}}

@article{Shen:2004,
	Abstract = {Neural stem cells are reported to lie in a vascular niche, but there is no direct evidence for a functional relationship between the stem cells and blood vessel component cells. We show that endothelial cells but not vascular smooth muscle cells release soluble factors that stimulate the self-renewal of neural stem cells, inhibit their differentiation, and enhance their neuron production. Both embryonic and adult neural stem cells respond, allowing extensive production of both projection neuron and interneuron types in vitro. Endothelial coculture stimulates neuroepithelial cell contact, activating Notch and Hes 1 to promote self-renewal. These findings identify endothelial cells as a critical component of the neural stem cell niche.},
	Author = {Shen, Qin and Goderie, Susan K. and Jin, Li and Karanth, Nithin and Sun, Yu and Abramova, Natalia and Vincent, Peter and Pumiglia, Kevin and Temple, Sally},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Cell Differentiation;Signal Transduction;Astrocytes;Animals;Cells, Cultured;Endothelial Cells;Oligodendroglia;Cell Communication;Fibroblast Growth Factor 2;Embryo;03 Adult neurogenesis progenitor source;Cell Line;Cell Lineage;Coculture;Cerebral Cortex;Neurons;Cattle;Cell Adhesion;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Muscle, Smooth, Vascular;Stem Cells;Clone Cells;Myocytes, Smooth Muscle;Endothelium, Vascular},
	Month = {5},
	Nlm_Id = {0404511},
	Number = {5675},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA.},
	Pages = {1338-40},
	Pii = {1095505},
	Pubmed = {15060285},
	Title = {Endothelial cells stimulate self-renewal and expand neurogenesis of neural stem cells},
	Uuid = {3B051C69-009A-4A6F-8430-9366D36D453E},
	Volume = {304},
	Year = {2004},
	url = {papers/Shen_Science2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1095505}}

@article{Shetty:1998,
	Abstract = {Neural stem cells proliferate in vitro and form neurospheres in the presence of epidermal growth factor (EGF), and are capable of differentiating into both neurons and glia when exposed to a substrate. We hypothesize that specific neurotrophic factors induce differentiation of stem cells from different central nervous system (CNS) regions into particular fates. We investigated differentiation of stem cells from the postnatal mouse hippocampus in culture using the following trophic factors (20 ng/mL): brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and glial-derived neurotrophic factor (GDNF). Without trophic factors, 32\%of stem cells differentiated into neurons by 4 days in vitro (DIV), decreasing to 10\%by 14 DIV. Addition of BDNF (starting at either day 0 or day 3) significantly increased neuron survival (31-43\%by 14 DIV) and differentiation. Morphologically, many well-differentiated neurons resembled hippocampal pyramidal neurons. 5'-Bromodeoxyuridine labeling demonstrated that the pyramidal-like neurons originated from stem cells which had proliferated in EGF-containing cultures. However, similar application of NT-3 and GDNF did not exert such a differentiating effect. Addition of BDNF to stem cells from the postnatal cerebellum, midbrain, and striatum did not induce these neuronal phenotypes, though similar application to cortical stem cells yielded pyramidal-like neurons. Thus, BDNF supports survival of hippocampal stem cell-derived neurons and also can induce differentiation of these cells into pyramidal-like neurons. The presence of pyramidal neurons in BDNF-treated hippocampal and cortical stem cell cultures, but not in striatal, cerebellar, and midbrain stem cell cultures, suggests that stem cells from different CNS regions differentiate into region-specific phenotypic neurons when stimulated with an appropriate neurotrophic factor.},
	Author = {Shetty, A. K. and Turner, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Neurons;Cell Differentiation;Hippocampus;Epidermal Growth Factor;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Cell Line;Cell Survival;Animals, Newborn;Research Support, U.S. Gov't, Non-P.H.S.;Brain-Derived Neurotrophic Factor;Mice;Animals;24 Pubmed search results 2008;Cells, Cultured;Mice, Inbred Strains},
	Medline = {98287718},
	Month = {6},
	Nlm_Id = {0213640},
	Number = {4},
	Organization = {Department of Surgery (Neurosurgery) and Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA. ashok.shetty\@duke.edu},
	Pages = {395-425},
	Pii = {10.1002/(SICI)1097-4695(19980615)35:4<395::AID-NEU7>3.0.CO;2-U},
	Pubmed = {9624622},
	Title = {In vitro survival and differentiation of neurons derived from epidermal growth factor-responsive postnatal hippocampal stem cells: inducing effects of brain-derived neurotrophic factor},
	Uuid = {4A58599D-CE28-442B-AF7A-F045F4F06758},
	Volume = {35},
	Year = {1998}}

@article{Shibata:1997,
	Abstract = {The glutamate transporter GLAST is localized on the cell membrane of mature astrocytes and is also expressed in the ventricular zone of developing brains. To characterize and follow the GLAST-expressing cells during development, we examined the mouse spinal cord by in situ hybridization and immunohistochemistry. At embryonic day (E) 11 and E13, cells expressing GLAST mRNA were present only in the ventricular zone, where GLAST immunoreactivity was associated with most of the cell bodies of neuroepithelial cells. In addition, GLAST immunoreactivity was detected in radial processes running through the mantle and marginal zones. From this characteristic cytology, GLAST-expressing cells at early stages were judged to be radial glia cells. At E15, cells expressing GLAST mRNA first appeared in the mantle zone, and GLAST-immunopositive punctate or reticular protrusions were formed along the radial processes. From E18 to postnatal day (P) 7, GLAST mRNA or its immunoreactivity gradually decreased from the ventricular zone and disappeared from radial processes, whereas cells with GLAST mRNA spread all over the mantle zone and GLAST-immunopositive punctate/reticular protrusions predominated in the neuropils. At P7, GLAST-expressing cells were immunopositive for glial fibrillary acidic protein, an intermediate filament specific to astrocytes. Therefore, the glutamate transporter GLAST is expressed from radial glia through astrocytes during spinal cord development. Furthermore, the distinct changes in the cell position and morphology suggest that both the migration and transformation of radial glia cells begin in the spinal cord between E13 and E15, when the active stage of neuronal migration is over.},
	Author = {Shibata, T. and Yamada, K. and Watanabe, M. and Ikenaka, K. and Wada, K. and Tanaka, K. and Inoue, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci},
	Keywords = {Spinal Cord/cytology/embryology/*metabolism;RNA, Messenger/biosynthesis;G;Neuroglia/*metabolism;Nerve Tissue Proteins/*metabolism;*Gene Expression Regulation, Developmental;ABC Transporters/*biosynthesis/genetics;Glial Fibrillary Acidic Protein/analysis;Astrocytes/metabolism;Animal;11 Glia;Mice, Inbred C57BL;Cell Movement;Support, Non-U.S. Gov't;Cell Lineage;Mice;Amino Acid Sequence;Molecular Sequence Data;Gestational Age},
	Number = {23},
	Organization = {Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan.},
	Pages = {9212-9.},
	Title = {Glutamate transporter GLAST is expressed in the radial glia-astrocyte lineage of developing mouse spinal cord},
	Uuid = {2FB65D68-F4EE-42CE-A85D-3F4F46237375},
	Volume = {17},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9364068}}

@article{Shieh:1998,
	Abstract = {The role of human immunodeficiency virus (HIV) strain variability remains a key unanswered question in HIV dementia, a condition affecting around 20\%of infected individuals. Several groups have shown that viruses within the central nervous system (CNS) of infected patients constitute an independently evolving subset of HIV strains. A potential explanation for the replication and sequestration of viruses within the CNS is the preferential use of certain chemokine receptors present in microglia. To determine the role of specific chemokine coreceptors in infection of adult microglial cells, we obtained a small panel of HIV type 1 brain isolates, as well as other HIV strains that replicate well in cultured microglial cells. These viruses and molecular clones of their envelopes were used in infections, in cell-to-cell fusion assays, and in the construction of pseudotypes. The results demonstrate the predominant use of CCR5, at least among the major coreceptors, with minor use of CCR3 and CXCR4 by some of the isolates or their envelope clones.},
	Author = {Shieh, J. T. and Albright, A. V. and Sharron, M. and Gartner, S. and Strizki, J. and Doms, R. W. and Gonz{\'a}lez-Scarano, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Tumor Cells, Cultured;Transfection;HIV-1;Receptors, CCR5;Research Support, Non-U.S. Gov't;Adult;Membrane Fusion;Virus Replication;Research Support, U.S. Gov't, P.H.S.;Cytopathogenic Effect, Viral;11 Glia;Microglia;Cells, Cultured;Receptors, CXCR4;Brain;Receptors, Chemokine;Humans},
	Medline = {98216792},
	Month = {5},
	Nlm_Id = {0113724},
	Number = {5},
	Organization = {Department of Neurology, University of Pennsylvania Medical Center, Philadelphia 19104-6146, USA.},
	Pages = {4243-9},
	Pubmed = {9557714},
	Title = {Chemokine receptor utilization by human immunodeficiency virus type 1 isolates that replicate in microglia},
	Uuid = {8914F6A6-8EBD-4ACA-B4BB-7C54DE0E8A37},
	Volume = {72},
	Year = {1998},
	url = {papers/Shieh_JVirol1998.pdf}}

@article{Shieh:2000,
	Abstract = {Microglia are the main reservoir for human immunodeficiency virus type 1 (HIV-1) in the central nervous system (CNS), and multinucleated giant cells, the result of fusion of HIV-1-infected microglia and brain macrophages, are the neuropathologic hallmark of HIV dementia. One potential explanation for the formation of syncytia is viral adaptation for these CD4(+) CNS cells. HIV-1(BORI-15), a virus adapted to growth in microglia by sequential passage in vitro, mediates high levels of fusion and replicates more efficiently in microglia and monocyte-derived-macrophages than its unpassaged parent (J. M. Strizki, A. V. Albright, H. Sheng, M. O'Connor, L. Perrin, and F. Gonzalez-Scarano, J. Virol. 70:7654-7662, 1996). Since the interaction between the viral envelope glycoprotein and CD4 and the chemokine receptor mediates fusion and plays a key role in tropism, we have analyzed the HIV-1(BORI-15) env as a fusogen and in recombinant and pseudotyped viruses. Its syncytium-forming phenotype is not the result of a switch in coreceptor use but rather of the HIV-1(BORI-15) envelope-mediated fusion of CD4(+)CCR5(+) cells with greater efficiency than that of its parental strain, either by itself or in the context of a recombinant virus. Genetic analysis indicated that the syncytium-forming phenotype was due to four discrete amino acid differences in V1/V2, with a single-amino-acid change between the parent and the adapted virus (E153G) responsible for the majority of the effect. Additionally, HIV-1(BORI-15) env-pseudotyped viruses were less sensitive to decreases in the levels of CD4 on transfected 293T cells, leading to the hypothesis that the differences in V1/V2 alter the interaction between this envelope and CD4 or CCR5, or both. In sum, the characterization of the envelope of HIV-1(BORI-15), a highly fusogenic glycoprotein with genetic determinants in V1/V2, may lead to a better understanding of the relationship between HIV replication and syncytium formation in the CNS and of the importance of this region of gp120 in the interaction with CD4 and CCR5.},
	Author = {Shieh, J. T. and Mart{\'\i}n, J. and Baltuch, G. and Malim, M. H. and Gonz{\'a}lez-Scarano, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Gene Products, env;Human;HIV-1;Cells, Cultured;Humans;Phenotype;Cell Line, Transformed;Microglia;Cell Fusion;Antigens, CD4;11 Glia;Giant Cells;Leukocytes, Mononuclear;Research Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Tumor Cells, Cultured;Recombination, Genetic;Adult;Support, U.S. Gov't, P.H.S.;Receptors, CCR5;Virus Replication;Chromosome Mapping;Research Support, Non-U.S. Gov't},
	Medline = {20091324},
	Month = {1},
	Nlm_Id = {0113724},
	Number = {2},
	Organization = {Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA.},
	Pages = {693-701},
	Pubmed = {10623731},
	Title = {Determinants of syncytium formation in microglia by human immunodeficiency virus type 1: role of the V1/V2 domains},
	Uuid = {12B98C7C-433A-11DB-A5D2-000D9346EC2A},
	Volume = {74},
	Year = {2000},
	url = {papers/Shieh_JVirol2000.pdf}}

@article{Shigematsu:1992,
	Abstract = {Kainic acid lesions of rat striatum caused an elevation of amyloid precursor protein (APP) immunoreactivity in neurons and neurites, some of which were then phagocytosed by reactive microglia/macrophages. Immunoexpression of APP was observed in neurites and neurons 1 day after the kainic injection. Four days after lesioning, immunoreactivity was still concentrated in thick and distorted neurites, but it began to appear in microglia/macrophages and in the tissue matrix. The cells were identified as microglia/macrophages by the phenotypic markers Ia (OX6), leukocyte common antigen (OX1), C3bi receptor (OX42), and macrophage marker (ED1). They were negative for the astrocytic marker glial fibrillary acidic protein (GFAP). APP immunoreactivity in these phagocytic cells was most prominent between 1 week and 1 month postlesioning. No extracellular amyloid fibrils were detectable. These results suggest that APP production is rapidly upregulated in damaged neurons and accumulates in degenerating axons. However, phagocytosis of APP by reactive microglia/macrophages in this rat model does not result in production of Alzheimer type amyloid deposits.},
	Author = {Shigematsu, K. and McGeer, P. L. and Walker, D. G. and Ishii, T. and McGeer, E. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Phagocytosis;Animals;Macrophages;Rats;Nervous System Diseases;Axons;Rats, Inbred Strains;Neurites;Not relevant;11 Glia;Kainic Acid;Antibodies;Amyloid beta-Protein Precursor;Male;Support, Non-U.S. Gov't;Neurons;Neuroglia;Perfusion;Amino Acid Sequence;Molecular Sequence Data},
	Medline = {92349469},
	Month = {3},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, Vancouver, Canada.},
	Pages = {443-53},
	Pubmed = {1640496},
	Title = {Reactive microglia/macrophages phagocytose amyloid precursor protein produced by neurons following neural damage},
	Uuid = {08CB9713-521C-4AC3-B50C-1990938B467D},
	Volume = {31},
	Year = {1992}}

@article{Shih:2006,
	Author = {Shih, Andy Y. and Fernandes, Herman B. and Choi, Fiona Y. and Kozoriz, Michael G. and Liu, Yingru and Li, Ping and Cowan, Catherine M. and Klegeris, Andis},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {comment;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {15},
	Organization = {Graduate Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, V6T 1Z3, Canada. ashih\@interchange.ubc.ca},
	Pages = {3887-8},
	Pii = {26/15/3887},
	Pubmed = {16611803},
	Title = {Policing the police: astrocytes modulate microglial activation},
	Uuid = {9B6294E5-D3CC-4BEC-BC59-F83659A08311},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0936-06.2006}}

@article{Shihabuddin:1997,
	Abstract = {The adult rat brain contains progenitor cells that can be induced to proliferate in vitro in response to FGF-2. In the present study we explored whether similar progenitor cells can be cultured from different levels (cervical, thoracic, lumbar, and sacral) of adult rat spinal cord and whether they give rise to neurons and glia as well as spinal cord-specific neurons (e.g., motoneurons). Cervical, thoracic, lumbar, and sacral areas of adult rat spinal cord (>3 months old) were microdissected and neural progenitors were isolated and cultured in serum-free medium containing FGF-2 (20 ng/ml) through multiple passages. Although all areas generated rapidly proliferating cells, the cultures were heterogeneous in nature and cell morphology varied within a given area as well as between areas. A percentage of cells from all areas of the spinal cord differentiate into cells displaying antigenic properties of neuronal, astroglial, and oligodendroglial lineages; however, the majority of cells from all regions expressed the immature proliferating progenitor marker vimentin. In established multipassage cultures, a few large, neuron-like cells expressed immunoreactivity for p75NGFr and did not express GFAP. These cells may be motoneurons. These results demonstrate that FGF-2 is mitogenic for progenitor cells from adult rat spinal cord that have the potential to give rise to glia and neurons including motoneurons.},
	Author = {Shihabuddin, L. S. and Ray, J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {Exp Neurol},
	Keywords = {Rats;Female;Animal;02 Adult neurogenesis migration;Glial Fibrillary Acidic Protein/analysis;Stem Cells/*cytology/drug effects;Spinal Cord/*cytology/growth &development;Fibroblast Growth Factor, Basic/*pharmacology;Neuroglia/*cytology/drug effects;03 Adult neurogenesis progenitor source;Rats, Inbred F344;BB abstr;Support, Non-U.S. Gov't;Organ Specificity;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Neurons/*cytology/drug effects;Cell Division/drug effects},
	Number = {2},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {577-86.},
	Title = {FGF-2 is sufficient to isolate progenitors found in the adult mammalian spinal cord},
	Uuid = {9DF363D5-B190-4B9A-B25D-73F1B3E2556C},
	Volume = {148},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9417834}}

@article{Shihabuddin:1995,
	Abstract = {The chronic survival and differentiation of the conditionally immortalized neuronal cell line, RN33B, was examined following transplantation into the adult and neonatal rat hippocampus and cerebral cortex. In clonal culture, differentiated RN33B cells express p75NTR and trkB mRNA and protein, and respond to brain-derived neurotrophic factor treatment by inducing c-fos mRNA. Transplanted cells, identified using immunohistochemistry to detect beta-galactosidase expression, were seen in most animals up to 24 weeks posttransplantation (the latest time point examined). Stably integrated cells with various morphologies consistent with their transplantation site were observed. In the cerebral cortex, many RN33B cells differentiated with morphologies similar to pyramidal neurons and stellate cells. In the hippocampal formation, many RN33B cells assumed morphologies similar to pyramidal neurons characteristic of CA1 and CA3 regions, granular cell layer neurons of the dentate gyrus, and polymorphic neurons of the hilar region. Identical morphologies were observed in both adult and neonatal hosts, although a greater percentage of beta-galactosidase immunoreactive cells had differentiated in the neonatal brains. These results suggest that RN33B cells have the developmental plasticity to respond to local microenvironmental signals and that the adult brain retains the capacity to direct the differentiation of neuronal precursor cells in a direction that is consistent with that of endogenous neurons. eng Journal Article},
	Author = {Shihabuddin, L. S. and Hertz, J. A. and Holets, V. R. and Whittemore, S. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Cell Differentiation;Rats, Inbred Lew;Rats;Neurons/*cytology/enzymology/*transplantation;Cell Line, Transformed;beta-Galactosidase/metabolism;Aging/physiology;Female;Animal;Stem Cells/*cytology/enzymology/*transplantation;17 Transplant Regeneration;Time Factors;Hippocampus/*physiology;Animals, Newborn;Support, Non-U.S. Gov't;L abstr;Support, U.S. Gov't, P.H.S.;Cerebral Cortex/*physiology},
	Number = {10},
	Organization = {Neuroscience Program, University of Miami School of Medicine, Florida 33136, USA.},
	Pages = {6666-78.},
	Title = {The adult CNS retains the potential to direct region-specific differentiation of a transplanted neuronal precursor cell line},
	Uuid = {D0081226-FB61-44C2-841C-F48FA20236A3},
	Volume = {15},
	Year = {1995}}

@article{Shihabuddin:2000,
	Abstract = {The adult rat spinal cord contains cells that can proliferate and differentiate into astrocytes and oligodendroglia in situ. Using clonal and subclonal analyses we demonstrate that, in contrast to progenitors isolated from the adult mouse spinal cord with a combination of growth factors, progenitors isolated from the adult rat spinal cord using basic fibroblast growth factor alone display stem cell properties as defined by their multipotentiality and self-renewal. Clonal cultures derived from single founder cells generate neurons, astrocytes, and oligodendrocytes, confirming the multipotent nature of the parent cell. Subcloning analysis showed that after serial passaging, recloning, and expansion, these cells retained multipotentiality, indicating that they are self-renewing. Transplantation of an in vitro-expanded clonal population of cells into the adult rat spinal cord resulted in their differentiation into glial cells only. However, after heterotopic transplantation into the hippocampus, transplanted cells that integrated in the granular cell layer differentiated into cells characteristic of this region, whereas engraftment into other hippocampal regions resulted in the differentiation of cells with astroglial and oligodendroglial phenotypes. The data indicate that clonally expanded, multipotent adult progenitor cells from a non- neurogenic region are not lineage-restricted to their developmental origin but can generate region-specific neurons in vivo when exposed to the appropriate environmental cues.},
	Author = {Shihabuddin, L. S. and Horner, P. J. and Ray, J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:56:59 -0400},
	Journal = {J Neurosci},
	Keywords = {Stem Cells/drug effects/*transplantation;Cell Differentiation;Fibroblast Growth Factor, Basic/pharmacology;Clone Cells/transplantation;Cells, Cultured;Hippocampus/cytology/surgery;Rats;Neurons/*cytology;Dentate Gyrus/*cytology/surgery;Phenotype;Animal;02 Adult neurogenesis migration;Transplantation, Heterotopic;Spinal Cord/*cytology/*transplantation;Neck;Support, Non-U.S. Gov't;Cell Lineage;B;Support, U.S. Gov't, P.H.S.;Immunohistochemistry;Graft Survival;Bromodeoxyuridine;Neuroglia/cytology},
	Number = {23},
	Organization = {The Salk Institute, Laboratory of Genetics, La Jolla, California 92037, USA.},
	Pages = {8727-35.},
	Title = {Adult spinal cord stem cells generate neurons after transplantation in the adult dentate gyrus},
	Uuid = {E19753CA-98F3-4AD6-B196-4C5FAB2E6F0A},
	Volume = {20},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11102479%20http://www.jneurosci.org/cgi/content/full/20/23/8727%20http://www.jneurosci.org/cgi/content/abstract/20/23/8727}}

@article{Shimada:1996,
	Abstract = {Various cortical dysplasias, such as agyria-lissencephalia, pachygyria, micropolygyria, neuronal heterotopia and so on, have become relatively common neuropathological findings among the children with intactable epilepsy and mental and/or physical handicap. Together with various environmental factors, gene abnormalities are recently increasing as a cause in various cortical dysplasias. However, details of the pathogenesis still remain unknown. Experimental studies using animal models indicated that inhibition of neuron production, disorders of neuron-glia and neuron-neuron contact, and plastic and unbalanced synaptogenesis subsequent to abnormal neuron production play an important role either separately or in combination in the pathogenesis of various cortical dysplasias.},
	Author = {Shimada, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0029-0831},
	Journal = {No To Hattatsu},
	Keywords = {21 Epilepsy;24 Pubmed search results 2008;21 Neurophysiology;English Abstract;Animals;Humans;Brain;review;Abnormalities},
	Medline = {97003966},
	Month = {3},
	Nlm_Id = {0215224},
	Number = {2},
	Organization = {Department of Pediatrics, Shiga University of Medical Science, Otsu.},
	Pages = {93-101},
	Pubmed = {8851277},
	Title = {[Chaos in pathogenesis of brain dysgenesis]},
	Uuid = {427C05E9-0B3C-4579-BA3F-CAAC3AA315E7},
	Volume = {28},
	Year = {1996}}

@article{Shimazaki:2001,
	Abstract = {The cytokines that signal through the common receptor subunit gp130, including ciliary neurotrophic factor (CNTF), interleukin-6, leukemia inhibitory factor (LIF) and oncostatin M, have pleiotropic functions in CNS development. Given the restricted expression domain of the CNTF receptor alpha (CNTFR) in the developing forebrain germinal zone and adult forebrain periventricular area, we have examined the putative role of CNTFR/LIFR/gp130-mediated signaling in regulating forebrain neural stem cell fate in vivo and in vitro. Analysis of LIFR-deficient mice revealed that a decreased level of LIFR expression results in a reduction in the number of adult neural stem cells. In adult LIFR heterozygote (+/-) mice, the number of neural stem cells and their progeny in the forebrain subependyma and TH-immunoreactive neurons in the olfactory bulb were significantly reduced. Intraventricular infusion of CNTF into the adult mouse forebrain, in the absence or presence of epidermal growth factor (EGF), enhanced self-renewal of neural stem cells in vivo. Analyses of EGF-responsive neural stem cells proliferating in vitro found that CNTF inhibits lineage restriction of neural stem cells to glial progenitors, which in turn results in enhanced expansion of stem cell number. These results suggest that CNTFR/LIFR/gp130-mediated signaling supports the maintenance of forebrain neural stem cells, likely by suppressing restriction to a glial progenitor cell fate.},
	Author = {Shimazaki, T. and Shingo, T. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation/drug effects;Heterozygote;Receptor, Ciliary Neurotrophic Factor/genetics/*metabolism;Neurons/cytology/*metabolism;Cells, Cultured;Olfactory Bulb/cytology/metabolism;Ciliary Neurotrophic Factor/metabolism/pharmacology;Receptors, Cytokine/deficiency/genetics;Cell Count;Animal;C abstr;Antigens, CD/metabolism;Prosencephalon/cytology/*metabolism;Injections, Intraventricular;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Tyrosine 3-Monooxygenase/biosynthesis;Cell Lineage;Mice, Knockout;Macromolecular Systems;04 Adult neurogenesis factors;Stem Cells/cytology/drug effects/*metabolism;Membrane Glycoproteins/metabolism;Mice;Signal Transduction/physiology;Neuroglia/cytology/metabolism},
	Number = {19},
	Organization = {Genes &Development Research Group, Department of Cell Biology and Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1.},
	Pages = {7642-53.},
	Title = {The ciliary neurotrophic factor/leukemia inhibitory factor/gp130 receptor complex operates in the maintenance of mammalian forebrain neural stem cells},
	Uuid = {4B11047F-8810-448B-B29C-AE8BCB1DE87A},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11567054%20http://www.jneurosci.org/cgi/content/full/21/19/7642%20http://www.jneurosci.org/cgi/content/abstract/21/19/7642}}

@article{Shin:2004,
	Abstract = {How to minimize brain inflammation is pathophysiologically important, since inflammation induced by microglial activation can exacerbate brain damage. In the present report, we show that injection of lipopolysaccharide (LPS) into the rat cortex led to increased levels of interleukin-13 (IL-13) and to IL-13 immunoreactivity, followed by the substantial loss of microglia at 3 days post-LPS. IL-13 levels in LPS-injected cortex reached a peak at 12 h post-injection, remained elevated at 24 h, and returned to basal levels at day 4. In parallel, IL-13 immunoreactivity was detected as early as 12 h post-LPS and maintained up to 24 h; it disappeared at 4 days. Surprisingly, IL-13 immunoreactivity was detected exclusively in microglia, but not in neurons or astrocytes. Following treatment with LPS in vitro, IL-13 expression was also induced in microglia in the presence of neurons, but not in the presence of astrocytes or in cultured pure microglia alone. In experiments designed to determine the involvement of IL-13 in microglia cell death, IL-13-neutralizing antibodies significantly increased survival of activated microglia at 3 days post-LPS. Consistent with these results, the expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-alpha) was sustained in activated microglia and neuronal cell death was consequently increased. Taken together, the present study is the first to demonstrate the endogenous expression of IL-13 in LPS-activated microglia in vivo, and to demonstrate that neurons may be required for IL-13 expression in microglia. Our data strongly suggest that IL-13 may control brain inflammation by inducing the death of activated microglia in vivo, resulting in an enhancement of neuronal survival.},
	Author = {Shin, Won Ho and Lee, Da-Yong Y. and Park, Keun Woo and Kim, Seung Up and Yang, Myung-Soon S. and Joe, Eun-Hye H. and Jin, Byung Kwan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Cell Survival;Tumor Necrosis Factor;Animals;Cells, Cultured;Rats;Apoptosis;Female;Cell Communication;Rats, Sprague-Dawley;Microglia;Nitric-Oxide Synthase;Not relevant;11 Glia;Lipopolysaccharides;Alpha;Antibodies;Support, Non-U.S. Gov't;Interleukin-13;Cerebral Cortex;Neurons;Gene Expression},
	Month = {4},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea.},
	Pages = {142-52},
	Pubmed = {15042582},
	Title = {Microglia expressing interleukin-13 undergo cell death and contribute to neuronal survival in vivo},
	Uuid = {8CFF8DC3-8555-4047-9CC4-313191388D26},
	Volume = {46},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10357}}

@article{Shin:2000,
	Abstract = {Reconstruction of complex neocortical and other CNS circuitry may be possible via transplantation of appropriate neural precursors, guided by cellular and molecular controls. Although cellular repopulation and complex circuitry repair may make possible new avenues of treatment for degenerative, developmental, or acquired CNS diseases, functional integration may depend critically on specificity of neuronal synaptic integration and appropriate neurotransmitter/receptor phenotype. The current study investigated neurotransmitter and receptor phenotypes of newly incorporated neurons after transplantation in regions of targeted neuronal degeneration of cortical callosal projection neurons (CPNs). Donor neuroblasts were compared to the population of normal endogenous CPNs in their expression of appropriate neurotransmitters (glutamate, aspartate, and GABA) and receptors (kainate-R, AMPA-R, NMDA-R. and GABA-R), and the time course over which this phenotype developed after transplantation. Transplanted immature neuroblasts from embryonic day 17 (E17) primary somatosensory (S1) cortex migrated to cortical layers undergoing degeneration, differentiated to a mature CPN phenotype, and received synaptic input from other neurons. In addition, 23.1 +/- 13.6\%of the donor-derived neurons extended appropriate long-distance callosal projections to the contralateral S1 cortex. The percentage of donor-derived neurons expressing appropriate neurotransmitters and receptors showed a steady increase with time, reaching numbers equivalent to adult endogenous CPNs by 4-16 weeks after transplantation. These results suggest that previously demonstrated changes in gene expression induced by synchronous apoptotic degeneration of adult CPNs create a cellular and molecular environment that is both permissive and instructive for the specific and appropriate maturation of transplanted neuroblasts. These experiments demonstrate, for the first time, that newly repopulating neurons can undergo directed differentiation with high fidelity of their neurotransmitter and receptor phenotype, toward reconstruction of complex CNS circuitry.},
	Author = {Shin, J. J. and Fricker-Gates, R. A. and Perez, F. A. and Leavitt, B. R. and Zurakowski, D. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Lasers;Cell Differentiation;Animals;Stem Cell Transplantation;Synapses;Microinjections;Receptors, Cell Surface;Phenotype;Neocortex;Female;Cell Movement;Mice, Inbred C57BL;Male;Microspheres;Research Support, U.S. Gov't, P.H.S.;Neurons;Neurotransmitters;Porphyrins;Mice;24 Pubmed search results 2008;Stem Cells;Graft Survival;Corpus Callosum;Research Support, Non-U.S. Gov't},
	Medline = {20482310},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {19},
	Organization = {Division of Neuroscience, Children's Hospital, Department of Neurology and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {7404-16},
	Pubmed = {11007899},
	Title = {Transplanted neuroblasts differentiate appropriately into projection neurons with correct neurotransmitter and receptor phenotype in neocortex undergoing targeted projection neuron degeneration},
	Uuid = {5ADF41D1-FD71-408C-B448-8671E5994261},
	Volume = {20},
	Year = {2000}}

@article{Shingo:2001,
	Abstract = {Recent studies have shown that neurogenesis is enhanced after hypoxia and that erythropoietin (EPO), an inducible cytokine, is produced in the brain as part of the intrinsic hypoxia response. Thus, we asked whether EPO might regulate neurogenesis by forebrain neural stem cells (NSCs). We found that EPO receptors are expressed in the embryonic germinal zone during neurogenesis as well as in the adult subventricular zone, which continues to generate neurons throughout adulthood. Cultured NSCs exposed to a modest hypoxia produced two- to threefold more neurons, which was associated with an elevation in EPO gene expression. The enhanced neuron production attributable to hypoxia was mimicked by EPO and blocked by coadministration of an EPO neutralizing antibody. EPO appears to act directly on NSCs, promoting the production of neuronal progenitors at the expense of multipotent progenitors. EPO infusion into the adult lateral ventricles resulted in a decrease in the numbers of NSCs in the subventricular zone, an increase in newly generated cells migrating to the olfactory bulb, and an increase in new olfactory bulb interneurons. Infusion of anti-EPO antibodies had the opposite effect: an increase in the number of NSCs in the subventricular zone and a decrease in the number of newly generated cells migrating to the bulb. These findings suggest that EPO is an autocrine-paracrine factor, capable of regulating the production of neuronal progenitor cells by forebrain NSCs.},
	Author = {Shingo, T. and Sorokan, S. T. and Shimazaki, T. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurosci},
	Keywords = {Olfactory Bulb/cytology/drug effects;Paracrine Communication/physiology;Cells, Cultured;NF-kappa B/antagonists &inhibitors/metabolism;Transcription Factors/biosynthesis;Cell Hypoxia/physiology;Interneurons/cytology/drug effects;Cell Movement/drug effects;Animal;Cell Count;Peptides/pharmacology;Cell Division/drug effects/physiology;C abstr;Injections, Intraventricular;Epidermal Growth Factor/pharmacology;Active Transport, Cell Nucleus/drug effects;Erythropoietin/antagonists &inhibitors/*metabolism/pharmacology;Support, Non-U.S. Gov't;Neurons/cytology/drug effects/*metabolism;Antibodies/administration &dosage/pharmacology;04 Adult neurogenesis factors;Stem Cells/cytology/drug effects/*metabolism;DNA-Binding Proteins/biosynthesis;Spheroids/cytology/drug effects;Mice;Lateral Ventricles/cytology/drug effects/physiology;Autocrine Communication/physiology;Prosencephalon/cytology/embryology/*metabolism},
	Number = {24},
	Organization = {Genes &Development Research Group, Department of Cell Biology and Anatomy, University of Calgary, Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1.},
	Pages = {9733-43.},
	Title = {Erythropoietin regulates the in vitro and in vivo production of neuronal progenitors by mammalian forebrain neural stem cells},
	Uuid = {260F91B6-358D-4281-8311-A7F8F1E223C1},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11739582%20http://www.jneurosci.org/cgi/content/full/21/24/9733%20http://www.jneurosci.org/cgi/content/abstract/21/24/9733}}

@article{Shingo:2003,
	Abstract = {Neurogenesis occurs in the olfactory system of the adult brain throughout life, in both invertebrates and vertebrates, but its physiological regulation is not understood. We show that the production of neuronal progenitors is stimulated in the forebrain subventricular zone of female mice during pregnancy and that this effect is mediated by the hormone prolactin. The progenitors then migrate to produce new olfactory interneurons, a process likely to be important for maternal behavior, because olfactory discrimination is critical for recognition and rearing of offspring. Neurogenesis occurs even in females that mate with sterile males. These findings imply that forebrain olfactory neurogenesis may contribute to adaptive behaviors in mating and pregnancy. 1095-9203 Journal Article},
	Author = {Shingo, T. and Gregg, C. and Enwere, E. and Fujikawa, H. and Hassam, R. and Geary, C. and Cross, J. C. and Weiss, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Science},
	Keywords = {Pregnancy;Cell Differentiation;Signal Transduction;Choroid Plexus/metabolism;Olfactory Bulb/*cytology;Animals;Cells, Cultured;Neurons/cytology/*physiology;Pseudopregnancy;Estradiol/administration &dosage/pharmacology;Female;Cell Movement;Dentate Gyrus/cytology;Progesterone/administration &dosage/pharmacology;Stem Cells/*cytology;Male;Epidermal Growth Factor/pharmacology;Prosencephalon/*cytology/*physiology;Support, Non-U.S. Gov't;C;Interneurons/cytology/*physiology;Prolactin/administration &dosage/blood/pharmacology/*physiology;04 Adult neurogenesis factors;Receptors, Prolactin/genetics/metabolism;Cell Division;Mice},
	Number = {5603},
	Organization = {Genes &Development Research Group, Department of Cell Biology and Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1.},
	Pages = {117-20},
	Pubmed = {12511652},
	Title = {Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin},
	Uuid = {F096B588-6F39-48AC-A5AF-E4FE8C37E5A3},
	Volume = {299},
	Year = {2003},
	url = {papers/Shingo_Science2003.pdf}}

@article{Shojaei:2005,
	Abstract = {The molecular basis governing functional behavior of human hematopoietic stem cells (HSCs) is largely unknown. Here, using in vitro and in vivo assays, we isolate and define progenitors versus repopulating HSCs from multiple stages of human development for global gene expression profiling. Accounting for both the hierarchical relationship between repopulating cells and their progenitors, and the enhanced HSC function unique to early stages of ontogeny, the human homologs of Hairy Enhancer of Split-1 (HES-1) and Hepatocyte Leukemia Factor (HLF) were identified as candidate regulators of HSCs. Transgenic human hematopoietic cells expressing HES-1 or HLF demonstrated enhanced in vivo reconstitution ability that correlated to increased cycling frequency and inhibition of apoptosis, respectively. Our report identifies regulatory factors involved in HSC function that elicit their effect through independent systems, suggesting that a unique orchestration of pathways fundamental to all human cells is capable of controlling stem cell behavior.},
	Author = {Shojaei, Farbod and Trowbridge, Jennifer and Gallacher, Lisa and Yuefei, Lou and Goodale, David and Karanu, Francis and Levac, Krysta and Bhatia, Mickie},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1534-5807},
	Journal = {Dev Cell},
	Keywords = {22 Stem cells;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {101120028},
	Number = {5},
	Organization = {Stem Cell Biology and Regenerative Medicine, Robarts Research Institute, London, Ontario, Canada.},
	Pages = {651-63},
	Pii = {S1534-5807(05)00088-2},
	Pubmed = {15866157},
	Title = {Hierarchical and ontogenic positions serve to define the molecular basis of human hematopoietic stem cell behavior},
	Uuid = {67E6BBB7-D2F7-4159-89E5-0CD153FE8557},
	Volume = {8},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.devcel.2005.03.004}}

@article{Shors:2001,
	Abstract = {The vertebrate brain continues to produce new neurons throughout life. In the rat hippocampus, several thousand are produced each day, many of which die within weeks. Associative learning can enhance their survival; however, until now it was unknown whether new neurons are involved in memory formation. Here we show that a substantial reduction in the number of newly generated neurons in the adult rat impairs hippocampal-dependent trace conditioning, a task in which an animal must associate stimuli that are separated in time. A similar reduction did not affect learning when the same stimuli are not separated in time, a task that is hippocampal-independent. The reduction in neurogenesis did not induce death of mature hippocampal neurons or permanently alter neurophysiological properties of the CA1 region, such as long-term potentiation. Moreover, recovery of cell production was associated with the ability to acquire trace memories. These results indicate that newly generated neurons in the adult are not only affected by the formation of a hippocampal-dependent memory, but also participate in it.},
	Author = {Shors, T. J. and Miesegaes, G. and Beylin, A. and Zhao, M. and Rydel, T. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nature},
	Keywords = {A-12},
	Number = {6826},
	Organization = {Department of Psychology and Center for Collaborative Neuroscience, Rutgers University, Piscataway, New Jersey 08854, USA.},
	Pages = {372-6.},
	Title = {Neurogenesis in the adult is involved in the formation of trace memories},
	Uuid = {A4A47235-CDEF-11D9-B244-000D9346EC2A},
	Volume = {410},
	Year = {2001},
	url = {papers/Shors_Nature2001.pdf}}

@article{Shrikant:1996,
	Abstract = {It is well established that the two major glial cells in the central nervous system (CNS), astrocytes and microglia, are key participants in mediating the neurologic dysfunction associated with HIV infection of the CNS. In this study, we investigated the ability of the major envelope glycoprotein of HIV, glycoprotein 120 (gp120), to regulate intercellular adhesion molecule-1 (ICAM-1) expression in glial cells, because ICAM-1 is important in mediating immune responsiveness in the CNS, facilitating entry of HIV-infected cells into the CNS, and promoting syncytia formation. Our results indicate that gp120 enhances ICAM-1 gene expression in primary rat astrocytes, primary human astrocytes, a human astroglioma cell line CRT, and primary rat microglia. The signal transduction events involved in gp120-mediated enhancement of ICAM-1 appear to involve activation of both protein kinase C and tyrosine kinase, because inhibitors of protein kinase C and tyrosine kinase abrogate gp120-mediated ICAM-1 expression in both astrocytes and microglia. Moreover, gp120 induces tyrosine phosphorylation of signal transducer and activator of transcription (STAT-1 alpha) as well as the Janus kinase (JAK2) in glial cells. We also demonstrate that gp120-mediated ICAM-1 expression has functional significance, as it enhances the ability of monocytic cells to bind to gp120-stimulated human astrocytes in an ICAM-1/beta 2 integrin-dependent fashion. These results provide new insights into how gp120 can influence the involvement of glial cells in the pathogenesis of AIDS dementia complex.},
	Author = {Shrikant, P. and Benos, D. J. and Tang, L. P. and Benveniste, E. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Antigens, CD18;Human;Signal Transduction;Protein Kinase C;HIV-1;DNA-Binding Proteins;Intercellular Adhesion Molecule-1;Trans-Activators;Monocytes;Rats;Astrocytes;Animals;Microglia;viral;Phosphorylation;Humans;Macrophage Activation;11 Glia;RNA, Messenger;Cell Line;Research Support, U.S. Gov't, P.H.S.;Cell Adhesion;Tumor Cells, Cultured;Astrocytoma;Neuroglia;Support, U.S. Gov't, P.H.S.;Proto-Oncogene Proteins;Protein-Tyrosine Kinase;HIV Envelope Protein gp120},
	Medline = {96144358},
	Month = {2},
	Nlm_Id = {2985117R},
	Number = {3},
	Organization = {Department of Cell Biology, University of Alabama, Birmingham 35294, USA.},
	Pages = {1307-14},
	Pubmed = {8558011},
	Title = {HIV glycoprotein 120 enhances intercellular adhesion molecule-1 gene expression in glial cells. Involvement of Janus kinase/signal transducer and activator of transcription and protein kinase C signaling pathways},
	Uuid = {B52CBE71-9253-45C9-BE67-D0565F5FA0E5},
	Volume = {156},
	Year = {1996}}

@article{Shu:2006,
	Abstract = {The mechanisms controlling neurogenesis during brain development remain relatively unknown. Through a differential protein screen with developmental versus mature neural tissues, we identified a group of developmentally enriched microtubule-associated proteins (MAPs) including doublecortin-like kinase (DCLK), a protein that shares high homology with doublecortin (DCX). DCLK, but not DCX, is highly expressed in regions of active neurogenesis in the neocortex and cerebellum. Through a dynein-dependent mechanism, DCLK regulates the formation of bipolar mitotic spindles and the proper transition from prometaphase to metaphase during mitosis. In cultured cortical neural progenitors, DCLK RNAi Lentivirus disrupts the structure of mitotic spindles and the progression of M phase, causing an increase of cell-cycle exit index and an ectopic commitment to a neuronal fate. Furthermore, both DCLK gain and loss of function in vivo specifically promote a neuronal identity in neural progenitors. These data provide evidence that DCLK controls mitotic division by regulating spindle formation and also determines the fate of neural progenitors during cortical neurogenesis.},
	Author = {Shu, Tianzhi and Tseng, Huang-Chun C. and Sapir, Tamar and Stern, Patrick and Zhou, Ying and Sanada, Kamon and Fischer, Andre and Coquelle, Fr{\'e}d{\'e}ric M. and Reiner, Orly and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Cell Differentiation;research support, n.i.h., extramural ;Animals;Cells, Cultured;Humans;Microtubule-Associated Proteins;Mitosis;Nervous System;Mitotic Spindle Apparatus;Embryonic Development;Protein-Serine-Threonine Kinases;research support, non-u.s. gov't;Prometaphase;research support, non-u.s. gov't ;Microtubules;Cerebral Cortex;Neurons;research support, n.i.h., extramural;Mice;Dynein ATPase;24 Pubmed search results 2008;Cell Division;Stem Cells},
	Month = {1},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {25-39},
	Pii = {S0896-6273(05)01007-X},
	Pubmed = {16387637},
	Title = {Doublecortin-like kinase controls neurogenesis by regulating mitotic spindles and M phase progression},
	Uuid = {AD94642C-A1E0-42DA-B940-559D38F46450},
	Volume = {49},
	Year = {2006},
	url = {papers/Shu_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.10.039}}

@article{Shuaib:1994,
	Abstract = {Hypothyroidism protects the brain from the effects of transient forebrain ischemia in gerbils. The mechanism for this protection is not fully understood. In this study we looked at the release of glutamate during ischemia in gerbils exposed to surgical hypothyroidism (n = 7), chemical hypothyroidism (n = 8), and surgical hypothyroidism thyroxine-treated (n = 3) and compared them to control euthyroid animals (n = 8). The duration of ischemia was 10 min. Glutamate release was measured with in vivo microdialysis. Microdialysis analysis began 2 h after the placement of the probes (to stabilize the baseline) and collections were obtained in 10-min samples. During ischemia, there was an increase in the release of glutamate that returned to the baseline within 20 min following the insult. In animals made hypothyroid surgically and chemically, the extent of glutamate release was significantly lower than that in the controls. The release of glutamate in the surgically hypothyroid thyroxine-treated animals was similar to that in controls. The attenuated glutamate release could be a mechanism of protection during ischemia in hypothyroid gerbils. 0014-4886 Journal Article},
	Author = {Shuaib, A. and Ijaz, S. and Hemmings, S. and Galazka, P. and Ishaqzay, R. and Liu, L. and Ravindran, J. and Miyashita, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Exp Neurol},
	Keywords = {Male;Propylthiouracil;Thyroidectomy;Brain Ischemia/*metabolism;Triiodothyronine/blood;06 Adult neurogenesis injury induced;Microdialysis;Glutamates/*metabolism;Gerbillinae;D pdf;Animals;Support, Non-U.S. Gov't;Thyroxine/blood/pharmacology;Hypothyroidism/chemically induced/etiology/*metabolism;Glutamic Acid},
	Number = {2},
	Organization = {Department of Medicine (Neurology), Saskatchewan Stroke Research Centre, Saskatoon, Canada.},
	Pages = {260-5},
	Pubmed = {7915676},
	Title = {Decreased glutamate release during hypothyroidism may contribute to protection in cerebral ischemia},
	Uuid = {444C4195-79C0-4CB7-B6B8-639C7EAF917E},
	Volume = {128},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7915676}}

@article{Shuaib:1994a,
	Abstract = {The mechanisms by which brain cells die after brief episodes of cerebral ischemia are not fully understood. In certain brain regions this damage may not be apparent for days. Hypothyroidism is known to decrease cerebral metabolism. We postulated that this slowing in cerebral metabolism may be neuroprotective after transient cerebral ischemia. To test this hypothesis, a total of 10 gerbils had thyroidectomies performed 2 weeks prior to ischemia. Six gerbils served as euthyroid controls. All animals were exposed to 5 min of transient ischemia and sacrificed 7 days after the insult. Silver degeneration staining was used for histological evaluation. Hippocampal damage [subiculum (P <0.001), CA1 (P = 0. <.001), CA3 (P <0.05), and CA4 (P <0.001)] was significantly less in the hypothyroid animals. There was also significantly less damage in the cerebral cortex (P <0.05) and thalamus (P <0.05) in the hypothyroid animals. The exact mechanism of this protection is not fully understood but could be secondary to a decrease in the metabolic activity, or a reduced generation of free radicals (as is seen with protection from ischemia in kidney and liver under hypothyroid conditions). Further studies are required in order to gain a better understanding of the protective effects of hypothyroidism on cerebral ischemia. 0014-4886 Journal Article},
	Author = {Shuaib, A. and Ijaz, S. and Mazagri, R. and Kalra, J. and Hemmings, S. and Senthilsvlvan, A. and Crosby, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Exp Neurol},
	Keywords = {control;Insulin/blood;Animals;Triiodothyronine/blood;Ischemic Attack, Transient/*pathology/physiopathology/*prevention &;Gerbillinae;Brain/*pathology;Pyramidal Cells/pathology;Hippocampus/pathology;D pdf;gamma-Glutamyltransferase/blood/metabolism;Hypothyroidism/blood/pathology/*physiopathology;Reference Values;Ketone Bodies/blood;Male;Time Factors;Liver/enzymology;Support, Non-U.S. Gov't;Blood Glucose/metabolism;Thyroidectomy;06 Adult neurogenesis injury induced;Thyroxine/blood;Cerebral Cortex/pathology;Thalamus/pathology},
	Number = {1},
	Organization = {Department of Medicine (Neurology), College of Medicine, University of Saskatchewan, Canada.},
	Pages = {119-25},
	Pubmed = {7911086},
	Title = {Hypothyroidism protects the brain during transient forebrain ischemia in gerbils},
	Uuid = {6BF481B6-8019-4071-BFEF-3B9BE40B494B},
	Volume = {127},
	Year = {1994},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7911086}}

@article{Si:2003,
	Abstract = {Synapse-specific facilitation requires rapamycin-dependent local protein synthesis at the activated synapse. In Aplysia, rapamycin-dependent local protein synthesis serves two functions: (1) it provides a component of the mark at the activated synapse and thereby confers synapse specificity and (2) it stabilizes the synaptic growth associated with long-term facilitation. Here we report that a neuron-specific isoform of cytoplasmic polyadenylation element binding protein (CPEB) regulates this synaptic protein synthesis in an activity-dependent manner. Aplysia CPEB protein is upregulated locally at activated synapses, and it is needed not for the initiation but for the stable maintenance of long-term facilitation. We suggest that Aplysia CPEB is one of the stabilizing components of the synaptic mark. 0092-8674 Journal Article},
	Author = {Si, K. and Giustetto, M. and Etkin, A. and Hsu, R. and Janisiewicz, A. M. and Miniaci, M. C. and Kim, J. H. and Zhu, H. and Kandel, E. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Cell},
	Keywords = {10 Development;F pdf},
	Number = {7},
	Organization = {Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, 722 West 168th Street, New York, NY 10032, USA. ks560\@columbia.edu},
	Pages = {893-904},
	Pubmed = {14697206},
	Title = {A neuronal isoform of CPEB regulates local protein synthesis and stabilizes synapse-specific long-term facilitation in aplysia},
	Uuid = {364054C6-97A5-4275-8596-AC37647E9495},
	Volume = {115},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14697206}}

@article{Si:2003a,
	Abstract = {Prion proteins have the unusual capacity to fold into two functionally distinct conformations, one of which is self-perpetuating. When yeast prion proteins switch state, they produce heritable phenotypes. We report prion-like properties in a neuronal member of the CPEB family (cytoplasmic polyadenylation element binding protein), which regulates mRNA translation. Compared to other CPEB family members, the neuronal protein has an N-terminal extension that shares characteristics of yeast prion-determinants: a high glutamine content and predicted conformational flexibility. When fused to a reporter protein in yeast, this region confers upon it the epigenetic changes in state that characterize yeast prions. Full-length CPEB undergoes similar changes, but surprisingly it is the dominant, self-perpetuating prion-like form that has the greatest capacity to stimulate translation of CPEB-regulated mRNA. We hypothesize that conversion of CPEB to a prion-like state in stimulated synapses helps to maintain long-term synaptic changes associated with memory storage. 0092-8674 Journal Article},
	Author = {Si, K. and Lindquist, S. and Kandel, E. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Cell},
	Keywords = {10 Development;F pdf},
	Number = {7},
	Organization = {Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, 722 West 168th Street, New York, NY 10032, USA. ks560\@columbia.edu},
	Pages = {879-91},
	Pubmed = {14697205},
	Title = {A neuronal isoform of the aplysia CPEB has prion-like properties},
	Uuid = {74754E0D-2FC2-40E2-85C8-532AE54B1588},
	Volume = {115},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14697205}}

@article{Si:2002,
	Abstract = {Significant numbers of patients with acquired immunodeficiency syndrome (AIDS) develop CNS infection primarily in macrophages and microglial cells. Therefore, the regulation of human immunodeficiency virus type 1 (HIV-1) infection and activation of the brain mononuclear phagocytes subsequent to infection are important areas of investigation. In the current report, we studied the role of granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage-CSF (M-CSF) in the expression of antiviral beta-chemokines and HIV-1 p24 in cultures of primary human fetal microglia. We found that stimulation with GM-CSF or M-CSF induced macrophage inflammatory proteins (MIP-1alpha and MIP-1beta) and augmented RANTES expression, after HIV-1 infection of microglia. This was not due to the effect of GM-CSF on viral expression because GM-CSF was neither necessary nor stimulatory for viral infection, nor did GM-CSF enhance the expression of env-pseudotyped reporter viruses. Blocking GM-CSF-induced microglial proliferation by nocodazole had no effect on beta-chemokine or p24 expression. The functional significance of the GM-CSF-induced beta-chemokines was suggested by the finding that, in the presence of GM-CSF, exogenous beta-chemokines lost their anti-HIV-1 effects. We further show that although HIV-1-infected microglia produced M-CSF, they failed to produce GM-CSF. In vivo, GM-CSF expression was localized to activated astrocytes and some inflammatory cells in HIV-1 encephalitis, suggesting paracrine activation of microglia through GM-CSF. Our results demonstrate a complex interplay between CSFs, chemokines, and virus in microglial cells and may have bearing on the interpretation of data derived in vivo and in vitro.},
	Author = {Si, Qiusheng and Cosenza, Melissa and Zhao, Meng-Liang L. and Goldstein, Harris and Lee, Sunhee C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Fetus;Dose-Response Relationship, Drug;Pregnancy;HIV-1;Humans;Cells, Cultured;Adjuvants, Immunologic;Brain;Microglia;Female;Macrophage Activation;Recombinant Fusion Proteins;Granulocyte-Macrophage Colony-Stimulating Factor;11 Glia;Chemokines, CC;Research Support, U.S. Gov't, P.H.S.;RANTES;Heat;Macrophage Colony-Stimulating Factor;Macrophage Inflammatory Protein-1;HIV Core Protein p24;Virus Replication;Cell Division;AIDS Dementia Complex},
	Medline = {22106033},
	Month = {8},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.},
	Pages = {174-83},
	Pubmed = {12112368},
	Title = {GM-CSF and M-CSF modulate beta-chemokine and HIV-1 expression in microglia},
	Uuid = {4DDF3FDD-1CC9-4D3A-9141-DCFFB649C288},
	Volume = {39},
	Year = {2002},
	url = {papers/Si_Glia2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10095}}

@article{Sieburth:2005,
	Abstract = {Chemical synapses are complex structures that mediate rapid intercellular signalling in the nervous system. Proteomic studies suggest that several hundred proteins will be found at synaptic specializations. Here we describe a systematic screen to identify genes required for the function or development of Caenorhabditis elegans neuromuscular junctions. A total of 185 genes were identified in an RNA interference screen for decreased acetylcholine secretion; 132 of these genes had not previously been implicated in synaptic transmission. Functional profiles for these genes were determined by comparing secretion defects observed after RNA interference under a variety of conditions. Hierarchical clustering identified groups of functionally related genes, including those involved in the synaptic vesicle cycle, neuropeptide signalling and responsiveness to phorbol esters. Twenty-four genes encoded proteins that were localized to presynaptic specializations. Loss-of-function mutations in 12 genes caused defects in presynaptic structure.},
	Author = {Sieburth, Derek and Ch'ng, QueeLim and Dybbs, Michael and Tavazoie, Masoud and Kennedy, Scott and Wang, Duo and Dupuy, Denis and Rual, Jean-Fran\c{c}ois F. and Hill, David E. and Vidal, Marc and Ruvkun, Gary and Kaplan, Joshua M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Fluorescence;research support, n.i.h., extramural ;Animals;Phorbol Esters;Synapses;Microfilament Proteins;Caenorhabditis elegans;research support, u.s. gov't, p.h.s. ;Synaptic Transmission;Protein Transport;Mutation;Synaptic Vesicles;Cluster Analysis;RNA Interference;Gene Expression Profiling;Neuropeptides;research support, non-u.s. gov't ;Neuromuscular Junction;21 Neurophysiology;Cytoskeleton;Aldicarb;Caenorhabditis elegans Proteins;Motor Neurons;24 Pubmed search results 2008;Drug Resistance;Membrane Proteins;Nerve Tissue Proteins;R-SNARE Proteins},
	Month = {7},
	Nlm_Id = {0410462},
	Number = {7050},
	Organization = {Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.},
	Pages = {510-7},
	Pii = {nature03809},
	Pubmed = {16049479},
	Title = {Systematic analysis of genes required for synapse structure and function},
	Uuid = {B9FEB382-FB29-4ACB-9B53-D0B469B377C7},
	Volume = {436},
	Year = {2005},
	url = {papers/Sieburth_Nature2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03809}}

@article{Sieczkarski:2003,
	Abstract = {Enveloped viruses often enter cells via endocytosis; however, specific endocytic trafficking pathway(s) for many viruses have not been determined. Here we demonstrate, through the use of dominant-negative Rab5 and Rab7, that influenza virus (Influenza A/WSN/33 (H1N1) and A/X-31 (H3N2)) requires both early and late endosomes for entry and subsequent infection in HeLa cells. Time-course experiments, monitoring viral ribonucleoprotein colocalization with endosomal markers, indicated that influenza exhibits a conventional endocytic uptake pattern--reaching early endosomes after approximately 10 min, and late endosomes after 40 min. Detection with conformation-specific hemagglutinin antibodies indicated that hemagglutinin did not reach a fusion-competent form until the virus had trafficked beyond early endosomes. We also examined two other enveloped viruses that are also pH-dependent for entry--Semliki Forest virus and vesicular stomatitis virus. In contrast to influenza virus, infection with both Semliki Forest virus and vesicular stomatitis virus was inhibited only by the expression of dominant negative Rab5 and not by dominant negative Rab7, indicating an independence of late endosome function for infection by these viruses. As a whole, these data provide a definitive characterization of influenza virus endocytic trafficking and show differential requirements for endocytic trafficking between pH-dependent enveloped viruses.},
	Author = {Sieczkarski, Sara B. and Whittaker, Gary R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {1398-9219},
	Journal = {Traffic},
	Keywords = {Rhabdoviridae Infections;Semliki forest virus;Research Support, Non-U.S. Gov't;Hela Cells;Research Support, U.S. Gov't, P.H.S.;rab GTP-Binding Proteins;Endosomes;Orthomyxoviridae Infections;rab5 GTP-Binding Proteins;Vesicular stomatitis-Indiana virus;Endocytosis;Orthomyxoviridae;Humans;15 Retrovirus mechanism;24 Pubmed search results 2008;Alphavirus Infections},
	Medline = {22601024},
	Month = {5},
	Nlm_Id = {100939340},
	Number = {5},
	Organization = {Department of Microbiology & Immunology, Cornell University, Ithaca, NY, USA.},
	Pages = {333-43},
	Pii = {090},
	Pubmed = {12713661},
	Title = {Differential requirements of Rab5 and Rab7 for endocytosis of influenza and other enveloped viruses},
	Uuid = {8BE28386-C1C1-4517-A039-1D0643763B31},
	Volume = {4},
	Year = {2003}}

@article{Sierra:2007,
	Abstract = {Microglia play a critical role in neurodegenerative diseases and in the brain aging process. Yet, little is known about the functional dynamics of microglia during aging. Thus, using young and aging transgenic mice expressing enhanced-green fluorescent protein (EGFP) under the promoter of the c-fms gene for macrophage-colony stimulating factor receptor, we evaluated invivo-induced inflammatory responses of EGFP-expressing microglia sorted by flow cytometry. Aging microglia were characterized by the presence of lipofuscin granules, decreased processes complexity, altered granularity, and increased mRNA expression of both pro-inflammatory (TNFalpha, IL-1beta, IL-6) and anti-inflammatory (IL-10, TGFbeta1) cytokines. Following lipopolysaccharide (LPS) challenge (1 mg/kg, 3 h), aging microglia exhibit increased basal expression of TNFalpha, IL-1beta, IL-6, and IL-10. Yet, the fold-over-basal LPS response remained constant across age, implying that the inflammatory machinery in aging microglia is functional and adjusted to the basal state. Gender differences were not overall observed across the treatments (age, LPS). The low but sustained production of pro-inflammatory cytokines by aging microglia may have a profound impact in the brain aging process. (c) 2007 Wiley-Liss, Inc.},
	Author = {Sierra, and Gottfried-Blackmore, and McEwen, and Bulloch,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8806785},
	Organization = {Laboratory of Neuroendocrinology, Rockefeller University, New York, New York.},
	Pubmed = {17203473},
	Title = {Microglia derived from aging mice exhibit an altered inflammatory profile},
	Uuid = {52724559-8B15-4022-BBB5-89AC382C61F4},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20468}}

@article{Sievers:2003,
	Abstract = {Wallerian degeneration, the disintegration of the distal part of an injured axon, is an important event in many neurodegenerative diseases. We studied Wallerian degeneration in dorsal root ganglion (DRG) explants in culture by separating neurites from their cell bodies with a scalpel. The severed neurites showed Annexin V positive staining, that spreads distally with a rate comparable to that of slow axonal transport in intact neurons in vivo. Moreover, the injured neurites showed loss of mitochondrial membrane potential. These features resemble those seen when cells undergo apoptosis. These data contribute to a new understanding of the mechanism of axonal degeneration, have implications for the response of stromal cells in central nervous system (CNS) and raise the prospect of new pharmacological treatments for those neurodegenerative pathologies where the protection of the cell body alone does not alleviate the disease.},
	Author = {Sievers, Caroline and Platt, Nick and Perry, V. Hugh and Coleman, Michael P. and Conforti, Laura},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0168-0102},
	Journal = {Neurosci Res},
	Keywords = {Cell Culture Techniques;Animals;Osmolar Concentration;Ganglia, Spinal;Enzyme Inhibitors;Comparative Study;Cycloheximide;Apoptosis;Mitochondria;Neurites;Protein Synthesis Inhibitors;Staurosporine;Wallerian Degeneration;Annexin A5;Axotomy;Membrane Potentials;Mice;24 Pubmed search results 2008;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {22653026},
	Month = {6},
	Nlm_Id = {8500749},
	Number = {2},
	Organization = {Center for Molecular Medicine (ZMMK) and Institute for Genetics, University of Cologne, Germany.},
	Pages = {161-9},
	Pii = {S0168010203000397},
	Pubmed = {12767479},
	Title = {Neurites undergoing Wallerian degeneration show an apoptotic-like process with Annexin V positive staining and loss of mitochondrial membrane potential},
	Uuid = {3DFC333D-D198-4149-9824-BBBF6FD1F2D2},
	Volume = {46},
	Year = {2003}}

@article{Sijen:2001,
	Abstract = {We have investigated the role of trigger RNA amplification during RNA interference (RNAi) in Caenorhabditis elegans. Analysis of small interfering RNAs (siRNAs) produced during RNAi in C. elegans revealed a substantial fraction that cannot derive directly from input dsRNA. Instead, a population of siRNAs (termed secondary siRNAs) appeared to derive from the action of a cellular RNA-directed RNA polymerase (RdRP) on mRNAs that are being targeted by the RNAi mechanism. The distribution of secondary siRNAs exhibited a distinct polarity (5'-->3'on the antisense strand), suggesting a cyclic amplification process in which RdRP is primed by existing siRNAs. This amplification mechanism substantially augments the potency of RNAi-based surveillance, while ensuring that the RNAi machinery will focus on expressed mRNAs. 0092-8674 Journal Article},
	Author = {Sijen, T. and Fleenor, J. and Simmer, F. and Thijssen, K. L. and Parrish, S. and Timmons, L. and Plasterk, R. H. and Fire, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Cell},
	Keywords = {Ribonuclease III;Animals;Transcription Factors/genetics/*physiology;Endoribonucleases/physiology;Animals, Genetically Modified;23 Technique;RNA, Small Interfering;RNA, Double-Stranded/*physiology;Support, Non-U.S. Gov't;Recombinant Fusion Proteins/physiology;RNA-Directed DNA Polymerase/*physiology;Sequence Deletion;RNA, Untranslated/*physiology;T abstr;RNA, Helminth/*physiology;Support, U.S. Gov't, P.H.S.;*Models, Genetic;Helminth Proteins/genetics/*physiology;Caenorhabditis elegans/embryology/*genetics;Gene Silencing/*physiology;Transgenes},
	Number = {4},
	Organization = {Hubrecht Laboratory, Center for Biomedical Genetics, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.},
	Pages = {465-76},
	Pubmed = {11719187},
	Title = {On the role of RNA amplification in dsRNA-triggered gene silencing},
	Uuid = {ADDC3CDA-DBBA-4A89-BA04-4685BCEA6F0A},
	Volume = {107},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11719187}}

@article{Silva:2002,
	Abstract = {Progenitor cells in the early developing nervous system can divide symmetrically, giving rise to two daughter cells that divide again, or asymmetrically, giving rise to one cell that differentiates and one that divides again. It has been suggested that the orientation of the cell cleavage plane during mitosis determines the type of division. A marker of early cell differentiation, the RA4 antigen, was used to identify regions of the developing chick retina with and without differentiating cells, and the orientation of the cleavage plane was characterized for mitotic figures in each region. No difference was found in the frequency of any orientation between the regions with or without differentiating cells. Furthermore, in the region of the retina with differentiating cells, the RA4 antigen was present in mitotic figures with every possible orientation. Thus, the orientation of the cleavage plane appears to be unrelated to whether or not a division produces a cell that differentiates. It has also been suggested that the intracellular protein Numb mediates neurogenesis via asymmetric localization during cell division. Numb localization was compared with expression of markers of early cell differentiation, the RA4 antigen and Delta. Differentiating and nondifferentiating cells were found both with and without Numb expression. Cells with a cleavage plane parallel to the retinal surface were polarized, such that Numb and/or the RA4 antigen, when present, were only in the daughter cell farthest from the ventricle. These findings indicate a need to reconsider current hypotheses regarding the key features underlying symmetric and asymmetric divisions in the developing nervous system. 22184307 1529-2401 Journal Article},
	Author = {Silva, A. O. and Ercole, C. E. and McLoon, S. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:58 -0400},
	Journal = {J Neurosci},
	Keywords = {Juvenile Hormones/*biosynthesis;Cell Division/physiology;10 Development;Mitosis/physiology;Cell Differentiation/*physiology;Retina/*cytology/*embryology/metabolism;Immunohistochemistry;F both;Antigens, Differentiation/biosynthesis;Cell Polarity/physiology;Chick Embryo;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Specific Pathogen-Free Organisms},
	Number = {17},
	Organization = {Department of Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455, USA.},
	Pages = {7518-25},
	Title = {Plane of cell cleavage and numb distribution during cell division relative to cell differentiation in the developing retina},
	Uuid = {1BA9346B-06BD-4A6F-9BBC-D35814A77BD2},
	Volume = {22},
	Year = {2002},
	url = {papers/Silva_JNeurosci2002.pdf}}

@article{Silver:2004,
	Abstract = {1471-003x Journal Article},
	Author = {Silver, J. and Miller, J. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {G, L pdf;11 Glia},
	Number = {2},
	Organization = {Department of Neurosciences, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio 44106, USA. jxs10\@cwru.edu},
	Pages = {146-56},
	Title = {Regeneration beyond the glial scar},
	Uuid = {C45FF0A6-E32E-43C6-879F-1F4074B3F210},
	Volume = {5},
	Year = {2004},
	url = {papers/Silver_NatRevNeurosci2004.pdf}}

@article{Sim:2006,
	Abstract = {Central neurocytoma (CN) is a rare periventricular tumor, whose derivation, lineage potential, and molecular regulation have been mostly unexplored. We noted that CN cells exhibited an antigenic profile typical of neuronal progenitor cells in vivo, yet in vitro generated neurospheres, divided in response to bFGF (basic fibroblast growth factor), activated the neuroepithelial enhancer of the nestin gene, and gave rise to both neuron-like cells and astrocytes. When CN gene expression was compared with that of both normal adult VZ (ventricular zone) and E/nestin:GFP (green fluorescent protein)-sorted native neuronal progenitors, significant overlap was noted. Marker analysis suggested that the gene expression pattern of CN was that of a proneuronal population; glial markers were conspicuously absent, suggesting that the emergence of astroglia from CN occurred only with passage. The expression pattern of CN was distinguished from that of native progenitor cells by a cohort of differentially expressed genes potentially involved in both the oncogenesis and phenotypic restriction of neurocytoma. These included both IGF2 and several components of its signaling pathway, whose sharp overexpression implicated dysregulated autocrine IGF2 signaling in CN oncogenesis. Both receptors and effectors of canonical wnt signaling, as well as GDF8 (growth differentiation factor 8), PDGF-D, and neuregulin, were differentially overexpressed by CN, suggesting that CN is characterized by the concurrent overactivation of these pathways, which may serve to drive neurocytoma expansion while restricting tumor progenitor phenotype. This strategy of comparing the gene expression of tumor cells to that of the purified native progenitors from which they derive may provide a focused approach to identifying transcripts important to stem and progenitor cell oncogenesis.},
	Author = {Sim, Fraser J. and Keyoung, H. Michael and Goldman, James E. and Kim, Dong Kyu and Jung, Hee-Won W. and Roy, Neeta S. and Goldman, Steven A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Tumor Cells, Cultured;Adult;Neurocytoma;Stem Cells;comparative study;research support, n.i.h., extramural;Humans;Male;24 Pubmed search results 2008;Neurons},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {48},
	Organization = {Department of Neurology, University of Rochester Medical Center, Rochester, New York 14642, USA.},
	Pages = {12544-55},
	Pii = {26/48/12544},
	Pubmed = {17135416},
	Title = {Neurocytoma is a tumor of adult neuronal progenitor cells},
	Uuid = {271E2B6E-0735-4776-9D0C-C8983709D86C},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0829-06.2006}}

@article{Simard:2004,
	Abstract = {Pluripotent stem cells can differentiate into a variety of cell types during tissue development and regeneration. However, it is still unclear whether bone marrow-derived stem cells can migrate across the blood-brain barrier in many regions of the central nervous system (CNS) and if these cells can readily differentiate into functional parenchymal microglia. We thus studied the differentiation fate of bone marrow stem cells upon immigration into the CNS. To this end, we systemically transplanted stem cells that express green fluorescent protein (GFP) into lethally irradiated mice and found that these cells immigrated into the brain parenchyma of many regions of the CNS. Nearly all of the infiltrating cells had a highly ramified morphology and colocalized with the microglial marker iba1. Moreover, these cells expressed high levels of the protein CD11c, indicating that microglia of bone marrow origin may be potent antigen presenting cells. These data suggest that microglia of blood origin could activate cells of the adaptive immune system and cause harm to the CNS. Therefore, these results may have great clinical relevance for both immune-derived neuronal disorders and cancer patients undergoing allogeneic hematopoietic stem-cell transplantation.},
	Author = {Simard, Alain R. and Rivest, Serge},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;Central Nervous System;Bone Marrow Cells;Multipotent Stem Cells;Mice, Inbred C57BL;Stem Cells;Bone Marrow Transplantation;11 Glia;Microglia;Antigen-Presenting Cells;Animals;Cell Movement;Mice;Stem Cell Transplantation;Cell Lineage},
	Month = {6},
	Nlm_Id = {8804484},
	Number = {9},
	Organization = {Laboratory of Molecular Endocrinology, CHUL Research Center and Department of Anatomy and Physiology, Laval University, Qu{\'e}bec, Canada.},
	Pages = {998-1000},
	Pii = {04-1517fje},
	Pubmed = {15084516},
	Title = {Bone marrow stem cells have the ability to populate the entire central nervous system into fully differentiated parenchymal microglia},
	Uuid = {8481DE10-D3B7-11D9-A0E9-000D9346EC2A},
	Volume = {18},
	Year = {2004},
	url = {papers/Simard_FASEBJ2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.04-1517fje}}

@article{Simard:2006,
	Abstract = {Microglia are the immune cells of the brain. Here we show a massive infiltration of highly ramified and elongated microglia within the core of amyloid plaques in transgenic mouse models of Alzheimer's disease (AD). Many of these cells originate from the bone marrow, and the beta-amyloid-40 and -42 isoforms are able to trigger this chemoattraction. These newly recruited cells also exhibit a specific immune reaction to both exogenous and endogenous beta-amyloid in the brain. Creation of a new AD transgenic mouse that expresses the thymidine kinase protein under the control of the CD11b promoter allowed us to show that blood-derived microglia and not their resident counterparts have the ability to eliminate amyloid deposits by a cell-specific phagocytic mechanism. These bone marrow-derived microglia are thus very efficient in restricting amyloid deposits. Therapeutic strategies aiming to improve their recruitment could potentially lead to a new powerful tool for the elimination of toxic senile plaques.},
	Author = {Simard, Alain R. and Soulet, Denis and Gowing, Genevieve and Julien, Jean-Pierre P. and Rivest, Serge},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Alzheimer Disease;research support, non-u.s. gov't ;Peptide Fragments;Disease Models, Animal;24 Pubmed search results 2008;Green Fluorescent Proteins;Amyloid beta-Protein Precursor;Immunohistochemistry;Lysosomal-Associated Membrane Protein 2;Calcium-Binding Proteins;Animals;Cells, Cultured;Age Factors;Phagocytosis;Whole-Body Irradiation;Injections, Intraventricular;comparative study ;Amyloid beta-Protein;Imaging, Three-Dimensional;Gene Expression;Presenilin-1;Interleukin-1;Bone Marrow Transplantation;Mice, Inbred C57BL;RNA, Messenger;In Situ Hybridization;Toll-Like Receptor 2;Senile Plaques;11 Glia;comparative study;Tumor Necrosis Factor-alpha;Antigens, CD46;Indoles;Time Factors;Membrane Proteins;Bone Marrow Cells;Microglia;research support, non-u.s. gov't;Microscopy, Confocal;Mice;Humans;Mice, Transgenic},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Laboratory of Molecular Endocrinology, CHUL Research Center and Department of Anatomy and Physiology, Laval University, 2705 Laurier boul., Qu{\'e}bec G1V 4G2, Canada.},
	Pages = {489-502},
	Pii = {S0896-6273(06)00075-4},
	Pubmed = {16476660},
	Title = {Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer's disease},
	Uuid = {E2375546-D015-4E0A-A2ED-F431F11D6B00},
	Volume = {49},
	Year = {2006},
	url = {papers/Simard_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.01.022}}

@article{Simpson:2000,
	Abstract = {Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) characterised by perivascular inflammatory cell infiltrates and plaques of demyelination. Chemokines have been shown to play an important role in the activation and directional migration of cells to sites of CNS inflammation. The action of chemokines requires the expression of their complementary chemokine receptors by their target cells. We have examined the expression of the beta-chemokine receptors CCR2, CCR3 and CCR5 in post-mortem MS CNS tissue using single- and double-labelling immunocytochemistry techniques. Low levels of CCR2, CCR3 and CCR5 were expressed by microglial cells throughout control CNS tissue. In chronic active MS lesions CCR2, CCR3 and CCR5 were associated with foamy macrophages and activated microglia. CCR2 and CCR5 were also present on large numbers of infiltrating lymphocytes. A smaller number of CCR3-positive lymphocytes were present, but we also noted CCR3 and CCR5 on astrocytes in five of the 14 cases of MS investigated, particularly associated with processes around vessels and at the glia limitans. Ligands for CCR2 and CCR3 include MCP-1 and MCP-3 which were co-localised around vessels with the infiltrating leukocytes, but were also present in unaffected areas of cortex. The elevated expression of CCR2, CCR3 and CCR5 in the CNS in MS suggests these beta-chemokine receptors and their ligands play a role in the pathogenesis of MS.},
	Author = {Simpson, J. and Rezaie, P. and Newcombe, J. and Cuzner, M. L. and Male, D. and Woodroofe, M. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Ligands;Research Support, Non-U.S. Gov't;Multiple Sclerosis;Astrocytes;Humans;Macrophages;Middle Aged;Disease Progression;Microglia;Female;11 Glia;Chemotaxis, Leukocyte;Chronic Disease;Male;Aged;Monocyte Chemoattractant Proteins;Antibody Specificity;Matched-Pair Analysis;Receptors, Chemokine;Aged, 80 and over;Adult;Receptors, CCR5;CD4-Positive T-Lymphocytes;Central Nervous System;Monocyte Chemoattractant Protein-1;Immunohistochemistry;Inflammation;Recurrence;Cytokines},
	Medline = {20361893},
	Month = {8},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Biomedical Research Centre and Division of Biomedical Sciences, Sheffield Hallam University, City Campus, Pond Street, South Yorkshire, S1 1WB, Sheffield, UK.},
	Pages = {192-200},
	Pii = {S0165572800002745},
	Pubmed = {10900353},
	Title = {Expression of the beta-chemokine receptors CCR2, CCR3 and CCR5 in multiple sclerosis central nervous system tissue},
	Uuid = {1A944190-B640-4087-8951-1EF4E40A2CB9},
	Volume = {108},
	Year = {2000}}

@article{Sinclair:1999,
	Abstract = {The yield of surviving dopamine cells in nigral grafts is typically low. It is unclear whether the dopamine neurons that do survive are postmitotic at the time of implantation, or are precursor cells that differentiate into dopamine neurons following transplantation in the host brain. We have therefore compared the survival of dopamine neurons in grafts that have been labelled with BrdU at different times prior to or following implantation in order to identify those cells that undergo final cell division at each stage of the procedure. Seven groups of rats were prepared with unilateral nigrostriatal lesions. Three groups received nigral grafts derived from E14 embryos labelled with BrdU in utero on either E12, E13 or E14 days of embryonic age (the E14 injection made 2 h prior to preparation of the graft cell suspension). Three further groups received nigral grafts from untreated E14 embryos, and then dividing cells within the grafts were labelled by injection of BrdU into the host lateral ventricle, 2 h, 1 day or 2 days after implantation (equivalent to E14, E15 and E16 days of embryonic age). The control group received standard (unlabelled) E14 grafts. Five weeks after the transplantation surgery, the host brains were processed using double immunohistochemical techniques to detect tyrosine hydroxylase (TH)-positive neurons which had incorporated BrdU. In the grafts labelled with BrdU prior to implantation, there was an increasing proportion of double-labelled cells (out of the total TH-positive cells surviving in the grafts) with birth dates on E12, E13 and E14 (1\%, 12\%and 10\%per day, respectively). By contrast, grafts labelled following implantation, although containing many dividing neurons, had very few of these BrdU-labelled cells expressing a dopaminergic phenotype; < 1\%surviving TH-positive cells were double-labelled from the 2 h post-transplant injection, and < 0.1\%from each subsequent injection. This suggests not only that the great majority of TH-positive neurons in nigral grafts were already differentiated at the time of implantation, but also that transplantation of E14 ventral mesencephalic tissue either kills dopaminergic precursors or (more likely in our opinion) prevents their differentiation into a dopaminergic phenotype. Precursor cells that would differentiate into dopaminergic neurons beyond E14 if left in situ in the intact ventral mesencephalon do not readily differentiate into mature dopamine neurons following transplantation. If we are to enhance yields of functional dopamine-rich transplants, then we must identify strategies both to protect predifferentiated dopamine neurons in the grafts and to promote differentiation of a dopaminergic phenotype in precursor cells that continue to divide within the grafts following transplantation into an adult host environment.},
	Author = {Sinclair, S. R. and Fawcett, J. W. and Dunnett, S. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Survival;Cell Differentiation;Dopamine;Animals;Brain Tissue Transplantation;Rats;Female;Substantia Nigra;Fetal Tissue Transplantation;Embryo;Rats, Inbred F344;Neurons;Tyrosine 3-Monooxygenase;Cell Division;24 Pubmed search results 2008;Bromodeoxyuridine;Immunohistochemistry;Graft Survival;Oxidopamine;Research Support, Non-U.S. Gov't},
	Medline = {20062501},
	Month = {12},
	Nlm_Id = {8918110},
	Number = {12},
	Organization = {Center for Brain Repair, Cambridge, UK.},
	Pages = {4341-8},
	Pii = {ejn867},
	Pubmed = {10594660},
	Title = {Dopamine cells in nigral grafts differentiate prior to implantation},
	Uuid = {B35168F2-42EC-4DD6-8B29-3EB1773D37C2},
	Volume = {11},
	Year = {1999}}

@article{Sinclair:1997,
	Abstract = {Retroviral vectors have had limited success in mediating gene transfer to hematopoietic stem cells, particularly in primates, due in part to low or absent expression of the amphotropic receptor (RAM-1). We have been interested in determining whether retrovirus pseudotyped with vesicular stomatitis virus G protein (VSV-G) would allow more efficient gene delivery to hematopoietic stem cells as the VSV-G receptors appear to be ubiquitously present phospholipids. However, we previously found that completion of retroviral vector reverse transcription does not occur in CD34+ CD38- hematopoietic stem cells that were exposed to VSV-G pseudotyped retrovirus. To determine at which stage the block to infection of CD34+ CD38- cells occurs, we confirmed by FACS analysis that VSV-G pseudotyped viral particles could bind to CD34+ CD38- cells. Virus binding to CD34+ cells was saturable at 4 degrees C but nonsaturable at 37 degrees C, up to a multiplicity of infection of 1080. This suggests that surface levels of phospholipid receptors available for viral binding are limiting on CD34+ cells. Cytokine stimulation increased virus binding to CD34+ cells. However, no increase in the level of surface phosphatidylserine (PS), a strong candidate for the VSV-G receptor, was seen as detected by the PS-specific reagent, annexin V. This suggests that another molecule is serving as the VSV-G receptor on CD34+ cells. Here, we show that once virus binding to cytokine-stimulated CD34+ CD38- cells has occurred, virus fusion proceeds efficiently as determined by octadecyl rhodamine (R18) fusion assays. Taken together with our previous observation that reverse transcription does not occur in CD34+ CD38- cells, we suggest that there are intracellular mechanisms leading to blockage of complete reverse transcription of the retrovirus in CD34+ CD38- cells. This has important implications for retrovirus-mediated gene transfer to quiescent stem cells.},
	Author = {Sinclair, A. M. and Agrawal, Y. P. and Elbar, E. and Agrawal, R. and Ho, A. D. and Levine, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Flow Cytometry;Virus Diseases;Research Support, Non-U.S. Gov't;ADP-ribosyl Cyclase;Hematopoietic Stem Cells;Antigens, Differentiation;Research Support, U.S. Gov't, P.H.S.;Annexin A5;Retroviridae;Antigens, CD;Antigens, CD34;Vesicular stomatitis-Indiana virus;Gene Therapy;NAD+ Nucleosidase;Humans;15 Retrovirus mechanism;Genetic Vectors},
	Medline = {98010141},
	Month = {9},
	Nlm_Id = {9421525},
	Number = {9},
	Organization = {Department of Haematology, University of Cambridge, MRC Center, UK.},
	Pages = {918-27},
	Pubmed = {9349428},
	Title = {Interaction of vesicular stomatitis virus-G pseudotyped retrovirus with CD34+ and CD34+ CD38- hematopoietic progenitor cells},
	Uuid = {15A95DC0-C7C0-4ED1-A32C-6F4641519503},
	Volume = {4},
	Year = {1997},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3300479}}

@article{Singh:2008,
	Abstract = {The mechanisms that regulate the pruning of mammalian axons are just now being elucidated. Here, we describe a mechanism by which, during developmental sympathetic axon competition, winning axons secrete brain-derived neurotrophic factor (BDNF) in an activity-dependent fashion, which binds to the p75 neurotrophin receptor (p75NTR) on losing axons to cause their degeneration and, ultimately, axon pruning. Specifically, we found that pruning of rat and mouse sympathetic axons that project to the eye requires both activity-dependent BDNF and p75NTR. p75NTR and BDNF are also essential for activity-dependent axon pruning in culture, where they mediate pruning by directly causing axon degeneration. p75NTR, which is enriched in losing axons, causes axonal degeneration by suppressing TrkA-mediated signaling that is essential for axonal maintenance. These data provide a mechanism that explains how active axons can eliminate less-active, competing axons during developmental pruning by directly promoting p75NTR-mediated axonal degeneration.},
	Author = {Singh, Karun K. and Park, Katya J. and Hong, Elizabeth J. and Kramer, Bianca M. and Greenberg, Michael E. and Kaplan, David R. and Miller, Freda D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Cholera Toxin;Dose-Response Relationship, Drug;Nerve Degeneration;Animals;Cells, Cultured;Gene Expression Regulation, Developmental;Rats;Enzyme Inhibitors;Nerve Growth Factor;Brain-Derived Neurotrophic Factor;Visual Pathways;Axons;Rats, Sprague-Dawley;Mice, Transgenic;Mice, Inbred C57BL;Potassium Chloride;research support, non-u.s. gov't;Green Fluorescent Proteins;Stilbamidines;Animals, Newborn;Axotomy;Neurons;Superior Cervical Ganglion;Receptor, Nerve Growth Factor;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Drug Interactions},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Organization = {Developmental and Stem Cell Biology, Hospital for Sick Children, 555 University Avenue, Toronto, Canada M5G 1X8.},
	Pages = {649-58},
	Pii = {nn.2114},
	Pubmed = {18382462},
	Title = {Developmental axon pruning mediated by BDNF-p75NTR-dependent axon degeneration},
	Uuid = {F293B6FC-FAFF-4823-B0EF-F8D81450C953},
	Volume = {11},
	Year = {2008},
	url = {papers/Singh_NatNeurosci2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn.2114}}

@article{Singh:1996,
	Abstract = {Vectors based on murine C-type retroviruses are commonly used in biology. The efficiency of viral infection is normally increased by a facilitator, for example polybrene, DEAE-dextran or a liposome. The receptor for ecotropic viruses is a transporter for basic amino acids; we therefore explored the use of a highly basic protein, histone type IIA, as a facilitator. We show in several cell types that histone is as efficient as the other agents tested, and in some cases more so. This readily available reagent is thus likely to be useful in the wide range of studies that employ retroviral vectors. 0305-1048 Journal Article},
	Author = {Singh, D. and Rigby, P. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nucleic Acids Res},
	Keywords = {*Gene Transfer Techniques;*Genetic Vectors;*Receptors, Virus;Biological Transport/drug effects;Amino Acids, Diamino/metabolism;*Membrane Glycoproteins;Membrane Proteins/drug effects;Carrier Proteins/drug effects;J;Gammaretrovirus/*genetics/pathogenicity;15 Retrovirus mechanism;Cells, Cultured;Animals;Support, Non-U.S. Gov't;Mice;Histones/*pharmacology},
	Number = {15},
	Organization = {Division of Eukaryotic Molecular Genetics, MRC National Institute for Medical Research, London, UK.},
	Pages = {3113-4},
	Pubmed = {8760902},
	Title = {The use of histone as a facilitator to improve the efficiency of retroviral gene transfer},
	Uuid = {6103ABFA-20B2-4ADB-B4CF-60DA80F3D161},
	Volume = {24},
	Year = {1996},
	url = {papers/Singh_NucleicAcidsRes1996.pdf}}

@article{Siolas:2005,
	Abstract = {Designing potent silencing triggers is key to the successful application of RNA interference (RNAi) in mammals. Recent studies suggest that the assembly of RNAi effector complexes is coupled to Dicer cleavage. Here we examine whether transfection of optimized Dicer substrates results in an improved RNAi response. Dicer cleavage of chemically synthesized short hairpin RNAs (shRNAs) with 29-base-pair stems and 2-nucleotide 3' overhangs produced predictable homogeneous small RNAs comprising the 22 bases at the 3' end of the stem. Consequently, direct comparisons of synthetic small interfering RNAs and shRNAs that yield the same small RNA became possible. We found synthetic 29-mer shRNAs to be more potent inducers of RNAi than small interfering RNAs. Maximal inhibition of target genes was achieved at lower concentrations and silencing at 24 h was often greater. These studies provide the basis for an improved approach to triggering experimental silencing via the RNAi pathway.},
	Author = {Siolas, Despina and Lerner, Cara and Burchard, Julja and Ge, Wei and Linsley, Peter S. and Paddison, Patrick J. and Hannon, Gregory J. and Cleary, Michele A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {23 RNAi;23 Technique},
	Month = {2},
	Nlm_Id = {9604648},
	Number = {2},
	Organization = {[1] Program in Genetics, Stony Brook University, Stony Brook, New York 11794, USA. [2] Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA.},
	Pages = {227-31},
	Pii = {nbt1052},
	Pubmed = {15619616},
	Title = {Synthetic shRNAs as potent RNAi triggers},
	Uuid = {2956939B-1F08-404B-846C-5F52A9EF2C64},
	Volume = {23},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt1052}}

@article{Sioud:2006,
	Author = {Sioud, Mouldy},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {news;Models, Biological;RNA, Messenger;RNA, Small Interfering;23 Technique;Inflammation;Cell Line;Signal Transduction;RNA Interference;comment;RNA, Viral;Animals;Humans;24 Pubmed search results 2008;Immune System;Cytoplasm},
	Month = {5},
	Nlm_Id = {9604648},
	Number = {5},
	Pages = {521-2},
	Pii = {nbt0506-521},
	Pubmed = {16680132},
	Title = {RNA interference below the immune radar},
	Uuid = {81F9AFB3-C704-4FB5-9697-968D619E09D8},
	Volume = {24},
	Year = {2006},
	url = {papers/Sioud_NatBiotechnol2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt0506-521}}

@article{Sivasankaran:2004,
	Abstract = {Successful axon regeneration in the mammalian central nervous system (CNS) is at least partially compromised due to the inhibitors associated with myelin and glial scar. However, the intracellular signaling mechanisms underlying these inhibitory activities are largely unknown. Here we provide biochemical and functional evidence that conventional isoforms of protein kinase C (PKC) are key components in the signaling pathways that mediate the inhibitory activities of myelin components and chondroitin sulfate proteoglycans (CSPGs), the major class of inhibitors in the glial scar. Both the myelin inhibitors and CSPGs induce PKC activation. Blocking PKC activity pharmacologically and genetically attenuates the ability of CNS myelin and CSPGs to activate Rho and inhibit neurite outgrowth. Intrathecal infusion of a PKC inhibitor, Go6976, into the site of dorsal hemisection promotes regeneration of dorsal column axons across and beyond the lesion site in adult rats. Thus, perturbing PKC activity could represent a therapeutic approach to stimulating axon regeneration after brain and spinal cord injuries. 1097-6256 Journal Article},
	Author = {Sivasankaran, R. and Pei, J. and Wang, K. C. and Zhang, Y. P. and Shields, C. B. and Xu, X. M. and He, Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nat Neurosci},
	Keywords = {G, L pdf;17 Transplant Regeneration;11 Glia},
	Number = {3},
	Organization = {Division of Neuroscience, 320 Longwood Avenue, Children's Hospital, Boston, Massachusetts 02115, USA.},
	Pages = {261-8},
	Title = {PKC mediates inhibitory effects of myelin and chondroitin sulfate proteoglycans on axonal regeneration},
	Uuid = {67533739-7F6A-4536-A114-79F3D1C4B090},
	Volume = {7},
	Year = {2004},
	url = {papers/Sivasankaran_NatNeurosci2004.pdf}}

@article{Skeen:1986,
	Abstract = {Quantitative morphometric methods were used in mice to study the effect postnatal olfactory deprivation has on tufted cell size and number. The two layers containing tufted cells, the external plexiform and glomerular layers, are considerably smaller in the deprived olfactory bulbs than in the contralateral, experienced olfactory bulbs. While most of this volumetric deficit may be due to an attenuation of synaptogenesis and dendritic elaboration, an additional factor contributing to the reduced volume of these bulbar layers is a substantial loss of tufted cells. Since tufted cells are generated prenatally, their reduced number in the postnatally deprived olfactory bulb is probably a consequence of retarded migration or cell death. eng Journal Article},
	Author = {Skeen, L. C. and Due, B. R. and Douglas, F. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Journal = {Neurosci Lett},
	Keywords = {Olfactory Bulb/*cytology/physiology;*Cell Count;Animals, Newborn/*physiology;Cell Survival;Animal;Mice, Inbred ICR;Support, U.S. Gov't, P.H.S.;I abstr;Neurons/physiology;Mice;Cell Movement;13 Olfactory bulb anatomy;Sensory Deprivation/*physiology},
	Number = {1},
	Pages = {5-10.},
	Title = {Neonatal sensory deprivation reduces tufted cell number in mouse olfactory bulbs},
	Uuid = {A5CAD779-A840-4370-93EC-75D76E904547},
	Volume = {63},
	Year = {1986}}

@article{Skinner:2001,
	Abstract = {Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disease caused by the expression of mutant ataxin-1 that contains an expanded polyglutamine tract. Overexpression of mutant ataxin-1 in Purkinje cells of transgenic mice results in a progressive ataxia and Purkinje cell pathology that are very similar to those seen in SCA1 patients. Two prominent aspects of pathology in the SCA1 mice are the presence of cytoplasmic vacuoles and dendritic atrophy. We found that the vacuoles in Purkinje cells seem to originate as large invaginations of the outer cell membrane. The cytoplasmic vacuoles contained proteins from the somatodendritic membrane, including mGluR1, GluRDelta1/Delta2, GluR2/3, and protein kinase C (PKC) gamma. Further examination of PKCgamma revealed that its sequestration into cytoplasmic vacuoles was accompanied by concurrent loss of PKCgamma localization at the Purkinje cell dendritic membrane and decreased detection of PKCgamma by Western blot analysis. In addition, the vacuoles were immunoreactive for components of the ubiquitin/proteasome degradative pathway. These findings present a link between vacuole formation and loss of dendrites in Purkinje cells of SCA1 mice and indicate that altered somatodendritic membrane trafficking and loss of proteins including PKCgamma, are a part of the neuronal dysfunction in SCA1 transgenic mice.},
	Author = {Skinner, P. J. and Vierra-Green, C. A. and Clark, H. B. and Zoghbi, H. Y. and Orr, H. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Protein Kinase C;Purkinje Cells;Tissue Distribution;Animals;Ubiquitins;Cytoplasm;Mice, Transgenic;Cysteine Endopeptidases;Not relevant;11 Glia;Multienzyme Complexes;Dendrites;Support, U.S. Gov't, P.H.S.;Nuclear Proteins;Mice;Receptors, Metabotropic Glutamate;Isoenzymes;Intracellular Membranes;Nerve Tissue Proteins;Membrane Proteins},
	Medline = {21433386},
	Month = {9},
	Nlm_Id = {0370502},
	Number = {3},
	Organization = {Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota 55455, USA.},
	Pages = {905-13},
	Pubmed = {11549583},
	Title = {Altered trafficking of membrane proteins in purkinje cells of SCA1 transgenic mice},
	Uuid = {1168F850-1F71-4671-AE9F-E6B32973047B},
	Volume = {159},
	Year = {2001},
	url = {papers/Skinner_AmJPathol2001.pdf}}

@article{Skupski:1999,
	Abstract = {During 1998 the primary focus of the Genome Sequence DataBase (GSDB; http://www.ncgr.org/gsdb ) located at the National Center for Genome Resources (NCGR) has been to improve data quality, improve data collections, and provide new methods and tools to access and analyze data. Data quality has been improved by extensive curation of certain data fields necessary for maintaining data collections and for using certain tools. Data quality has also been increased by improvements to the suite of programs that import data from the International Nucleotide Sequence Database Collaboration (IC). The Sequence Tag Alignment and Consensus Knowledgebase (STACK), a database of human expressed gene sequences developed by the South African National Bioinformatics Institute (SANBI), became available within the last year, allowing public access to this valuable resource of expressed sequences. Data access was improved by the addition of the Sequence Viewer, a platform-independent graphical viewer for GSDB sequence data. This tool has also been integrated with other searching and data retrieval tools. A BLAST homology search service was also made available, allowing researchers to search all of the data, including the unique data, that are available from GSDB. These improvements are designed to make GSDB more accessible to users, extend the rich searching capability already present in GSDB, and to facilitate the transition to an integrated system containing many different types of biological data.},
	Author = {Skupski, M. P. and Booker, M. and Farmer, A. and Harpold, M. and Huang, W. and Inman, J. and Kiphart, D. and Kodira, C. and Root, S. and Schilkey, F. and Schwertfeger, J. and Siepel, A. and Stamper, D. and Thayer, N. and Thompson, R. and Wortman, J. and Zhuang, J. J. and Harger, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0305-1048},
	Journal = {Nucleic Acids Res},
	Keywords = {Computational Biology;Base Sequence;Databases, Factual;Human;Sequence Alignment;Genome, Human;Gene Expression;Support, U.S. Gov't, Non-P.H.S.;Genome;Animals;Information Storage and Retrieval;Consensus Sequence;23 Technique},
	Medline = {99063647},
	Month = {1},
	Nlm_Id = {0411011},
	Number = {1},
	Organization = {National Center for Genome Resources, 1800 Old Pecos Trail, Suite A, Santa Fe, NM 87505, USA.},
	Pages = {35-8},
	Pii = {gkc104},
	Pubmed = {9847136},
	Title = {The Genome Sequence DataBase: towards an integrated functional genomics resource},
	Uuid = {3E6094C4-D474-42AA-94E3-9340C922F20B},
	Volume = {27},
	Year = {1999}}

@article{Slobodov:2001,
	Abstract = {Injury and demyelinating diseases result in the disruption of the myelin sheath that surrounds axons in the nervous system. The removal of degenerating myelin by macrophages and microglia is central to repair mechanisms that follow. The efficiency of myelin removal depends on magnitudes and rates of myelin phagocytosis and degradation. In the present study we test whether environmental conditions within a tissue can control patterns of myelin removal. We document that macrophages that are recruited to the same tissue but by distinct inflammatory stimuli differ in their ability to phagocytose and degrade myelin. These observations may apply to the nervous system where different pathological conditions that involve distinct inflammatory stimuli may induce different functional states in microglia and macrophages.},
	Author = {Slobodov, U. and Reichert, F. and Mirski, R. and Rotshenker, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Macrophages, Peritoneal;Phagocytosis;Animals;Myelin Sheath;Cells, Cultured;Myelin Basic Proteins;Mice, Inbred C57BL;Not relevant;11 Glia;Microscopy, Fluorescence;Cell Adhesion;Support, Non-U.S. Gov't;Macrophage-1 Antigen;Support, U.S. Gov't, Non-P.H.S.;Mice;Enzyme-Linked Immunosorbent Assay;Immunohistochemistry;Inflammation},
	Medline = {21099727},
	Month = {2},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.},
	Pages = {401-9},
	Pii = {S0014488600975599},
	Pubmed = {11161629},
	Title = {Distinct inflammatory stimuli induce different patterns of myelin phagocytosis and degradation in recruited macrophages},
	Uuid = {7F35B0EE-801B-4275-8642-7729784263A0},
	Volume = {167},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/exnr.2000.7559}}

@article{Smith:1998,
	Abstract = {The anterior portion of the neonatal telencephalic subventricular zone (SVZa) contains proliferating cells that generate an immense number of neurons destined to become the granule and periglomerular cells of the olfactory bulb. In contrast to other immature neurons in the central nervous system, cells arising in the SVZa maintain the ability to divide as they traverse the rostral migratory stream to their final destinations despite expressing an antigenic marker of differentiated neurons (Menezes et al. [1995] Molec. Cell. Neurosci. 6:496-508). Because of their considerable proliferative capacities and unusual mitotic behavior, we decided to determine the cell cycle length of proliferating cells within the SVZa and within the migratory pathway used by SVZa-derived cells. Following the methodology of Nowakowski et al. [1989](J. Neurocytol. 18:311-318), postnatal day 2 rat pups were exposed to 5'-bromo-2'deoxyuridine (BrdU) for increasing periods of time before perfusion. By plotting the percentage of nuclei undergoing DNA synthesis in the SVZa at each time versus the BrdU labeling interval, we determined that approximately 15\%of the SVZa population is actively dividing and that these cells have a cycle length of approximately 14 hr, significantly less than the 18.6 hr determined to be the cycle length of dividing cells in more posterior, glia- generating regions of the subventricular zone (Thomaidou et al. [1997] J. Neurosci. 17:1075-1085). The cycle length of cells dividing in the mid portion of the rostral migratory stream, however, is considerably longer: 17.3 hr. This may reflect the need for these cells to coordinate the processes of migration and division. Our studies also suggest that there may be regional differences in the types of descendants produced by the proliferating cells. Retroviral lineage tracing studies showed that those cells that divide within the rostral migratory stream, like proliferating cells within the SVZa, make cells destined for the olfactory bulb. Unlike the progenitors that divide within the SVZa and generate more granule cells than periglomerular cells, the proliferating cells within the migratory pathway generate more periglomerular cells than granule cells. Collectively the proliferating cells of the SVZa and migratory pathway produce a large number of olfactory bulb interneurons. Our work suggests that this may be achieved in part by the relatively rapid divisions of progenitor cells within the SVZa and in part by the ongoing division of migrating cells en route to the olfactory bulb.},
	Author = {Smith, C. M. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Dev Dyn},
	Keywords = {Pregnancy;Olfactory Bulb/*cytology/growth &development/metabolism;BB;beta-Galactosidase/genetics/metabolism;Rats;Cell Cycle;Female;Animal;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Interneurons/cytology/metabolism;Cell Movement;Male;Genetic Vectors;Stem Cells/cytology/metabolism;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;Bromodeoxyuridine/metabolism;DNA/biosynthesis;Retroviridae/genetics;Animals, Newborn;Lac Operon;Support, U.S. Gov't, P.H.S.},
	Number = {2},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {220-7.},
	Title = {Cell cycle length of olfactory bulb neuronal progenitors in the rostral migratory stream},
	Uuid = {8E5676D7-421D-4881-B445-E8D7C3BC22EE},
	Volume = {213},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9786422}}

@article{Smith:1999,
	Abstract = {Neuronal heterotopia is a malformation of cortical development that is closely associated with epilepsy in humans. Despite emerging interest in the structure and function of the heterotopic cortex, little is known about the membrane properties and synaptic connections of these displaced neurons. We used whole-cell patch-clamp and extracellular field potential recordings from heterotopic neurons in slices from young adult rats with experimentally induced cortical dysgenesis to determine if local synaptic connections were present in nodular heterotopia. Complex synaptic responses were observed after electrical stimulation of adjacent white matter. The results suggest that neurons in nodular heterotopic gray matter can form local excitatory and inhibitory synaptic connections and may participate in epileptiform events. Copyright Copyright 1999 S. Karger AG, Basel},
	Author = {Smith, B. N. and Dudek, F. E. and Roper, S. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Electrophysiology;Animals;Synapses;Rats;Periaqueductal Gray;Synaptic Transmission;Brain;Female;21 Epilepsy;Rats, Sprague-Dawley;21 Dysplasia-heterotopia;Brain Diseases;Bicuculline;Research Support, U.S. Gov't, P.H.S.;21 Neurophysiology;Neurons;24 Pubmed search results 2008;Choristoma},
	Medline = {20044660},
	Month = {11},
	Nlm_Id = {7809375},
	Number = {3-5},
	Organization = {Department of Anatomy and Neurobiology, Colorado State University College of Veterinary Medicine and Biomedical Sciences, Fort Collins, CO, USA.},
	Pages = {365-73},
	Pii = {dne21365},
	Pubmed = {10575260},
	Title = {Synaptic responses of neurons in heterotopic gray matter in an animal model of cortical dysgenesis},
	Uuid = {51428AA5-1DD1-442E-A086-CDFEF8737718},
	Volume = {21},
	Year = {1999},
	url = {papers/Smith_DevNeurosci1999.pdf}}

@article{Smith:2006,
	Abstract = {Neurogenesis in the adult mammalian hippocampus resulting in long-term persistence of new neurons with features of capacity for functional activation is recognized. Many stimuli are capable of increasing the rate of neurogenesis, including seizure activity. Whether these insults result in an increased number of new functionally active neurons over and above the baseline rate of neurogenesis is not known. The rapid electrical amygdala kindling (REAK) model of seizures isolates the effects of seizures alone in the absence of neuronal death and the resulting seizures induce expression of c-Fos in the vast majority of dentate gyrus (DG) granule cells. C57BL/6 mice were exposed to REAK then injected with bromodeoxyuridine (BrDU) to label dividing cells, then re-exposed to REAK after a delay period to allow detection of functional activation in new neurons by measurement c-Fos expression in response to seizures. Adult subgranular zone cells migrated into the DG granule cell layer (GCL), assumed a neuronal phenotype and demonstrated seizure-dependent responsiveness. Larger absolute numbers of new neurons demonstrating seizure-dependent activation were found in the GCL of previously kindled mice. Seizures are capable of increasing the number of new neurons with the capacity for functional activation laid down in the postseizure period and incorporated into seizure-activated circuitry.},
	Author = {Smith, Paul D. and McLean, Karen J. and Murphy, Michael A. and Turnley, Ann M. and Cook, Mark J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {8918110},
	Number = {11},
	Organization = {Centre for Clinical Neurosciences and Neurological Research, St Vincent's Hospital, Melbourne, VIC, Australia 3065.},
	Pages = {3195-203},
	Pii = {EJN5205},
	Pubmed = {17156380},
	Title = {Functional dentate gyrus neurogenesis in a rapid kindling seizure model},
	Uuid = {FDF65D35-1F27-4DE1-B4FB-B98CDC4CFA4E},
	Volume = {24},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2006.05205.x}}

@article{Smith:2004,
	Abstract = {Viruses replicate within living cells and use the cellular machinery for the synthesis of their genome and other components. To gain access, they have evolved a variety of elegant mechanisms to deliver their genes and accessory proteins into the host cell. Many animal viruses take advantage of endocytic pathways and rely on the cell to guide them through a complex entry and uncoating program. In the dialogue between the cell and the intruder, the cell provides critical cues that allow the virus to undergo molecular transformations that lead to successful internalization, intra-cellular transport, and uncoating.},
	Author = {Smith, Alicia E. and Helenius, Ari},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Viral Proteins;Signal Transduction;Animals;review, tutorial;review;15 Retrovirus mechanism;Virion;Carbohydrates;Membrane Microdomains;Active Transport, Cell Nucleus;Membrane Fusion;Cells;Genome, Viral;Cytosol;Viral Physiology;Receptors, Virus;Cell Nucleus;Cell Physiology;Endocytosis;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Month = {4},
	Nlm_Id = {0404511},
	Number = {5668},
	Organization = {Institute of Biochemistry, Swiss Federal Institute of Technology-Zurich, CH-8093 Zurich, Switzerland.},
	Pages = {237-42},
	Pii = {304/5668/237},
	Pubmed = {15073366},
	Title = {How viruses enter animal cells},
	Uuid = {9D42FF5C-60AF-47C0-B1E5-39CB6735B563},
	Volume = {304},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1094823}}

@article{Snyder:2002,
	Abstract = {1078-8956 Comment News},
	Author = {Snyder, E. Y. and Park, K. I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nat Med},
	Keywords = {06 Adult neurogenesis injury induced;Human;Rats;Radiation Injuries, Experimental/physiopathology;Regeneration/*physiology;Cell Division;Bone Marrow Transplantation;Neuroglia/cytology/physiology/radiation effects;Bromodeoxyuridine/analysis/metabolism;Neuronal Plasticity/*physiology;Neurons/radiation effects;Brain/*physiology/radiation effects;Animals;Cells, Cultured;Stem Cells/*physiology/radiation effects;D pdf;Brain Diseases/*physiopathology},
	Number = {9},
	Pages = {928-30},
	Title = {Limitations in brain repair},
	Uuid = {D34149FB-6706-4CA2-9996-C7F917637C19},
	Volume = {8},
	Year = {2002},
	url = {papers/Snyder_NatMed2002.pdf}}

@article{Snyder:1997,
	Abstract = {Neurons undergoing targeted photolytic cell death degenerate by apoptosis. Clonal, multipotent neural precursor cells were transplanted into regions of adult mouse neocortex undergoing selective degeneration of layer II/III pyramidal neurons via targeted photolysis. These precursors integrated into the regions of selective neuronal death; 15 +/- 7\%differentiated into neurons with many characteristics of the degenerated pyramidal neurons. They extended axons and dendrites and established afferent synaptic contacts. In intact and kainic acid- lesioned control adult neocortex, transplanted precursors differentiated exclusively into glia. These results suggest that the microenvironmental alterations produced by this synchronous apoptotic neuronal degeneration in adult neocortex induced multipotent neural precursors to undergo neuronal differentiation which ordinarily occurs only during embryonic corticogenesis. Studying the effects of this defined microenvironmental perturbation on the differentiation of clonal neural precursors may facilitate identification of factors involved in commitment and differentiation during normal development. Because photolytic degeneration simulates some mechanisms underlying apoptotic neurodegenerative diseases, these results also suggest the possibility of neural precursor transplantation as a potential cell replacement or molecular support therapy for some diseases of neocortex, even in the adult.},
	Author = {Snyder, E. Y. and Yoon, C. and Flax, J. D. and Macklis, J. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {beta-Galactosidase/biosynthesis;*Nerve Degeneration;Cell Differentiation;Pyramidal Cells/*cytology/physiology;Afferent Pathways;Dendrites/physiology/ultrastructure;Photolysis;Animal;Brain Tissue Transplantation/pathology/*physiology;Mice, Inbred C57BL;Stem Cells/*cytology;Axons/physiology/ultrastructure;*Apoptosis;Support, Non-U.S. Gov't;06 Adult neurogenesis injury induced;Neurons/*cytology/*transplantation/ultrastructure;Support, U.S. Gov't, P.H.S.;Mice;Neocortex/*cytology/*physiology;Genes, Reporter;D-5;Synapses/physiology/ultrastructure},
	Number = {21},
	Organization = {Department of Neurology, Harvard Medical School, and Division of Neuroscience, Children's Hospital, 320 Longwood Avenue, Boston, MA 02115, USA.},
	Pages = {11663-8.},
	Title = {Multipotent neural precursors can differentiate toward replacement of neurons undergoing targeted apoptotic degeneration in adult mouse neocortex},
	Uuid = {366767C2-EC80-11DA-8605-000D9346EC2A},
	Volume = {94},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9326667}}

@article{Solecki:2006,
	Abstract = {We review studies on the polarity of developing cerebellar granule, showing that the centrosome localizes to the pole of the neuron that extrudes the nascent axon, and the Rho GTPase Cdc42 (cell division cycle 42) activates the mPar6alpha/Par3 (Par for partitioning defective) complex to coordinate actin dynamics in the growth cone. Subsequently, mPar6alpha signaling controls the migration of immature granule neurons down the Bergmann glial fibers into the internal granule cell layer in which they establish synaptic connections.},
	Author = {Solecki, David J. and Govek, Eve-Ellen E. and Hatten, Mary E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Synapses;24 Pubmed search results 2008;Cell Cycle Proteins;Neuroglia;Membrane Proteins;Cerebellum;Protein Isoforms;research support, n.i.h., extramural;Animals;Cell Movement;Humans;review;Proteins},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {42},
	Organization = {Laboratory of Developmental Neurobiology, The Rockefeller University, New York, New York 10021, USA.},
	Pages = {10624-5},
	Pii = {26/42/10624},
	Pubmed = {17050699},
	Title = {mPar6 alpha controls neuronal migration},
	Uuid = {E4CD48E6-AA37-4C1A-8C15-E72DAD9B9CA6},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4060-06.2006}}

@article{Soloveva:1979,
	Abstract = {The brains of 7--12 week embryos, developing in normal and mentally ill females (normal--14, schizophrenia--12, other mental disorders--10) were studied by means of electron microscopy. It was established that the cells of the microglia type may be encountered in the brain of embryos beginning from 7 weeks. In the brain of embryos from normal females these cells had mainly a round or oval form (globose microglia). Axons were encountered relatively rarely. Some of the cells had protrusions of the pseudopodia-like type. In the brain of embryos from mentally ill females the cells of the microglia type have diverse, sometimes sticklike forms; they form multiple thin axons, actively fagocyte. The ultrastructure in such conditions was not destructed. These changes are considered to be the result of an increased activity of microglial cells under the influence of factors of the pathological process.},
	Author = {Solov'eva, Zh V. h. V. and Orlovskaia, D. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0044-4588},
	Journal = {Zh Nevropatol Psikhiatr Im S S Korsakova},
	Keywords = {Maternal-Fetal Exchange;Neuroglia;Female;Human;Microscopy, Electron;English Abstract;Not relevant;11 Glia;Pregnancy;Mental Disorders;Schizophrenia;Phagocytosis;Brain},
	Medline = {79231744},
	Nlm_Id = {8710066},
	Number = {7},
	Pages = {852-7},
	Pubmed = {465151},
	Title = {[Microglia-type cells in normal and pathologic human embryonic brains]},
	Uuid = {35E732B9-6FBB-4BE1-A2E3-3DB60FE343DF},
	Volume = {79},
	Year = {1979}}

@article{Sommer:2002,
	Abstract = {Normal CNS development involves the sequential differentiation of multipotent stem cells. Alteration of the numbers of stem cells, their self-renewal ability, or their proliferative capacity will have major effects on the appropriate development of the nervous system. In this review, we discuss different mechanisms that regulate neural stem cell differentiation. Proliferation signals and cell cycle regulators may regulate cell kinetics or total number of cell divisions. Loss of trophic support and cytokine receptor activation may differentially contribute to the induction of cell death at specific stages of development. Signaling from differentiated progeny or asymmetric distribution of specific molecules may alter the self-renewal characteristics of stem cells. We conclude that the final decision of a cell to self-renew, differentiate or remain quiescent is dependent on an integration of multiple signaling pathways and at each instant will depend on cell density, metabolic state, ligand availability, type and levels of receptor expression, and downstream cross-talk between distinct signaling pathways. 21896379 0301-0082 Journal Article Review Review, Tutorial},
	Author = {Sommer, L. and Rao, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Prog Neurobiol},
	Keywords = {B-25;02 Adult neurogenesis migration;Cell Differentiation;Human;Apoptosis;Signal Transduction;Cell Division;Cell Count;Central Nervous System/cytology/*embryology/*growth &development;Animal;Neurons/*cytology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Stem Cells/*cytology},
	Number = {1},
	Organization = {Institute of Cell Biology, Swiss Federal Institute of Technology, ETH-Hoenggerberg HPM E38, CH-8093 Zurich, Switzerland. lukas.sommer\@cell.biol.ethz.ch},
	Pages = {1-18},
	Pubmed = {11897403},
	Title = {Neural stem cells and regulation of cell number},
	Uuid = {E22C73E3-6FAB-4251-B4AC-D3F679404C7F},
	Volume = {66},
	Year = {2002},
	url = {papers/Sommer_ProgNeurobiol2002}}

@article{Song:2004a,
	Abstract = {Allogeneic stem cell-based transplants may be limited by allograft rejection, as is seen with conventional organ transplantation. One way to avert such a response is to use autologous stem cells, but that may carry the risk of recurrence of the original disease, particularly in the context of a genetic defect. We investigated the potential for gene modification of autologous stem cells to avoid both problems, using recombinant adenoassociated virus vector expressing human alpha1-antitrypsin in murine liver progenitor cells. We showed that recombinant adenoassociated virus 1 was the most efficient vector for liver progenitor cell transduction among five different serotypes of recombinant adenoassociated virus vectors. Ex vivo infected green fluorescent protein-positive liver progenitor cells from C57BL/6 mice with recombinant adenoassociated virus 1-vector-expressing human alpha1 antitrypsin were transplanted into the liver of monocrotaline-treated and partial-hepatectomized C57BL/6 recipients. Using green fluorescent protein as a donor marker, we were able to determine that at 18 weeks after transplantation, approximately 40\%to 50\%of the regenerated liver was green fluorescent protein positive. In addition, transgene expression (serum human alpha1-antitrypsin) was sustained for the length of the study (18 weeks after transplantation). Immunostaining revealed approximately 5\%to 10\%of repopulating liver cells expressing human alpha1-antitrypsin. In conclusion, this study demonstrated the feasibility of long-term engraftment and stability of transgene expression from genetically modified liver progenitor cells with a recombinant adenoassociated virus vector and implies a novel approach to gene therapy for treatment of liver diseases, such as alpha1-antitrypsin deficiency.},
	Author = {Song, Sihong and Witek, Rafal P. and Lu, Yuanqing and Choi, Young-Kook K. and Zheng, Donghang and Jorgensen, Marda and Li, Chengwen and Flotte, Terence R. and Petersen, Byron E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0270-9139},
	Journal = {Hepatology},
	Keywords = {Transgenes;Transduction, Genetic;Animals;Stem Cell Transplantation;Female;Liver;alpha 1-Antitrypsin;Mice, Inbred C57BL;Liver Diseases;alpha 1-Antitrypsin Deficiency;11 Glia;Green Fluorescent Proteins;Research Support, U.S. Gov't, P.H.S.;Hepatectomy;Gene Therapy;Mice;Luminescent Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {10},
	Nlm_Id = {8302946},
	Number = {4},
	Organization = {Department of Pharmaceutics, University of Florida, Gainesville, FL 32610, USA. shsong\@ufl.edu},
	Pages = {918-24},
	Pubmed = {15382177},
	Title = {Ex vivo transduced liver progenitor cells as a platform for gene therapy in mice},
	Uuid = {668A72DE-10C8-49FD-8E2A-6C806230C7DC},
	Volume = {40},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/hep.20404}}

@article{Song:2002a,
	Abstract = {Neural stem cells are present both in the developing nervous system and in the adult nervous system of all mammals, including humans. Little is known, however, about the extent to which stem cells in adults can give rise to new neurons. We used immunocytochemistry, electron microscopy, fluorescence microscopy (FM imaging) and electrophysiology to demonstrate that progeny of adult rat neural stem cells, when co- cultured with primary neurons and astrocytes from neonatal hippocampus, develop into electrically active neurons and integrate into neuronal networks with functional synaptic transmission. We also found that functional neurogenesis from adult stem cells is possible in co-culture with astrocytes from neonatal and adult hippocampus. These studies show that neural stem cells derived from adult tissues, like those derived from embryonic tissues, retain the potential to differentiate into functional neurons with essential properties of mature CNS neurons.},
	Author = {Song, H. J. and Stevens, C. F. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nat Neurosci},
	Keywords = {02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;BB abstr},
	Number = {5},
	Organization = {[1] Molecular Neurobiology Laboratory, Howard Hughes Medical Institute at the Salk Institute, 10010 N. Torrey Pines Road, La Jolla, California 92037, USA [2] Laboratory of Genetics, The Salk Institute, 10010 N. Torrey Pines Road, La Jolla, California 92037, USA.},
	Pages = {438-445.},
	Title = {Neural stem cells from adult hippocampus develop essential properties of functional CNS neurons},
	Uuid = {EBAF0E0A-5A02-4BE2-B816-785AEE3D7070},
	Volume = {5},
	Year = {2002},
	url = {papers/Song_NatNeurosci2002.pdf}}

@article{Song:2004,
	Abstract = {The generation of distinct cell types during development depends on the competence of progenitor populations to differentiate along specific lineages. Here we investigate the mechanisms that regulate competence of rodent cortical progenitors to differentiate into astrocytes in response to ciliary neurotrophic factor (CNTF). We found that fibroblast growth factor 2 (FGF2), which by itself does not induce astrocyte-specific gene expression, regulates the ability of CNTF to induce expression of glial fibrillary acidic protein (GFAP). FGF2 facilitates access of the STAT/CBP (signal transducer and activator of transcription/CRE binding protein) complex to the GFAP promoter by inducing Lys4 methylation and suppressing Lys9 methylation of histone H3 at the STAT binding site. Histone methylation at this site is specific to the cell's state of differentiation. In progenitors, the promoter is bound by Lys9-methylated histones, and in astrocytes, it is bound by Lys4-methylated histones, indicating that astrocyte differentiation in vivo involves this switch in chromatin state. Our observations indicate that extracellular signals can regulate access of transcription factors to genomic promoters by local chromatin modification, and thereby regulate developmental competence. 1097-6256 Journal Article},
	Author = {Song, M. R. and Ghosh, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Journal = {Nat Neurosci},
	Keywords = {04 Adult neurogenesis factors;C, G pdf},
	Number = {3},
	Organization = {Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, Maryland 21205, USA.},
	Pages = {229-35},
	Title = {FGF2-induced chromatin remodeling regulates CNTF-mediated gene expression and astrocyte differentiation},
	Uuid = {169AD8FB-1C1B-4356-98E0-BFF15C1E97DA},
	Volume = {7},
	Year = {2004},
	url = {papers/Song_NatNeurosci2004.pdf}}

@article{Song:2002,
	Abstract = {During an investigation of the mechanisms through which the local environment controls the fate specification of adult neural stem cells, we discovered that adult astrocytes from hippocampus are capable of regulating neurogenesis by instructing the stem cells to adopt a neuronal fate. This role in fate specification was unexpected because, during development, neurons are generated before most of the astrocytes. Our findings, together with recent reports that astrocytes regulate synapse formation and synaptic transmission, reinforce the emerging view that astrocytes have an active regulatory role--rather than merely supportive roles traditionally assigned to them--in the mature central nervous system. 0028-0836 Journal Article},
	Author = {Song, H. and Stevens, C. F. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:39:59 -0400},
	Journal = {Nature},
	Keywords = {Cell Survival;Animals;Culture Media, Serum-Free;Cells, Cultured;Neurons/*cytology/metabolism;Rats;Hippocampus/cytology/growth &development;Comparative Study;*Cell Differentiation;Stem Cells/*cytology/metabolism;Fibroblasts;Spinal Cord/cytology/growth &development;02 Adult neurogenesis migration;Aging/*physiology;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;BB pdf;Astrocytes/*physiology;Cell Lineage;Organ Specificity;Coculture;Rats, Inbred F344;Laminin/metabolism;Support, U.S. Gov't, P.H.S.;Oligodendroglia/physiology;Cell Division;Animals, Newborn;Bromodeoxyuridine},
	Number = {6884},
	Organization = {Molecular Neurobiology Laboratory, Howard Hughes Medical Institute at the Salk Institute, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.},
	Pages = {39-44},
	Title = {Astroglia induce neurogenesis from adult neural stem cells},
	Uuid = {82134804-2BA5-47B1-ADD0-8CAE96A4230C},
	Volume = {417},
	Year = {2002},
	url = {papers/Song_Nature2002}}

@article{Sorensen:1996,
	Abstract = {The purpose of the present study was to study if the connectivity of fetal neocortical tissue blocks placed in ischemic brain infarcts of adult rats would be enhanced in rats housed in an enriched environment. We also investigated whether the enriched housing conditions could enhance the postischemic and postgrafting functional outcome, in terms of motor behavior. This part of the study has been published recently. The middle cerebral artery was ligated on the right side in 37 inbred, adult male spontaneously hypertensive rats. The rats were placed at random either in an enriched environment (groups A and B) or in standard laboratory cages (group C). Three weeks after the artery occlusion, blocks of fetal sensorimotor cortex (embryonic day 17) were transplanted into the infarct cavity of rats from groups B and C. After 9 weeks all transplanted rats received an injection, into the graft, of a mixture containing the two tracers Fluoro-Gold and biotinylated Dextran amine. The transplants revealed a structured morphology with whorls and bands of cells reminiscent of normal neocortex. Tracing of efferent transplant to host fibers with biotinylated Dextran amine showed pronounced intrinsic transplant projections, as well as fibers, although significantly fewer, to the host ipsilateral sensorimotor cortex, striatum, and thalamus. Host to transplant projections were revealed by Fluoro-Gold-labeled cells found in the ipsilateral host sensorimotor cortex, the basal nucleus of Meynert, the thalamic ventrobasal, ventrolateral and posterior nuclei, and in the dorsal raphe nuclei. We conclude that fetal frontal neocortical block grafts placed in brain infarcts of adult rats develop a morphology reminiscent of normal neocortex and that both afferent and efferent neural connections, although sparse, are established with the host brain, whether the rats are reared under enriched housing conditions or not. 0014-4886 Journal Article},
	Author = {Sorensen, J. C. and Grabowski, M. and Zimmer, J. and Johansson, B. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Exp Neurol},
	Keywords = {Fluorescent Dyes;Animals;Neural Pathways/pathology/physiopathology;Rats;Dextrans;*Fetal Tissue Transplantation;Rats, Inbred SHR;Microscopy, Fluorescence;17 Transplant Regeneration;*Stilbamidines;Male;Support, Non-U.S. Gov't;Biotin/analogs &derivatives;L abstr;Brain/pathology/*physiopathology;Cerebral Infarction/pathology/*physiopathology/*surgery;*Brain Tissue Transplantation;Graft Survival},
	Number = {2},
	Organization = {Department of Neurobiology, Aarhus University, Denmark.},
	Pages = {227-35},
	Pubmed = {8620921},
	Title = {Fetal neocortical tissue blocks implanted in brain infarcts of adult rats interconnect with the host brain},
	Uuid = {21025CEF-756A-4B81-A56D-3F2703383E75},
	Volume = {138},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8620921}}

@article{Soria:2004,
	Abstract = {The subventricular zone (SVZ) is one of the sources of adult neural stem cells (ANSCs) in the mouse brain. Precursor cells proliferate in the SVZ and migrate through the rostral migratory stream (RMS) to the olfactory bulb (OB), where they differentiate into granule and periglomerular cells. Few transcription factors are known to be responsible for regulating NSC proliferation, migration, and differentiation processes; even fewer have been found to be responsible for the organization of the SVZ and RMS. For this reason, we studied the ventral anterior homeobox (Vax1) gene in NSC proliferation and in SVZ organization. We found that Vax1 is strongly expressed in the SVZ and in the RMS and that, in the absence of Vax1, embryonic precursor cells proliferate 100 times more than wild-type controls, in vitro. The SVZ of Vax1(-/-) brains is hyperplastic and mostly disorganized, and the RMS is missing, causing a failure of precursor cell migration to the OBs, which as a result are severely hypoplastic. Moreover, we found that Vax1 is essential for the correct differentiation of ependyma and astrocytes. Together, these data indicate that Vax1 is a potent regulator of SVZ organization and NSC proliferation, with important consequences on postnatal neurogenesis.},
	Author = {Soria, Jos{\'e} Miguel and Taglialatela, Paola and Gil-Perotin, Sara and Galli, Rossella and Gritti, Angela and Verdugo, Jos{\'e} Manuel Garcia and Bertuzzi, Stefano},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {49},
	Organization = {Dulbecco Telethon Institute at Consiglio Nazionale delle Ricerche-Istituto di Tecnologie Biomediche, 20090 Segrate, Milan, Italy.},
	Pages = {11171-81},
	Pii = {24/49/11171},
	Pubmed = {15590934},
	Title = {Defective postnatal neurogenesis and disorganization of the rostral migratory stream in absence of the Vax1 homeobox gene},
	Uuid = {AD8B1B66-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {24},
	Year = {2004},
	url = {papers/Soria_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3248-04.2004}}

@article{Sossey-Alaoui:1998,
	Abstract = {Subcortical band heterotopia (SBH) and classical lissencephaly (LIS) result from deficient neuronal migration which causes mental retardation and epilepsy. A single LIS/SBH locus on Xq22.3-q24 was mapped by linkage analysis and physical mapping of the breakpoint in an X;2 translocation. A recently identified gene, doublecortin ( DCX ), is expressed in fetal brain and mutated in LIS/SBH patients. We have identified four novel missense mutations in the gene, one familial mutation with LIS in a male and SBH in the carrier females, one de novo mutation in an SBH female, and two mutations in sporadic SBH female patients. The DCX gene is found to be expressed exclusively at a very high level in the adult frontal lobe. We have also cloned the X-linked mouse doublecortin (Dcx) gene. It encodes isoforms of a highly hydrophilic 40 kDa protein, homologous to its human counterpart and containing several potential phosphorylation sites. Both human and mouse DCX proteins are homologous to a CNS protein containing a Ca2+/calmodulin kinase domain, suggesting that the DCX protein may belong to a novel class of intracellular proteins involved in neuronal migration through Ca2+-dependent signaling.},
	Author = {Sossey-Alaoui, K. and Hartung, A. J. and Guerrini, R. and Manchester, D. K. and Posar, A. and Puche-Mira, A. and Andermann, E. and Dobyns, W. B. and Srivastava, A. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0964-6906},
	Journal = {Hum Mol Genet},
	Keywords = {10 Development;Signal Transduction;Animals;Microtubule-Associated Proteins;Humans;Sequence Homology, Amino Acid;Female;Epilepsy;Cell Movement;Mental Retardation;Calcium;Male;Neuropeptides;Linkage (Genetics);Research Support, U.S. Gov't, P.H.S.;X Chromosome;Neurons;Adult;Mice;Amino Acid Sequence;Molecular Sequence Data},
	Medline = {98334553},
	Month = {8},
	Nlm_Id = {9208958},
	Number = {8},
	Organization = {J. C. Self Research Institute of Human Genetics, Greenwood Genetic Center, Greenwood, SC 29646, USA.},
	Pages = {1327-32},
	Pii = {ddb156},
	Pubmed = {9668176},
	Title = {Human doublecortin (DCX) and the homologous gene in mouse encode a putative Ca2+-dependent signaling protein which is mutated in human X-linked neuronal migration defects},
	Uuid = {C9480CCC-F0DE-400C-98C8-3794697DCC1A},
	Volume = {7},
	Year = {1998},
	url = {papers/Sossey-Alaoui_HumMolGenet1998.pdf}}

@article{Sotelo:1991,
	Abstract = {Repair of adult 'point-to-point'systems by neural grafting is possible only when grafted neurons succeed in synaptically replacing the host's missing neurons, thus re-establishing the anatomical and functional integrity of the impaired circuits. Grafting experiments carried out on the cerebellum of the adult pcd (Purkinje-cell-degeneration) mutant mouse (an animal model of hereditary degenerative ataxia) reveal that embryonic Purkinje cells, by some unknown sorting mechanism, selectively invade the deprived cerebellar cortex. These neurons migrate to their proper domains and, inducing axonal sprouting of specific populations of host neurons, they become integrated synaptically within the pcd cerebellar cortex. However, the re-establishment of the corticonuclear projection is achieved only rarely, and this is the current experimental limit for the complete reconstruction of the cerebellar circuit. 0166-2236 Journal Article Review Review, Tutorial},
	Author = {Sotelo, C. and Alvarado-Mallart, R. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Trends Neurosci},
	Keywords = {Mice;Nerve Degeneration/physiology;Purkinje Cells/physiology/transplantation;17 Transplant Regeneration;Human;Dendrites/physiology;L abstr;Support, Non-U.S. Gov't;Animals;Cerebellum/*surgery/transplantation;Mice, Neurologic Mutants;Brain Tissue Transplantation/physiology},
	Number = {8},
	Organization = {Laboratory of Neuromorphology, INSERM U 106, Hopital de la Salpetriere, France.},
	Pages = {350-5},
	Pubmed = {1721740},
	Title = {The reconstruction of cerebellar circuits},
	Uuid = {9B1EF6E8-3226-4877-9496-443FF742F309},
	Volume = {14},
	Year = {1991},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1721740}}

@article{Spassky:2005,
	Abstract = {Ependymal cells on the walls of brain ventricles play essential roles in the transport of CSF and in brain homeostasis. It has been suggested that ependymal cells also function as stem cells. However, the proliferative capacity of mature ependymal cells remains controversial, and the developmental origin of these cells is not known. Using confocal or electron microscopy (EM) of adult mice that received bromodeoxyuridine (BrdU) or [3H]thymidine for several weeks, we found no evidence that ependymal cells proliferate. In contrast, ependymal cells were labeled by BrdU administration during embryonic development. The majority of them are born between embryonic day 14 (E14) and E16. Interestingly, we found that the maturation of ependymal cells and the formation of cilia occur significantly later, during the first postnatal week. We analyzed the early postnatal ventricular zone at the EM and found a subpopulation of radial glia in various stages of transformation into ependymal cells. These cells often had deuterosomes. To directly test whether radial glia give rise to ependymal cells, we used a Cre-lox recombination strategy to genetically tag radial glia in the neonatal brain and follow their progeny. We found that some radial glia in the lateral ventricular wall transform to give rise to mature ependymal cells. This work identifies the time of birth and early stages in the maturation of ependymal cells and demonstrates that these cells are derived from radial glia. Our results indicate that ependymal cells are born in the embryonic and early postnatal brain and that they do not divide after differentiation. The postmitotic nature of ependymal cells strongly suggests that these cells do not function as neural stem cells in the adult.},
	Author = {Spassky, Nathalie and Merkle, Florian T. and Flames, Nuria and Tramontin, Anthony D. and Garc{\'\i}a-Verdugo, Jos{\'e} Manuel and Alvarez-Buylla, Arturo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {1},
	Organization = {Department of Neurological Surgery and Program in Developmental and Stem Cell Biology, University of California San Francisco, San Francisco, California 94143, USA.},
	Pages = {10-8},
	Pii = {25/1/10},
	Pubmed = {15634762},
	Title = {Adult ependymal cells are postmitotic and are derived from radial glial cells during embryogenesis},
	Uuid = {FBA68663-053C-4DA7-ADEA-96E594E7F24D},
	Volume = {25},
	Year = {2005},
	url = {papers/Spassky_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1108-04.2005}}

@article{Spiegel:2006,
	Abstract = {The formation of the myelin sheath in the CNS is the endpoint of a defined developmental program along which oligodendrocytes progress. However, the molecular signals required for the initiation of myelination are largely unknown. Ishibashi et al. report in this issue of Neuron that ATP released by axons as a result of electrical stimulation serves as an important myelination signal. Surprisingly, they found that ATP does not act directly on oligodendrocytes but rather on astrocytes, causing the release of leukemia inhibitory factor (LIF), which in turns affects promyelinating oligodendrocytes. These findings uncover a novel role for astrocytes in mediating the intricate communication between axons and myelinating glial cells.},
	Author = {Spiegel, Ivo and Peles, Elior},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {comment;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel.},
	Pages = {777-8},
	Pii = {S0896-6273(06)00167-X},
	Pubmed = {16543121},
	Title = {A new player in CNS myelination},
	Uuid = {6FD68E86-F5BA-44F2-97D5-DFC12E0DB100},
	Volume = {49},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.03.001}}

@article{Spradling:2001,
	Abstract = {The concept that stem cells are controlled by particular microenvironments known as 'niches'has been widely invoked. But niches have remained largely a theoretical construct because of the difficulty of identifying and manipulating individual stem cells and their surroundings. Technical advances now make it possible to characterize small zones that maintain and control stem cell activity in several organs, including gonads, skin and gut. These studies are beginning to unify our understanding of stem cell regulation at the cellular and molecular levels, and promise to advance efforts to use stem cells therapeutically. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Spradling, A. and Drummond-Barbosa, D. and Kai, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Nature},
	Keywords = {Testis/cytology;F abstr;10 Development;Intestines/cytology;Ovary/cytology;Female;Hematopoietic Stem Cells/cytology;Mammals;Epithelial Cells;*Stem Cells;Caenorhabditis elegans/cytology;Endoderm/cytology;Drosophila/cytology;Skin/cytology;Animals;Male},
	Number = {6859},
	Organization = {HHMI/Department of Embryology, Carnegie Institution of Washington, Baltimore, Maryland 21210, USA.},
	Pages = {98-104},
	Pubmed = {11689954},
	Title = {Stem cells find their niche},
	Uuid = {82B836D0-B729-4ADA-A323-073B5D18A71F},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689954}}

@article{Staber:1978,
	Author = {Staber, F. G. and Schl{\"a}fli, E. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {15 ERVs retroelements;Cell Differentiation;Hematopoietic Stem Cells;Retroviridae;Antigens, Surface;15 Retrovirus mechanism;Animals;Spleen;Mice;Antigens, Viral;24 Pubmed search results 2008},
	Medline = {79032157},
	Month = {10},
	Nlm_Id = {0410462},
	Number = {5681},
	Pages = {669-71},
	Pubmed = {212682},
	Title = {Expression of endogenous C-type viral antigen on normal mouse haemopoietic stem cells},
	Uuid = {86028F6A-8C08-4E8C-94A2-5F619E39A0EA},
	Volume = {275},
	Year = {1978}}

@article{Stables:2002,
	Abstract = {PURPOSE: The workshop explored the current problems, needs, and potential usefulness of existing methods of discovery of new therapies to treat epilepsy patients. Resistance to medical therapy (pharmacoresistance) and the development of epilepsy (epileptogenesis) are recognized as two of the major problems in epilepsy treatment today. At the same time, there is growing awareness that the development of new therapies has slowed, a trend that has economic and scientific roots. To move toward new and more effective therapies, novel approaches to therapy discovery are needed. METHODS: A workshop was held in March 2001 with the charge to develop a plan to move the exploration and discovery process forward. Participants from academia, government, and industry reviewed the current status of epilepsy therapy and explored the identification of potential new therapies. RESULTS: At the end of the 2-day meeting, the panel made a series of recommendations. The two major recommendations were (a) to establish a means for continuing the examination of new approaches to therapy discovery, and (b) to identify models and approaches to therapy discovery that may identify treatments that are more successful than those available. Further recommendations were made to support the development of technology (miniaturization, computerization, video monitoring, etc.) to facilitate the use of the new models and to identify the mechanisms of therapy success and failure. CONCLUSIONS: Understanding the epidemiology of therapy resistance and providing support for new approaches to therapy development were identified as key issues for introduction of new and more effective treatments.},
	Author = {Stables, James P. and Bertram, Edward H. and White, H. Steve and Coulter, Douglas A. and Dichter, Marc A. and Jacobs, Margaret P. and Loscher, Wolfgang and Lowenstein, Daniel H. and Moshe, Solomon L. and Noebels, Jeffrey L. and Davis, Mirian},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Epilepsy;Technology, Pharmaceutical;24 Pubmed search results 2008;21 Epilepsy;Anticonvulsants;21 Neurophysiology;consensus development conference;Child, Preschool;Drug Resistance;Humans;Animals;Disease Models, Animal;review;consensus development conference, nih},
	Medline = {22310892},
	Month = {11},
	Nlm_Id = {2983306R},
	Number = {11},
	Organization = {National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892, USA. stablesj\@ninds.nih.gov},
	Pages = {1410-20},
	Pii = {epi06702},
	Pubmed = {12423393},
	Title = {Models for epilepsy and epileptogenesis: report from the NIH workshop, Bethesda, Maryland},
	Uuid = {6259E419-9A1B-459F-8E40-A364535106BE},
	Volume = {43},
	Year = {2002}}

@article{Stagaard:1987,
	Abstract = {The population of microglial cells in the subependymal layer of the subcommissural organ is sparse in normal adult rats. The number of microglial cells was substantially increased in this area following intraventricular injection of the serotonin neurotoxin 5,6-dihydroxytryptamine (5,6-DHT). In sections of plastic embedded material, 1 micron thick, the majority of phagocytic cells scattered in the subependymal layer had an appearance similar to that described in classical studies of microglial cells. At the electron microscopic level microglial cells exhibited the characteristic elongate nucleus with peripheral chromatin condensation. The perikaryon was scanty, containing strands of rough endoplasmic reticulum. The abundant organelles in the processes included Golgi complexes, mitochondria, rough and smooth endoplasmic reticulum as well as dense and multivesicular bodies. In addition, the processes contained phagocytosed axon terminals originating from the dense serotoninergic input to the subcommissural organ, which had degenerated on accumulating the serotonin neurotoxin. A fraction of the phagocytosed material was contained in subependymal subcommissural organ cells, astrocytes and oligodendrocytes. At the light microscopic level the phagocytosed terminals were visualized histochemically with Schmorl's reaction, which resulted in Prussian Blue precipitates. This allowed screening of microglial cells in complete series of sections through the well-defined subependymal layer of the subcommissural organ.},
	Author = {Stagaard, M. and Balslev, Y. and Lundberg, J. J. and M\ollg\r{a}rd, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Brain Diseases;Neuroglia;5,6-Dihydroxytryptamine;Rats;Microscopy, Electron;Subcommissural Organ;Serotonin;Not relevant;Female;11 Glia;Injections, Intraventricular;Neurosecretory Systems;Animals;Phagocytosis;Rats, Inbred Strains},
	Medline = {87225061},
	Month = {2},
	Nlm_Id = {0364620},
	Number = {1},
	Pages = {131-42},
	Pubmed = {3585416},
	Title = {Microglia in the hypendyma of the rat subcommissural organ following brain lesion with serotonin neurotoxin},
	Uuid = {78D23D6E-AC73-42C2-A846-630AAB05BB4D},
	Volume = {16},
	Year = {1987}}

@article{Stagi:2005,
	Abstract = {The mechanism of axonal injury in inflammatory brain diseases is still unclear. Increased microglial production of nitric oxide (NO) is a common early sign in neuroinflammatory diseases. We found by fluorescence correlation spectroscopy that synaptophysin tagged with enhanced green fluorescence protein (synaptophysin-EGFP) moves anterogradely in axons of cultured neurons. Activated microglia focally inhibited the axonal movement of synaptophysin-EGFP in a NO synthase-dependent manner. Direct application of a NO donor to neurons resulted in inhibition of axonal transport of synaptophysin-EGFP and synaptotagmin I tagged with EGFP, mediated via phosphorylation of c-jun NH2-terminal kinase (JNK). Thus, overt production of reactive NO by activated microglia blocks the axonal transport of synaptic vesicle precursors via phosphorylation of JNK and could cause axonal and synaptic dysfunction.},
	Author = {Stagi, Massimiliano and Dittrich, Petra S. and Frank, Nadja and Iliev, Asparouh I. and Schwille, Petra and Neumann, Harald},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:32 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {2},
	Organization = {Neuroimmunology Group, European Neuroscience Institute G{\"o}ttingen, 37073 G{\"o}ttingen, Germany.},
	Pages = {352-62},
	Pii = {25/2/352},
	Pubmed = {15647478},
	Title = {Breakdown of axonal synaptic vesicle precursor transport by microglial nitric oxide},
	Uuid = {A6FAE162-80E4-4B25-805A-EBBCD4A31A25},
	Volume = {25},
	Year = {2005},
	url = {papers/Stagi_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3887-04.2005}}

@article{Steele:2006,
	Abstract = {The misfolding of the prion protein (PrP(c)) is a central event in prion diseases, yet the normal function of PrP(c) remains unknown. PrP(c) has putative roles in many cellular processes including signaling, survival, adhesion, and differentiation. Given the abundance of PrP(c) in the developing and mature mammalian CNS, we investigated the role of PrP(c) in neural development and in adult neurogenesis, which occurs constitutively in the dentate gyrus (DG) of the hippocampus and in the olfactory bulb from precursors in the subventricular zone (SVZ)/rostral migratory stream. In vivo, we find that PrP(c) is expressed immediately adjacent to the proliferative region of the SVZ but not in mitotic cells. In vivo and in vitro studies further find that PrP(c) is expressed in multipotent neural precursors and mature neurons but is not detectable in glia. Loss- and gain-of-function experiments demonstrate that PrP(c) levels correlate with differentiation of multipotent neural precursors into mature neurons in vitro and that PrP(c) levels positively influence neuronal differentiation in a dose-dependent manner. PrP(c) also increases cellular proliferation in vivo; in the SVZ, PrP(c) overexpresser (OE) mice have more proliferating cells compared with wild-type (WT) or knockout (KO) mice; in the DG, PrP(c) OE and WT mice have more proliferating cells compared with KO mice. Our results demonstrate that PrP(c) plays an important role in neurogenesis and differentiation. Because the final number of neurons produced in the DG is unchanged by PrP(c) expression, other factors must control the ultimate fate of new neurons.},
	Author = {Steele, Andrew D. and Emsley, Jason G. and Ozdinler, P. Hande and Lindquist, Susan and Macklis, Jeffrey D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Aging;Cell Differentiation;Research Support, Non-U.S. Gov't;Mice, Knockout;Gene Expression Regulation, Developmental;Cell Proliferation;Stem Cells;Research Support, N.I.H., Extramural;Prions;Nervous System;Animals;Cells, Cultured;Mice;Neurons;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {9},
	Organization = {Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, 02142, USA.},
	Pages = {3416-21},
	Pii = {0511290103},
	Pubmed = {16492732},
	Title = {Prion protein (PrPc) positively regulates neural precursor proliferation during developmental and adult mammalian neurogenesis},
	Uuid = {239C09C9-FF6E-4170-B55B-F27787B04639},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0511290103}}

@article{Steffan:1994,
	Abstract = {Feline immunodeficiency virus (FIV) provokes a disease in cats characterized by histopathological lesions similar to those observed in AIDS patients. In order to determine whether endothelial cells from brain microvessels are involved in the central nervous system disease to the same extent as macrophages and microglia, cells were isolated from healthy cat brains, cultured and infected in vitro with the FIV Villefranche IFFA 1/88 strain. The isolated cells displayed typical endothelial cell ultrastructural features and were characterized further by von Willebrand factor-labelling and the binding of specific lectins such as Ulex europaeus lectin on their membrane. They were also able to take up acetylated low density lipoproteins. Two weeks after infection, significant amounts of FIV p24 antigen were detected by indirect immunofluorescence in syncytia and single cells. Concomitantly, the same antigen could be detected in the culture medium of the infected cells by an ELISA technique. Numerous viral particles as well as different steps in the process of viral budding were observed under transmission electron microscopy. The synthesis of FIV p24 antigens still occurred in cells in which replication was blocked in the G2 phase with taxol. Our results suggest the possibility of a productive infection of brain microvascular endothelial cells by FIV in vivo, which could lead to important perturbations in the functions of the blood-brain barrier.},
	Author = {Steffan, A. M. and Lafon, M. E. and Gendrault, J. L. and Koehren, F. and De Monte, M. and Royer, C. and Kirn, A. and Gut, J. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0022-1317},
	Journal = {J Gen Virol},
	Keywords = {Animals;Cells, Cultured;Immunodeficiency Virus, Feline;Receptors, Cell Surface;Brain;Paclitaxel;Gene Products, gag;Culture Media, Conditioned;Lipoproteins, LDL;G2 Phase;11 Glia;Receptors, Mitogen;Microcirculation;Virus Replication;Microscopy, Electron;Cats;von Willebrand Factor;Endothelium, Vascular},
	Medline = {95088615},
	Month = {12},
	Nlm_Id = {0077340},
	Organization = {Intitut National de la Sant{\'e} et de la Recherche M{\'e}dicale U74, Institut de Virologie de la Facult{\'e} de M{\'e}decine, Strasbourg, France.},
	Pages = {3647-53},
	Pubmed = {7996160},
	Title = {Feline immunodeficiency virus can productively infect cultured endothelial cells from cat brain microvessels},
	Uuid = {EE946C60-4A4D-4AEF-9099-45142B484E01},
	Volume = {75 ( Pt 12)},
	Year = {1994}}

@article{Stein:2005,
	Abstract = {Feline immunodeficiency virus (FIV)-based lentiviral vectors can be targeted to restricted cell types by pseudotyping with envelopes from other viruses. An FIV vector expressing bacterial beta-galactosidase (beta-gal) and pseudotyped with lymphocytic choriomeningitis virus (LCMV) envelope glycoprotein was injected into postnatal mouse brain striatum to determine neural cell-type transduction. After 3 or 7.5 weeks, the beta-gal-expressing cells included astrocytes in the striatum and in the subventricular zone (SVZ), neuroblasts along the rostral migratory stream, and neurons in the olfactory bulb. This pattern was suggestive of transduction of neural stem cells/progenitors that reside in the SVZ and continually generate olfactory bulb neurons. To test for transduction of SVZ type B astrocyte/stem cells, LCMV-pseudotyped FIV encoding Cre recombinase driven by an astrocyte-specific promoter was injected into the striatum of ROSA26 Cre reporter mice. beta-Gal expression in these mice depends on Cre recombinase-mediated DNA recombination. beta-Gal-expressing neuroblasts and neurons were detected in the rostral migratory stream and olfactory bulb, respectively, indicating that these cells derived from an astrocytic-type stem cell. Thus, LCMV (WE54)-pseudotyped FIV provides a novel vector for transducing neural stem cells/progenitors in vivo and may prove valuable as a gene transfer vector for therapy of neurodegenerative diseases.},
	Author = {Stein, Colleen S. and Martins, In\^{e}s and Davidson, Beverly L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1525-0016},
	Journal = {Mol Ther},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {100890581},
	Number = {3},
	Organization = {Program in Gene Therapy, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242, USA.},
	Pages = {382-9},
	Pii = {S1525-0016(04)01531-X},
	Pubmed = {15727934},
	Title = {The lymphocytic choriomeningitis virus envelope glycoprotein targets lentiviral gene transfer vector to neural progenitors in the murine brain},
	Uuid = {29D68708-3E78-4401-BBEB-B692F93B1D97},
	Volume = {11},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ymthe.2004.11.008}}

@article{Steiner:2004,
	Abstract = {In adult hippocampal neurogenesis, new neurons appear to originate from a cell with astrocytic properties expressing glial fibrillary acidic protein (GFAP). Also, new astrocytes are generated in the adult dentate gyrus. Whereas the putative astrocyte-like progenitor cells are consistently S-100beta-negative, many new astrocytes are S-100beta-positive. Thus, it is unclear whether the GFAP-positive progenitor cells are astrocytes in a general sense or rather neural progenitor cells with certain astrocytic characteristics. We therefore investigated the development of GFAP-expressing cells in the context of adult hippocampal neurogenesis. Proliferating cells could be either GFAP-positive or doublecortin-positive (DCX), but never both, indicating two independent populations of dividing cells in the glial and neuronal lineages. Two distinct populations of cells with astroglial properties were detected-one expressing GFAP, the other co-expressing GFAP and S-100beta. We never found S-100beta-cells to be in S-phase. No overlap between neuronal and glial markers was seen at any time point. Thus, astrogenesis occurred in parallel and to some degree independent of adult neurogenesis. The uninterrupted GFAP expression in this lineage, and neuronal markers in the other lineage, argue against a late common precursor for neurogenesis and gliogenesis in the adult hippocampus. Very few newly generated microglia and no new oligodendrocytes were detected. Environmental enrichment and voluntary wheel running-two experimental paradigms with robust stimulatory effects on adult hippocampal neurogenesis-affected hippocampal astrogenesis differentially: Running, but not enrichment, strongly induced net astrogenesis (GFAP/S-100beta), but also GFAP-positive S-100beta-negative cells, which thus appear to be a transiently amplifiable intermediate population within the glial lineage. 0894-1491 Journal Article},
	Author = {Steiner, B. and Kronenberg, G. and Jessberger, S. and Brandt, M. D. and Reuter, K. and Kempermann, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {Glia},
	Keywords = {02 Adult neurogenesis migration;03 Adult neurogenesis progenitor source;BB, G},
	Number = {1},
	Organization = {Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch, Berlin, Germany.},
	Pages = {41-52},
	Title = {Differential regulation of gliogenesis in the context of adult hippocampal neurogenesis in mice},
	Uuid = {8DA2A2F9-0018-4FB3-B703-42E83BBE9DEA},
	Volume = {46},
	Year = {2004},
	url = {papers/Steiner_Glia2004.pdf}}

@article{Stence:2001,
	Abstract = {The dynamics of microglial cell activation was studied in freshly prepared rat brain tissue slices. Microglia became activated in the tissue slices, as evidenced by their conversion from a ramified to amoeboid form within several hours in vitro. To define better the cytoarchitectural dynamics underlying microglial activation, we performed direct three-dimensional time-lapse confocal imaging of microglial cells in live brain slices. Microglia in tissue slices were stained with a fluorescent lectin conjugate, FITC-IB(4), and stacks of confocal optical sections through the tissue were collected repeatedly at intervals of 2-5 min for several hours at a time. Morphometric analysis of cells from time-lapse sequences revealed that ramified microglia progress to amoeboid macrophages through a stereotypical sequence of steps. First, in the withdrawal stage, the existing ramified branches of activating microglia do not actively extend or engulf other cells, but instead retract back (mean rate, 0.5-1.5 microm/min) and are completely resorbed into the cell body. Second, in the motility stage, a new set of dynamic protrusions, which can exhibit cycles of rapid extension and retraction (both up to 4 microm/min), abruptly emerges. Sometimes new processes begin to emerge even before the old branches are completely withdrawn. Third, in the locomotory stage, microglia begin translocating within the tissue (up to 118 microm/h) only after the new protrusions emerge. We conclude that the rapid conversion of resting ramified microglia to active amoeboid macrophages is accomplished not by converting quiescent branches to dynamic ones, but rather by replacing existing branches with an entirely new set of highly motile protrusions. This suggests that the ramified branches of resting microglia are normally incapable of rapid morphological dynamics necessary for activated microglial function. More generally, our time-lapse observations identify changes in the dynamic behavior of activating microglia and thereby help define distinct temporal and functional stages of activation for further investigation.},
	Author = {Stence, N. and Waite, M. and Dailey, M. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Microscopy, Confocal;Research Support, Non-U.S. Gov't;Image Processing, Computer-Assisted;Rats;Hippocampus;Microscopy, Video;11 Glia;Microglia;Organ Culture Techniques;Animals;Cell Movement;24 Pubmed search results 2008},
	Medline = {21135754},
	Month = {3},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Biological Sciences, 355 Biology Building, University of Iowa, Iowa City, IA 52242, USA.},
	Pages = {256-66},
	Pii = {10.1002/1098-1136(200103)33:3<256::AID-GLIA1024>3.0.CO;2-J},
	Pubmed = {11241743},
	Title = {Dynamics of microglial activation: a confocal time-lapse analysis in hippocampal slices},
	Uuid = {8E346440-972E-4CF4-BD61-6267EDF701FB},
	Volume = {33},
	Year = {2001},
	url = {papers/Stence_Glia2001.pdf}}

@article{Stenman:2003a,
	Abstract = {We showed previously that the orphan nuclear receptor Tlx is required for the correct establishment of the pallio-subpallial boundary. Loss of Tlx results in a dorsal expansion of ventral markers (e.g., the homeodomain protein GSH2) into the ventralmost pallial region, i.e., the ventral pallium. We also observed a disproportionate reduction in the size of the Tlx mutant lateral ganglionic eminence (LGE) from embryonic day 14.5 onward. Here we show that this reduction is caused, at least in large part, by a proliferation defect. Interestingly, in Tlx mutants, the LGE derivatives are differentially affected. Although the development of the Tlx mutant striatum is compromised, an apparently normal number of olfactory bulb interneurons are observed. Consistent with this observation, we found that Tlx is required for the normal establishment of the ventral LGE that gives rise to striatal projection neurons. This domain is reduced by the dorsal and ventral expansion of molecular markers normally confined to progenitor domains flanking the ventral LGE. Finally, we investigated possible genetic interactions between Gsh2 and Tlx in lateral telencephalic development. Our results show that, although Gsh2 and Tlx have additive effects on striatal development, they differentially regulate the establishment of ventral pallial identity.},
	Author = {Stenman, Jan M. and Wang, Bei and Campbell, Kenneth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008;10 Development;Telencephalon;Research Support, Non-U.S. Gov't;Receptors, Cytoplasmic and Nuclear;Antigens, Differentiation;Research Support, U.S. Gov't, P.H.S.;Corpus Striatum;Cell Division;Mice, Mutant Strains;Body Patterning;Animals;Mice;Nervous System Malformations;Homeodomain Proteins;Bromodeoxyuridine},
	Medline = {22989841},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {33},
	Organization = {Division of Developmental Biology, Children's Hospital Research Foundation, Cincinnati, Ohio 45229-3039, USA.},
	Pages = {10568-76},
	Pii = {23/33/10568},
	Pubmed = {14627641},
	Title = {Tlx controls proliferation and patterning of lateral telencephalic progenitor domains},
	Uuid = {F1ABB797-2B7E-48E4-9BCB-F87ADF9D4768},
	Volume = {23},
	Year = {2003}}

@article{Stevens:2007,
	Abstract = {During development, the formation of mature neural circuits requires the selective elimination of inappropriate synaptic connections. Here we show that C1q, the initiating protein in the classical complement cascade, is expressed by postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina. Mice deficient in complement protein C1q or the downstream complement protein C3 exhibit large sustained defects in CNS synapse elimination, as shown by the failure of anatomical refinement of retinogeniculate connections and the retention of excess retinal innervation by lateral geniculate neurons. Neuronal C1q is normally downregulated in the adult CNS; however, in a mouse model of glaucoma, C1q becomes upregulated and synaptically relocalized in the adult retina early in the disease. These findings support a model in which unwanted synapses are tagged by complement for elimination and suggest that complement-mediated synapse elimination may become aberrantly reactivated in neurodegenerative disease.},
	Author = {Stevens, Beth and Allen, Nicola J. and Vazquez, Luis E. and Howell, Gareth R. and Christopherson, Karen S. and Nouri, Navid and Micheva, Kristina D. and Mehalow, Adrienne K. and Huberman, Andrew D. and Stafford, Benjamin and Sher, Alexander and Litke, Alan M. and Lambris, John D. and Smith, Stephen J. and John, Simon W. M. and Barres, Ben A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Long-Term Synaptic Depression;10 Development;Retina;Animals;Astrocytes;Synapses;Up-Regulation;Complement C1q;RNA, Messenger;research support, non-u.s. gov't;10 circuit formation;Animals, Newborn;Mice, Knockout;Mice, Inbred DBA;Complement Activation;research support, n.i.h., extramural;Mice;Central Nervous System;24 Pubmed search results 2008;Complement C3;Geniculate Bodies;Glaucoma;Retinal Ganglion Cells},
	Month = {12},
	Nlm_Id = {0413066},
	Number = {6},
	Organization = {Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA. beths\@standfordmedalumni.org},
	Pages = {1164-78},
	Pii = {S0092-8674(07)01355-4},
	Pubmed = {18083105},
	Title = {The classical complement cascade mediates CNS synapse elimination},
	Uuid = {66D0A897-7431-4778-BDD1-B5E9D6693967},
	Volume = {131},
	Year = {2007},
	url = {papers/Stevens_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2007.10.036}}

@article{Stevenson:2001,
	Abstract = {In Drosophila syncytial blastoderm embryos, centrosomes specify the position of actin-based interphase caps and mitotic furrows. Mutations in the scrambled locus prevent assembly of mitotic furrows, but do not block actin cap formation. The scrambled gene encodes a protein that localizes to the mitotic furrows and centrosomes. Sced localization, actin reorganization from caps into mitotic furrows, and centrosome-coordinated assembly of actin caps are not blocked by microtubule disruption. Our results indicate that centrosomes may coordinate assembly of cortical actin caps through a microtubule-independent mechanism, and that Scrambled mediates a second microtubule-independent process that drives mitotic furrow assembly. 1465-7392 Journal Article},
	Author = {Stevenson, V. A. and Kramer, J. and Kuhn, J. and Theurkauf, W. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {Nat Cell Biol},
	Keywords = {Animals;Microtubules/drug effects/*genetics/ultrastructure;Insect Proteins/*genetics/metabolism;Centrosome/*metabolism/ultrastructure;Colchicine/pharmacology;EE pdf;Actins/*genetics/ultrastructure;Cell Cycle Proteins/*genetics/metabolism;08 Aberrant cell cycle;Cytochalasin D/pharmacology;Mitosis/drug effects/*physiology;Embryo/cytology/*embryology/metabolism;Polymers/metabolism;Mutation/physiology;Cytoskeleton/genetics/metabolism/ultrastructure;*Drosophila Proteins;Support, U.S. Gov't, P.H.S.;Drosophila/cytology/*embryology/genetics;Blastoderm/cytology/metabolism;Interphase/physiology},
	Number = {1},
	Organization = {Program in Molecular Medicine and the Department of Molecular Genetics and Microbiology, University of Massachusetts Medical Center, 373 Plantation Street, Worcester, Massachusetts 01605, USA.},
	Pages = {68-75},
	Title = {Centrosomes and the Scrambled protein coordinate microtubule-independent actin reorganization},
	Uuid = {FD9B7455-DE2C-472A-9E4C-6054DDD8F36A},
	Volume = {3},
	Year = {2001},
	url = {papers/Stevenson_NatCellBiol2001.pdf}}

@article{Stewart:2002,

@article{Stewart:1999,
	Abstract = {The progenitor cells from the anterior part of the neonatal subventricular zone, the SVZa, are unusual in that, although they undergo division, they have a neuronal phenotype. To characterize the electrophysiological properties of the SVZa precursor cells, recordings were made of potassium and sodium currents from SVZa cells that were removed from postnatal day 0-1 rats and cultured for 1 day. The properties of the delayed rectifier and A-type potassium currents were described by classical Hodgkin and Huxley analyses of activation and inactivation. In addition, cells were assessed under current clamp for their ability to generate action potentials. The A-type potassium current (IK(A)) was completely inactivated at a holding potential of - 50 mV. The remaining potassium current resembled the delayed rectifier current (IK(DR)) in that it was blocked by tetraethylammonium (TEA; IC50 4.1 mM) and activated and inactivated slowly compared with IK(A). The conductance-voltage (G-V) curve revealed that G increased continuously from 0.2 nS at -40 mV to a peak of 2.6 nS at +10 or +20 mV, and then decreased for voltages above +30 mV. Activation time constants were largest at -40 mV ( approximately 11 ms) and smallest at 100 mV ( approximately 1.5 ms). The properties of IK(A) were studied in the presence of 20 mM TEA, to block IK(DR), and from a holding potential of -15 mV, to inactivate both IK(DR) and IK(A). IK(A) was then allowed to recover from inactivation to negative potentials during 200- to 800-ms pulses. Recovery from inactivation was fastest at -130 mV ( approximately 21 ms) and slowest at -90 mV ( approximately 135 ms). Inactivation was voltage independent from -60 to +60 mV with a time constant of approximately 15 ms. At steady state, IK(A) was half inactivated at -90 mV. GK(A) increased from 0.2 nS at -60 mV to a peak of 2.4 nS at +40 mV. Finally, the activation time constants ranged from approximately 1.9 ms at -50 mV to 0.7 ms at +60 mV. The properties of IK(A) resembled those of IK(A) found in differentiating cerebellar granule neurons. Most SVZa cells had sodium currents (28/32 cells). However, in current clamp 11 of 12 cells were incapable of generating action potentials from voltages of -30 to -100 mV, suggesting that the available current densities were too low to support excitability.},
	Author = {Stewart, R. R. and Zigova, T. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:59 -0400},
	Journal = {J Neurophysiol},
	Keywords = {Electric Stimulation;Tetraethylammonium Compounds/pharmacology;Membrane Potentials/physiology;Prosencephalon/cytology/*metabolism;Rats;Cerebral Ventricles/cytology/*metabolism;Animals, Newborn/*physiology;Animal;Potassium Channels/*metabolism;Support, U.S. Gov't, P.H.S.;Electrophysiology;Patch-Clamp Techniques;13 Olfactory bulb anatomy;I both},
	Number = {1},
	Organization = {Laboratory of Molecular and Cellular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892-8115, USA.},
	Pages = {95-102.},
	Title = {Potassium currents in precursor cells isolated from the anterior subventricular zone of the neonatal rat forebrain},
	Uuid = {A1258A3B-A961-4498-A579-92A084C02800},
	Volume = {81},
	Year = {1999},
	url = {papers/Stewart_JNeurophysiol1999.pdf}}

@article{Stiene-Martin:2001,
	Abstract = {Accumulating evidence, obtained largely in vitro, indicates that opioids regulate the genesis of neurons and glia and their precursors in the nervous system. Despite this evidence, few studies have assessed opioid receptor expression in identified cells within germinal zones or examined opioid effects on gliogenesis in vivo. To address this question, the role of opioids was explored in the subventricular zone (SVZ) and/or striatum of 2-5-day-old and/or adult ICR mice. The results showed that subpopulations of neurons, astrocytes, and oligodendrocytes in the SVZ and striatum differentially express mu-, delta-, and/or kappa-receptor immunoreactivity in a cell type-specific and developmentally regulated manner. In addition, DNA synthesis was assessed by examining 5-bromo-2'-deoxyuridine (BrdU) incorporation into glial and nonglial precursors. Morphine (a preferential mu-agonist) significantly decreased the number of BrdU-labeled GFAP(+) cells compared with controls or mice co-treated with naltrexone plus morphine. Alternatively, in S100beta(+) cells, morphine did not significantly decrease BrdU incorporation; however, significant differences were noted between mice treated with morphine and those treated with morphine plus naltrexone. Most cells were GFAP(- )/S100beta(-). When BrdU incorporation was assessed within the total population (glia and nonglia), morphine had no net effect, but naltrexone alone markedly increased BrdU incorporation. This finding suggests that DNA synthesis in GFAP(-)/S100beta(-) cells is tonically suppressed by endogenous opioids. Assuming that S100beta and GFAP, respectively, distinguish among younger and older astroglia, this implies that astroglial replication becomes increasingly sensitive to morphine during maturation, and suggests that opioids differentially regulate the development of distinct subpopulations of glia and glial precursors.},
	Author = {Stiene-Martin, A. and Knapp, P. E. and Martin, K. and Gurwell, J. A. and Ryan, S. and Thornton, S. R. and Smith, F. L. and Hauser, K. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Glia},
	Keywords = {Glial Fibrillary Acidic Protein/metabolism;Receptors, Opioid/drug effects/*metabolism;Lateral Ventricles/cytology/*growth &development/metabolism;Comparative Study;Calcium-Binding Proteins/metabolism;Antigens, Differentiation/metabolism;Aging/physiology;Antigens, Surface/metabolism;Animal;Mice, Inbred ICR/anatomy &histology/growth &development/metabolism;11 Glia;G abstr;Naltrexone/pharmacology;Morphine/pharmacology;Neostriatum/cytology/*growth &development/metabolism;Opioid Peptides/metabolism;Animals, Newborn/anatomy &histology/growth &development/metabolism;Oligodendroglia/cytology/drug effects/*metabolism;Cell Differentiation/drug effects/physiology;Nerve Growth Factors/metabolism;Support, U.S. Gov't, P.H.S.;Amino Acid Transport System X-AG/metabolism;Mice;Astrocytes/cytology/drug effects/*metabolism;Immunohistochemistry;Bromodeoxyuridine/pharmacokinetics;Cell Division/drug effects/*physiology;Neurons/cytology/drug effects/*metabolism},
	Number = {1},
	Organization = {Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, Kentucky, USA.},
	Pages = {78-88.},
	Title = {Opioid system diversity in developing neurons, astroglia, and oligodendroglia in the subventricular zone and striatum: impact on gliogenesis in vivo},
	Uuid = {C174C104-3215-4351-9563-46D0653D403B},
	Volume = {36},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11571786}}

@article{Stockinger:2005,
	Abstract = {Male-specific fruitless (fru) products (Fru(M)) are both necessary and sufficient to "hardwire" the potential for male courtship behavior into the Drosophila nervous system. Fru(M) is expressed in approximately 2\%of neurons in the male nervous system, but not in the female. We have targeted the insertion of GAL4 into the fru locus, allowing us to visualize and manipulate the Fru(M)-expressing neurons in the male as well as their counterparts in the female. We present evidence that these neurons are directly and specifically involved in male courtship behavior and that at least some of them are interconnected in a circuit. This circuit includes olfactory neurons required for the behavioral response to sex pheromones. Anatomical differences in this circuit that might account for the dramatic differences in male and female sexual behavior are not apparent.},
	Author = {Stockinger, Petra and Kvitsiani, Duda and Rotkopf, Shay and Tiri{\'a}n, L{\'a}szl{\'o} and Dickson, Barry J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Institute of Molecular Biotechnology of the Austrian Academy of Sciences, A-1030 Vienna, Austria.},
	Pages = {795-807},
	Pii = {S0092-8674(05)00406-X},
	Pubmed = {15935765},
	Title = {Neural circuitry that governs Drosophila male courtship behavior},
	Uuid = {3A1E6911-8603-4A53-A001-586DD633A397},
	Volume = {121},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2005.04.026}}

@article{Stott:2006,
	Abstract = {In vivo application of viral vectors for gene transfer is a commonly used tool in anatomical and functional studies, as well as in development of neuroprotective and restorative strategies for therapy. Although the most common route of administration is via direct injection into the brain parenchyma in adult animals, a number of short-term studies have been performed in the developing central nervous system. Here we investigated the long-term transgene expression following in utero delivery of a retroviral vector encoding for the green fluorescent protein (GFP) marker gene at embryonic days 14.5-17.5 using an ultrasound-guided injection system. Intraparenchymal injections of the ganglionic eminence were compared with vector delivery to the intracerebroventricular space. Injections into the ganglionic eminences resulted in a predominantly unilateral transduction localized to the forebrain, giving rise to GFP-positive (GFP+) neurons and astrocytes in the striatum, olfactory bulb, cortex and hippocampus. When the vector was injected into the lateral ventricle, on the other hand, widespread expression of GFP was seen throughout the brain. The total number of GFP+ cells in the striatum was estimated to be between 20,000 and 50,000 cells using a computerized stereological quantification tool. Phenotypic characterization of these transduced cells using confocal microscopical analysis showed that 64\%were NeuN+ neurons, 14\%APC+ oligodendrocytes and 15\%glial cells labelled with GFAP, S100beta and Iba1, when the vector injection was performed at E14.5. Delivery into later embryos resulted in a reduction in neuronal profiles with a reciprocal increase in glial cells.},
	Author = {Stott, Simon R. W. and Kirik, Deniz},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Microtubule-Associated Proteins;Pregnancy;Transduction, Genetic;Animals;Gene Expression Regulation, Developmental;Rats;comparative study;Brain;Phosphopyruvate Hydratase;Female;Cell Count;Rats, Sprague-Dawley;Ki-67 Antigen;23 Technique;Retroviridae;research support, non-u.s. gov't;Green Fluorescent Proteins;Genetic Vectors;Embryo;Neuropeptides;Sialic Acids;Somatostatin;Age Factors;Neural Cell Adhesion Molecule L1;24 Pubmed search results 2008;Immunohistochemistry;Uterus},
	Month = {10},
	Nlm_Id = {8918110},
	Number = {7},
	Organization = {CNS Disease Modelling Unit, Section of Neuroscience, Department of Experimental Medical Science, Lund University, Sweden. Simon.Stott\@med.lu.se},
	Pages = {1897-906},
	Pii = {EJN5095},
	Pubmed = {17067293},
	Title = {Targeted in utero delivery of a retroviral vector for gene transfer in the rodent brain},
	Uuid = {A614A7B6-07EC-4EDF-8514-9D489739AFE5},
	Volume = {24},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2006.05095.x}}

@article{Stoye:2001,
	Abstract = {Embedded in the genomes of all vertebrates are the proviral remnants of previous retroviral infections. Although the overwhelming majority has suffered inactivating mutations, current research suggests that members of one family of human retroelements may still be capable of movement.},
	Author = {Stoye, J. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {15 ERVs retroelements;Humans;Endogenous Retroviruses;24 Pubmed search results 2008;Evolution, Molecular;Terminal Repeat Sequences;DNA, Viral;comment;15 Retrovirus mechanism;Animals;Proviruses;Recombination, Genetic;review;Virus Integration},
	Medline = {21575979},
	Month = {11},
	Nlm_Id = {9107782},
	Number = {22},
	Organization = {National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK. jstoye\@nimr.mrc.ac.uk},
	Pages = {R914-6},
	Pii = {S0960-9822(01)00553-X},
	Pubmed = {11719237},
	Title = {Endogenous retroviruses: still active after all these years?},
	Uuid = {ADFF7686-AFD5-4602-891B-286245325D63},
	Volume = {11},
	Year = {2001}}

@article{Stoye:1983,
	Abstract = {Germ line DNA from all strains of mice contains numerous endogenous retroviruses. One of these viruses, a virus with xenotropic host range is induced from lymphocytes of most strains by treatment with B cell mitogens. Virus induction is amplified by 5-bromo-2'-deoxyuridine (BrdU) treatment. We report here studies of the genetic control of retrovirus induction from lymphocytes in crosses between BALB/cTif mice and noninducible 129/Rrj mice. We identify a novel locus, Bdv-1, which controls the expression of a reverse transcriptase-positive, defective retrovirus in BALB/cTif lymphocytes. In addition, we confirm previous reports that xenotropic virus is controlled by a locus, Bxv-1, mapping to chromosome 1. The two loci are nonlinked and respond differently to inducing stimuli. Bxv-1 is induced mainly by BrdU and only marginally by mitogen; in contrast, Bdv-1 is induced by mitogen and BrdU has little effect. The induction of these two loci is discussed with respect to B cell differentiation.},
	Author = {Stoye, J. P. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0022-1007},
	Journal = {J Exp Med},
	Keywords = {23 dNTPs-Brdu;Mice, Inbred BALB C;Animals;Lymphocytes;Lipopolysaccharides;Female;15 Retrovirus mechanism;Lymphocyte Activation;RNA-Directed DNA Polymerase;23 Technique;Retroviridae;11 Glia;Male;Crosses, Genetic;Virus Activation;Retroviridae Infections;Mice;24 Pubmed search results 2008;Bromodeoxyuridine;Spleen},
	Medline = {83215084},
	Month = {5},
	Nlm_Id = {2985109R},
	Number = {5},
	Pages = {1660-74},
	Pubmed = {6189943},
	Title = {Endogenous retrovirus expression in stimulated murine lymphocytes. Identification of a new locus controlling mitogen induction of a defective virus},
	Uuid = {624D3349-27FE-48D0-8970-AF3E156BB75F},
	Volume = {157},
	Year = {1983},
	url = {papers/Stoye_JExpMed1983.pdf}}

@article{Stoye:1984,
	Abstract = {In addition to the known induction of xenotropic endogenous virus in B-mitogen-stimulated murine lymphocyte cultures, distinguishable defective viruses were also induced in different mouse strains (NFS/N, 129, BALB/c). AKR cells produced xenotropic virus and also, in contrast to BALB/c, ecotropic virus. The drug bromodeoxyuridine appeared to have differential effects on virus expression, amplifying xenotropic virus induction but inhibiting the spontaneous production of the ecotropic virus in AKR cultures and of the defective virus in NFS/N cells. Infecting stimulated BALB/c or AKR cultures with Friend leukaemia virus resulted in the production of ecotropic-xenotropic pseudotype viruses, indicating that the infecting ecotropic virus replicates in the cells in which xenotropic virus is induced. No pseudotypes or recombinants were observed following infection of spleen cells releasing defective viruses. Friend leukaemia virus and xenotropic virus with an ecotropic envelope replicated equally well in stimulated lymphocytes from the different strains examined. Taken together, these findings indicate that the non-infectious viruses are encoded by defective proviruses, rather than resulting from faulty, host cell-controlled, virus maturation.},
	Author = {Stoye, J. P. and Moroni, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0022-1317},
	Journal = {J Gen Virol},
	Keywords = {15 ERVs retroelements;Animals;Lipopolysaccharides;Species Specificity;Phenotype;Comparative Study;Cell Line;Lymphocytes;Rats;Gammaretrovirus;15 Retrovirus mechanism;Mink;Mice;Bromodeoxyuridine;24 Pubmed search results 2008;Lymphocyte Activation;Mice, Inbred Strains},
	Medline = {84113551},
	Month = {2},
	Nlm_Id = {0077340},
	Pages = {317-26},
	Pubmed = {6319577},
	Title = {Phenotypic mixing of retroviruses in mitogen-stimulated lymphocytes: analysis of xenotropic and defective endogenous mouse viruses},
	Uuid = {115EE463-75EB-4503-AA19-EC84199E9EDD},
	Volume = {65 ( Pt 2)},
	Year = {1984}}

@article{Stoye:2000,
	Author = {Stoye, J. P. and Coffin, J. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {15 ERVs retroelements;Pregnancy Proteins;Endogenous Retroviruses;24 Pubmed search results 2008;Female;Gene Products, env;Evolution, Molecular;Membrane Fusion;Placenta;Trophoblasts;comment;Pregnancy;Animals;Humans;Proviruses;15 Retrovirus mechanism;news},
	Medline = {20155452},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {6771},
	Pages = {715, 717},
	Pubmed = {10693785},
	Title = {A provirus put to work},
	Uuid = {693791A2-7637-4343-B342-1E1229596A0F},
	Volume = {403},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35001700}}

@article{Stranahan:2006,
	Abstract = {Social isolation can exacerbate the negative consequences of stress and increase the risk of developing psychopathology. However, the influence of living alone on experiences generally considered to be beneficial to the brain, such as physical exercise, remains unknown. We report here that individual housing precludes the positive influence of short-term running on adult neurogenesis in the hippocampus of rats and, in the presence of additional stress, suppresses the generation of new neurons. Individual housing also influenced corticosterone levels-runners in both housing conditions had elevated corticosterone during the active phase, but individually housed runners had higher levels of this hormone in response to stress. Moreover, lowering corticosterone levels converted the influence of short-term running on neurogenesis in individually housed rats from negative to positive. These results suggest that, in the absence of social interaction, a normally beneficial experience can exert a potentially deleterious influence on the brain.},
	Author = {Stranahan, Alexis M. and Khalil, David and Gould, Elizabeth},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {9809671},
	Number = {4},
	Organization = {Department of Psychology, Princeton University, Princeton NJ 08544.},
	Pages = {526-33},
	Pii = {nn1668},
	Pubmed = {16531997},
	Title = {Social isolation delays the positive effects of running on adult neurogenesis},
	Uuid = {15965441-45DA-426F-8B7D-C5B750F0ADBD},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1668}}

@article{Streit:2002,
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0947-6075},
	Journal = {Ernst Schering Res Found Workshop},
	Keywords = {Brain Injuries;Human;Not relevant;Alzheimer Disease;Microglia;review, tutorial;11 Glia;Animals;review;Neurons},
	Medline = {22062110},
	Nlm_Id = {9422786},
	Number = {39},
	Organization = {Department of Neuroscience, P.O. Box 100244, Building 59, University of Florida, College of Medicine, 100 Newell Drive, Gainesville, FL 32611, USA. streit\@ufbi.ufl.edu},
	Pages = {11-24},
	Pubmed = {12066409},
	Title = {Microglia and the response to brain injury},
	Uuid = {EE8FC4E7-225E-4E59-BC3A-B36BC86EF60C},
	Year = {2002}}

@article{Streit:1994,
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0937-4477},
	Journal = {Eur Arch Otorhinolaryngol},
	Keywords = {Facial Nerve;Cytokines;Rats;Nerve Regeneration;Motor Neurons;Not relevant;11 Glia;Microglia;Animals;Major Histocompatibility Complex},
	Medline = {20236131},
	Month = {12},
	Nlm_Id = {9002937},
	Organization = {Department of Neuroscience, U of F Health Service Center, University of Florida College of Medicine, Gainesville 32610-0244, USA.},
	Pages = {S69-70},
	Pubmed = {10774316},
	Title = {The role of microglia in regeneration},
	Uuid = {063BDC33-57FB-495A-8DFA-A94C1707F726},
	Year = {1994}}

@article{Streit:1989,
	Abstract = {The expression of immune-associated (MHC class II) antigen was studied immunohistochemically over several months in the rat facial nucleus after nerve transection and after intraneural injection of toxic ricin. Cells expressing Ia antigen were of a perivascular type and parenchymal ramified microglia. In the first few weeks after nerve lesions we observed a gradual increase in the number of Ia-immunoreactive cells starting with an initial appearance of Ia-positive perivascular cells which were succeeded by increasing numbers of Ia-positive ramified microglia. In long-term animals Ia expression was almost exclusively found in microglia. We propose (a) the existence of a population of immunocompetent perivascular cells normally present in adult rat brain that can be stimulated to express Ia antigen, and (b) the existence of a subpopulation of ramified microglia that arises through transformation of Ia-positive perivascular cells in the adult under pathological conditions.},
	Author = {Streit, W. J. and Graeber, M. B. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Reference Values;Neuroglia;Motor Neurons;Nerve Regeneration;Nerve Degeneration;Rats;Histocompatibility Antigens Class II;Facial Nerve;Time Factors;Cell Survival;11 Glia;Not relevant;Denervation;Animals;Brain;Rats, Inbred Strains},
	Medline = {89325514},
	Month = {8},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Neuromorphology, Max Planck Institute for Psychiatry, Martinsried, Federal Republic of Germany.},
	Pages = {115-26},
	Pubmed = {2753113},
	Title = {Expression of Ia antigen on perivascular and microglial cells after sublethal and lethal motor neuron injury},
	Uuid = {B141CD81-502A-4FA0-9DA4-72057B4DDD6A},
	Volume = {105},
	Year = {1989}}

@article{Streit:1988,
	Abstract = {The present review summarizes recently acquired data in vivo, which support a role of CNS microglia as a source of defense cells in the CNS capable of carrying out certain immune functions autonomously. We have kept the following discussion restricted to microglial cells and have not included work on the immunological functions of astrocytes, which has been recently reviewed elsewhere (Fontana et al.: Immunological Reviews 137:3521-3527, 1987). Resting microglia are scattered uniformly throughout the CNS forming a network of potential immunoeffector cells, which can be activated by stimuli ranging from peripheral nerve injury over viral infections to direct mechanical brain trauma. The term "activated microglia" is used here to describe proliferating cells that demonstrate changes in their immunophenotype but have not undergone transformation into brain macrophages. Such a transformation can be stimulated by neuronal death but not by sublethal neuronal injury. Microglia may function as antigen-presenting cells and may thus represent the effector cell responsible for the recruitment of lymphocytes to the brain resulting in an inflammatory reaction. The recent developments in the understanding of microglial cell function may lead to a redefinition of the often cited "immune privilege" of the brain.},
	Author = {Streit, W. J. and Graeber, M. B. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Neuroglia;Human;Neuroimmunomodulation;Not relevant;11 Glia;Antigen-Presenting Cells;Macrophages;review, tutorial;Animals;Brain;Humans;review;Axons},
	Medline = {89154609},
	Nlm_Id = {8806785},
	Number = {5},
	Organization = {Department of Neuromorphology, Max Planck Institute of Psychiatry, Martinsried, Federal Republic of Germany.},
	Pages = {301-7},
	Pubmed = {2976393},
	Title = {Functional plasticity of microglia: a review},
	Uuid = {543D5E72-FB86-4332-A76B-AA39BA9B0DA5},
	Volume = {1},
	Year = {1988}}

@article{Streit:1993,
	Abstract = {We reflect here on the development of a neuroimmunological concept which has been formulated over the past 5 years through studying microglial cell responses in the facial nerve system. A simple axotomy of the adult rat facial nerve which causes regeneration of facial motor neurons and little, if any, cell death can activate microglial cells just as easily as a full-blown degeneration of the entire nucleus induced by toxic ricin. In both instances, the prompt microglial reaction is characterized by a series of structural and phenotypic changes which are in many ways similar to an immune response, e.g., there is cell proliferation and upregulation of MHC antigens. However, since white blood cells do not participate in the retrograde response of facial motor neurons, we have adopted a notion which views microglia as a CNS-wide network of immunocompetent cells whose morphological dissimilarities from leukocytes are a result of their unique adaptation to the CNS architecture. We have continued our in vivo investigations of the phagocytic and immunophenotypic properties of microglial and perivascular cells during the retrograde reaction of facial motor neurons by using intra-neural injections of fluorogold (FG) and ricin followed by lectin and immunostaining for microglia. Two new findings can be added to the microglial neuroimmune network: (1) Microglia take up FG only after motor neuron degeneration, whereas perivascular cells may take up FG under nondegenerating conditions. (2) Immunologically important molecules, such as MHC class II, CD4, and leukocyte common antigens, are expressed by different microglial subpopulations. Thus there is functional and phenotypic heterogeneity among immunocompetent cells of the CNS.},
	Author = {Streit, W. J. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Neuroglia;Facial Nerve;Antigens;Lectins;Not relevant;Denervation;Plant Lectins;11 Glia;review, tutorial;Blood Vessels;Injections;Animals;review;Axons},
	Medline = {93138746},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida, Gainesville 32610.},
	Pages = {68-74},
	Pubmed = {8423064},
	Title = {Heterogeneity of microglial and perivascular cell populations: insights gained from the facial nucleus paradigm},
	Uuid = {9B7A7571-3081-45D7-B136-90667365E8FD},
	Volume = {7},
	Year = {1993}}

@article{Streit:2002a,
	Abstract = {The role of glial cells is to support and sustain proper neuronal function and microglia are no exception to this. This viewpoint article emphasizes the fundamental interdependence of microglia and neurons and takes a look at the possibility of what could happen if microglial cells became dysfunctional as a result of aging, genetics, or epigenetics. Could microglial senescence be a factor in the pathogenesis of Alzheimer's and other neurodegenerative diseases? The cautious answer to that question is 'yes'. Future studies along these lines may provide novel insights into microglial involvement in neurodegenerative disease pathogenesis.},
	Author = {Streit, Wolfgang J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Endothelium, Vascular;Neuroglia;Central Nervous System;Interleukins;Endocrine System;Cytokines;Human;Signal Transduction;Not relevant;Chemokines;11 Glia;Microglia;review, tutorial;Animals;review;Neurons},
	Medline = {22267059},
	Month = {11},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Neuroscience, University of Florida College of Medicine and McKnight Brain Institute, Gainesville, Florida 32611, USA. streit\@mbi.ufl.edu},
	Pages = {133-9},
	Pubmed = {12379901},
	Title = {Microglia as neuroprotective, immunocompetent cells of the CNS},
	Uuid = {852A2CEC-B241-44B3-B5BC-6675C54FD470},
	Volume = {40},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10154}}

@article{Streit:2004a,
	Abstract = {We have studied microglial morphology in the human cerebral cortex of two nondemented subjects using high-resolution LN-3 immunohistochemistry. Several abnormalities in microglial cytoplasmic structure, including deramification, spheroid formation, gnarling, and fragmentation of processes, were identified. These changes were determined to be different from the morphological changes that occur during microglial activation and they were designated collectively as microglial dystrophy. Quantitative evaluation of dystrophic changes in microglia revealed that these were much more prevalent in the older subject (68-year-old) than in the younger one (38-year-old). Thus, we conclude that microglial dystrophy is a sign of microglial cell senescence. We hypothesize that microglial senescence could be important for understanding age-related declines in cognitive function.},
	Author = {Streit, Wolfgang J. and Sammons, Nicole W. and Kuhns, Amanda J. and Sparks, D. Larry},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Aging;Cognition Disorders;Aged;Adult;Immunohistochemistry;Cell Aging;Human;Not relevant;Biological Markers;Atrophy;11 Glia;Microglia;Oligosaccharides;Male;Cerebral Cortex},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Neuroscience, PO Box 100244, University of Florida College of Medicine, Building 59, 100 Newell Drive, Gainesville, FL 32610, USA. streit\@mbi.ufl.edu},
	Pages = {208-12},
	Pubmed = {14730714},
	Title = {Dystrophic microglia in the aging human brain},
	Uuid = {4B6FD6C0-C06C-4DBE-A3ED-FD1A1F4015BE},
	Volume = {45},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10319}}

@article{Streit:1993a,
	Abstract = {The question of whether activated microglial cells are potentially harmful or beneficial to injured central nervous system neurons is being addressed by examining in vivo and in vitro findings. While observations made in vivo suggest that microglial activation is triggered by injured neurons and may aid in regeneration, in vitro data show production of neurotoxic agents by cultured microglia. An effort is made to find a common denominator in these apparently conflicting findings by discussing microglial activation during motor neuron regeneration and during delayed neuronal death occurring as a consequence of global forebrain ischemia.},
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0891-0618},
	Journal = {J Chem Neuroanat},
	Keywords = {Cell Communication;Hippocampus;Models, Neurological;Get paper from library;11 Glia;Microglia;review, tutorial;Spinal Cord;Cells, Cultured;Brain;Animals;Neurons;review},
	Medline = {94000514},
	Nlm_Id = {8902615},
	Number = {4},
	Organization = {Department of Neuroscience, University of Florida, Gainesville 32610.},
	Pages = {261-6},
	Pubmed = {8397924},
	Title = {Microglial-neuronal interactions},
	Uuid = {6A2FC7F4-983A-4EDD-8FB3-A8726C557A03},
	Volume = {6},
	Year = {1993}}

@article{Streit:1988a,
	Abstract = {The injection of toxic lectin from Ricinus communis into the rat facial nerve resulted in suicide transport and rapid degeneration of facial motor neurons. The reaction of glial cells to neuronal death in comparison with nerve crush lesions was studied by using lectin-HRP conjugates derived from Griffonia simplicifolia for the selective staining of microglial cells at both light and electron microscopic levels. In addition, the proliferative activity of microglia was assessed by quantification of 3H-thymidine incorporation. The astrocytic response was evaluated by light microscopic immunocytochemistry for glial fibrillary acidic protein. In the degenerating facial nucleus local microglial cells responded by rapid proliferation and phagocytosis of neuronal debris. After nerve crush, no phagocytes were observed, but microglial proliferation and perineuronal satellitosis were prominent. The astrocytic expression of glial fibrillary acidic protein in response to nerve crush proceeded gradually over a period of several weeks after which it declined, contrasting with accelerated astrocytic hypertrophy and permanent glial scarring after neuronal degeneration. These results show that the expression of glial fibrillary acidic protein by fibrous astrocytes is intensified after lethal neuronal injury compared to sublethal insults. In the absence of any observations indicating participation of hematogenous elements, it is proposed that local microglial cells transform into brain macrophages.},
	Author = {Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Ricin;Neuroglia;Facial Nerve;Nerve Degeneration;Motor Neurons;Rats;Not relevant;Cell Division;Cell Survival;11 Glia;Nerve Crush;Animals;Rats, Inbred Strains},
	Medline = {88198671},
	Month = {2},
	Nlm_Id = {0406041},
	Number = {2},
	Organization = {Department of Neuromorphology, Max Planck Institute of Psychiatry, Martinsried n. Munich, Federal Republic of Germany.},
	Pages = {248-63},
	Pubmed = {3360987},
	Title = {Response of endogenous glial cells to motor neuron degeneration induced by toxic ricin},
	Uuid = {5FF02678-1890-4EB5-ACA3-043CA29F2F5A},
	Volume = {268},
	Year = {1988}}

@article{Streit:1990,
	Abstract = {A simple method for the lectin histochemical visualization of rat microglial cells is described. Advantages include ease of fixation of brain tissue using paraformaldehyde, and rapidity of tissue processing by vibratome sectioning. Furthermore, in addition to providing good structural preservation, the method achieves improved lectin binding, resulting in complete labeling of all microglial cells and in superior visualization of cellular processes. The lectin histochemical technique for rat microglia has the potential to be adapted to any mammalian species, and should prove valuable for neuroscientists interested in studying this glial cell type.},
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0022-1554},
	Journal = {J Histochem Cytochem},
	Keywords = {Neuroglia;Rats;Lectins;Not relevant;11 Glia;Spinal Cord;Histocytochemistry;Male;Brain;Rats, Inbred Strains;Animals},
	Medline = {91010649},
	Month = {11},
	Nlm_Id = {9815334},
	Number = {11},
	Organization = {Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610.},
	Pages = {1683-6},
	Pubmed = {2212623},
	Title = {An improved staining method for rat microglial cells using the lectin from Griffonia simplicifolia (GSA I-B4)},
	Uuid = {491054E2-FCDC-4E58-8615-31F149C99443},
	Volume = {38},
	Year = {1990}}

@article{Streit:1997,
	Abstract = {Activated microglial cells are concentrated in senile plaques characteristic of Alzheimer's disease. Such accumulations of activated microglia may contribute towards neurodegeneration via production of cytokines and free radicals. Studies suggesting a link between Alzheimer's disease and heart disease led us to study microglia immunohistochemically, using monoclonal antibody LN-3, in age-matched nondemented humans with and without heart disease. Using a qualitative staging system for assessing morphological changes occurring in microglia, we found higher microglial activation in the brains of subjects with heart disease than in those without it. Lectin histochemical examination of brains from rabbits maintained on a high-cholesterol diet also revealed increased microglial activation and leukocyte infiltration. Collectively our observations from humans and rabbits suggest that hypercholesterolemia and heart disease accelerate brain aging, and that the formation of senile plaques may be the end result of progressive microglial activation that occurs with aging.},
	Author = {Streit, W. J. and Sparks, D. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0946-2716},
	Journal = {J Mol Med},
	Keywords = {Aging;Aged;Human;Immunohistochemistry;Heart Diseases;Not relevant;Alzheimer Disease;Hypercholesterolemia;Middle Aged;Rabbits;Microglia;Animals;Brain;11 Glia},
	Medline = {97237452},
	Month = {2},
	Nlm_Id = {9504370},
	Number = {2},
	Organization = {Department of Neuroscience, University of Florida Brain Institute, Gainesville 32610-0244, USA.},
	Pages = {130-8},
	Pubmed = {9083930},
	Title = {Activation of microglia in the brains of humans with heart disease and hypercholesterolemic rabbits},
	Uuid = {0A5C01E1-FB37-4E55-8863-45A05944D8EB},
	Volume = {75},
	Year = {1997}}

@article{Streit:1987,
	Abstract = {Conjugates of the B4 isolectin from Griffonia simplicifolia seeds and horseradish peroxidase were used as a histochemical reagent for the specific visualization of microglial cells in the rat CNS. Resident microglia bearing galactose-containing glycoconjugates were stained throughout the brainstem and cerebellum. In the first week following axotomy of the facial nerve, a profound and rapid accumulation of reactive microglia, as evidenced by increasing lectin reactivity, was seen to take place in the facial nucleus. Light microscopy of paraffin sections demonstrated binding of lectin-horseradish peroxidase conjugates to microglial cytoplasmic processes. When ultrastructural cytochemistry was performed, reaction product was found localized on microglial plasma membranes, as well as on intracytoplasmic membranes. The glial reaction to axotomy was studied further with double labelling of microglia and astrocytes by lectin histochemistry and immunostaining for glial fibrillary acidic protein, respectively. Our results demonstrated the presence of membrane-associated glycoconjugates containing terminal alpha-D-galactose residues on microglia, but not on other glial cell types. The possible nature and function of these glycoconjugates are discussed.},
	Author = {Streit, W. J. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {G;Brain Stem;Neuroglia;Binding Sites;Carbohydrates;Rats;Microscopy, Electron;Lectins;Not relevant;11 Glia;Histocytochemistry;Animals;Male;Horseradish Peroxidase;Rats, Inbred Strains;Support, Non-U.S. Gov't},
	Medline = {87310543},
	Month = {4},
	Nlm_Id = {0364620},
	Number = {2},
	Pages = {249-60},
	Pubmed = {3625239},
	Title = {Lectin binding by resting and reactive microglia},
	Uuid = {FAC8D6E0-E092-11DA-9DD9-000D9346EC2A},
	Volume = {16},
	Year = {1987}}

@article{Streit:1989a,
	Abstract = {Proliferation of central nervous system (CNS) glia in response to peripheral nerve injury occurs without apparent participation of cells of the immune system. It is shown here that following transection of the rat facial nerve there is strongly elevated expression of class I, and to a lesser extent, class II antigens of the major histocompatibility complex (MHC) in the facial nucleus. It is demonstrated by double-immunofluorescence studies that the cells responsible for increased levels of MHC class I antigens are endogenous brain microglia. These findings emphasize the thought that microglia are immunocompetent cells, but, at the same time, raise the possibility for a non-immunological function of MHC antigens under conditions of neural regeneration.},
	Author = {Streit, W. J. and Graeber, M. B. and Kreutzberg, G. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Neuroglia;Facial Nerve;Immunohistochemistry;Histocompatibility Antigens Class II;Rats;Not relevant;Biological Markers;11 Glia;Histocompatibility Antigens Class I;Animals;Male;Brain;Rats, Inbred Strains},
	Medline = {89109521},
	Month = {2},
	Nlm_Id = {8109498},
	Number = {2-3},
	Organization = {Department of Neuromorphology, Max Planck Institute of Psychiatry, Martinsried, F.R.G.},
	Pages = {117-23},
	Pubmed = {2913044},
	Title = {Peripheral nerve lesion produces increased levels of major histocompatibility complex antigens in the central nervous system},
	Uuid = {3CE2FC37-F898-482D-A7FB-29412A6B15AB},
	Volume = {21},
	Year = {1989}}

@article{Streit:2004,
	Abstract = {Microglia make up the innate immune system of the central nervous system and are key cellular mediators of neuroinflammatory processes. Their role in central nervous system diseases, including infections, is discussed in terms of a participation in both acute and chronic neuroinflammatory responses. Specific reference is made also to their involvement in Alzheimer's disease where microglial cell activation is thought to be critically important in the neurodegenerative process.},
	Author = {Streit, and Mrak, and Griffin,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1742-2094},
	Journal = {J Neuroinflammation},
	Keywords = {Not relevant;11 Glia},
	Month = {7},
	Nlm_Id = {101222974},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida College of Medicine, P,O, Box 100244, Gainesville, Florida 32610, USA. streit\@mbi.ufl.edu},
	Pages = {14},
	Pii = {1742-2094-1-14},
	Pubmed = {15285801},
	Title = {Microglia and neuroinflammation: a pathological perspective},
	Uuid = {1FD141C6-DC56-4E2C-911A-E37542B17397},
	Volume = {1},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1742-2094-1-14}}

@article{Streit:2000,
	Abstract = {Using reverse transcription polymerase chain reaction (RT-PCR), we have studied the temporal expression of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), transforming growth factor-beta 1 (TGF-beta 1), and tumor necrosis factor-alpha (TNF-alpha) mRNAs in three axotomy paradigms with distinct functional outcomes. Axotomy of adult rat facial motoneurons results in neuronal regeneration, axotomy of neonatal facial motoneurons results in neuronal apoptosis, and axotomy of rubrospinal neurons results in neuronal atrophy. Our RT-PCR findings show that a significant and sustained upregulation of IL-6 mRNA is associated uniquely with the regeneration of adult facial motoneurons. Histochemical studies using IL-6 immunohistochemistry show intense IL-6 immunoreactivity in axotomized adult facial motoneurons. Assessment of reactive glial changes with astroglial and microglial markers reveals that the reactive gliosis following adult facial nerve axotomy is more intense than that observed in either of the other two paradigms. Exposure of cultured microglial cells to IL-6 stimulates microglial proliferation in a dose-dependent manner. Cultured microglia also show expression of IL-6 receptor mRNA, as determined by RT-PCR. Our findings support the idea that reactive gliosis is required for neuron regeneration to occur, and more specifically, they suggest that neuron-derived IL-6 serves as a signalling molecule that induces microglial proliferation during motoneuron regeneration.},
	Author = {Streit, W. J. and Hurley, S. D. and McGraw, T. S. and Semple-Rowland, S. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Tumor Necrosis Factor;Nerve Degeneration;Signal Transduction;Animals;Rats;Transforming Growth Factor beta;Comparative Study;Microglia;Female;Cell Communication;Rats, Wistar;Not relevant;11 Glia;RNA, Messenger;Male;Nerve Regeneration;Receptors, Interleukin-6;Support, Non-U.S. Gov't;Neurons;Axotomy;Interleukin-1;Support, U.S. Gov't, P.H.S.;Gliosis;Age Factors;Cell Division;Interleukin-6;Facial Nerve;Lectins;Gene Expression},
	Medline = {20321007},
	Month = {7},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida College of Medicine and Brain Institute, Gainesville 32611, Florida, USA. streit\@ufbi.ufl.edu},
	Pages = {10-20},
	Pii = {10.1002/1097-4547(20000701)61:1<10::AID-JNR2>3.0.CO;2-E},
	Pubmed = {10861795},
	Title = {Comparative evaluation of cytokine profiles and reactive gliosis supports a critical role for interleukin-6 in neuron-glia signaling during regeneration},
	Uuid = {43892833-7542-4488-B497-5E8ED2645EE5},
	Volume = {61},
	Year = {2000}}

@article{Streit:2004b,
	Abstract = {The most visible and, until very recently, the only hypothesis regarding the involvement of microglial cells in Alzheimer's disease (AD) pathogenesis is centered around the notion that activated microglia are neurotoxin-producing immune effector cells actively involved in causing the neurodegeneration that is the cause for AD dementia. The concept of detrimental neuroinflammation has gained a strong foothold in the AD arena and is being expanded to other neurodegenerative diseases. This review takes a comprehensive and critical look at the overall evidence supporting the neuroinflammation hypothesis and points out some weaknesses. The current work also reviews evidence for an alternative theory, the microglial dysfunction hypothesis, which, although eliminating some of the shortcomings, does not necessarily negate the amyloid/neuroinflammation theory. The microglial dysfunction theory offers a different perspective on the identity of activated microglia and their role in AD pathogenesis taking into account the most recent insights gained from studying basic microglial biology.},
	Author = {Streit, Wolfgang J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Amyloid beta-Protein;Encephalitis;Neurofibrillary Tangles;Cell Aging;Human;Neurotoxins;Models, Neurological;Gliosis;Alzheimer Disease;Microglia;review, tutorial;11 Glia;Not relevant;Animals;review},
	Month = {7},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida College of Medicine, Gainesville, Florida 32610-0244, USA. streit\@mbi.ufl.edu},
	Pages = {1-8},
	Pubmed = {15197750},
	Title = {Microglia and Alzheimer's disease pathogenesis},
	Uuid = {F13FB3E2-F91B-4EF5-82FC-A6FAD9F0BA31},
	Volume = {77},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20093}}

@article{Streit:2001,
	Abstract = {In recent years, increasing attention has been focused on chemokines as inflammatory mediators in the CNS. The limited number of studies that have investigated chemokine and chemokine receptor expression in Alzheimer's disease (AD) brain and in cell culture models seem to support a role for inflammation in AD pathogenesis. Here we provide a review of these studies, but in addition, point out the possible role of chemokines as communication molecules between neurons and microglia. Understanding neuron-microglia interactions is essential for understanding AD pathogenesis, and disturbances in chemokine-mediated intercellular communication may contribute toward a generalized impairment of microglial cell function.},
	Author = {Streit, W. J. and Conde, J. R. and Harrison, J. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0197-4580},
	Journal = {Neurobiol Aging},
	Keywords = {Human;Not relevant;Chemokines;Alzheimer Disease;Microglia;review, tutorial;11 Glia;Brain Chemistry;review},
	Medline = {21630088},
	Nlm_Id = {8100437},
	Number = {6},
	Organization = {Department of Neuroscience, University of Florida College of Medicine and McKnight Brain Institute, Gainesville, FL 32611, USA. streit\@ufbi.ufl.edu},
	Pages = {909-13},
	Pii = {S0197458001002901},
	Pubmed = {11754998},
	Title = {Chemokines and Alzheimer's disease},
	Uuid = {046ADE1C-B3DB-440C-A352-AFA227CB3A04},
	Volume = {22},
	Year = {2001}}

@article{Streit:1994a,
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Glioma;Rats;Human;Phenotype;Not relevant;11 Glia;Microglia;Transforming Growth Factor beta;Brain Neoplasms;Animals;Immunity, Cellular;Major Histocompatibility Complex},
	Medline = {94352547},
	Month = {4},
	Nlm_Id = {7609829},
	Number = {2},
	Organization = {Department of Neuroscience, University of Florida, Gainesville 32610.},
	Pages = {205-6},
	Pubmed = {8072665},
	Title = {Cellular immune response in brain tumors},
	Uuid = {6B8518E3-6DF8-4BC3-93EA-D67BCA55BCB9},
	Volume = {20},
	Year = {1994}}

@article{Streit:1992,
	Abstract = {Delayed neuronal death induced by transient forebrain ischemia in the rat hippocampus is preceded by a prominent microglial reaction which begins within minutes after the ischemic injury. In the present study we have examined the effect of the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 on microglial activation and neuronal survival. Using lectin histochemistry to detect microglia, we show that the systemic administration of MK-801 prior to ischemia prevents microglial activation, as well as delayed death of CA1 pyramidal neurons. The results demonstrate that early blockage of the glutamate cascade prevents microglial activation, and could suggest a role for microglia in mediating ischemic injury.},
	Author = {Streit, W. J. and Morioka, T. and Kalehua, A. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0959-4965},
	Journal = {Neuroreport},
	Keywords = {Hippocampus;Rats;Female;Not relevant;11 Glia;Mesoderm;Prosencephalon;Receptors, N-Methyl-D-Aspartate;Animals;Rats, Inbred Strains;Ischemic Attack, Transient;Dizocilpine Maleate},
	Medline = {92322929},
	Month = {2},
	Nlm_Id = {9100935},
	Number = {2},
	Organization = {Department of Neuroscience, University of Florida, Gainesville 32610.},
	Pages = {146-8},
	Pubmed = {1535800},
	Title = {MK-801 prevents microglial reaction in rat hippocampus after forebrain ischemia},
	Uuid = {D99BF86D-75DC-4B65-8D0F-941426FF8120},
	Volume = {3},
	Year = {1992}}

@article{Streit:1996,
	Abstract = {Microglial cells are exquisitely sensitive to neuronal damage. Neurons which have been damaged by an injury or a neurotoxicant will stimulate microglia in their immediate vicinity to become activated and undergo a series of morphologic and phenotypic changes. The changes occurring on microglial cells can be documented quite readily using histochemical methods, and it is suggested that the histological demonstration of microglial activation can serve as a very sensitive biological marker for neuron damage. While the functional significance of microglial activation is unknown, there is evidence to suggest that microglia may exert both neurotrophic and neurotoxic effects. However, proving that these functions are indeed carried out by microglia in vivo remains a formidable challenge for future investigations.},
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0161-813X},
	Journal = {Neurotoxicology},
	Keywords = {Nerve Degeneration;Not relevant;11 Glia;Microglia;review, tutorial;Animals;Brain Injuries;review},
	Medline = {97241088},
	Nlm_Id = {7905589},
	Number = {3-4},
	Organization = {Department of Neuroscience, University of Florida, Gainesville 32610, USA.},
	Pages = {671-8},
	Pubmed = {9086488},
	Title = {The role of microglia in brain injury},
	Uuid = {97F8632E-714B-4C9F-9E91-4C0DC0D80BCA},
	Volume = {17},
	Year = {1996}}

@article{Streit:2001a,
	Abstract = {An understanding of microglial functions during normal CNS development is prerequisite for understanding developmental neurotoxicology. This review provides a brief summary of previous work regarding the origin of microglia and addresses differences and similarities between microglia and brain macrophages. Current concepts and ideas which implicate microglia in diverse developmental processes, such as apoptosis, axon growth, and vasculogenesis are discussed. The study of reactive microgliosis may prove useful in the histopathological analysis of neurotoxicant-induced brain damage during development.},
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0161-813X},
	Journal = {Neurotoxicology},
	Keywords = {Central Nervous System;Comparative Study;Human;Not relevant;11 Glia;Microglia;Macrophages;review, tutorial;Animals;review},
	Medline = {21626810},
	Month = {10},
	Nlm_Id = {7905589},
	Number = {5},
	Organization = {Department of Neuroscience, University of Florida College of Medicine and McKnight Brain Institute, Gainesville 32611, USA. streit\@ufbi.ufl.edu},
	Pages = {619-24},
	Pubmed = {11770883},
	Title = {Microglia and macrophages in the developing CNS},
	Uuid = {D100E2D1-37E7-43DD-8014-D27C2C6C4316},
	Volume = {22},
	Year = {2001}}

@article{Streit:1996a,
	Author = {Streit, W. J. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0079-6336},
	Journal = {Prog Histochem Cytochem},
	Keywords = {Aging;Adult;Human;Infection;Regeneration;Not relevant;11 Glia;Microglia;review, tutorial;Humans;Animals;Central Nervous System Diseases;review},
	Medline = {97048470},
	Nlm_Id = {0253725},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida Brain Institute Gainesville 32610, USA.},
	Pages = {1-89},
	Pubmed = {8893306},
	Title = {Microglia: a pictorial},
	Uuid = {A7A07CDA-C1F9-4FEE-892B-30F7483D9929},
	Volume = {31},
	Year = {1996}}

@article{Streit:1999,
	Abstract = {Damage to the central nervous system (CNS) elicits the activation of both astrocytes and microglia. This review is focused on the principal features that characterize the activation of microglia after CNS injury. It provides a critical discussion of concepts regarding microglial biology that include the relationship between microglia and macrophages, as well as the role of microglia as immunocompetent cells of the CNS. Mechanistic and functional aspects of microgliosis are discussed primarily in the context of microglial neuronal interactions. The controversial issue of whether reactive microgliosis is a beneficial or a harmful process is addressed, and a resolution of this dilemma is offered by suggesting different interpretations of the term 'activated microglia' depending on its usage during in vivo or in vitro experimentation.},
	Author = {Streit, W. J. and Walter, S. A. and Pennell, N. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0301-0082},
	Journal = {Prog Neurobiol},
	Keywords = {Neurons;Cell Communication;review, academic;Human;Gliosis;Not relevant;11 Glia;Microglia;Animals;review;Immunocompetence},
	Medline = {99236971},
	Month = {4},
	Nlm_Id = {0370121},
	Number = {6},
	Organization = {Department of Neuroscience, University of Florida College of Medicine and Brain Institute, Gainesville 32610, USA. streit\@ufbi.ufl.edu},
	Pages = {563-81},
	Pii = {S0301008298000690},
	Pubmed = {10221782},
	Title = {Reactive microgliosis},
	Uuid = {108CE8D3-7786-4625-89D3-97E8B0B9BA1F},
	Volume = {57},
	Year = {1999}}

@article{Streit:1995,
	Author = {Streit, W. J. and Kincaid-Colton, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0036-8733},
	Journal = {Sci Am},
	Keywords = {Cytokines;Human;AIDS Dementia Complex;Immunity;Not relevant;Alzheimer Disease;Microglia;Down Syndrome;review, tutorial;11 Glia;Brain;review},
	Medline = {97113064},
	Month = {11},
	Nlm_Id = {0404400},
	Number = {5},
	Organization = {University of Florida Brain Institute, USA.},
	Pages = {54-5, 58-61},
	Pubmed = {8966536},
	Title = {The brain's immune system},
	Uuid = {2181400D-779F-406C-8A16-03258FF63EAE},
	Volume = {273},
	Year = {1995}}

@article{Streit:2000a,
	Abstract = {In addition to astrocytes and oligodendrocytes, microglia represent the third major population of glial cells within the central nervous system (CNS). Microglia are distributed ubiquitously throughout the brain and spinal cord, and one of their main functions is to monitor and sustain neuronal health. Microglial cells are quite sensitive to even minor disturbances in CNS homeostasis, and they become readily activated during most neuropathologic conditions, including peripheral nerve injury, trauma and stroke, inflammatory disease, and neurotoxicant-induced neuronal injury. During activation, microglia display conspicuous functional plasticity, which involves changes in cell morphology, cell number, cell surface receptor expression, and production of growth factors and cytokines. The many changes occurring in activated cells reflect the altered functional states of microglia that are induced by signals arising from injured neurons. Thus, neuronal-microglial signaling plays a fundamental role in understanding how the CNS responds to injury. Reactive microgliosis should be viewed as a cellular effort to initiate ameliorative and reparative measures in the injured brain.},
	Author = {Streit, W. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0192-6233},
	Journal = {Toxicol Pathol},
	Keywords = {Human;Gliosis;Not relevant;11 Glia;Microglia;review, tutorial;Animals;Brain Injuries;review},
	Medline = {20132471},
	Nlm_Id = {7905907},
	Number = {1},
	Organization = {Department of Neuroscience, University of Florida College of Medicine and Brain Institute, Gainesville 32610-0244, USA. streit\@ufbi.ufl.edu},
	Pages = {28-30},
	Pubmed = {10668987},
	Title = {Microglial response to brain injury: a brief synopsis},
	Uuid = {3C6F6228-8000-4D04-9959-A7C6D499306C},
	Volume = {28},
	Year = {2000}}

@article{Strizki:1997,
	Abstract = {We used a monoclonal antibody (12G5) directed against an extracellular domain of CXCR-4 to investigate the role of this receptor in infection of immortalized lymphoid cell lines, peripheral blood mononuclear cells (PBMCs), and primary brain microglia with a dual-tropic strain of human immunodeficiency virus (HIV-1(89.6)) and a T-tropic strain (HIV-1(IIIB)). Addition of antibody 12G5 to cells prior to and during infection with HIV-1(89.6) inhibited p24 production 100- to 10,000-fold in CEMx174 and 174-CD4 cells and about 10-fold in PBMC cultures but had no activity against infection of either monocyte-derived macrophages or brain microglia. In contrast, 12G5 had little or no effect on infection of CEMx174 cells with HIV-1(IIIB) or HIV-1(HxB). To identify the region of the HIV-1(89.6) envelope that confers sensitivity to 12G5, we used chimeric molecular clones. Chimeras containing the V3 loop region of HIV-1(89.6) were inhibited by 12G5 to the same degree as wild-type HIV-1(89.6) whereas replication of those viruses containing the V3 loop of HIV-1(HxB) was not inhibited by the antibody. A similar pattern was seen in infections of a U87 glioblastoma line that coexpresses CD4 and CXCR-4. Antibody 12G5 was also able to block fusion between HeLa-CD4 cells and CEMx174 cells chronically infected with HIV-1(89.6) but had no effect on fusion mediated by cells chronically infected with HIV-1(IIIB). Taken together, these results suggest that different strains of HIV-1 may interact with different sites on CXCR-4 or may have different binding affinities for the coreceptor.},
	Author = {Strizki, J. M. and Turner, J. D. and Collman, R. G. and Hoxie, J. and Gonz{\'a}lez-Scarano, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {T-Lymphocytes;Receptors, CXCR4;HIV-1;Humans;Cells, Cultured;Microglia;Receptors, HIV;Cell Fusion;Antigens, CD4;11 Glia;Hela Cells;Cell Line;Research Support, U.S. Gov't, P.H.S.;Peptide Fragments;Antibodies, Monoclonal;Tumor Cells, Cultured;HIV Core Protein p24;Membrane Proteins;HIV Envelope Protein gp120},
	Medline = {97332414},
	Month = {7},
	Nlm_Id = {0113724},
	Number = {7},
	Organization = {Department of Neurology and Microbiology, University of Pennsylvania Medical Center, Philadelphia 19104-6146, USA.},
	Pages = {5678-83},
	Pubmed = {9188648},
	Title = {A monoclonal antibody (12G5) directed against CXCR-4 inhibits infection with the dual-tropic human immunodeficiency virus type 1 isolate HIV-1(89.6) but not the T-tropic isolate HIV-1(HxB)},
	Uuid = {319AEF9D-2CC3-4CBF-AF69-FB2E41571557},
	Volume = {71},
	Year = {1997}}

@article{Struble:2001,
	Abstract = {Olfactory receptor neurons can regenerate from basal stem cells. Receptor neuron lesion causes degenerative changes in the olfactory bulb followed by regeneration as new olfactory receptor axons innervate the olfactory bulb. To our knowledge, parametric analyses of morphometric changes in the olfactory bulb during degeneration and regeneration do not exist except in abstract form. To better characterize olfactory bulb response, we performed morphometric analysis in rats following reversible olfactory nerve lesion with diethyldithiocarbamate. We also performed anterograde tracing of the olfactory nerve with wheatgerm agglutinin linked to horseradish peroxidase. Results of morphometry and tracing were complementary. The glomerular layer and external plexiform layer showed shrinkage of 45 and 26\%, respectively, at 9 days. No significant shrinkage occurred in any other layer. Individual glomeruli shrank by 40-50\%at 3 and 9 days following lesion. These data show that degenerative changes occur both in the glomeruli and transneuronally in the external plexiform layer. Olfactory nerve regeneration (identified by WGA-HRP transport) paralleled volumetric recovery. Recovery occurred first in ventral and lateral glomeruli between 9 and 16 days followed by recovery in medial and dorsal glomeruli. These data indicate substantial transynaptic degeneration in the olfactory bulb and a heretofore unrecognized gradient in olfactory nerve regeneration that can be used to systematically study recovery of a cortical structure.},
	Author = {Struble, R. G. and Beckman, S. L. and Fesser, E. and Nathan, B. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {Chem Senses},
	Keywords = {I pdf;13 Olfactory bulb anatomy},
	Number = {8},
	Organization = {Center for Alzheimer Disease and Related Disorders, PO Box 19682, Southern Illinois University School of Medicine, Springfield, IL 62794, USA. Department of Biological Sciences, Eastern Illinois University, Charleston, IL 61920, USA.},
	Pages = {971-81.},
	Title = {Volumetric and horseradish peroxidase tracing analysis of rat olfactory bulb following reversible olfactory nerve lesions},
	Uuid = {CDCE0028-60A1-4399-B30D-40B5C894ADC2},
	Volume = {26},
	Year = {2001},
	url = {papers/Struble_ChemSenses2001}}

@article{Stuckmann:2001,
	Abstract = {To identify molecules involved in neurogenesis, we have raised monoclonal antibodies against embryonic day 12.5 mouse telencephalon. One antibody, monoclonal antibody 25H11, stains predominantly the ventricular zone of the anterior and lateral telencephalon. Purification of the 25H11 antigen, a 47 kDa integral membrane protein, from approximately 2500 mouse telencephali reveals its identity with ephrin B1. Ephrin B1 appears at the onset of neocortical neurogenesis, being first expressed in neuron-generating neuroepithelial cells and rapidly thereafter in virtually all neuroepithelial cells. Expression of ephrin B1 persists through the period of neocortical neurogenesis and is downregulated thereafter. Ephrin B1 is present on the ventricular as well as basolateral plasma membrane of neuroepithelial cells and exhibits an ventricular-high to pial-low gradient across the ventricular zone. Expression of ephrin B1 is also detected on radial glial cells, extending all the way to their pial endfeet, and on neurons in the mantle/intermediate zone but not in the cortical plate. Our results suggest that ephrin B1, presumably via ephrin-Eph receptor signaling, has a role in neurogenesis. Given the ventricular-to-pial gradient of ephrin B1 on the neuroepithelial cell surface and its known role in cell migration in other systems mediated by its repulsive properties, we propose that ephrin B1 may be involved in the migration of newborn neurons out from the ventricular zone toward the neocortex.},
	Author = {Stuckmann, I. and Weigmann, A. and Shevchenko, A. and Mann, M. and Huttner, W. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurosci},
	Keywords = {Neocortex/cytology/embryology/metabolism;Cell Membrane/metabolism;Neurons/cytology/*metabolism;Gene Expression Regulation, Developmental;Rats;Animal;Telencephalon/cytology/*embryology/*metabolism;Epithelial Cells/cytology/*metabolism;Support, Non-U.S. Gov't;Antibody Specificity;Mice, Inbred Strains;Membrane Proteins/*biosynthesis/chemistry/metabolism;Organ Specificity;C;Pia Mater/cytology/embryology/metabolism;04 Adult neurogenesis factors;Cell Movement/physiology;Mice;Morphogenesis/physiology;Antibodies, Monoclonal/isolation &purification/metabolism;Antigens, Differentiation/biosynthesis/chemistry/immunology;Molecular Weight;Cerebral Ventricles/cytology/embryology/metabolism;Signal Transduction/physiology;Neuroglia/cytology/metabolism},
	Number = {8},
	Organization = {Department of Neurobiology, University of Heidelberg, D-69120 Heidelberg, Germany.},
	Pages = {2726-37.},
	Title = {Ephrin B1 is expressed on neuroepithelial cells in correlation with neocortical neurogenesis},
	Uuid = {7F029820-46DC-4CDC-A474-A3477D4792A8},
	Volume = {21},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11306625%20http://www.jneurosci.org/cgi/content/full/21/8/2726%20http://www.jneurosci.org/cgi/content/abstract/21/8/2726}}

@article{Studer:2000,
	Abstract = {Standard cell culture systems impose environmental oxygen (O(2)) levels of 20\%, whereas actual tissue O(2) levels in both developing and adult brain are an order of magnitude lower. To address whether proliferation and differentiation of CNS precursors in vitro are influenced by the O(2) environment, we analyzed embryonic day 12 rat mesencephalic precursor cells in traditional cultures with 20\%O(2) and in lowered O(2) (3 +/- 2\%). Proliferation was promoted and apoptosis was reduced when cells were grown in lowered O(2), yielding greater numbers of precursors. The differentiation of precursor cells into neurons with specific neurotransmitter phenotypes was also significantly altered. The percentage of neurons of dopaminergic phenotype increased to 56\%in lowered O(2) compared with 18\%in 20\%O(2). Together, the increases in total cell number and percentage of dopaminergic neurons resulted in a ninefold net increase in dopamine neuron yield. Differential gene expression analysis revealed more abundant messages for FGF8, engrailed-1, and erythropoietin in lowered O(2). Erythropoietin supplementation of 20\%O(2) cultures partially mimicked increased dopaminergic differentiation characteristic of CNS precursors cultured in lowered O(2). These data demonstrate increased proliferation, reduced cell death, and enhanced dopamine neuron generation in lowered O(2), making this method an important advance in the ex vivo generation of specific neurons for brain repair.},
	Author = {Studer, L. and Csete, M. and Lee, S. H. and Kabbani, N. and Walikonis, J. and Wold, B. and McKay, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Cell Differentiation;Animals;Dopamine;Rats;Oxygen;Research Support, U.S. Gov't, Non-P.H.S.;Antigens, Differentiation;Apoptosis;Cell Hypoxia;23 Technique;Fibroblast Growth Factor 2;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;In Situ Nick-End Labeling;Cell Division;Central Nervous System;Bromodeoxyuridine;Stem Cells;Erythropoietin},
	Medline = {20482307},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {19},
	Organization = {Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.},
	Pages = {7377-83},
	Pubmed = {11007896},
	Title = {Enhanced proliferation, survival, and dopaminergic differentiation of CNS precursors in lowered oxygen},
	Uuid = {3031270F-5455-4E6C-A5C1-465BFFBC78BC},
	Volume = {20},
	Year = {2000}}

@article{Stumm:2003,
	Abstract = {The chemotactic factors directing interneuron migration during cerebrocortical development are essentially unknown. Here we identify the CXC chemokine receptor 4 (CXCR4) in interneuron precursors migrating from the basal forebrain to the neocortex and demonstrate that stromal cell-derived factor-1 (SDF-1) is a potent chemoattractant for isolated striatal precursors. In addition, we show that CXCR4 is present in early generated Cajal-Retzius cells of the cortical marginal zone. In mice with a null mutation in CXCR4 or SDF-1, interneurons were severely underrepresented in the superficial layers and ectopically placed in the deep layers of the neocortex. In contrast, the submeningeal positioning of Cajal-Retzius cells was unaffected. Thus, our findings suggest that SDF-1, which is highly expressed in the embryonic leptomeninx, selectively regulates migration and layer-specific integration of CXCR4-expressing interneurons during neocortical development.},
	Author = {Stumm, Ralf K. and Zhou, Chun and Ara, Toshiaki and Lazarini, Fran\c{c}oise and Dubois-Dalcq, Monique and Nagasawa, Takashi and H{\"o}llt, Volker and Schulz, Stefan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Receptors, CXCR4;Signal Transduction;Animals;Gene Expression Regulation, Developmental;Rats;Neocortex;Cell Count;Cell Movement;Cell Adhesion Molecules, Neuronal;Mice, Inbred C57BL;Rats, Wistar;Serine Endopeptidases;RNA, Messenger;In Situ Hybridization;Extracellular Matrix Proteins;Nervous System Malformations;Mice, Knockout;Chemokines, CXC;Mice;Interneurons;24 Pubmed search results 2008;Immunohistochemistry;Stem Cells;Nerve Tissue Proteins;Choristoma;Research Support, Non-U.S. Gov't},
	Medline = {22716536},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Department of Pharmacology and Toxicology, Otto-von-Guericke University, 39120 Magdeburg, Germany.},
	Pages = {5123-30},
	Pii = {23/12/5123},
	Pubmed = {12832536},
	Title = {CXCR4 regulates interneuron migration in the developing neocortex},
	Uuid = {F892B6ED-E9CA-45B4-A3AD-977216D6CE59},
	Volume = {23},
	Year = {2003}}

@article{Sturrock:1988,
	Abstract = {Macrophages were found in the meningeal sheath of the human optic nerve at all ages from 8 to 18 weeks post-conception. At 8 weeks the majority of macrophages contained few cytoplasmic organelles or vacuoles, but even at this age a small number of cells packed with small dense bodies were present. With increasing age the number of organelles increased and some vacuolated macrophages were present. The morphology of macrophages largely depended on the part of the meninges in which they were situated. Those lying in the subarachnoid space or loose outer layers of the dura were irregularly shaped and often vacuolated, whereas those lying in the tightly packed layer of arachnoid at its junction with the dura were elongated and contained few, if any, vacuoles. A few meningeal macrophages were observed apparently migrating along the fibrous septa which carry blood vessels into the substance of the nerve. The main structural differences between meningeal macrophages and optic nerve microglia (Sturrock, 1984) were the presence in the latter of numerous small vacuoles and long strands of endoplasmic reticulum. These structural differences may be the result of microglia being actively engaged in phagocytosis of the large number of degenerating axons which are present in the optic nerve between 8 and 10 weeks post-conception.},
	Author = {Sturrock, R. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0021-8782},
	Journal = {J Anat},
	Keywords = {Gestational Age;Human;Microscopy, Electron;Meninges;Not relevant;11 Glia;Macrophages;Optic Nerve},
	Medline = {89066390},
	Month = {4},
	Nlm_Id = {0137162},
	Organization = {Department of Anatomy, University of Dundee, Scotland.},
	Pages = {145-51},
	Pubmed = {3198475},
	Title = {An electron microscopic study of macrophages in the meninges of the human embryonic optic nerve},
	Uuid = {BBC675A2-8700-456C-B970-45620D9DC789},
	Volume = {157},
	Year = {1988}}

@article{Sudo:1998,
	Abstract = {Although microglial cells are well known to become activated in the pathological brain, mechanisms underlying the microglial activation are not fully understood. In the present study, with an aim to elucidate whether neurons are involved in the microglial activation, we compared the morphology and the superoxide anion (O2-)-generating activity of rat microglial cells in pure culture with those of cells cocultured with rat primary cortical neurons. Microglial cells in pure culture in serum-free Eagle's minimum essential medium on poly-L-lysine-coated coverslips displayed ramified morphology and suppressed activity of O2- generation. In contrast, microglial cells in neuron-microglia coculture under the same conditions as those for the pure culture displayed ameboid shape and upregulated activity of O2- generation. Electron microscopic observation revealed that microglial cells in coculture were more abundant in Golgi apparatus and secretory granules than those in pure culture and that some of microglial cells in the vicinity of neurites exhibited membrane specialization reminiscent of a junctional apparatus with high electron density between a microglial soma and a neurite. Microglial cells in coculture tended to tie neurites in bundles by extending processes. Medium conditioned by neurons significantly enhanced O2- generation by microglia, but microglial cells in contact with or in close apposition to cocultured neurons were much more intensely activated than those remote from the neurons. Furthermore, the membrane fraction of cortical neurons activated microglial cells, and this effect was abolished by treating the neuronal membrane with trypsin or neuraminidase. In conclusion, neuronal-microglial contact may be necessary to mediate microglial activation. The present findings suggest that the contact of microglia with damaged neurons in the brain is a plausible cause to activate microglia in the neuropathological processes.},
	Author = {Sudo, S. and Tanaka, J. and Toku, K. and Desaki, J. and Matsuda, S. and Arai, T. and Sakanaka, M. and Maeda, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Neuraminidase;Animals;Astrocytes;Cells, Cultured;Serine;Rats;N-Acetylneuraminic Acid;Microglia;Cell Communication;Superoxides;Culture Media, Conditioned;Trypsin;11 Glia;Alpha;Animals, Newborn;Support, Non-U.S. Gov't;Tetradecanoylphorbol Acetate;Cerebral Cortex;Cell Size;Neurons;Carcinogens;Glycine;Anions;Cell Culture;Microscopy, Electron},
	Medline = {99096824},
	Month = {12},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Anesthesiology and Resuscitology, School of Medicine, Ehime University, Shigenobu, Ehime, 791-0295, Japan.},
	Pages = {499-510},
	Pii = {S0014488698969114},
	Pubmed = {9878185},
	Title = {Neurons induce the activation of microglial cells in vitro},
	Uuid = {1BF1DD64-EE31-11DA-8605-000D9346EC2A},
	Volume = {154},
	Year = {1998},
	url = {papers/Sudo_ExpNeurol1998.pdf}}

@article{Sugama:2003,
	Abstract = {Dopaminergic neurons in the substantia nigra pars compacta undergo apoptosis after transection of the medial forebrain bundle. We have assessed the temporal and sequential activities of microglia in these events by examining the complement-3 (OX-42), major histocompatibility complex class II antigen presentation (OX-6) and phagocytic activity (ED1), and correlating these indicators with dopaminergic neuronal loss. Microglia in the ipsilateral substantia nigra pars reticulata evinced activation morphology at 12 h postaxotomy. Phagocytic microglia apposed dying dopaminergic neurons in the pars compacta starting at 3 days postlesion; their number increased through 14 days and slowly decreased. Nuclear chromatin condensation and significant loss of tyrosine hydroxylase-positive dopaminergic neurons occurred around 7 days postlesion. In contrast to microglial expression of interleukin-1beta and inducible nitric oxide synthase at the axotomy site, nigral microglia were interleukin-1beta and inducible nitric oxide synthase-negative. Consistently, RNase protection assays showed that interleukin-1beta and inducible nitric oxide synthase transcripts in nigra were equivocal. The present data support the idea that phagocytosis of axotomized neurons by activated microglia is not limited to dead neurons but includes dying neurons probably without cytotoxic effects of inflammatory substances, such as interleukin-1beta or nitric oxide.},
	Author = {Sugama, S. and Cho, B. P. and Degiorgio, L. A. and Shimizu, Y. and Kim, S. S. and Kim, Y. S. and Shin, D. H. and Volpe, B. T. and Reis, D. J. and Cho, S. and Joh, T. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Nitric-Oxide Synthase;Substantia Nigra;Cytokines;Comparative Study;Rats;Apoptosis;Not relevant;Time Factors;Rats, Wistar;11 Glia;Microglia;Tyrosine 3-Monooxygenase;Animals;Male;Support, Non-U.S. Gov't;Medial Forebrain Bundle;Axotomy},
	Medline = {22506139},
	Nlm_Id = {7605074},
	Number = {4},
	Organization = {Laboratory of Molecular Neurobiology, The W M Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA.},
	Pages = {925-33},
	Pii = {S0306452202005729},
	Pubmed = {12617934},
	Title = {Temporal and sequential analysis of microglia in the substantia nigra following medial forebrain bundle axotomy in rat},
	Uuid = {042AB9F4-4074-43EE-83CB-3015FC2AADA3},
	Volume = {116},
	Year = {2003},
	url = {papers/Sugama_Neuroscience2003.pdf}}

@article{Sugiyama:1995,
	Abstract = {Multiple subpial transection (MST) is an effective surgical therapy for patients with intractable seizures whose epileptogenic lesions lie in the cortex and are unresectable. Morrell developed this procedure and reported clinical results obtained using it. However, only the disappearance of epileptiform discharges after MST in an experimental model of epilepsy has been demonstrated. The aim of this study was to establish the histological changes caused by MST and evaluate the effects of this procedure on interneuronal discharge spread in an epilepsy model, i.e. acute cortical kindling in rabbits. Histologically, vertical cracks in the transected cortex with mild gliosis and very little tissue disruption were observed. Horizontal fibers across the crack had been transected, whereas vertical fibers and neuronal cell bodies were preserved. The stimulation-induced after-discharges (ADs) were analyzed: cortical hyperactivity across the transected zone was reduced significantly earlier than that in the control group. Propagation of ADs induced by the kindling effect was also inhibited. These results suggest that MST interrupts not only neuronal synchronization, but also excitatory interneuronal conduction, in this epilepsy model.},
	Author = {Sugiyama, S. and Fujii, M. and Ito, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Issn = {0920-1211},
	Journal = {Epilepsy Res},
	Keywords = {Epilepsy;Electric Stimulation;Electroencephalography;24 Pubmed search results 2008;21 Epilepsy;21 Neurophysiology;Female;Neural Conduction;Kindling (Neurology);Parietal Lobe;Electrophysiology;Interneurons;Animals;Male;Cerebral Cortex;Rabbits;Frontal Lobe},
	Medline = {95369222},
	Month = {5},
	Nlm_Id = {8703089},
	Number = {1},
	Organization = {Department of Neurosurgery, Yamaguchi University School of Medicine, Japan.},
	Pages = {1-9},
	Pii = {092012119500003S},
	Pubmed = {7641670},
	Title = {The electrophysiological effects of multiple subpial transection (MST) in an experimental model of epilepsy induced by cortical stimulation},
	Uuid = {03E256C4-A807-4DAF-A13E-BE86F08EC6BC},
	Volume = {21},
	Year = {1995}}

@article{Suhonen:1996,
	Abstract = {Neurogenesis continues throughout adulthood in discrete regions. Proliferative zones include the subependymal zone, from where progenitors migrate along the rostral migratory pathway to differentiate into neurons in the olfactory bulb, and the hippocampal subgranular zone, where they migrate and differentiate into granule neurons. Progenitors isolated from adult subependymal zone exhibit in vitro neurogenesis when stimulated with epidermal or fibroblast growth factor. Cultured adult rat hippocampal progenitors (AHPs) grafted to adult rat hippocampus show site-specific neuronal differentiation. Here we investigate determinants of multipotentiality in the adult central nervous system, by grafting AHPs into homotypic (hippocampus) or heterotypic (the rostral migratory pathway) neurogenic sites or a heterotypic, non-neurogenic site (the cerebellum). We found that grafts into neurogenic, but not nonneurogenic sites, showed neuronal differentiation. Furthermore, AHPs grafted in the rostral migratory pathway migrated into the olfactory bulb, differentiating into tyrosine- hydroxylase-positive neurons, a non-hippocampus phenotype. These results reveal that AHP populations can respond to persistent neuronal differentiation cues in the adult central nervous system.},
	Author = {Suhonen, J. O. and Peterson, D. A. and Ray, J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:41 -0400},
	Journal = {Nature},
	Keywords = {Human;Cell Differentiation;Stem Cells/cytology/transplantation;Cells, Cultured;Rats;Neurons/*cytology;Cerebellum/cytology;Female;Animal;Cell Movement;Rats, Inbred F344;Olfactory Pathways/*cytology;B;Olfactory Bulb/cytology;Support, Non-U.S. Gov't;Adult;Support, U.S. Gov't, P.H.S.;Hippocampus/*cytology},
	Number = {6601},
	Organization = {Laboratory of Genetics, The Salk Institute, La Jolla, California 92037- 1099, USA.},
	Pages = {624-7.},
	Title = {Differentiation of adult hippocampus-derived progenitors into olfactory neurons in vivo},
	Uuid = {AD8B0CAA-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {383},
	Year = {1996},
	url = {papers/Suhonen_Nature1996.pdf}}

@article{Sun:1997,
	Abstract = {The features of a glial cell population in the developing brain of mice prenatally exposed to 60Co gamma-irradiation at the most radiosensitive stage were studied with immunohistochemistry for anti-midkine (MK), anti-vimentin (Vim), and anti-GFAP antibodies. Anti-MK- and anti-Vim- positive radial glial fibers distributed in a similar radial fashion; these fibers were observed primarily in the embryonic period and disappeared after birth. Anti-MK- and anti-Vim-stained radial fibers ran perpendicular to the pial surface in controls, whereas such fibers were disorganized 6 hours (h) after irradiation. This finding provided new evidence that the migratory pathways of young neurons were interrupted beginning a few hours after irradiation. By E17 the ectopic cell masses formed so as to replace the parts of the ventricular zone where no anti-MK immunoreactive radial fibers were present, but where anti-GFAP-stained fibrillary astrocytes emerged in the ectopic cell masses from the early postnatal period. The results suggested a twofold source of the generated astrocytes: either directly from a separate precursor of the astrocytes, or due to the transformation of the classic radial glial cells. In the newborn, numerous protoplasmic transitional forms displaced by astrocytes in irradiated brains indicated that reactive gliosis was a powerful response of a brain exposed to irradiation.},
	Author = {Sun, X. Z. and Inouye, M. and Fukui, Y. and Hisano, S. and Sawada, K. and Muramatsu, H. and Muramatsu, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {G;Pregnancy;Glial Fibrillary Acidic Protein/metabolism;Female;Animal;Neuroglia/*metabolism/pathology;*Prenatal Exposure Delayed Effects;11 Glia;Mice, Inbred ICR;Support, Non-U.S. Gov't;Carrier Proteins/metabolism;Vimentin/metabolism;Brain/embryology/*metabolism/pathology;Nerve Fibers/metabolism/pathology;Fetus/*radiation effects;Mice;Immunohistochemistry;*Gamma Rays},
	Number = {12},
	Organization = {Department of Anatomy, School of Medicine, Tokushima University, Japan.},
	Pages = {1339-48.},
	Title = {An immunohistochemical study of radial glial cells in the mouse brain prenatally exposed to gamma-irradiation},
	Uuid = {81091F1C-8E21-458D-AB13-CA7994840C5C},
	Volume = {56},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9413282}}

@article{Sun:2005,
	Abstract = {It has been debated whether asymmetric distribution of cell surface receptors during mitosis could generate asymmetric cell divisions by yielding daughters with different environmental responsiveness and, thus, different fates. We have found that in mouse embryonic forebrain ventricular and subventricular zones, the EGFR can distribute asymmetrically during mitosis in vivo and in vitro. This occurs during divisions yielding two Nestin+ progenitor cells, via an actin-dependent mechanism. The resulting sibling progenitor cells respond differently to EGFR ligand in terms of migration and proliferation. Moreover, they express different phenotypic markers: the EGFRhigh daughter usually has radial glial/astrocytic markers, while its EGFRlow sister lacks them, indicating fate divergence. Lineage trees of cultured cortical glioblasts reveal repeated EGFR asymmetric distribution, and asymmetric divisions underlie formation of oligodendrocytes and astrocytes in clones. These data suggest that asymmetric EGFR distribution contributes to forebrain development by creating progenitors with different proliferative, migratory, and differentiation responses to ligand.},
	Author = {Sun, Yu and Goderie, Susan K. and Temple, Sally},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Cell Differentiation;Animals;Receptor, Epidermal Growth Factor;Astrocytes;Cells, Cultured;Phenotype;Mitosis;Oligodendroglia;Cell Movement;Cell Proliferation;Prosencephalon;Research Support, U.S. Gov't, P.H.S.;Cell Lineage;Cerebral Cortex;Intermediate Filament Proteins;Epidermal Growth Factor;Mice;Actins;Stem Cells;Nerve Tissue Proteins;Biological Markers;Receptor Aggregation},
	Month = {3},
	Nlm_Id = {8809320},
	Number = {6},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, New York 12208, USA.},
	Pages = {873-86},
	Pii = {S0896-6273(05)00114-5},
	Pubmed = {15797549},
	Title = {Asymmetric distribution of EGFR receptor during mitosis generates diverse CNS progenitor cells},
	Uuid = {15F32482-C69A-48AA-A4A3-A39DD8B9096A},
	Volume = {45},
	Year = {2005},
	url = {papers/Sun_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.01.045}}

@article{Sun:2006,
	Abstract = {Rett syndrome (RTT) is an X-linked postnatal neurodevelopmental disorder, which is primarily caused by mutations in the gene encoding methyl-CpG binding protein 2 (MeCP2). A number of MeCP2 target genes have been identified, including the neurotrophic factor BDNF; however, the functional relevance of these targets has not been established. In this issue of Neuron, Chang et al. provide the first in vivo evidence for a functional interaction between BDNF and MeCP2.},
	Author = {Sun, Yi E. and Wu, Hao},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Models, Biological;Methyl-CpG-Binding Protein 2;21 Neurophysiology;Rett Syndrome;comment;Brain-Derived Neurotrophic Factor;Animals;Humans;24 Pubmed search results 2008;review},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Psychiatry and Biobehavioral Sciences, Neuropsychiatric Institute, University of California, Los Angeles, 635 Charles E. Young Drive South, Los Angeles, California 91301, USA.},
	Pages = {321-3},
	Pii = {S0896-6273(06)00043-2},
	Pubmed = {16446133},
	Title = {The ups and downs of BDNF in Rett syndrome},
	Uuid = {F4AA2220-E345-4E6B-9107-30602C3E9B02},
	Volume = {49},
	Year = {2006},
	url = {papers/Sun_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2006.01.014}}

@article{Sundholm-Peters:2004,
	Abstract = {During development radial glia (RG) are neurogenic, provide a substrate for migration, and transform into astrocytes. Cells in the RG lineage are functionally and biochemically heterogeneous in subregions of the brain. In the subventricular zone (SVZ) of the adult, astrocyte-like cells exhibit stem cell properties. During examination of the response of SVZ astrocytes to brain injury in adult mice, we serendipitously found a population of cells in the walls of the ventral lateral ventricle (LV) that were morphologically similar to RG. The cells expressed vimentin, glial fibrillary acidic protein (GFAP), intermediate filament proteins expressed by neural progenitor cells, RG and astrocytes. These RG-like cells had long processes extending ventrally into the nucleus accumbens, ventromedial striatum, ventrolateral septum, and the bed nucleus of the stria terminalis. The RG-like cell processes were associated with a high density of doublecortin-positive cells. Lesioning the cerebral cortex did not change the expression of vimentin and GFAP in RG-like cells, nor did it alter their morphology. To study the ontogeny of these cells, we examined the expression of molecules associated with RG during development: vimentin, astrocyte-specific glutamate transporter (GLAST), and brain lipid-binding protein (BLBP). As expected, vimentin was expressed in RG in the ventral LV embryonically (E16, E19) and during the first postnatal week (P0, P7). At P14, P21, P28 as well as in the adult (8-12 weeks), the ventral portion of the LV retained vimentin immunopositive RG-like cells, whereas RG largely disappeared in the dorsal two-thirds of the LV. GLAST and BLBP were expressed in RG of the ventral LV embryonically and through P7. In contrast to vimentin, at later stages BLBP and GLAST were found in RG-like cell somata but not in their processes. Our results show that cells expressing vimentin and GFAP (in the radial glia-astrocyte lineage) are heterogeneous dorsoventrally in the walls of the LV. The results suggest that not all RG in the ventral LV complete the transformation into astrocytes and that the ventral SVZ may be functionally dissimilar from the rest of the SVZ. 0300-4864 Journal Article},
	Author = {Sundholm-Peters, N. L. and Yang, H. K. and Goings, G. E. and Walker, A. S. and Szele, F. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:59 -0400},
	Journal = {J Neurocytol},
	Keywords = {B, G pdf;02 Adult neurogenesis migration},
	Number = {1},
	Organization = {2430 N. Halsted, No. 209, CMIER Neurobiology Program, Children's Memorial Hospital, Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60614-3394, USA.},
	Pages = {153-64},
	Title = {Radial glia-like cells at the base of the lateral ventricles in adult mice},
	Uuid = {6D0C4FC8-156F-425A-8C2C-0EC4FCDD7A5A},
	Volume = {33},
	Year = {2004},
	url = {papers/Sundholm-Peters_JNeurocytol2004.pdf}}

@article{Sunnemark:2005,

@article{Super:1998,
	Abstract = {During neural development, specific recognition molecules provide the cues necessary for the formation of initial projection maps, which are reshaped later in development. In some systems, guiding cues for axonal pathfinding and target selection are provided by specific cells that are present only at critical times. For instance, the floor plate guides commissural axons in the spinal cord, and the subplate is involved in the formation of thalamocortical connections. Here we study the development of entorhinal and commissural connections to the murine hippocampus, which in the adult terminate in nonoverlapping layers. We show that two groups of pioneer neurons, Cajal-Retzius cells and GABAergic neurons, form layer-specific scaffolds that overlap with distinct hippocampal afferents at embryonic and early postnatal stages. Furthermore, at postnatal day 0 (P0)-P5, before the dendrites of pyramidal neurons develop, these pioneer neurons are preferential synaptic targets for hippocampal afferents. Birthdating analysis using 5'-bromodeoxyuridine (BrdU) pulses showed that most such early-generated neurons disappear at late postnatal stages, most likely by cell death. Together with previous studies, these findings indicate that distinct pioneer neurons are involved in the guidance and targeting of different hippocampal afferents.},
	Author = {Sup\`{e}r, H. and Mart{\'\i}nez, A. and Del R{\'\i}o, J. A. and Soriano, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Aging;Synapses;Research Support, Non-U.S. Gov't;Hippocampus;Neural Pathways;Time Factors;Animals, Newborn;Neurons, Afferent;Animals;Mice;24 Pubmed search results 2008;Mice, Inbred Strains;Neurons},
	Medline = {98279072},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Department of Animal and Plant Cell Biology, Faculty of Biology, University of Barcelona, Barcelona 08028, Spain.},
	Pages = {4616-26},
	Pubmed = {9614236},
	Title = {Involvement of distinct pioneer neurons in the formation of layer-specific connections in the hippocampus},
	Uuid = {1F27319A-561A-4919-B256-159F499A9621},
	Volume = {18},
	Year = {1998}}

@article{Surani:2001,
	Abstract = {Most cells contain the same set of genes and yet they are extremely diverse in appearance and functions. It is the selective expression and repression of genes that determines the specific properties of individual cells. Nevertheless, even when fully differentiated, any cell can potentially be reprogrammed back to totipotency, which in turn results in re-differentiation of the full repertoire of adult cells from a single original cell of any kind. Mechanisms that regulate this exceptional genomic plasticity and the state of totipotency are being unravelled, and will enhance our ability to manipulate stem cells for therapeutic purposes. 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Surani, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Nature},
	Keywords = {Stem Cells/*physiology;*Genome;F abstr;10 Development;Genomic Imprinting;Human;Oocytes;Zygote;Support, Non-U.S. Gov't;Animals;Cell Differentiation/*genetics;Cell Nucleus;Germ Cells},
	Number = {6859},
	Organization = {Wellcome CRC Institute of Cancer and Developmental Biology and Physiology Laboratory, University of Cambridge, UK. as10021\@mole.bio.cam.ac.uk},
	Pages = {122-8},
	Pubmed = {11689958},
	Title = {Reprogramming of genome function through epigenetic inheritance},
	Uuid = {3A677250-E697-4F1C-B670-CEFB61206F58},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689958}}

@article{Suter:2007,
	Abstract = {The projection neurons of the neocortex are produced in the pseudostratified ventricular epithelium (PVE) lining the embryonic lateral ventricles. Over a 7 d period in mouse, these neurons arise in an overlapping layer VI-to-II sequence and in an anterolateral to posteromedial gradient [the transverse neurogenetic gradient (TNG)]. At any time in the 7 d neurogenetic interval, a given PVE cell must know what class of precursor cell or neuron to form next. How this information is encoded in the PVE is not known. With comparative experiments in wild-type and double-transgenic mice, overexpressing the cell cycle inhibitor p27(Kip1), we show that a gradient of expression of Lhx2 (inferred from its mRNA levels), a LIM homeodomain transcription factor, together with a gradient in duration of the G1 phase of the cell cycle (T(G1)), are sufficient to specify a positional mapping system that informs the PVE cell what class of neuron to produce next. Lhx2 likely is representative of an entire class of transcription factors expressed along the TNG. This mapping system consisting of a combination of signals from two different sources is a novel perspective on the source of positional information for neuronal specification in the developing CNS.},
	Author = {Suter, Bernhard and Nowakowski, Richard S. and Bhide, Pradeep G. and Caviness, Verne S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {40},
	Organization = {Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.},
	Pages = {10777-84},
	Pii = {27/40/10777},
	Pubmed = {17913911},
	Title = {Navigating neocortical neurogenesis and neuronal specification: a positional information system encoded by neurogenetic gradients},
	Uuid = {5B2DA9CC-AE09-498B-8143-B8432B055AFD},
	Volume = {27},
	Year = {2007},
	url = {papers/Suter_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3091-07.2007}}

@article{Sutton:2007,
	Abstract = {Activity-dependent regulation of dendritic protein synthesis is critical for enduring changes in synaptic function, but how the unique features of distinct activity patterns are decoded by the dendritic translation machinery remains poorly understood. Here, we identify eukaryotic elongation factor-2 (eEF2), which catalyzes ribosomal translocation during protein synthesis, as a biochemical sensor in dendrites that is specifically and locally tuned to the quality of neurotransmission. We show that intrinsic action potential (AP)-mediated network activity in cultured hippocampal neurons maintains eEF2 in a relatively dephosphorylated (active) state, whereas spontaneous neurotransmitter release (i.e., miniature neurotransmission) strongly promotes the phosphorylation (and inactivation) of eEF2. The regulation of eEF2 phosphorylation is responsive to bidirectional changes in miniature neurotransmission and is controlled locally in dendrites. Finally, direct spatially controlled inhibition of eEF2 phosphorylation induces local translational activation, suggesting that eEF2 is a biochemical sensor that couples miniature synaptic events to local translational suppression in neuronal dendrites.},
	Author = {Sutton, Michael A. and Taylor, Anne M. and Ito, Hiroshi T. and Pham, Anh and Schuman, Erin M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Excitatory Amino Acid Antagonists;Animals;Cells, Cultured;Rats;Transfection;Synaptic Transmission;Diagnostic Imaging;Patch-Clamp Techniques;Eukaryotic Initiation Factor-2;Hippocampus;Tetrodotoxin;research support, non-u.s. gov't;Green Fluorescent Proteins;Dendrites;Analysis of Variance;Animals, Newborn;Action Potentials;21 Neurophysiology;Neurons;research support, n.i.h., extramural;Protein Biosynthesis;24 Pubmed search results 2008;Excitatory Postsynaptic Potentials},
	Month = {8},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Division of Biology 114-96, California Institute of Technology, Pasadena, CA 91125, USA.},
	Pages = {648-61},
	Pii = {S0896-6273(07)00575-2},
	Pubmed = {17698016},
	Title = {Postsynaptic decoding of neural activity: eEF2 as a biochemical sensor coupling miniature synaptic transmission to local protein synthesis},
	Uuid = {A6A4F575-59BB-4F16-B992-762EDA3428FE},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.07.030}}

@article{Suzuki:2002,
	Abstract = {Neuronal progenitor cells (NPC) are particularly suited as the target population for genetic and cellular therapy of neurological disorders such as Parkinson's disease or stroke. However, genetic modification of these cells using retroviral vectors remains a great challenge because of the low transduction rate and the need for fetal calf serum (FCS) during the transduction process that induces the cell differentiation to mature neurons. To overcome these problems, we developed a new retrovirus production system in which the simplified retroviral vector GCDNsap engineered to be resistant to denovo methylation was packaged in the vesicular stomatitis virus G protein (VSV-G), concentrated by centrifugation, and resuspended in serum-free medium (StemPro-34 SFM). In transduction experiments using enhanced green fluorescent protein (EGFP) as a marker, the concentrated FCS-free virus supernatant infected NPC at a high rate, while maintaining the ability of these cells to self-renew and differentiate in vitro. When such cells were grafted into mouse brains, EGFP-expressing NPC were detected in the region around the injection site at 8 weeks post transplantation. These findings suggest that the gene transfer system described here may provide a useful tool to genetically modify NPC for treatments of neurological disorders.},
	Author = {Suzuki, A. and Obi, K. and Urabe, T. and Hayakawa, H. and Yamada, M. and Kaneko, S. and Onodera, M. and Mizuno, Y. and Mochizuki, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Transduction, Genetic;Animals;Corpus Striatum;Cells, Cultured;Stem Cell Transplantation;Feasibility Studies;Nervous System Diseases;Mice, Inbred C57BL;Retroviridae;11 Glia;Male;Genetic Vectors;Viral Envelope Proteins;Membrane Glycoproteins;Gene Therapy;Mice;Genes, Reporter;Graft Survival;Clone Cells;Luminescent Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Medline = {22246909},
	Month = {8},
	Nlm_Id = {2985190R},
	Number = {4},
	Organization = {Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.},
	Pages = {953-60},
	Pii = {1048},
	Pubmed = {12358801},
	Title = {Feasibility of ex vivo gene therapy for neurological disorders using the new retroviral vector GCDNsap packaged in the vesicular stomatitis virus G protein},
	Uuid = {5DD24BD8-12E3-4EA0-9756-C5FF2E0E63E3},
	Volume = {82},
	Year = {2002}}

@article{Suzuki:2003,
	Abstract = {Neural progenitors in the subventricular zone (SVZ) of the postnatal rat forebrain give rise to either olfactory interneurons or glia. To investigate the overall patterns of progenitor movement, we labeled neonatal rat SVZ cells by stereotactic injection of a GFP-encoding retrovirus into the SVZ at various coronal levels. We then studied the movements of labeled cells by time-lapse videomicroscopy in living brain slices cut in different orientations. We observed two migration patterns: (1) progenitors migrated radially into the overlying white matter and cortex, but only at the level of viral injection; these were previously shown to give rise to astrocytes and oligodendrocytes, (2) progenitors migrated in a bidirectional, rostrocaudal pattern along the entire extent of the SVZ; many of these cells eventually migrated into the olfactory bulb and developed into interneurons, but they did not turn to migrate radially out of the SVZ until they reached the olfactory bulb. Video imaging showed apparent boundaries to migration between the SVZ and adjacent structures. These observations indicate that there are at least two distinct migratory pathways within the SVZ used differentially by immature neurons and glia. 1529-2401 Journal Article},
	Author = {Suzuki, S. O. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {J Neurosci},
	Keywords = {B both;Microscopy, Video;Neuroglia/cytology/physiology/virology;Stem Cells/cytology/physiology/virology;Animals;Rats;Cell Movement/*physiology;Vimentin/analysis;Neurons/cytology/physiology/virology;02 Adult neurogenesis migration;Kinetics;Rats, Sprague-Dawley;Brain/cytology/embryology/virology;Time Factors;Injections, Intraventricular;Prosencephalon/*cytology/physiology/virology;Cell Line;Animals, Newborn;Oligodendroglia/cytology/physiology;3T3 Cells;Olfactory Bulb/cytology/physiology/virology;Frontal Lobe/cytology/physiology/virology;Support, U.S. Gov't, P.H.S.;Mice;Cell Differentiation/physiology;Luminescent Proteins/metabolism;Astrocytes/cytology/physiology/virology},
	Number = {10},
	Organization = {Department of Pathology and the Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA. sosuzuki\@np.med.kyushu-u.ac.jp},
	Pages = {4240-50},
	Title = {Multiple cell populations in the early postnatal subventricular zone take distinct migratory pathways: a dynamic study of glial and neuronal progenitor migration},
	Uuid = {E8D656A3-B86A-11DA-93EA-000D9346EC2A},
	Volume = {23},
	Year = {2003},
	url = {papers/Suzuki_JNeurosci2003.pdf}}

@article{Svendsen:2001,
	Abstract = {It is now possible to grow stem cells from a wide variety of tissues. Some of these cells have been shown to differentiate into presumptive neurons in vitro, or after transplantation into the developing or adult brain. When stem cells derived directly from the brain are induced to differentiate, there is a high probability that some of the resulting cells will be neurons. However, when stem cells from one tissue (for example, bone marrow or skin) take on the phenotype of another (for example, brain), rigorous criteria are required to define neurons. The aim of this review is to discuss the various techniques that are used to identify a cell as a neuron.},
	Author = {Svendsen, C. N. and Bhattacharyya, A. and Tai, Y. T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {02 Adult neurogenesis migration;B},
	Number = {11},
	Organization = {Clive N. Svendsen, Anita Bhattacharyya and Yu-Tzu Tai are members of the Stem Cell Research Program, Waisman Center and Departments of Anatomy and Neurology, University of Wisconsin, Madison, Wisconsin 53705-2280, USA.},
	Pages = {831-4.},
	Title = {Neurons from stem cells: preventing an identity crisis},
	Uuid = {FC0CA5A8-4BD6-4280-BD2C-0E4AB71F250C},
	Volume = {2},
	Year = {2001},
	url = {papers/Svendsen_NatRevNeurosci2001.pdf}}

@article{Sweeney:2008,
	Abstract = {The sticky/citron kinase protein is a conserved regulator of cell-cycle progression from invertebrates to humans. While this kinase is essential for completion of cytokinesis, sticky/citron kinase phenotypes disrupting neurogenesis and cell differentiation suggest additional non-cell-cycle functions. However, it is not known whether these phenotypes are an indirect consequence of sticky mutant cell-cycle defects or whether they define a novel function for this kinase. We have isolated a temperature-sensitive allele of the Drosophila sticky gene and we show that sticky/citron kinase is required for histone H3-K9 methylation, HP1 localization, and heterochromatin-mediated gene silencing. sticky genetically interacts with Argonaute 1 and sticky mutants exhibit context-dependent Su(var) and E(var) activity. These observations indicate that sticky/citron kinase functions to regulate both actin-myosin-mediated cytokinesis and epigenetic gene silencing, possibly linking cell-cycle progression to heterochromatin assembly and inheritance of gene expression states.},
	Author = {Sweeney, Sarah J. and Campbell, Paula and Bosco, Giovanni},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0016-6731},
	Journal = {Genetics},
	Keywords = {Chromosomal Proteins, Non-Histone;Animals;Cell Cycle;Female;Mutation;Protein-Serine-Threonine Kinases;Models, Genetic;Methylation;Heterochromatin;research support, non-u.s. gov't;Eye;Temperature;Alleles;Drosophila melanogaster;Histones;Gene Silencing;Intracellular Signaling Peptides and Proteins;research support, n.i.h., extramural;Ploidies;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;Ovarian Follicle;Drosophila Proteins;Genes, Insect},
	Month = {3},
	Nlm_Id = {0374636},
	Number = {3},
	Organization = {Department of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona 85721, USA.},
	Pages = {1311-25},
	Pii = {genetics.107.082511},
	Pmc = {PMC2278101},
	Pubmed = {18245345},
	Title = {Drosophila sticky/citron kinase is a regulator of cell-cycle progression, genetically interacts with Argonaute 1 and modulates epigenetic gene silencing},
	Uuid = {9681BE33-E73A-4AEB-81CF-149933CA044F},
	Volume = {178},
	Year = {2008},
	url = {papers/Sweeney_Genetics2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.107.082511}}

@article{Sychowa:1968,
	Author = {Sychowa, B. and Stepie\'{n}, L. and Stepie\'{n}, I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0365-0820},
	Journal = {Acta Biol Exp (Warsz)},
	Keywords = {Nerve Degeneration;Neural Pathways;Dogs;Thalamus;Animals;24 Pubmed search results 2008;Frontal Lobe},
	Medline = {69255827},
	Nlm_Id = {1246764},
	Number = {4},
	Pages = {383-99},
	Pubmed = {5732769},
	Title = {Degeneration in the thalamus following medial frontal lesions in the dog},
	Uuid = {04E5FE10-B69E-4C3D-8B9E-CE30AF6FEAB2},
	Volume = {28},
	Year = {1968}}

@article{Szele:1996,
	Abstract = {The subventricular zone (SVZ) bordering the lateral ventricle is one of the few regions of adult brain that contains dividing cells. These cells can differentiate into neurons in vivo after migration into the olfactory bulb and in vitro in the presence of appropriate growth factors. Little is known, however, about the fate of these cells in vivo after brain injury in adults. We examined cell number and expression of differentiation markers in the SVZ of adult rats after cortical lesions. Aspiration lesions of the sensorimotor cortex in adult rats induced a transient doubling of the number of cells in the SVZ at the level of the striatum without consistent increases in bromodeoxyuridine-labeled cells. Immunoreactivity to the polysialylated neural cell adhesion molecule, expressed by the majority of cells of the SVZ during development, increased dramatically after lesion. In contrast, immunolabeling for molecules found in mature neurons and glia did not increase in the SVZ after lesion, and immunoreactivity for growth factors that induce differentiation of SVZ cells in vitro decreased or remained undetectable, suggesting that lack of appropriate growth factor expression may contribute to the lack of differentiation of the newly accumulated cells in vivo. The data reveal that cells of the SVZ are capable of plasticity in the adult rat after brain injury in vivo and that the newly accumulated cells retain characteristics seen during development.},
	Author = {Szele, F. G. and Chesselet, M. F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Comp Neurol},
	Keywords = {B-6;Growth Substances/biosynthesis;Rats;Neural Cell Adhesion Molecules/analysis/*biosynthesis;Cell Movement/*physiology;Animal;Neuroglia/chemistry;02 Adult neurogenesis migration;Cell Count;Male;Cerebral Ventricles/*chemistry/*cytology;Neostriatum/chemistry/cytology;Support, U.S. Gov't, P.H.S.;Rats, Sprague-Dawley/*physiology;Intermediate Filament Proteins/analysis;Immunohistochemistry;Biological Markers;Bromodeoxyuridine;Neurons/chemistry;Sialic Acids/analysis/*biosynthesis},
	Number = {3},
	Organization = {Department of Pharmacology, University of Pennsylvania, Philadelphia 19104, USA.},
	Pages = {439-54.},
	Title = {Cortical lesions induce an increase in cell number and PSA-NCAM expression in the subventricular zone of adult rats},
	Uuid = {78CB2857-3612-41F5-BB01-D946A0D8ABA5},
	Volume = {368},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8725350}}

@article{Tabar:2005,
	Abstract = {Human embryonic stem (hES) cells provide a potentially unlimited cell source for regenerative medicine. Recently, differentiation strategies were developed to direct hES cells towards neural fates in vitro. However, the interaction of hES cell progeny with the adult brain environment remains unexplored. Here we report that hES cell-derived neural precursors differentiate into neurons, astrocytes and oligodendrocytes in the normal and lesioned brain of young adult rats and migrate extensively along white matter tracts. The differentiation and migration behavior of hES cell progeny was region specific. The hES cell-derived neural precursors integrated into the endogenous precursor pool in the subventricular zone, a site of persistent neurogenesis. Like adult neural stem cells, hES cell-derived precursors traveled along the rostral migratory stream to the olfactory bulb, where they contributed to neurogenesis. We found no evidence of cell fusion, suggesting that hES cell progeny are capable of responding appropriately to host cues in the subventricular zone.},
	Author = {Tabar, and Panagiotakos, and Greenberg, and Chan, and Sadelain, and Gutin, and Studer,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {22 Stem cells},
	Month = {4},
	Nlm_Id = {9604648},
	Number = {5},
	Organization = {[1] Developmental Biology, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, New York 10021, USA. [2] Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, New York 10021, USA.},
	Pages = {601-6},
	Pii = {nbt1088},
	Pubmed = {15852001},
	Title = {Migration and differentiation of neural precursors derived from human embryonic stem cells in the rat brain},
	Uuid = {330CEE8B-271F-400D-9623-8CB5613FC5C4},
	Volume = {23},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt1088}}

@article{Tabata:2003,
	Abstract = {Two distinct modes of radial neuronal migration, locomotion and somal translocation, have been reported in the developing cerebral cortex. Although these two modes of migration have been well documented, the cortical intermediate zone contains abundant multipolar cells, and they do not resemble the cells migrating by locomotion or somal translocation. Here, we report that these multipolar cells express neuronal markers and extend multiple thin processes in various directions independently of the radial glial fibers. Time-lapse analysis of living slices revealed that the multipolar cells do not have any fixed cell polarity, and that they very dynamically extend and retract multiple processes as their cell bodies slowly move. They do not usually move straight toward the pial surface during their radial migration, but instead frequently change migration direction and rate; sometimes they even remain in almost the same position, especially when they are in the subventricular zone. Occasionally, the multipolar cells jump tangentially during their radial migration. Because the migration modality of these cells clearly differs from locomotion or somal translocation, we refer to their novel type of migration as "multipolar migration."In view of the high proportion of cells exhibiting multipolar migration, this third mode of radial migration must be an important type of migration in the developing cortex. 1529-2401 Journal Article},
	Author = {Tabata, H. and Nakajima, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurosci},
	Keywords = {Gene Transfer Techniques;Genes, Reporter;10 Development;Luminescent Proteins/biosynthesis/genetics;Interneurons/cytology/metabolism;Antigens, Differentiation/biosynthesis;In Vitro;Lateral Ventricles/cytology;Mice, Inbred ICR;Neurons/*cytology/metabolism;Electroporation;Cell Movement/*physiology;Animals;Support, Non-U.S. Gov't;Mice;Cerebral Cortex/*cytology/*embryology;F pdf},
	Number = {31},
	Organization = {Department of Anatomy, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.},
	Pages = {9996-10001},
	Pubmed = {14602813},
	Title = {Multipolar migration: the third mode of radial neuronal migration in the developing cerebral cortex},
	Uuid = {EEBB8283-067E-49E2-B145-850E95463409},
	Volume = {23},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14602813}}

@article{Takagi:1999,
	Abstract = {We investigated the proliferation of neuronal progenitor cells by labeling dividing cells by systemic application of the thymidine analog 5-bromodeoxyuridine (BrdU) during transient forebrain ischemia in mice. At 3 (n=6), 7 (n=6), 10 (n=6), and 17 days (n=6) after reperfusion, BrdU-labeled cells were detected in the dentate gyrus and paraventricle lesion. After ischemia-reperfusion, BrdU-labeled cells in the dentate gyrus significantly increased in number but not in the paraventricle lesion. These observations may help to clarify the mechanism of functional recovery after stroke. 0006-8993 Journal Article},
	Author = {Takagi, Y. and Nozaki, K. and Takahashi, J. and Yodoi, J. and Ishikawa, M. and Hashimoto, N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Brain Res},
	Keywords = {Mice;Male;Dentate Gyrus/*pathology;D abstr;In Situ Nick-End Labeling;Prosencephalon/*blood supply;Ischemic Attack, Transient/*pathology;Cell Division/physiology;Time Factors;Mice, Inbred C57BL;06 Adult neurogenesis injury induced;Animals;Bromodeoxyuridine;Support, Non-U.S. Gov't;Neurons/*pathology;Stem Cells/*pathology},
	Number = {1-2},
	Organization = {Department of Neurosurgery, Graduate School of Medicine, Kyoto University, Sakyo, Kyoto, Japan.},
	Pages = {283-7},
	Pubmed = {10412007},
	Title = {Proliferation of neuronal precursor cells in the dentate gyrus is accelerated after transient forebrain ischemia in mice},
	Uuid = {1F5F517B-EC81-11DA-8605-000D9346EC2A},
	Volume = {831},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10412007}}

@article{Takahashi:1990,
	Abstract = {Cells of astroglial lineage in the murine cerebrum undergo a succession of transformations during prenatal and early postnatal development. The bipolar radial cell, the earliest astroglial form to appear, provides a radially aligned, parallel array of fibers that serves as a guide to neuronal migration. The multipolar astrocyte is the representative of this lineage that persists in the adult cerebrum. The processes of the multipolar astrocytes form a complex reticulum, which is considered critical to the development, function, and maintenance of neural circuits. A monopolar radial cell appears to be transitional between the two. The shift from the radial glial fiber system to a diffuse glial network is achieved largely in the E17-P2 interval in the mouse. This phenomenon has been studied qualitatively and quantitatively by staining cerebral tissue with monoclonal antibody RC2, a specific and sensitive ligand for cells of astroglial lineage in the mouse. Elongation and branching of glial processes contribute to the glial transformation. Elongation of radial fibers occurs under the guidance of other radial glial fibers (fasciculated elongation) or independently of other fibers (nonfasciculated elongation). Fasciculated elongation results in an increase in the density of radial glial fibers that span the cortical layers. Nonfasciculated elongation appears to be associated with process branching. This is the initial event in transformation of the bipolar radial cells to monopolar radial or multipolar cells. Only nonfasciculated elongation is characteristic of processes of the monopolar radial cells and multipolar astrocytes. Branching of the processes of all three cell forms appears to occur both by bifurcation at the elongating tip and by sprouting from the fiber shaft. Elongating fibers are tipped by growth cones that are relatively simple in shape as compared to those observed at the tips of elongating axons. Growth cones at the tips of nonfasciculated fibers are more complex in form than those at the tips of radial fibers elongating in contact with other radial fibers.},
	Author = {Takahashi, T. and Misson, J. P. and Caviness, V. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Astrocytes/chemistry/*ultrastructure;Animal;11 Glia;Cell Differentiation/physiology;Support, U.S. Gov't, P.H.S.;Immunoenzyme Techniques;Support, Non-U.S. Gov't;G;Mice;Fetal Development/physiology;Cerebral Cortex/embryology/growth &development/*ultrastructure},
	Number = {1},
	Organization = {Department of Neurology, Massachusetts General Hospital, Boston 02114.},
	Pages = {15-28.},
	Title = {Glial process elongation and branching in the developing murine neocortex: a qualitative and quantitative immunohistochemical analysis},
	Uuid = {A6DF4110-A5F4-4192-9381-249C147316E3},
	Volume = {302},
	Year = {1990},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=2086612}}

@article{Takahashi:1999,
	Abstract = {ABSTRACT: The adult rat hippocampus contains fibroblast growth factor 2- responsive stem cells that are self-renewing and have the ability to generate both neurons and glia in vitro, but little is known about the molecular events that regulate stem cell differentiation. Hippocampus- derived stem cell clones were used to examine the effects of retinoic acid (RA) on neuronal differentiation. Exposure to RA caused an immediate up-regulation of NeuroD, increased p21 expression, and concurrent exit from cell cycle. These changes were accompanied by a threefold increase in the number of cells differentiating into immature neurons. An accompanying effect of RA was to sustain or up-regulate trkA, trkB, trkC, and p75NGFR expression. Without RA treatment, cells were minimally responsive to neurotrophins (NTs), whereas the sequential application of RA followed by brain-derived neurotrophic factor or NT-3 led to a significant increase in neurons displaying mature y-a-minobutyric acid, acetylcholinesterase, tyrosine hydroxylase, or calbindin phenotypes. Although NTs promoted maturation, they had little effect on the total number of neurons generated, suggesting that RA and neurotrophins acted at distinct stages in neurogenesis. RA first promoted the acquisition of a neuronal fate, and NTs subsequently enhanced maturation by way of RA-dependent expression of the Trk receptors. In combination, these sequential effects were sufficient to stimulate stem cell-derived progenitors to differentiate into neurons displaying a variety of transmitter phenotypes.},
	Author = {Takahashi, J. and Palmer, T. D. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurobiol},
	Keywords = {Cell Differentiation/drug effects;Proto-Oncogene Proteins/drug effects/metabolism;Receptor, trkA;Stem Cells/*drug effects/physiology;Tretinoin/*pharmacology;Up-Regulation (Physiology);Gene Expression Regulation, Developmental;Receptor Protein-Tyrosine Kinases/drug effects/metabolism;Rats;Neurons/cytology/*drug effects;Nerve Growth Factors/pharmacology;Animal;C abstr;Hippocampus;Reverse Transcriptase Polymerase Chain Reaction;Support, Non-U.S. Gov't;Fibroblast Growth Factor/pharmacology;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Receptors, Nerve Growth Factor/*drug effects/metabolism},
	Number = {1},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {65-81.},
	Title = {Retinoic acid and neurotrophins collaborate to regulate neurogenesis in adult-derived neural stem cell cultures},
	Uuid = {2C8D170B-D877-4B0E-A18C-03B639004C7F},
	Volume = {38},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10027563}}

@article{Takahashi:1995,
	Abstract = {Neurons destined for the cerebral neocortex are formed in the pseudostratified ventricular epithelium (PVE) lining the ventricular cavity of the developing cerebral wall. The present study, based upon cumulative S-phase labeling with bromodeoxyuridine, is an analysis of cell cycle parameters of the PVE. It is undertaken in the dorsomedial cerebral wall of mouse embryos from the eleventh to the seventeenth gestational day (E11-E17, day of conception = E0) corresponding to the complete period of neuronogenesis. The growth fraction (fraction of cells in the population which is proliferating) is virtually 1.0 from E11 through E16. The length of the cell cycle increases from 8.1 to 18.4 hr, which corresponds to a sequence of 11 integer cell cycles over the course of neuronal cytogenesis in mice. The increase in the length of the cell cycle is due essentially to a fourfold increase in the length of G1 phase which is the only phase of the cell cycle which varies systematically. Thus, the G1 phase is most likely to be the phase of the cell cycle which is modulated by extrinsically and intrinsically acting mechanisms involved in the regulation of neuronal cytogenesis.},
	Author = {Takahashi, T. and Nowakowski, R. S. and Caviness, V. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Embryonic and Fetal Development;Epithelium;Research Support, U.S. Gov't, P.H.S.;Cell Cycle;Research Support, U.S. Gov't, Non-P.H.S.;Mice;Animals;Cerebral Ventricles;Mice, Inbred Strains;Bromodeoxyuridine},
	Medline = {95395589},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {9},
	Organization = {Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA.},
	Pages = {6046-57},
	Pubmed = {7666188},
	Title = {The cell cycle of the pseudostratified ventricular epithelium of the embryonic murine cerebral wall},
	Uuid = {5D68872E-541F-4423-B128-0742A44DEAA3},
	Volume = {15},
	Year = {1995}}

@article{Takahashi:1995a,
	Abstract = {The present report is an analysis of the proliferative behavior of the secondary proliferative population (SPP) of the dorsomedial region of the embryonic mouse cerebral wall. It is based upon experiments undertaken on embryonic days 14-16 (E14-E16) and exploits methods in which proliferative cells are labeled in S phase with either or both bromodeoxyuridine and tritiated thymidine. The SPP, which arises from the PVE by E13, is principally the progenitor population to the neuroglial population of the mature neocortex and subjacent cerebral wall. By the end of E14 the SPP comes to be distributed diffusely from the outer margin of the ventricular zone throughout subventricular zone and intermediate zone. The length of the cell cycle of the SPP is constant at approximately 15 hr throughout this interval; thus, this population undergoes 1.6 cell cycles/24 hr or 3.2 cycles in the course of the 48 hr period, E14-E16. Over this 48 hr period, the SPP increases from 11\%to 35\%of the total proliferative population of the dorsomedial cerebral wall. The absolute size of the SPP increases nearly sixfold. With these values taken together it may be estimated that approximately 87\%of postmitotic cells of the SPP reenter S phase after each cell division in this interval which means that only approximately 13\%of the proliferative population exits the cycle. These findings illustrate the massive expansion of the SPP antecedent to the explosive diffusion of glial cells through the neocortex and subjacent cerebral wall as neuronal migration comes to completion and neocortical growth and differentiation accelerate.},
	Author = {Takahashi, T. and Nowakowski, R. S. and Caviness, V. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Thymidine;Research Support, Non-U.S. Gov't;Embryonic and Fetal Development;S Phase;Research Support, U.S. Gov't, P.H.S.;Cell Division;Cell Cycle;Research Support, U.S. Gov't, Non-P.H.S.;Animals;Bromodeoxyuridine;Brain;Mice;24 Pubmed search results 2008},
	Medline = {95395590},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {9},
	Organization = {Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA.},
	Pages = {6058-68},
	Pubmed = {7666189},
	Title = {Early ontogeny of the secondary proliferative population of the embryonic murine cerebral wall},
	Uuid = {E59F52BF-6524-4EEC-885D-CD2156382C5B},
	Volume = {15},
	Year = {1995}}

@article{Takasawa:2002,
	Abstract = {Recent studies demonstrated that neurogenesis in the adult hippocampus increased after transient global ischemia; however, the molecular mechanism underlying increased neurogenesis after ischemia remains unclear. The finding that proliferation of progenitor cells occurred at least a week after ischemic insult suggests that the stimulus was not an ischemic insult to progenitor cells. To clarify whether focal ischemia increases the rate of neurogenesis in the remote area, the authors examined the contralateral hemisphere in rats subjected to permanent occlusion of the middle cerebral artery. In the subgranular zone of the hippocampal dentate gyrus, the numbers of bromodeoxyuridine (BrdU)-positive cells increased approximately sixfold 7 days after ischemia. In double immunofluorescence staining, more than 80\%of newborn cells expressed Musashi1, a marker of neural stem/progenitor cells, but only approximately 10\%of BrdU-positive cells expressed glial fibrillary acidic protein (GFAP), a marker of astrocytes. The number of BrdU-positive cells markedly decreased 28 days after BrdU administration after ischemia, but it was still elevated compared with that of sham-operated rats. In double immunofluorescence staining, 80\%of newborn cells expressed NeuN, a marker of differentiated neurons, and 10\%of BrdU-positive cells expressed GFAP. However, in the other areas of the contralateral hemisphere including the rostral subventricular zone, the number of BrdU-positive cells remained unchanged. These results showed that focal ischemia stimulated the proliferation of neuronal progenitor cells, but did not support survival of newborn cells in the contralateral hippocampus. 0271-678x Journal Article},
	Author = {Takasawa, K. and Kitagawa, K. and Yagita, Y. and Sasaki, T. and Tanaka, S. and Matsushita, K. and Ohstuki, T. and Miyata, T. and Okano, H. and Hori, M. and Matsumoto, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Cereb Blood Flow Metab},
	Keywords = {Brain/*pathology;Dentate Gyrus/*pathology;Laterality;D abstr;Ischemic Attack, Transient/*pathology;Middle Cerebral Artery;Rats;Stem Cells/*cytology/*pathology;Rats, Wistar;Cell Survival;Hippocampus/*pathology;06 Adult neurogenesis injury induced;Support, Non-U.S. Gov't;Brain Ischemia/pathology;Animals;Neurons/*pathology;Male},
	Number = {3},
	Organization = {Division of Strokology, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan.},
	Pages = {299-307},
	Pubmed = {11891435},
	Title = {Increased proliferation of neural progenitor cells but reduced survival of newborn cells in the contralateral hippocampus after focal cerebral ischemia in rats},
	Uuid = {7B974738-EC81-11DA-8605-000D9346EC2A},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11891435}}

@article{Takemura:2002,
	Abstract = {BACKGROUND: Glial fibrillary acidic protein (GFAP) is the principal component of intermediate filaments (IFs) in mature astrocytes in the central nervous system (CNS). Like other IF proteins, GFAP has multiple phosphorylation sites in the N-terminal head domain. The distribution of phospho-GFAP in vivo has not been elucidated. RESULTS: We generated Gfap(hwt) knock-in mice, in which the coding region for the head domain of GFAP is replaced with the corresponding human sequence. In combination with a series of monoclonal antibodies (mAbs) reactive to human phospho-GFAP, we visualized the distribution of phospho-GFAP in vivo in mice. GFAP phosphorylated at Thr7, Ser8 and/or Ser13 increased postnatally in the CNS of these mice. Limited populations of GFAP-positive astrocytes were labelled with anti-phospho-GFAP mAbs in most brain areas, whereas almost all the astrocytes in the optic nerve and spinal cord were labelled. Astrocytes in the subventricular zone and rostral migratory stream preferentially contained phospho-GFAP. In a cold injury model of the cerebral cortex, we detected phospho-GFAP in reactive astrocytes at 2-3 weeks after the injury. CONCLUSIONS: Phospho-GFAP provides a molecular marker indicating the heterogeneity of astrocytes, and Gfap(hwt) knock-in mice will aid in monitoring intracellular conditions of astrocytes, under various conditions. Our results suggest that the phosphorylation of GFAP plays a role in non-dividing astrocytes in vivo. 1356-9597 Journal Article},
	Author = {Takemura, M. and Nishiyama, H. and Itohara, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Genes Cells},
	Keywords = {Organ Specificity;Glial Fibrillary Acidic Protein/genetics/*metabolism;Central Nervous System/*metabolism;G abstr;Immunohistochemistry;Animals, Genetically Modified;11 Glia;Astrocytes/*metabolism;Animals;Support, Non-U.S. Gov't;Mice;Phosphotransferases/*metabolism;Phosphorylation},
	Number = {3},
	Organization = {Laboratory for Behavioural Genetics, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako 351-0198, Japan.},
	Pages = {295-307},
	Pubmed = {11918673},
	Title = {Distribution of phosphorylated glial fibrillary acidic protein in the mouse central nervous system},
	Uuid = {6DD56C00-56B7-4887-A0FD-D9900D524E00},
	Volume = {7},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11918673}}

@article{Takeuchi:2005,
	Abstract = {Recent studies suggest that excitotoxicity may contribute to neuronal damage in neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Activated microglia have been observed around degenerative neurons in these diseases, and they are thought to act as effector cells in the degeneration of neural cells in the central nervous system. Neuritic beading, focal bead-like swellings in the dendrites and axons, is a neuropathological sign in epilepsy, trauma, ischemia, aging and neurodegenerative diseases. Previous reports showed that neuritic beading is induced by various stimuli including glutamate or nitric oxide and is a neuronal response to harmful stimuli. However, the precise physiologic significance of neuritic beading is unclear. We provide evidence that neuritic beading induced by activated microglia is a feature of neuronal cell dysfunction toward neuronal death, and the neurotoxicity of activated microglia is mediated through N-methyl-D-aspartate (NMDA) receptor signaling. Neuritic beading occurred concordant with a rapid drop in intracellular ATP levels and preceded neuronal death. The actual neurite beads consisted of collapsed cytoskeletal proteins and motor proteins arising from impaired neuronal transport secondary to cellular energy loss. The drop in intracellular ATP levels was due to the inhibition of mitochondrial respiratory chain complex IV activity downstream of NMDA receptor signaling. Blockage of NMDA receptors nearly completely abrogated mitochondrial dysfunction and neurotoxicity. Thus, neuritic beading induced by activated microglia occurs through NMDA receptor signaling and represents neuronal cell dysfunction preceding neuronal death. Blockage of NMDA receptors may be an effective therapeutic approach for neurodegenerative diseases.},
	Author = {Takeuchi, and Mizuno, and Zhang, and Wang, and Kawanokuchi, and Kuno, and Suzumura,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {2985121R},
	Organization = {Department of Neuroimmunology, Nagoya University Research Institute of Environmental Medicine, Nagoya 464-8601.},
	Pii = {M413863200},
	Pubmed = {15640150},
	Title = {Neuritic beading induced by activated microglia is an early feature of neuronal dysfunction toward neuronal death by inhibition of mitochondrial respiration and axonal transport},
	Uuid = {3AE25662-A663-4495-AACE-C5159906F3F0},
	Year = {2005},
	url = {papers/Takeuchi_JBiolChem2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1074/jbc.M413863200}}

@article{Takeuchi:2006,
	Abstract = {MAM (meprin/A5 protein/receptor protein tyrosine phosphatase mu) domain glycosylphosphatidylinositol anchor 1 (MDGA1), a unique cell surface glycoprotein, is similar to Ig-containing cell adhesion molecules that influence neuronal migration and process outgrowth. We show in postnatal mice that MDGA1 is expressed by layer 2/3 neurons throughout the neocortex. During development, MDGA1 is expressed in patterns consistent with its expression by migrating layer 2/3 neurons, suggesting a role for MDGA1 in controlling their migration and settling in the superficial cortical plate. To test this hypothesis, we performed loss-of-function studies using RNA interference (RNAi) targeting different sequences of mouse MDGA1. RNAi or empty vectors were coelectroporated with an enhanced green fluorescent protein reporter in utero into the lateral ventricle at embryonic day 15.5 to transfect progenitors of superficial layer neurons; the distributions of transfected neurons were analyzed late on postnatal day 0. We found a direct correlation between effectiveness of an RNAi in suppressing MDGA1 expression and disrupting migration of superficial layer neurons. An RNAi with no effect on MDGA1 expression has no effect on the migration. In contrast, an RNAi that suppresses MDGA1 expression also blocks proper migration of transfected superficial layer neurons, with essentially all transfected cells found deep in the cortical plate or beneath it. This migration defect is rescued by cotransfection of a rat MDGA1 expression construct along with the effective RNAi, confirming that the RNAi effect is specific to diminishing mouse MDGA1 expression. RNAi transfections of deep layer neurons that do not express MDGA1 do not significantly affect their migration. We conclude that MDGA1 acts cell autonomously to control the migration of MDGA1-expressing superficial layer cortical neurons.},
	Author = {Takeuchi, Akihide and O'Leary, Dennis D. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {17},
	Organization = {Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, California 92037, USA.},
	Pages = {4460-4},
	Pii = {26/17/4460},
	Pubmed = {16641224},
	Title = {Radial migration of superficial layer cortical neurons controlled by novel Ig cell adhesion molecule MDGA1},
	Uuid = {35D564D0-E31B-4E0D-ABDC-2929062E5766},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4935-05.2006}}

@article{Takeuchi:2001,
	Abstract = {In a previous study, we have demonstrated that damaged neurons within a boundary area around necrosis fall into delayed neuronal death owing to the cytotoxic effect of microglial nitric oxide (NO), and these neurons are finally eliminated by activated microglia. In this process, microglia are activated to release NO, increase in number, and accumulate toward the damaged area. In this study, we investigated the expression of macrophage colony-stimulating factor (M-CSF, also called colony stimulating factor-1; CSF-1) and other cytokines, which are reported to relate to activation, proliferation, or migration of microglia. The mRNA of M-CSF arose biphasically from 30 min to 1 hr and from 6 to 72 hr after the injury, as demonstrated by semiquantitative RT-PCR. However, another cytokine of granulocyte-macrophage CSF (GM-CSF) or interleukin-3 (IL-3), which causes proliferation of microglia in vitro, was not detected. From immunohistochemical studies, positive staining of M-CSF was observed mainly in neuron-specific enolase (NSE)-positive cells from 1 to 12 hr after the injury, and after that M-CSF became positive in Griffonia simplicifolia isolectin-B4 (GSA-I-B4)-positive cells from 24 to 72 hr in the boundary area around necrosis. These results suggest that neurons around the damaged area express M-CSF in the early phase after injury, which may initially activate microglia, and these activated microglia also express M-CSF later, causing further proliferation or migration of microglia themselves to eliminate damaged neurons or necrotic brain tissue.},
	Author = {Takeuchi, A. and Miyaishi, O. and Kiuchi, K. and Isobe, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Nerve Degeneration;Astrocytes;Stereotaxic Techniques;Encephalitis;Rats;Ethanol;Animals;Microglia;Central Nervous System Depressants;RNA, Messenger;Not relevant;11 Glia;Support, Non-U.S. Gov't;Fusobacterium Infections;Neurons;Macrophage Colony-Stimulating Factor;Gene Expression;Nitric Oxide},
	Medline = {21326332},
	Month = {7},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Basic Gerontology, National Institute for Longevity Sciences, Oobu-city, Aichi, Japan.},
	Pages = {38-44},
	Pubmed = {11433427},
	Title = {Macrophage colony-stimulating factor is expressed in neuron and microglia after focal brain injury},
	Uuid = {9466DE13-65EB-4E2B-8F7C-2D097CBA0535},
	Volume = {65},
	Year = {2001},
	url = {papers/Takeuchi_JNeurosciRes2001.pdf}}

@article{Taleisnik:1981,
	Author = {Taleisnik, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0361-7742},
	Journal = {Prog Clin Biol Res},
	Keywords = {24 Pubmed search results 2008;Electrochemistry;Research Support, Non-U.S. Gov't;Gonadotropins;Neurotransmitters;Neural Pathways;Humans;Cerebral Cortex;review;Frontal Lobe},
	Medline = {82106093},
	Nlm_Id = {7605701},
	Pages = {249-57},
	Pubmed = {6119701},
	Title = {Role of the frontal lobe cortex in the regulation of gonadotropin secretion},
	Uuid = {3A0C2937-BDFD-4794-98F1-39384857A262},
	Volume = {74},
	Year = {1981}}

@article{Tamaki:2002,
	Abstract = {Direct isolation of human central nervous system stem cells (CNS-SC) based on cell surface markers yields a highly purified stem cell population that can extensively expand in vitro and exhibit multilineage differentiation potential both in vitro and in vivo. The CNS-SC were isolated from fetal brain tissue using the cell surface markers CD133(+), CD34(-), CD45(-), and CD24(-/lo) (CD133(+) cells). Fluorescence-activated cell sorted (FACS) CD133(+) cells continue to expand exponentially as neurospheres while retaining multipotential differentiation capacity for >10 passages. CD133(-), CD34(-), and CD45(-) sorted cells (approximately 95\%of total fetal brain tissue) fail to initiate neurospheres. Neurosphere cells transplanted into neonatal immunodeficient NOD-SCID mice proliferated, migrated, and differentiated in a site-specific manner. However, it has been difficult to evaluate human cell engraftment, because many of the available monoclonal antibodies against neural cells (beta-tubulin III and glial fibrillary acidic protein) are not species specific. To trace the progeny of human cells after transplantation, CD133(+)-derived neurosphere cells were transduced with lentiviral vectors containing enhanced green fluorescent protein (eGFP) expressed downstream of the phosphoglycerate kinase promoter. After transduction, GFP(+) cells were enriched by FACS, expanded, and transplanted into the lateral ventricular space of neonatal immunodeficient NOD-SCID brain. The progeny of transplanted cells were detected by either GFP fluorescence or antibody against GFP. GFP(+) cells were present in the subventricular zone-rostral migrating stream, olfactory bulb, and hippocampus as well as nonneurogenic sites, such as cerebellum, cerebral cortex, and striatum. Antibody against GFP revealed that some of the cells displayed differentiating dendrites and processes with neurons or glia cells. Thus, marking human CNS-SC with reporter genes introduced by lentiviral vectors is a useful tool with which to characterize migration and differentiation of human cells in this mouse transplantation model.},
	Author = {Tamaki, Stanley and Eckert, Karl and He, Dongping and Sutton, Richard and Doshe, Monika and Jain, Gitanjali and Tushinski, Robert and Reitsma, Michael and Harris, Brent and Tsukamoto, Ann and Gage, Fred and Weissman, Irving and Uchida, Nobuko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Differentiation;Transduction, Genetic;Mice, Inbred NOD;Corpus Striatum;Animals;Brain Tissue Transplantation;Humans;Cell Separation;Stem Cell Transplantation;Lentivirus;Indicators and Reagents;Mice, SCID;Hippocampus;Cell Movement;Green Fluorescent Proteins;Fetal Tissue Transplantation;11 Glia;Genetic Vectors;Injections, Intraventricular;Olfactory Pathways;Neurons;Mice;Cell Division;Luminescent Proteins;Stem Cells;Corpus Callosum},
	Medline = {22194586},
	Month = {9},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {StemCells, Inc., Palo Alto, California.},
	Pages = {976-86},
	Pubmed = {12205691},
	Title = {Engraftment of sorted/expanded human central nervous system stem cells from fetal brain},
	Uuid = {F22E1447-6E7A-4E23-B983-8F308A7FD6D3},
	Volume = {69},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10412}}

@article{Tamamaki:2001,
	Abstract = {Neocortical neurons are produced by cell division of neural stem cells in the ventricular zone of the cerebral cortex. We investigated the production of neurons by infecting neuroepithelial cells with a modified GFP-recombinant adenovirus. The adenovirus DNA is inherited by only one daughter cell at each cell division and travels one way from the progenitor to the progeny. Since the ventricular zone (VZ) of the embryo neocortex expressed an adenovirus receptor, CAR ubiquitously, morphology and cell-lineage of cells in the VZ could be revealed by the adenovirus infection. Radial glias, cells with a bipolar shape, and spherical cells were found as modified-GFP-positive (mGFP+) in the VZ. The bipolar cells (radial cells) had a radial process not in contact with the pia mater and a growth-cone-like structure at the edge of their radial process, while the radial glias had a process spanning all the cortical layers. Ten hours after viral infection, most mGFP+ cells were radial cells. In the following 8 h, the percentage of mGFP+ radial glias in mGFP+ neocortical cells increased from 18 to 50\%, while that in radial/spherical cells decreased from 75 to 19\%. The radial glias often divided asymmetrically and produced spherical cells and neuronal precursors. The spherical cells seemed to become radial cells by extending a radial process. The spherical cells, radial cells and radial glias seemed to constitute a proliferating cell cycle during which postmitotic neuronal precursors are produced. The neuronal precursors that inherited the radial processes migrated radially and developed into neocortical neurons. Four days after the viral infection, 97\%of mGFP+ cells were neocortical neurons. Here, we propose that the radial glia is a progenitor of neocortical neurons, and that a significant number of radially migrating neurons is guided by their own radial processes connected to the pia mater.},
	Author = {Tamamaki, N. and Nakamura, K. and Okamoto, K. and Kaneko, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0168-0102},
	Journal = {Neurosci Res},
	Keywords = {Fetus;Cell Differentiation;Animals;Aging;Indicators and Reagents;Cell Movement;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Genetic Vectors;Cell Lineage;Cerebral Cortex;Neurons;Neuroglia;Receptors, Virus;Mice;Cell Division;Microscopy, Electron;Growth Cones;Stem Cells;Luminescent Proteins;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {21427498},
	Month = {9},
	Nlm_Id = {8500749},
	Number = {1},
	Organization = {Department of Morphological Brain Science, Graduate School of Medicine, Kyoto University, Yoshida Konoecho, Sakyoku, 606-8501, Kyoto, Japan. tamamaki\@mbs.med.kyoto-u.ac.jp},
	Pages = {51-60},
	Pii = {S0168010201002590},
	Pubmed = {11535293},
	Title = {Radial glia is a progenitor of neocortical neurons in the developing cerebral cortex},
	Uuid = {A7D165DA-76BE-445F-A376-5B8632C9B1FD},
	Volume = {41},
	Year = {2001}}

@article{Tamura:2007,
	Abstract = {In the adult mammalian brain, multipotent stem or progenitor cells involved in reproduction of neurons and glial cells have been well investigated only in very restricted regions; the subventricular zone of the lateral ventricle and the dentate gyrus in the hippocampal formation. In the neocortex, a series of in vitro studies has suggested the possible existence of neural progenitor cells possessing neurogenic and/or gliogenic potential in adult mammals. However, the cellular properties of the cortical progenitor cells in vivo have not been fully elucidated. Using 5'-bromodeoxyuridine labeling and immunohistochemical analysis of cell differentiation markers, we found that a subpopulation of NG2-immunopositive cells co-expressing doublecortin (DCX), an immature neuron marker, ubiquitously reside in the adult rat neocortex. Furthermore, these cells are the major population of proliferating cells in the region. The DCX(+)/NG2(+) cells reproduced the same daughter cells, or differentiated into DCX(+)/NG2(-) (approximately 1\%) or DCX(-)/NG2(+) (approximately 10\%) cells within 2 weeks after cell division. The DCX(+)/NG2(-) cells were also immunopositive for TUC-4, a neuronal linage marker, suggesting that these cells were committed to neuronal cell differentiation, whereas the DCX(-)/NG2(+) cells showed faint immunoreactivity for glutathione S-transferase (GST)-pi, an oligodendrocyte lineage marker, in the cytoplasm, suggesting glial cell lineage, and thereafter the cells differentiated into NG2(-)/GST-pi(+) mature oligodendrocytes after a further 2 weeks. These findings indicate that DCX(+)/NG2(+) cells ubiquitously exist as 'multipotent progenitor cells' in the neocortex of adult rats.},
	Author = {Tamura, Yasuhisa and Kataoka, Yosky and Cui, Yilong and Takamori, Yasuharu and Watanabe, Yasuyoshi and Yamada, Hisao},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Microtubule-Associated Proteins;Cell Differentiation;Animals;Rats;Multipotent Stem Cells;Phosphopyruvate Hydratase;Models, Biological;Neocortex;Cell Count;research support, non-u.s. gov't;Time Factors;Neuropeptides;Male;01 Adult neurogenesis general;Glutathione Transferase;Versicans;Immunohistochemistry;24 Pubmed search results 2008;Bromodeoxyuridine;Nerve Tissue Proteins},
	Month = {6},
	Nlm_Id = {8918110},
	Number = {12},
	Organization = {Department of Anatomy and Cell Science, KMU 21C COE Project, Kansai Medical University, Osaka, Japan.},
	Pages = {3489-98},
	Pii = {EJN5617},
	Pubmed = {17610569},
	Title = {Multi-directional differentiation of doublecortin- and NG2-immunopositive progenitor cells in the adult rat neocortex in vivo},
	Uuid = {2B39259E-FB93-4DB5-A031-AF1DA7DD5477},
	Volume = {25},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2007.05617.x}}

@article{Tanaka:2006a,
	Abstract = {The doublecortin (Dcx) and doublecortin-like kinase 1 (Dclk) genes are developmentally expressed neuronal microtubule-associated proteins. Humans with DCX mutations show a severe defect in hippocampal development, but targeted deletion in mouse shows only a defect in pyramidal neuron lamination. There is significant sequence overlap between Dcx and Dclk, suggesting functional redundancy. Here we show that the two genes display overlapping expression patterns in developing mouse hippocampus. Targeted deletion of Dclk shows no appreciable developmental defect in the hippocampus, but removal of both genes shows severe hippocampal lamination defects involving the entire cornu ammonis and dentate gyrus fields that mimic the human phenotype. These results suggest these genes are partially functionally redundant in the formation of the murine hippocampus.},
	Author = {Tanaka, Teruyuki and Koizumi, Hiroyuki and Gleeson, Joseph G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {Microtubule-Associated Proteins;Cell Differentiation;Animals;Aging;Cell Movement;Hippocampus;Protein-Serine-Threonine Kinases;research support, non-u.s. gov't;Neuropeptides;Animals, Newborn;Nerve Net;Mice, Knockout;Neurons;Cell Aggregation;Organogenesis;research support, n.i.h., extramural;Body Patterning;Mice;24 Pubmed search results 2008;in vitro},
	Month = {7},
	Nlm_Id = {9110718},
	Organization = {Neurogenetics Laboratory, Department of Neurosciences, University of California, San Diego, CA, USA.},
	Pages = {i69-73},
	Pii = {16/suppl_1/i69},
	Pubmed = {16766710},
	Title = {The doublecortin and doublecortin-like kinase 1 genes cooperate in murine hippocampal development},
	Uuid = {DFBB8848-D8DB-46D9-9EF7-66355ED1F17E},
	Volume = {16 Suppl 1},
	Year = {2006},
	url = {papers/Tanaka_CerebCortex2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhk005}}

@article{Tanaka:2002a,
	Abstract = {The mrf-1 gene has been isolated from microglia exposed to cultured cerebellar granule neurons undergoing apoptosis. We have shown that mrf-1 is upregulated in response to neuronal death and degeneration both in vitro and in vivo. However, the exact role of MRF-1 remains unknown. Here we show that MRF-1 is released from cultured rat microglia, and its release is greatly enhanced under inflammatory conditions. When microglia were treated with ATP, the amount of MRF-1 that was released increased 10-fold compared to the basal level of release. Enhanced MRF-1 release was induced within 10 min and peaked within 1 h; after approximately 4 h, the MRF-1 release had returned to normal. MRF-1 release was stimulated by 2-methyl-thio-ATP (five-fold) and a P2X(7) selective agonist, 2'- and 3'-O-(4-benzoylbenzoyl)-ATP (ten-fold). Moreover, the ATP-stimulated MRF-1 release was inhibited by a P2X(7) selective antagonist, oxidized ATP (oATP), and also under a Ca(2+)-free condition. These results indicate that the effects of ATP are dependent on Ca(2+) influx through P2X(7) receptors. MRF-1 release was enhanced by Ca(2+)-ionophore A23187 (sixfold), thapsigargin (threefold); however, it was not enhanced by glutamate or lipopolysaccharide. Moreover, a platelet-activating factor enhanced microglial MRF-1 release in a dose-dependent manner. We also showed that a conditioned medium from cerebellar granule neurons undergoing apoptosis markedly increased MRF-1 release from microglia; that effect was significantly inhibited by oATP. These results indicate that selective inflammatory stimulations, including ATP and PAF, enhance MRF-1 release from microglia through a Ca(2+)-dependent mechanism and suggest that MRF-1 may play a role in cell-cell interactions under inflammatory conditions.},
	Author = {Tanaka, Shuuitsu and Koike, Tatsuro},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Calcium Signaling;Animals;Cells, Cultured;Encephalitis;Rats;Enzyme Inhibitors;Up-Regulation;Chemotaxis;Microglia;Cell Communication;Rats, Sprague-Dawley;Culture Media, Conditioned;11 Glia;Ionophores;Adenosine Triphosphate;Animals, Newborn;Support, Non-U.S. Gov't;Platelet Activating Factor;Neurons;Inflammation Mediators;Gliosis;Nerve Tissue Proteins;Receptors, Purinergic P2},
	Medline = {22307125},
	Month = {12},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Molecular Neurobiology Laboratory, Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo, Japan. shtanaka\@sci.hokudai.ac.jp},
	Pages = {360-71},
	Pubmed = {12420315},
	Title = {Selective inflammatory stimulations enhance release of microglial response factor (MRF)-1 from cultured microglia},
	Uuid = {583C5467-7ACD-4493-8201-9E431D77D847},
	Volume = {40},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10142}}

@article{Tanaka:1999,
	Abstract = {Notch family molecules are thought to be negative regulators of neuronal differentiation in early brain development. After expression in the embryonic period, Notch2 continues to be expressed postnatally in the specific regions in the rodent brain. Here, we examined Notch2 expression in the postnatal mouse brain using lacZ knockin animals at the Notch2 locus. Notch2 expression was observed in the developing cerebellum and hippocampus, characteristic regions where neurogenesis persists after birth. Double staining of sections revealed that Notch2 was expressed by Bergmann glia in the cerebellum, radial glia in the hippocampus, and some astrocytes in both regions. Notch2 expression by glial cells was clearly confirmed in dissociated cell cultures. Interestingly, neocortical glia, many of which did not express Notch2 in vivo, did express Notch2 in a dissociated culture condition. The triple staining of dissociated cell cultures revealed that stronger Notch2 expression correlated with the immature type of glial gene expressions: stronger vimentin and weaker glial fibrillary acidic protein expressions. In addition, Notch2 expression correlated with the incorporation of bromodeoxyuridine both in vivo and in vitro. Thus, these findings demonstrate that Notch2 is expressed not only by neuronal cells in the embryonic brain, but also by glial cells in the postnatal brain, and that its expression negatively correlates with glial differentiation, proposing its novel function as a negative regulator of glial differentiation in mammalian brain development.},
	Author = {Tanaka, M. and Kadokawa, Y. and Hamada, Y. and Marunouchi, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurobiol},
	Keywords = {G;Cell Differentiation;Aging;Cerebellum/cytology/growth &development/metabolism;Brain/cytology/growth &development/*metabolism;*Gene Expression Regulation, Developmental;Female;Animal;Glial Fibrillary Acidic Protein/analysis;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;beta-Galactosidase/genetics;Crosses, Genetic;Receptors, Cell Surface/analysis/*genetics;Male;Neuroglia/cytology/*physiology;In Situ Hybridization;Support, Non-U.S. Gov't;Mice},
	Number = {4},
	Organization = {Division of Cell Biology, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi 470-1192, Japan.},
	Pages = {524-39.},
	Title = {Notch2 expression negatively correlates with glial differentiation in the postnatal mouse brain},
	Uuid = {B7CC0E42-C7B1-487B-A7D3-82B10561BD8F},
	Volume = {41},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10590176}}

@article{Tanaka:2002,
	Abstract = {An ischemia-induced gene was screened using a differential display technique in mouse transient forebrain ischemia. One of the ischemia-responsive clones was found to encode mouse hsp40. HSP40 has a critical regulatory function in the HSC70 ATPase activity. Expression of hsp40 mRNA was low in the nonischemic mouse hippocampus, but it was significantly upregulated 4 hr after ischemia by Northern blot analysis. In situ hybridization analysis revealed hsp40 mRNA induction in the neuron. HSP40 protein expression was also enhanced in the pyramidal and dentate granular neurons from 2 to 4 days after ischemia. The temporal expression and distribution profile of HSC70 protein was similar to that of HSP40, and both proteins were colocalized in ischemic hippocampal neurons. In the gerbil transient forebrain ischemia model, both HSP40 and HSC70 proteins were expressed strongly in ischemia-resistant CA3 neurons and dentate granule cells 1 day after 5 min ischemia, but were not expressed in vulnerable CA1 neurons. However, both proteins were in parallel expressed in the tolerance-acquired CA1 neurons. Based on the current observation that both HSP40 and HSC70 proteins were synergistically expressed in the ischemia-resistant and tolerance-acquired neurons, cochaperone HSP40 may play a significant role against postischemic neuronal response and lead to cell survival through interaction with simultaneously induced HSC70. 21624013 0360-4012 Journal Article},
	Author = {Tanaka, S. and Kitagawa, K. and Ohtsuki, T. and Yagita, Y. and Takasawa, K. and Hori, M. and Matsumoto, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Up-Regulation/genetics;Neurons/*metabolism/pathology;Gene Expression Regulation/physiology;Gerbillinae;*Ischemic Preconditioning;Hippocampus/*metabolism/pathology/physiopathology;Heat-Shock Proteins/*genetics/metabolism;Nerve Degeneration/genetics/metabolism/physiopathology;Animal;C abstr;Mice, Inbred C57BL;Disease Models, Animal;Heat-Shock Proteins 70/*genetics/metabolism;Cell Survival/genetics;Reperfusion Injury/*genetics/metabolism/physiopathology;Male;Support, Non-U.S. Gov't;Brain Ischemia/*genetics/metabolism/physiopathology;04 Adult neurogenesis factors;Mice;Immunohistochemistry;RNA, Messenger/metabolism},
	Number = {1},
	Organization = {Division of Strokology, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Osaka, Japan. brain\@medone.med.osaka-u.ac.jp},
	Pages = {37-47},
	Pubmed = {11754079},
	Title = {Synergistic induction of HSP40 and HSC70 in the mouse hippocampal neurons after cerebral ischemia and ischemic tolerance in gerbil hippocampus},
	Uuid = {BD6D4C61-6613-43F1-94E4-ACF5937BA88D},
	Volume = {67},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11754079}}

@article{Tanaka:2006,
	Abstract = {We used lipopolysaccharide (LPS) to activate microglia that play an important role in the brain immune system. LPS injected into the rat hippocampus CA1 region activated microglial cells resulting in an increased production of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha in the hippocampus during the initial stage of treatment. Immunostaining for IL-1beta was increased at 6 hr after LPS injection. IL-1beta-immunopositive cells were co-localized with immunostaining for CD11b. Subacute treatment with LPS by the same route for 5 days caused long-term activation of microglia and induced learning and memory deficits in animals when examined with a step-through passive avoidance test, but histochemical analysis showed that neuronal cell death was not observed under these experimental conditions. The increased expression of the heme oxygenase-1 (HO-1) gene, an oxidative stress maker, was observed. However, the genetic expression of brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, decreased during the course of LPS treatment. We found decreases in [(3)H]MK801 binding in the hippocampus CA1 region by LPS-treatment for 5 days. The data shows that glutamatergic transmission was attenuated in the LPS-treated rats. These results suggest that long-term activation of microglia induced by LPS results in a decrease of glutamatergic transmission that leads to learning and memory deficits without neuronal cell death. The physiologic significance of these findings is discussed. (c) 2006 Wiley-Liss, Inc.},
	Author = {Tanaka, and Ide, and Shibutani, and Ohtaki, and Numazawa, and Shioda, and Yoshida,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {11 Glia},
	Month = {1},
	Nlm_Id = {7600111},
	Organization = {Department of Biochemical Toxicology, School of Pharmaceutical Sciences.},
	Pubmed = {16429444},
	Title = {Lipopolysaccharide-induced microglial activation induces learning and memory deficits without neuronal cell deathin rats},
	Uuid = {01D200C6-4B27-4416-BC9E-21349BCF7F9C},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20752}}

@article{Tanaka:2003,
	Abstract = {Brain ischemia induces a marked response of resident microglia and hematopoietic cells including monocytes/macrophages. The present study was designed to assess the distribution of microglia/macrophages in cerebral ischemia using bone marrow chimera mice known to express enhanced green fluorescent protein (EGFP). At 24 h after middle cerebral artery occlusion (MCAO), many round-shaped EGFP-positive cells migrated to the ischemic core and peri-infarct area. At 48-72 h after MCAO, irregular round- or oval-shaped EGFP/ionized calcium-binding adapter molecule 1 (Iba 1)-positive cells increased in the transition zone, while many amoeboid-shaped or large-cell-body EGFP/Iba 1-positive cells were increased in number in the innermost area of ischemia. At 7 days after MCAO, many process-bearing ramified shaped EGFP/Iba 1-positive cells were detected in the transition to the peri-infarct area, while phagocytic cells were distributed in the transition to the core area of the infarction. The distribution of these morphologically variable EGFP/Iba 1-positive cells was similar up to 14 days from MCAO. The present study directly showed the migration and distribution of bone marrow-derived monocytes/macrophages and the relationship between resident microglia and infiltrated hematogenous element in ischemic mouse brain. It is important to study the distribution of intrinsic and extrinsic microglia/macrophage in ischemic brain, since such findings may allow the design of appropriate gene-delivery system using exogenous microglia/macrophages to the ischemic brain area.},
	Author = {Tanaka, R. and Komine-Kobayashi, M. and Mochizuki, H. and Yamada, M. and Furuya, T. and Migita, M. and Shimada, T. and Mizuno, Y. and Urabe, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Microtubule-Associated Proteins;Animals;Macrophages;Chimera;Whole-Body Irradiation;Comparative Study;Infarction, Middle Cerebral Artery;Microglia;Cell Count;Mice, Transgenic;Cell Movement;11 Glia;Green Fluorescent Proteins;Time Factors;Immunosuppressive Agents;Bone Marrow;Fluorouracil;Calcium-Binding Proteins;Brain Ischemia;Transplants;Mice;Luminescent Proteins;Central Nervous System;Immunohistochemistry;Dose-Response Relationship, Radiation;Research Support, Non-U.S. Gov't},
	Medline = {22506166},
	Nlm_Id = {7605074},
	Number = {3},
	Organization = {Department of Neurology, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.},
	Pages = {531-9},
	Pii = {S0306452202009545},
	Pubmed = {12617960},
	Title = {Migration of enhanced green fluorescent protein expressing bone marrow-derived microglia/macrophage into the mouse brain following permanent focal ischemia},
	Uuid = {7E8946AA-A893-411B-BCA0-24D6462F6192},
	Volume = {117},
	Year = {2003}}

@article{Tanaka:2004a,
	Abstract = {BACKGROUND AND PURPOSE: Gene therapy may show promise for stroke patients, but invasive techniques such as intraventricular or intracerebral injection of therapeutic genes may have limited applicability. The purpose of this study is to develop systemic gene therapy using macrophages infiltrating the infarct to deliver and express the gene. METHODS: After permanent middle cerebral artery occlusion in rats, an enhanced green fluorescent protein (EGFP) plasmid conjugate in liposomes was injected via the femoral vein. We also constructed a bicistronic plasmid vector for fibroblast growth factor-2 (FGF-2) as well as EGFP, administering it in other rats with middle cerebral artery occlusion. RESULTS: EGFP expression in normal brain was absent but was strong in macrophages accumulating along the infarct border. FGF-2 protein production was induced in macrophages along the infarct border after injection of bicistronic FGF-2 and EGFP plasmid vector; this stimulated proliferation of neural progenitors in the subventricular zone in the ischemic hemisphere compared with control plasmid vectors (61.7+/-5.2 versus 42.2+/-5.5 cells per mm2, n=4 each, P<0.01). CONCLUSIONS: Systemic gene transfer by liposome to macrophages infiltrating an infarct may prove useful for gene therapy in stroke.},
	Author = {Tanaka, Shigeru and Kitagawa, Kazuo and Sugiura, Shiro and Matsuoka-Omura, Emi and Sasaki, Tsutomu and Yagita, Yoshiki and Hori, Masatsugu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1524-4628},
	Journal = {Stroke},
	Keywords = {Animals;Genes, erbB-1;Rats;Macrophages;Infarction, Middle Cerebral Artery;Cell Movement;Liposomes;Cerebral Infarction;Not relevant;Cell Proliferation;Male;Genetic Vectors;11 Glia;Green Fluorescent Proteins;Disease Models, Animal;Plasmids;Fibroblast Growth Factor 2;Rats, Wistar;Gene Therapy;Gene Transfer Techniques;Neurons;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {8},
	Nlm_Id = {0235266},
	Number = {8},
	Organization = {Division of Strokology, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Osaka, Japan.},
	Pages = {1968-73},
	Pii = {01.STR.0000133685.59556.a7},
	Pubmed = {15192242},
	Title = {Infiltrating macrophages as in vivo targets for intravenous gene delivery in cerebral infarction},
	Uuid = {AFEB2555-3643-4BED-9880-DC0E68791B55},
	Volume = {35},
	Year = {2004},
	url = {papers/Tanaka_Stroke2004a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.STR.0000133685.59556.a7}}

@article{Tanaka:2004,
	Abstract = {BACKGROUND AND PURPOSE: Neurogenesis has been observed in the dentate gyrus of the adult hippocampus; however, the mechanisms involved in this process are still only partly understood. In this study, we visualized the proliferation, migration, and differentiation of neuronal progenitor cells in the dentate gyrus induced by ischemic stress using improved retroviral vector. METHODS: Improved retroviral vector expressing enhanced green fluorescent protein (EGFP) as a transgene was injected into the dentate gyrus of adult Mongolian gerbils. After 48 hours, transient global ischemia (TGI) was induced by bilateral common carotid artery occlusion for 5 minutes using aneurysm clips. The morphological and immunohistological features of newly-generated cells in the dentate gyrus were analyzed at various times thereafter. RESULTS: At 48 hours after viral injection, almost all EGFP-positive dividing cells were found in the subgranule layer (SGL). These cells proliferated and migrated to the granule cell layer (GCL), expressing the developing neuronal markers polysialic acid and doublecortin, and differentiated to neuronal nuclei-positive or calbindin-positive mature granule cells at 30 days after TGI or sham-operation. The number of GFP-positive cells in the GCL was significantly higher (P<0.05) in the ischemic animals at 30 days than in sham-operated gerbils. CONCLUSIONS: We saw neurogenesis in the adult dentate gyrus. Furthermore, we showed that ischemic stress promoted the proliferation and normal development of neurons at this site.},
	Author = {Tanaka, Ryota and Yamashiro, Kazuo and Mochizuki, Hideki and Cho, Nei and Onodera, Masafumi and Mizuno, Yoshikuni and Urabe, Takao},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1524-4628},
	Journal = {Stroke},
	Keywords = {Genetic Vectors;Indicators and Reagents;Cell Differentiation;Luminescent Proteins;Animals;Dentate Gyrus;Stem Cells;Retroviridae;Cell Division;06 Adult neurogenesis injury induced;Gerbillinae;Male;Cell Movement;Support, Non-U.S. Gov't;Neurons;Ischemic Attack, Transient},
	Month = {6},
	Nlm_Id = {0235266},
	Number = {6},
	Organization = {Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Tokyo, Japan.},
	Pages = {1454-9},
	Pii = {01.STR.0000126480.40967.b3},
	Pubmed = {15073392},
	Title = {Neurogenesis after transient global ischemia in the adult hippocampus visualized by improved retroviral vector},
	Uuid = {E59FC3FD-200C-4F66-BEA8-4E01B0F28C23},
	Volume = {35},
	Year = {2004},
	url = {papers/Tanaka_Stroke2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.STR.0000126480.40967.b3}}

@article{Tanapat:1998,
	Abstract = {The granule cell population of the dentate gyrus is produced predominantly during the postnatal period in rats. Previous studies have shown that experimental increases in the levels of adrenal steroids suppress the proliferation of granule cell precursors during the first postnatal week, the time of maximal neurogenesis in the dentate gyrus. These findings raise the possibility that stressful experiences that elevate adrenal steroid levels may inhibit the production of granule neurons, and thus alter the development of the dentate gyrus. To test this possibility, we exposed naive rat pups to the odors of a known predator, adult male rats, and examined both plasma corticosterone levels and the number of 3H-thymidine labeled cells in the dentate gyrus. A single exposure of rat pups to adult male rat odor elevated corticosterone levels immediately and diminished the number of 3H-thymidine labeled cells in the granule cell layer by 24 h later. These results suggest that stressful experiences suppress the production of granule neurons in the developing dentate gyrus.},
	Author = {Tanapat, P. and Galea, L. A. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Int J Dev Neurosci},
	Keywords = {Animals, Newborn/*growth &development;Odors;Cell Division/physiology;Rats, Sprague-Dawley;Stress/blood/etiology/*pathology;Embryo/pathology;Rats;C;Aging/physiology;Animal;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Male;Dentate Gyrus/*embryology/*growth &development/pathology;Neurons/*pathology;Fetal Development/physiology;Stem Cells/*pathology},
	Number = {3-4},
	Organization = {Department of Psychology, Princeton University, NJ 08544, USA.},
	Pages = {235-9.},
	Pubmed = {9785120},
	Title = {Stress inhibits the proliferation of granule cell precursors in the developing dentate gyrus},
	Uuid = {C9E0E1A1-2EF7-4D41-9BF2-A15FADFFBDA4},
	Volume = {16},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=9785120&dopt=Citation}}

@article{Tanapat:1999,
	Abstract = {To determine whether a sex difference exists in the production of hippocampal cells during adulthood, we examined proliferating cells and their progeny in adult rats using the thymidine analog bromodeoxyuridine (BrdU) combined with immunohistochemistry for markers of neurons and glia. Additionally, to determine whether ovarian hormones affect cell proliferation, we examined the numbers of BrdU- labeled cells at different estrous cycle stages and after ovarian steroid manipulation. Stereological analyses of the numbers of BrdU- labeled cells revealed that females produced more cells than males in the dentate gyrus but not in the subventricular zone. The production of new hippocampal cells in females appears to be affected by ovarian hormone levels; ovariectomy diminished the number of BrdU-labeled cells, an effect reversed by estrogen replacement. A natural fluctuation in cell proliferation was also noted; females produced more cells during proestrus (when estrogen levels are highest) compared with estrus and diestrus. Many of these cells acquired neuronal characteristics, including the formation of dendrites and expression of Turned-On-After-Division 64 kDa, a marker of immature granule neurons, and the calcium-binding protein calbindin, a marker of mature granule neurons. However, examination of the numbers of pyknotic cells and the numbers of BrdU-labeled cells at longer survival times revealed that many new cells in the dentate gyrus eventually degenerate. Consistently the number of labeled cells in females is no longer higher than that observed in males by 2 weeks after the last BrdU injection. These findings suggest that estrogen-enhanced cell proliferation during proestrus results in more immature neurons in the hippocampal formation of females compared with males and present the possibility that these new cells exert an important influence on hippocampal function.},
	Author = {Tanapat, P. and Hastings, N. B. and Reeves, A. J. and Gould, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Neurosci},
	Keywords = {Rats;Estrus/*physiology;Microscopy, Confocal;C-9;Female;Animal;Rats, Sprague-Dawley;Nerve Tissue Proteins/analysis;Dentate Gyrus/*cytology;Male;Estradiol/*pharmacology/physiology;Neuroglia/*cytology/drug effects;Sex Characteristics;04 Adult neurogenesis factors;Ovariectomy;Support, U.S. Gov't, P.H.S.;Bromodeoxyuridine;Hippocampus/*cytology;Cell Division/drug effects;Neurons/*cytology/drug effects},
	Number = {14},
	Organization = {Department of Psychology, Princeton University, Princeton, New Jersey 08544, USA.},
	Pages = {5792-801.},
	Title = {Estrogen stimulates a transient increase in the number of new neurons in the dentate gyrus of the adult female rat},
	Uuid = {8428E986-0BF2-45C5-8C60-259AE0A994D2},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10407020%20http://www.jneurosci.org/cgi/content/full/19/14/5792%20http://www.jneurosci.org/cgi/content/abstract/19/14/5792}}

@article{Tanigaki:2001,
	Abstract = {Notch1 has been shown to induce glia in the peripheral nervous system. However, it has not been known whether Notch can direct commitment to glia from multipotent progenitors of the central nervous system. Here we present evidence that activated Notch1 and Notch3 promotes the differentiation of astroglia from the rat adult hippocampus-derived multipotent progenitors (AHPs). Quantitative clonal analysis indicates that the action of Notch is likely to be instructive. Transient activation of Notch can direct commitment of AHPs irreversibly to astroglia. Astroglial induction by Notch signaling was shown to be independent of STAT3, which is a key regulatory transcriptional factor when ciliary neurotrophic factor (CNTF) induces astroglia. These data suggest that Notch provides a CNTF-independent instructive signal of astroglia differentiation in CNS multipotent progenitor cells. 0896-6273 Journal Article},
	Author = {Tanigaki, K. and Nogaki, F. and Takahashi, J. and Tashiro, K. and Kurooka, H. and Honjo, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Neuron},
	Keywords = {Astrocytes/*metabolism;Clone Cells/drug effects;Cell Differentiation/drug effects;Proto-Oncogene Proteins/*metabolism/pharmacology;Animals;Cells, Cultured;Membrane Proteins/*metabolism/pharmacology;Rats;10 Development;Ciliary Neurotrophic Factor/metabolism/pharmacology;Trans-Activators/metabolism;Signal Transduction/drug effects;Cell Lineage/drug effects;Neurons/cytology/drug effects/metabolism;DNA-Binding Proteins/metabolism;Support, Non-U.S. Gov't;Stem Cells/cytology/drug effects/*metabolism;Hippocampus/cytology/metabolism;Fibroblast Growth Factor 2/*metabolism/pharmacology;F},
	Number = {1},
	Organization = {Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe Sakyo, 606-8501, Kyoto, Japan.},
	Pages = {45-55},
	Pubmed = {11182080},
	Title = {Notch1 and Notch3 instructively restrict bFGF-responsive multipotent neural progenitor cells to an astroglial fate},
	Uuid = {CAC346CF-76C9-43DF-ABE8-8C0353B8EEBC},
	Volume = {29},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11182080}}

@article{Taniguchi:2001,
	Abstract = {Reciprocal dendrodendritic synapses between mitral and granule cells in the accessory olfactory bulb have been implicated in a specialized form of olfactory learning in mice, in which a female forms a memory to the pheromonal signal of the male that mates with her. Relatively little is known, however, about the mechanism of synaptic transmission at the reciprocal synapses. We analyzed synaptic currents generated in accessory olfactory bulb mitral cells in slice preparations with the patch-clamp technique in nystatin-perforated whole-cell configuration. A brief (5-20-ms) depolarizing voltage step from -70 to 0 mV applied to a single mitral cell evoked GABA(A) receptor-mediated inhibitory postsynaptic currents. The inhibitory postsynaptic currents persisted in the presence of tetrodotoxin, indicating that the inhibitory postsynaptic current in mitral cells can be elicited through purely dendritic interactions. The inhibitory postsynaptic currents were greatly enhanced by washout of extracellular Mg(2+). In Mg(2+)-free solution, the N-methyl-D-aspartate (NMDA) receptor antagonist D,L-2- amino-5-phosphonovaleric acid greatly reduced the inhibitory postsynaptic currents, whereas the non-NMDA receptor antagonist 6-cyano- 7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) slightly reduced them.These data demonstrate that NMDA receptors play an important role in the generation of dendrodendritic inhibition in mitral cells of the mouse accessory olfactory bulb.},
	Author = {Taniguchi, M. and Kaba, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Neuroscience},
	Keywords = {I abstr;13 Olfactory bulb anatomy},
	Number = {3},
	Pages = {365-70.},
	Title = {Properties of reciprocal synapses in the mouse accessory olfactory bulb},
	Uuid = {7AADD09A-71E4-43F5-9EC9-7F0C71DD0A0A},
	Volume = {108},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11738251}}

@article{Tansey:1998,
	Abstract = {The present study addresses a controversy over the abilities of astrocytes to perform phagocytosis. Primary glial-cell cultures were prepared from the brains of neonatal rats and were incubated with fluorescently-labeled dextran beads (molecular weights approximately 10 and approximately 40 kDa). Astrocytes and oligodendrocytes were double-labeled by immunofluorescence staining of cell-specific markers, and microglia by lectin histochemistry. Cells were permitted to take up beads for 1 h, fixed, and incubated with primary antibodies, followed by fluorescent secondary antibodies or fluorescently-labeled lectin. Macrophages and astrocytes internalized beads of both sizes. In astrocyte processes the beads appeared to line up along glial filaments. The results, which provide direct evidence for uptake of beads by astrocytes in vitro and against equally rapid, if any, uptake by oligodendrocytes, bear upon issues of acid/base balance and glial cell development and are relevant to neuropathological observations in human disease.},
	Author = {Tansey, F. A. and Cammer, W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Research Support, Non-U.S. Gov't;Fluorescent Antibody Technique, Indirect;Astrocytes;Animals;Macrophages;Rats;Dextrans;Cells, Cultured;Brain;Microglia;Oligodendroglia;Rats, Sprague-Dawley;11 Glia;Microspheres;Research Support, U.S. Gov't, P.H.S.;Animals, Newborn;Neuroglia;Lectins;Glial Fibrillary Acidic Protein},
	Medline = {98316905},
	Month = {6},
	Nlm_Id = {7600130},
	Number = {3},
	Organization = {Department of Neurology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.},
	Pages = {159-62},
	Pii = {S0304394098003735},
	Pubmed = {9654333},
	Title = {Differential uptake of dextran beads by astrocytes, macrophages and oligodendrocytes in mixed glial-cell cultures from brains of neonatal rats},
	Uuid = {890553FC-08E5-4044-9568-ADEDDEF0B207},
	Volume = {248},
	Year = {1998}}

@article{Tao:2004,
	Abstract = {Genetic modification of hematopoietic stem and progenitor cells has the potential to treat diseases affecting blood cells. Oncoretroviral vectors have been used for gene therapy; however, clinical success has been limited in part by low gene transfer efficiencies. We found that the presence of stromal-derived factor 1 (SDF-1alpha)/CXCL12 during retroviral transduction significantly enhanced, in a dose-dependent fashion, gene transfer into immature subsets of high proliferative human and murine hematopoietic progenitor cells. Murine mononuclear bone marrow cells and purified c-Kit(+)Lin(-) bone marrow cells were prestimulated and transduced with the bicistronic retroviral vector MIEG3 on Retronectin-coated surfaces in the presence and absence of SDF-1. SDF-1 enhanced gene transduction of murine bone marrow and c-Kit(+)Lin(-) cells by 35 and 29\%, respectively. Moreover, SDF-1 enhanced transduction of progenitors in these populations by 121 and 107\%, respectively. SDF-1 also enhanced transduction of human immature subsets of high proliferative progenitors present in either nonadherent mononuclear or CD34(+) umbilical cord blood cells. Transduction of hematopoietic progenitors was further increased by preloading Retronectin-coated plates with retrovirus using low-speed centrifugation followed by increasing cell-virus interactions through brief centrifugation during the transduction procedure. These results may be of clinical relevance.},
	Author = {Tao, W. and Hangoc, G. and Cooper, S. and Broxmeyer, H. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Genetic Vectors;Transduction, Genetic;Research Support, Non-U.S. Gov't;Luminescent Proteins;Hematopoietic Stem Cells;Research Support, U.S. Gov't, P.H.S.;Mice, Inbred C57BL;Retroviridae;Gene Expression;11 Glia;Gene Therapy;Chemokines, CXC;Mice;Animals;Green Fluorescent Proteins;Humans;Hematologic Diseases},
	Month = {1},
	Nlm_Id = {9421525},
	Number = {1},
	Organization = {Department of Microbiology and Immunology, The Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202-5181, USA.},
	Pages = {61-9},
	Pii = {3302127},
	Pubmed = {14681698},
	Title = {SDF-1alpha/CXCL12 enhances retroviral-mediated gene transfer into immature subsets of human and murine hematopoietic progenitor cells},
	Uuid = {53107025-7E51-473F-BEB8-E2A29231D1AF},
	Volume = {11},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj.gt.3302127}}

@article{Tao:1999,
	Abstract = {Immature motoneurons are highly susceptible to degeneration following axon injury. The response of perineuronal glia to axon injury may significantly influence neuronal survival and axon regeneration. We have examined the central reactions to neonatal facial nerve transection with emphasis on the expression of complement component C3 (C3) and the multifunctional apolipoprotein J (ApoJ). Axotomy was performed on one-day-old rats. Animals were perfused from eight hours to two weeks after the lesion. The astroglial marker, glial fibrillary acidic protein (GFAP) was increased from one day and the microglial marker OX-42 from two days after injury. ApoJ immunoreactivity was increased in axotomized neuronal perikarya and astroglial cells from one day postaxotomy, but no C3 immunoreactive profiles were found at any postoperative survival time. Cell proliferation as judged by bromodeoxyuridine labeling and immunoreactivity for the cyclin Ki-67 antigen (antibody MIB5) occurred only at two days after injury. Double immunostaining revealed that the vast majority of proliferating cells were microglia, although occasional cells double labeled astrocytes were found as well. Our results indicate that the non-neuronal response in neonatal animals differ from that of adult ones as follows: 1) microglia transform rapidly into phagocytes in parallel with the degeneration of axotomized neurons, 2) despite the presence of neuronal degeneration, no expression of C3 was found, and the upregulation of the expression of the complement C3 receptor (CR3) is delayed, 3) ApoJ is strongly upregulated in perineuronal astrocytes as well as in the axotomized motoneurons. The marked upregulation of ApoJ in both instances suggests a general role of this protein in the neuronal response to axotomy.},
	Author = {Tao, R. and Aldskogius, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Glycoproteins;Nerve Degeneration;Fluorescent Antibody Technique, Indirect;Astrocytes;Gene Expression Regulation;Aging;Rats;Animals;Microglia;Oligodendroglia;Rats, Sprague-Dawley;Nerve Regeneration;Animals, Newborn;Neuroglia;Molecular Chaperones;Axotomy;Neurons;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Complement 3;Facial Nerve;Research Support, Non-U.S. Gov't},
	Medline = {20261710},
	Month = {7},
	Nlm_Id = {0364620},
	Number = {7},
	Organization = {Department of Neuroscience, Division of Neuroanatomy, Biomedical Center, P.O. Box 587, SE-751 23 Uppsala, Sweden.},
	Pages = {559-70},
	Pubmed = {10800205},
	Title = {Glial cell responses, complement and apolipoprotein J expression following axon injury in the neonatal rat},
	Uuid = {62BA6F7E-C329-44ED-88EB-5DDBACE6610E},
	Volume = {28},
	Year = {1999}}

@article{Tarantal:2001,
	Abstract = {Many life-threatening conditions that can be diagnosed early in gestation may be treatable in utero using gene therapy. In order to determine in utero gene transfer efficiency and safety, studies were conducted with fetal rhesus monkeys as a model for the human. Included in these studies were Moloney murine leukemia virus (MLV)-based amphotropic retrovirus, vesicular stomatitis virus-G (VSV-G) pseudotyped MLV, and a VSV-G pseudotyped HIV-1-based vector, all expressing the enhanced green fluorescent protein (EGFP) as a reporter gene and driven by a cytomegalovirus-immediate early promoter (N = 16). Rhesus monkey fetuses were administered viral vector supernatant preparations by the intraperitoneal (ip) (N = 14) or intrahepatic (ih) (N = 2) routes via ultrasound guidance at 55 +/- 5 days gestation (late first trimester; term 165 +/- 10 days). Fetuses were monitored sonographically, specimens were collected prenatally and postnatally, and tissue harvests were performed at birth or 3 or 6 months postnatal age (3-10 months post-gene transfer). PCR analyses demonstrated that transduced cells were present at approximately 1.2\%in peripheral blood mononuclear cells from fetuses administered amphotropic MLV, <0.5\%in fetuses receiving MLV/VSV-G, and approximately 4.2\%for the lentiviral vector, which decreased to 2\%at birth. Hematopoietic progenitors showed that overall (mean of all time points assessed), approximately 25\%of the collected colonies were positive for the EGFP transgene with the lentiviral vector, which was significantly greater than results achieved with the MLV-based vector systems (4-9\%; P <or = 0.001-0.016). At necropsy, 0.001-10\%of the total genomic DNA was positive for EGFP in most tissues for all groups. EGFP-positive fluorescent cells were found in cell suspensions of thymus, liver, spleen, lymph nodes, cerebral cortex, and bone marrow (0.5-6\%). Overall, the results of these studies have shown: (1) healthy infants expressing vector sequences up to 10 months post-gene transfer, (2) fetal primate administration of retroviral vectors results in gene transfer to multiple organ systems, (3) the highest level of gene transfer to hematopoietic progenitors was observed with the lentiviral vector system, and (4) there was no evidence of transplacental transfer of vector sequences into the dams. The rhesus monkey is an important preclinical primate model system for exploring gene transfer approaches for future applications in humans.},
	Author = {Tarantal, A. F. and O'Rourke, J. P. and Case, S. S. and Newbound, G. C. and Li, J. and Lee, C. I. and Baskin, C. R. and Kohn, D. B. and Bunnell, B. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1525-0016},
	Journal = {Mol Ther},
	Keywords = {Moloney murine leukemia virus;Genetic Vectors;Cytomegalovirus;Green Fluorescent Proteins;Male;Gene Therapy;Luminescent Proteins;Models, Genetic;Animals;Flow Cytometry;Genes, Reporter;Research Support, U.S. Gov't, P.H.S.;Tissue Distribution;Promoter Regions (Genetics);Azacitidine;11 Glia;Leukocytes, Mononuclear;Viral Envelope Proteins;Macaca mulatta;Membrane Glycoproteins;Gene Transfer Techniques;Retroviridae;Time Factors;Female;Dose-Response Relationship, Drug;HIV-1;Polymerase Chain Reaction;Lentivirus;Research Support, Non-U.S. Gov't;Humans;Reverse Transcriptase Polymerase Chain Reaction},
	Medline = {21138540},
	Month = {2},
	Nlm_Id = {100890581},
	Number = {2},
	Organization = {California Regional Primate Research Center, University of California at Davis, 95616-8542, USA. aftarantal\@primate.ucdavis.edu},
	Pages = {128-38},
	Pii = {S1525001600902557},
	Pubmed = {11237669},
	Title = {Rhesus monkey model for fetal gene transfer: studies with retroviral- based vector systems},
	Uuid = {DDAB4716-4A7D-4BCA-A164-D45554EA8CCB},
	Volume = {3},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/mthe.2000.0255}}

@article{Tashiro:2007,
	Abstract = {Neural circuits in the dentate gyrus are continuously modified by adult neurogenesis, whose level is affected by the animal's experience. However, it is not known whether this experience-dependent anatomical modification alters the functional properties of the dentate gyrus. Here, using the expression of immediate early gene products, c-fos and Zif268, as indicators of recently activated neurons, we show that previous exposure to an enriched environment increases the total number of new neurons and the number of new neurons responding to reexposure to the same environment. The increase in the density of activated new neurons occurred specifically in response to exposure to the same environment but not to a different experience. Furthermore, we found that these experience-specific modifications are affected exclusively by previous exposure around the second week after neuronal birth but not later than 3 weeks. Thus, the animal's experience within a critical period during an immature stage of new neurons determines the survival and population response of the new neurons and may affect later neural representation of the experience in the dentate gyrus. This experience-specific functional modification through adult neurogenesis could be a mechanism by which new neurons exert a long-term influence on the function of the dentate gyrus related to learning and memory.},
	Author = {Tashiro, Ayumu and Makino, Hiroshi and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;Cell Differentiation;research support, non-u.s. gov't;Critical Period (Psychology);Dentate Gyrus;Environment;Mice, Inbred C57BL;Cell Survival;research support, u.s. gov't, non-p.h.s.;comparative study;research support, n.i.h., extramural;Animals, Newborn;Age Factors;Animals;Mice;Neurons;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {3252-9},
	Pii = {27/12/3252},
	Pubmed = {17376985},
	Title = {Experience-specific functional modification of the dentate gyrus through adult neurogenesis: a critical period during an immature stage},
	Uuid = {233B8C83-B663-40D8-913A-5A075CA6F732},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4941-06.2007}}

@article{Tattersfield:2004,
	Abstract = {The presence of ongoing neurogenesis in the adult mammalian brain raises the exciting possibility that endogenous progenitor cells may be able to generate new neurons to replace cells lost through brain injury or neurodegenerative disease. We have recently demonstrated increased cell proliferation and the generation of new neurons in the Huntington's disease human brain. In order to better understand the potential role of endogenous neuronal replacement in neurodegenerative disorders and extend our initial observations in the human Huntington's disease brain, we examined the effect of striatal cell loss on neurogenesis in the subventricular zone (SVZ) of the adult rodent forebrain using the quinolinic acid (QA) lesion rat model of Huntington's disease. Cell proliferation and neurogenesis were assessed with bromodeoxyuridine (BrdU) labeling and immunocytochemistry for cell type-specific markers. BrdU labeling demonstrated increased cell proliferation in the SVZ ipsilateral to the QA-lesioned striatum, resulting in expansion of the SVZ in the lesioned hemisphere. Quantification revealed that QA lesion-induced striatal cell loss produced a significant increase in the area of BrdU-immunoreactivity in the SVZ ipsilateral to the lesioned hemisphere between 1 and 14 days post-lesion compared with sham-lesioned animals, with the greatest increase observed at 7 days post-lesion. These changes were associated with an increase in cells in the anterior SVZ ipsilateral to the lesioned striatum expressing the antigenic marker for SVZ neuroblasts, doublecortin (Dcx). Importantly, we observed Dcx-positive cells extending from the SVZ into the QA-lesioned striatum where a subpopulation of newly generated cells expressed markers for immature and mature neurons. This study demonstrates that loss of GABAergic medium spiny projection neurons following QA striatal lesioning of the adult rat brain increases SVZ neurogenesis, leading to the putative migration of neuroblasts to damaged areas of the striatum and the formation of new neurons.},
	Author = {Tattersfield, A. S. and Croon, R. J. and Liu, Y. W. and Kells, A. P. and Faull, R. L. M. and Connor, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Research Support, Non-U.S. Gov't;gamma-Aminobutyric Acid;Cell Differentiation;Neurotoxins;Animals;Corpus Striatum;Up-Regulation;Rats;Microtubule-Associated Proteins;Denervation;Cell Movement;Reaction Time;Rats, Wistar;Disease Models, Animal;Male;Neuropeptides;Nerve Regeneration;Quinolinic Acid;Neurons;Huntington Disease;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Biological Markers;Bromodeoxyuridine;Cell Death;Stem Cells},
	Nlm_Id = {7605074},
	Number = {2},
	Organization = {Department of Pharmacology and Clinical Pharmacology, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand.},
	Pages = {319-32},
	Pii = {S0306452204003483},
	Pubmed = {15262322},
	Title = {Neurogenesis in the striatum of the quinolinic acid lesion model of Huntington's disease},
	Uuid = {57CE5186-2375-450A-8B66-A14E4D2803D5},
	Volume = {127},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2004.04.061}}

@article{Taupin:2007,
	Abstract = {Bromodeoxyuridine (BrdU) is a thymidine analog that incorporates DNA of dividing cells during the S-phase of the cell cycle. As such, BrdU is used for birth dating and monitoring cell proliferation. BrdU immunohistochemistry has been instrumental for the study of the development of the nervous system, and to confirm that neurogenesis occurs in the adult mammalian brain, including in human. However, the use of BrdU for studying neurogenesis is not without pitfalls and limitations. BrdU is a toxic and mutagenic substance. It triggers cell death, the formation of teratomas, alters DNA stability, lengthens the cell cycle, and has mitogenic, transcriptional and translational effects on cells that incorporate it. All of which have profound consequences on neurogenesis. BrdU is not a marker of the S-phase of the cell cycle. As a thymidine analog, it is a marker of DNA synthesis. Therefore, studying neurogenesis with BrdU requires distinguishing cell proliferation and neurogenesis from other events involving DNA synthesis, like DNA repair, abortive cell cycle reentry and gene duplication. BrdU labeling is currently the most used technique for studying adult neurogenesis in situ. However in many instances, appropriate controls have been overlooked and events reported as the generation of new neuronal cells in the adult brain misinterpreted, which makes BrdU labeling one of the most misused techniques in neuroscience.},
	Author = {Taupin, Philippe},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0165-0173},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8908638},
	Number = {1},
	Organization = {National Neuroscience Institute, Singapore. obgpjt\@nus.edu.sg <obgpjt\@nus.edu.sg>},
	Pages = {198-214},
	Pii = {S0165-0173(06)00104-4},
	Pubmed = {17020783},
	Title = {BrdU immunohistochemistry for studying adult neurogenesis: paradigms, pitfalls, limitations, and validation},
	Uuid = {C68C4E8B-D702-474F-A84A-B0CF90F722EB},
	Volume = {53},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainresrev.2006.08.002}}

@article{Taupin:2000,
	Abstract = {We have purified and characterized a factor, from the conditioned medium of neural stem cell cultures, which is required for fibroblast growth factor 2's (FGF-2) mitogenic activity on neural stem cells. This autocrine/paracrine cofactor is a glycosylated form of cystatin C (CCg), whose N-glycosylation is required for its activity. We further demonstrated that, both in vitro and in vivo, neural stem cells undergoing cell division are immunopositive for cystatin C. Finally, we showed in vivo functional activity of CCg by demonstrating that the combined delivery of FGF-2 and CCg to the adult dentate gyrus stimulated neurogenesis. We propose that the process of neurogenesis is controlled by the cooperation between trophic factors and autocrine/paracrine cofactors, of which CCg is a prototype. 0896-6273 Journal Article},
	Author = {Taupin, P. and Ray, J. and Fischer, W. H. and Suhr, S. T. and Hakansson, K. and Grubb, A. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Neuron},
	Keywords = {Hippocampus/cytology/drug effects/metabolism;10 Development;Animals;Stem Cell Transplantation;Cells, Cultured;Rats;Autocrine Communication/drug effects;Paracrine Communication/drug effects;Cystatins/*chemistry/genetics/*metabolism/pharmacology;Glycosylation;Support, Non-U.S. Gov't;Fibroblast Growth Factor 2/genetics/*metabolism/pharmacology;Neurons/cytology/drug effects/*metabolism;Dentate Gyrus/cytology/drug effects;Sequence Analysis, Protein;Stem Cells/cytology/drug effects/*metabolism;Support, U.S. Gov't, P.H.S.;Protein Processing, Post-Translational;Molecular Weight;Molecular Sequence Data;F;Culture Media, Conditioned/chemistry;Cell Division/drug effects},
	Number = {2},
	Organization = {Laboratory of Genetics, The Salk Institute, La Jolla, California 92037, USA.},
	Pages = {385-97},
	Pubmed = {11144350},
	Title = {FGF-2-responsive neural stem cell proliferation requires CCg, a novel autocrine/paracrine cofactor},
	Uuid = {A93AFF42-8CEF-42C4-9352-B08B9C84F46B},
	Volume = {28},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11144350}}

@article{Tavazoie:2005,
	Abstract = {Mutations in the TSC1 or TSC2 tumor suppressor genes lead to tuberous sclerosis complex (TSC), a dominant hamartomatous disorder that often presents with mental retardation, epilepsy and autism. The etiology of these neurological symptoms is unclear and the function of the TSC pathway in neurons is unknown. We found that in post-mitotic, hippocampal pyramidal neurons of mice and rats, loss of Tsc1 or Tsc2 triggered enlargement of somas and dendritic spines and altered the properties of glutamatergic synapses. Furthermore, loss of a single copy of the Tsc1 gene was sufficient to perturb dendritic spine structure. Morphological changes required regulation of the actin-depolymerization factor cofilin at a conserved LIM-kinase phosphorylation site, the phosphorylation of which was increased by loss of Tsc2. Thus, the TSC pathway regulates growth and synapse function in neurons, and perturbations of neuronal structure and function are likely to contribute to the pathogenesis of the neurological symptoms of TSC.},
	Author = {Tavazoie, Sohail F. and Alvarez, Veronica A. and Ridenour, Dennis A. and Kwiatkowski, David J. and Sabatini, Bernardo L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Cell Differentiation;research support, n.i.h., extramural ;Animals;Humans;Gene Expression Regulation, Developmental;Rats;Phosphorylation;Tuberous Sclerosis;Cofilin 1;research support, u.s. gov't, non-p.h.s. ;Dendritic Spines;Brain;Rats, Sprague-Dawley;Hippocampus;Pyramidal Cells;Mice, Transgenic;research support, non-u.s. gov't ;Cell Line;Mice, Knockout;21 Neurophysiology;Cell Shape;Neurons;Mice;Tumor Suppressor Proteins;24 Pubmed search results 2008},
	Month = {12},
	Nlm_Id = {9809671},
	Number = {12},
	Organization = {Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.},
	Pages = {1727-34},
	Pii = {nn1566},
	Pubmed = {16286931},
	Title = {Regulation of neuronal morphology and function by the tumor suppressors Tsc1 and Tsc2},
	Uuid = {CEEDF056-1F1F-4622-B0A0-0FB3DE2433F8},
	Volume = {8},
	Year = {2005},
	url = {papers/Tavazoie_NatNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1566}}

@article{Taylor:2002,
	Abstract = {A key feature of myogenesis is the fusion of myoblasts to form multinucleate myotubes. Recent work in Drosophila has uncovered a collection of genes that operate at different stages of this process. Some interactions between them have been described that begin to define links from outside the cell via the plasma membrane to the cytoskeleton. Future studies will establish the extent to which the molecular mechanisms of myoblast fusion are conserved between Drosophila and other animals, as found in other aspects of myogenesis.},
	Author = {Taylor, Michael V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {Cell Membrane;Cell Differentiation;Cell Fusion;Gene Expression Regulation, Developmental;Muscles;Embryo, Nonmammalian;Sodium Channels;08 Aberrant cell cycle;Drosophila Proteins;Insect Proteins;Drosophila;review, tutorial;Mesoderm;Animals;Cytoplasm;review},
	Medline = {21906656},
	Month = {3},
	Nlm_Id = {9107782},
	Number = {6},
	Organization = {Cardiff School of Biosciences, Cardiff University, UK. TaylorMV\@cf.ac.uk},
	Pages = {R224-8},
	Pii = {S0960982202007571},
	Pubmed = {11909553},
	Title = {Muscle differentiation: how two cells become one},
	Uuid = {6D9AB901-B180-413D-8C17-8B1E5F449A96},
	Volume = {12},
	Year = {2002},
	url = {papers/Taylor_CurrBiol2002.pdf}}

@article{Taylor:1999,
	Abstract = {The role of glycoprotein membrane-spanning domains in the process of membrane fusion is poorly understood. It has been demonstrated that replacing all or part of the membrane-spanning domain of a viral fusion protein with sequences that encode signals for glycosylphosphatidylinositol linkage attachment abrogates membrane fusion activity. It has been suggested, however, that the actual amino acid sequence of the membrane-spanning domain is not critical for the activity of viral fusion proteins. We have examined the function of Moloney murine leukemia virus envelope proteins with substitutions in the membrane-spanning domain. Envelope proteins bearing substitutions for proline 617 are processed and incorporated into virus particles normally and bind to the viral receptor. However, they possess greatly reduced or undetectable capacities for the promotion of membrane fusion and infectious virus particle formation. Our results imply a direct role for the residues in the membrane-spanning domain of the murine leukemia virus envelope protein in membrane fusion and its regulation. They also support the thesis that membrane-spanning domains possess a sequence-dependent function in other protein-mediated membrane fusion events.},
	Author = {Taylor, G. M. and Sanders, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1059-1524},
	Journal = {Mol Biol Cell},
	Keywords = {Proline;Glycoproteins;Conserved Sequence;Animals;Gene Products, env;Mutation;Virus Assembly;Cell Fusion;Amino Acid Substitution;15 Retrovirus mechanism;Giant Cells;08 Aberrant cell cycle;Cell Line;Support, Non-U.S. Gov't;Moloney murine leukemia virus;Membrane Fusion;Support, U.S. Gov't, P.H.S.;Receptors, Virus;Mice;Protein Processing, Post-Translational;Amino Acid Sequence;Molecular Sequence Data;Membrane Proteins},
	Medline = {99402792},
	Month = {9},
	Nlm_Id = {9201390},
	Number = {9},
	Organization = {Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392, USA.},
	Pages = {2803-15},
	Pubmed = {10473628},
	Title = {The role of the membrane-spanning domain sequence in glycoprotein-mediated membrane fusion},
	Uuid = {C07717A5-EC27-4151-BBF3-F7A6F137E119},
	Volume = {10},
	Year = {1999},
	url = {papers/Taylor_MolBiolCell1999.pdf}}

@article{Taylor:2004,
	Abstract = {The programmed cell death (PCD) of neurons is generally thought to be cell autonomous and not to require a death signal from other cells. A recent study by Mar{\'\i}n-Teva et al., in this issue of Neuron, brings this theory into question and suggests that neighboring microglia actively participate in the PCD of Purkinje cells in the cerebellum.},
	Author = {Taylor, Anna R. and Oppenheim, Ronald W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Membrane Lipids;Purkinje Cells;Alpha;Cell Communication;Apoptosis;Signal Transduction;Not relevant;11 Glia;Microglia;comment;Animals;Caspases;news},
	Month = {2},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.},
	Pages = {491-3},
	Pii = {S0896627304000790},
	Pubmed = {14980198},
	Title = {The kiss of death},
	Uuid = {02F2AA1E-4C90-4FEE-A8E4-477F13C0BFF9},
	Volume = {41},
	Year = {2004}}

@article{Tchantchou:2007,
	Abstract = {Standardized Ginkgo biloba extract EGb 761 exhibits beneficial effects to patients with Alzheimer's disease (AD). It was previously demonstrated that EGb 761 inhibits amyloid beta (Abeta) oligomerization in vitro, protects neuronal cells against Abeta toxicity, and improves cognitive defects in a mouse model of AD (Tg 2576). In this study, the neurogenic potential of EGb 761 and its effect on cAMP response element binding protein (CREB) were examined in a double transgenic mouse model (TgAPP/PS1). EGb 761 significantly increases cell proliferation in the hippocampus of both young (6 months) and old (22 months) TgAPP/PS1 mice, and the total number of neuronal precursor cells in vitro in a dose-dependent manner. Furthermore, Abeta oligomers inhibit phosphorylation of CREB and cell proliferation in the hippocampus of TgAPP/PS1 mice. Administration of EGb 761 reduces Abeta oligomers and restores CREB phosphorylation in the hippocampus of these mice. The present findings suggest that 1) enhanced neurogenesis by EGb 761 may be mediated by activation of CREB, 2) stimulation of neurogenesis by EGb 761 may contribute to its beneficial effects in AD patients and improved cognitive functions in the mouse model of AD, and 3) EGb 761 has therapeutic potential for the prevention and improved treatment of AD.--Tchantchou, F., Xu, Y., Wu, Y., Christen, Y., Luo, Y. EGb 761 enhances adult hippocampal neurogenesis and phosphorylation of CREB in transgenic mouse model of Alzheimer's disease.},
	Author = {Tchantchou, and Xu, and Wu, and Christen, and Luo,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1530-6860},
	Journal = {FASEB J},
	Keywords = {04 Adult neurogenesis factors;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8804484},
	Organization = {*Department of Pharmaceutical Sciences, School of Pharmacy,Center for Integrative Medicine, School of Medicine, University of Maryland, Baltimore, Maryland, USA; andIpsen, Paris, France.},
	Pii = {fj.06-7649com},
	Pubmed = {17356006},
	Title = {EGb 761 enhances adult hippocampal neurogenesis and phosphorylation of CREB in transgenic mouse model of Alzheimer's disease},
	Uuid = {2A129A89-A49E-4F0F-BD2F-5863B80CE0CB},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.06-7649com}}

@article{Teich:1973,
	Author = {Teich, N. and Lowy, D. R. and Hartley, J. W. and Rowe, W. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {15 ERVs retroelements;Radiation Effects;Immune Sera;Animals;Idoxuridine;DNA;Ultraviolet Rays;Thymidine;15 Retrovirus mechanism;Time Factors;Leukemia Virus, Murine;Cell Line;Cytarabine;Light;Mice;Floxuridine;24 Pubmed search results 2008;Bromodeoxyuridine;Virus Replication;Clone Cells;Plaque Assay;Mice, Inbred AKR},
	Medline = {73086525},
	Month = {1},
	Nlm_Id = {0110674},
	Number = {1},
	Pages = {163-73},
	Pii = {0042-6822(73)90376-0},
	Pubmed = {4346294},
	Title = {Studies of the mechanism of induction of infectious murine leukemia virus from AKR mouse embryo cell lines by 5-iododeoxyuridine and 5-bromodeoxyuridine},
	Uuid = {833A299F-4326-11DB-A5D2-000D9346EC2A},
	Volume = {51},
	Year = {1973}}

@article{Temple:1999,
	Abstract = {Over the past year, evidence has accrued that adult CNS stem cells are a widespread progenitor cell type. These cells may normally replace neurons and/or glia in the adult brain and spinal cord. Advances have been made in understanding the signals that regulate stem cell proliferation and differentiation. A deeper understanding of the structure of germinal zones has helped us move towards identifying stem cells in vivo. Recent studies suggest that the fate of stem cell progeny in vivo may be linked to the complexity of the animal's environment.},
	Author = {Temple, S. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {Curr Opin Neurobiol},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration;Stem Cells/*cytology/*drug effects;Rats;03 Adult neurogenesis progenitor source;Animal;Fibroblast Growth Factor, Basic/pharmacology;Support, U.S. Gov't, P.H.S.;Cell Differentiation/drug effects;Epidermal Growth Factor/pharmacology;Central Nervous System/*cytology;Mice;A, BB pdf;Age Factors},
	Number = {1},
	Organization = {Department of Pharmacology and Neuroscience A-60 The Albany Medical College Albany New York 12208 USA. TempleS\@mail.amc.edu},
	Pages = {135-41.},
	Title = {Stem cells in the adult mammalian central nervous system},
	Uuid = {F3D117FD-6F19-42D4-BF1E-6B7E5C23FDBB},
	Volume = {9},
	Year = {1999},
	url = {papers/Temple_CurrOpinNeurobiol1999.pdf}}

@article{Temple:2001,
	Author = {Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:11:59 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {Blastocyst/cytology;Cell Lineage;02 Adult neurogenesis migration;Cell Differentiation/*physiology;Neurons/cytology;Brain/cytology/*embryology;03 Adult neurogenesis progenitor source;Human;Phenotype;Chick Embryo;BB both;Animal;Neuronal Plasticity/*physiology;Stem Cells/*cytology/*transplantation;Mice;Fetal Tissue Transplantation;Transplantation Chimera},
	Number = {7},
	Organization = {Center for Neuropharmacology and Neuroscience, Albany Medical College, 43 New Scotland Avenue, Albany, New York 12208, USA. temples\@mail.amc.edu},
	Pages = {513-20.},
	Title = {Stem cell plasticity--building the brain of our dreams},
	Uuid = {75E82E95-3AB9-4DB7-B9BC-8A377BDA025E},
	Volume = {2},
	Year = {2001},
	url = {papers/Temple_NatRevNeurosci2001.pdf}}

@article{Temple:2001a,
	Abstract = {The discovery of stem cells that can generate neural tissue has raised new possibilities for repairing the nervous system. A rush of papers proclaiming adult stem cell plasticity has fostered the notion that there is essentially one stem cell type that, with the right impetus, can create whatever progeny our heart, liver or other vital organ desires. But studies aimed at understanding the role of stem cells during development have led to a different view - that stem cells are restricted regionally and temporally, and thus not all stem cells are equivalent. Can these views be reconciled? 0028-0836 Journal Article Review Review, Tutorial},
	Author = {Temple, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Forecasting;Cell Differentiation;Human;Animals;Stem Cells/cytology/*physiology;Humans;10 Development;review, tutorial;Nervous System;review;Nervous System Diseases;Nervous System/*cytology/growth &development;Nervous System Diseases/therapy;Embryo/cytology;Embryo;Cell Lineage;22 Stem cells;Stem Cells;F},
	Medline = {21548546},
	Month = {11},
	Nlm_Id = {0410462},
	Number = {6859},
	Organization = {Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA. temples\@mail.amc.edu},
	Pages = {112-7},
	Pii = {35102174},
	Pubmed = {11689956},
	Title = {The development of neural stem cells},
	Uuid = {06502141-75BF-425A-9844-9CC25B7B857E},
	Volume = {414},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/35102174},
	Bdsk-Url-2 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689956}}

@article{Terada:2002,
	Abstract = {Recent studies have demonstrated that transplanted bone marrow cells can turn into unexpected lineages including myocytes, hepatocytes, neurons and many others. A potential problem, however, is that reports discussing such 'transdifferentiation'in vivo tend to conclude donor origin of transdifferentiated cells on the basis of the existence of donor-specific genes such as Y-chromosome markers. Here we demonstrate that mouse bone marrow cells can fuse spontaneously with embryonic stem cells in culture in vitro that contains interleukin-3. Moreover, spontaneously fused bone marrow cells can subsequently adopt the phenotype of the recipient cells, which, without detailed genetic analysis, might be interpreted as 'dedifferentiation'or transdifferentiation. 0028-0836 Journal Article},
	Author = {Terada, N. and Hamazaki, T. and Oka, M. and Hoki, M. and Mastalerz, D. M. and Nakano, Y. and Meyer, E. M. and Morel, L. and Petersen, B. E. and Scott, E. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {Nature},
	Keywords = {Animals;Cells, Cultured;*Cell Differentiation;Phenotype;Antigens, Differentiation;Female;EE pdf;Mice, Transgenic;Interleukin-3/pharmacology;Embryo/cytology;Stem Cells/*cytology;Male;Reverse Transcriptase Polymerase Chain Reaction;*Cell Fusion;Karyotyping;Bone Marrow Cells/*cytology;Ploidies;Support, U.S. Gov't, P.H.S.;Mice;Luminescent Proteins/genetics;Genetic Markers},
	Number = {6880},
	Organization = {Department of Pathology, University of Florida College of Medicine, Gainesville, Florida 32610, USA. terada\@pathology.ufl.edu},
	Pages = {542-5},
	Title = {Bone marrow cells adopt the phenotype of other cells by spontaneous cell fusion},
	Uuid = {6D02513A-CCCF-11D9-8C77-000D9346EC2A},
	Volume = {416},
	Year = {2002},
	url = {papers/Terada_Nature2002.pdf}}

@article{Terai:2003,
	Abstract = {The plasticity of bone marrow cells (BMCs) remains controversial. The present study found that persistent injury induces efficient trans-differentiation of BMCs into functional hepatocytes. Mice with liver cirrhosis induced by carbon tetrachloride were injected with 1 x 10(5) non-treated green fluorescent protein (GFP)-positive BMCs via the tail vein. In these mice, transplanted GFP-positive BMCs efficiently migrated into the peri-portal area of liver lobules after one day, repopulating 25\%of the recipient liver by 4 weeks. In contrast, no GFP-positive BMCs were detected following transplantation into control mice with undamaged livers. BMCs trans-differentiated into functional mature hepatocytes via immature hepatoblasts. Serum albumin levels were significantly elevated to compensate for chronic liver failure in BMC transplantation. These results reveal that recipient conditions and microenvironments represent key factors for successful cell therapy using BMCs.},
	Author = {Terai, Shuji and Sakaida, Isao and Yamamoto, Naoki and Omori, Kaoru and Watanabe, Tomomi and Ohata, Shinya and Katada, Toshiaki and Miyamoto, Koji and Shinoda, Koh and Nishina, Hiroshi and Okita, Kiwamu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0021-924X},
	Journal = {J Biochem (Tokyo)},
	Keywords = {Research Support, Non-U.S. Gov't;Cell Differentiation;Cell Culture Techniques;Animals;Cells, Cultured;Cell Movement;Fibrosis;Liver;Mice, Inbred C57BL;11 Glia;Time Factors;Microscopy, Fluorescence;Green Fluorescent Proteins;Bone Marrow Cells;Mice;Luminescent Proteins;Immunohistochemistry;Hepatocytes;Albumins;Carbon Tetrachloride},
	Medline = {22969963},
	Month = {10},
	Nlm_Id = {0376600},
	Number = {4},
	Organization = {Department of Molecular Science &Applied Medicine (Gastroenterology &Hepatology), Yamaguchi University School of Medicine, Minami Kogushi 1-1-1, Ube, Yamaguchi 755-8505. terais\@yamaguchi-u.ac.jp},
	Pages = {551-8},
	Pubmed = {14607982},
	Title = {An in vivo model for monitoring trans-differentiation of bone marrow cells into functional hepatocytes},
	Uuid = {78E76360-71DD-493C-B04E-06D1373809AE},
	Volume = {134},
	Year = {2003}}

@article{Tettoni:1996,
	Abstract = {In order to analyze the structural organization of complex axonal arbors reconstructed from histological serial sections, and to investigate the functional implications of their geometrical properties, we developed software providing the following facilities: (1) direct importation of data files generated by a commercially available 3-D light-microscopic reconstruction system, including routine procedures for identification and correction of data acquisition errors; (2) real-time 3-D rotations of the arbors in the stack of serial sections; (3) multiple interactive display modes; (4) possibility of modifying diameter and/or connectivity of different branches; (5) simulation of the invasion of the arbor by a single action potential initiated at any chosen point, and visualization of spatio-temporal profiles of activation; (6) extraction of quantitative data converted to standard file formats compatible with available mathematical software. All these tools can be applied to single or multiple axons, individually or simultaneously. The software, called Maxsim, is a highly flexible C-written program running on graphical workstations using the UNIX operating system and X-Window environment.},
	Author = {Tettoni, L. and Lehmann, P. and Houzel, J. C. and Innocenti, G. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0165-0270},
	Journal = {J Neurosci Methods},
	Keywords = {Neurosciences;Software;Not relevant;11 Glia;Support, Non-U.S. Gov't;Animals;Neurons;Axons},
	Medline = {97001527},
	Month = {7},
	Nlm_Id = {7905558},
	Number = {1},
	Organization = {Institut d'Anatomie, Lausanne, Switzerland.},
	Pages = {1-9},
	Pii = {016502709500095X},
	Pubmed = {8844519},
	Title = {Maxsim, software for the analysis of multiple axonal arbors and their simulated activation},
	Uuid = {47C26FEF-2C85-40C4-8B4B-CF8E56B0D1EA},
	Volume = {67},
	Year = {1996}}

@article{Thalmeier:2001,
	Abstract = {BACKGROUND: CD34(-) stem cells are apparently the earliest progenitors of hematopoiesis and mesenchymal tissues. The majority of those progeny rests in the BM as fibroblast-like cells, but can also circulate the peripheral blood. Nevertheless, CD34(-), fibroblast-like cells can be isolated from BM aspirates and PBMC, mediated by their ability to adhere to the plastic surface of tissue culture flasks. In standard colony assays, CD34(-), fibroblast-like cells produce a significant number of colony-forming-units (CFUs), mainly CFU-F (fibroblast). METHODS: Despite advanced cell-culture techniques and the application of various growth factors, the life span of those multipotent stem cells is limited. Therefore, we immortalized and cloned fibroblast-like, CD34(-) stem cells and used retroviral constructs containing the green-fluorescence protein (GFP) to determine the gene-transfer efficiency and their use for gene marking prior to transplantation into NOD/SCID mice. RESULTS: We could demonstrate a highly efficient retroviral gene transfer into those immortalized CD34(-), fibroblast-like hematopoietic cells (up to 95\%transduced cells), maintaining their ability to produce CFUs, as well as a distinct organ distribution after transplantation into the recipient animals, functioning as SCID-repopulating cells (SRC). Transplanted cells could be detected in the BM, as well as other parenchymal organs, such as the lung, liver, skin, small intestine and brain. DISCUSSION: CD34(-), fibroblast-like progenitor cells can give rise to hematopoietic progeny, but also home to mesenchymal organ sites in recipient animals. There is increasing evidence that pluripotent CD34(-) stem cells can be isolated from various sources and still maintain their capabilities to generate progeny of different tissues. This could be a promising approach to using peripheral-blood derived stem cells for cellreplacement therapy and tissue engineering.},
	Author = {Thalmeier, K. and Huss, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1465-3249},
	Journal = {Cytotherapy},
	Keywords = {Lung;Transduction, Genetic;Mice, Inbred NOD;Animals;Viscera;Cell Line, Transformed;Fibroblasts;Female;Indicators and Reagents;Antigens, CD34;Retroviridae;11 Glia;Green Fluorescent Proteins;Genetic Vectors;Hematopoietic Stem Cell Transplantation;Male;Bone Marrow Cells;Gene Transfer Techniques;Mice;Hematopoietic Stem Cells;Luminescent Proteins;Graft Survival;Dogs;Spleen;Research Support, Non-U.S. Gov't},
	Medline = {22162136},
	Nlm_Id = {100895309},
	Number = {4},
	Organization = {Institute of Pathology, University of Munich, Germany.},
	Pages = {245-51},
	Pubmed = {12171712},
	Title = {Highly efficient retroviral gene transfer into immortalized CD34(-) cells and organ distribution after transplantation into NOD/SCID mice},
	Uuid = {30A39EDD-A11C-4DC8-8765-10CA222FC8F9},
	Volume = {3},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1080/146532401317070871}}

@article{Thanos:1992,
	Abstract = {Understanding of neuron-glial interactions in neurodegenerative diseases remains limited, but is of crucial importance for unravelling the etiology of such disorders both in humans and in animals. The present work employed a new, function-dependent technique for examining the role of microglia in rats afflicted with inherited retinal photoreceptor degeneration (strain: royal college of surgeons, RCS). In this rat strain, which served as a surrogate for human inherited retinal photoreceptor dystrophy, the optic nerve was cut and the ganglion cells were retrogradely labelled with the fluorescent dye 4Di-10ASP. The experiment was performed under three different conditions: (1) at the 50th day of postnatal age (P50) when there is ongoing degeneration of photoreceptor cells, (2) at P110 when most photoreceptors were degenerated and (3) at P50 in non-dystrophic rats of the Sprague-Dawley strain. After axotomy-induced ganglion cell death and labelling of activated microglia by phagocytosis of the ganglion cell debris, this study monitored whether the labelled and therefore identifiable microglial cells within the severed ganglion cell layer (GCL) are prompted to migrate and to participate in phagocytosis of debris produced within the endogenously degenerating photoreceptor cell layer (PRL). Massive migration of microglial cells from the GCL to the PRL occurred in dystrophic animals with optic nerve transection at P50. Double-labelling of microglial cells with the fluorescent dye ingested within the GCL and with lipofuscin ingested within the PRL indicated the ability of these cells to perform double-phagocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)},
	Author = {Thanos, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Axons;Retina;Neuroglia;Rats, Sprague-Dawley;Nerve Degeneration;Retinitis;Rats;Photoreceptors;Not relevant;Retinal Degeneration;11 Glia;Retinal Ganglion Cells;Animals;Disease Models, Animal;Phagocytosis;Rats, Inbred Strains;Support, Non-U.S. Gov't},
	Medline = {93007098},
	Month = {8},
	Nlm_Id = {0045503},
	Number = {1},
	Organization = {Department of Ophthalmology, University of T{\"u}bingen, School of Medicine, FRG.},
	Pages = {21-8},
	Pubmed = {1393569},
	Title = {Sick photoreceptors attract activated microglia from the ganglion cell layer: a model to study the inflammatory cascades in rats with inherited retinal dystrophy},
	Uuid = {F13F51D0-1D7A-4A42-AD24-2F8B20B2238F},
	Volume = {588},
	Year = {1992}}

@article{Thanos:1991,

@article{Thanos:1992a,
	Abstract = {The present work was undertaken to assess the fate of ganglion cell debris in the axotomized retina of adult rats and employed a new technique to label phagocytosing microglia via the internalized material. In the main experiment, transection axotomy was performed on the intraorbital segment of the optic nerve, and a fast-transported, vital fluorescent styryl dye (4Di-10ASP) was deposited at the ocular stump of the nerve in order to pre-label retrogradely the ganglion cells destined to die because of the axotomy. Optic nerve transection resulted in progressive degradation of ganglion cell axons, perikarya, and dendrites within the retina and in release of fluorescent material, which was then incorporated into cells identified as microglia. No other retinal cells stained, although astrocytes and M{\"u}ller's cells also responded to neuron degeneration by accumulating glial fibrillary acidic protein. Incorporation of labelled material into microglia topo-chronologically paralleled the ganglion cell degeneration starting within the optic fibre layer (OFL) and proceeding towards the ganglion cell layer (GCL) and the inner plexiform layer (IPL) of the affected retina. Long-term labelling of microglia monitored up to 3 months after optic nerve transection indicated that labelled microglial cells persisted within the retina. Microglia displayed a strong territorial arrangement within the GCL and IPL, and staggered, bilaminated distribution in both layers. These studies directly prove that microglia in the retina can be transcellularly labelled during traumatic degeneration of ganglion cells. The findings suggest that microglial cells play an important role in axotomy-induced wound healing and removal of cell debris.},
	Author = {Thanos, S. and Pavlidis, C. and Mey, J. and Thiel, H. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0014-4835},
	Journal = {Exp Eye Res},
	Keywords = {Fluorescent Dyes;Thiamine Pyrophosphatase;Nerve Degeneration;Animals;Phagocytosis;Rats;Female;Cell Count;Optic Nerve;Rats, Inbred Strains;Staining and Labeling;Not relevant;Get paper from library;Time Factors;11 Glia;Dendrites;Support, Non-U.S. Gov't;Carbocyanines;Retinal Ganglion Cells},
	Medline = {93011730},
	Month = {7},
	Nlm_Id = {0370707},
	Number = {1},
	Organization = {Department of Ophthalmology, University of T{\"u}bingen, School of Medicine, Germany.},
	Pages = {101-17},
	Pubmed = {1383017},
	Title = {Specific transcellular staining of microglia in the adult rat after traumatic degeneration of carbocyanine-filled retinal ganglion cells},
	Uuid = {71778C4C-8AE1-4E25-917B-BE569C0FAE84},
	Volume = {55},
	Year = {1992},
	url = {papers/Thanos_ExpEyeRes1992.PDF}}

@article{Thanos:1993,
	Abstract = {To monitor the cascade of events initiated by injury of adult neurons, and to explore whether and how neighboring microglial cells contribute to the degradation of lesioned neurons, axotomy-induced ganglion cell degeneration was investigated in adult rats. Suppression of macrophage and microglia activity during the weeks following transection of the optic nerve was performed with the immunoglobulin-derived tripeptide Thr-Lys-Pro, which is a macrophage inhibitory factor (MIF) and retards the activity of cells of monocytic origin. Single or repeated injection of MIF into the vitreous body during and after transection of the optic nerve resulted in significant retardation of axotomy-induced ganglion cell degradation in the retina as detected by specific labeling with the retrogradely transported fluorescent dye 4Di-10ASP. MIF specifically altered the morphology of labeled microglial cells from a ramified to an oval, less ramified shape, indicating that these cells were targets of its activity. Injection of the tetrapeptide macrophage stimulating factor, also known as tuftsin (Thr-Lys-Pro-Arg), revealed effects opposite to those described for the MIF: it increased the number of labeled microglial cells and enhanced the devastating effects of axotomy on ganglion cells. The viability of rescued ganglion cells in retinas treated with the various drugs was assessed both in vivo and in vitro. (1) Intravitreal injection of MIF to prevent degradation of neurons combined with transplantation of autologous peripheral nerve grafts, which facilitate regrowth of the transected neurites, revealed that significantly more ganglion cells contributed to axonal regeneration (17.1\%) than in untreated controls (9.5\%). (2) Explantation of retinas that were pretreated with MIF in situ revealed higher incidence of axonal outgrowth in organ cultures than untreated control explants or retinas treated with either the basic fibroblast growth factor or brain-derived neurotrophic factor. The present results demonstrate that axotomy initializes a cascade of microglia-mediated autodestructive retinal responses, which culminate in degradation of "sick," but obviously viable neurons. We postulate that the retinal microglial system has a key role in recognizing and eliminating severed neurons.},
	Author = {Thanos, S. and Mey, J. and Wild, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;Research Support, Non-U.S. Gov't;Nerve Degeneration;Animals;Macrophages;Rats;Oligopeptides;Female;Denervation;Rats, Sprague-Dawley;Optic Nerve;Axons;11 Glia;Nerve Regeneration;Axonal Transport;Macrophage Migration-Inhibitory Factors;Neuroglia;Tuftsin;24 Pubmed search results 2008;Amino Acid Sequence;Molecular Sequence Data;Retinal Ganglion Cells},
	Medline = {93147920},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {2},
	Organization = {Department of Ophthalmology, University of T{\"u}bingen, School of Medicine, Germany.},
	Pages = {455-66},
	Pubmed = {7678855},
	Title = {Treatment of the adult retina with microglia-suppressing factors retards axotomy-induced neuronal degradation and enhances axonal regeneration in vivo and in vitro},
	Uuid = {54E4FFC1-8FE6-40EC-A9C0-81F5FC086B51},
	Volume = {13},
	Year = {1993}}

@article{Thanos:1994,
	Abstract = {The nature of the interactions between dying neurons and microglial cells within the developing and injured CNS remains controversial. A new technique for labelling microglial cells is available, which enables further studies of such interactions in a direct way. The value of the method relies on retrograde filling of neurons with vital fluorescent dye, subsequent degeneration of the neurons due to either naturally occurring cell death or as the result of axotomy, and phagocytotic removal of the fluorescent cell debris by microglial cells, which thus become identifiable. The fluorescent dye can be visualized in whole-mounted tissue or after sectioning. Photoconversion of the dye into electron-dense material permits examination of the microglial and dying ganglion-cell interactions at the ultrastructural level. This new principle of the function-dependent, selective fluorescent labelling of phagocytosing microglial cells, which might now be extended to other dyes and to other neurodegenerative models, promises to shed light onto the function of microglial cells within the brain.},
	Author = {Thanos, S. and Kacza, J. and Seeger, J. and Mey, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0166-2236},
	Journal = {Trends Neurosci},
	Keywords = {23 Technique;Alpha;Not relevant;Fluorescent Dyes;11 Glia;Microglia;Microscopy, Fluorescence;Retinal Ganglion Cells;Neurology;Animals;Phagocytosis;G;24 Pubmed search results 2008},
	Medline = {94337417},
	Month = {5},
	Nlm_Id = {7808616},
	Number = {5},
	Organization = {Dept of Ophthalmology, University of T{\"u}bingen, School of Medicine, Germany.},
	Pages = {177-82},
	Pubmed = {7520197},
	Title = {Old dyes for new scopes: the phagocytosis-dependent long-term fluorescence labelling of microglial cells in vivo},
	Uuid = {9187B582-3592-4B4F-90D2-9D8D60C3EE18},
	Volume = {17},
	Year = {1994}}

@article{Thery:1994,
	Abstract = {Brain macrophages (BM), a subpopulation of microglia, have the ability to kill neurons by producing reactive oxygen intermediates. Cocultures of neurons and macrophages derived from the cerebral cortex of rat embryos were used to look for regulation of BM neurotoxicity. Isoproterenol (10(-7) M), a beta-adrenergic agonist, induced a significant inhibition of BM neurotoxicity and this effect was abolished in the presence of propranolol, a beta-adrenergic antagonist. BM neurotoxicity was also reduced in the presence of prostaglandin E2 (10(-8), 10(-6) M), a metabolite derived from arachidonic acid. These results suggest endogenous mechanisms of neuroprotection operating either during development or following lesions.},
	Author = {Th{\'e}ry, C. and Dobbertin, A. and Mallat, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Down-Regulation;Propranolol;Support, Non-U.S. Gov't;Adrenergic beta-Agonists;Rats;Reactive Oxygen Species;Not relevant;11 Glia;Dinoprostone;Cell Death;Macrophages;Isoproterenol;Microtubule-Associated Proteins;Brain;Neurons;Animals},
	Medline = {95048682},
	Month = {8},
	Nlm_Id = {8806785},
	Number = {4},
	Organization = {INSERM U.114, Chaire de Neuropharmacologie, Coll\`{e}ge de France, Paris, France.},
	Pages = {383-6},
	Pubmed = {7960041},
	Title = {Downregulation of in vitro neurotoxicity of brain macrophages by prostaglandin E2 and a beta-adrenergic agonist},
	Uuid = {7DDB487C-FE27-43C0-A4F4-79776DE7ABB6},
	Volume = {11},
	Year = {1994}}

@article{Thery:1990,
	Abstract = {We have investigated the expression of macrophage-colony stimulating factor (M-CSF) gene in mouse brain during development. Northern blot analysis of cerebral RNA evidenced a 4.5-kb M-CSF transcript from day 14 of gestation until 2 weeks after birth. The cell type responsible for this transcription was studied using in vitro cell cultures. The 4.5-kb M-CSF transcript was found both in astrocyte primary cultures and in immortalized astrocytic cell lines. M-CSF mRNA was also detected in lipopolysaccharide-stimulated brain macrophage cultures. These results suggest that M-CSF is involved in the outgrowth of microglia during ontogenesis.},
	Author = {Th{\'e}ry, C. and H{\'e}tier, E. and Evrard, C. and Mallat, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Embryo and Fetal Development;Macrophage Colony-Stimulating Factor;Cerebral Cortex;Animals;Nucleic Acid Hybridization;Gene Expression Regulation;Astrocytes;11 Glia;Colony-Stimulating Factors;Support, Non-U.S. Gov't;Molecular Weight;Cells, Cultured;RNA, Messenger;Mice},
	Medline = {90294329},
	Month = {5},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Inserum U.114, Chaire de Neuropharmacologie, Coll\`{e}ge de France, Paris.},
	Pages = {129-33},
	Pubmed = {2193167},
	Title = {Expression of macrophage colony-stimulating factor gene in the mouse brain during development},
	Uuid = {373B1E3D-94A4-4CC6-934E-D13F18CF2AF1},
	Volume = {26},
	Year = {1990}}

@article{Thinakaran:1993,
	Abstract = {Skeletal myoblasts undergo terminal differentiation when maintained under low-mitogen conditions. We have examined the expression of c-jun, one of the growth-factor-inducible immediate-early genes, during myogenic differentiation of L6 myoblasts. The steady-state levels of c-jun mRNA, c-Jun polypeptide, and activator protein 1 binding activity were not markedly altered in L6 cells undergoing myogenic differentiation. Although expression of c-jun is induced by serum mitogens in fibroblasts and other cell lines, addition of high serum to proliferating myoblasts resulted in the activation of another immediate early gene junB, but not c-jun mRNA expression. These results indicate that regulation of c-jun may differ from that of other immediate early genes in L6 cells. Manipulation of myogenesis by exposing L6 cells to dimethyl sulfoxide also suggested that expression of myogenin and muscle differentiation could occur in the presence of high levels of c-Jun. Furthermore, expression of c-jun from Moloney murine leukaemia viral long-terminal repeat in transfected L6 cells confirmed that constitutive expression of c-jun does not interfere with myogenesis in L6 myoblasts. Therefore, regulation of c-jun expression in rat L6 cells differs from that in the mouse C2 cell line. 0829-8211 Journal Article},
	Author = {Thinakaran, G. and Bag, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Biochem Cell Biol},
	Keywords = {Cell Differentiation/drug effects/*genetics;Animals;Base Sequence;Rats;Transfection;Repetitive Sequences, Nucleic Acid;Muscles/*cytology;*Gene Expression;Moloney murine leukemia virus/genetics;*Genes, jun;Proto-Oncogene Proteins c-jun/metabolism;DNA/metabolism;EE, DMSO, abstr;08 Aberrant cell cycle;Myogenin/genetics;Dimethyl Sulfoxide/pharmacology;Cell Line;Half-Life;Support, Non-U.S. Gov't;RNA, Messenger/metabolism;Blood;Transcription, Genetic},
	Number = {5-6},
	Organization = {Department of Molecular Biology and Genetics, University of Guelph, ON, Canada.},
	Pages = {260-9},
	Pubmed = {8274267},
	Title = {Expression of the protooncogene c-jun is maintained during myogenic differentiation in rat L6 myoblasts},
	Uuid = {E16197A5-16D8-471E-966A-5BD7AD63AC02},
	Volume = {71},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8274267}}

@article{Thomas:1999,
	Abstract = {Pericytes are a unique cell group intimately associated with the vasculature and that appear to be present in most tissues. Their presence is generally considered to be restricted to the microvessels - arterioles, venules and particularly capillaries, where there is little or no smooth muscle. Morphologically, the pericytes exhibit a small, oval cell body with multiple processes extending for some distance along the vessel axis; these primary processes then give rise to orthogonal secondary branches which encircle the vascular wall. Through this morphology and their close association with the vasculature, the contour of the cells conforms to that of the adjacent vascular element; also, they are usually enclosed within the basal lamina of the microvasculature. While many earlier studies suggested brain pericytes as a source of macrophage activity, recent results substantiate this functional role; these recent findings include the demonstration of macrophage markers, phagocytosis and antigen presentation. Coupled with current knowledge on the entry of lymphoblasts into brain tissue and perivascular areas as potentially being the primary site of cellular interactions for production of immune responses, this places the pericytes in a position to significantly contribute to central nervous system (CNS) immune mechanisms. They may in fact be the population of brain macrophages most instrumental in the initiation of an immune response. Although these cells constitutively express several macrophage properties, they are also capable of up-regulation to display the full range of macrophage functional activity. At least, some of the pericytic macrophages are located on the surface of the basal lamina as opposed to completely within it; however, their potential transformation into microglia of the parenchyma remains an open issue. In addition to their function as macrophages, pericytes appear to serve a host of other functional roles. They are contractile and seem to serve as a smooth muscle equivalent in the capillaries performing vasoconstriction; they regulate endothelial cell properties and contribute to the stability and maintenance of blood vessels; and they appear to directly participate in coagulation through the extrinsic pathway. Also, pericytes have been suggested to be pluripotential and serve as precursors for a variety of other cell types. From these functional roles, comes their involvement in various disease processes. In association with the macrophage function, they are involved in numerous autoimmune and infectious diseases. Through their vascular role, they are involved in diabetic retinopathy and inflammation. Also, the pericytes appear to have involvement in Alzheimer's as well as other diseases. Thus, these cells are presented not only as macrophages but as a group with broad functional activities and significant potential for contributing to disease states.},
	Author = {Thomas, W. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0165-0173},
	Journal = {Brain Res Brain Res Rev},
	Keywords = {Endothelium, Vascular;Pericytes;Rats;Research Support, U.S. Gov't, P.H.S.;11 Glia;Macrophages;Animals;Brain;Mice;review;Humans},
	Medline = {20079001},
	Month = {12},
	Nlm_Id = {8908638},
	Number = {1},
	Organization = {Department of Biological Sciences, 308 Hovey Hall, Illinois State University, Normal, IL 61790-4000, USA.},
	Pages = {42-57},
	Pii = {S0165017399000247},
	Pubmed = {10611494},
	Title = {Brain macrophages: on the role of pericytes and perivascular cells},
	Uuid = {C4DF02CF-A154-4521-8EC3-A8FEEC24F48D},
	Volume = {31},
	Year = {1999}}

@article{Thomas:1996,
	Abstract = {The subependymal zone (SEZ) of the lateral ventricle of adult rodents has long been known to be mitotically active. There has been increased interest in the SEZ, since it has been demonstrated that neuroepithelial stem cells residing there generate neurons in addition to glia in vitro. In the present study, we have examined parasagittal sections of the adult mouse brain using immunocytochemistry for extracellular matrix (ECM) molecules (tenascin and chondroitin sulfate- containing proteoglycans), glial fibrillary acidic protein (GFAP, a cytoskeletal protein prominently expressed by immature and reactive astrocytes), RC-2 (a radial glial and immature astrocyte cytoskeletal marker), TuJ1 (a class III beta-tubulin isoform expressed solely by postmitotic and adult neurons), nestin (a cytoskeletal protein associated with stem cells), neuron-specific enolase, and bromodeoxyuridine (BrdU, which is taken up by dividing cells). Our results demonstrate that a population of young neurons reside within an ECM-rich, GFAP-positive astrocyte pathway from the rostral SEZ all the way into the olfactory bulb. Furthermore, BrdU labeling studies indicate that there is a high level of cell division along the entire length of this path, and double-labeling studies indicate that neurons committed to a neuronal lineage (i.e., TuJ1+) take up BrdU (suggesting they are in the DNA synthesis phase of the cell cycle), again along the entire length of the SEZ "migratory pathway."Thus, the SEZ appears to retain the ability to produce neurons and glia throughout the life of the animal, functioning as a type of "brain marrow."The implications of these findings are discussed in relation to the role that such a glial/ ECM-rich boundary (as seen in the embryonic cortical subplate and other developing areas) may play in: confining the migratory populations and maintaining them in a persistent state of immaturity; facilitating their migration to the olfactory bulb, where they are incorporated into established adult circuitries; and potentially altering SEZ cell cycle dynamics that eventually lead to cell death.},
	Author = {Thomas, L. B. and Gates, M. A. and Steindler, D. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Glia},
	Keywords = {Astrocytes/*physiology;02 Adult neurogenesis migration;Neurons/*physiology;Extracellular Matrix/*physiology;Immunohistochemistry;Brain/*anatomy &histology;Animal;Mice, Inbred ICR;Support, U.S. Gov't, P.H.S.;B abstr;Cell Division/*physiology;Support, Non-U.S. Gov't;Mice;Neural Pathways/*anatomy &histology},
	Number = {1},
	Organization = {Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163, USA.},
	Pages = {1-14.},
	Title = {Young neurons from the adult subependymal zone proliferate and migrate along an astrocyte, extracellular matrix-rich pathway},
	Uuid = {03B34F82-139C-40D9-B918-1C561E6AD7D5},
	Volume = {17},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8723838}}

@article{Thomas:2007,
	Abstract = {Factors modulating neurogenesis may contribute to the pathophysiology of affective disorders such as major depression. Environmental stressors in animal models have been proposed to alter neurogenesis, suggesting a mechanism for this contribution. The effect of an acute psychosocial stressor on either proliferation or survival (immediate, short term, and long term) was examined along with subsequent neuronal differentiation in the hippocampus of adult male Sprague Dawley rats. Subjects were exposed to a widely used social dominance paradigm that elicits behavioral and physiological responses to an acute psychosocial stressor. This social dominance paradigm may mimic human relational stress more realistically than laboratory stressors and provides a socially relevant model. We found that exposure to an acute psychosocial stressor at the time of cell generation resulted in a decreased number of newly generated cells in the hippocampus. By using sequential thymidine analog administration to provide temporal discrimination of DNA replication, we showed that short-term survival but not initial proliferation or immediate survival was altered in response to stress. Furthermore, we determined that stress experienced subsequent to proliferation also diminished long-term survival of cells. Thus, an acute episode of a social stress produces long-lasting effects on the incorporation of new hippocampal neurons by reducing their survival.},
	Author = {Thomas, Rosanne M. and Hotsenpiller, Gregory and Peterson, Daniel A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {02 Adult neurogenesis migration;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {11},
	Organization = {Neural Repair and Neurogenesis Laboratory, Department of Neuroscience, The Chicago Medical School at Rosalind Franklin University of Medicine and Science, North Chicago, Illinois 60064, USA.},
	Pages = {2734-43},
	Pii = {27/11/2734},
	Pubmed = {17360895},
	Title = {Acute psychosocial stress reduces cell survival in adult hippocampal neurogenesis without altering proliferation},
	Uuid = {BE14073E-F66E-4C7F-B9A0-8805BC384D87},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3849-06.2007}}

@article{Threadgill:1997,
	Abstract = {The acquisition of cell type-specific morphologies is a central feature of neuronal differentiation and has important consequences for nervous system function. To begin to identify the underlying molecular mechanisms, we have explored the role of Rho-related GTPases in the dendritic development of cortical neurons. Expression of dominant negative mutants of Rac or Cdc42, the Rho-inhibitory molecule C3 transferase, or the GTPase-activating protein RhoGAP p190 causes a marked reduction in the number of primary dendrites in nonpyramidal (multipolar) neurons and in the number of basal dendrites in neurons with pyramidal morphologies. Conversely, the expression of constitutively active mutants of Rho, Rac, or Cdc42 leads to an increase in the number of primary and basal dendrites. In cortical cultures, as in vivo, dendritic remodeling leads to an apparent transformation from pyramidal to nonpyramidal morphologies over time. Strikingly, this shift in favor of nonpyramidal morphologies is also inhibited by the expression of dominant negative mutants of Cdc42 and Rac and by RhoGAP p190. These observations indicate that Rho, Rac, and Cdc42 play a central role in dendritic development and suggest that differential activation of Rho-related GTPases may contribute to the generation of morphological diversity in the developing cortex.},
	Author = {Threadgill, R. and Bobb, K. and Ghosh, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;GTP-Binding Proteins;Cell Cycle Proteins;Signal Transduction;Animals;Gene Expression Regulation, Developmental;Rats;Transfection;10 Structural plasticity;Phenotype;Proteins;Neocortex;cdc42 GTP-Binding Protein;Cells, Cultured;Beta;Rats, Inbred Strains;RNA, Messenger;Pyramidal Cells;Mutagenesis;GTP Phosphohydrolases;Dendrites;rhoA GTP-Binding Protein;GTPase-Activating Proteins;10 Spiny stellate;Support, Non-U.S. Gov't;Plasmids;Neurotransmitters;Interneurons},
	Medline = {97470893},
	Month = {9},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.},
	Pages = {625-34},
	Pubmed = {9331353},
	Title = {Regulation of dendritic growth and remodeling by Rho, Rac, and Cdc42},
	Uuid = {BA40C7D5-7DE2-4BEE-A133-C6702FCF0CC6},
	Volume = {19},
	Year = {1997},
	url = {papers/Threadgill_Neuron1997.pdf}}

@article{Tian:2003,
	Abstract = {BACKGROUND: Host immune responses to foreign gene products have been shown to lead to the elimination of genetically modified cells, and are a major barrier to successful therapeutic gene therapy. We have shown that immunological tolerance to retrovirally transduced cell surface proteins can be induced by expressing the gene encoding these products in bone marrow derived cells. Here, we investigate if expression of foreign gene products in bone marrow derived cells can be used to induce tolerance to cytoplasmic proteins. METHODS: Balb/c mice were reconstituted with syngeneic bone marrow cells transduced with retrovirus carrying the gene encoding enhanced green fluorescent protein (eGFP), or mock-transduced bone marrow cells. After reconstitution, mice were immunized with cells expressing eGFP, and T cells were tested for the ability to kill eGFP-expressing targets in in vitro cytotoxic T lymphocyte (CTL) assays. RESULTS: T cells from Balb/c mice reconstituted with mock-transduced bone marrow were able to kill target cells expressing eGFP. In contrast, T cells from mice reconstituted with eGFP-transduced bone marrow were unable to kill targets expressing eGFP. In addition, we observed that T cell responses to eGFP in C57BL/6 mice were minimal even under highly immunogenic conditions. CONCLUSIONS: These data suggest that expression of foreign gene products in bone marrow derived cells is capable of inducing T cell tolerance to proteins expressed exclusively in the cytoplasm.},
	Author = {Tian, Chaorui and Bagley, Jessamyn and Kaye, Joel and Iacomini, John},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1099-498X},
	Journal = {J Gene Med},
	Keywords = {T-Lymphocytes;Mice, Inbred BALB C;Animals;Bone Marrow Transplantation;Cytoplasm;Female;Cell Membrane;Recombinant Fusion Proteins;Retroviridae;11 Glia;Green Fluorescent Proteins;Immune Tolerance;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Gene Transfer Techniques;Gene Therapy;T-Lymphocytes, Cytotoxic;Flow Cytometry;Mice;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22616074},
	Month = {5},
	Nlm_Id = {9815764},
	Number = {5},
	Organization = {Transplantation Biology Research Center, Massachusetts General Hospital and Harvard Medical School, MGH-East, Building 149, 13th St., Boston 02129, USA.},
	Pages = {359-65},
	Pubmed = {12731084},
	Title = {Induction of T cell tolerance to a protein expressed in the cytoplasm through retroviral-mediated gene transfer},
	Uuid = {87A96FFB-89E3-4557-97CF-2C37DDA55689},
	Volume = {5},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jgm.363}}

@article{Tillmann:1994,
	Abstract = {Retroviruses have been implicated as causative agents of a variety of human diseases including malignancy, immune system dysfunction, and neurologic disorders. Despite the isolation of various retroviral agents from patients suffering from malignant neoplasias and neurologic disorders, only the human T-cell lymphotropic virus type I (HTLV-I) and the human immunodeficiency virus (HIV) have been definitively accepted as etiologic agents of human disease (Hjelle, 1991; Gessain and Gout, 1992; Rosenblatt, 1993). Because of their increasingly defined roles in disease progression, the replication of HTLV-I and HIV is an important focus for understanding the pathogenic processes resulting from viral infection. Of particular interest are the molecular mechanisms by which expression of retroviral genomes is regulated by their regulatory units, the long terminal repeats (LTR), in a manner specific to the cellular targets which they infect.},
	Author = {Tillmann, M. and Krebs, F. C. and Wessner, R. and Pomeroy, S. M. and Goodenow, M. M. and Wigdahl, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0960-5428},
	Journal = {Adv Neuroimmunol},
	Keywords = {Trans-Activation (Genetics);Transcription, Genetic;Transcription Factors;Gene Expression Regulation, Viral;HIV-1;Humans;Base Sequence;Repetitive Sequences, Nucleic Acid;Cells, Cultured;review, tutorial;Human T-lymphotropic virus 1;review;Microglia;Models, Biological;HIV Long Terminal Repeat;Gene Products, tax;Recombinant Fusion Proteins;11 Glia;Research Support, U.S. Gov't, P.H.S.;Genome, Viral;Neuroglia;Molecular Sequence Data;AIDS Dementia Complex},
	Medline = {95179422},
	Nlm_Id = {9108376},
	Number = {3},
	Organization = {Department of Microbiology and Immunology, Pennsylvania State University, College of Medicine, Hershey 17033.},
	Pages = {305-18},
	Pubmed = {7874399},
	Title = {Neuroglial-specific factors and the regulation of retrovirus transcription},
	Uuid = {DABFF682-D9FC-499C-982C-68AF62CF45AF},
	Volume = {4},
	Year = {1994}}

@article{Tiveron:2006,
	Abstract = {Most cortical interneurons are generated in the subpallial ganglionic eminences and migrate tangentially to their final destinations in the neocortex. Within the cortex, interneurons follow mainly stereotype routes in the subventricular zone/intermediate zone (SVZ/IZ) and in the marginal zone. It has been suggested that interactions between invading interneurons and locally generated projection neurons are implicated in the temporal and spatial regulation of the invasion process. However, so far experimental evidence for such interactions is lacking. We show here that the chemokine stromal-derived factor 1 (SDF-1; CXCL12) is expressed in the main invasion route for cortical interneurons in the SVZ/IZ. Most SDF-1-positive cells are proliferating and express the homeodomain transcription factors Cux1 and Cux2. Using MASH-1 mutant mice in concert with the interneuron marker DLX, we exclude that interneurons themselves produce the chemokine in an autocrine manner. We conclude that the SDF-1-expressing cell population represents the precursors of projection neurons during their transition and amplification in the SVZ/IZ. Using mice lacking the SDF-1 receptor CXCR4 or Pax6, we demonstrate that SDF-1 expression in the cortical SVZ/IZ is essential for recognition of this pathway by interneurons. These results represent the first evidence for a molecular interaction between precursors of projection neurons and invading interneurons during corticogenesis.},
	Author = {Tiveron, Marie-Catherine C. and Rossel, Mireille and Moepps, Barbara and Zhang, Yong Li and Seidenfaden, Ralph and Favor, Jack and K{\"o}nig, Norbert and Cremer, Harold},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Receptors, CXCR4;Signal Transduction;Animals;comparative study;Neural Pathways;Cell Communication;Mice, Transgenic;Cell Movement;Mice, Inbred C57BL;research support, non-u.s. gov't;Cerebral Ventricles;Cerebral Cortex;Neurons;Chemokines, CXC;Mice;Interneurons;24 Pubmed search results 2008;Stem Cells},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {51},
	Organization = {Institut de Biologie du D{\'e}veloppement de Marseille Luminy, Centre National de la Recherche Scientifique/Universit{\'e} de Mediterran{\'e}e, 13288 Marseille, France.},
	Pages = {13273-8},
	Pii = {26/51/13273},
	Pubmed = {17182777},
	Title = {Molecular interaction between projection neuron precursors and invading interneurons via stromal-derived factor 1 (CXCL12)/CXCR4 signaling in the cortical subventricular zone/intermediate zone},
	Uuid = {275C5222-106C-4A4C-80CC-EF344200A075},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4162-06.2006}}

@article{Todaro:1972,
	Author = {Todaro, G. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0090-0028},
	Journal = {Nat New Biol},
	Keywords = {Tritium;24 Pubmed search results 2008;Mice, Inbred BALB C;Animals;RNA Viruses;15 Retrovirus mechanism;RNA-Directed DNA Polymerase;Retroviridae;Embryo;Cell Line;Thymine Nucleotides;Mice;Virus Replication;Microscopy, Electron;Clone Cells;15 ERVs retroelements;Cell Transformation, Neoplastic;Oncogenic Viruses},
	Medline = {73061740},
	Month = {11},
	Nlm_Id = {0410463},
	Number = {100},
	Pages = {157-60},
	Pubmed = {4118366},
	Title = {Spontaneous release of type C viruses from clonal lines of spontaneously transformed Blab-3T3 cells},
	Uuid = {8DFF9FC6-4328-11DB-A5D2-000D9346EC2A},
	Volume = {240},
	Year = {1972}}

@article{Toggas:1994,
	Abstract = {Many people infected with human immunodeficiency virus type 1 (HIV-1) develop neurological complications that can culminate in dementia and paralysis. The discrepancy between the severity of impairment and the paucity of detectable HIV-1 within neurons has led to an intense search for diffusible virus- and host-derived factors that might be neurotoxic (see ref. 2 for review). The HIV-1 envelope glycoprotein gp120 is an extracellular protein that is shed from infected cells and so has the potential to diffuse and interact with distant uninfected brain cells. Studies on cultured immature cells suggest that gp120 induces neurotoxicity (reviewed in refs 2, 4), and systemic injection of gp120 in neonatal rats and intracerebroventricular injection in adult rats results in deleterious effects on the brain. To assess the pathogenic potential of gp120 in the intact brain, we have now produced gp120 in the brains of transgenic mice and found a spectrum of neuronal and glial changes resembling abnormalities in brains of HIV-1-infected humans. The severity of damage correlated positively with the brain level of gp120 expression. These results provide in vivo evidence that gp120 plays a key part in HIV-1-associated nervous system impairment. This model should facilitate the evaluation and development of therapeutic strategies aimed at HIV-brain interactions.},
	Author = {Toggas, S. M. and Masliah, E. and Rockenstein, E. M. and Rall, G. F. and Abraham, C. R. and Mucke, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Research Support, Non-U.S. Gov't;AIDS Dementia Complex;Animals;HIV-1;Astrocytes;Base Sequence;Humans;Brain;Microglia;Mice, Transgenic;Recombinant Fusion Proteins;11 Glia;Research Support, U.S. Gov't, P.H.S.;Neurons;Mice;Molecular Sequence Data;HIV Envelope Protein gp120;Glial Fibrillary Acidic Protein},
	Medline = {94159078},
	Month = {1},
	Nlm_Id = {0410462},
	Number = {6459},
	Organization = {Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037.},
	Pages = {188-93},
	Pubmed = {8114918},
	Title = {Central nervous system damage produced by expression of the HIV-1 coat protein gp120 in transgenic mice},
	Uuid = {3BAC6409-FCA9-4A2D-A6F1-7B3CADDE6FE7},
	Volume = {367},
	Year = {1994},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/367188a0}}

@article{Toida:1998,
	Abstract = {The present study analyzed three-dimensional structural features and synaptic contacts of morphologically and chemically identified calbindin D28K-immunoreactive neurons in the glomerular layer of the rat main olfactory bulb by means of combined confocal laser scanning light microscopy, high-voltage electron microscopy and electron microscopic serial section/three-dimensional reconstruction. Most of calbindin D28K-immunoreactive neurons were identified as the periglomerular cell type by combined high-voltage electron microscopic and confocal laser scanning light microscopic observations, and the minority were the short-axon cell type and others. The combined confocal laser scanning light microscopic and electron microscopic study revealed that the calbindin D28K-immunoreactive neurons exhibited unique synaptic contact patterns; they received asymmetrical synapses from presumed mitral/tufted dendrites and made conversely symmetrical synapses with them. About 30\%of asymmetrical postsynaptic sites and about 40\%of symmetrical presynaptic sites formed reciprocal pairs of synapses. Calbindin D28K-immunoreactive dendrites and somata also received synapses from GABA-like-immunoreactive profiles containing numerous pleomorphic, and a few dense-cored, vesicles. On the other hand, surprisingly, calbindin D28K-immunoreactive neurons had almost no synaptic contacts from olfactory nerve terminals. The present study clearly revealed that calbindin D28K-immunoreactive neurons are a type of periglomerular cell involving unique synaptic contacts that have not been reported so far, and thus indicated that so-called periglomerular cells should be heterogeneous in their synaptic connections as well as in their chemical and structural features.},
	Author = {Toida, K. and Kosaka, K. and Heizmann, C. W. and Kosaka, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Journal = {J Comp Neurol},
	Keywords = {I;Calcium-Binding Protein, Vitamin D-Dependent/*analysis;Rats;Microscopy, Electron;Immunohistochemistry;Neurons/classification/*cytology/ultrastructure;Rats, Wistar;Animal;Nerve Tissue Proteins/*analysis;Olfactory Bulb/*cytology;Support, Non-U.S. Gov't;Models, Structural;GABA/analysis;Synapses/physiology/*ultrastructure;13 Olfactory bulb anatomy},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, Kyushu University Faculty of Medicine, Higashiku, Fukuoka, Japan. toida\@a3rd.med.kyushu-u.ac.jp},
	Pages = {179-98.},
	Title = {Chemically defined neuron groups and their subpopulations in the glomerular layer of the rat main olfactory bulb: III. Structural features of calbindin D28K-immunoreactive neurons},
	Uuid = {C19AA732-2AED-40E9-BA81-1AD1F1A823CC},
	Volume = {392},
	Year = {1998},
	url = {papers/Toida_JCompNeurol1998.pdf}}

@article{Toida:1996,
	Abstract = {Neurons containing a calcium-binding protein parvalbumin in the external plexiform layer of the rat olfactory bulb were identified light microscopically with the pre-embedding immunocytochemistry and were subsequently analysed with the electron microscopic serial- sectioning and three-dimensional reconstructions. In the present study we chose several different types of parvalbumin-immunoreactive neurons identified light microscopically as Van Gehuchten cell type, superficial short-axon cell type and multipolar cell type. Parvalbumin- immunoreactive somata were similar to one another in their ultrastructural characteristics, showing nuclear indentations, moderately developed Golgi apparatus and abundant mitochondria; these structural features appeared to resemble those of the short axon cells around the glomeruli and in the granule cell layer reported in previous electron microscopic studies. All neurons analysed in the present study made symmetrical synapses on to dendrites and somata of presumed mitral/tufted cells and received asymmetrical synapses from them, and occasionally formed reciprocal synapses with them. On the parvalbumin- immunoreactive processes, the asymmetrical synapses nearly equalled the symmetrical ones in number and about 30-50\%of them were identified as reciprocal pairs. In contrast, no presynaptic sites were observed on parvalbumin-immunoreactive somata, and thick portions (more than approximately 2 microns in diameter) of the proximal dendrites, where they were occasionally postsynaptic in some asymmetrical and symmetrical synapses from parvalbumin-immunonegative profiles. Characteristically, parvalbumin-immunoreactive process frequently make direct contacts with one another; processes regarded light microscopically as arising from a soma or a dendrite or parvalbumin- immunoreactive neurons were sometimes revealed to be separate but directly contacting processes with electron microscopic examinations. Although puncta adherentia were occasionally observed between these contact sites, so far neither gap junctions nor chemical synapses were observed. Until now, it has been believed that in the external plexiform layer only granule cells form reciprocal synapses with mitral/tufted cells. However, the present study clearly demonstrates that interneurons different from granule cells, namely GABAergic neurons containing a calcium-binding protein parvalbumin, also make reciprocal synapses with mitral/tufted cells in the external plexiform layer. Therefore, neuronal processes making reciprocal synapses with mitral/tufted cells in the external plexiform layer cannot be determined a priori as granule cell processes.},
	Author = {Toida, K. and Kosaka, K. and Heizmann, C. W. and Kosaka, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Neuroscience},
	Keywords = {I;Interneurons/metabolism/ultrastructure;Image Processing, Computer-Assisted;Immunohistochemistry;Microscopy, Electron;Rats;Parvalbumins/*metabolism;Rats, Wistar;Animal;Olfactory Bulb/*metabolism/*ultrastructure;Support, Non-U.S. Gov't;Mitochondria/metabolism/ultrastructure;Neurons/*metabolism/*ultrastructure;Male;13 Olfactory bulb anatomy},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.},
	Pages = {449-66.},
	Title = {Electron microscopic serial-sectioning/reconstruction study of parvalbumin-containing neurons in the external plexiform layer of the rat olfactory bulb},
	Uuid = {36346847-0E50-490A-B29C-E5D61E89A9C5},
	Volume = {72},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8737415}}

@article{Toida:2000,
	Abstract = {Synapses of intraglomerular processes of tyrosine hydroxylase- immunoreactive neurons in the rat main olfactory bulb were examined by electron microscopic immunocytochemistry. Prominent characteristics of intraglomerular synapses of tyrosine hydroxylase-immunoreactive elements were that the vast majority (about 80\%) of their synaptic inputs were asymmetrical synapses from olfactory nerve terminals and, though far smaller in proportion, one half of the remaining were asymmetrical synapses from mitral/tufted cell dendrites and the other half were symmetrical synapses from gamma-aminobutyric acid-like immunoreactive elements. So far, we have observed no typical reciprocal synapses between tyrosine hydroxylase-immunoreactive processes and mitral/tufted dendrites; however, we have often identified serial synapses; that is, asymmetrical synapses from olfactory nerve terminals or mitral/tufted cell dendrites to tyrosine hydroxylase-immunoreactive processes, and then symmetrical synapses from the latter to different mitral/tufted cell dendrites. These synaptic connections of tyrosine hydroxylase-immunoreactive neurons were very different from those of Calbindin-D(28k)-immunoreactive neurons, which received no synaptic contact directly from olfactory nerve terminals but formed reciprocal synapses with mitral/tufted cells as we analysed previously.Thus, our present and previous electron microscopic studies combined with confocal laser scanning light microscopy clearly indicated for the first time the heterogeneity of periglomerular neurons, not only in their chemical and morphological features, but also in their synaptic organization in the olfactory glomerulus. Using Smart Source Parsing},
	Author = {Toida, K. and Kosaka, K. and Aika, Y. and Kosaka, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Neuroscience},
	Keywords = {I;Olfactory Bulb/*metabolism/ultrastructure;Olfactory Nerve/metabolism/ultrastructure;Tyrosine 3-Monooxygenase/*metabolism;Smell/physiology;Rats;Cell Size/physiology;Neural Pathways/*metabolism/ultrastructure;Neurons/*metabolism/ultrastructure;Rats, Wistar;Animal;Support, Non-U.S. Gov't;Male;13 Olfactory bulb anatomy;Dendrites/metabolism/ultrastructure;Synapses/*metabolism/ultrastructure},
	Number = {1},
	Organization = {Department of Anatomy and Neurobiology, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, 812-8582, Japan. toida\@basic.med.tokushima-u.ac.jp},
	Pages = {11-7},
	Title = {Chemically defined neuron groups and their subpopulations in the glomerular layer of the rat main olfactory bulb--IV. Intraglomerular synapses of tyrosine hydroxylase-immunoreactive neurons},
	Uuid = {88DF0CD8-AB61-4569-9B31-2C214F3A6FA8},
	Volume = {101},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11068132}}

@article{Tomita:2004,
	Abstract = {Choroidal neovascularization (CNV) is a known cause of age-related macular degeneration (ARMD). Moreover, the most common cause of blindness in the elderly in advanced countries is ARMD with CNV. It has recently been shown that bone marrow cells (BMCs) can differentiate into various cell lineages in vitro and in vivo. Adults maintain a reservoir of hematopoietic stem cells included in BMCs that can enter the circulation to reach various organs in need of regeneration. It has recently been reported that endothelial progenitor cells (EPCs) included in BMCs are associated with neovascularization. We examine the role of BMCs in CNV using a model of CNV in adult mice. Using methods consisting of fractionated irradiation (6.0 Gy x 2) followed by bone marrow transplantation (BMT), adult mice were engrafted with whole BMCs isolated from transgenic mice expressing enhanced green fluorescent protein (EGFP). Three months after BMT, we confirmed that the hematopoietic cells in the recipients had been completely replaced with donor cells. We then carried out laser photocoagulation to induce CNV in chimeric mice (donor cells >95\%). Two weeks after the laser photocoagulation, by which time CNV had occurred, immunohistochemical examination was carried out. The vascular wall cells of the CNV expressed both EGFP and CD31. These findings indicate that newly developed blood vessels in the CNV are derived from the BMCs and suggest that the inhibition of EPC mobilization from the bone marrow to the eyes could be a new approach to the fundamental treatment of CNV in ARMD.},
	Author = {Tomita, Minoru and Yamada, Haruhiko and Adachi, Yasushi and Cui, Yunze and Yamada, Eri and Higuchi, Akiko and Minamino, Keizo and Suzuki, Yasuhiko and Matsumura, Miyo and Ikehara, Susumu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {Cell Differentiation;Animals;Macular Degeneration;Endothelial Cells;Choroidal Neovascularization;Mice, Transgenic;Cell Movement;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Disease Models, Animal;Hematopoietic Stem Cell Transplantation;Antigens, CD31;Radiation Chimera;Male;Cell Lineage;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Graft Survival;Light Coagulation;Blood Vessels},
	Nlm_Id = {9304532},
	Number = {1},
	Organization = {First Department of Pathology, Kansai Medical University, Moriguchi City, Osaka, Japan.},
	Pages = {21-6},
	Pubmed = {14688388},
	Title = {Choroidal neovascularization is provided by bone marrow cells},
	Uuid = {48E22B41-9141-4206-BFD2-B4A5D2D61E36},
	Volume = {22},
	Year = {2004}}

@article{Tomita:2006,
	Abstract = {Retinal progenitor cells (RPCs) are immature precursors that can differentiate into retinal neurons, including photoreceptors. Recently, it has been reported that bone marrow-derived cells may also be capable of differentiation into cells of central nervous system lineage, including retinal neurons. We compared these two cell types to evaluate their potential as a source of cells for retinal transplantation. Marrow stromal cells (MSCs) and macrophages were isolated from enhanced green fluorescence protein mice. MSCs were cultured with brain-derived neurotrophic factor, nerve growth factor, and basic fibroblast growth factor to induce neuronal differentiation. RPCs were cultured under the same conditions or with 10\%fetal bovine serum. Neuronal marker expression was examined and compared between MSCs and RPCs. MSCs, macrophages, and RPCs were also cultured with explanted retinas from rhodopsin knockout mice to study their potential for retinal integration. MSCs expressed neuronal and retina-specific markers by reverse transcription-polymerase chain reaction and immunocytochemistry. Both types of cells migrated into retinal explants and expressed neurofilament 200, glial fibrillary acidic protein, protein kinase C-alpha, and recoverin. RPCs expressed rhodopsin, a photoreceptor marker we never detected in MSCs. A majority of bone marrow derived-macrophages differentiated into cells that resembled microglia, rather than neural cells, in the explanted retina. This study shows that RPCs are likely to be a preferred cell type for retinal transplantation studies, compared with MSCs. However, MSCs may remain an attractive candidate for autologous transplantation.},
	Author = {Tomita, Minoru and Mori, Taisuke and Maruyama, Kazuichi and Zahir, Tasneem and Ward, Matthew and Umezawa, Akihiro and Young, Michael J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {Retina;Cell Differentiation;Cell Culture Techniques;Animals;Cells, Cultured;Macrophages;comparative study;Stem Cell Transplantation;Rhodopsin;Microglia;Cell Movement;Mice, Inbred C57BL;research support, non-u.s. gov't;Bone Marrow Cells;Mice, Knockout;Neurons;research support, n.i.h., extramural;Mice;24 Pubmed search results 2008;Stem Cells;Stromal Cells;research support, u.s. gov't, non-p.h.s.},
	Month = {10},
	Nlm_Id = {9304532},
	Number = {10},
	Organization = {The Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, 20 Staniford St., Boston, Massachusetts 02114, USA. tomita\@vision.eri.harvard.edu},
	Pages = {2270-8},
	Pii = {24/10/2270},
	Pubmed = {17008430},
	Title = {A comparison of neural differentiation and retinal transplantation with bone marrow-derived cells and retinal progenitor cells},
	Uuid = {91D0229C-51AC-4588-A1EF-4A41621925F1},
	Volume = {24},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1634/stemcells.2005-0507}}

@article{Tonchev:2003a,
	Abstract = {We investigated the fate of proliferating cells in the adult monkey brain after global ischemia. We used the thymidine analogue bromodeoxyuridine (BrdU) to label S-phase cells and their progeny in Japanese macaques subjected to global cerebral ischemia for 20 min or to a sham operation. Subsequently, newly generated cells were identified by BrdU immunohistochemistry, and their immunophenotype was determined quantitatively, using specific markers. The ischemic insult significantly increased the number of proliferating cells in the hippocampus and temporal neocortex, where the majority BrdU-labeled cells expressed markers for microglia (Iba1, CD68, and Ham56) or astrocytes (S-100beta and glial fibrillary acidic protein [GFAP]). In contrast, the proliferation level in the parahippocampal region remained unchanged. This discrepancy prompted us to investigate the postischemic response in the olfactory bulb, a well-known site of adult cell generation that is anatomically distant from the above-mentioned regions but that is also subjected to the global ischemic insult. The olfactory bulb contained clusters of proliferating cells expressing markers for neural (Musashi1 and Nestin) and/or neuronal (class III beta-tubulin) progenitors; these were immunophenotypically distinct from other cell types. Their number and distribution were unaltered by ischemia. Our results demonstrate that cell proliferation and differentiation in the adult macaque brain and olfactory bulb are differentially affected by a common insult.},
	Author = {Tonchev, Anton B. and Yamashima, Tetsumori and Zhao, Liang and Okano, Hideyuki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Glial Fibrillary Acidic Protein;Research Support, Non-U.S. Gov't;Cell Differentiation;Animals;Astrocytes;Biological Markers;Comparative Study;Tubulin;Microglia;Female;Macaca;RNA-Binding Proteins;Nerve Regeneration;Olfactory Bulb;Antigens, CD56;Antibodies, Monoclonal;Calcium-Binding Proteins;Cerebral Cortex;Neurons;Intermediate Filament Proteins;Gliosis;Brain Ischemia;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine;Stem Cells;Nerve Tissue Proteins;S100 Proteins},
	Medline = {22560378},
	Month = {5},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Neurosurgery, Kanazawa University Graduate School of Medical Science, Kanazawa City, Japan.},
	Pages = {209-24},
	Pubmed = {12673828},
	Title = {Differential proliferative response in the postischemic hippocampus, temporal cortex, and olfactory bulb of young adult macaque monkeys},
	Uuid = {FE5A75A6-5FDA-4A8E-A339-3749732D16C5},
	Volume = {42},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10209}}

@article{Tonchev:2003,
	Abstract = {To investigate the effect of global cerebral ischemia on brain cell proliferation in young adult macaques, we infused 5-bromo-2'-deoxyuridine (BrdU), a DNA replication indicator, into monkeys subjected to ischemia or sham-operated. Subsequent quantification by BrdU immunohistochemistry revealed a significant postischemic increase in the number of BrdU-labeled cells in the hippocampal dentate gyrus, subventricular zone of the temporal horn of the lateral ventricle, and temporal neocortex. In all animals, 20-40\%of the newly generated cells in the dentate gyrus and subventricular zone expressed the neural progenitor cell markers Musashi1 or Nestin. A few BrdU-positive cells in postischemic monkeys were double-stained for markers of neuronal progenitors (class III beta-tubulin, TUC4, doublecortin, or Hu), neurons (NeuN), or glia (S100beta or GFAP). Our results suggest that ischemia activates endogenous neuronal and glial precursors residing in diverse locations of the adult primate central nervous system. 1044-7431 Journal Article},
	Author = {Tonchev, A. B. and Yamashima, T. and Zhao, L. and Okano, H. J. and Okano, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:33 -0400},
	Issn = {1044-7431},
	Journal = {Mol Cell Neurosci},
	Keywords = {Neuronal Plasticity/*physiology;Support, Non-U.S. Gov't;Dentate Gyrus;06 Adult neurogenesis injury induced;Research Support, Non-U.S. Gov't;24 Pubmed search results 2008;Immunohistochemistry;Dentate Gyrus/cytology/growth &development/metabolism;Nerve Regeneration;Bromodeoxyuridine/diagnostic use;Brain Ischemia;Animals;Telencephalon/cytology/*growth &development/metabolism;RNA-Binding Proteins/metabolism;Cell Division/physiology;Phenotype;Bromodeoxyuridine;Intermediate Filament Proteins;RNA-Binding Proteins;Cell Division;Lateral Ventricles;Nerve Regeneration/*physiology;Neuronal Plasticity;Biological Markers;Cell Death/physiology;DNA Damage/physiology;Macaca;D pdf;Cell Death;Neurons/cytology/*metabolism;Female;Telencephalon;Stem Cells/cytology/*metabolism;DNA Damage;Temporal Lobe;Lateral Ventricles/cytology/growth &development/metabolism;Stem Cells;Nerve Tissue Proteins/metabolism;Neurons;Brain Ischemia/*metabolism/physiopathology;Nerve Tissue Proteins;Temporal Lobe/cytology/growth &development/metabolism;Intermediate Filament Proteins/metabolism},
	Medline = {22697603},
	Month = {6},
	Nlm_Id = {9100095},
	Number = {2},
	Organization = {Department of Neurosurgery, Division of Neuroscience, Kanazawa University Graduate School of Medical Science, Kanazawa, 920-8641, Japan.},
	Pages = {292-301},
	Pii = {S1044743103000587},
	Pubmed = {12812760},
	Title = {Proliferation of neural and neuronal progenitors after global brain ischemia in young adult macaque monkeys},
	Uuid = {530E602F-EC81-11DA-8605-000D9346EC2A},
	Volume = {23},
	Year = {2003},
	url = {papers/Tonchev_MolCellNeurosci2003}}

@article{Toyo-oka:2003,
	Abstract = {Heterozygous deletions of 17p13.3 result in the human neuronal migration disorders isolated lissencephaly sequence (ILS) and the more severe Miller-Dieker syndrome (MDS). Mutations in PAFAH1B1 (the gene encoding LIS1) are responsible for ILS and contribute to MDS, but the genetic causes of the greater severity of MDS are unknown. Here, we show that the gene encoding 14-3-3epsilon (YWHAE), one of a family of ubiquitous phosphoserine/threonine-binding proteins, is always deleted in individuals with MDS. Mice deficient in Ywhae have defects in brain development and neuronal migration, similar to defects observed in mice heterozygous with respect to Pafah1b1. Mice heterozygous with respect to both genes have more severe migration defects than single heterozygotes. 14-3-3epsilon binds to CDK5/p35-phosphorylated NUDEL and this binding maintains NUDEL phosphorylation. Similar to LIS1, deficiency of 14-3-3epsilon results in mislocalization of NUDEL and LIS1, consistent with reduction of cytoplasmic dynein function. These results establish a crucial role for 14-3-3epsilon in neuronal development by sustaining the effects of CDK5 phosphorylation and provide a molecular explanation for the differences in severity of human neuronal migration defects with 17p13.3 deletions.},
	Author = {Toyo-oka, Kazuhito and Shionoya, Aki and Gambello, Michael J. and Cardoso, Carlos and Leventer, Richard and Ward, Heather L. and Ayala, Ramses and Tsai, Li-Huei H. and Dobyns, William and Ledbetter, David and Hirotsune, Shinji and Wynshaw-Boris, Anthony},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {Dynein ATPase;Immunoenzyme Techniques;24 Pubmed search results 2008;Green Fluorescent Proteins;Phosphoprotein Phosphatases;Male;Brain Diseases;Cyclin-Dependent Kinases;Luminescent Proteins;10 Development;Animals;Cell Cycle Proteins;Cells, Cultured;Protein Kinase C;Brain;Coatomer Protein;Cell Movement;1-Alkyl-2-acetylglycerophosphocholine Esterase;Mice, Inbred C57BL;research support, u.s. gov't, p.h.s.;Microtubule-Associated Proteins;Abnormalities, Multiple;14-3-3 Proteins;Enzyme Inhibitors;Female;Syndrome;research support, non-u.s. gov't;Mice;Neurons;Humans;Tyrosine 3-Monooxygenase;10 genetics malformation;Cyclin-Dependent Kinase 5},
	Month = {7},
	Nlm_Id = {9216904},
	Number = {3},
	Organization = {Department of Pediatrics, UCSD Cancer Center, University of California, San Diego School of Medicine, 9500 Gilman Drive, Mailstop 0627, La Jolla, California 92093-0627, USA.},
	Pages = {274-85},
	Pii = {ng1169},
	Pubmed = {12796778},
	Title = {14-3-3epsilon is important for neuronal migration by binding to NUDEL: a molecular explanation for Miller-Dieker syndrome},
	Uuid = {71E48F49-21C4-47E9-845C-8DDB07B7CD54},
	Volume = {34},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ng1169}}

@article{Tramontin:2003,
	Abstract = {The germinal neuroepithelium, or ventricular zone (VZ) of the developing fetal brain, was once thought to transform into the non-germinal ependymal zone of the postnatal and adult brain. Persistence of neural stem cells and neurogenesis throughout postnatal life, however, suggests a continuum between embryonic and adult germinal brain centers. Here, we suggest that developmental changes in anatomy and molecular marker expression in the ventricular walls (the principal germinal centers of the brain) may have misled us into current interpretations of VZ transformation from a germinal to a non-germinal epithelium. We review previous studies and present new data indicating that a germinal layer with characteristics similar to those of the embryonic VZ persists in lateral ventricular walls of the postnatal mouse brain, a region where the adult subventricular zone (SVZ) develops and where neurogenesis persists into adult life. The early postnatal VZ is largely composed of radial glial cell bodies that remain proliferative, display interkinetic nuclear migration and serve as progenitors of new neurons. Ependymal cells then progressively populate the walls of the lateral ventricle but a subpopulation of astrocytes, derived from radial glia, remain in contact with the ventricle lumen, into which they extend a single cilium similar to that found on neuroepithelial cells and radial cells. We propose that a VZ 'compartment'is retained postnatally and that this niche may be essential for stem cell function. 1047-3211 Journal Article Review Review, Tutorial},
	Author = {Tramontin, A. D. and Garcia-Verdugo, J. M. and Lim, D. A. and Alvarez-Buylla, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {Cereb Cortex},
	Keywords = {01 Adult neurogenesis general;Neuroglia/*cytology/*physiology;Stem Cells/*cytology/physiology;Cerebral Ventricles/*cytology/embryology/*growth &development/physiology;Cell Differentiation/physiology;Animals, Newborn;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Animals;Mice;A pdf;Neurons/cytology/physiology},
	Number = {6},
	Organization = {Department of Neurosurgery Research, University of California, San Francisco, CA 94143, USA. tonyt\@itsa.ucsf.edu},
	Pages = {580-7},
	Pubmed = {12764031},
	Title = {Postnatal development of radial glia and the ventricular zone (VZ): a continuum of the neural stem cell compartment},
	Uuid = {0DFAE8E1-06EC-47B7-AA0C-448A4150BA75},
	Volume = {13},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12764031}}

@article{Tran:2007,
	Abstract = {We previously demonstrated that chemokine receptors are expressed by neural progenitors grown as cultured neurospheres. To examine the significance of these findings for neural progenitor function in vivo, we investigated whether chemokine receptors were expressed by cells having the characteristics of neural progenitors in neurogenic regions of the postnatal brain. Using in situ hybridization we demonstrated the expression of CCR1, CCR2, CCR5, CXCR3, and CXCR4 chemokine receptors by cells in the dentate gyrus (DG), subventricular zone of the lateral ventricle, and olfactory bulb. The pattern of expression for all of these receptors was similar, including regions where neural progenitors normally reside. In addition, we attempted to colocalize chemokine receptors with markers for neural progenitors. In order to do this we used nestin-EGFP and TLX-LacZ transgenic mice, as well as labeling for Ki67, a marker for dividing cells. In all three areas of the brain we demonstrated colocalization of chemokine receptors with these three markers in populations of cells. Expression of chemokine receptors by neural progenitors was further confirmed using CXCR4-EGFP BAC transgenic mice. Expression of CXCR4 in the DG included cells that expressed nestin and GFAP as well as cells that appeared to be immature granule neurons expressing PSA-NCAM, calretinin, and Prox-1. CXCR4-expressing cells in the DG were found in close proximity to immature granule neurons that expressed the chemokine SDF-1/CXCL12. Cells expressing CXCR4 frequently coexpressed CCR2 receptors. These data support the hypothesis that chemokine receptors are important in regulating the migration of progenitor cells in postnatal brain. J. Comp. Neurol. 500:1007-1033, 2007. (c) 2006 Wiley-Liss, Inc.},
	Author = {Tran, Phuong B. and Banisadr, Ghazal and Ren, Dongjun and Chenn, Anjen and Miller, Richard J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0406041},
	Number = {6},
	Organization = {Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, Chicago, Illinois 60611.},
	Pages = {1007-34},
	Pubmed = {17183554},
	Title = {Chemokine receptor expression by neural progenitor cells in neurogenic regions of mouse brain},
	Uuid = {43EE2C8B-6E66-4C7A-BE20-ABDC81390E7C},
	Volume = {500},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.21229}}

@article{Tran:1998,
	Abstract = {There is increasing evidence that microglia serve as antigen presenters in the human CNS. Although the occurrence of MHC class II immunoreactive cells has been reported in astrocytic gliomas, the relative contribution of microglia to this cell population has not been studied in detail. Using computer-assisted image analysis, we have investigated the expression of MHC class II molecules and of the microglia/macrophage markers Ki-MIP, RCA-1, KP1 and iba1, in 97 astrocytic gliomas comprising all WHO grades to answer the question whether there is a correlation between tumour grade and the number of MHC class II positive microglia/macrophage profiles. Microglia expressing MHC class II were common in astrocytomas and anaplastic astrocytomas but rare in pilocytic tumours although there was significant variation within each group. MHC class II immunoreactivity was reduced in highly cellular areas of glioblastomas where large numbers of cells expressing macrophage markers were still present. Thus, there was no simple relationship between tumour grade and microglial/macrophage MHC class II expression. In addition, up to 55\%of astrocytic gliomas contained MHC class II immunoreactive tumour cells. Microglia but not tumour cells were found to express the BB1/B7 costimulator. We conclude that microglia in astrocytic gliomas are well equipped to function as antigen presenting cells. Yet, neoplastic astroglia appear to acquire the capacity to downregulate microglial MHC class II expression and, at the same time, may induce T-cell clonal anergy through aberrant expression of MHC class II molecules.},
	Author = {Tran, C. T. and Wolz, P. and Egensperger, R. and K{\"o}sel, S. and Imai, Y. and Bise, K. and Kohsaka, S. and Mehraein, P. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0305-1846},
	Journal = {Neuropathol Appl Neurobiol},
	Keywords = {Immunotherapy;Paraffin Embedding;Glioblastoma;Research Support, Non-U.S. Gov't;Antigen Presentation;Histocompatibility Antigens Class II;Astrocytes;T-Lymphocytes;11 Glia;Gene Expression Regulation, Neoplastic;Macrophages;Humans;Biopsy},
	Medline = {98448521},
	Month = {8},
	Nlm_Id = {7609829},
	Number = {4},
	Organization = {Institute of Neuropathology, Ludwig-Maximilians-University, Munich, Germany.},
	Pages = {293-301},
	Pubmed = {9775395},
	Title = {Differential expression of MHC class II molecules by microglia and neoplastic astroglia: relevance for the escape of astrocytoma cells from immune surveillance},
	Uuid = {C81D2502-B197-4FFE-880C-376E7B412F21},
	Volume = {24},
	Year = {1998}}

@article{Trapp:2006,
	Abstract = {Recent studies have described significant demyelination and microglial activation in the cerebral cortex of brains from multiple sclerosis patients. To date, however, experimental models of cortical demyelination or cortical inflammation have not been extensively studied. In this report we describe focal cortical inflammation induced by stereotaxic injection of killed bacteria (BCG), followed 1 month later by subcutaneous injection of the same antigen, a protocol that overcomes the immune privilege of the cortex. Intracerebral BCG injection produced focal microglial activation at the injection site (termed acute lesion). Ten days after peripheral challenge (termed immune-mediated lesion), larger areas and higher densities of activated microglia were found near the injection site. In both paradigms, activated microglia and/or their processes closely apposed neuronal perikarya and apical dendrites. In the immune-mediated lesions, approximately 45\%of the axosomatic synapses was displaced by activated microglia. Upon activation, therefore, cortical microglial migrate to and strip synapses from neuronal perikarya. Since neuronal pathology was not a feature of either the acute or immune-mediated lesion, synaptic stripping by activated microglia may have neuroprotective consequences. (c) 2006 Wiley-Liss, Inc.},
	Author = {Trapp, and Wujek, and Criste, and Jalabi, and Yin, and Kidd, and Stohlman, and Ransohoff,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {8806785},
	Organization = {Department of Neurosciences, Lerner Research Institute, The Cleveland Clinic, Cleveland, Ohio.},
	Pubmed = {17136771},
	Title = {Evidence for synaptic stripping by cortical microglia},
	Uuid = {318DF3A8-9F94-4C7E-88FD-F43E44F29407},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20462}}

@article{Trapp:1997,
	Abstract = {Previous studies have indicated that newly formed oligodendrocytes are dynamic cells whose production, survival, and differentiation depend upon axonal influences. This study has characterized the appearance and fate of newly formed oligodendrocytes in developing rat brain. Oligodendrocytes appear in predictable locations and radially extend DM-20-positive processes that cover 80-microm domains in the cortex and 40-microm domains in the corpus callosum. These premyelinating oligodendrocytes have one of two fates: they myelinate axons or degenerate. Between 7 and 21 d after birth, approximately 20\%of premyelinating oligodendrocytes identified in the cerebral cortex were degenerating. Oligodendrocytes that ensheathed axons expressed and selectively targeted proteolipid protein to compact myelin and did not degenerate. These observations support the hypothesis that axonal influences affect oligodendrocyte survival, differentiation, and expression of proteolipid protein gene products. 0021-9525 Journal Article},
	Author = {Trapp, B. D. and Nishiyama, A. and Cheng, D. and Macklin, W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:00 -0400},
	Journal = {J Cell Biol},
	Keywords = {Chromatin/chemistry;Cell Differentiation;Rats, Sprague-Dawley;Corpus Callosum/chemistry/cytology;Myelin Proteolipid Protein/*analysis;Rats;Oligodendroglia/*cytology/metabolism;11 Glia;Cell Death;Axons/metabolism;Cerebral Cortex/chemistry/cytology;Animals;Support, Non-U.S. Gov't;G;Brain/*cytology/growth &development;Support, U.S. Gov't, P.H.S.},
	Number = {2},
	Organization = {Department of Neurosciences, Research Institute, The Cleveland Clinic Foundation, Ohio 44195, USA.},
	Pages = {459-68},
	Pubmed = {9128255},
	Title = {Differentiation and death of premyelinating oligodendrocytes in developing rodent brain},
	Uuid = {DE9AF883-2B2A-4DC0-A753-0288235C4E25},
	Volume = {137},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9128255}}

@article{Tripp:2001,
	Abstract = {Chemokines are chemoattractant proteins that are divided into subfamilies based upon cysteine signature motifs termed C, CC, CXC and CX3C. Chemokines have roles in immunity and inflammation that affect cell trafficking and activation of T cells as well as cells of the innate immune system. We report here CX3C chemokine mimicry for the G glycoprotein of respiratory syncytial virus (RSV) and show binding to CX3CR1--the specific receptor for the CX3C chemokine fractalkine--and induction of leukocyte chemotaxis. We also show that CX3CR1 facilitates RSV infection of cells. Thus, G glycoprotein interaction with CX3CR1 probably plays a key role in the biology of RSV infection.},
	Author = {Tripp, R. A. and Jones, L. P. and Haynes, L. M. and Zheng, H. and Murphy, P. M. and Anderson, L. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1529-2908},
	Journal = {Nat Immunol},
	Keywords = {Chemokines, CX3C;Respiratory Syncytial Viruses;Molecular Sequence Data;Chemotaxis, Leukocyte;Immunity, Natural;T-Lymphocytes;Viral Proteins;11 Glia;Glycoproteins;15 Retrovirus mechanism;Mice;Animals;Lymphocyte Activation;24 Pubmed search results 2008},
	Medline = {21370260},
	Month = {8},
	Nlm_Id = {100941354},
	Number = {8},
	Organization = {National Centers for Infectious Diseases, Division of Viral and Rickettsial Diseases, Respiratory and Enteric Virus Branch, Mailstop G-09, 1600 Clifton Rd., Atlanta, GA, USA. rgt3\@cdc.gov},
	Pages = {732-8},
	Pii = {90675},
	Pubmed = {11477410},
	Title = {CX3C chemokine mimicry by respiratory syncytial virus G glycoprotein},
	Uuid = {41114BD2-EE15-11DA-8605-000D9346EC2A},
	Volume = {2},
	Year = {2001},
	url = {papers/Tripp_NatImmunol2001.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/90675}}

@article{Tropepe:1999,
	Abstract = {Multipotent, self-renewing neural stem cells reside in the embryonic mouse telencephalic germinal zone. Using an in vitro neurosphere assay for neural stem cell proliferation, we demonstrate that FGF-responsive neural stem cells are present as early as E8.5 in the anterior neural plate, but EGF-responsive neural stem cells emerge later in development in a temporally and spatially specific manner. By separately blocking EGF and FGF2 signaling, we also show that EGF alone and FGF2 alone can independently elicit neural stem cell proliferation and at relatively high cell densities separate cell nonautonomous effects can substantially enhance the mitogen-induced proliferation. At lower cell densities, neural stem cell proliferation is additive in the presence of EGF and FGF2 combined, revealing two different stem cell populations. However, both FGF-responsive and EGF-responsive neural stem cells retain their self-renewal and multilineage potential, regardless of growth factor conditions. These results support a model in which separate, lineage-related EGF- and FGF-responsive neural stem cells are present in the embryonic telencephalic germinal zone. 99177151 0012-1606 Journal Article},
	Author = {Tropepe, V. and Sibilia, M. and Ciruna, B. G. and Rossant, J. and Wagner, E. F. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Dev Biol},
	Keywords = {Cell Differentiation;Chimera;Telencephalon/*embryology;Embryo and Fetal Development;Neurons/*metabolism;Animal;C-12b;Epidermal Growth Factor/*pharmacology;Fibroblast Growth Factors/*pharmacology;Receptor, Epidermal Growth Factor/metabolism;Support, Non-U.S. Gov't;Intermediate Filament Proteins/metabolism;Ploidies;04 Adult neurogenesis factors;Receptors, Fibroblast Growth Factor/metabolism;Mice;Immunohistochemistry;Gestational Age;Signal Transduction/physiology;Cell Division/drug effects;Stem Cells/*metabolism},
	Number = {1},
	Organization = {Department of Anatomy and Cell Biology, University of Toronto, Toronto, M5S 1A8, Canada. v.tropepe\@utoronto.ca},
	Pages = {166-88},
	Pubmed = {10075850},
	Title = {Distinct neural stem cells proliferate in response to EGF and FGF in the developing mouse telencephalon},
	Uuid = {BEC16883-816D-47FE-BECB-34FDD727D05E},
	Volume = {208},
	Year = {1999},
	url = {papers/Tropepe_DevBiol1999}}

@article{Tropepe:1997,
	Abstract = {The adult mammalian forebrain subependyma contains neural stem cells and their progeny, the constitutively proliferating progenitor cells. Using bromodeoxyuridine labeling to detect mitotically active cells, we demonstrate that the endogenous expression of transforming growth factor-alpha (TGFalpha) is necessary for the full proliferation of progenitor cells localized to the dorsolateral corner of the subependyma and the full production of the neuronal progenitors that migrate to the olfactory bulbs. Proliferation of these progenitor cells also is diminished with age (in 23- to 25-months-old compared with 2- to 4-months-old mice), likely because of a lengthening of the cell cycle. Senescence or the absence of endogenous TGFalpha does not affect the numbers of neural stem cells isolated in vitro in the presence of epidermal growth factor. These results suggest that endogenous TGFalpha and the effects of senescence may regulate the proliferation of progenitor cells in the adult subependyma, but that the number of neural stem cells is maintained throughout life. 97461629 0270-6474 Journal Article},
	Author = {Tropepe, V. and Craig, C. G. and Morshead, C. M. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {J Neurosci},
	Keywords = {Prosencephalon/*cytology;Mice, Knockout/genetics;Tissue Culture;Neurons/*cytology/physiology;Cell Cycle;Animal;Cell Count;Cell Movement;Ependyma/*cytology;Aging/*physiology;Stem Cells/*cytology;Time Factors;Male;Support, Non-U.S. Gov't;C-5b;Olfactory Bulb/cytology;Transforming Growth Factor alpha/*deficiency/genetics;04 Adult neurogenesis factors;Mice;Cell Division},
	Number = {20},
	Organization = {Neurobiology Research Group, Department of Anatomy and Cell Biology, University of Toronto, Toronto, Ontario M5S 1A8, Canada.},
	Pages = {7850-9},
	Pubmed = {9315905},
	Title = {Transforming growth factor-alpha null and senescent mice show decreased neural progenitor cell proliferation in the forebrain subependyma},
	Uuid = {A8ABEE22-19ED-4EC9-B845-16D783654795},
	Volume = {17},
	Year = {1997},
	url = {papers/Tropepe_JNeurosci1997.pdf}}

@article{Tropepe:2001,
	Abstract = {Little is known about how neural stem cells are formed initially during development. We investigated whether a default mechanism of neural specification could regulate acquisition of neural stem cell identity directly from embryonic stem (ES) cells. ES cells cultured in defined, low-density conditions readily acquire a neural identity. We characterize a novel primitive neural stem cell as a component of neural lineage specification that is negatively regulated by TGFbeta-related signaling. Primitive neural stem cells have distinct growth factor requirements, express neural precursor markers, generate neurons and glia in vitro, and have neural and non-neural lineage potential in vivo. These results are consistent with a default mechanism for neural fate specification and support a model whereby definitive neural stem cell formation is preceded by a primitive neural stem cell stage during neural lineage commitment. 21243067 0896-6273 Journal Article},
	Author = {Tropepe, V. and Hitoshi, S. and Sirard, C. and Mak, T. W. and Rossant, J. and van der Kooy, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {10 Development;Neurons/*cytology/metabolism;Nervous System/cytology/*embryology/*growth &development;Body Patterning/drug effects/*physiology;Animal;Chimera/embryology/genetics/metabolism;Cell Differentiation/drug effects/*physiology;Cell Size/genetics;DNA-Binding Proteins/genetics/metabolism;Cells, Cultured/cytology/drug effects/metabolism;Mammals/*embryology/metabolism;Culture Media, Serum-Free/pharmacology;Signal Transduction/drug effects/physiology;Stem Cells/*cytology/drug effects/metabolism;Growth Substances/deficiency;Support, Non-U.S. Gov't;Cell Lineage/drug effects/*physiology;Intermediate Filament Proteins/drug effects/metabolism;Trans-Activators/genetics/metabolism;Growth Inhibitors/pharmacology;Lymphokines/pharmacology;Transforming Growth Factor beta/drug effects/metabolism;Mice;F},
	Number = {1},
	Organization = {Department of Anatomy &Cell Biology, University of Toronto, Ontario M5S 1A8, Toronto, Canada.},
	Pages = {65-78},
	Pubmed = {11343645},
	Title = {Direct neural fate specification from embryonic stem cells: a primitive mammalian neural stem cell stage acquired through a default mechanism},
	Uuid = {7C53C390-FFEE-476B-9E2C-E0AC12E1A71C},
	Volume = {30},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11343645}}

@article{Trujillo:2007,
	Abstract = {Although protein receptors on the plasma membrane involved in the initial steps of productive HIV-1 infection have been well characterized, little is known about interactions between cellular carbohydrate receptors and HIV-1. Here, we report the involvement of a carbohydrate receptor, the macrophage mannose receptor (MR), and its role in supporting HIV-1 binding and entry. HIV-1 can enter the cytoplasm of human macrophages and microglia as well as murine macrophages by MR, although no subsequent viral replication was observed. Correspondingly, HIV-1 entry into Cos-7 cells after induction of expression of MR by transfection with MR-cDNA did not demonstrate viral replication. Our studies suggest that whereas MR may serve as a binding and an entry site, the MR-mediated pathway does not lead to productive HIV-1 infection. In addition, we report that recombinant HIV-1 gp120 blocks MR-mediated phagocytosis in human and murine alveolar macrophages and microglial cells. Therefore, characterization of the HIV-1 noninfectious MR-mediated phagocytic pathway may foster advances in HIV-1 vaccine design and an improved understanding of HIV-1/AIDS pathogenesis and host defenses.},
	Author = {Trujillo, and Rogers, and Molina, and Dangond, and McLane, and Essex, and Brain,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7505876},
	Organization = {Molecular and Integrative Physiological Sciences, Department of Environmental Health, Department of Immunology and Infectious Diseases, and Biomedical Imaging Laboratory, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115.},
	Pii = {0611263104},
	Pubmed = {17360361},
	Title = {Noninfectious entry of HIV-1 into peripheral and brain macrophages mediated by the mannose receptor},
	Uuid = {21F7E793-F954-48AB-852F-59A667AB2679},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0611263104}}

@article{Truman:2004,
	Abstract = {In Drosophila most thoracic neuroblasts have two neurogenic periods: an initial brief period during embryogenesis and a second prolonged phase during larval growth. This study focuses on the adult-specific neurons that are born primarily during the second phase of neurogenesis. The fasciculated neurites arising from each cluster of adult-specific neurons express the cell-adhesion protein Neurotactin and they make a complex scaffold of neurite bundles within the thoracic neuropils. Using MARCM clones, we identified the 24 lineages that make up the scaffold of a thoracic hemineuromere. Unlike the early-born neurons that are strikingly diverse in both form and function, the adult specific cells in a given lineage are remarkably similar and typically project to only one or two initial targets, which appear to be the bundled neurites from other lineages. Correlated changes in the contacts between the lineages in different segments suggest that these initial contacts have functional significance in terms of future synaptic partners. This paper provides an overall view of the initial connections that eventually lead to the complex connectivity of the bulk of the thoracic neurons.},
	Author = {Truman, James W. and Schuppe, Hansj{\"u}rgen and Shepherd, David and Williams, Darren W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Membrane Glycoproteins;Research Support, Non-U.S. Gov't;Central Nervous System;Larva;Research Support, U.S. Gov't, P.H.S.;Drosophila Proteins;Drosophila;Animals;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8701744},
	Number = {20},
	Organization = {Department of Biology, University of Washington, Seattle, WA 98195, USA. jwt\@u.washington.edu},
	Pages = {5167-84},
	Pii = {131/20/5167},
	Pubmed = {15459108},
	Title = {Developmental architecture of adult-specific lineages in the ventral CNS of Drosophila},
	Uuid = {FFA13D7A-3CC6-4033-BF89-E50E1BA2E7BE},
	Volume = {131},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.01371}}

@article{Tsai:2005,
	Abstract = {Mutations in the human LIS1 gene cause the smooth brain disease classical lissencephaly. To understand the underlying mechanisms, we conducted in situ live cell imaging analysis of LIS1 function throughout the entire radial migration pathway. In utero electroporation of LIS1 small interference RNA and short hairpin dominant negative LIS1 and dynactin cDNAs caused a dramatic accumulation of multipolar progenitor cells within the subventricular zone of embryonic rat brains. This effect resulted from a complete failure in progression from the multipolar to the migratory bipolar state, as revealed by time-lapse analysis of brain slices. Surprisingly, interkinetic nuclear oscillations in the radial glial progenitors were also abolished, as were cell divisions at the ventricular surface. Those few bipolar cells that reached the intermediate zone also exhibited a complete block in somal translocation, although, remarkably, process extension persisted. Finally, axonal growth also ceased. These results identify multiple distinct and novel roles for LIS1 in nucleokinesis and process dynamics and suggest that nuclear position controls neural progenitor cell division.},
	Author = {Tsai, Jin-Wu W. and Chen, Yu and Kriegstein, Arnold R. and Vallee, Richard B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0021-9525},
	Journal = {J Cell Biol},
	Keywords = {10 Development},
	Month = {9},
	Nlm_Id = {0375356},
	Number = {6},
	Organization = {Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.},
	Pages = {935-45},
	Pii = {jcb.200505166},
	Pubmed = {16144905},
	Title = {LIS1 RNA interference blocks neural stem cell division, morphogenesis, and motility at multiple stages},
	Uuid = {49B2E577-3563-452C-81C2-B653D20A5571},
	Volume = {170},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1083/jcb.200505166}}

@article{Tsai:2007,
	Abstract = {During brain development, neural precursor cells migrate along radial glial fibers to populate the neocortex. RNA interference (RNAi) of the lissencephaly gene LIS1 (also known as PAFAH1b1) inhibits somal movement but not process extension of neural precursors in live brain slices. Here we report imaging of the subcellular events accompanying neural precursor migration and the effects of LIS1, cytoplasmic dynein and myosin II inhibition. Centrosomes move continuously and often far in advance of nuclei, which show extreme saltatory behavior. LIS1 and dynein RNAi inhibit centrosomal and nuclear movement independently, whereas myosin II inhibition blocks only nuclear translocation. Imaging of the microtubule end-binding protein 3 (EB3) reveals a centrosome-centered array of microtubules in live neural precursors under all conditions examined. Dynein is concentrated both at a swelling in the leading process reported to initiate each migratory cycle and in the soma. Thus, dynein pulls on the microtubule network from the swelling. The nucleus is transported along the trailing microtubules by dynein assisted by myosin II.},
	Author = {Tsai, Jin-Wu W. and Bremner, K. Helen and Vallee, Richard B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Microtubule-Associated Proteins;Animals;Humans;Rats;Myosin Type II;Microscopy, Confocal;Intracellular Space;Electroporation;Cell Movement;Organ Culture Techniques;research support, non-u.s. gov't;Time Factors;Embryo;Cerebral Cortex;Neurons;Heterocyclic Compounds with 4 or More Rings;research support, n.i.h., extramural;Mice;Dynein ATPase;24 Pubmed search results 2008;Luminescent Proteins;Stem Cells;Nerve Tissue Proteins;Oligonucleotides, Antisense;in vitro},
	Month = {8},
	Nlm_Id = {9809671},
	Number = {8},
	Organization = {Integrated Program in Cellular, Molecular and Biophysical Studies, Columbia University, 630 W 168th Street, New York, New York 10032, USA.},
	Pages = {970-9},
	Pii = {nn1934},
	Pubmed = {17618279},
	Title = {Dual subcellular roles for LIS1 and dynein in radial neuronal migration in live brain tissue},
	Uuid = {37271B18-460C-4C14-8380-55CEBF98FE84},
	Volume = {10},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1934}}

@article{Tsai:2005a,
	Abstract = {Neuronal migration is a critical phase of nervous system development and can be divided into two distinct phases: extension of the leading process and movement of the cell body and nucleus (nucleokinesis). Nucleokinesis appears to require many of the same cytoskeletal and signaling molecules used in cell mitosis. Converging studies suggest it requires cytoplasmic dynein, cell polarity genes, and microtubule-associated proteins that coordinate microtubule remodeling. These coordinate first the positioning of the centrosome (microtubule organizing center) in the leading process in front of the nucleus and then the movement of the nucleus towards the centrosome. The positioning of the centrosome and the dynamic regulation that couples and uncouples the nucleus underlies directed migration of neurons.},
	Author = {Tsai, Li-Huei H. and Gleeson, Joseph G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;24 Pubmed search results 2008},
	Month = {5},
	Nlm_Id = {8809320},
	Number = {3},
	Organization = {Department of Pathology, Harvard Medical School, Howard Hughes Medical Institute, 77 Avenue Louis Pasteur, Room 858C, Boston, Massachusetts 02115.},
	Pages = {383-8},
	Pii = {S0896-6273(05)00349-1},
	Pubmed = {15882636},
	Title = {Nucleokinesis in neuronal migration},
	Uuid = {D5CC1906-6426-4CFF-A303-F399BE26AA81},
	Volume = {46},
	Year = {2005},
	url = {papers/Tsai_Neuron2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.04.013}}

@article{Tsuchida:1974,
	Abstract = {0042-6822 Journal Article},
	Author = {Tsuchida, N. and Green, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Virology},
	Keywords = {Nucleic Acid Denaturation;Phosphorus Radioisotopes;*Moloney murine leukemia virus;Mice;RNA, Viral/*analysis;EE, DMSO, abstr;Rats;Cell Line;08 Aberrant cell cycle;*Cell Transformation, Neoplastic;Electrophoresis, Polyacrylamide Gel;Tritium;Animals;Dimethyl Sulfoxide;Nucleic Acid Hybridization;Hamsters;Centrifugation, Density Gradient},
	Number = {1},
	Pages = {258-65},
	Pubmed = {4826208},
	Title = {Intracellular and virion 35 S RNA species of murine sarcoma and leukemia viruses},
	Uuid = {67D425E1-3206-4E3F-9696-7A2CD7699548},
	Volume = {59},
	Year = {1974},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=4826208}}

@article{Tsuchiya:2005,
	Abstract = {We derived microglia from mouse embryonic stem cells (ES cells) at very high density. Using the markers Mac1(+)/CD45(low) and Mac1(+)/CD45(high) to define microglia and macrophages, respectively, we show that Mac1(+) cells are induced by GM-CSF stimulation following neuronal differentiation of mouse ES cells using a five-step method. CD45(low) expression was high and CD45(high) expression was low on induced cells. We used a density gradient method to obtain a large amount of microglia-like cells, approximately 90\%of Mac1(+) cells. Microglia-like cells expressed MHC class I, class II, CD40, CD80, CD86, and IFN-gammaR. The expression level of these molecules on microglia-like cells was barely enhanced by IFN-gamma. Intravenously transferred GFP(+) microglia derived from GFP(+) ES cells selectively accumulated in brain but not in peripheral tissues such as spleen and lymph node. GFP(+) cells were detected mainly in corpus callosum and hippocampus but were rarely seen in cerebral cortex, where Iba1, another marker of microglia, is primarily expressed. Furthermore, both GFP(+) and Iba1(+) cells exhibited a ramified morphology characteristic of mature microglia. These studies suggest that ES cell-derived microglia-like cells obtained using our protocol are functional and migrate selectively into the brain but not into peripheral tissues after intravenous transplantation.},
	Author = {Tsuchiya, Takahiro and Park, Kae Chang and Toyonaga, Shinichi and Yamada, Shoko M. and Nakabayashi, Hiromichi and Nakai, Eiichi and Ikawa, Naoki and Furuya, Masato and Tominaga, Akira and Shimizu, Keiji},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Month = {3},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Neurosurgery, Kochi Medical School, Kochi University, Kohasu, Okoh-cho, Nankoku, Kochi 783-8505 Japan.},
	Pages = {210-8},
	Pii = {S0165-5728(04)00404-7},
	Pubmed = {15710475},
	Title = {Characterization of microglia induced from mouse embryonic stem cells and their migration into the brain parenchyma},
	Uuid = {BAA1C220-C26D-11DA-969D-000D9346EC2A},
	Volume = {160},
	Year = {2005},
	url = {papers/Tsuchiya_JNeuroimmunol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jneuroim.2004.10.025}}

@article{Turlejski:2002,
	Abstract = {In this chapter we provide an extensive review of 100 years of research on the stability of neurons in the mammalian brain, with special emphasis on humans. Although Cajal formulated the Neuronal Doctrine, he was wrong in his beliefs that adult neurogenesis did not occur and adult neurons are dying throughout life. These two beliefs became accepted "common knowledge" and have shaped much of neuroscience research and provided much of the basis for clinical treatment of age-related brain diseases. In this review, we consider adult neurogenesis from a historical and evolutionary perspective. It is concluded, that while adult neurogenesis is a factor in the dynamics of the dentate gyrus and olfactory bulb, it is probably not a major factor during the life-span in most brain areas. Likewise, the acceptance of neuronal death as an explanation for normal age-related senility is challenged with evidence collected over the last fifty years. Much of the problem in changing this common belief of dying neurons was the inadequacies of neuronal counting methods. In this review we discuss in detail implications of recent improvements in neuronal quantification. We conclude: First, age-related neuronal atrophy is the major factor in functional deterioration of existing neurons and could be slowed down, or even reversed by various pharmacological interventions. Second, in most cases neuronal degeneration during aging is a pathology that in principle may be avoided. Third, loss of myelin and of the white matter is more frequent and important than the limited neuronal death in normal aging.},
	Author = {Turlejski, Kris and Djavadian, Ruzanna},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0079-6123},
	Journal = {Prog Brain Res},
	Keywords = {Aging;24 Pubmed search results 2008;Cell Differentiation;Research Support, Non-U.S. Gov't;Central Nervous System;Nerve Degeneration;Cell Division;Cell Death;Nerve Fibers, Myelinated;Humans;Animals;Neurons;review},
	Medline = {22139342},
	Nlm_Id = {0376441},
	Organization = {Department of Neurophysiology, Nencki Institute of Experimental Biology, 3 Pasteur Street, 02-093 Warsaw, Poland. krist\@nencki.gov.pl},
	Pages = {39-65},
	Pubmed = {12143397},
	Title = {Life-long stability of neurons: a century of research on neurogenesis, neuronal death and neuron quantification in adult CNS},
	Uuid = {C4AF9723-3E39-4F72-92C5-987DBCA729E1},
	Volume = {136},
	Year = {2002}}

@article{Ueyama:2004,
	Abstract = {Protein kinase C (PKC) plays a prominent role in immune signaling. To elucidate the signal transduction in a respiratory burst and isoform-specific function of PKC during FcgammaR-mediated phagocytosis, we used live, digital fluorescence imaging of mouse microglial cells expressing GFP-tagged molecules. betaI PKC, epsilonPKC, and diacylglycerol kinase (DGK) beta dynamically and transiently accumulated around IgG-opsonized beads (BIgG). Moreover, the accumulation of p47(phox), an essential cytosolic component of NADPH oxidase and a substrate for betaI PKC, at the phagosomal cup/phagosome was apparent during BIgG ingestion. Superoxide (O(2)(-)) production was profoundly inhibited by G{\"o}6976, a cPKC inhibitor, and dramatically increased by the DGK inhibitor, R59949. Ultrastructural analysis revealed that BIgG induced O(2)(-) production at the phagosome but not at the intracellular granules. We conclude that activation/accumulation of betaI PKC is involved in O(2)(-) production, and that O(2)(-) production is primarily initiated at the phagosomal cup/phagosome. This study also suggests that DGKbeta plays a prominent role in regulation of O(2)(-) production during FcgammaR-mediated phagocytosis.},
	Author = {Ueyama, Takehiko and Lennartz, Michelle R. and Noda, Yukiko and Kobayashi, Toshihiro and Shirai, Yasuhito and Rikitake, Kyoko and Yamasaki, Tomoko and Hayashi, Shigeto and Sakai, Norio and Seguchi, Harumichi and Sawada, Makoto and Sumimoto, Hideki and Saito, Naoaki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Phagocytosis;Protein Kinase C;Oxidants;Animals;Humans;Comparative Study;Cell Line, Transformed;Microglia;Superoxides;11 Glia;Phagocytes;Green Fluorescent Proteins;Microspheres;Phagosomes;Mice;Receptors, IgG;Isoenzymes;Luminescent Proteins;Diacylglycerol Kinase;Research Support, Non-U.S. Gov't},
	Month = {10},
	Nlm_Id = {2985117R},
	Number = {7},
	Organization = {Laboratory of Molecular Pharmacology, Biosignal Research Center, Kobe University, Kobe, Japan.},
	Pages = {4582-9},
	Pii = {173/7/4582},
	Pubmed = {15383592},
	Title = {Superoxide production at phagosomal cup/phagosome through beta I protein kinase C during Fc gamma R-mediated phagocytosis in microglia},
	Uuid = {C3AE759E-D686-490F-91D0-A8E8173E9BA4},
	Volume = {173},
	Year = {2004}}

@article{Ule:2005,
	Abstract = {Alternative RNA splicing greatly increases proteome diversity and may thereby contribute to tissue-specific functions. We carried out genome-wide quantitative analysis of alternative splicing using a custom Affymetrix microarray to assess the role of the neuronal splicing factor Nova in the brain. We used a stringent algorithm to identify 591 exons that were differentially spliced in the brain relative to immune tissues, and 6.6\%of these showed major splicing defects in the neocortex of Nova2-/- mice. We tested 49 exons with the largest predicted Nova-dependent splicing changes and validated all 49 by RT-PCR. We analyzed the encoded proteins and found that all those with defined brain functions acted in the synapse (34 of 40, including neurotransmitter receptors, cation channels, adhesion and scaffold proteins) or in axon guidance (8 of 40). Moreover, of the 35 proteins with known interaction partners, 74\%(26) interact with each other. Validating a large set of Nova RNA targets has led us to identify a multi-tiered network in which Nova regulates the exon content of RNAs encoding proteins that interact in the synapse.},
	Author = {Ule, Jernej and Ule, Aljaz and Spencer, Joanna and Williams, Alan and Hu, Jing-Shan S. and Cline, Melissa and Wang, Hui and Clark, Tyson and Fraser, Claire and Ruggiu, Matteo and Zeeberg, Barry R. and Kane, David and Weinstein, John N. and Blume, John and Darnell, Robert B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {Antigens, Neoplasm;Synapses;10 Development;Mice, Knockout;Research Support, Non-U.S. Gov't;Nerve Tissue Proteins;Alternative Splicing;Research Support, U.S. Gov't, P.H.S.;Neocortex;Oligonucleotide Array Sequence Analysis;Research Support, N.I.H., Extramural;RNA-Binding Proteins;Animals;Mice;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {9216904},
	Number = {8},
	Organization = {Howard Hughes Medical Institute and Laboratory of Molecular Neuro-Oncology, The Rockefeller University, New York, New York, USA.},
	Pages = {844-52},
	Pii = {ng1610},
	Pubmed = {16041372},
	Title = {Nova regulates brain-specific splicing to shape the synapse},
	Uuid = {B45FE5B2-123E-4E77-8AFC-466C0FFA3363},
	Volume = {37},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ng1610}}

@article{Ulfig:2004,
	Abstract = {Whereas several studies have addressed the activation of microglia (the resident mononuclear phagocytes of the brain) and macrophages within the nervous system in experimental animal models of congenital and induced hydrocephalus, little is known of their state of activation or regional distribution in human fetal hydrocephalus. This investigation aimed to address such questions. Ten human fetal cases [20-36 gestational weeks (GW) at postmortem] previously diagnosed with hydrocephalus on ultrasound examination in utero, and 10 non-hydrocephalic controls (22-38 GW at postmortem) were assessed immufcnohistochemically with antibodies directed against MHC class II and CD68 antigens, and lectin histochemistry with Lycopersicon esculentum (tomato lectin). Adjacent sections were also immunoreacted with an antiserum to laminin to detect cerebral blood vessels. Eight out of the 10 hydrocephalus cases showed numerous CD68 and tomato lectin-positive macrophages located at focal regions along the ependymal lining of the lateral ventricles (particularly within the occipital horn). However, only five of these cases demonstrated MHC class II positive macrophages associated with the ventricular lining. Microglial reactivity within periventricular regions could also be identified using the lectin in four cases, two of which were also immunoreactive with CD68 (but not with MHC class II). By comparison, in control cases five out of 10 fetal brains (aged between 20 and 24 GW) showed few or no ependymal or supraependymal macrophages. One case at 28 GW, and cases at 32 and 38 GW (two of which were diagnosed with intrauterine hypoxic-ischemia) did, however, show some MHC class II (CD68 negative) cells located at the ependymal surface. Nevertheless, these were not as numerous or intensely immunoreactive as in the hydrocephalus cases. Microglia interspersed throughout the intermediate zone and circumscribing the basal ganglia were within normal confines in all cases examined. Hydrocephalic cases additionally showed focal regions of hypovascularization or alterations in the structure and orientation of capillaries within periventricular areas, compared to controls. The macrophage response detected at the ependymal lining of the ventricles and within the periventricular area in hydrocephalus may be related both to the severity of hydrocephalus and the age of the fetus.},
	Author = {Ulfig, Norbert and Bohl, J{\"u}rgen and Neud{\"o}rfer, Frank and Rezaie, Payam},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0387-7604},
	Journal = {Brain Dev},
	Keywords = {Pregnancy;Plant Lectins;case reports;Antigens, Differentiation, Myelomonocytic;Macrophages;Humans;Brain;Microglia;Female;Antigens, CD;Hydrocephalus;Cerebrovascular Circulation;11 Glia;Laminin;Male;Cause of Death;Genes, MHC Class II;Adult;Immunohistochemistry;Gestational Age;Fetal Diseases},
	Month = {8},
	Nlm_Id = {7909235},
	Number = {5},
	Organization = {Neuroembryonic Research Laboratory, Institute of Anatomy, University of Rostock, Gertrudenstrasse 9, D-18055 Rostock, Germany. norbert.ulfig\@med.uni-rostock.de},
	Pages = {307-15},
	Pii = {S0387760403001724},
	Pubmed = {15165671},
	Title = {Brain macrophages and microglia in human fetal hydrocephalus},
	Uuid = {CC6C46C7-FEBE-41D3-88C6-327087194652},
	Volume = {26},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/S0387-7604(03)00172-4}}

@article{Umeda:1996,
	Abstract = {The development of macrophage populations in osteopetrosis (op) mutant mice defective in production of functional macrophage colony-stimulating factor (M-CSF) and the response of these cell populations to exogenous M-CSF were used to classify macrophages into four groups: 1) monocytes, monocyte-derived macrophages, and osteoclasts, 2) MOMA-1-positive macrophages, 3) ER-TR9-positive macrophages, and 4) immature tissue macrophages. Monocytes, monocyte-derived macrophages, osteoclasts in bone, microglia in brain, synovial A cells, and MOMA-1- or ER-TR9-positive macrophages were deficient in op/op mice. The former three populations expanded to normal levels in op/op mice after daily M-CSF administration, indicating that they are developed and differentiated due to the effect of M-CSF supplied humorally. In contrast, the other cells did not respond or very slightly responded to M-CSF, and their development seems due to either M-CSF produced in situ or expression of receptor for M-CSF. Macrophages present in tissues of the mutant mice were immature and appear to be regulated by either granulocyte/macrophage colony-stimulating factor and/or interleukin-3 produced in situ or receptor expression. Northern blot analysis revealed different expressions of GM-CSF and IL-3 mRNA in various tissues of the op/op mice. However, granulocyte/macrophage colony-stimulating factor and interleukin-3 in serum were not detected by enzyme-linked immunosorbent assay. The immature macrophages differentiated and matured into resident macrophages after M-CSF administration, and some of these cells proliferated in response to M-CSF.},
	Author = {Umeda, S. and Takahashi, K. and Shultz, L. D. and Naito, M. and Takagi, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Animals;Monocytes;Osteopetrosis;Mice, Mutant Strains;Macrophages;Antigens, Differentiation;Cell Count;Interleukin-3;Liver;Mice, Inbred C57BL;11 Glia;RNA, Messenger;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Blotting, Northern;Antibodies, Monoclonal;Flow Cytometry;Macrophage Colony-Stimulating Factor;Mice;Microscopy, Electron;Stem Cells;Immunohistochemistry;Spleen;Research Support, Non-U.S. Gov't},
	Medline = {96312859},
	Month = {8},
	Nlm_Id = {0370502},
	Number = {2},
	Organization = {Second Department of Pathology, Kumamoto University School of Medicine, Japan.},
	Pages = {559-74},
	Pubmed = {8701995},
	Title = {Effects of macrophage colony-stimulating factor on macrophages and their related cell populations in the osteopetrosis mouse defective in production of functional macrophage colony-stimulating factor protein},
	Uuid = {EB9BA219-003D-43B3-B2AA-33648C1FABF7},
	Volume = {149},
	Year = {1996}}

@article{Unal-Cevik:2004,
	Abstract = {NeuN immunoreactivity is used as a specific marker for neurons. The number of NeuN-positive cells decreases under pathological conditions. This finding is usually considered as an evidence of neuronal loss. However, decrease in NeuN labeling may also be caused by depletion of the protein or loss of its antigenicity. Hence, we have investigated the morphological features of neurons that lost NeuN immunoreactivity and the NeuN protein levels in mouse brain after cerebral ischemia. The number of NeuN-labeled cells was decreased 6 h after a mild ischemic insult (30 min middle cerebral artery occlusion) in penumbral and core regions. Hematoxylin and eosin (H&E) staining of adjacent sections showed that neurons in the penumbra were not disintegrated but displayed early ischemic changes. The nuclear NeuN staining was dramatically reduced or lost in some neurons. However, Hoechst 33258 staining of the same sections revealed that these nuclei were preserved with an intact membrane. Labeling of neurons that had lost NeuN-positivity with antibodies against caspase-3-p20, which is constitutively not present but emerges in neurons after ischemia, disclosed that these neurons still preserved their integrity. Moreover, Western blots showed that NeuN protein levels were not decreased, suggesting that reduced NeuN antigenicity accounted for loss of immunoreactivity in this mild brain injury model. Supporting this idea, NeuN labeling was partially restored after antigenic retrieval. In conclusion, since NeuN immunoreactivity readily decreases after metabolic perturbations, reduced NeuN labeling should not be taken as an indicator of neuronal loss and, quantitative analysis based on NeuN-positivity should be used cautiously after central nervous system (CNS) injury.},
	Author = {Unal-Cevik, Isin and Kilin\c{c}, M{\"u}nire and G{\"u}rsoy-Ozdemir, Yasemin and Gurer, Gunfer and Dalkara, Turgay},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Brain Chemistry;01 Adult neurogenesis general;Brain Ischemia;Comparative Study;Immunohistochemistry;Nerve Tissue Proteins;Biological Markers;evaluation studies;Antigens, Nuclear;Nuclear Proteins;Cell Death;Animals;Brain;Support, Non-U.S. Gov't;Neurons;Mice},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Institute of Neurological Sciences and Psychiatry, and Faculty of Medicine, Department of Neurology, Hacettepe University, Sihhiye Ankara 06100, Turkey.},
	Pages = {169-74},
	Pii = {S000689930400616X},
	Pubmed = {15223381},
	Title = {Loss of NeuN immunoreactivity after cerebral ischemia does not indicate neuronal cell loss: a cautionary note},
	Uuid = {5AC49152-D378-11D9-A0E9-000D9346EC2A},
	Volume = {1015},
	Year = {2004},
	url = {papers/Unal-Cevik_BrainRes2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainres.2004.04.032}}

@article{Unger:1993,
	Abstract = {In five female bone marrow transplant (BMT) recipients of sex-mismatched donor marrow, Y-chromosome specific in situ hybridization was performed on formalin-fixed, paraffin-embedded sections of the medulla to detect the male donor marrow-derived cells. Y-chromosome-bearing cells (Y-cells), thereby donor-derived, were matched with leukocyte common antigen (LCA)-reactive cells in adjacent sections immunostained with anti-LCA antibody. Y-cells included mononuclear leukocytes (MNL) within the vessel lumen and infiltrating the perivascular space and parenchyma, and "perivascular cells." We have, therefore, concluded that donor marrow-derived MNL, though limited in number, do enter the normal-appearing brain and can transform to "perivascular cells" in human BMT recipients. It remains, however, to be confirmed whether MNL entering the normal adult CNS parenchyma transform to ramified microglia.},
	Author = {Unger, E. R. and Sung, J. H. and Manivel, J. C. and Chenggis, M. L. and Blazar, B. R. and Krivit, W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Adolescent;Colorimetry;Antigens, CD45;Follow-Up Studies;Child, Preschool;Humans;Bone Marrow Transplantation;Brain;Female;Child;Sex Factors;11 Glia;Polymorphism, Restriction Fragment Length;Male;Aged;In Situ Hybridization;Research Support, U.S. Gov't, P.H.S.;Adult;Y Chromosome;Immunohistochemistry;Research Support, Non-U.S. Gov't},
	Medline = {93367517},
	Month = {9},
	Nlm_Id = {2985192R},
	Number = {5},
	Organization = {Department of Pathology, Emory University, Atlanta, Georgia.},
	Pages = {460-70},
	Pubmed = {8103085},
	Title = {Male donor-derived cells in the brains of female sex-mismatched bone marrow transplant recipients: a Y-chromosome specific in situ hybridization study},
	Uuid = {5F287E74-851E-4885-8432-FB73DFED1564},
	Volume = {52},
	Year = {1993}}

@article{Upender:1999,
	Abstract = {Neuronal elimination in the developing CNS is accomplished by an orderly type of cellular suicide called programmed cell death. The principal non-neuronal cells implicated in regulating programmed cell death and subsequent phagocytosis of dying neurons are the brain's macrophage population, the microglia. Little is known about the signaling between microglia and neurons during programmed cell death. However, macrophages in non-neural tissues express receptors for immunoglobulin (IgG) and complement, and these molecules help regulate phagocytosis of dying cells and foreign organisms. Since many of the neurons generated early in CNS development are transient cell types that are immunoreactive for IgG [Upender et al.: J Comp Neurol 1997; 384:271-282], we hypothesized that IgG might alter the phagocytic properties of microglia within the developing nervous system and potentiate engulfment of dying cells. To begin to address this hypothesis, we first asked whether cortical neurons immunoreactive for IgG or calbindin-D28k exhibit morphological evidence of programmed cell death in the cerebral cortex of neonatal rat pups. Secondly, we quantified the incidence of contacts made by microglia on IgG- vs. calbindin-immunoreactive neurons. Thirdly, perturbation experiments were performed to elevate intracortical levels of IgG and the incidence of microglia:neuron contacts were determined. We found that although the nuclei of some IgG-immunoreactive neurons exhibited condensation and fragmentation characteristic of programmed cell death, we did not observe pyknotic calbindin-immunoreactive neurons. IgG-immunoreactive neurons were also more likely to be contacted by microglia than calbindin-immunoreactive neurons. Elevating intracortical levels of IgG experimentally led to a dramatic increase in the expression of microglia complement receptors throughout the cerebral cortex. Taken together, these results suggest that IgG normally present within neuronal subsets in the developing cerebral cortex could serve to locally regulate the expression of complement receptors on microglia.},
	Author = {Upender, M. B. and Naegele, J. R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {Phagocytosis;Rats, Long-Evans;Animals;Up-Regulation;Rats;Immunoglobulin G;Immunity, Maternally-Acquired;Apoptosis;Female;Cell Communication;Microglia;Not relevant;Calcium-Binding Protein, Vitamin D-Dependent;11 Glia;Male;Receptors, Complement;Membrane Glycoproteins;Cerebral Cortex;Neurons;Support, U.S. Gov't, Non-P.H.S.},
	Medline = {20108839},
	Nlm_Id = {7809375},
	Number = {6},
	Organization = {Biology Department and Program in Neuroscience and Behavior, Wesleyan University, Middletown, CT, USA.},
	Pages = {491-505},
	Pii = {dne21491},
	Pubmed = {10640867},
	Title = {Activation of microglia during developmentally regulated cell death in the cerebral cortex},
	Uuid = {7EC8699F-EE25-11DA-8605-000D9346EC2A},
	Volume = {21},
	Year = {1999},
	url = {papers/Upender_DevNeurosci1999.pdf}}

@article{Vaillant:1999,
	Abstract = {In this report, we have examined the mechanisms whereby neurotrophins and neural activity coordinately regulate neuronal survival, focussing on sympathetic neurons, which require target-derived NGF and neural activity for survival during development. When sympathetic neurons were maintained in suboptimal concentrations of NGF, coincident depolarization with concentrations of KCl that on their own had no survival effect, synergistically enhanced survival. Biochemical analysis revealed that depolarization was sufficient to activate a Ras-phosphatidylinositol 3-kinase-Akt pathway (Ras-PI3-kinase-Akt), and function-blocking experiments using recombinant adenovirus indicated that this pathway was essential for approximately 50\%of depolarization-mediated neuronal survival. At concentrations of NGF and KCl that promoted synergistic survival, these two stimuli converged to promote increased PI3-kinase-dependent Akt phosphorylation. This convergent PI3-kinase-Akt pathway was essential for synergistic survival. In contrast, inhibition of calcium/calmodulin-dependent protein kinase II revealed that, while this molecule was essential for depolarization-induced survival, it had no role in KCl- induced Akt phosphorylation, nor was it important for synergistic survival by NGF and KCl. Thus, NGF and depolarization together mediate survival of sympathetic neurons via intracellular convergence on a Ras-PI3-kinase-Akt pathway. This convergent regulation of Akt may provide a general mechanism for coordinating the effects of growth factors and neural activity on neuronal survival throughout the nervous system. 0021-9525 Journal Article},
	Author = {Vaillant, A. R. and Mazzoni, I. and Tudan, C. and Boudreau, M. and Kaplan, D. R. and Miller, F. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Cell Biol},
	Keywords = {Protein-Tyrosine Kinase/antagonists &inhibitors/metabolism;Potassium Chloride/pharmacology;Drug Synergism;Neurons/*cytology/drug effects/enzymology;Membrane Potentials/drug effects/physiology;Receptor, trkA;Rats;Proto-Oncogene Proteins/antagonists &inhibitors/*metabolism/physiology;Cells, Cultured;Apoptosis/drug effects;Receptor Protein-Tyrosine Kinases/antagonists &inhibitors/physiology;Animals;Nerve Growth Factors/*pharmacology;Sympathetic Nervous System/cytology;Cell Survival/drug effects;C abstr;Rats, Sprague-Dawley;Enzyme Activation/drug effects;Ca(2+)-Calmodulin Dependent Protein Kinase/antagonists &;Animals, Newborn;inhibitors/metabolism;Receptors, Nerve Growth Factor/antagonists &inhibitors/physiology;Phosphorylation/drug effects;Protein-Serine-Threonine Kinases/antagonists &inhibitors/metabolism;04 Adult neurogenesis factors;1-Phosphatidylinositol 3-Kinase/antagonists &inhibitors/*metabolism;Proto-Oncogene Protein p21(ras)/metabolism;Mitogen-Activated Protein Kinase Kinases;Signal Transduction/*drug effects},
	Number = {5},
	Organization = {Center for Neuronal Survival, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada H3A 2B4.},
	Pages = {955-66},
	Pubmed = {10477751},
	Title = {Depolarization and neurotrophins converge on the phosphatidylinositol 3-kinase-Akt pathway to synergistically regulate neuronal survival},
	Uuid = {15095E6A-C86D-4D95-B5AE-E72D75BCE5A3},
	Volume = {146},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10477751}}

@article{Vallieres:2002,
	Abstract = {Postnatal neurogenesis can be modulated after brain injury, but the role of the attendant expression of inflammatory mediators in such responses remains to be determined. Here we report that transgenically directed production of interleukin-6 (IL-6) by astroglia decreased overall neurogenesis by 63\%in the hippocampal dentate gyrus of young adult transgenic mice. The proliferation, survival, and differentiation of neural progenitor cells labeled with the thymidine analog bromodeoxyuridine were all reduced in the granule cell layer of these mice, whereas their distribution and gliogenesis appeared normal. These effects were not a consequence of general toxicity of the IL-6 transgene, because they were manifested in the absence of neuronal death and of major changes in glial cell number and morphology. These findings suggest that long-term exposure of the brain to proinflammatory mediators such as IL-6, as is seen in certain degenerative disorders and infections, can interfere with adult neurogenesis.},
	Author = {Vallieres, L. and Campbell, I. L. and Gage, F. H. and Sawchenko, P. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Neurosci},
	Keywords = {Fluorescent Dyes;Cell Differentiation/genetics;Phenotype;Animal;Cell Count;Mice, Transgenic;Hippocampus/cytology/*metabolism;Cell Survival/genetics;Astrocytes/cytology/*metabolism;Support, Non-U.S. Gov't;Cell Division/genetics;*Neurons/cytology;C;04 Adult neurogenesis factors;Interleukin-6/*biosynthesis/genetics;Support, U.S. Gov't, P.H.S.;Mice;Dentate Gyrus/cytology/metabolism;Immunohistochemistry;Genes, Reporter;Gene Expression;Bromodeoxyuridine;Transgenes},
	Number = {2},
	Organization = {Laboratories of Neuronal Structure and Function, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {486-92.},
	Title = {Reduced hippocampal neurogenesis in adult transgenic mice with chronic astrocytic production of interleukin-6},
	Uuid = {759FAA48-64F3-4659-9D50-36C9B6058CE6},
	Volume = {22},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11784794%20http://www.jneurosci.org/cgi/content/full/22/2/486%20http://www.jneurosci.org/cgi/content/abstract/22/2/486}}

@article{Vallieres:2003,
	Abstract = {Cytogenesis in the adult brain can result from the recruitment of circulating precursors, but the proposal that some such cells transdifferentiate into neural elements is controversial. We have reinvestigated this issue by following the phenotypic fate of bone marrow cells expressing the green fluorescent protein transplanted into the systemic circulation of irradiated mice. Thousands of donor-derived cells were detected throughout brains of recipients killed 1-12 months after transplantation, but none displayed neuronal, macroglial, or endothelial characteristics, even after injury. Among those that crossed the endothelium of the cerebral cortex, >99.7\%were identified as perivascular macrophages. Newly formed parenchymal microglia were found in significant numbers only in the cerebellum and at injury sites. Therefore, bone marrow does supply the mature brain with new specialized cells; however, mesenchymal precursors neither adopt neural phenotypes nor contribute to cerebral vascular remodeling. This continuous traffic of macrophages across the blood-brain barrier provides a vehicle to introduce therapeutic genes into the nervous system.},
	Author = {Valli\`{e}res, Luc and Sawchenko, Paul E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Animals;Macrophages;Bone Marrow Transplantation;Phenotype;Brain;Microglia;Cell Count;Mice, Transgenic;Mice, Inbred C57BL;Male;Blood-Brain Barrier;Time;Bone Marrow Cells;Brain Injuries;Cell Lineage;Hematopoietic System;Support, Non-U.S. Gov't;Support, U.S. Gov't, P.H.S.;Mice;Cell Division;Genes, Reporter;Cerebral Decortication;Luminescent Proteins},
	Medline = {22716544},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Laboratoire d'Endocrinologie Mol{\'e}culaire, Centre de Recherche du Centre Hospitalier de l'Universit{\'e} Laval, Universit{\'e} Laval, Qu{\'e}bec, Qu{\'e}bec, G1V 4G2, Canada. Luc.Vallieres\@crchul.ulaval.ca},
	Pages = {5197-207},
	Pii = {23/12/5197},
	Pubmed = {12832544},
	Title = {Bone marrow-derived cells that populate the adult mouse brain preserve their hematopoietic identity},
	Uuid = {8481E025-D3B7-11D9-A0E9-000D9346EC2A},
	Volume = {23},
	Year = {2003}}

@article{Van-De-Bor:2002,
	Abstract = {Neurons and glial cells depend on similar developmental pathways and often originate from common precursors; however, the differentiation of one or the other cell type depends on the activation of cell-specific pathways. In Drosophila, the differentiation of glial cells depends on a transcription factor, Glide/Gcm. This glial-promoting factor is both necessary and sufficient to induce the central and peripheral glial fates at the expense of the neuronal fate. In a screen for mutations affecting the adult peripheral nervous system, we have found a dominant mutation inducing supernumerary sensory organs. Surprisingly, this mutation is allelic to glide/gcm and induces precocious glide/gcm expression, which, in turn, activates the proneural genes. As a consequence, sensory organs are induced. Thus, temporal misregulation of the Glide/Gcm glial-promoting factor reveals a novel potential for this cell fate determinant. At the molecular level, this implies unpredicted features of the glide/gcm pathway. These findings also emphasize the requirement for both spatial and temporal glide/gcm regulation to achieve proper cell specification within the nervous system.},
	Author = {Van De Bor, V. and Heitzler, P. and Leger, S. and Plessy, C. and Giangrande, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Genetics},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {3},
	Organization = {Institut de Genetique et Biologie Moleculaire et Cellulaire IGBMC/CNRS/ULP/INSERM-BP 163 67404 Illkirch, c.u. de Strasbourg, France.},
	Pages = {1095-106.},
	Title = {Precocious expression of the glide/gcm glial-promoting factor in Drosophila induces neurogenesis},
	Uuid = {3EC4E8BE-EB75-4BE3-9982-2F1A529E9429},
	Volume = {160},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11901125%20http://www.genetics.org/cgi/content/full/160/3/1095%20http://www.genetics.org/cgi/content/abstract/160/3/1095}}

@article{Van-Hoeven:2005,
	Abstract = {BACKGROUND: Retrovirus infection depends on binding of the retroviral envelope (Env) protein to specific cell-surface protein receptors. Interference, or superinfection resistance, is a frequent consequence of retroviral infection, and occurs when newly-synthesized Env binds to receptor proteins resulting in a block to entry by retroviruses that use the same receptors. Three groups of viruses demonstrate a non-reciprocal pattern of interference (NRI), which requires the existence of both a common receptor utilized by all viruses within the group, and a specific receptor that is used by a subset of viruses. In the case of amphotropic and 10A1 murine leukemia viruses (MLV), the common and specific receptors are the products of two related genes. In the case of avian sarcoma and leukosis virus types B, D, and E, the two receptors are distinct protein products of a single gene. NRI also occurs between xenotropic and polytropic MLV. The common receptor, Xpr1, has been identified, but a specific receptor has yet to be described. RESULTS: Using chimeric receptor proteins and interference studies, we have identified a region of Xpr1 that is uniquely utilized by xenotropic MLV and show that this receptor domain is required for non-reciprocal interference. CONCLUSION: We propose a novel pattern of receptor usage by xenotropic and polytropic MLV to explain the NRI observed between these viruses. We propose that the specific and common receptor determinants for xenotropic and polytropic viruses are simultaneously present in discreet domains of a single Xpr1 protein.},
	Author = {Van Hoeven, Neal S. and Miller, A. Dusty},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1742-4690},
	Journal = {Retrovirology},
	Keywords = {15 PS VSVG receptor;15 Retrovirus mechanism;24 Pubmed search results 2008},
	Nlm_Id = {101216893},
	Number = {1},
	Organization = {Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. nvanhoeven\@cdc.gov},
	Pages = {76},
	Pii = {1742-4690-2-76},
	Pubmed = {16354307},
	Title = {Use of different but overlapping determinants in a retrovirus receptor accounts for non-reciprocal interference between xenotropic and polytropic murine leukemia viruses},
	Uuid = {4655D5C7-9073-4FE7-827D-935AD2507FC1},
	Volume = {2},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/1742-4690-2-76}}

@article{Van-Kampen:2004,
	Abstract = {Abstract Discrete regions of the adult CNS, including the subventricular zone (SVZ), do retain the capacity for neurogenesis. These progenitor cells may represent a potential new source of cells for replacement therapies in neuroregenerative diseases. An understanding of the microenvironmental signals regulating neurogenesis in the adult brain would facilitate the development of such therapeutic approaches. A particularly strong expression of dopamine D(3) receptor mRNA occurs in the proliferative SVZ during prenatal and early postnatal ontogeny. Although its expression diminishes following development, a restricted D(3) receptor expression persists in this region through adulthood, coincident with continued proliferation in this region. Here, we demonstrate a two-fold induction of cell proliferation (BrdU incorporation) in the SVZ and rostral migratory stream of the adult Sprague-Dawley rat brain following intrasubventricular administration of the dopamine D(3) receptor agonist, 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) for 2 weeks. The number of BrdU-positive cells was elevated ten-fold from very low baseline levels in the neighbouring neostriatum, another region known to express D(3) receptors. These striatal BrdU-positive cells appeared within 3 days following intracerebral infusion of 7-OH-DPAT and were distributed homogeneously throughout the striatum following systemic administration. This suggests that these cells originate from resident progenitor cells rather than the SVZ. Dopamine D(3) receptor activation may serve as a proneuronal differentiation signal as 60-70\%of the new cells had neuronal markers following 7-OH-DPAT infusion. These results suggest that the dopamine D(3) receptor may be a good drug target for cell replacement strategies, particularly because of the fact that its expression is almost exclusively limited to the nervous system. 0953-816x Journal Article},
	Author = {Van Kampen, J. M. and Hagg, T. and Robertson, H. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Eur J Neurosci},
	Keywords = {01 Adult neurogenesis general;A, C, D pdf},
	Number = {9},
	Organization = {Department Pharmacology, Dalhousie University, Tupper Building, 5850 College St., Halifax, Nova Scotia, B3H 15X Canada.},
	Pages = {2377-87},
	Title = {Induction of neurogenesis in the adult rat subventricular zone and neostriatum following dopamine D receptor stimulation},
	Uuid = {EA0E369E-923A-4B68-8913-C62C74BDDB8B},
	Volume = {19},
	Year = {2004},
	url = {papers/VanKampen_EurJNeurosci2004.pdf}}

@article{Vanek:1998,
	Abstract = {Myelin contains potent inhibitors of neurite growth which have been implicated in the failure of long-distance regeneration of nerve fibres within the CNS. These myelin-associated neurite growth inhibitors may also be involved in the stabilization of neural connections by suppressing sprouting and fibre growth. After lesions of the CNS in neonatal animals, extensive rearrangements of the remaining fibre systems have been observed. In the rat, this plasticity of neuronal connections is severely restricted following the first few weeks of postnatal life, coincident with the progression of myelination of the nervous system. A well-studied example of postnatal plasticity is the sprouting of one corticospinal tract (CST) into the denervated half of the spinal cord after unilateral motor cortex or pyramidal lesions. In the hamster and rat, significant CST sprouting is restricted to the first 10 postnatal days. Here we show that very extensive sprouting of corticospinal fibres occurs after deafferentations as late as P21 if myelination is prevented by neonatal X-irradiation in the rat lumbar spinal cord. Sprouted fibres from the intact CST cross the midline and develop large terminal arbors in the denervated spinal cord, suggesting the establishment of synaptic connections. Our results suggest that myelin and its associated neurite growth inhibitors play an important role in the termination of neurite growth permissive periods during postnatal CNS development. Corticospinal sprouting subsequent to lesions early in life, i.e. in the absence of myelin-associated neurite growth inhibitors may explain the frequent occurrence of mirror movements in patients with hemiplegic cerebral palsy.},
	Author = {Vanek, P. and Thallmair, M. and Schwab, M. E. and Kapfhammer, J. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:42 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate;Nerve Fibers;Research Support, Non-U.S. Gov't;Rats, Inbred Lew;Neurites;Nerve Regeneration;Rats;Myelin Sheath;Neuronal Plasticity;Denervation;Pyramidal Tracts;Myelin Proteins;Animals, Newborn;Animals;24 Pubmed search results 2008},
	Medline = {98424034},
	Month = {1},
	Nlm_Id = {8918110},
	Number = {1},
	Organization = {Institut f{\"u}r Hirnforschung, Universit{\"a}t Z{\"u}rich, Switzerland.},
	Pages = {45-56},
	Pubmed = {9753112},
	Title = {Increased lesion-induced sprouting of corticospinal fibres in the myelin-free rat spinal cord},
	Uuid = {FFB42372-63A0-4B34-B99F-02D8BD9713CA},
	Volume = {10},
	Year = {1998}}

@article{Varki:2006,
	Abstract = {The remarkable structural diversity of glycans in nature, and their roles in cellular processes, host-pathogen interactions, biological diversity and speciation can be explained by evolutionary processes.},
	Author = {Varki, Ajit},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {24 Pubmed search results 2008;Glycosyltransferases;Membrane Glycoproteins;Protein Transport;Glycosylation;Gene Expression Regulation, Enzymologic;09 Evolutionary dynamics;Evolution, Molecular;Genetic Speciation;Glycoproteins;Animals;Humans;Orthomyxoviridae;Polysaccharides;Protein Processing, Post-Translational},
	Month = {9},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Glycobiology Research and Training Center, Departments of Medicine and Cellular & Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA. a1varki\@ucsd.edu},
	Pages = {841-5},
	Pii = {S0092-8674(06)01089-0},
	Pubmed = {16959563},
	Title = {Nothing in glycobiology makes sense, except in the light of evolution},
	Uuid = {1584ECEC-236C-485E-8BA6-BB00847C5FC5},
	Volume = {126},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2006.08.022}}

@article{Vasquez:1997,
	Abstract = {Previous studies demonstrated that nanomolar concentrations of nocodazole can block cells in mitosis without net microtubule disassembly and resulted in the hypothesis that this block was due to a nocodazole-induced stabilization of microtubules. We tested this hypothesis by examining the effects of nanomolar concentrations of nocodazole on microtubule dynamic instability in interphase cells and in vitro with purified brain tubulin. Newt lung epithelial cell microtubules were visualized by video-enhanced differential interference contrast microscopy and cells were perfused with solutions of nocodazole ranging in concentration from 4 to 400 nM. Microtubules showed a loss of the two-state behavior typical of dynamic instability as evidenced by the addition of a third state where they exhibited little net change in length (a paused state). Nocodazole perfusion also resulted in slower elongation and shortening velocities, increased catastrophe, and an overall decrease in microtubule turnover. Experiments performed on BSC-1 cells that were microinjected with rhodamine-labeled tubulin, incubated in nocodazole for 1 h, and visualized by using low-light-level fluorescence microscopy showed similar results except that nocodazole-treated BSC-1 cells showed a decrease in catastrophe. To gain insight into possible mechanisms responsible for changes in dynamic instability, we examined the effects of 4 nM to 12 microM nocodazole on the assembly of purified tubulin from axoneme seeds. At both microtubule plus and minus ends, perfusion with nocodazole resulted in a dose-dependent decrease in elongation and shortening velocities, increase in pause duration and catastrophe frequency, and decrease in rescue frequency. These effects, which result in an overall decrease in microtubule turnover after nocodazole treatment, suggest that the mitotic block observed is due to a reduction in microtubule dynamic turnover. In addition, the in vitro results are similar to the effects of increasing concentrations of GDP-tubulin (TuD) subunits on microtubule assembly. Given that nocodazole increases tubulin GTPase activity, we propose that nocodazole acts by generating TuD subunits that then alter dynamic instability. 1059-1524 Journal Article},
	Author = {Vasquez, R. J. and Howell, B. and Yvon, A. M. and Wadsworth, P. and Cassimeris, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Mol Biol Cell},
	Keywords = {Dose-Response Relationship, Drug;Animals;Cells, Cultured;EE, T abstr;Mitotic Spindle Apparatus/*drug effects;Sea Urchins;Swine;08 Aberrant cell cycle;Male;Tubulin/*drug effects;Guanosine Triphosphate/metabolism;Sperm Tail/ultrastructure;Macromolecular Systems;Microtubules/*drug effects;EE, T pdf;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Nocodazole/*administration &dosage;Salamandridae},
	Number = {6},
	Organization = {Department of Biological Sciences, Lehigh University, Bethlehem, Pennsylvania 18015, USA.},
	Pages = {973-85},
	Pubmed = {9201709},
	Title = {Nanomolar concentrations of nocodazole alter microtubule dynamic instability in vivo and in vitro},
	Uuid = {8F586F86-0A17-475E-BD21-7CF78CECA579},
	Volume = {8},
	Year = {1997},
	url = {papers/Vasquez_MolBiolCell1997.pdf}}

@article{Vassilopoulos:2003,
	Abstract = {Results from several experimental systems suggest that cells from one tissue type can form other tissue types after transplantation. This could be due to the presence of multipotential or several types of adult stem cells in donor tissues, or alternatively, to fusion of donor and recipient cells. In a model of tyrosinaemia type I, mice with mutations in the fumarylacetoacetate hydrolase gene (Fah-/-) regain normal liver function after transplantation of Fah+/+ bone marrow cells, and form regenerating liver nodules with normal histology that express Fah. Here we show that these hepatic nodules contain more mutant than wild-type Fah alleles, and that their hepatocytes express both donor and host genes, consistent with polyploid genome formation by fusion of host and donor cells. Using bone marrow cells marked with integrated foamy virus vectors that express green fluorescent protein, we identify common proviral junctions in hepatic nodules and haematopoietic cells. We also show that the haematopoietic donor genome adopts a more hepatocyte-specific expression profile after cell fusion, as the wild-type Fah gene was activated and the pan-haematopoietic CD45 marker was no longer expressed. 0028-0836 Journal Article},
	Author = {Vassilopoulos, G. and Wang, P. R. and Russell, D. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Nature},
	Keywords = {Cell Differentiation;Animals;Heterozygote;Liver/cytology/metabolism;Gene Expression Regulation;Hematopoietic Stem Cells/cytology/metabolism;*Liver Regeneration;Hybrid Cells/*cytology/metabolism;DNA/analysis/genetics;Bone Marrow Cells/*cytology/metabolism;Female;EE pdf;Cell Fusion;Gene Deletion;Mice, Inbred C57BL;08 Aberrant cell cycle;Hepatocytes/*cytology/metabolism/*transplantation;Male;Diploidy;Hydrolases/genetics;Support, Non-U.S. Gov't;Homozygote;Organ Specificity;RNA, Messenger/genetics/metabolism;Polyploidy;Mice;*Bone Marrow Transplantation},
	Number = {6934},
	Organization = {Division of Hematology, University of Washington, Seattle, Washington 98195, USA.},
	Pages = {901-4},
	Pubmed = {12665833},
	Title = {Transplanted bone marrow regenerates liver by cell fusion},
	Uuid = {E40348A5-C829-431D-A5D0-B0AAA995A968},
	Volume = {422},
	Year = {2003},
	url = {papers/Vassilopoulos_Nature2003.pdf}}

@article{Venter:2004,
	Abstract = {We have applied "whole-genome shotgun sequencing" to microbial populations collected en masse on tangential flow and impact filters from seawater samples collected from the Sargasso Sea near Bermuda. A total of 1.045 billion base pairs of nonredundant sequence was generated, annotated, and analyzed to elucidate the gene content, diversity, and relative abundance of the organisms within these environmental samples. These data are estimated to derive from at least 1800 genomic species based on sequence relatedness, including 148 previously unknown bacterial phylotypes. We have identified over 1.2 million previously unknown genes represented in these samples, including more than 782 new rhodopsin-like photoreceptors. Variation in species present and stoichiometry suggests substantial oceanic microbial diversity.},
	Author = {Venter, J. Craig and Remington, Karin and Heidelberg, John F. and Halpern, Aaron L. and Rusch, Doug and Eisen, Jonathan A. and Wu, Dongying and Paulsen, Ian and Nelson, Karen E. and Nelson, William and Fouts, Derrick E. and Levy, Samuel and Knap, Anthony H. and Lomas, Michael W. and Nealson, Ken and White, Owen and Peterson, Jeremy and Hoffman, Jeff and Parsons, Rachel and Baden-Tillson, Holly and Pfannkoch, Cynthia and Rogers, Yu-Hui H. and Smith, Hamilton O.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1095-9203},
	Journal = {Science},
	Keywords = {Synechococcus Group;Ecosystem;Cyanobacteria;Sequence Analysis, DNA;Seawater;Rhodopsin;Photosynthesis;Atlantic Ocean;Water Microbiology;Phylogeny;Genome, Archaeal;Genomics;Computational Biology;23 Technique;Bacteria;Biodiversity;Genome, Bacterial;Plasmids;Support, Non-U.S. Gov't;Genes, rRNA;Genes, Archaeal;Archaea;Support, U.S. Gov't, Non-P.H.S.;Genes, Bacterial;Molecular Sequence Data;Bacteriophages;Eukaryotic Cells},
	Month = {4},
	Nlm_Id = {0404511},
	Number = {5667},
	Organization = {Institute for Biological Energy Alternatives, 1901 Research Boulevard, Rockville, MD 20850, USA. jcventer\@tcag.org},
	Pages = {66-74},
	Pii = {1093857},
	Pubmed = {15001713},
	Title = {Environmental genome shotgun sequencing of the Sargasso Sea},
	Uuid = {A2FBE27F-4440-43AA-B8DA-F7449CD9CC3D},
	Volume = {304},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1093857}}

@article{Vercelli:2003,
	Abstract = {The parafascicular nucleus (PFN) of the rat, homologous to the human centre m{\'e}dian, is an intralaminar nucleus of the thalamus, classically considered as part of the ascending activating system. We have previously demonstrated that it is also connected to several subcortical nuclei. To obtain a more detailed picture of the connectivity of the PFN, the organization and the topography of the reciprocal parafascicular-telencephalic relationships were studied in both adult and developing rats, using anterograde and retrograde neuronal tracers. In the adult rat, the ascending parafascicular projections were densest to the striatum, dense to the frontal and least dense to cingulate cortex, and were strictly ipsilateral. They displayed a loose topography, with the more medial parafascicular neurons projecting to the medial frontal and cingulate cortex and medial striatum, and the more lateral neurons projecting to the lateral frontal cortex and lateral striatum. All these connections were already present at embryonic day 19. Parafascicular neurons projecting to the telencephalon in adult rats were mostly of the multipolar type, with a few bipolar neurons. In neonatal rats they showed a bipolar morphology at birth; they became mostly multipolar later on, with an increasing complexity of the dendritic arbor up to postnatal day 10. Neurons in the frontal cortex retrogradely labelled from the PFN were more numerous perinatally, and decreased as early as postnatal day 5. The telencephalic connections of the PFN were found to be more discrete and restricted than previously thought, thus suggesting a more specific functional role for the nucleus than cortical recruitment.},
	Author = {Vercelli, Alessandro and Marini, Gabriella and Tredici, Giovanni},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;Rats;Neural Pathways;Fluorescent Dyes;Lysine;Rats, Wistar;Microscopy, Fluorescence;Animals;Intralaminar Thalamic Nuclei;24 Pubmed search results 2008;Neurons},
	Medline = {22770073},
	Month = {7},
	Nlm_Id = {8918110},
	Number = {2},
	Organization = {Department of Anatomy, Pharmacology and Forensic Medicine, University of Torino, corso M. D'Azeglio 52, 10126 Torino, Italy. alessandro.vercelli\@unito.it},
	Pages = {275-89},
	Pii = {2743},
	Pubmed = {12887409},
	Title = {Anatomical organization of the telencephalic connections of the parafascicular nucleus in adult and developing rats},
	Uuid = {D4B83FDF-C216-4370-9692-6077DC559160},
	Volume = {18},
	Year = {2003}}

@article{Vercelli:2004,
	Abstract = {The apical dendrites of the pyramidal neurons of the cerebral cortex form radial bundles in all species and areas. Using microtubule-associated protein (MAP)2 immunostaining and Voronoi tessellation analysis in the rat visual cortex, we obtained objective criteria to define dendritic bundles in tangential sections: in supragranular layers of the rat visual cortex we found bundles of 6-6.4 dendrites, at a density of 1929 bundles/mm(2) and a centre-to-centre distance of 27 micro m. Using lipophilic tracers to label different pyramidal cell populations, based on the same criteria as in MAP2-immunostained material, we found that in the rat visual cortex the bundles consist of neurons with specific targets. Neurons projecting to the ipsi- or contralateral cortex form bundles together and with neurons projecting to the striatum, but not with those projecting to the superior colliculus, dorsal division of the lateral geniculate nucleus or through the cerebral peduncle. The latter neurons form bundles with neurons projecting to the striatum. Thus, the cerebral cortex is organized in minicolumns of output neurons visible at the earliest ages studied (P3), which might have a higher probability of being interconnected than those outside.},
	Author = {Vercelli, Alessandro E. and Garbossa, Diego and Curtetti, Roberta and Innocenti, Giorgio M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Not relevant;11 Glia},
	Month = {7},
	Nlm_Id = {8918110},
	Number = {2},
	Organization = {Department of Anatomy, Pharmacology and Forensic Medicine, corso M. d'Azeglio 52, 10126 Torino, Italy. alessandro.vercelli\@unito.it},
	Pages = {495-502},
	Pii = {EJN3483},
	Pubmed = {15233758},
	Title = {Somatodendritic minicolumns of output neurons in the rat visual cortex},
	Uuid = {F2876FE2-126A-49DD-B4CE-02C8FC9C596F},
	Volume = {20},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1460-9568.2004.03483.x}}

@article{Vergano-Vera:2006,
	Abstract = {During the embryonic period, many olfactory bulb (OB) interneurons arise in the lateral ganglionic eminence (LGE) from precursor cells expressing Dlx2, Gsh2 and Er81 transcription factors. Whether GABAergic and dopaminergic interneurons are also generated within the embryonic OB has not been studied thoroughly. In contrast to abundant Dlx2 and Gsh2 expression in ganglionic eminences (GE), Dlx2 and Gsh2 proteins are not expressed in the E12.5-13.5 mouse OB, whereas the telencephalic pallial domain marker Pax6 is abundant. We found GABAergic and dopaminergic neurons originating from dividing precursor cells in E13.5 OB and in short-term dissociated cultures prepared from the rostral half of E13.5 OB. In OB cultures, 22\%of neurons were GAD+, of which 53\%were Dlx2+, whereas none expressed Gsh2. By contrast, 70\%of GAD+ cells in GE cultures were Dlx2+ and 16\%expressed Gsh2. In E13.5 OB slices transplanted with EGFP-labeled E13.5 OB precursor cells, 31.7\%of EGFP+ cells differentiated to GABAergic neurons. OB and LGE precursors transplanted into early postnatal OB migrated and differentiated in distinct patterns. Transplanted OB precursors gave rise to interneurons with dendritic spines in close proximity to synaptophysin-positive boutons. Interneurons were also abundant in differentiating OB neural stem cell cultures; the neurons responded to the neurotrophin Bdnf and expressed presynaptic proteins. In vivo, the Bdnf receptor TrkB colocalized with synaptic proteins at the glomeruli. These findings suggest that, in addition to receiving interneurons from the LGE, the embryonic OB contains molecularly distinct local precursor cells that generate mature GABAergic and dopaminergic neurons.},
	Author = {Verga\~{n}o-Vera, Eva and Yusta-Boyo, Mar{\'\i}a J. and de Castro, Fernando and Bernad, Antonio and de Pablo, Flora and Vicario-Abej{\'o}n, Carlos},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {8701744},
	Number = {21},
	Organization = {Instituto Cajal, Consejo Superior de Investigaciones Cient{\'\i}ficas (CSIC), Spain.},
	Pages = {4367-79},
	Pii = {133/21/4367},
	Pubmed = {17038521},
	Title = {Generation of GABAergic and dopaminergic interneurons from endogenous embryonic olfactory bulb precursor cells},
	Uuid = {50B0BC5F-C574-49F4-89F7-D15F22132D3B},
	Volume = {133},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.02601}}

@article{Verstegen:1998,
	Abstract = {In vivo expansion and multilineage outgrowth of human immature hematopoietic cell subsets from umbilical cord blood (UCB) were studied by transplantation into hereditary immunodeficient (SCID) mice. The mice were preconditioned with Cl2MDP-liposomes to deplete macrophages and 3.5 Gy total body irradiation (TBI). As measured by immunophenotyping, this procedure resulted in high levels of human CD45(+) cells in SCID mouse bone marrow (BM) 5 weeks after transplantation, similar to the levels of human cells observed in NOD/SCID mice preconditioned with TBI. Grafts containing approximately 10(7) unfractionated cells, approximately 10(5) purified CD34+ cells, or 5 x 10(3) purified CD34+CD38- cells yielded equivalent numbers of human CD45+ cells in the SCID mouse BM, which contained human CD34+ cells, monocytes, granulocytes, erythroid cells, and B lymphocytes at different stages of maturation. Low numbers of human GpA+ erythroid cells and CD41+ platelets were observed in the peripheral blood of engrafted mice. CD34+CD38+ cells (5 x 10(4)/mouse) failed to engraft, whereas CD34- cells (10(7)/mouse) displayed only low levels of chimerism, mainly due to mature T lymphocytes. Transplantation of graded numbers of UCB cells resulted in a proportional increase of the percentages of CD45+ and CD34+ cells produced in SCID mouse BM. In contrast, the number of immature, CD34+CD38- cells produced in vivo showed a second-order relation to CD34+ graft size, and mice engrafted with purified CD34+CD38- grafts produced 10-fold fewer CD34+ cells without detectable CD34+CD38- cells than mice transplanted with equivalent numbers of unfractionated or purified CD34+ cells. These results indicate that SCID repopulating CD34+CD38- cells require CD34+CD38+ accessory cell support for survival and expansion of immature cells, but not for production of mature multilineage progeny in SCID mouse BM. These accessory cells are present in the purified, nonrepopulating CD34+CD38+ subset as was directly proven by the ability of this fraction to restore the maintenance and expansion of immature CD34+CD38- cells in vivo when cotransplanted with purified CD34+CD38- grafts. The possibility to distinguish between maintenance and outgrowth of immature repopulating cells in SCID mice will facilitate further studies on the regulatory functions of accessory cells, growth factors, and other stimuli. Such information will be essential to design efficient stem cell expansion procedures for clinical use.},
	Author = {Verstegen, M. M. and van Hennik, P. B. and Terpstra, W. and van den Bos, C. and Wielenga, J. J. and van Rooijen, N. and Ploemacher, R. E. and Wagemaker, G. and Wognum, A. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Mice, Inbred NOD;ADP-ribosyl Cyclase;Humans;Macrophages;Animals;Transplantation, Heterologous;Comparative Study;Antigens, Differentiation;Female;Antigens, CD;NAD+ Nucleosidase;Mice, SCID;Antigens, CD34;11 Glia;Specific Pathogen-Free Organisms;Radiation Chimera;Hematopoietic Stem Cell Transplantation;Hematopoiesis;Cell Lineage;Mice;Transplantation Conditioning;Fetal Blood;Graft Survival;Hematopoietic Stem Cells;Clodronic Acid;Research Support, Non-U.S. Gov't},
	Medline = {98158631},
	Month = {3},
	Nlm_Id = {7603509},
	Number = {6},
	Organization = {Institute of Hematology, Erasmus University Rotterdam, Rotterdam, The Netherlands.},
	Pages = {1966-76},
	Pubmed = {9490679},
	Title = {Transplantation of human umbilical cord blood cells in macrophage-depleted SCID mice: evidence for accessory cell involvement in expansion of immature CD34+CD38- cells},
	Uuid = {2BD00B5D-2C6C-4A50-AD1C-7EB559BDAD14},
	Volume = {91},
	Year = {1998}}

@article{Vicario-Abejon:1995,
	Abstract = {Restrictions in neuronal fate occur during the transition from a multipotential to a postmitotic cell. This and later steps in neuronal differentiation are determined by extracellular signals. We report that basic fibroblast growth factor is mitogenic for stem cells and is a differentiation factor for calbindin-expressing hippocampal neurons. The neurotrophin NT-3 is a differentiation factor for the same neurons but does not affect proliferation. NT-3 and brain-derived neurotrophic factor promote the maturation of neurons derived from stem cells that have been grown in vitro. These results define functions for basic fibroblast growth factor and neurotrophins in the differentiation processes that direct a multipotential stem cell to a specific neuronal fate.},
	Author = {Vicario-Abejon, C. and Johe, K. K. and Hazel, T. G. and Collazo, D. and McKay, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {Cell Differentiation/drug effects;Nerve Growth Factors/*pharmacology;Hippocampus/*cytology/drug effects;Rats;C-4;Neurons/cytology/*drug effects;Stem Cells/cytology/drug effects;Brain-Derived Neurotrophic Factor;Neurotrophin 3;Animal;Cell Count;Rats, Sprague-Dawley;Calcium-Binding Protein, Vitamin D-Dependent/drug effects;Fibroblast Growth Factor, Basic/*pharmacology;Nerve Tissue Proteins/drug effects/*pharmacology;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Cells, Cultured/cytology/drug effects;Biological Markers},
	Number = {1},
	Organization = {Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.},
	Pages = {105-14.},
	Title = {Functions of basic fibroblast growth factor and neurotrophins in the differentiation of hippocampal neurons},
	Uuid = {FF169870-A6ED-489A-B864-CAFF6EA9CA9B},
	Volume = {15},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=7619514}}

@article{Vicario-Abejon:1995a,
	Abstract = {During the development of the CNS, a salient issue is whether neuronal phenotype is defined by the lineage or by the environment of precursor cells. Transplants permit these two possibilities to be tested, as cell fate can be examined in a new location. Dissociated cerebellar cells from newborn rats treated with tritiated thymidine or from NSE-lacZ transgenic mice were grafted into the dentate gyrus of the developing hippocampus. Implanted cells integrated into the granule cell layer, which contains the cell bodies of host granule neurons. Immunohistochemistry showed that grafted cells in the granule cell layer, like the host hippocampal granule neurons, were calbindin positive and upregulated FOS in a seizure paradigm. Electron microscopic analysis also showed that cells grafted to the dentate gyrus share features with host dentate neurons. These assays indicate that transplanted cerebellar cells acquired morphological and antigenic features characteristic of hippocampal neurons. These results show that metencephalic precursors are capable of differentiating in response to signals in the telencephalon, suggesting that the environment controls the regional fate of neuronal precursor cells during neurogenesis.},
	Author = {Vicario-Abej{\'o}n, C. and Cunningham, M. G. and McKay, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0270-6474},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;10 Development;Research Support, Non-U.S. Gov't;Rats, Sprague-Dawley;Cell Transplantation;Rats;10 Hippocampus;Hippocampus;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Dentate Gyrus;Cerebellum;Mice, Transgenic;Animals, Newborn;Mice;Animals;Neurons},
	Medline = {96033731},
	Month = {10},
	Nlm_Id = {8102140},
	Number = {10},
	Organization = {Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139, USA.},
	Pages = {6351-63},
	Pubmed = {7472400},
	Title = {Cerebellar precursors transplanted to the neonatal dentate gyrus express features characteristic of hippocampal neurons},
	Uuid = {DB225F9F-D7BC-432D-99B8-CAF1F783FA29},
	Volume = {15},
	Year = {1995}}

@article{Vignery:2000,
	Abstract = {Membrane fusion is a ubiquitous event that occurs in a wide range of biological processes. While intracellular membrane fusion mediating organelle trafficking is well understood, much less is known about cell-cell fusion mediating sperm cell-oocyte, myoblast-myoblast and macrophage-macrophage fusion. In the case of mononuclear phagocytes, their fusion is not only associated with the differentiation of osteoclasts, cells which play a key role in the pathogenesis of osteoporosis, but also of giant cells that are present in chronic inflammatory reactions and in tumours. Despite the biological and pathophysiological importance of intercellular fusion events, the actual molecular mechanism of macrophage fusion is still unclear. One of the main research themes in my laboratory has been to investigate the molecular mechanism of mononuclear phagocyte fusion. Our hypothesis has been that macrophage-macrophage fusion, similar to virus-cell fusion, is mediated by specific cell surface proteins. But, in contrast with myoblasts and sperm cells, macrophage fusion is a rare event that occurs in specific instances. To test our hypothesis, we established an in vitro cell-cell fusion assay as a model system which uses alveolar macrophages. Upon multinucleation, these macrophages acquire the osteoclast phenotype. This indicates that multinucleation of macrophages leads to a specific and novel functional phenotype in macrophages. To identify the components of the fusion machinery, we generated four monoclonal antibodies (mAbs) which block the fusion of alveolar macrophages and purified the unique antigen recognized by these mAbs. This led us to the cloning of MFR (Macrophage Fusion Receptor). MFR was cloned simultaneously as P84/SHPS-1/SIRPalpha/BIT by other laboratories. We subsequently showed that the recombinant extracellular domain of MFR blocks fusion. Most recently, we identified a lower molecular weight form of MFR that is missing two extracellular immunoglobulin (Ig) C domains. Shortly after we cloned MFR, CD47 was reported to be a ligand for P84/SIRPalpha. We have since generated preliminary results which suggest that CD47 interacts with MFR during adhesion/fusion and is a member of the fusion machinery. We also identified CD44 as a plasma membrane protein which, like MFR, is highly expressed at the onset of fusion. The recombinant soluble extracellular domain of CD44 blocks fusion by interacting with a cell-surface binding site. We now propose a model in which both forms of MFR, CD44, and CD47 mediate macrophage adhesion/fusion and therefore the differentiation of osteoclasts and giant cells.},
	Author = {Vignery, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0959-9673},
	Journal = {Int J Exp Pathol},
	Keywords = {Humans;Carrier Proteins;Macrophages;review;Antigens, CD47;Antigens, Differentiation;Antigens, CD;Cell Fusion;Antigens, CD44;Receptors, Immunologic;Giant Cells;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Membrane Glycoproteins;Viral Physiology;Neural Cell Adhesion Molecule L1;24 Pubmed search results 2008;Osteoclasts;Neural Cell Adhesion Molecules},
	Medline = {21094981},
	Month = {10},
	Nlm_Id = {9014042},
	Number = {5},
	Organization = {Yale University School of Medicine, Department of Orthopaedics and Rehabilitation, New Haven, CT 06510, USA. agnes.vignery\@yale.edu},
	Pages = {291-304},
	Pii = {iep164},
	Pubmed = {11168677},
	Title = {Osteoclasts and giant cells: macrophage-macrophage fusion mechanism},
	Uuid = {2AEABBC4-E9E0-11DA-920C-000D9346EC2A},
	Volume = {81},
	Year = {2000},
	url = {papers/Vignery_IntJExpPathol2000.pdf}}

@article{Vignery:2005,
	Abstract = {The fusion of cells is a fundamental biological event that is essential for a variety of developmental and homeostatic processes. Fusion is required for the formation of multinucleated osteoclasts and giant cells, although the mechanisms that govern these processes are poorly understood. A new study now reveals an unexpected role for the receptor, dendritic cell-specific transmembrane protein (DC-STAMP), in this process. The potential mechanism by which DC-STAMP governs fusion and the implications of this finding will be discussed.},
	Author = {Vignery, Agn\`{e}s},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0022-1007},
	Journal = {J Exp Med},
	Keywords = {11 Glia},
	Month = {8},
	Nlm_Id = {2985109R},
	Number = {3},
	Organization = {Yale University School of Medicine, New Haven, CT 06510.},
	Pages = {337-40},
	Pii = {jem.20051123},
	Pubmed = {16061722},
	Title = {Macrophage fusion: the making of osteoclasts and giant cells},
	Uuid = {81CCBB7C-99E0-4320-94C7-F85DD9630C4B},
	Volume = {202},
	Year = {2005},
	url = {papers/Vignery_JExpMed2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1084/jem.20051123}}

@article{Vignery:2005a,
	Abstract = {Macrophages are present in all tissues and can fuse with themselves to differentiate into multinucleate osteoclasts or giant cells that play a central role in osteoporosis and chronic inflammatory diseases, respectively. Yet, the mechanism by which they fuse remains uncharacterized. The macrophage fusion receptor (MFR) and its ligand CD47 might mediate homotypic fusion of macrophages and allow for their recognition as 'self' before fusion. Although a novel process and controversial idea, macrophages might exploit a similar mechanism for fusion with somatic cells or tumor cells, with resultant organ repair or metastasis, respectively. Hence, macrophages might be the 'double-edged swords' of tissues.},
	Author = {Vignery, Agn\`{e}s},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0962-8924},
	Journal = {Trends Cell Biol},
	Keywords = {Membrane Glycoproteins;Cell Fusion;Alpha;Cell Proliferation;Antigens, Differentiation;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Antigens, CD;Tumor Stem Cells;Research Support, N.I.H., Extramural;11 Glia;review, tutorial;Macrophages;Humans;Receptors, Immunologic;review},
	Month = {4},
	Nlm_Id = {9200566},
	Number = {4},
	Organization = {Yale University School of Medicine, Dept of Orthopaedics and Rehabilitation, TMP534, 310 Cedar Street, New Haven CT 06510, USA. agnes.vignery\@yale.edu},
	Pages = {188-93},
	Pii = {S0962-8924(05)00052-8},
	Pubmed = {15817374},
	Title = {Macrophage fusion: are somatic and cancer cells possible partners?},
	Uuid = {6CE27E5F-E9C0-11DA-920C-000D9346EC2A},
	Volume = {15},
	Year = {2005},
	url = {papers/Vignery_TrendsCellBiol2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tcb.2005.02.008}}

@article{Vincent:2002,
	Abstract = {Macrophage colony stimulating factor (M-CSF) is a microglial activator expressed at increased levels in the brain in Alzheimer's disease. In monotypic microglial cultures, M-CSF strongly augments amyloid beta (Abeta) induced microglial production of proinflammatory cytokines and nitric oxide. However, this augmentation could be due to strong autocrine and paracrine effects in monotypic cultures. We used hippocampal organotypic cultures to test M-CSF/Abeta augmentation in a system modeling intact brain. Combined M-CSF/Abeta treatment increased interleukin-1 (IL-1) and macrophage inflammatory protein 1-alpha expression by microglia, whereas inducible nitric oxide synthase (iNOS) expression was localized primarily to astroglia. Induction of cytokines and iNOS was also observed after lipopolysaccharide treatment of organotypic hippocampal cultures, but iNOS expression was localized mainly to microglia rather than astrocytes. Treatment with M-CSF/Abeta did not result in neuronal death. These results demonstrate that combined M-CSF/Abeta treatment results in a strong inflammatory response in the organotypic environment without inducing neurotoxicity.},
	Author = {Vincent, Valerie A. M. and Selwood, Simon P. and Murphy, Greer M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0197-4580},
	Journal = {Neurobiol Aging},
	Keywords = {Animals;Astrocytes;Amyloid beta-Protein;Rats;Comparative Study;Adjuvants, Immunologic;Microglia;Enzyme Induction;Lipopolysaccharides;Rats, Sprague-Dawley;Hippocampus;Drug Combinations;11 Glia;Nitric-Oxide Synthase;RNA, Messenger;Support, Non-U.S. Gov't;Peptide Fragments;Neurons;Interleukin-1;Support, U.S. Gov't, P.H.S.;Macrophage Colony-Stimulating Factor;Macrophage Inflammatory Protein-1;Interleukin-6;Inflammation;Cell Death;Organ Culture;Nitric Oxide},
	Medline = {21956959},
	Nlm_Id = {8100437},
	Number = {3},
	Organization = {Department of Psychiatry and Behavioral Sciences, Neuroscience Research Laboratories, Stanford University School of Medicine, Stanford, CA 94305-5485, USA.},
	Pages = {349-62},
	Pii = {S0197458001003384},
	Pubmed = {11959396},
	Title = {Proinflammatory effects of M-CSF and A beta in hippocampal organotypic cultures},
	Uuid = {B957C0EA-922C-4CB1-84CF-44BB6C194D31},
	Volume = {23},
	Year = {2002}}

@article{Virag:2003,
	Abstract = {Granulation tissue formation is a critical step in infarct repair, however, the kinetics of cell replication and the molecules that regulate this process are poorly understood. In uninjured mouse hearts and at 2 days post-infarction, very little DNA synthesis (measured by incorporation of a BrdU pulse) was detected in any cell type. Four days after permanent coronary occlusion, the rates of myofibroblast (smooth muscle alpha-actin and BrdU double-positive) and endothelial cell (CD31 and BrdU double-positive) proliferation were 15.4 +/- 1.1\%and 2.9 +/- 0.5\%, respectively. Most proliferating cells were located at the interface of the infarct and viable tissue. By 1 week, fibroblast and endothelial cell proliferation declined to 4.1 +/- 0.6\%and 0.7 +/- 0.1\%, respectively. In the 2-week infarct, the remaining necrosis had been phagocytosed, and fibroblast and endothelial cell proliferation were <0.5\%. Although leukocytes were abundant throughout infarct repair, no significant proliferation was detected at any time in cells expressing CD45 or mac-3. Infarct size at 4 days was 38 +/- 5\%of the left ventricle and contracted to 20 +/- 4\%by 4 weeks. After 4 days, the chamber dilated to four times that of the control hearts and remained so for the duration of the time course. The vascular density (per mm(2)) declined from 3643 +/- 82 in control hearts to 2716 +/- 197 at 1 week and 1010 +/- 47 at 4 weeks post-myocardial infarction (MI). The average percent area occupied by vessels did not change significantly between the groups but the area/vessel ( micro m(2)) increased from 14.1 +/- 0.3 in control hearts to 16.9 +/- 1.9 at 1 week and 38.7 +/- 7.9 at 4 weeks post-MI. These data indicate that mitogens for fibroblasts and endothelial cells peak within 4 days of infarction in the mouse heart. This provides the basis for identifying the responsible molecules and developing strategies to alter wound repair and improve cardiac function. 0002-9440 Journal Article},
	Author = {Virag, J. I. and Murry, C. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Am J Pathol},
	Keywords = {EE;Muscle, Smooth/*pathology;Endothelial Cells/pathology;08 Aberrant cell cycle;Time Factors;Cell Division;Mice, Inbred C57BL;Myocardium/*pathology;Chronic Disease;*Wound Healing;Support, U.S. Gov't, P.H.S.;Animals;Mice;Leukocytes/pathology;Fibroblasts/*pathology;Myocardial Infarction/*pathology/*physiopathology},
	Number = {6},
	Organization = {Department of Pathology, University of Washington, Seattle, Washington 98195, USA.},
	Pages = {2433-40},
	Pubmed = {14633615},
	Title = {Myofibroblast and endothelial cell proliferation during murine myocardial infarct repair},
	Uuid = {8DC42CD4-49A0-4A95-BD3E-DA8B7109291F},
	Volume = {163},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14633615}}

@article{Vitry:2003,
	Abstract = {Finding ways to enhance remyelination is a major challenge in treating demyelinating diseases. Recent studies have suggested that circulating bone marrow cells can home in brain and transdifferentiate into neural cells. To ask whether hematopoietic precursors can form myelinating cells, we investigated the neuropoietic potential of embryonic precursors sorted from the mouse aorta-gonads-mesonephros (AGM) region. This cell fraction is capable of long-term hematopoietic reconstitution and generates colonies containing multipotential precursors and lymphoid or erythro-myeloid progenies. When cultured in hematopoietic growth conditions, a fraction of CD45-positive AGM cells coexpress neural markers such as nestin, the polysialylated form of neural cell adhesion molecule, the betaIII tubulin isoform, and glial fibrillary acidic protein. However, when hematopoietic precursors containing green fluorescent protein were cocultured with embryonic striatal precursors into neurospheres, they maintained their hematopoietic phenotype without undergoing differentiation into neurons, astrocytes, or oligodendrocytes. After intraventricular grafting, hematopoietic precursors integrated into the brain of wild-type or hypomyelinated newborn shiverer mice and gave rise to microglia but not neurons or glia. In contrast, when wild-type embryonic striatal neurospheres were grafted in shiverer, they formed numerous myelin internode patches. Even when neural and hematopoietic precursors were grafted together into shiverer mice, only neural precursors generated myelin-forming cells and synthesized myelin. Thus, embryonic neurospheres have myelin repair properties not shown by embryonic hematopoietic precursors. This suggests that the use of multipotential neural precursors to generate myelin-forming cells remains one of the most promising avenues toward remyelination therapies.},
	Author = {Vitry, Sandrine and Bertrand, Julien Y. and Cumano, Ana and Dubois-Dalcq, Monique},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Cell Culture Techniques;Myelin Sheath;Cells, Cultured;Gonads;Mesonephros;Animals;Cell Separation;Antigens, Differentiation;Mice, Inbred C3H;Female;Microglia;Mice, Transgenic;Mice, Inbred C57BL;Mice, Neurologic Mutants;Oligodendroglia;Crosses, Genetic;Male;Aorta;Hematopoietic Stem Cell Transplantation;Animals, Newborn;Neurons;Flow Cytometry;Hematopoietic Stem Cells;Mice;24 Pubmed search results 2008;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {22989858},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {33},
	Organization = {Unit{\'e} de Neurovirologie et R{\'e}g{\'e}n{\'e}ration du Syst\`{e}me Nerveux Centre National de la Recherche Scientifique 1961, Institut Pasteur, 75724, Paris, Cedex 15, France.},
	Pages = {10724-31},
	Pii = {23/33/10724},
	Pubmed = {14627658},
	Title = {Primordial hematopoietic stem cells generate microglia but not myelin-forming cells in a neural environment},
	Uuid = {153FF7C6-93F4-474C-B0F4-B06FEDF89C5E},
	Volume = {23},
	Year = {2003}}

@article{Vives:2003,
	Abstract = {S100B, the EF-hand Ca(++)-binding protein with gliotrophic and neurotrophic properties implicated in the pathogenesis of Alzheimer's disease, is coined as a glial marker, despite its documented presence in rodent brain neurons. We have generated a transgenic mouse whose EGFP reporter, controlled by the -1,669/+3,106 sequence of the murine S100B gene, allows the direct microscopic observation of most S100B-expressing cells in the central nervous system (CNS). From embryonic day 13 onward, EGFP expression was targeted to selected neuroepithelial, glial, and neuronal cells, indicating that cell-specific expression of S100B is regulated at the transcriptional level during development. In adult mice, the highest level of EGFP expression was found in ependymocytes; astrocytes; and spinal, medullar, pontine, and deep cerebellar S100B neurons. Our results, thus, agree with earlier reports suggesting that S100B is not a CNS glial-specific marker. In addition, we detected EGFP and S100B in forebrain neurons previously thought not to express S100B in the mouse, including neurons of primary motor and somatosensory neocortical areas, the ventral pallidum and prerubral field. Another interesting finding was the selected EGFP targeting to neonatal S100B oligodendrocytes and adult NG2 progenitors as opposed to mature S100B oligodendrocytes. This finding suggests that, except for oligodendrocytes at the last stage of myelin maturation, the -1,669/+3,106 sequence of the S100B gene is a useful reagent for driving expression of transgenes in most S100B-expressing cells of mouse brain. 0021-9967 Journal Article},
	Author = {Vives, V. and Alonso, G. and Solal, A. C. and Joubert, D. and Legraverend, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Comp Neurol},
	Keywords = {02 Adult neurogenesis migration;Nerve Growth Factors/*metabolism;Neurons/*metabolism;BB pdf;03 Adult neurogenesis progenitor source;Central Nervous System/*metabolism;Neuroglia/*metabolism;Mice, Transgenic;Luminescent Proteins/genetics/*metabolism;S100 Proteins/*metabolism;Fluorescent Antibody Technique;Blotting, Western;Animals;Support, Non-U.S. Gov't;Mice},
	Number = {4},
	Organization = {Institut National de la Sante et de la Recherche Medicale U469, Centre CNRS-INSERM de Pharmacologie et d'Endocrinologie, F-34094 Montpellier Cedex 05, France.},
	Pages = {404-19},
	Pubmed = {12561079},
	Title = {Visualization of S100B-positive neurons and glia in the central nervous system of EGFP transgenic mice},
	Uuid = {97243622-E035-4D16-B39B-71D05CF0EB1F},
	Volume = {457},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12561079}}

@article{Wagers:2004,
	Abstract = {Recent years have seen much excitement over the possibility that adult mammalian stem cells may be capable of differentiating across tissue lineage boundaries, and as such may represent novel, accessible, and very versatile effectors of therapeutic tissue regeneration. Yet studies proposing such "plasticity"of adult somatic stem cells remain controversial, and in general, existing evidence suggests that in vivo such unexpected transformations are exceedingly rare and in some cases can be accounted for by equally unexpected alternative explanations. 0092-8674 Journal Article},
	Author = {Wagers, A. J. and Weissman, I. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Cell},
	Keywords = {22 Stem cells;S pdf},
	Number = {5},
	Organization = {Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. awagers\@stanford.edu},
	Pages = {639-48},
	Title = {Plasticity of adult stem cells},
	Uuid = {F8F1B3E8-9F63-11DA-8D49-000D9346EC2A},
	Volume = {116},
	Year = {2004},
	url = {papers/Wagers_Cell2004.pdf}}

@article{Wagner:1999,
	Abstract = {Mounting evidence indicates that extracellular factors exert proliferative effects on neurogenetic precursors in vivo. Recently we found that systemic levels of basic fibroblast growth factor (bFGF) regulate neurogenesis in the brain of newborn rats, with factors apparently crossing the blood-brain barrier (BBB) to stimulate mitosis. To determine whether peripheral bFGF affects proliferation during adulthood, we focused on regions in which neurogenesis persists into maturity, the hippocampus and the forebrain subventricular zone (SVZ). In postnatal day 1 (P1) rats, 8 hr after subcutaneous injection (5 ng/gm body weight), bFGF increased [(3)H]thymidine incorporation 70\%in hippocampal and SVZ homogenates and elicited twofold increases in mitotic nuclei in the dentate gyrus and the dorsolateral SVZ, detected by bromodeoxyuridine immunohistochemistry. Because approximately 25\%of proliferating hippocampal cells stimulated in vivo expressed neuronal traits in culture, bFGF-induced mitosis may reflect increased neurogenesis. bFGF effects were not restricted to the perinatal period; hippocampal DNA synthesis was stimulated by peripheral factor in older animals (P7-P21), indicating the persistence of bFGF-responsive cells and activity of peripheral bFGF into late development. To begin defining underlying mechanisms, pharmacokinetic studies were performed in P28 rats; bFGF transferred from plasma to CSF rapidly, levels rising in both compartments in parallel, indicating that peripheral factor crosses the BBB during maturity. Consequently, we tested bFGF in adults; peripheral bFGF increased the number of mitotic nuclei threefold in the SVZ and olfactory tract, regions exhibiting persistent neurogenesis. Our observations suggest that bFGF regulates ongoing neurogenesis via a unique, endocrine-like pathway, potentially coordinating neuron number and body growth, and potentially providing new approaches for treating damaged brain during development and adulthood.},
	Author = {Wagner, J. P. and Black, I. B. and DiCicco-Bloom, E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Neurosci},
	Keywords = {C-11;Fibroblast Growth Factor, Basic/administration &dosage/*pharmacology;Hippocampus/cytology/drug effects/growth &development;Cells, Cultured;Aging;Rats;Microtubule-Associated Proteins/analysis;Thymidine/metabolism;Neurons/cytology/*drug effects;Mitosis;Animal;Rats, Sprague-Dawley;Glial Fibrillary Acidic Protein/analysis;Prosencephalon/cytology/drug effects;Cattle;Animals, Newborn;Injections, Subcutaneous;Brain/cytology/*drug effects/growth &development;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Cell Division/drug effects},
	Number = {14},
	Organization = {Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.},
	Pages = {6006-16.},
	Title = {Stimulation of neonatal and adult brain neurogenesis by subcutaneous injection of basic fibroblast growth factor},
	Uuid = {FD1BBD1E-0F76-4F67-B2A2-73BE3EF82AFE},
	Volume = {19},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10407038%20http://www.jneurosci.org/cgi/content/full/19/14/6006%20http://www.jneurosci.org/cgi/content/abstract/19/14/6006}}

@article{Wahlers:2001,
	Abstract = {Using retroviral vectors encoding enhanced green fluorescent protein (EGFP), we addressed to what extent expression of retroviral transgenes in hematopoietic cells depends on the multiplicity of infection (MOI) and on the half-life of the encoded protein. We show that an elevation of the MOI not only elevates the frequency of transduced cells, but also increases transgene expression levels and reduces interanimal variability in vivo (hematopoietic cells of C57BL/6J mice analyzed 13 weeks after transplantation). This suggests that the MOI has to be carefully controlled and should be adapted as desired for clinical studies when evaluating vector performance in preclinical models. The impact of protein stability is demonstrated by comparing vectors expressing EGFP or a destabilized variant with a C-terminal PEST-sequence, d2EGFP. The loss of expression with d2EGFP was more pronounced in terminally differentiated cells of the peripheral blood (>30 fold) than in progenitor cells (five- to 10-fold), indicating a stronger transcription of the retroviral promoter in progenitor cells and a predominant role of protein inheritance over de novo synthesis of transgenic protein in mature blood cells. This analysis reveals an important and differentiation-dependent contribution of protein half-life to the expression of retroviral vectors in hematopoietic cells, establishes d2EGFP as a more accurate reporter for determination of vector transcription, and also suggests that preclinical data obtained under conditions of high transduction rates or with vectors expressing stable reporter proteins require careful interpretation.},
	Author = {Wahlers, A. and Schwieger, M. and Li, Z. and Meier-Tackmann, D. and Lindemann, C. and Eckert, H. G. and von Laer, D. and Baum, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {T-Lymphocytes;Transcription, Genetic;Animals;Humans;Mice, Inbred C57BL;Retroviridae;Antigens, CD34;11 Glia;Time Factors;Green Fluorescent Proteins;Genetic Vectors;Half-Life;Bone Marrow Cells;Gene Therapy;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Gene Expression;Research Support, Non-U.S. Gov't},
	Medline = {21214797},
	Month = {3},
	Nlm_Id = {9421525},
	Number = {6},
	Organization = {Department Cell and Virus Genetics, Heinrich-Pette-Institute, Hamburg, Germany.},
	Pages = {477-86},
	Pubmed = {11313827},
	Title = {Influence of multiplicity of infection and protein stability on retroviral vector-mediated gene expression in hematopoietic cells},
	Uuid = {8A80C570-12D8-4309-9B55-74A834F9CB2E},
	Volume = {8},
	Year = {2001},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/sj/gt/3301426}}

@article{Wakselman:2008,
	Abstract = {In several brain regions, microglia actively promote neuronal apoptosis during development. However, molecular actors leading microglia to trigger death remain mostly unknown. Here, we show that, in the developing hippocampus, apoptotic neurons are contacted by microglia expressing both the integrin CD11b and the immunoreceptor DAP12. We demonstrate that developmental apoptosis decreases in mice deficient for CD11b or DAP12. In addition, function-blocking antibodies directed against CD11b decrease neuronal death when injected into wild-type neonates, but have no effect when injected into DAP12-deficient littermates. This demonstrates that DAP12 and CD11b act in converging pathways to induce neuronal death. Finally, we show that DAP12 and CD11b control the production of microglial superoxide ions, which kill the neurons. Thus, our data show that the process of developmental neuronal death triggered by microglia is similar to the elimination of pathogenic cells by the innate immune cells.},
	Author = {Wakselman, Shirley and B{\'e}chade, Catherine and Roumier, Anne and Bernard, Delphine and Triller, Antoine and Bessis, Alain},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008;research support, non-u.s. gov't;Mice, Knockout;Immunity, Natural;Cell Communication;Hippocampus;Apoptosis;Mice, Mutant Strains;Adaptor Proteins, Signal Transducing;Antigens, CD11b;Microglia;Animals;Mice;Superoxides;Neurons;Receptors, Immunologic},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {32},
	Organization = {Laboratoire de Biologie Cellulaire de la Synapse, Institut National de Sant{\'e} et de Recherche M{\'e}dicale, Unit{\'e} 789, 75230 Paris Cedex 05, France.},
	Pages = {8138-43},
	Pii = {28/32/8138},
	Pubmed = {18685038},
	Title = {Developmental neuronal death in hippocampus requires the microglial CD11b integrin and DAP12 immunoreceptor},
	Uuid = {24CD4BEB-E75B-43F4-A4C6-0A03BAC6C81F},
	Volume = {28},
	Year = {2008},
	url = {papers/Wakselman_JNeurosci2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1006-08.2008}}

@article{Walczak:2004,
	Abstract = {Hematopoietic progenitors are cells, which under challenging experimental conditions can develop unusual phenotypic properties, rather distant from their original mesodermal origin. As previously reported, cells derived from human umbilical cord blood (HUCB) or human bone marrow (BM) under certain in vivo or in vitro conditions can manifest neural features that resemble features of neural-derived cells, immunocytochemically and in some instances also morphologically. The present study explored how hematopoietic-derived cells would respond to neurogenic signals from the subventricular zone (SVZ) of adult and aged (6 and 16 months old) rats. The mononuclear fraction of HUCB cells was transplanted into the SVZ of immunosuppressed (single cyclosporin or three-drug treatment) animals. The triple-suppression paradigm allowed us to protect transplanted human cells within the brain and to explore further their phenotypic and migratory properties. One week after implantation, many surviving HUCB cells were located within the SVZ and the vertical limb of the rostral migratory stream (RMS). The migration of HUCB cells was restricted exclusively to the pathway leading to the olfactory bulb. In younger animals, grafted cells navigated almost halfway through the vertical limb, whereas, in the older animals, the migration was less pronounced. The overall cell survival was greater in younger animals than in older ones. Immunocytochemistry for surface CD antigen expression showed that many HUCB cells, either cultured or within the brain parenchyma, retained their hematopoietic identity. A few cells, identified by using human-specific antibodies (anti-human nuclei, or mitochondria) expressed nestin and doublecortin, markers of endogenous neural progenitors. Therefore, it is believed that the environment of the neurogenic SVZ, even in aged animals, was able to support survival, "neuralization," and migratory features of HUCB-derived cells.},
	Author = {Walczak, P. and Chen, N. and Hudson, J. E. and Willing, A. E. and Garbuzova-Davis, S. N. and Song, S. and Sanberg, P. R. and Sanchez-Ramos, J. and Bickford, P. C. and Zigova, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Differentiation;Cerebral Ventricles;Cell Survival;Immunohistochemistry;Green Fluorescent Proteins;Luminescent Proteins;Antigens, CD45;Male;Animals;Cells, Cultured;Age Factors;Environment;Research Support, U.S. Gov't, P.H.S.;Cell Movement;Phenotype;Cell Count;Antigens, CD;Mice, Inbred C57BL;Hematopoietic Stem Cells;Tubulin;Immunosuppressive Agents;11 Glia;Multipotent Stem Cells;Antigens, Neoplasm;Blood Proteins;Comparative Study;Rats, Inbred F344;Membrane Glycoproteins;Antigens, Surface;Glial Fibrillary Acidic Protein;Indoles;Rats;Bone Marrow Cells;Avian Proteins;Mice;Research Support, Non-U.S. Gov't;Neurons;Humans;Mice, Transgenic;Cord Blood Stem Cell Transplantation},
	Month = {4},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Center of Excellence for Aging and Brain Repair, Department of Neurosurgery, University of South Florida College of Medicine, Tampa, Florida 33612, USA. pwalczak\@hsc.usf.edu},
	Pages = {244-54},
	Pubmed = {15048922},
	Title = {Do hematopoietic cells exposed to a neurogenic environment mimic properties of endogenous neural precursors?},
	Uuid = {EBB68EBA-EC4B-479B-954F-7C8C414CA2BF},
	Volume = {76},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20042}}

@article{Walker:1999,
	Abstract = {The brain contains two populations of macrophages: the microglia of brain parenchyma, and the central nervous system (CNS) macrophages located in the perivascular spaces, the leptomeninges and the choroid plexus. The microglia are characterized, in part, by their paucity of major histocompatibility complex (MHC) molecules and lack of constitutive antigen (Ag)-presenting activity for na{\"\i}ve CD4+ T-cells. Some CNS macrophages, on the other hand, constitutively express MHC molecules and present Ag to na{\"\i}ve CD4+ T-cells. We have reported that mouse brain contains precursor cells that, in the presence of colony-stimulating factor-1, the macrophage growth factor, give rise to clones of cells that differ in their ability to constitutively present Ag to naive CD4+ T cells. Here we report that this population of precursor cells can be separated into two discrete subpopulations based on differences in cell density and that the two cell populations give rise to progeny that differ in their content of cells constitutively expressing MHC class II and CD86 molecules, and the ability to present Ag to na{\"\i}ve CD4+ T-cells. A comparison of the level of CD45 staining of the progeny, an indication of a microglial or a CNS macrophage origin, suggests that one population of precursor cells yields immunologically immature microglia and the other CNS macrophages.},
	Author = {Walker, W. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Neuroimmunomodulation;Antigens, CD45;Animals;Cell Separation;Macrophages;Brain;Microglia;Mice, Inbred C3H;Antigens, CD;Mice, Transgenic;11 Glia;Immunophenotyping;Research Support, U.S. Gov't, P.H.S.;Membrane Glycoproteins;Antibodies, Monoclonal;Antigen Presentation;Hematopoietic Stem Cells;CD4-Positive T-Lymphocytes;Mice;Clone Cells;Spleen;Histocompatibility Antigens Class II;Research Support, Non-U.S. Gov't},
	Medline = {99303438},
	Month = {2},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105-2794, USA. bill.walker\@st.jude.org},
	Pages = {127-33},
	Pubmed = {10376945},
	Title = {Separate precursor cells for macrophages and microglia in mouse brain: immunophenotypic and immunoregulatory properties of the progeny},
	Uuid = {323F4DB7-5239-4E0A-8F72-031FDB5CE398},
	Volume = {94},
	Year = {1999}}

@article{Walker:2007,
	Abstract = {Doublecortin (DCX) has recently been promulgated as a selective marker of cells committed to the neuronal lineage in both the developing and the adult brain. To explore the potential of DCX-positive (DCX+) cells more stringently, these cells were isolated by flow cytometry from the brains of transgenic mice expressing green fluorescent protein under the control of the DCX promoter in embryonic, early postnatal, and adult animals. It was found that virtually all of the cells (99.9\%) expressing high levels of DCX (DCX(high)) in the embryonic brain coexpressed the neuronal marker betaIII-tubulin and that this population contained no stem-like cells as demonstrated by lack of neurosphere formation in vitro. However, the DCX+ population from the early postnatal brain and the adult subventricular zone and hippocampus, which expressed low levels of DCX (DCX(low)), was enriched for neurosphere-forming cells, with only a small subpopulation of these cells coexpressing the neuronal markers betaIII-tubulin or microtubule-associated protein 2. Similarly, the DCX(low) population from embryonic day 14 (E14) brain contained neurosphere-forming cells. Only the postnatal cerebellum and adult olfactory bulb contained some DCX(high) cells, which were shown to be similar to the E14 DCX(high) cells in that they had no stem cell activity. Electrophysiological studies confirmed the heterogeneous nature of DCX+ cells, with some cells displaying characteristics of immature or mature neurons, whereas others showed no neuronal characteristics whatsoever. These results indicate that DCX(high) cells, regardless of location, are restricted to the neuronal lineage or are bone fide neurons, whereas some DCX(low) cells retain their multipotentiality.},
	Author = {Walker, Tara L. and Yasuda, Takahiro and Adams, David J. and Bartlett, Perry F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;02 Adult neurogenesis migration;research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {Queensland Brain Institute, The University of Queensland, Brisbane, Queensland 4072, Australia.},
	Pages = {3734-42},
	Pii = {27/14/3734},
	Pubmed = {17409237},
	Title = {The doublecortin-expressing population in the developing and adult brain contains multipotential precursors in addition to neuronal-lineage cells},
	Uuid = {ECF0D1B3-7FC5-4B75-87DD-D16C57475BE2},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.5060-06.2007}}

@article{Walsh:1998,
	Author = {Walsh, C. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1061-4036},
	Journal = {Nat Genet},
	Keywords = {Mice;Microtubule-Associated Proteins;Proteins;Mice, Knockout;10 Development;21 Neurophysiology;21 Dysplasia-heterotopia;24 Pubmed search results 2008;Abnormalities, Multiple;comment;1-Alkyl-2-acetylglycerophosphocholine Esterase;Animals;Disease Models, Animal;Cerebral Cortex;Humans;news},
	Month = {8},
	Nlm_Id = {9216904},
	Number = {4},
	Pages = {307-8},
	Pubmed = {9697681},
	Title = {LISsen up!},
	Uuid = {9A52B650-A150-411B-8F7E-D0CEDCFFD70C},
	Volume = {19},
	Year = {1998},
	url = {papers/Walsh_NatGenet1998.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/1186}}

@article{Walton:2006,
	Abstract = {Microglia are increasingly implicated as a source of non-neural regulation of postnatal neurogenesis and neuronal development. To evaluate better the contributions of microglia to neural stem cells (NSCs) of the subventricular neuraxis, we employed an adherent culture system that models the continuing proliferation and differentiation of the dissociated neuropoietic subventricular tissues. In this model, neuropoietic cells retain the ability to self-renew and form multipotent neurospheres, but progressively lose the ability to generate committed neuroblasts with continued culture. Neurogenesis in highly expanded NSCs can be rescued by coculture with microglial cells or microglia-conditioned medium, indicating that microglia provide secreted factor(s) essential for neurogenesis, but not NSC maintenance, self-renewal, or propagation. Our findings suggest an instructive role for microglial cells in contributing to postnatal neurogenesis in the largest neurogenic niche of the mammalian brain. (c) 2006 Wiley-Liss, Inc.},
	Author = {Walton, and Sutter, and Laywell, and Levkoff, and Kearns, and Marshall, and Scheffler, and Steindler,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {14 Immune;11 Glia;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {8806785},
	Number = {8},
	Organization = {Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, Florida.},
	Pages = {815-825},
	Pubmed = {16977605},
	Title = {Microglia instruct subventricular zone neurogenesis},
	Uuid = {BC51FD76-894E-4B57-AF26-AC0304A877FD},
	Volume = {54},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20419}}

@article{Wang:1997,
	Abstract = {Glutamate metabotropic receptor mediated mechanisms have been implicated in both neuroprotection and neurotoxicity. To characterize these mechanisms further in vivo, the effects of an intrastriatally injected metabotropic receptor agonist, trans-(1S,3R)-1-amino-1,3- cyclopentanedicarboxylic acid (1S,3R-ACPD), were studied alone and together with N-methyl-D-aspartate (NMDA) or kainic acid (KA) receptor agonists on DNA fragmentation and nerve cell death. 1S,3R-ACPD induced internucleosomal DNA fragmentation of striatal cells in a dose- dependent manner. TUNEL and propidium iodide staining showed DNA fragmentation and profound nuclear condensation around the injection site. Fragmented nuclei were occasionally seen under light microscopy. Internucleosomal DNA fragmentation induced by 1S,3R-ACPD was attenuated by the protein synthesis inhibitor cycloheximide as well as by the non- selective and selective metabotropic receptor antagonists L-(+)-2-amino- 3-phosphonopionic acid (L-AP3), (RS)-aminoindan-1,5-dicarboxylic acid and (RS)-alpha-methylserine-o-phosphate monophenyl ester, respectively. The 1S,3R-ACPD (100-900 nmol) induced death of striatal neurons was suggested by the reduction in NMDA and D1 dopamine receptors by up to 13\%(P <0.05) and 20\%(P <0.05) as well as by the decline in GAD67 mRNA (25\%, P <0.01) and proenkephalin mRNA levels (35\%, P <0.01). Interestingly, 1S,3R-ACPD attenuated internucleosomal DNA fragmentation induced by NMDA, but potentiated that induced by KA. These results suggest that metabotropic receptor stimulation leads to the death of striatal neurons by a mechanism having the biochemical stigmata of apoptosis. Moreover, metabotropic receptor stimulation evidently exerts opposite effects on pre- or postsynaptic mechanisms contributing to the NMDA and KA-induced apoptotic-like death of these neurons.},
	Author = {Wang, Y. and Qin, Z. H. and Nakai, M. and Chase, T. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Brain Res},
	Keywords = {Alanine/analogs &derivatives/pharmacology;Neurotoxins/*toxicity;Rats;Excitatory Amino Acid Antagonists/pharmacology;07 Excitotoxicity Apoptosis;Electrophoresis, Agar Gel;Animal;Rats, Sprague-Dawley;Receptors, Metabotropic Glutamate/*agonists;In Situ Hybridization;E-6;Nucleosomes/*drug effects;Cell Death/drug effects;Protein Synthesis Inhibitors/pharmacology;Cycloleucine/*analogs &derivatives/toxicity;Autoradiography;*DNA Fragmentation;Histocytochemistry/methods},
	Number = {1-2},
	Organization = {Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892-1406, USA.},
	Pages = {45-56.},
	Title = {Glutamate metabotropic receptor agonist 1S,3R-ACPD induces internucleosomal DNA fragmentation and cell death in rat striatum},
	Uuid = {669F7C41-F6D9-4D3C-8F11-FDCF8C3BF5FB},
	Volume = {772},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9406954}}

@article{Wang:2007,
	Abstract = {Human type 1 lissencephaly is a severe brain malformation associated with cognitive dysfunction and intractable epilepsy. Mutant mice with a heterozygous deletion of LIS1 show varying degrees of hippocampal abnormality and enhanced excitability. Whether a reduction of LIS1 function affects adult hippocampal neurogenesis, and if so, whether aberrant neurogenesis contributes to the generation of a disorganized hippocampus remain unknown. Previous reports indicate the presence of multiple pyramidal cell layers and granule cell dispersion in LIS1 mutant mice. Here we observed disruption of the subgranular zone and glial fibrillary acidic protein-immunoreactive radial astrocytes in the dentate gyrus of adult LIS1 mice. Using pulse-chase bromodeoxyuridine (BrdU) labeling combined with neuronal and glial antibody staining we provide evidence for ectopic adult neurogenesis in LIS1 mice. A gradually decreased survival rate for these newborn granule cells was also demonstrated in LIS1 mice 7 days after BrdU injection. This reduced survival rate was associated with impaired neuronal differentiation 28 days after BrdU administration. Thus, LIS1 haploinsufficiency can lead to abnormal cell proliferation, migration and differentiation in the adult dentate gyrus.},
	Author = {Wang, Yanling and Baraban, Scott C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Nlm_Id = {7809375},
	Number = {1-2},
	Organization = {Epilepsy Research Laboratory in the Department of Neurological Surgery and PIBS Graduate Program in Neuroscience, University of California, San Francisco, San Francisco, CA 94143, USA.},
	Pages = {91-8},
	Pii = {DNE20070291_2091},
	Pubmed = {17148952},
	Title = {Granule cell dispersion and aberrant neurogenesis in the adult hippocampus of an LIS1 mutant mouse},
	Uuid = {78F60B17-E715-45E1-913B-611694FD8901},
	Volume = {29},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000096214}}

@article{Wang:1996,
	Abstract = {The present study examined the expression of different antigens in amoeboid microglial cells (AMC) in fetal rat brain extending from 12 to 20 d postconception (E12-E20) using a panel of monoclonal antibodies which recognised the major histocompatibility complex (MHC) class I (OX-18) and class II (OX-6) antigens, leucocyte common antigen (OX-1), CD4 receptor (OX-35), complement type 3 receptor (OX-42) or macrophage antigens of unknown function (ED1 and ED2). Of the above-mentioned antigens, ED1 and ED2-labelled AMC were observed in the neuroepithelia as early as embryonic day 12 (E12); other antigens were not detected at this stage. At E14, except for MHC class I antigen, all other antigens were expressed by AMC distributed predominantly in the developing white matter. At E16, AMC in the intermediate zone lateral to the striatum were endowed with all the above-mentioned antigens including MHC class I. At E18, the immunoreactivities of AMC stained with OX-6, OX-18, OX-35 and OX-42 antigens were noticeably reduced when compared with those cells at E16. At E20, amoeboid microglial cells exhibited full complement of antigen expression similar to those cells at E16; some of the labelled cells emitted a variable number of cytoplasmic processes. It is suggested that the successive and differential expression of various macrophage related antigens on AMC in fetal brain is related to the specific requirement of local environment in different stages of development.},
	Author = {Wang, C. C. and Wu, C. H. and Shieh, J. Y. and Wen, C. Y. and Ling, E. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0021-8782},
	Journal = {J Anat},
	Keywords = {Gestational Age;Immunophenotyping;Rats;Macrophage-1 Antigen;Histocompatibility Antigens Class II;Not relevant;Antigens, CD45;Antigens;11 Glia;Antigens, CD4;Macrophages;Microglia;Histocompatibility Antigens Class I;Support, Non-U.S. Gov't;Brain;Animals;G},
	Medline = {97137495},
	Month = {12},
	Nlm_Id = {0137162},
	Organization = {Department of Anatomy, College of Medicine, National Taiwan University, Taipei.},
	Pages = {567-74},
	Pubmed = {8982832},
	Title = {Immunohistochemical study of amoeboid microglial cells in fetal rat brain},
	Uuid = {6B98C3D3-EE25-11DA-8605-000D9346EC2A},
	Volume = {189 ( Pt 3)},
	Year = {1996}}

@article{Wang:2003,
	Abstract = {Previous studies have reported the presence of neuronal progenitors in the subventricular zone (SVZ) and rostral migratory stream (RMS) of the postnatal mammalian brain. Although many studies have examined the survival and migration of progenitors after transplantation and the factors influencing their proliferation or differentiation, no information is available on the electrophysiological properties of these progenitors in a near-intact environment. Thus we performed whole cell and cell-attached patch-clamp recordings of progenitors in brain slices containing either the SVZ or the RMS from postnatal day 15 to day 25 mice. Both regions displayed strong immunoreactivity for nestin and neuron-specific class III beta-tubulin, and recorded cells displayed a morphology typical of the neuronal progenitors known to migrate throughout the SVZ and RMS to the olfactory bulb. Recorded progenitors had depolarized zero-current resting potentials (mean more depolarized than -28 mV), very high input resistances (about 4 GOmega), and lacked action potentials. Using the reversal potential of K+ currents through a cell-attached patch a mean resting potential of -59 mV was estimated. Recorded progenitors displayed Ca2+-dependent K+ currents and TEA-sensitive-delayed rectifying K+ (KDR) currents, but lacked inward K+ currents and transient outward K+ currents. KDR currents displayed classical kinetics and were also sensitive to 4-aminopyridine and alpha-dendrotoxin, a blocker of Kv1 channels. Na+ currents were found in about 60\%of the SVZ neuronal progenitors. No developmental changes were observed in the passive membrane properties and current profile of neuronal progenitors. Together these data suggest that SVZ neuronal progenitors display passive membrane properties and an ionic signature distinct from that of cultured SVZ neuronal progenitors and mature neurons. 0022-3077 Journal Article},
	Author = {Wang, D. D. and Krueger, D. D. and Bordey, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {J Neurophysiol},
	Keywords = {Lateral Ventricles/drug effects/*growth &development;01 Adult neurogenesis general;Stem Cells/drug effects/*physiology;Support, U.S. Gov't, P.H.S.;Neurons/drug effects/*physiology;Animals, Newborn;Ion Channels/physiology;In Vitro;Biophysics;Corpus Striatum/drug effects/*growth &development;Calcium/pharmacology/physiology;Corpus Callosum/drug effects/*growth &development;Support, Non-U.S. Gov't;Animals;Mice;A pdf},
	Number = {4},
	Organization = {Department of Neurosurgery and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520-8082, USA.},
	Pages = {2291-302},
	Pubmed = {12801891},
	Title = {Biophysical properties and ionic signature of neuronal progenitors of the postnatal subventricular zone in situ},
	Uuid = {67D1AD48-4093-4DAB-90E2-0865A87749B5},
	Volume = {90},
	Year = {2003},
	url = {papers/Wang_JNeurophysiol2003.pdf}}

@article{Wang:1999,
	Abstract = {We report that neurons in the central nervous system express colony stimulating factor-1 receptor (CSF-1R) mRNA and protein and that the expression has regional specificity. The presence of CSF-1R in neurons was demonstrated by the use of four different types of antibodies to CSF-1R and the presence of CSF-1R mRNA by in situ hybridization using oligonucleotide probe. In the steady state in most areas of the brain, CSF-1R is weakly expressed in only a few neurons. In the cerebellum, brainstem, and spinal cord, however, CSF-1R is expressed constitutively in greater numbers of neurons. After cerebral cortex ischemic injury, neurons in the area next to the ischemic lesion markedly upregulate CSF-1R. It is also upregulated in the contralateral cortex and in many other areas of the brain and spinal cord. We demonstrated that in cultures the ligand CSF-1 binds to its receptor (CSF-1R) in neurons and that reduction of the number of apoptotic neurons and potentiation of neuron survival is CSF-1 dose dependent. We propose that CSF-1/CSF-1R signaling is an important regulatory pathway between neurons, microglia, and astrocytes.},
	Author = {Wang, Y. and Berezovska, O. and Fedoroff, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Survival;Human;Animals;Gene Expression Regulation;Cells, Cultured;Recombinant Proteins;Apoptosis;Receptor, Macrophage Colony-Stimulating Factor;Mice, Inbred C3H;Translation, Genetic;Brain;RNA, Messenger;11 Glia;Male;Embryo;Spinal Cord;Support, Non-U.S. Gov't;Cerebral Cortex;Neurons;Brain Ischemia;Macrophage Colony-Stimulating Factor;Mice;Transcription, Genetic},
	Medline = {99393594},
	Month = {9},
	Nlm_Id = {7600111},
	Number = {5},
	Organization = {Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.},
	Pages = {616-32},
	Pii = {10.1002/(SICI)1097-4547(19990901)57:5<616::AID-JNR4>3.0.CO;2-E},
	Pubmed = {10462686},
	Title = {Expression of colony stimulating factor-1 receptor (CSF-1R) by CNS neurons in mice},
	Uuid = {EBC46FB9-09D4-4A12-9F5C-B060F9CEA961},
	Volume = {57},
	Year = {1999}}

@article{Wang:1991,
	Abstract = {The complementary DNA sequence encoding the cell-surface receptor for ecotropic host-range murine retroviruses (ecoR) shows that it contains 622 amino acids and 14 hydrophobic potentially membrane-spanning sequences. Because this receptor occurs on many or all murine cells and is probably essential for viability of cultured fibroblasts, its normal function might be to transport an essential metabolite. We expressed ecoR in Xenopus laevis oocytes by injecting RNA transcribed from the cloned cDNA. These oocytes specifically bound the gp70 envelope glycoprotein from an ecotropic murine leukaemia virus. An inward current was recorded electrophysiologically when a mixture of amino-acids was applied: this resulted from a stereoselective, saturable uptake of lysine, arginine and ornithine; it was independent of sodium and not substantially altered by gp70. Cysteine and homoserine were also taken up, but sodium was necessary for their transport. These properties of ecoR correspond to those of the y+ amino-acid transporter. Our results demonstrate the subversion of a ubiquitous cell membrane protein, in this case a basic amino acid transporter, for use as a retroviral receptor.},
	Author = {Wang, H. and Kavanaugh, M. P. and North, R. A. and Kabat, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Arginine;Animals;Electric Conductivity;In Vitro;Lysine;Cloning, Molecular;Cations;Biological Transport;Recombinant Proteins;15 Retrovirus mechanism;Kinetics;Xenopus laevis;Viral Envelope Proteins;Research Support, U.S. Gov't, P.H.S.;Moloney murine leukemia virus;Membrane Glycoproteins;Receptors, Virus;Membrane Transport Proteins;24 Pubmed search results 2008;Ornithine},
	Medline = {91343002},
	Month = {8},
	Nlm_Id = {0410462},
	Number = {6337},
	Organization = {Department of Biochemistry, Oregon Health Sciences University, Portland 97201.},
	Pages = {729-31},
	Pubmed = {1908564},
	Title = {Cell-surface receptor for ecotropic murine retroviruses is a basic amino-acid transporter},
	Uuid = {0B790250-EE2C-11DA-8605-000D9346EC2A},
	Volume = {352},
	Year = {1991},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/352729a0}}

@article{Wang:2003a,
	Abstract = {Evidence suggests that haematopoietic stem cells might have unexpected developmental plasticity, highlighting therapeutic potential. For example, bone-marrow-derived hepatocytes can repopulate the liver of mice with fumarylacetoacetate hydrolase deficiency and correct their liver disease. To determine the underlying mechanism in this murine model, we performed serial transplantation of bone-marrow-derived hepatocytes. Here we show by Southern blot analysis that the repopulating hepatocytes in the liver were heterozygous for alleles unique to the donor marrow, in contrast to the original homozygous donor cells. Furthermore, cytogenetic analysis of hepatocytes transplanted from female donor mice into male recipients demonstrated 80,XXXY (diploid to diploid fusion) and 120,XXXXYY (diploid to tetraploid fusion) karyotypes, indicative of fusion between donor and host cells. We conclude that hepatocytes derived form bone marrow arise from cell fusion and not by differentiation of haematopoietic stem cells. 0028-0836 Journal Article},
	Author = {Wang, X. and Willenbring, H. and Akkari, Y. and Torimaru, Y. and Foster, M. and Al-Dhalimy, M. and Lagasse, E. and Finegold, M. and Olson, S. and Grompe, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Nature},
	Keywords = {In Situ Hybridization, Fluorescence;Cell Differentiation;Heterozygote;Animals;Hybrid Cells/*cytology/metabolism;Hematopoietic Stem Cells/*cytology;Female;EE pdf;Cell Fusion;Hepatocytes/*cytology/metabolism/*transplantation;Male;Diploidy;Support, Non-U.S. Gov't;Alleles;Homozygote;Karyotyping;Bone Marrow Cells/*cytology;Support, U.S. Gov't, P.H.S.;Polyploidy;Mice},
	Number = {6934},
	Organization = {Department of Molecular and Medical Genetics, Oregon Health &Science University, Portland, Oregon 97239, USA.},
	Pages = {897-901},
	Pubmed = {12665832},
	Title = {Cell fusion is the principal source of bone-marrow-derived hepatocytes},
	Uuid = {E8A87491-CEDB-11D9-B244-000D9346EC2A},
	Volume = {422},
	Year = {2003},
	url = {../../Volumes/Vega/Users/ackman/James/Endnotelibraries/OMEGAoldpdfs/EE-aberrantcellcyclepdfs/cellfusion2-nat03.pdf}}

@article{Wang:2000,
	Author = {Wang, S. and Barres, B. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {Cell Differentiation/*physiology;Schwann Cells/cytology;Ligands;Embryonic Induction;11 Glia;Neurons/*cytology;Cerebral Cortex/cytology/embryology/metabolism;Signal Transduction/*physiology;Neuroglia/*cytology/*metabolism;G;Membrane Proteins/metabolism;Retina/cytology/embryology/metabolism;Stem Cells/*cytology/metabolism},
	Number = {2},
	Organization = {Stanford University School of Medicine, Department of Neurobiology, California 94305, USA. songli\@stanford.edu},
	Pages = {197-200.},
	Title = {Up a notch: instructing gliogenesis},
	Uuid = {CDE8488E-6408-4705-8464-ABA05E395AC0},
	Volume = {27},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10985340}}

@article{Wang:2001,
	Abstract = {Compared to neurons, the intracellular mechanisms that control glial differentiation are still poorly understood. We show here that oligodendrocyte lineage cells express the helix-loop-helix proteins Mash1 and Id2. Although Mash1 has been found to regulate neuronal development, we found that in the absence of Mash1 oligodendrocyte differentiation occurs normally. In contrast, we found that overexpression of Id2 powerfully inhibits oligodendrocyte differentiation, that Id2 normally translocates out of the nucleus at the onset of differentiation, and that absence of Id2 induces premature oligodendrocyte differentiation in vitro. These findings demonstrate that Id2 is a component of the intracellular mechanism that times oligodendrocyte differentiation and point to the existence of an as yet unidentified MyoD-like bHLH protein necessary for oligodendrocyte differentiation.},
	Author = {Wang, S. and Sdrulla, A. and Johnson, J. E. and Yokota, Y. and Barres, B. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {G;Platelet-Derived Growth Factor/pharmacology;*Helix-Loop-Helix Motifs;Cells, Cultured;Rats;*Cell Differentiation;Oligodendroglia/chemistry/*cytology/metabolism;DNA-Binding Proteins/analysis/deficiency/genetics/*physiology;Transcription Factors/analysis/deficiency/physiology;Animal;11 Glia;Time Factors;RNA, Messenger/analysis;Support, Non-U.S. Gov't;Mice, Knockout;Triiodothyronine/pharmacology;Support, U.S. Gov't, P.H.S.;Polymerase Chain Reaction;Mice;Cell Division;Immunohistochemistry;Gene Expression;Optic Nerve/cytology;Stem Cells/chemistry/*cytology/metabolism},
	Number = {3},
	Organization = {Stanford University School of Medicine, Department of Neurobiology, Sherman Fairchild Science Building D231, 299 Campus Drive, Stanford, CA 94305, USA.},
	Pages = {603-14.},
	Title = {A role for the helix-loop-helix protein Id2 in the control of oligodendrocyte development},
	Uuid = {F09FD640-6216-44BB-AE75-BB5D68AA545B},
	Volume = {29},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11301021}}

@article{Ward:2003,
	Abstract = {Although neuronal migration is an essential process in development, how neural precursors reach their final destination in the nervous system is not well understood. Secreted molecules that are known to be involved in axon guidance are likely to play important roles in regulating neuronal migration, but an important issue that remains unclear is whether such molecules act as directional guidance cues or as motility regulators in neuronal migration. The secreted protein Slit was initially suggested to be a repellent for migrating neurons (Wu et al., 1999). However, it was concluded recently that Slit plays an inhibitory rather than a repulsive role in neuronal migration (Mason et al., 2001). We have developed a series of assays that allow us to differentiate between repulsive and inhibitory effects of secreted molecules, and we demonstrate that Slit is a repellent capable of reversing the direction of neurons migrating either in culture or in their native pathways. We also show that although Slit reduces migratory speed under certain conditions, it can function as a repellent without concurrent inhibition of neuronal migration. This is the first study to clearly demonstrate that migrating neurons can be directionally guided by secreted molecules. These findings provide a basis to understand the physiological roles of secreted molecules in the developing nervous system and have implications on how they could be applied therapeutically. Our results also indicate that it should be possible to determine the specific action of other molecules as directional guidance cues or as motility regulators of cell migration. 1529-2401 Journal Article},
	Author = {Ward, M. and McCann, C. and DeWulf, M. and Wu, J. Y. and Rao, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {J Neurosci},
	Keywords = {B pdf;Nerve Tissue Proteins/pharmacology/*physiology/secretion;02 Adult neurogenesis migration;Culture Media, Conditioned/pharmacology;Human;Cell Movement/drug effects/*physiology;Rats;Time Factors;Glycoproteins/pharmacology/*physiology/secretion;Coculture;Lateral Ventricles/cytology;Kidney/cytology/metabolism/secretion;Support, U.S. Gov't, P.H.S.;Cells, Cultured;Animals;Support, Non-U.S. Gov't;Neurons/*cytology/drug effects/*physiology},
	Number = {12},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.},
	Pages = {5170-7},
	Pubmed = {12832541},
	Title = {Distinguishing between directional guidance and motility regulation in neuronal migration},
	Uuid = {7422A521-5EE1-4B8A-9B28-16D2FADC1DC5},
	Volume = {23},
	Year = {2003},
	url = {papers/Ward_JNeurosci2003.pdf}}

@article{Warner-Schmidt:2007,
	Abstract = {The neural mechanisms underlying the cellular and behavioral responses to antidepressants are not yet known. Up-regulation of growth factors and adult neurogenesis suggest a role for one or more of these factors in the action of antidepressants. One candidate of interest is vascular endothelial growth factor (VEGF), which was initially characterized for its role in angiogenesis, but also exerts direct mitogenic effects on neural progenitors in vitro. Results of this study demonstrate that VEGF is induced by multiple classes of antidepressants at time points consistent with the induction of cell proliferation and therapeutic action of these treatments. We find that VEGF signaling through the Flk-1 receptor is required for antidepressant-induced cell proliferation. We also show that VEGF-Flk-1 signaling is required and sufficient for behavioral responses in two chronic and two subchronic antidepressant models. Taken together, these studies identify VEGF and VEGF-Flk-1 signaling as mediators of antidepressant actions and potential targets for therapeutic intervention.},
	Author = {Warner-Schmidt, Jennifer L. and Duman, Ronald S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {04 Adult neurogenesis factors;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {7505876},
	Number = {11},
	Organization = {Departments of Psychiatry and Pharmacology, Yale University School of Medicine, New Haven, CT 06508.},
	Pages = {4647-52},
	Pii = {0610282104},
	Pubmed = {17360578},
	Title = {VEGF is an essential mediator of the neurogenic and behavioral actions of antidepressants},
	Uuid = {8AA57953-429D-4417-A1BF-F10757AB3865},
	Volume = {104},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0610282104}}

@article{Warren:1973,
	Abstract = {0008-5472 Journal Article},
	Author = {Warren, J. and Sacksteder, M. R. and Ellis, B. M. and Schwartz, R. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Cancer Res},
	Keywords = {Mice, Inbred BALB C;Injections, Intraperitoneal;Animals;Cells, Cultured;Virus Replication/drug effects;*Moloney murine leukemia virus/drug effects;Injections, Intramuscular;Fibroblasts;EE, DMSO, abstr;08 Aberrant cell cycle;Time Factors;Embryo;*Sarcoma Viruses, Avian/drug effects;Dimethyl Sulfoxide/*administration &dosage/pharmacology;Mice;Administration, Oral;Sarcoma, Avian/pathology;Quail;Sarcoma, Experimental/*etiology/pathology},
	Number = {3},
	Pages = {618-22},
	Pubmed = {4347720},
	Title = {Enhancement of viral oncogenicity by the prior administration of dimethyl sulfoxide},
	Uuid = {4AFDA350-3E66-4344-AEA8-5CBF77023B03},
	Volume = {33},
	Year = {1973},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=4347720}}

@article{Watanabe:2002,
	Abstract = {A8 virus (A8-V) is a molecular clone of the neuropathogenic FrC6 virus derived from the Friend murine leukemia virus (F-MuLV). The A8-V infects endothelia and microglia in the brain. We constructed a gene transfer system with the A8-V gene. Pseudotyped virus carrying the surface protein of A8-V (A8-SU) transduced the beta-glactosidase gene incorporated in the retroviral vector efficiently to cultured microglial cells derived from newborn rats. Ex vivo gene transferred microglial cells were then injected into the right hemisphere of 3-day-old and 3-week-old rat brains. All of the rats examined at 4 weeks after the injection contained the labeled microglial cells in the brain (7/7 and 5/5 of the rats injected at 3 days and 3 weeks, respectively). None of the rats showed pathological changes in the whole body investigated, including the central nervous system, 4 weeks after transplantation of the labeled microglial cells.},
	Author = {Watanabe, Rihito and Takase-Yoden, Sayaka and Fukumitsu, Hidefumi and Nakajima, Kazuyuki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0963-6897},
	Journal = {Cell Transplant},
	Keywords = {Research Support, Non-U.S. Gov't;Rats, Inbred Lew;Rats;Retroviridae;11 Glia;Microglia;Cells, Cultured;Brain;Animals;Genetic Vectors},
	Medline = {22270118},
	Nlm_Id = {9208854},
	Number = {5},
	Organization = {Institute of Life Science, Soka University, Hachioji, Tokyo, Japan. rihito\@t.soka.ac.jp},
	Pages = {471-3},
	Pubmed = {12382676},
	Title = {Cell transplantation to the brain with microglia labeled by neuropathogenic retroviral vector system},
	Uuid = {B7759AB5-C05D-4D4C-A3F1-AA819A161070},
	Volume = {11},
	Year = {2002},
	url = {papers/Watanabe_CellTransplant2002.pdf}}

@article{Watson:2003,
	Abstract = {Human Ntera-2 (NT2) cells can be differentiated in vitro into well-characterized populations of NT2N neurons that engraft and mature when transplanted into the adult CNS of rodents and humans. They have shown promise as treatments for neurologic disease, trauma, and ischemic stroke. Although these features suggest that NT2N neurons would be an excellent platform for ex vivo gene therapy in the CNS, stable gene expression has been surprisingly difficult to achieve in these cells. In this report we demonstrate stable, efficient, and nontoxic gene transfer into undifferentiated NT2 cells using a pseudotyped lentiviral vector encoding the human elongation factor 1-alpha promoter and the reporter gene eGFP. Expression of eGFP was maintained when the NT2 cells were differentiated into NT2N neurons after treatment with retinoic acid. When transplanted into the striatum of adult nude mice, transduced NT2N neurons survived, engrafted, and continued to express the reporter gene for long-term time points in vivo. Furthermore, transplantation of NT2N neurons genetically modified to express nerve growth factor significantly attenuated cognitive dysfunction following traumatic brain injury in mice. These results demonstrate that defined populations of genetically modified human NT2N neurons are a practical and effective platform for stable ex vivo gene delivery into the CNS.},
	Author = {Watson, Deborah J. and Longhi, Luca and Lee, Edward B. and Fulp, Carl T. and Fujimoto, Scott and Royo, Nicolas C. and Passini, Marco A. and Trojanowski, John Q. and Lee, Virginia M. Y. and McIntosh, Tracy K. and Wolfe, John H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Cell Differentiation;Animals;Stem Cell Transplantation;Gene Expression Regulation;Nerve Growth Factor;Treatment Outcome;Rats;Recovery of Function;Humans;Research Support, U.S. Gov't, Non-P.H.S.;Lentivirus;Female;11 Glia;PC12 Cells;Green Fluorescent Proteins;Mice, Nude;Genetic Vectors;Brain Injuries;Research Support, U.S. Gov't, P.H.S.;Gene Therapy;Gene Transfer Techniques;Neurons;Mice;Peptide Elongation Factor 1;Luminescent Proteins;Graft Survival;Stem Cells;Tretinoin;Research Support, Non-U.S. Gov't},
	Medline = {22606053},
	Month = {4},
	Nlm_Id = {2985192R},
	Number = {4},
	Organization = {Department of Pathobiology, Center for Comparative Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA.},
	Pages = {368-80},
	Pubmed = {12722829},
	Title = {Genetically modified NT2N human neuronal cells mediate long-term gene expression as CNS grafts in vivo and improve functional cognitive outcome following experimental traumatic brain injury},
	Uuid = {493ABD0F-6F42-4FE9-BA8F-EA1DAA2382CD},
	Volume = {62},
	Year = {2003}}

@article{Watt:2001,
	Abstract = {Expression of the p75 low-affinity neurotrophin receptor (p75NTR) was investigated immunocytochemically at the light and ultrastructural level during the axonal degeneration that follows partial denervation of the rat neural lobe (NL) and following systemic administration of lipopolysaccharide (LPS). A significant increase in the intensity and extent of p75NTR immunoreactivity in the NL of partially denervated animals compared with age-matched, sham-operated controls was observed at 5-10 days postdenervation, with immunoreactivity returning to control values by 35 days. Dual-label confocal comparison of p75NTR localization with that of the C3bi complement receptor, a microglial marker, and S100, an astrocyte-specific Ca2+-binding protein, revealed no colocalization. Immunoelectron-microscopic examination demonstrated that the p75NTR immunoreactivity is present in a subpopulation of cells located within the extensive perivascular space of the NL. No examples of p75NTR-immunoreactive pituicytes or endothelia were observed at the light or ultrastructural level. Dense p75NTR immunoreactivity was frequently observed surrounding endocytotic omega profiles of plasmalemma engulfing extracellular debris as well as lining vacuoles within the cytoplasm of perivascular cells. The association of p75NTR with phagocytosis was confirmed by confocal microscopy, showing the presence of p75NTR in all cells expressing the ED-1 antigen, which is restricted to the lysosomal membrane of phagocytes (Damoiseaux et al. 1994). Likewise, a marked increase in p75NTR and ED-1 immunoreactivity was observed in the NL following systemic administration of LPS. These results suggest a strong correlation between modulation of p75NTR immunoreactivity and conditions that induce high levels of phagocytic activity by perivascular cells in the NL of the rat. Implications for understanding the mechanisms by which phagocytes may support compensatory responses to neuronal injury are discussed.},
	Author = {Watt, J. A. and Paden, C. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0302-766X},
	Journal = {Cell Tissue Res},
	Keywords = {Lysosomes;Phagocytosis;Animals;Microscopy, Immunoelectron;Up-Regulation;Rats;Microglia;Denervation;Pituitary Gland, Posterior;Rats, Sprague-Dawley;Lipopolysaccharides;Not relevant;11 Glia;Male;Receptors, Complement;Antigens;Support, U.S. Gov't, P.H.S.;Receptor, Nerve Growth Factor;Immunohistochemistry;Complement 3b;S100 Proteins},
	Medline = {21130734},
	Month = {1},
	Nlm_Id = {0417625},
	Number = {1},
	Organization = {Department of Cell Biology and Neuroscience, Montana State University, Bozeman 59717-0346, USA. jwatt\@montana.edu},
	Pages = {81-91},
	Pubmed = {11236007},
	Title = {Upregulation of the p75 low-affinity neurotrophin receptor by phagocytically active perivascular active cells in the rat neural lobe},
	Uuid = {8AE248B5-5D00-4AEE-8D77-FDA67AC7510D},
	Volume = {303},
	Year = {2001}}

@article{Watts:2004,
	Abstract = {Developmental axon pruning is widely used in constructing the nervous system. Accordingly, diverse mechanisms are likely employed for various forms of axon pruning. In the Drosophila mushroom bodies (MB), gamma neurons initially extend axon branches into both the dorsal and medial MB axon lobes in larvae. Through a well-orchestrated set of developmental events during metamorphosis, axon branches to both lobes degenerate prior to the formation of adult connections. Here, we analyze ultrastructural changes underlying axon pruning by using a genetically encoded electron microscopic (EM) marker to selectively label gamma neurons. By inhibiting axon pruning in combination with the use of this EM marker, we demonstrate a causal link between observed cellular events and axon pruning. These events include changes in axon ultrastructure, synaptic degeneration, and engulfment of degenerating axon fragments by glia for their subsequent breakdown via the endosomal-lysosomal pathway. Interestingly, glia selectively invade MB axon lobes at the onset of metamorphosis; this increase in cell number is independent of axon fragmentation. Our study reveals a key role for glia in the removal of axon fragments during developmental axon pruning.},
	Author = {Watts, Ryan J. and Schuldiner, Oren and Perrino, John and Larsen, Camilla and Luo, Liqun},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0960-9822},
	Journal = {Curr Biol},
	Keywords = {Models, Biological;Mushroom Bodies;Neuroglia;Research Support, Non-U.S. Gov't;Nerve Degeneration;Comparative Study;Microscopy, Electron;Research Support, U.S. Gov't, P.H.S.;Drosophila;Lysosomes;Motor Neurons, Gamma;Fluorescent Antibody Technique;Metamorphosis, Biological;Endocytosis;Animals;24 Pubmed search results 2008;Axons},
	Month = {4},
	Nlm_Id = {9107782},
	Number = {8},
	Organization = {Department of Biological Sciences, Stanford University, Stanford, CA 94305 USA.},
	Pages = {678-84},
	Pii = {S0960982204002143},
	Pubmed = {15084282},
	Title = {Glia engulf degenerating axons during developmental axon pruning},
	Uuid = {A226E904-0E69-487B-8954-7200DEC6B273},
	Volume = {14},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2004.03.035}}

@article{Wegiel:1998,
	Abstract = {The numerical density of microglial cells is reduced by 47\%in the corpus callosum, by 37\%in the parietal cortex and by 34\%in the frontal cortex of mice mutant at the op locus which are totally devoid of colony stimulating factor-1 (CSF-1), the major growth factor for macrophages. Moreover, microglia in the frontal cortex of the op/op mice are smaller and have shorter cytoplasmic processes compared to control mice. Study suggests that CSF-1 plays a role in vivo in the formation and maturation of microglia and has little or no effect on perivascular cells.},
	Author = {Wegiel, J. and Wi\'{s}niewski, H. M. and Dziewiatkowski, J. and Tarnawski, M. and Kozielski, R. and Trenkner, E. and Wiktor-Jedrzejczak, W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Brain;Macrophage Colony-Stimulating Factor;Mutation;Mice;Osteopetrosis;Frontal Lobe;Immunohistochemistry;Cell Count;11 Glia;Microglia;Parietal Lobe;Support, Non-U.S. Gov't;Male;Animals;Mice, Inbred Strains;Corpus Callosum},
	Medline = {98398418},
	Month = {8},
	Nlm_Id = {0045503},
	Number = {1},
	Organization = {New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA.},
	Pages = {135-9},
	Pii = {S0006899398006180},
	Pubmed = {9729335},
	Title = {Reduced number and altered morphology of microglial cells in colony stimulating factor-1-deficient osteopetrotic op/op mice},
	Uuid = {D3F404B1-3EFF-4A75-B1EB-49258DF6387A},
	Volume = {804},
	Year = {1998}}

@article{Wehner:2003,
	Abstract = {Differentiation of bone marrow (BM) cells into astroglia expressing the glial fibrillary acidic protein (GFAP) has been reported in vitro and after intracerebral or systemic BM transplantation. In contrast, recent data suggest that astrocytic differentiation does not occur from BM-derived cells in vivo. Using transgenic mice that express the enhanced green fluorescent protein (GFP) under the control of the human glial fibrillary acidic protein (GFAP) promoter, we investigated the potential of adult murine BM-derived cells to differentiate into macroglia. In the brains of GFAP-GFP transgenic mice, astrocytes were brightly fluorescent from the expression of GFP. When BM from these animals was transplanted into lethally irradiated wild-type animals, the transgene was detected in the reconstituted hematopoietic system, but no GFP expression was found in the nervous system. In contrast, GFAP-GFP neuroectodermal anlage grafted into adult wild-type striatum gave rise to GFP-expressing astrocytes. Because cerebral ischemia has been suggested to promote the differentiation of BM-derived cells into astrocytes, BM chimeric mice were subjected to focal cerebral ischemia. No GFP-positive cells were found in the ischemic or contralateral hemispheres of these brains. Even after direct injection of GFAP-GFP transgenic BM cells into wild-type striatum, no GFP-expressing astroglia were detected. To test the hypothesis that the in vitro environment might be more permissible for astroglial differentiation, we cultured BM from mice that constitutively express GFP, BM cells expressing GFP from a retroviral vector, and BM from GFAP-GFP transgenic mice on astrocytes and on organotypic hippocampal slices. In all experimental paradigms, BM-derived cells were found to differentiate into ramified microglia but not into GFAP-expressing astrocytes.},
	Author = {Wehner, Tim and B{\"o}ntert, Matthias and Ey{\"u}poglu, Ilker and Prass, Konstantin and Prinz, Marco and Klett, Francisco Fern{\'a}ndez and Heinze, Matthias and Bechmann, Ingo and Nitsch, Robert and Kirchhoff, Frank and Kettenmann, Helmut and Dirnagl, Ulrich and Priller, Josef},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Glial Fibrillary Acidic Protein;Cell Differentiation;Animals;Astrocytes;In Vitro;Coculture Techniques;Brain Tissue Transplantation;Cells, Cultured;Humans;Stem Cell Transplantation;Brain;Microglia;Mice, Transgenic;Hippocampus;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Radiation Chimera;Bone Marrow Cells;Promoter Regions (Genetics);Mice;Ischemic Attack, Transient;Graft Survival;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22716523},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {12},
	Organization = {Department of Neurology, Charit{\'e}, Humboldt-University, 10117 Berlin, Germany.},
	Pages = {5004-11},
	Pii = {23/12/5004},
	Pubmed = {12832523},
	Title = {Bone marrow-derived cells expressing green fluorescent protein under the control of the glial fibrillary acidic protein promoter do not differentiate into astrocytes in vitro and in vivo},
	Uuid = {F2F9AA7C-800D-460C-86AF-AFAFE2F04DF6},
	Volume = {23},
	Year = {2003},
	url = {papers/Wehner_JNeurosci2003.pdf}}

@article{Weimann:2003,
	Abstract = {Heterokaryons are the product of cell fusion without subsequent nuclear or chromosome loss. Decades of research using Sendai-virus or polyethylene glycol (PEG)-mediated fusion in tissue culture showed that the terminally differentiated state of a cell could be altered. But whether stable non-dividing heterokaryons could occur in animals has remained unclear. Here, we show that green fluorescent protein (GFP)-positive bone-marrow-derived cells (BMDCs) contribute to adult mouse Purkinje neurons through cell fusion. The formation of heterokaryons increases in a linear manner over 1.5 years and seems to be stable. The dominant Purkinje neurons caused the BMDC nuclei within the resulting heterokaryons to enlarge, exhibit dispersed chromatin and activate a Purkinje neuron-specific transgene, L7-GFP. The observed reprogrammed heterokaryons that form in brain may provide insights into gene regulation associated with cell-fate plasticity.},
	Author = {Weimann, James M. and Johansson, Clas B. and Trejo, Angelica and Blau, Helen M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1465-7392},
	Journal = {Nat Cell Biol},
	Keywords = {Research Support, Non-U.S. Gov't;In Situ Hybridization, Fluorescence;Purkinje Cells;Animals;Chromatin;Bone Marrow Transplantation;Cell Fusion;Mice, Transgenic;Mice, Inbred C57BL;Green Fluorescent Proteins;08 Aberrant cell cycle;17 Transplant Regeneration;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Flow Cytometry;Mice;22 Stem cells;24 Pubmed search results 2008;Luminescent Proteins;Transgenes},
	Medline = {22954634},
	Month = {11},
	Nlm_Id = {100890575},
	Number = {11},
	Organization = {Baxter Laboratory in Genetic Pharmacology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. jweimann\@stanford.edu},
	Pages = {959-66},
	Pii = {ncb1053},
	Pubmed = {14562057},
	Title = {Stable reprogrammed heterokaryons form spontaneously in Purkinje neurons after bone marrow transplant},
	Uuid = {52FC753E-E9C3-11DA-920C-000D9346EC2A},
	Volume = {5},
	Year = {2003},
	url = {papers/Weimann_NatCellBiol2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/ncb1053}}

@article{Weimann:2003a,
	Abstract = {We show here that cells within human adult bone marrow can contribute to cells in the adult human brain. Cerebellar tissues from female patients with hematologic malignancies, who had received chemotherapy, radiation, and a bone marrow transplant, were analyzed. Brain samples were obtained at autopsy from female patients who received male (sex-mismatched) or female (sex-matched, control) bone marrow transplants. Cerebella were evaluated in 10-microm-thick, formaldehyde-fixed, paraffin-embedded sections that encompassed up to approximately 50\%of a human Purkinje nucleus. A total of 5,860 Purkinje cells from sex-mismatched females and 3,202 Purkinje cells from sex-matched females were screened for Y chromosomes by epifluorescence. Confocal laser scanning microscopy allowed definitive identification of the sex chromosomes within the morphologically distinct Purkinje cells. In the brains of females who received male bone marrow, four Purkinje neurons were found that contained an X and a Y chromosome and two other Purkinje neurons contained more than a diploid number of sex chromosomes. No Y chromosomes were detected in the brains of sex-matched controls. The total frequency of male bone marrow contribution to female Purkinje cells approximated 0.1\%. This study demonstrates that although during human development Purkinje neurons are no longer generated after birth, cells within the bone marrow can contribute to these CNS neurons even in adulthood. The underlying mechanism may be caused either by generation de novo of Purkinje neurons from bone marrow-derived cells or by fusion of marrow-derived cells with existing recipient Purkinje neurons.},
	Author = {Weimann, James M. and Charlton, Carol A. and Brazelton, Timothy R. and Hackman, Robert C. and Blau, Helen M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {In Situ Hybridization;Chromosomes, Human, Y;Purkinje Cells;Research Support, Non-U.S. Gov't;Adult;17 Transplant Regeneration;Cell Fusion;Female;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Bone Marrow Transplantation;22 Stem cells;Humans;Brain;24 Pubmed search results 2008;Neurons},
	Medline = {22480347},
	Month = {2},
	Nlm_Id = {7505876},
	Number = {4},
	Organization = {Baxter Laboratory for Genetic Pharmacology, Stanford University School of Medicine, Stanford, CA 94305, USA.},
	Pages = {2088-93},
	Pii = {0337659100},
	Pubmed = {12576546},
	Title = {Contribution of transplanted bone marrow cells to Purkinje neurons in human adult brains},
	Uuid = {52FC79D0-E9C3-11DA-920C-000D9346EC2A},
	Volume = {100},
	Year = {2003},
	url = {papers/Weimann_ProcNatlAcadSciUSA2003.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0337659100}}

@article{Weimer:2006,
	Abstract = {Dynamic regulation of neuronal cytoskeletal machinery in response to extracellular cues enables distinct changes in neuronal development in the cerebral cortex. In this issue of Neuron, three related studies on doublecortin-like kinase, a microtubule-associated protein related to doublecortin, by Shu et al., Koizumi et al., and Deuel et al., provide evidence that doublecortin-like kinase is essential for proper neurogenesis, neuronal migration, and axonal wiring.},
	Author = {Weimer, Jill M. and Anton, E. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Aging;Embryonic Development;Embryo;10 Development;24 Pubmed search results 2008;Embryo, Nonmammalian;Neuropeptides;Drug Synergism;Protein-Serine-Threonine Kinases;Animals, Newborn;comment;Animals;Microtubule-Associated Proteins;Cerebral Cortex;review;Embryo, Mammalian},
	Month = {1},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Neuroscience Center, Department of Cell and Molecular Physiology, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA.},
	Pages = {3-4},
	Pii = {S0896-6273(05)01104-9},
	Pubmed = {16387632},
	Title = {Doubling up on microtubule stabilizers: synergistic functions of doublecortin-like kinase and doublecortin in the developing cerebral cortex},
	Uuid = {105DC4E6-8E15-41CD-8565-E4D900FB3206},
	Volume = {49},
	Year = {2006},
	url = {papers/Weimer_Neuron2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2005.12.016}}

@article{Weinberg:1980,
	Author = {Weinberg, R. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {15 ERVs retroelements;24 Pubmed search results 2008;Species Specificity;Virus Replication;Retroviridae;DNA, Viral;15 Retrovirus mechanism;Animals;Chickens;Cell Transformation, Viral;Mice;Recombination, Genetic},
	Month = {12},
	Nlm_Id = {0413066},
	Number = {3},
	Pages = {643-4},
	Pii = {0092-8674(80)90537-1},
	Pubmed = {7460007},
	Title = {Origins and roles of endogenous retroviruses},
	Uuid = {3CDEDFDA-6B1D-4B89-84E1-DAA420324201},
	Volume = {22},
	Year = {1980},
	url = {papers/Weinberg_Cell1980.pdf}}

@article{Weinberg:1991,
	Abstract = {Human immunodeficiency virus type 1 (HIV-1) infection of T lymphocytes requires cellular proliferation and DNA synthesis. Human monocytes were shown to have low DNA synthesis rates, yet the monocytotropic BaL isolate of HIV-1 was able to infect these cells efficiently. Monocytes that were irradiated to assure no DNA synthesis could also be readily infected with HIV-1BaL. Such infections were associated with the integration of HIV-1BaL DNA into the high molecular weight, chromosomal DNA of monocytes. Thus, normal, nonproliferating monocytes differ from T lymphocytes in that a productive HIV-1 infection can occur independently of cellular DNA synthesis. These results suggest that normal nonproliferating mononuclear phagocytes, which are relatively resistant to the destructive effects of this virus, may serve as persistent and productive reservoirs for HIV-1 in vivo.},
	Author = {Weinberg, J. B. and Matthews, T. J. and Cullen, B. R. and Malim, M. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0022-1007},
	Journal = {J Exp Med},
	Keywords = {Monocytes;Macrophage Colony-Stimulating Factor;HIV Core Protein p24;RNA-Directed DNA Polymerase;Research Support, Non-U.S. Gov't;HIV-1;HIV-1 Reverse Transcriptase;Research Support, U.S. Gov't, P.H.S.;Granulocyte-Macrophage Colony-Stimulating Factor;DNA;DNA, Viral;11 Glia;Research Support, U.S. Gov't, Non-P.H.S.;Cells, Cultured;Humans;Proteins},
	Medline = {92078858},
	Month = {12},
	Nlm_Id = {2985109R},
	Number = {6},
	Organization = {Department of Medicine, Veterans Affairs, Medical Center, Durham, North Carolina.},
	Pages = {1477-82},
	Pubmed = {1720811},
	Title = {Productive human immunodeficiency virus type 1 (HIV-1) infection of nonproliferating human monocytes},
	Uuid = {25CDFB48-B3DB-477C-98C9-C92E93B4F3CF},
	Volume = {174},
	Year = {1991}}

@article{Weinstein:1972,
	Author = {Weinstein, I. B. and Gebert, R. and Stadler, U. C. and Orenstein, J. M. and Axel, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0036-8075},
	Journal = {Science},
	Keywords = {Bromodeoxyuridine;Liver Neoplasms;RNA, Viral;Animals;RNA Viruses;Cells, Cultured;Leukosis Virus, Avian;Rats;Dimethyl Sulfoxide;Deoxyribonucleotides;15 Retrovirus mechanism;Uridine;Retroviridae;DNA Nucleotidyltransferases;Carcinoma, Hepatocellular;Fluorenes;24 Pubmed search results 2008;Tritium;Neoplasms, Experimental;15 ERVs retroelements;Microscopy, Electron;Oncogenic Viruses},
	Medline = {73042831},
	Month = {12},
	Nlm_Id = {0404511},
	Number = {65},
	Pages = {1098-100},
	Pubmed = {4343844},
	Title = {Type C virus from cell cultures of chemically induced rat hepatomas},
	Uuid = {8DFFB51B-4328-11DB-A5D2-000D9346EC2A},
	Volume = {178},
	Year = {1972}}

@article{Weiss:2003a,
	Abstract = {Immune rejection of transplanted material is a potential complication of organ donation. In response to tissue transplantation, immune rejection has two components: a host defense directed against the grafted tissue and an immune response from the grafted tissue against the host (graft vs host disease). To treat immune rejection, transplant recipients are typically put on immunosuppression therapy. Complications may arise from immune suppression or from secondary effects of immunosuppression drugs. Our preliminary work indicated that stem cells may be xenotransplanted without immunosuppression therapy. Here, we investigated the survival of pig stem cells derived from umbilical cord mucous connective tissue (UCM) after transplantation into rats. Our data demonstrate that UCM cells survive at least 6 weeks without immune suppression of the host animals after transplantation into either the brain or the periphery. In the first experiment, UCM cells were transplanted into the rat brain and recovered in that tissue 2-6 weeks posttransplantation. At 4 weeks posttransplantation, the UCM cells engrafted into the brain along the injection tract. The cells were small and roughly spherical. The transplanted cells were positively immunostained using a pig-specific antibody for neuronal filament 70 (NF70). In contrast, 6 weeks posttransplantation, about 10\%of the UCM cells that were recovered had migrated away from the injection site into the region just ventral to the corpus callosum; these cells also stained positively for NF70. In our second experiment, UCM cells that were engineered to constitutively express enhanced green fluorescent protein (eGFP) were transplanted. These cells were recovered 2-4 weeks after brain transplantation. Engrafted cells expressing eGFP and positively staining for NF70 were recovered. This finding indicates a potential for gene therapy. In the third experiment, to determine whether depositing the graft into the brain protected UCM cells from immune detection/clearance, UCM cells were injected into the tail vein and/or the semitendinosis muscle in a group of animals. UCM cells were recovered from the muscle or within the kidney 3 weeks posttransplantation. In control experiments, rat brains were injected with PKH 26-labeled UCM cells that had been lysed by repeated sonic disruption. One and 2 weeks following injection, no PKH 26-labeled neurons or glia were observed. Taken together, these data indicate that UCM cells can survive xenotransplantation and that a subset of the UCM cells respond to local signals to differentiate along a neural lineage.},
	Author = {Weiss, M. L. and Mitchell, K. E. and Hix, J. E. and Medicetty, S. and El-Zarkouny, S. Z. and Grieger, D. and Troyer, D. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0014-4886},
	Journal = {Exp Neurol},
	Keywords = {Cell Survival;Fluorescent Dyes;Rats, Inbred Lew;Animals;Stem Cell Transplantation;Cells, Cultured;Rats;Transfection;Umbilical Cord;Brain;Swine;Rats, Sprague-Dawley;Neurosurgical Procedures;Neurofilament Proteins;11 Glia;Green Fluorescent Proteins;Organic Chemicals;Research Support, U.S. Gov't, P.H.S.;Mesoderm;Immunohistochemistry;Stem Cells;Graft Survival;Injections;Luminescent Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22777794},
	Month = {8},
	Nlm_Id = {0370712},
	Number = {2},
	Organization = {Department of Anatomy and Physiology, Kansas State University, College of Veterinary Medicine, Manhattan, KS 66506-5602, USA. weiss\@vet.ksu.edu},
	Pages = {288-99},
	Pii = {S0014488603001286},
	Pubmed = {12895440},
	Title = {Transplantation of porcine umbilical cord matrix cells into the rat brain},
	Uuid = {87B7FBD5-BC09-4081-93A9-4D0EC90D2528},
	Volume = {182},
	Year = {2003}}

@article{Weiss:2002,
	Abstract = {Viruses use specific cell surface receptors to bind to and subsequently gain entry into their host cells. Some retroviruses such as HIV-1 and HIV-2 utilize one receptor for high-affinity binding (CD4), and a separate coreceptor to mediate fusion of the viral envelope with the cell membrane (CCR5 or CXCR4). The identification of these receptors explains the cellular tropism of HIV, and hence its pathogenesis leading to immune deficiency (T-helper cell depletion), the wasting syndrome (macrophage infection), and dementia (microglia infection). HIV can infect cells by membrane fusion at the cell surface and by receptor-mediated endocytosis. Knowledge of the HIV receptors has led to practical developments such as inhibitory drugs, reasons for genetic resistance to infection, and should inform the judicious choice of candidate vaccines.},
	Author = {Weiss, Robin A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {1521-6543},
	Journal = {IUBMB Life},
	Keywords = {Receptors, CXCR4;Animals;HIV-1;Humans;Protein Binding;review, tutorial;review;Acquired Immunodeficiency Syndrome;Models, Biological;Cell Membrane;Antigens, CD4;11 Glia;Epitopes;Receptors, CCR5;DNA, Complementary;Mice;Microscopy, Electron;HIV-2;HIV Envelope Protein gp120;Research Support, Non-U.S. Gov't},
	Medline = {22115640},
	Nlm_Id = {100888706},
	Number = {4-5},
	Organization = {Department of Immunology and Molecular Pathology, University College London, United Kingdom. r.weiss\@ucl.ac.uk},
	Pages = {201-5},
	Pubmed = {12120995},
	Title = {HIV receptors and cellular tropism},
	Uuid = {0E629AAA-0747-453F-A924-AAE6A6187973},
	Volume = {53},
	Year = {2002}}

@article{Weiss:2003,
	Abstract = {We studied the postnatal development of the radial glial scaffold in the dentate gyrus of reeler mice, lacking the extracellular matrix protein Reelin, in scrambler mice, deficient in the intracellular adaptor protein disabled1 (Dab1), which is required for the transmission of the Reelin signal into the cell, and in mutant mice lacking the Reelin receptors apolipoprotein receptor 2 (ApoER2) and/or the very low density lipoprotein receptor (VLDLR), known to transmit the Reelin signal via Dab1. By immunolabeling for the glial fibrillary acidic protein (GFAP), we show that a regular dentate radial glial scaffold fails to form in mutants deficient of Reelin, Dab1, and VLDLR and ApoER2. Mutant mice lacking only one of the Reelin receptors, VLDLR or ApoER2, display a gradual expression of the radial glial defects seen in mutants that lack both receptors. Our results suggest that Reelin signaling via ApoER2, VLDLR, and Dab1 is required for the formation of a regular radial glial scaffold in the dentate gyrus.},
	Author = {Weiss, Karl Heinz and Johanssen, Celine and Tielsch, Albrecht and Herz, Joachim and Deller, Thomas and Frotscher, Michael and F{\"o}rster, Eckart},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Male;Mice;10 Development;Mice, Knockout;Research Support, Non-U.S. Gov't;Neuroglia;Receptors, Lipoprotein;10 Hippocampus;Comparative Study;Female;Dentate Gyrus;Animals;Cell Movement;Nervous System Malformations;Receptors, LDL;Mice, Neurologic Mutants},
	Medline = {22573054},
	Month = {5},
	Nlm_Id = {0406041},
	Number = {1},
	Organization = {Anatomisches Institut, Universit{\"a}t Freiburg, D-79104 Freiburg, Germany.},
	Pages = {56-65},
	Pubmed = {12687696},
	Title = {Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice},
	Uuid = {87E33153-CFF4-4447-A081-C523F00D71B9},
	Volume = {460},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/cne.10644}}

@article{Weiss:1986,
	Abstract = {Striatal neurons were cultured from the fetal mouse brain and maintained in serum-free medium for 14-21 days in vitro (DIV). Pretreatment of the culture dishes successively with a polycation followed by fetal calf serum resulted in rapid neuron attachment and neurite proliferation. After 9-10 DIV, electron microscope observations revealed the presence of vesicles in axon terminals forming mature synapses with axons and perikarya of adjacent neurons and in varicosities along extended axons. Synapsin I, a synaptic vesicle-specific protein, was present only in neuronal perikarya after 3 DIV, in perikarya and in varicosities along extended axons after 6 DIV, and in varicosities and contact points between axon terminals and adjacent axons or perikarya after 11-14 DIV. Neurotransmitter-stimulated intracellular formation of cAMP decreased markedly during neuronal differentiation. Inositol phosphate formation in response to neurotransmitters, however, increased significantly throughout the period of striatal neuronal development. K+ (56 mM) depolarization resulted in a 2-fold increase in endogenous gamma-aminobutyric acid (GABA) release from striatal neurons, 50\%of which was Ca2+-dependent, between 3 and 11 DIV. Between 11 and 14 DIV, subsequent to synapse formation (as revealed by electron microscope observations), GABA release evoked by 56 mM K+ increased up to 5-fold, 75\%of which was Ca2+-dependent. It appears that the complete differentiation of striatal neurons in serum-free medium may provide a suitable model for the study of the physiological and regulatory mechanisms involved in nerve cell development. 0027-8424 Journal Article},
	Author = {Weiss, S. and Pin, J. P. and Sebben, M. and Kemp, D. E. and Sladeczek, F. and Gabrion, J. and Bockaert, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Nerve Tissue Proteins/metabolism;Cell Differentiation;T both;Inositol Phosphates/metabolism;Corpus Striatum/*cytology/embryology;Vasoactive Intestinal Peptide/pharmacology;Microscopy, Electron, Scanning;Synapses/*ultrastructure;Time Factors;Cyclic AMP/metabolism;Synapsins;gamma-Aminobutyric Acid/metabolism;Mice;Animals;Cells, Cultured;23 Technique;Support, Non-U.S. Gov't},
	Number = {7},
	Pages = {2238-42},
	Title = {Synaptogenesis of cultured striatal neurons in serum-free medium: a morphological and biochemical study},
	Uuid = {E6E66F3D-ACB5-42C1-8D94-C20DABACA2CA},
	Volume = {83},
	Year = {1986},
	url = {papers/Weiss_ProcNatlAcadSciUSA1986.pdf}}

@article{Weissman:2004,
	Abstract = {The majority of neurons in the adult neocortex are produced embryonically during a brief but intense period of neuronal proliferation. The radial glial cell, a transient embryonic cell type known for its crucial role in neuronal migration, has recently been shown to function as a neuronal progenitor cell and appears to produce most cortical pyramidal neurons. Radial glial cell modulation could thus affect neuron production, neuronal migration, and overall cortical architecture; however, signaling mechanisms among radial glia have not been studied directly. We demonstrate here that calcium waves propagate through radial glial cells in the proliferative cortical ventricular zone (VZ). Radial glial calcium waves occur spontaneously and require connexin hemichannels, P2Y1 ATP receptors, and intracellular IP3-mediated calcium release. Furthermore, we show that wave disruption decreases VZ proliferation during the peak of embryonic neurogenesis. Taken together, these results demonstrate a radial glial signaling mechanism that may regulate cortical neuronal production.},
	Author = {Weissman, Tamily A. and Riquelme, Patricio A. and Ivic, Lidija and Flint, Alexander C. and Kriegstein, Arnold R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-22 16:00:02 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {10 Development;Calcium Signaling;Animals;Rats;Neocortex;Cell Communication;Rats, Sprague-Dawley;Receptors, Cytoplasmic and Nuclear;Cell Movement;Calcium;Connexins;Research Support, U.S. Gov't, P.H.S.;Neuroglia;Neurons;Calcium Channels;Cell Division;Stem Cells;Receptors, Purinergic P2;Research Support, Non-U.S. Gov't; Spontaneous activity; calcium imaging; neurogenesis; 21 Activity-development; Structure-Activity Relationship; visual cortex; ideas; Grants},
	Month = {9},
	Nlm_Id = {8809320},
	Number = {5},
	Organization = {Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.},
	Pages = {647-61},
	Pii = {S0896627304004970},
	Pubmed = {15339647},
	Title = {Calcium waves propagate through radial glial cells and modulate proliferation in the developing neocortex},
	Uuid = {5906C5F8-FEC2-46D5-A30D-14BC3558B601},
	Volume = {43},
	Year = {2004},
	url = {papers/Weissman_Neuron2004.pdf},
	Bdsk-File-2 = {papers/Weissman_Neuron2004a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2004.08.015}}

@article{Weller:1993,
	Abstract = {The effects of DNA substitution by the thymidine analogue 5-bromodeoxyuridine (BrdU) on cell cycle progression and micronucleus induction were studied in different mammalian cell cultures. Simultaneous flow cytometric measurements of DNA content and side scatter of nuclei in Chinese hamster embryo (CHE) cells revealed a concentration-dependent temporary block in the G2/M phase of the first cell cycle. NIH 3T3 cells and human amniotic fluid fibroblast-like cells, on the contrary, did not show any cell cycle disturbances in the presence of BrdU. Micronucleus frequency increased as soon as CHE cells started to divide and reached a plateau when all cells have divided. The height of this plateau was almost equal for 60 and 100 microM BrdU. This saturation of micronucleus induction was due to a saturation of BrdU incorporation into DNA already at a doses of 60 microM as shown by the BrdU/Hoechst quenching technique. Indirect immunofluorescent staining of kinetochores with CREST antibodies revealed that nearly all BrdU-induced micronuclei were kinetochore-negative suggesting the presence of acentric chromosome fragments in these micronuclei. DNA distributions of micronuclei measured by flow cytometry showed several peaks representing micronuclei which contain DNA fragments of defined sizes induced by non-random breakage of chromosomes 1 and X as verified by flow karyotyping and C-banding.},
	Author = {Weller, E. M. and Dietrich, I. and Viaggi, S. and Beisker, W. and N{\"u}sse, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0267-8357},
	Journal = {Mutagenesis},
	Keywords = {Hamsters;Dose-Response Relationship, Drug;Animals;Humans;Cells, Cultured;Cell Cycle;DNA;Fibroblasts;Mutagens;Micronuclei, Chromosome-Defective;Chromosome Aberrations;15 Retrovirus mechanism;23 Technique;Cricetulus;01 Adult neurogenesis general;3T3 Cells;Karyotyping;Flow Cytometry;Mice;24 Pubmed search results 2008;Bromodeoxyuridine},
	Medline = {94049138},
	Month = {9},
	Nlm_Id = {8707812},
	Number = {5},
	Organization = {GSF-Institut f{\"u}r Biophysikalische Strahlenforschung, Arbeitsgruppe Durchflusszytometrie, Neuherberg, FRG.},
	Pages = {437-44},
	Pubmed = {8231825},
	Title = {Flow cytometric analysis of bromodeoxyuridine-induced micronuclei},
	Uuid = {FFF7B16C-013C-49C9-B5C7-2E4210F87DAC},
	Volume = {8},
	Year = {1993}}

@article{Wellman:2001,
	Abstract = {Chronic stress produces deficits in cognition accompanied by alterations in neural chemistry and morphology. For example, both stress and chronic administration of corticosterone produce dendritic atrophy in hippocampal neurons (Woolley C, Gould E, McEwen BS. 1990. Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons. Brain Res 531:225-231; Watanabe Y, Gould E, McEwen BS, 1992b. Stress induces atrophy of apical dendrites of hippocampal CA3 pyramidal neurons. Brain Res 588:341-345). Prefrontal cortex is also a target for glucocorticoids involved in the stress response (Meaney MJ, Aitken DH. 1985. [(3)H]Dexamethasone binding in rat frontal cortex. Brain Res 328:176-180); it shows neurochemical changes in response to stress (e.g., Luine VN, Spencer RL, McEwen BS. 1993. Effect of chronic corticosterone ingestion on spatial memory performance and hippocampal serotonergic function. Brain Res 616:55-70; Crayton JW, Joshi I, Gulati A, Arora RC, Wolf WA. 1996. Effect of corticosterone on serotonin and catecholamine receptors and uptake sites in rat frontal cortex. Brain Res 728:260-262; Takao K, Nagatani T, Kitamura Y, Yamawaki S. 1997. Effects of corticosterone on 5-HT(1A) and 5-HT(2) receptor binding and on the receptor-mediated behavioral responses of rats. Eur J Pharmacol 333:123-128; Sandi C, Loscertales M. 1999. Opposite effects on NCAM expression in the rat frontal cortex induced by acute vs. chronic corticosterone treatments. Brain Res 828:127-134), and mediates many of the behaviors that are altered by chronic corticosterone administration (e.g., Lyons DM, Lopez JM, Yang C, Schatzberg AF. 2000. Stress-level cortisol treatment impairs inhibitory control of behavior in monkeys. J Neurosci 20:7816-7821). To determine if glucocorticoid-induced morphological changes also occur in medial prefrontal cortex, the effects of chronic corticosterone administration on dendritic morphology in this corticolimbic structure were assessed. Adult male rats received s.c. injections of either corticosterone (10 mg in 250 microL sesame oil; n = 8) or vehicle (250 microL; n = 8) daily for 3 weeks. A third group of rats served as intact controls (n = 4). Brains were stained using a Golgi-Cox procedure and pyramidal neurons in layer II-III of medial prefrontal cortex were drawn; dendritic morphology was quantified in three dimensions. Sholl analyses demonstrated a significant redistribution of apical dendrites in corticosterone-treated animals: the amount of dendritic material proximal to the soma was increased relative to intact rats, while distal dendritic material was decreased relative to intact animals. Thus, chronic glucocorticoid administration dramatically reorganized apical arbors in medial prefrontal cortex. This reorganization likely reflects functional changes and may contribute to stress-induced changes in cognition.},
	Author = {Wellman, C. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Research Support, Non-U.S. Gov't;Dendrites;Rats, Sprague-Dawley;Rats;Pyramidal Cells;Prefrontal Cortex;Corticosterone;Stress;Cell Count;Male;Animals;24 Pubmed search results 2008},
	Medline = {21611752},
	Month = {11},
	Nlm_Id = {0213640},
	Number = {3},
	Organization = {Department of Psychology and Program in Neural Science, Indiana University, 1101 E. 10th Street, Bloomington, IN 47405, USA. wellmanc\@indiana.edu},
	Pages = {245-53},
	Pii = {10.1002/neu.1079},
	Pubmed = {11745662},
	Title = {Dendritic reorganization in pyramidal neurons in medial prefrontal cortex after chronic corticosterone administration},
	Uuid = {07CEEB33-DCF5-48E4-A7ED-878A16B6D90D},
	Volume = {49},
	Year = {2001}}

@article{Wen:2002,
	Abstract = {The functions of the presenilin-1 (PS-1) protein remain largely unknown. In adult brain PS-1 is expressed principally in neurons. However during development PS-1 is expressed more widely including in embryonic neural progenitors. To determine if PS-1 is expressed in neural progenitors in adult hippocampus we used bromodeoxyuridine (BrdU) labeling combined with immunostaining for BrdU, PS-1 and markers of neuronal or glial differentiation. Most BrdU labeled cells also expressed PS-1 at a time when few BrdU labeled cells expressed the early neuronal markers beta-III tubulin or TOAD-64 and none expressed mature neuronal (NeuN or calbindin) or astrocytic (GFAP) markers. Cells expressing PS-1 and the neural progenitor marker nestin were also found. Thus PS-1 is expressed in neural progenitor cells in adult hippocampus implying its possible role in neurogenesis in adult brain.},
	Author = {Wen, P. H. and Friedrich, V. L. and Shioi, J. and Robakis, N. K. and Elder, G. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neurosci Lett},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {2},
	Organization = {Department of Psychiatry, P.O. Box 1229, Mount Sinai School of Medicine, One Gustave Levy Place, 10029, New York, NY, USA},
	Pages = {53-6.},
	Title = {Presenilin-1 is expressed in neural progenitor cells in the hippocampus of adult mice},
	Uuid = {35B9AA18-E7DA-4A30-813D-105812FBAFD9},
	Volume = {318},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11796184}}

@article{Werner:1998,
	Abstract = {Intercellular adhesion molecule 1 (ICAM-1, CD54) is a widely expressed glycoprotein, which plays an important role in leukocyte extravasation and in the interaction of lymphocytes with antigen-presenting cells. In the current study we examined the regulation of ICAM-1 in the mouse facial motor nucleus after facial nerve transection, using immunohistochemistry, confocal laser microscopy and electron microscopy. In the normal facial nucleus ICAM-1 immunoreactivity was restricted to vascular endothelium. Transection of the facial nerve led to a strong and selective upregulation of ICAM-1 on activated microglia. Quantitation of microglial ICAM-1 immunoreactivity revealed a biphasic increase. The first peak 1-2 days post operation paralleling the early stage of microglial activation was followed by a decline at 4-7 days. The second induction of ICAM-1 occurred at day 14 accompanying the period of neuronal cell death and microglial phagocytosis of neuronal debris. Immunoelectron microscopy showed strong ICAM-1 reactivity on the cell membrane of activated microglia at day 2. During the second peak (day 14), ICAM-1 was also observed on lymphocytes adhering to phagocytotic microglia forming aggregates around neuronal debris. No immunolabelling was observed on neurons, astrocytes or oligodendroglia. These data suggest the involvement of ICAM-1 in the adhesion of activated microglia, in their phagocytosis of neuronal debris, and also in the interaction with infiltrating lymphocytes following this injury.},
	Author = {Werner, A. and Kloss, C. U. and Walter, J. and Kreutzberg, G. W. and Raivich, G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {Animals;Intercellular Adhesion Molecule-1;Fluorescent Antibody Technique;Microglia;Female;Axons;Not relevant;11 Glia;Blood-Brain Barrier;Nerve Regeneration;Facial Nerve Injuries;Support, Non-U.S. Gov't;Antibodies;Mice, Inbred Strains;Axotomy;Motor Neurons;Mice;Microscopy, Electron;Facial Nerve;Endothelium, Vascular},
	Medline = {20104427},
	Month = {4},
	Nlm_Id = {0364620},
	Number = {4},
	Organization = {Department of Neuromorphology, Max-Planck Institute of Neurobiology, Martinsried, Germany.},
	Pages = {219-32},
	Pubmed = {10640181},
	Title = {Intercellular adhesion molecule-1 (ICAM-1) in the mouse facial motor nucleus after axonal injury and during regeneration},
	Uuid = {8363E845-DFB2-4CAA-9930-35E22A298D8C},
	Volume = {27},
	Year = {1998}}

@article{Wernig:2004,
	Abstract = {Pluripotency and the potential for continuous self-renewal make embryonic stem (ES) cells an attractive donor source for neuronal cell replacement. Despite recent encouraging results in this field, little is known about the functional integration of transplanted ES cell-derived neurons on the single-cell level. To address this issue, ES cell-derived neural precursors exhibiting neuron-specific enhanced green fluorescent protein (EGFP) expression were introduced into the developing brain. Donor cells implanted into the cerebral ventricles of embryonic rats migrated as single cells into a variety of brain regions, where they acquired complex morphologies and adopted excitatory and inhibitory neurotransmitter phenotypes. Synaptic integration was suggested by the expression of PSD-95 (postsynaptic density-95) on donor cell dendrites, which in turn were approached by multiple synaptophysin-positive host axon terminals. Ultrastructural and electrophysiological data confirmed the formation of synapses between host and donor cells. Ten to 21 d after birth, all EGFP-positive donor cells examined displayed active membrane properties and received glutamatergic and GABAergic synaptic input from host neurons. These data demonstrate that, at the single-cell level, grafted ES cell-derived neurons undergo morphological and functional integration into the host brain circuitry. Antibodies to the region-specific transcription factors Bf1, Dlx, En1, and Pax6 were used to explore whether functional donor cell integration depends on the acquisition of a regional phenotype. Our data show that incorporated neurons frequently exhibit a lacking or ectopic expression of these transcription factors. Thus, the lack of an appropriate regional "code" does not preclude morphological and synaptic integration of ES cell-derived neurons.},
	Author = {Wernig, Marius and Benninger, Felix and Schmandt, Tanja and Rade, Monika and Tucker, Kerry L. and B{\"u}ssow, Heinrich and Beck, Heinz and Br{\"u}stle, Oliver},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Survival;Cell Differentiation;Animals;Stem Cell Transplantation;Cells, Cultured;Rats;Phenotype;Synaptic Transmission;Patch-Clamp Techniques;Antigens, Differentiation;Brain;Rats, Sprague-Dawley;Cell Movement;11 Glia;Green Fluorescent Proteins;17 Transplant Regeneration;Embryo;Injections, Intraventricular;Animals, Newborn;Embryo Research;Neurons;Neurotransmitters;Mice;22 Stem cells;Genes, Reporter;Graft Survival;Luminescent Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {22},
	Organization = {Institute of Reconstructive Neurobiology, University of Bonn Medical Center and Hertie Foundation, University of Bonn, D-53105 Bonn, Germany.},
	Pages = {5258-68},
	Pii = {24/22/5258},
	Pubmed = {15175396},
	Title = {Functional integration of embryonic stem cell-derived neurons in vivo},
	Uuid = {ED520BE0-526C-43BF-86CA-5CB4056D31D1},
	Volume = {24},
	Year = {2004},
	url = {papers/Wernig_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0428-04.200}}

@article{Whartenby:2002,
	Abstract = {Fas-mediated apoptosis is a major physiologic mechanism by which activated T cells are eliminated after antigen-stimulated clonal expansion generates a specific cellular immune response. Because activated T cells are the major effectors of allograft rejection, we hypothesized that genetically modifying allogeneic bone marrow (BM) cells prior to transplantation could provide some protection from host T-cell attack, thus enhancing donor cell engraftment in bone marrow transplantation (BMT). We undertook studies to determine the outcome of lentiviral vector-mediated transduction of Fas ligand (FasL) into lineage antigen-negative (lin(-)) mouse BM cells (lin(-) BMs), in an allogeneic BMT model. FasL-modified lin(-) BMs killed Fas-expressing T cells in vitro. Mice that received transplants of allogeneic FasL(+) lin(-) BMs had enhanced short-term engraftment, after nonmyeloablative conditioning, as compared to controls. We observed no major hepatic toxicity or hematopoietic or immune impairment in recipient mice at these time points. These results suggest potential therapeutic approaches by manipulating lymphohematopoietic stem-progenitor cells to express FasL or other immune-modulating genes in the context of BMT.},
	Author = {Whartenby, Katharine A. and Straley, Erin E. and Kim, Heeje and Racke, Frederick and Tanavde, Vivek and Gorski, Kevin S. and Cheng, Linzhao and Pardoll, Drew M. and Civin, Curt I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Apoptosis;Genetic Vectors;Models, Animal;Green Fluorescent Proteins;Luminescent Proteins;Gene Therapy;Listeria Infections;Animals;Lymphocyte Activation;Graft Enhancement, Immunologic;Disease Susceptibility;Tissue Donors;Base Sequence;Genes, Reporter;Mice, Inbred BALB C;Transfection;Molecular Sequence Data;Bone Marrow Transplantation;Mice, Inbred C57BL;Hematopoietic Stem Cells;Dendritic Cells;T-Lymphocytes;11 Glia;Membrane Glycoproteins;Transplantation, Homologous;Graft Survival;Radiation Chimera;Cell Lineage;Graft Rejection;Transplantation Conditioning;Recombinant Fusion Proteins;Lymphocyte Culture Test, Mixed;Mice;Lentivirus;Research Support, Non-U.S. Gov't;Mice, Transgenic},
	Medline = {22271094},
	Month = {11},
	Nlm_Id = {7603509},
	Number = {9},
	Organization = {Sidney Kimmel Comprehensive Cancer Center at JHU, School of Medicine, Johns Hopkins University, Bunting-Blaustein Cancer Research Building, Room 2M44, 1650 Orleans Street, Baltimore, MD 21231, USA. whartka\@jhmi.edu},
	Pages = {3147-54},
	Pubmed = {12384412},
	Title = {Transduction of donor hematopoietic stem-progenitor cells with Fas ligand enhanced short-term engraftment in a murine model of allogeneic bone marrow transplantation},
	Uuid = {E1D27FC0-8B68-4AF5-9CAB-2EE5C9F738AE},
	Volume = {100},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2002-01-0118}}

@article{White:2001,
	Abstract = {Rat neural crest stem cells (NCSCs) prospectively isolated from uncultured E14.5 sciatic nerve and transplanted into chick embryos generate fewer neurons than do NCSCs isolated from E10.5 neural tube explants. In addition, they differentiate primarily to cholinergic parasympathetic neurons, although in culture they can also generate noradrenergic sympathetic neurons. This in vivo behavior can be explained, at least in part, by a reduced sensitivity of sciatic nerve-derived NCSCs to the neurogenic signal BMP2 and by the observation that cholinergic neurons differentiate at a lower BMP2 concentration than do noradrenergic neurons in vitro. These results demonstrate that neural stem cells can undergo cell-intrinsic changes in their sensitivity to instructive signals, while maintaining multipotency and self-renewal capacity. They also suggest that the choice between sympathetic and parasympathetic fates may be determined by the local concentration of BMP2. 0896-6273 Journal Article},
	Author = {White, P. M. and Morrison, S. J. and Orimoto, K. and Kubu, C. J. and Verdi, J. M. and Anderson, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {10 Development;Norepinephrine/metabolism;Neurons/*cytology/drug effects/metabolism/transplantation;Animals;Cells, Cultured;Chimera;Rats;Transplantation, Heterologous;Phenotype;*Stem Cell Transplantation;Bone Morphogenetic Proteins/metabolism/pharmacology;Stem Cells/*cytology/drug effects;Cell Differentiation/drug effects/*physiology;Neurons, Afferent/cytology;Sympathetic Nervous System/cytology/embryology;Neural Crest/*cytology/embryology;Chick Embryo;Pelvis/embryology;Sciatic Nerve/cytology/embryology/transplantation;Acetylcholine/metabolism;Support, Non-U.S. Gov't;Autonomic Nervous System/cytology/embryology;Antigens, Differentiation/biosynthesis;F;Parasympathetic Nervous System/cytology/embryology},
	Number = {1},
	Organization = {Division of Biology 216-76, California Institute of Technology, Pasadena, CA 91125, USA.},
	Pages = {57-71},
	Pubmed = {11182081},
	Title = {Neural crest stem cells undergo cell-intrinsic developmental changes in sensitivity to instructive differentiation signals},
	Uuid = {F02A0284-B536-45A2-BB52-8352DA667692},
	Volume = {29},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11182081}}

@article{Whitman:2007,
	Abstract = {The adult mammalian olfactory bulb (OB) receives a continuing influx of new interneurons. Neuroblasts from the subventricular zone (SVZ) migrate into the OB and differentiate into granule cells and periglomerular cells that are presumed to integrate into the synaptic circuits of the OB. We have used retroviral infection into the SVZ of mice to label adult-generated granule cells and follow their differentiation and integration into OB circuitry. Using synaptic markers and electron microscopy, we show new granule cells integrating into the reciprocal circuitry of the external plexiform layer (EPL), beginning at 21 d postinfection (dpi). We further show that synapses are formed earlier, beginning at 10 dpi, on the somata and basal dendrites of new cells in the granule cell layer (GCL), before dendritic elaboration in the EPL. In the EPL, elaborate dendritic arbors with spines are first evident at 14 dpi. The density of spines increases from 14 to 28 dpi, and then decreases by 56 dpi. Despite the initial appearance of dendritic spines at 14 dpi in the EPL, no expression of presynaptic or postsynaptic markers is seen until 21 dpi. These data suggest that adult-generated granule cells are first innervated by centrifugal or mitral/tufted cell axon collaterals in the GCL and that these inputs may contribute to their differentiation, maturation, and synaptic integration into the dendrodendritic local circuits found in the EPL.},
	Author = {Whitman, Mary C. and Greer, Charles A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {37},
	Organization = {Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8082, USA.},
	Pages = {9951-61},
	Pii = {27/37/9951},
	Pubmed = {17855609},
	Title = {Synaptic integration of adult-generated olfactory bulb granule cells: basal axodendritic centrifugal input precedes apical dendrodendritic local circuits},
	Uuid = {7DC228E5-D617-4DDA-8D9F-9B05C5D96B2C},
	Volume = {27},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1633-07.2007}}

@article{Whittaker:2000,
	Abstract = {Because many viruses replicate in the nucleus of their host cells, they must have ways of transporting their genome and other components into and out of this compartment. For the incoming virus particle, nuclear entry is often one of the final steps in a complex transport and uncoating program. Typically, it involves recognition by importins (karyopherins), transport to the nucleus, and binding to nuclear pore complexes. Although all viruses take advantage of cellular signals and factors, viruses and viral capsids vary considerably in size, structure, and in how they interact with the nuclear import machinery. Influenza and adenoviruses undergo extensive disassembly prior to genome import; herpesviruses release their genome into the nucleus without immediate capsid disassembly. Polyoma viruses, parvoviruses, and lentivirus preintegration complexes are thought to enter in intact form, whereas the corresponding complexes of onco-retroviruses have to wait for mitosis because they cannot infect interphase nuclei. 1081-0706 Journal Article Review Review, Academic},
	Author = {Whittaker, G. R. and Kann, M. and Helenius, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Annu Rev Cell Dev Biol},
	Keywords = {J pdf;Viruses/*pathogenicity;Nuclear Envelope/virology;Human;Cytoplasm/virology;15 Retrovirus mechanism;Animals;*Viral Physiology;Cell Nucleus/*virology},
	Organization = {Department of Microbiology and Immunology, Cornell University, Ithaca New York, USA. grw7\@cornell.edu},
	Pages = {627-51},
	Pubmed = {11031249},
	Title = {Viral entry into the nucleus},
	Uuid = {9F8ACD09-1E43-409D-B6C5-6C2018B9523E},
	Volume = {16},
	Year = {2000},
	url = {papers/Whittaker_AnnuRevCellDevBiol2000.pdf}}

@article{Whittaker:1998,
	Abstract = {Many viruses replicate in the nucleus of their animal and plant host cells. Nuclear import, export, and nucleo-cytoplasmic shuttling play a central role in their replication cycle. Although the trafficking of individual virus proteins into and out of the nucleus has been well studied for some virus systems, the nuclear transport of larger entities such as viral genomes and capsids has only recently become a subject of molecular analysis. In this review, the general concepts emerging are discussed and a survey is provided of current information on both plant and animal viruses. Summarizing the main findings in this emerging field, it is evident that most viruses that enter or exit the nucleus take advantage of the cell's nuclear import and export machinery. With a few exceptions, viruses seem to cross the nuclear envelope through the nuclear pore complexes, making use of cellular nuclear import and export signals, receptors, and transport factors. In many cases, they capitalize on subtle control systems such as phosphorylation that regulate traffic of cellular components into and out of the nucleus. The large size of viral capsids and their composition (they contain large RNA and DNA molecules for which there are few precedents in normal nuclear transport) make the processes unique and complicated. Prior capsid disassembly (or deformation) is required before entry of viral genomes and accessory proteins can occur through nuclear pores. Capsids of different virus families display diverse uncoating programs which culminate in genome transfer through the nuclear pores. 0042-6822 Journal Article Review Review, Tutorial},
	Author = {Whittaker, G. R. and Helenius, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {Virology},
	Keywords = {Plant Viruses/physiology;Virus Replication/*physiology;*Genome, Viral;J pdf;Molecular Sequence Data;Amino Acid Sequence;Support, U.S. Gov't, P.H.S.;15 Retrovirus mechanism;Animals;Cell Nucleus/*virology},
	Number = {1},
	Organization = {Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, USA. grw7\@cornell.edu},
	Pages = {1-23},
	Pubmed = {9656989},
	Title = {Nuclear import and export of viruses and virus genomes},
	Uuid = {BE1C80A7-A056-477B-B27D-44B73B6780B5},
	Volume = {246},
	Year = {1998},
	url = {papers/Whittaker_Virology1998.pdf}}

@article{Whittemore:1999,
	Abstract = {The effects of specific mitogens and substrates on the proliferative capacity and the differentiated phenotypic plasticity of neural precursor cell populations isolated from the adult rat subventricular zone (SVZ) were examined. SVZ cells were grown on uncoated tissue culture plastic, extracellular matrix, or poly-D-ornithine with either laminin or fibronectin. SVZ neural precursor cells could not be generated with platelet-derived growth factor (PDGF), granulocyte macrophage colony stimulating factor, stem cell factor, heparin-binding epidermal growth factor (HB-EGF), granulocyte colony stimulating factor, or ciliary neurotrophic factor (CNTF), but could be with EGF, fibroblast growth factor 2 (FGF2), and FGF2 plus heparin. Varying combinations of substrate and mitogen resulted in very different expansion rates and/or lineage potential. Neurons, oligodendrocytes, and astrocytes differentiated from all cultures, but EGF-generated neural precursor cells were more restricted to an astrocytic lineage and FGF2-generated neural precursor cells had a greater capacity for neuronal differentiation. In both EGF- and FGF2-generated cell populations, CNTF increased the number of differentiated astrocytes, triiodothyronine oligodendrocytes, PDGF neurons, and brain-derived neurotrophic factor neurons only from EGF cells. Electrophysiological analysis of differentiated cells showed three distinct phenotypes, glial, neuronal, and presumed precursor cells, although the neuronal properties were immature. Collectively, these data indicate that CNS neural precursor cell populations isolated with different mitogens and substrates are intrinsically different and their characteristics cannot be directly compared. 0014-4827 Journal Article},
	Author = {Whittemore, S. R. and Morassutti, D. J. and Walters, W. M. and Liu, R. H. and Magnuson, D. S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Exp Cell Res},
	Keywords = {Neuroglia/cytology/drug effects/physiology;Heparin/pharmacology;Cell Differentiation/drug effects;Electrophysiology;Lateral Ventricles/*cytology;In Vitro;Animals;Rats;Phenotype;C abstr;Fibronectins/pharmacology;Epidermal Growth Factor/pharmacology;Support, Non-U.S. Gov't;Neurons/*cytology/*drug effects/physiology;Growth Substances/pharmacology;04 Adult neurogenesis factors;Fibroblast Growth Factor 2/pharmacology;Support, U.S. Gov't, P.H.S.;Mitogens/*pharmacology;Stem Cells/*cytology/*drug effects/physiology;Cell Division/drug effects},
	Number = {1},
	Organization = {The Miami Project, University of Miami School of Medicine, Miami, Florida 33136, USA. swhittemore\@louisville.edu},
	Pages = {75-95},
	Pubmed = {10502401},
	Title = {Mitogen and substrate differentially affect the lineage restriction of adult rat subventricular zone neural precursor cell populations},
	Uuid = {87F9709C-B9EA-4886-AF23-B15036754FEA},
	Volume = {252},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10502401}}

@article{Wickelgren:2002,
	Abstract = {1095-9203 News},
	Author = {Wickelgren, I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Journal = {Science},
	Keywords = {Neurons/*physiology;Human;Animals;Stem Cell Transplantation;Spinal Nerves/*physiology;Cyclic AMP/metabolism/therapeutic use;Chondroitin ABC Lyase/metabolism/therapeutic use;Recovery of Function;Stem Cells/physiology;Growth Substances/therapeutic use;Myelin Proteins/genetics/immunology/metabolism;Receptors, Cell Surface/antagonists &inhibitors/metabolism;Myelin-Associated Glycoprotein/metabolism;Olfactory Mucosa/cytology;Clinical Trials;01 Adult neurogenesis general;Neuroglia/physiology/transplantation;Methylprednisolone/therapeutic use;Spinal Cord Injuries/drug therapy/surgery/*therapy;Growth Inhibitors/antagonists &inhibitors/metabolism;Neuroprotective Agents/therapeutic use;*Nerve Regeneration;4-Aminopyridine/therapeutic use;Combined Modality Therapy;A both},
	Number = {5579},
	Pages = {178-81},
	Title = {Neuroscience. Animal studies raise hopes for spinal cord repair},
	Uuid = {26798064-237E-4B42-97C7-8E3669ED064C},
	Volume = {297},
	Year = {2002}}

@article{Wienecke:1997,
	Abstract = {The tuberous sclerosis-2 (TSC2) gene is linked to tuberous sclerosis (TSC), a dominantly inherited genetic syndrome in which inactivation of the normal TSC2 allele is associated with the development of mostly benign tumors and focal dysplasias. TSC2 encodes the protein tuberin, which is a widely expressed 180-kd polypeptide that exhibits specific GTPase activating activity toward Rap1 in vitro and co-localizes with Rap1 in cultured cells. In this study, we have performed immunohistochemical analyses, using affinity-purified anti-tuberin antibodies, to study the distribution of tuberin in a panel of normal human organs that are commonly affected by TSC. Cryosections indicated that tuberin is widely expressed at low levels. More intense staining of tuberin, in the cryosections and in paraffin sections, was observed in the small blood vessels of many organs, including the kidney, skin, and adrenal gland. High levels of tuberin were also detected in cortical neurons and cerebellar Purkinje cells. These findings imply that loss-of-function mutations in TSC2 might lead to the development of highly vascularized tumors, subcortical tubers, and focal atrophy of the cerebellar cortex, which are features commonly associated with TSC. Moreover, Rap1 was also found to be highly expressed in many of the same cells that contained high levels of tuberin, suggesting a functional interaction between tuberin and Rap1 in these tissues.},
	Author = {Wienecke, R. and Maize, J. C. and Reed, J. A. and de Gunzburg, J. and Yeung, R. S. and DeClue, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Tuberous Sclerosis;Tumor Suppressor Proteins;10 Development;research support, non-u.s. gov't;Repressor Proteins;Immunohistochemistry;GTP-Binding Proteins;rap GTP-Binding Proteins;10 genetics malformation;Myocardium;Kidney;Skin;Humans;Cerebral Cortex;24 Pubmed search results 2008;Genes, Tumor Suppressor},
	Month = {1},
	Nlm_Id = {0370502},
	Number = {1},
	Organization = {Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, Maryland 20892, USA.},
	Pages = {43-50},
	Pubmed = {9006320},
	Title = {Expression of the TSC2 product tuberin and its target Rap1 in normal human tissues},
	Uuid = {50EEB9BC-434D-4103-9BDE-C26A04DC263E},
	Volume = {150},
	Year = {1997}}

@article{Wilairat:1978,
	Abstract = {0024-3205 Journal Article},
	Author = {Wilairat, P. and Yuthavong, Y. and Khungvanlert, R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Life Sci},
	Keywords = {Erythrocytes/cytology/*drug effects;Female;EE, DMSO, abstr;08 Aberrant cell cycle;In Vitro;Cell Fusion/drug effects;Erythrocyte Membrane/metabolism;Dimethyl Sulfoxide/*pharmacology;Chickens;Animals},
	Number = {22},
	Pages = {1993-7},
	Pubmed = {672441},
	Title = {Effect of membrane modification on cell fusion of hen erythrocytes induced by dimethyl sulfoxide},
	Uuid = {0AD45407-4683-469F-8405-9EE6D1CA4649},
	Volume = {22},
	Year = {1978},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=672441}}

@article{Wilbrecht:2002,
	Abstract = {It is not known whether the addition of new neurons to the high vocal center (HVC) of juvenile zebra finches permits vocal learning or is the consequence of it. To tease apart these two, we performed surgery on 26- d-old juveniles. The operations were removal of both cochleae and unilateral or bilateral denervation of the syrinx. Ability to imitate a tutor song was little affected by unilateral syringeal denervation but was severely hindered by bilateral denervation or deafening. Recruitment of new HVC neurons was studied by injecting BrdU, a cell birth marker, on post-hatching days 61-65 and killing the animals 30 d later. Deafening or bilateral denervation did not alter the number of BrdU-labeled neurons in HVC, but unilateral denervation nearly doubled this number in the intact side. This doubling was transient, was blocked by deafening, and was not seen in birds that received BrdU injections earlier or later in vocal ontogeny. The adult number of HVC neurons was not affected by any of our surgical procedures. Apparently experience does not affect the total number of neurons in adult HVC, but some kinds of experience can, during narrowly defined times, influence the recruitment of new HVC neurons.},
	Author = {Wilbrecht, L. and Crionas, A. and Nottebohm, F.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:34 -0400},
	Journal = {J Neurosci},
	Keywords = {Drug Administration Schedule;Larynx/physiology;Songbirds;Neurons/cytology/*physiology;Deafness/physiopathology;Denervation;Cell Count;Animal;Brain/cytology/*physiology;Bromodeoxyuridine/administration &dosage/pharmacokinetics;Time Factors;Hearing/physiology;Male;01 Adult neurogenesis general;Support, Non-U.S. Gov't;Cochlea/innervation/physiology;Recruitment (Neurology)/*physiology;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Vocalization, Animal/*physiology;Learning/*physiology;A both},
	Number = {3},
	Organization = {Laboratory of Animal Behavior, The Rockefeller University, New York, New York 10021, USA. wilbrel\@mail.rockefeller.edu.},
	Pages = {825-31.},
	Title = {Experience affects recruitment of new neurons but not adult neuron number},
	Uuid = {99281C19-47C0-46B6-A552-A6D2BB070917},
	Volume = {22},
	Year = {2002},
	url = {papers/Wilbrecht_JNeurosci2002.pdf}}

@article{Wilkinson:2001,
	Abstract = {The control of cell movement during development is essential for forming and stabilizing the spatial organization of tissues and cell types. During initial steps of tissue patterning, distinct regional domains or cell types arise at appropriate locations, and the movement of cells is constrained in order to maintain spatial relationships during growth. In other situations, the guidance of migrating cells or neuronal growth cones to specific destinations underlies the establishment or remodeling of a pattern. Eph receptor tyrosine kinases and their ephrin ligands are key players in controlling these cell movements in many tissues and at multiple stages of patterning.},
	Author = {Wilkinson, D. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {1471-003X},
	Journal = {Nat Rev Neurosci},
	Keywords = {Neurons;Receptor Protein-Tyrosine Kinases;10 Development;Ligands;Membrane Proteins;Signal Transduction;10 circuit formation;Growth Cones;Receptor, EphA1;Body Patterning;Nervous System;Animals;Cell Movement;24 Pubmed search results 2008;review;Axons},
	Month = {3},
	Nlm_Id = {100962781},
	Number = {3},
	Organization = {Division of Developmental Neurobiology, National Institute for Medical Research, Ridgeway, Mill Hill, London NW7 1AA, UK. dwilkin\@nimr.mrc.ac.uk},
	Pages = {155-64},
	Pubmed = {11256076},
	Title = {Multiple roles of EPH receptors and ephrins in neural development},
	Uuid = {F526E1A8-2B4D-447B-859D-D14D0691868F},
	Volume = {2},
	Year = {2001}}

@article{Williams:2002,
	Abstract = {Brain perivascular macrophages are a major target of simian immunodeficiency virus (SIV) infection in rhesus macaques and HIV infection in humans. Perivascular macrophages are distinct from parenchymal microglia in their location, morphology, expression of myeloid markers, and turnover in the CNS. In contrast to parenchymal microglia, perivascular macrophages are continuously repopulated by blood monocytes, which undergo maturation to macrophages on entering the central nervous system (CNS). We studied differences in monocyte/macrophages in vivo that might account for preferential infection of perivascular macrophages by SIV. In situ hybridization for SIV and proliferating cellular nuclear antigen (PCNA) immunohistochemistry demonstrated that SIV-infected and PCNA-positive cells were predominantly found in perivascular cuffs of viremic animals and in histopathological lesions that characterize SIV encephalitis (SIVE) in animals with AIDS. Multilabel techniques including double-label immunohistochemistry and combined in situ hybridization and immunofluorescence confocal microscopy revealed numerous infected perivascular macrophages that were PCNA-positive. Outside the CNS, SIV-infected, PCNA-expressing macrophage subpopulations were found in the small intestine and lung of animals with AIDS. While PCNA is used as a marker of cell proliferation it is also strongly expressed in non-dividing cells undergoing DNA synthesis and repair. Therefore, more specific markers for cell proliferation including Ki-67, topoisomerase IIalpha, and bromodeoxyuridine (BrdU) incorporation were used which indicated that PCNA-positive cells within SIVE lesions were not proliferating. These observations are consistent with perivascular macrophages as terminally differentiated, non-dividing cells and underscores biological differences that could potentially define mechanisms of preferential, productive infection of perivascular macrophages in the rhesus macaque model of neuroAIDS. These studies suggest that within CNS and non-CNS tissues there exist subpopulations of macrophages that are SIV-infected and express PCNA.},
	Author = {Williams, Kenneth and Schwartz, Annette and Corey, Sarah and Orandle, Marlene and Kennedy, William and Thompson, Brendon and Alvarez, Xavier and Brown, Charlie and Gartner, Suzanne and Lackner, Andrew},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Research Support, Non-U.S. Gov't;Macaca mulatta;Research Support, U.S. Gov't, P.H.S.;Proliferating Cell Nuclear Antigen;Simian Acquired Immunodeficiency Syndrome;Cell Division;11 Glia;Macrophages;SIV;Animals;Brain},
	Medline = {22152816},
	Month = {8},
	Nlm_Id = {0370502},
	Number = {2},
	Organization = {Department of Medicine, Harvard Medical School, Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. kenneth\_williams\@hms.harvard.edu},
	Pages = {575-85},
	Pubmed = {12163382},
	Title = {Proliferating cellular nuclear antigen expression as a marker of perivascular macrophages in simian immunodeficiency virus encephalitis},
	Uuid = {4DD489F8-29A6-47A0-BCCA-F1111CBD6864},
	Volume = {161},
	Year = {2002}}

@article{Williams:2005b,
	Abstract = {Regressive events that refine exuberant or inaccurate connections are critical in neuronal development. We used multi-photon, time-lapse imaging to examine how dendrites of Drosophila dendritic arborizing (da) sensory neurons are eliminated during early metamorphosis, and how intrinsic and extrinsic cellular mechanisms control this deconstruction. Removal of the larval dendritic arbor involves two mechanisms: local degeneration and branch retraction. In local degeneration, major branch severing events entail focal disruption of the microtubule cytoskeleton, followed by thinning of the disrupted region, severing and fragmentation. Retraction was observed at distal tips of branches and in proximal stumps after severing events. The pruning program of da neuron dendrites is steroid induced; cell-autonomous dominant-negative inhibition of steroid action blocks local degeneration, although retraction events still occur. Our data suggest that steroid-induced changes in the epidermis may contribute to dendritic retraction. Finally, we find that phagocytic blood cells not only engulf neuronal debris but also attack and sever intact branches that show signs of destabilization.},
	Author = {Williams, Darren W. and Truman, James W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Cytoskeleton;Dendrites;Receptors, Steroid;Phagocytes;Research Support, U.S. Gov't, P.H.S.;Abdomen;Microscopy, Video;Drosophila melanogaster;Research Support, N.I.H., Extramural;Metamorphosis, Biological;Fluorescent Dyes;Neurons, Afferent;Animals;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {8701744},
	Number = {16},
	Organization = {Department of Biology, University of Washington, Seattle, WA 98195, USA. dww\@u.washington.edu},
	Pages = {3631-42},
	Pii = {dev.01928},
	Pubmed = {16033801},
	Title = {Cellular mechanisms of dendrite pruning in Drosophila: insights from in vivo time-lapse of remodeling dendritic arborizing sensory neurons},
	Uuid = {650F9964-00AB-11DB-9E68-000D9346EC2A},
	Volume = {132},
	Year = {2005},
	url = {papers/Williams_Development2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.01928}}

@article{Williams:2001,
	Abstract = {Perivascular cells are a heterogeneous population found in the central nervous system (CNS) and the peripheral nervous system (PNS). Several terms are used for these cells, including perivascular cells, perivascular macrophages, perivascular microglia, fluorescent granular perithelial cells (FGP), or Mato cells. Different terminology used may reflect subpopulations of perivascular cells within different anatomic regions and experimental paradigms, neuropathological conditions, and species studied. Different terminology also points to the lack of clear consensus of what cells are perivascular cells in different disease states and models, especially with breakdown of the blood-brain barrier (BBB). Despite this, there is consensus that perivascular cells, although a minor component of the CNS, are important immunoregulatory cells. Perivascular cells are bone marrow derived, continuously turn over in the CNS, and are found adjacent to CNS vessels. Thus, they are potential sensors of CNS and peripheral immune system perturbations; are activated in models of CNS inflammation, autoimmune disease, neuronal injury and death; and are implicated as phagocytic and pinocytotic cells in models of stroke and hypertension. Recent evidence from our laboratory implicate perivascular cells as primary targets of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infection in the CNS of humans and macaques. This article reviews current knowledge of perivascular cells, including anatomic location and nomenclature and putative immunoregulatory roles, and discusses new data on the infection of these cells by SIV, their accumulation after SIV infection, and a possible role of the immune system in SIV encephalitis.},
	Author = {Williams, K. and Alvarez, X. and Lackner, A. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Research Support, Non-U.S. Gov't;Central Nervous System;Nerve Degeneration;Bone Marrow Cells;AIDS Dementia Complex;Immunologic Surveillance;Research Support, U.S. Gov't, P.H.S.;11 Glia;Microglia;review, tutorial;Blood Vessels;Macrophages;Humans;Animals;Immune System;review},
	Medline = {21479411},
	Month = {11},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Medicine, Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. kenneth\_williams\@hms.harvard.edu},
	Pages = {156-64},
	Pii = {10.1002/glia.1105},
	Pubmed = {11596124},
	Title = {Central nervous system perivascular cells are immunoregulatory cells that connect the CNS with the peripheral immune system},
	Uuid = {5D113672-C206-45F0-9FB3-1B2349459B9D},
	Volume = {36},
	Year = {2001},
	url = {papers/Williams_Glia2001.pdf}}

@article{Williams:2005a,
	Abstract = {The genesis of dendritic shape during development sets in place key characteristics of a neuron's physiology and connectivity. During this construction, a cell interprets intrinsic cell-specific developmental programs and cues from the environment to generate its final phenotype. In insects that undergo complete metamorphosis certain neurons function in the larval nervous system and then remodel to generate an adult-specific arbor. By studying the dendrites of neurons that undergo such a cellular metamorphosis, one can explore the mechanisms that underlie both stereotyped pruning and local remodeling. Live imaging techniques in intact Drosophila have been especially useful in examining the outgrowth of the adult-specific dendritic arbors in remodeling dendritic arborizing (da) sensory neurons. These neurons show an initial scaffold-building phase during which the cell establishes the overall shape of the arbor and then switch to an elaboration phase where the arbor is filled out with higher order branches. The cellular machinery employed during these two phases is different, with branch retraction being a prominent feature of the scaffold building phase but absent from the elaboration phase. The transition between these two modes does not appear to be "hard-wired" but is plastic and under the extrinsic control of developmental hormones. This transition in branch dynamics may also involve changes in calcium signaling in the growing arbor. The potential relationship between hormone-induced transcriptional change and the calcium dynamics in dendritic morphogenesis is discussed.},
	Author = {Williams, D. W. and Truman, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0022-3034},
	Journal = {J Neurobiol},
	Keywords = {Dendrites;Insects;Research Support, U.S. Gov't, P.H.S.;Time Factors;Research Support, N.I.H., Extramural;Metamorphosis, Biological;Nervous System;Hormones;Animals;24 Pubmed search results 2008;review;Neurons},
	Month = {7},
	Nlm_Id = {0213640},
	Number = {1},
	Organization = {Department of Biology, University of Washington, Seattle, Washington 98195, USA.},
	Pages = {24-33},
	Pubmed = {15884009},
	Title = {Remodeling dendrites during insect metamorphosis},
	Uuid = {689B59D5-F466-4BED-AF06-D27CD81960F8},
	Volume = {64},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/neu.20151}}

@article{Williams:1992,
	Abstract = {We have compared phenotypic and functional properties of surgically derived adult human microglia to autologous and allogenic peripheral blood-derived monocytes and to astrocytes derived from the same surgical resection. We found that microglia differed from peripheral blood monocytes with respect to adhesion properties and survival rates in vitro. Microglia, similar to resident macrophages in different tissues, expressed many but not all (CD4, Leu-M3, non-specific esterase) monocyte/macrophage associated markers tested, a pattern similar to that of terminally differentiated cells of this lineage. As with other human tissue macrophages, but in contrast to astrocytes, microglia did not undergo DNA synthesis in vitro, assessed using BrdU incorporation. Under basal culture conditions the majority of microglia of all morphologic subtypes (ameboid, bipolar, ramified) expressed MHC class II molecules; by flow cytometric analysis, mean fluorescence intensity of these cells was less than that of blood monocytes (relative to isotype control). In vitro MHC class II antigen expression on microglia, under basal and interferon gamma activating conditions, was greater than on astrocytes. Freshly derived T cells cultured with 1-10\%autologous microglia plus Candida albicans underwent active proliferation, indicating the functional capacity of the microglia to serve as antigen-presenting cells.},
	Author = {Williams, K. and Bar-Or, A. and Ulvestad, E. and Olivier, A. and Antel, J. P. and Yong, V. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Monocytes;Research Support, Non-U.S. Gov't;Neuroglia;Phenotype;Histocompatibility Antigens Class II;Astrocytes;Comparative Study;Cell Division;Cell Survival;11 Glia;Humans;Cells, Cultured;Major Histocompatibility Complex},
	Medline = {92388944},
	Month = {9},
	Nlm_Id = {2985192R},
	Number = {5},
	Organization = {Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Quebec, Canada.},
	Pages = {538-49},
	Pubmed = {1517774},
	Title = {Biology of adult human microglia in culture: comparisons with peripheral blood monocytes and astrocytes},
	Uuid = {490AFE1B-1B85-4380-85BA-8DCB1AFFA090},
	Volume = {51},
	Year = {1992}}

@article{Williams:2004,
	Abstract = {In vivo time-lapse multiphoton microscopy was used to analyze the remodeling of the dendritic arborizing (da) sensory neuron known as dorsal dendritic arborizing neuron E (ddaE) during metamorphosis. After its larval processes have been removed, the cell body of ddaE repositions itself on the body wall between 25 and 40 hr after puparium formation (APF) and begins its adult outgrowth at 40 hr APF. The scaffold of the arbor is laid down between 40 and 54 hr APF, when growth is characterized by high filopodial activity at both terminal and interstitial positions and by branch retraction along with branch establishment. Later in development, filopodial activity remains high but is confined to terminal branches, and branch retraction is no longer seen. Treatment with the insect hormone juvenile hormone (JH), a key regulator of metamorphosis, alters the shape and complexity of the adult dendritic tree in a time-dependent manner. Early treatments with juvenile hormone mimic (JHm) appear to repress extension programs and maintain retraction programs. With later JHm treatments, extension programs appear normal, but retraction programs are maintained beyond their normal time. The JH treatments show the importance of retraction programs in establishing the overall arbor shape.},
	Author = {Williams, Darren W. and Truman, James W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Pupa;Dendrites;Cell Differentiation;Juvenile Hormones;Larva;Research Support, U.S. Gov't, P.H.S.;Pyridines;Time Factors;Animals, Genetically Modified;Drosophila;Metamorphosis, Biological;Microscopy, Fluorescence, Multiphoton;Neurons, Afferent;Genes, Reporter;Animals;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {7},
	Organization = {Department of Biology, University of Washington, Seattle, Washington 98195-1800, USA. dww\@u.washington.edu},
	Pages = {1541-50},
	Pii = {24/7/1541},
	Pubmed = {14973231},
	Title = {Mechanisms of dendritic elaboration of sensory neurons in Drosophila: insights from in vivo time lapse},
	Uuid = {6CA69234-AF45-42DE-BE44-1801785C662F},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4521-03.2004}}

@article{Williams:2005,
	Author = {Williams, Bryan R. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1087-0156},
	Journal = {Nat Biotechnol},
	Keywords = {23 RNAi;23 Technique},
	Month = {2},
	Nlm_Id = {9604648},
	Number = {2},
	Organization = {Bryan R.G. Williams is at the Cleveland Clinic Foundation, Department of Cancer Biology, NB40 The Lerner Research Institute, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA. williab\@ccf.org.},
	Pages = {181-2},
	Pii = {nbt0205-181},
	Pubmed = {15696144},
	Title = {Dicing with siRNA},
	Uuid = {C9FCF7D6-CA59-421C-B56F-A55F911A57C9},
	Volume = {23},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nbt0205-181}}

@article{Williams:2006,
	Abstract = {Pruning is important for sculpting neural circuits, as it removes excessive or inaccurate projections. Here we show that the removal of sensory neuron dendrites during pruning in Drosophila melanogaster is directed by local caspase activity. Suppressing caspase activity prevented dendrite removal, whereas a global activation of caspases within a neuron caused cell death. A new genetically encoded caspase probe revealed that caspase activity is confined to the degenerating dendrites of pruning neurons.},
	Author = {Williams, Darren W. and Kondo, Shu and Krzyzanowska, Agnieszka and Hiromi, Yasushi and Truman, James W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {research support, n.i.h., extramural ;Animals;Enzyme Activation;Ganglia, Spinal;Enzyme Inhibitors;Fluorescent Antibody Technique;Apoptosis;Neurons, Afferent;Animals, Genetically Modified;comparative study ;Caspases;Time Factors;Dendrites;research support, non-u.s. gov't ;Analysis of Variance;Drosophila melanogaster;24 Pubmed search results 2008;Drosophila Proteins},
	Month = {10},
	Nlm_Id = {9809671},
	Number = {10},
	Organization = {MRC Centre for Developmental Neurobiology, King's College London, London SE1 1UL, UK. darren.williams\@kcl.ac.uk},
	Pages = {1234-6},
	Pii = {nn1774},
	Pubmed = {16980964},
	Title = {Local caspase activity directs engulfment of dendrites during pruning},
	Uuid = {BAF58864-F066-4756-AF20-1930886FEB55},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1774}}

@article{Williams:1997,
	Abstract = {When exposed to platelet-derived growth factor (PDGF), uncommitted neuroepithelial cells from the developing cortex of embryonic day 14 (E14) rats develop into neurons. Outward signs of the neuronal phenotype are not observed for 4 days following exposure to PDGF. However, only a brief (2-3 hr) period of PDGF receptor activation is required to initiate neuronal development. During the window of receptor activation, RNA synthesis is essential, but protein synthesis is not. These observations indicate that specification of neuronal fate is mediated by an immediate early gene response. 0896-6273 Journal Article},
	Author = {Williams, B. P. and Park, J. K. and Alberta, J. A. and Muhlebach, S. G. and Hwang, G. Y. and Roberts, T. M. and Stiles, C. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {RNA/biosynthesis;Cell Differentiation;Gene Expression/*drug effects;Rats;Neurons/*cytology/drug effects;Cerebral Cortex/cytology/metabolism;Cerebral Ventricles/*cytology;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Platelet-Derived Growth Factor/metabolism/*pharmacology;Animals;Support, Non-U.S. Gov't;*Genes, Immediate-Early;C abstr;Stem Cells/*cytology},
	Number = {4},
	Organization = {Department of Microbiology and Molecular Genetics, Harvard Medical School and the Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA.},
	Pages = {553-62},
	Pubmed = {9136765},
	Title = {A PDGF-regulated immediate early gene response initiates neuronal differentiation in ventricular zone progenitor cells},
	Uuid = {DB9296BE-91D0-4B59-9430-2588A81C5A40},
	Volume = {18},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9136765}}

@article{Williams:1991,
	Abstract = {The role of edema in the pathogenesis of hypoxic-ischemic injury in the immature brain is controversial. We studied 15 chronically instrumented fetal sheep following transient cerebral ischemia, to estimate changes in extracellular space using an impedance technique, to quantify the electroencephalogram with real-time spectral analysis, and to assess histologic outcome 3 days after the insult. These measurements were made in the parasagittal cortex. There was a rapid loss of extracellular space from 5 +/- 2 minutes after the onset of ischemia. Following 10 minutes of ischemia (n = 7) the intracellular edema peaked but then quickly resolved (6 +/- 4 minutes), and mild selective neuronal loss was seen. In contrast, the swelling was biphasic after 30-40 minutes of ischemia (n = 8). The early edema resolved slowly (28 +/- 12 minutes) but incompletely, and secondary swelling began at 7 +/- 2 hours and peaked at 28 +/- 6 hours. The early swelling was the more severe. Postinsult epileptiform activity began at 8 +/- 2 hours and peaked at 10 +/- 3 hours; later there was laminar necrosis of the underlying cortex. The secondary decrease of extracellular space indicates that a progressive loss of membrane function started with the onset of postischemic epileptiform activity. The increased metabolic load of the epileptiform activity may have worsened this delayed deterioration.},
	Author = {Williams, C. E. and Gunn, A. and Gluckman, P. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0039-2499},
	Journal = {Stroke},
	Keywords = {Epilepsy;Electroencephalography;Research Support, Non-U.S. Gov't;21 Neurophysiology;Female;Brain Edema;Sheep;Pregnancy;Animals;Brain;24 Pubmed search results 2008;Ischemic Attack, Transient;21 Epilepsy},
	Medline = {91220353},
	Month = {4},
	Nlm_Id = {0235266},
	Number = {4},
	Organization = {Department of Paediatrics, University of Auckland, New Zealand.},
	Pages = {516-21},
	Pubmed = {2024281},
	Title = {Time course of intracellular edema and epileptiform activity following prenatal cerebral ischemia in sheep},
	Uuid = {C77742F3-EB39-4610-8D9F-AAB45B06C930},
	Volume = {22},
	Year = {1991}}

@article{Winship:2008,
	Abstract = {Functional mapping and microstimulation studies suggest that recovery after stroke damage can be attributed to surviving brain regions taking on the functional roles of lost tissues. Although this model is well supported by data, it is not clear how activity in single neurons is altered in relation to cortical functional maps. It is conceivable that individual surviving neurons could adopt new roles at the expense of their usual function. Alternatively, neurons that contribute to recovery may take on multiple functions and exhibit a wider repertoire of neuronal processing. In vivo two-photon calcium imaging was used in adult mice within reorganized forelimb and hindlimb somatosensory functional maps to determine how the response properties of individual neurons and glia were altered during recovery from ischemic damage over a period of 2-8 weeks. Single-cell calcium imaging revealed that the limb selectivity of individual neurons was altered during recovery from ischemia, such that neurons normally selective for a single contralateral limb processed information from multiple limbs. Altered limb selectivity was most prominent in border regions between stroke-altered forelimb and hindlimb macroscopic map representations, and peaked 1 month after the targeted insult. Two months after stroke, individual neurons near the center of reorganized functional areas became more selective for a preferred limb. These previously unreported forms of plasticity indicate that in adult animals, seemingly hardwired cortical neurons first adopt wider functional roles as they develop strategies to compensate for loss of specific sensory modalities after forms of brain damage such as stroke.},
	Author = {Winship, Ian R. and Murphy, Timothy H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Optics;Calcium Signaling;Photic Stimulation;Animals;Recovery of Function;Neuronal Plasticity;Afferent Pathways;Functional Laterality;Neurons, Afferent;Staining and Labeling;Mice, Inbred C57BL;research support, non-u.s. gov't;Male;Nerve Regeneration;Stroke;Adaptation, Physiological;Neurons;Brain Ischemia;Extremities;Somatosensory Cortex;Mice;24 Pubmed search results 2008;Brain Mapping},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {26},
	Organization = {Department of Psychiatry, Brain Research Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.},
	Pages = {6592-606},
	Pii = {28/26/6592},
	Pubmed = {18579732},
	Title = {In vivo calcium imaging reveals functional rewiring of single somatosensory neurons after stroke},
	Uuid = {4E4EFA22-1601-476A-8CBB-62260A35A732},
	Volume = {28},
	Year = {2008},
	url = {papers/Winship_JNeurosci2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0622-08.2008}}

@article{Winter:1995,
	Abstract = {Within the central nervous system (CNS) ciliary neurotrophic factor (CNTF) is expressed by astrocytes where it remains stored as an intracellular protein; its release and function as an extracellular ligand are thought to occur in the event of cellular injury. We find that overexpression of CNTF in transgenic mice recapitulates the glial response to CNS lesion, as does its injection into the uninjured brain. These results demonstrate that CNTF functions as an inducer of reactive gliosis, a condition associated with a number of neurological diseases of the CNS. 95320176 0027-8424 Journal Article},
	Author = {Winter, C. G. and Saotome, Y. and Levison, S. W. and Hirsh, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {*Nerve Degeneration/drug effects;Human;Ciliary Neurotrophic Factor;Rats;Glial Fibrillary Acidic Protein/analysis/biosynthesis;Macrophage-1 Antigen/analysis;Animal;Mice, Transgenic;G abstr;11 Glia;Neurons, Afferent/metabolism/pathology;Gliosis/chemically induced/pathology/*physiopathology;Support, Non-U.S. Gov't;Astrocytes/*physiology;Nerve Tissue Proteins/analysis/*biosynthesis/*pharmacology;DNA, Complementary;Mice;Gene Expression;Recombinant Proteins/pharmacology;Nerve Growth Factors/biosynthesis/pharmacology;Olfactory Bulb/metabolism/pathology},
	Number = {13},
	Organization = {Department of Biochemistry and Molecular Biophysics, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.},
	Pages = {5865-9},
	Pubmed = {7597043},
	Title = {A role for ciliary neurotrophic factor as an inducer of reactive gliosis, the glial response to central nervous system injury},
	Uuid = {B7469FB2-E4C2-4334-B8AB-3AD5A30F28D2},
	Volume = {92},
	Year = {1995},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7597043}}

@article{Witting:2000,
	Abstract = {Microglia, the tissue macrophages of the brain, play a crucial role in recognition and phagocytic removal of apoptotic neurons. The microglial receptors for recognition of apoptotic neurons are not yet characterized. Here we established a co-culture model of primary microglia and cerebellar granule neurons to examine the receptor systems involved in recognition/uptake of apoptotic neurons. Treatment with 100 microM S-nitrosocysteine induced apoptosis of cerebellar neurons as indicated by nuclear condensation and phosphatidylserine exposure to the exoplasmic leaflet of the plasma membrane. Microglial cells were added to neurons 2 h after apoptosis induction and co-cultured for 6 h in the presence of ligands that inhibit recognition by binding to respective receptors. Binding/phagocytosis was determined after combined 4', 6-diamidino-2-phenylindole/propidium iodide (for apoptotic/necrotic neurons) and lectin staining (for microglia). Uptake of apoptotic neurons was reduced by N-acetylglucosamine or galactose, suggesting that recognition involves asialoglycoprotein-like lectins. Furthermore, the inhibition of microglial binding/uptake of apoptotic neurons by RGDS peptide suggests a role of microglial vitronectin receptor. As microglia selectively bind lipid vesicles enriched in phosphatidylserine and O-phospho-L-serine interfered with the uptake of apoptotic neurons, an involvement of phosphatidylserine receptor is rather likely. Apoptotic neurons do not release soluble signals that serve to attract or activate microglia. Collectively, these results suggest that apoptotic neurons generate a complex surface signal recognized by different receptor systems on microglia.},
	Author = {Witting, A. and M{\"u}ller, P. and Herrmann, A. and Kettenmann, H. and Nolte, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0022-3042},
	Journal = {J Neurochem},
	Keywords = {Microscopy, Video;Phagocytosis;Animals;Cells, Cultured;Nitroso Compounds;Rats;Integrins;Macrophages;Receptors, Vitronectin;S-Nitrosothiols;Apoptosis;Microglia;Phosphatidylserines;Chemotaxis;Rats, Wistar;11 Glia;Cysteine;Support, Non-U.S. Gov't;Animals, Newborn;Coculture;Cerebral Cortex;Neurons;Cerebellum;Necrosis;Lectins},
	Medline = {20396180},
	Month = {9},
	Nlm_Id = {2985190R},
	Number = {3},
	Organization = {Max Delbr{\"u}ck Center for Molecular Medicine, Cellular Neurosciences, Berlin, Germany.},
	Pages = {1060-70},
	Pubmed = {10936187},
	Title = {Phagocytic clearance of apoptotic neurons by Microglia/Brain macrophages in vitro: involvement of lectin-, integrin-, and phosphatidylserine-mediated recognition},
	Uuid = {D3E13CC3-8DFE-4D64-8B81-BE1EBCE6C539},
	Volume = {75},
	Year = {2000},
	url = {papers/Witting_JNeurochem2000.pdf}}

@article{Wolf:2002,
	Abstract = {This study analyzes how the antigen specificity, the subtype, and the activation state of T cells modulate their recently discovered neuroprotective potential. We assessed the prevention from neuronal damage in organotypic entorhinal-hippocampal slice cultures after co-culture with Th1 and Th2 cells either specific for myelin basic protein (MBP) or ovalbumin (OVA). We found that MBP-specific Th2 cells were the most effective in preventing central nervous system (CNS) tissue from secondary injury. This neuroprotective T cell effect appears to be mediated by soluble factors. After stimulation with phorbol myristate acetate and ionomycin, all T cells were most effective in preventing neuronal death. Our data show that the T cell subtype and activation state are important features in determining the neuroprotective potential of these cells.},
	Author = {Wolf, Susanne A. and Fisher, Jasmin and Bechmann, Ingo and Steiner, Barbara and Kwidzinski, Erik and Nitsch, Robert},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0165-5728},
	Journal = {J Neuroimmunol},
	Keywords = {Mice, Inbred BALB C;Cell Survival;Contact Inhibition;Nerve Degeneration;Animals;Th2 Cells;Ovalbumin;Cytokines;Myelin Basic Proteins;Brain;11 Glia;Chemotaxis, Leukocyte;Brain Injuries;Animals, Newborn;Tetradecanoylphorbol Acetate;Neurons;Th1 Cells;Epitopes;Mice;Research Support, Non-U.S. Gov't},
	Medline = {22336842},
	Month = {12},
	Nlm_Id = {8109498},
	Number = {1-2},
	Organization = {Department of Cell and Neurobiology, Institute of Anatomy, Humboldt-University Hospital Charit\`{e}, 10098, Berlin, Germany.},
	Pages = {72-80},
	Pii = {S0165572802003673},
	Pubmed = {12446010},
	Title = {Neuroprotection by T-cells depends on their subtype and activation state},
	Uuid = {4B4E657A-0EC4-4056-BE35-1B9B26137914},
	Volume = {133},
	Year = {2002}}

@article{Wolf-Jurewicz:1982,
	Abstract = {Following destructions of the prefrontal medial brain area in dogs two basis changes were noticed: an increase in food intake (14 dogs--group I) and a decrease of food intake (16 dogs--group II). On the basis of a histological analysis one can conclude that the differences in size, site and depth of the lesions are responsible for the obtained results. The deep lesions involving the white and grey matter in FPG area between the III and V (Kreiner's atlas) frontal planes brought about the most pronounced increase in food intake. The lesions involving only the cortex or very broad lesions in the whole prefrontal medial area and also anterior lesions between the I and III frontal planes, or posterior lesions from the VI to VIII frontal planes decreased the food intake or caused no changes in it.},
	Author = {Wolf-Jurewicz, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0044-6033},
	Journal = {Acta Physiol Pol},
	Keywords = {Eating;Hyperphagia;Eating Disorders;Dogs;Animals;Humans;24 Pubmed search results 2008;Frontal Lobe},
	Medline = {83252335},
	Nlm_Id = {2985166R},
	Number = {4},
	Pages = {393-401},
	Pubmed = {6964027},
	Title = {The role of the medial prefrontal cortex in food intake in dogs},
	Uuid = {589EFF10-14A3-48F2-898D-C07A4AE8EFAC},
	Volume = {33},
	Year = {1982}}

@article{Won:2003,
	Abstract = {In this study, we examined the effect of the s.c. administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA) or saline on locomotor activity and Fos expression following the bilateral destruction of hippocampal dentate granule cells by colchicine in rats. The lesioned animals, when administered s.c. saline, showed a significantly greater increase in locomotor activity compared to the intact animals, and revealed a marginally significant level of increased locomotor activity compared to the sham-lesioned animals. In addition, when the lesioned animals were given s.c. saline or MDMA, there was a significant increase in Fos expression in the nucleus accumbens core, but not in the medial prefrontal cortex, dorsolateral prefrontal cortex, anterior cingulate cortex, piriform cortex, dorsal striatum, or nucleus accumbens shell, compared to the intact and sham-lesioned animals. Overall, these results suggest that the nucleus accumbens core may be involved in the enhancement of locomotor activity induced by the injection of saline alone (stress loading) or MDMA following bilateral destruction of hippocampal dentate granule cells by colchicine.},
	Author = {Won, Mujun and Minabe, Yoshio and Tani, Kunihiko and Suzuki, Katsuaki and Kawai, Masayoshi and Sekine, Yoshimoto and Ashby, Charles R. and Takei, Nori and Mori, Norio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0168-0102},
	Journal = {Neurosci Res},
	Keywords = {Neurons;Rats, Sprague-Dawley;07 Excitotoxicity Apoptosis;Behavior, Animal;Colchicine;Immunohistochemistry;Rats;Dentate Gyrus;Hallucinogens;06 Adult neurogenesis injury induced;Injections, Intraventricular;Animals;Male;N-Methyl-3,4-methylenedioxyamphetamine;Proto-Oncogene Proteins c-fos;Brain},
	Medline = {22653025},
	Month = {6},
	Nlm_Id = {8500749},
	Number = {2},
	Organization = {Department of Psychiatry and Neurology, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan.},
	Pages = {153-60},
	Pii = {S0168010203000415},
	Pubmed = {12767478},
	Title = {The effects of dentate granule cell destruction on behavioral activity and Fos protein expression induced by systemic MDMA in rats},
	Uuid = {1C698258-47AD-4483-B226-167177941838},
	Volume = {46},
	Year = {2003},
	url = {papers/Won_NeurosciRes2003}}

@article{Wong:2001,
	Abstract = {The Slit protein guides neuronal and leukocyte migration through the transmembrane receptor Roundabout (Robo). We report here that the intracellular domain of Robo interacts with a novel family of Rho GTPase activating proteins (GAPs). Two of the Slit-Robo GAPs (srGAPs) are expressed in regions responsive to Slit. Slit increased srGAP1- Robo1 interaction and inactivated Cdc42. A dominant negative srGAP1 blocked Slit inactivation of Cdc42 and Slit repulsion of migratory cells from the anterior subventricular zone (SVZa) of the forebrain. A constitutively active Cdc42 blocked the repulsive effect of Slit. These results have demonstrated important roles for GAPs and Cdc42 in neuronal migration. We propose a signal transduction pathway from the extracellular guidance cue to intracellular actin polymerization.},
	Author = {Wong, K. and Ren, X. R. and Huang, Y. Z. and Xie, Y. and Liu, G. and Saito, H. and Tang, H. and Wen, L. and Brady-Kalnay, S. M. and Mei, L. and Wu, J. Y. and Xiong, W. C. and Rao, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Cell},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, 660 South Euclid Avenue, 63110, Saint Louis, MO, USA},
	Pages = {209-21.},
	Title = {Signal transduction in neuronal migration. roles of gtpase activating proteins and the small gtpase cdc42 in the slit-robo pathway},
	Uuid = {BFD37879-2DAD-4318-91EA-23F78E0EBCBF},
	Volume = {107},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11672528}}

@article{Wong:2005,
	Abstract = {The human immunodeficiency virus type-1 (HIV-1) infects microglia, macrophages, and astrocytes in the central nervous system (CNS) and may cause severe neurological diseases, such as AIDS-related dementias or progressive encephalopathies, as a result of CNS inflammation and neurotrophin signaling defects associated with expression of viral antigens and HIV-1 replication in the brain. The HIV Tat protein can be endocytosed by surrounding uninfected cells; interacts with transcriptional coactivators/acetyltransferases, p300/CREB-binding protein, and p300/CREB-binding protein-associated factor (PCAF); and induces neuronal apoptosis. Since nerve growth factor (NGF) receptor and brain-derived neurotrophic factor receptor signaling through CREB requires p300 and PCAF histone acetyltransferases, we sought to determine whether HIV-1 Tat coactivator interactions interfere with neurotrophin receptor signaling in neuronal cells. Here, we demonstrate that Tat-coactivator interactions inhibit NGF- and brain-derived neurotrophic factor-responsive CRE trans-activation and neurotrophin protection against apoptosis in PC12 and IMR-32 neuroblastoma cells. Purified recombinant Tat or Tat-derived synthetic peptides, spanning p300- and PCAF-binding sequences, inhibit histone H3/H4 acetylation in vitro. A Tat mutant, TatK28A/K50A, defective for binding p300 and PCAF, neither repressed NGF-responsive CRE transactivation nor inhibited histone acetylation. HIV-1 Tat interacts in PCAF complexes in post-mortem CNS tissues from donor neuro-AIDS patients, as determined by fluorescence resonance energy transfer immunoconfocal microscopy. Importantly, these findings suggest that HIV-1 Tat-coactivator interactions may contribute to neurotrophin signaling impairments and neuronal apoptosis associated with HIV-1 infections of the CNS.},
	Author = {Wong, Kasuen and Sharma, Anima and Awasthi, Soumya and Matlock, Elizabeth F. and Rogers, Lowery and Van Lint, Carine and Skiest, Daniel J. and Burns, Dennis K. and Harrod, Robert},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {Molecular Sequence Data;Neuroblastoma;Cell Cycle Proteins;HIV-1;Signal Transduction;Humans;Rats;Transfection;Microscopy, Confocal;Acetylation;Animals;Gene Products, tat;Transcription Factors;Cell Line, Tumor;Recombinant Fusion Proteins;PC12 Cells;11 Glia;Nerve Growth Factors;DNA-Binding Protein, Cyclic AMP-Responsive;Histones;Virus Replication;Amino Acid Sequence;Fluorescence Resonance Energy Transfer;Acetyltransferases;Pheochromocytoma;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {2985121R},
	Number = {10},
	Organization = {Laboratory of Molecular Virology, Department of Biological Sciences, Southern Methodist University, Dallas, Texas 75275-0376, USA.},
	Pages = {9390-9},
	Pii = {M408643200},
	Pubmed = {15611041},
	Title = {HIV-1 Tat interactions with p300 and PCAF transcriptional coactivators inhibit histone acetylation and neurotrophin signaling through CREB},
	Uuid = {93049B5A-EA22-4589-8D19-6B1A1830343D},
	Volume = {280},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1074/jbc.M408643200}}

@article{Wood:1994,
	Abstract = {The use of viral vectors which infect and express genes in post-mitotic neurons is a potential strategy for the treatment of disorders affecting the central nervous system (CNS). However, the inflammatory consequences of such strategies have yet to be systematically examined. Preparations of non-replicating defective herpes simplex virus type 1 (HSV-1) amplicon vectors containing the lacZ gene were obtained by standard methods and stereotaxically injected into the adult rat dentate gyrus (DG). The consequent gene expression and inflammatory effects following microinjection were investigated. beta-Galactosidase activity was detected in neurons of the DG from 24 h to at least 12 days after vector injection. A strong inflammatory response developed within 2 days, characterized by diffuse up-regulation of major histocompatibility complex (MHC) class I antigens and the activation of microglia. After 4 days the recruitment of MHC class II+ cells, activated T lymphocytes and macrophages was detected. These features persisted for at least 31 days. Of importance was the finding of beta-galactosidase activity in a bilateral group of neurons in the supramammillary nuclei (SMN) of the posterior hypothalamus, known to send afferent projections to the DG. The onset of inflammation at this secondary site was delayed, but its cellular characteristics resembled those found at the primary site of injection. Thus, the use of preparations of defective HSV-1 vectors for gene transfer in the CNS has immunological implications both at primary and secondary sites within the CNS.(ABSTRACT TRUNCATED AT 250 WORDS)},
	Author = {Wood, M. J. and Byrnes, A. P. and Pfaff, D. W. and Rabkin, S. D. and Charlton, H. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0969-7128},
	Journal = {Gene Ther},
	Keywords = {Gene Transfer Techniques;Encephalitis;Rats;Lac Operon;Dentate Gyrus;Time Factors;Not relevant;Defective Viruses;Gene Expression;Support, U.S. Gov't, Non-P.H.S.;11 Glia;beta-Galactosidase;Gene Therapy;Support, Non-U.S. Gov't;Herpesvirus 1, Human;Animals;Genetic Vectors},
	Medline = {96050952},
	Month = {9},
	Nlm_Id = {9421525},
	Number = {5},
	Organization = {Department of Neurobiology and Behavior, Rockefeller University, New York 10021, USA.},
	Pages = {283-91},
	Pubmed = {7584093},
	Title = {Inflammatory effects of gene transfer into the CNS with defective HSV-1 vectors},
	Uuid = {B0CD275D-52CC-4301-A001-F982A0467D5D},
	Volume = {1},
	Year = {1994}}

@article{Woodbury:2000,
	Abstract = {Bone marrow stromal cells exhibit multiple traits of a stem cell population. They can be greatly expanded in vitro and induced to differentiate into multiple mesenchymal cell types. However, differentiation to non-mesenchymal fates has not been demonstrated. Here, adult rat stromal cells were expanded as undifferentiated cells in culture for more than 20 passages, indicating their proliferative capacity. A simple treatment protocol induced the stromal cells to exhibit a neuronal phenotype, expressing neuron-specific enolase, NeuN, neurofilament-M, and tau. With an optimal differentiation protocol, almost 80\%of the cells expressed NSE and NF-M. The refractile cell bodies extended long processes terminating in typical growth cones and filopodia. The differentiating cells expressed nestin, characteristic of neuronal precursor stem cells, at 5 hr, but the trait was undetectable at 6 days. In contrast, expression of trkA, the nerve growth factor receptor, persisted from 5 hr through 6 days. Clonal cell lines, established from single cells, proliferated, yielding both undifferentiated and neuronal cells. Human marrow stromal cells subjected to this protocol also differentiated into neurons. Consequently, adult marrow stromal cells can be induced to overcome their mesenchymal commitment and may constitute an abundant and accessible cellular reservoir for the treatment of a variety of neurologic diseases.},
	Author = {Woodbury, D. and Schwarz, E. J. and Prockop, D. J. and Black, I. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Differentiation;Bone Marrow;Research Support, Non-U.S. Gov't;Bone Marrow Cells;Neurofilament Proteins;08 Aberrant cell cycle;Research Support, U.S. Gov't, P.H.S.;Phosphopyruvate Hydratase;Rats;Culture Media;Mesoderm;Receptor, trkA;Cells, Cultured;Animals;Humans;Stromal Cells;Neurons},
	Medline = {20392108},
	Month = {8},
	Nlm_Id = {7600111},
	Number = {4},
	Organization = {Department of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA. woodburydl\@aol.com},
	Pages = {364-70},
	Pii = {10.1002/1097-4547(20000815)61:4<364::AID-JNR2>3.0.CO;2-C},
	Pubmed = {10931522},
	Title = {Adult rat and human bone marrow stromal cells differentiate into neurons},
	Uuid = {6DCB88C3-63B3-4586-9F23-95A255031CE7},
	Volume = {61},
	Year = {2000},
	url = {papers/Woodbury_JNeurosciRes2000.pdf}}

@article{Woodbury:2002,
	Abstract = {Bone marrow stromal stem cells (MSCs) normally differentiate into mesenchymal derivatives but recently have also been converted into neurons, classical ectodermal cells. To begin defining underlying mechanisms, we extended our characterization of MSCs and the differentiated neurons. In addition to expected mesodermal mRNAs, populations and clonal lines of MSCs expressed germinal, endodermal, and ectodermal genes. Thus, the MSCs are apparently "multidifferentiated" in addition to being multipotent. Conversely, the differentiating neurons derived from populations and clonal lines of MSCs expressed the specific markers beta-III tubulin, tau, neurofilament-M, TOAD-64, and synaptophysin de novo. The transmitter enzymes tyrosine hydroxylase and choline acetyltransferase were localized to neuronal subpopulations. Our observations suggest that MSCs are already multidifferentiated and that neural differentiation comprises quantitative modulation of gene expression rather than simple on-off switching of neural-specific genes.},
	Author = {Woodbury, Dale and Reynolds, Kathleen and Black, Ira B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Cell Differentiation;Animals;Ectoderm;Gene Expression Regulation, Developmental;Rats;Synaptic Transmission;Femur;08 Aberrant cell cycle;Bone Marrow Cells;Research Support, U.S. Gov't, P.H.S.;Mesoderm;Neuroglia;Neurons;Age Factors;Endoderm;Clone Cells;Stromal Cells;Nerve Tissue Proteins;Research Support, Non-U.S. Gov't},
	Medline = {22194578},
	Month = {9},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {Department of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA. woodburydl\@aol.com},
	Pages = {908-17},
	Pubmed = {12205683},
	Title = {Adult bone marrow stromal stem cells express germline, ectodermal, endodermal, and mesodermal genes prior to neurogenesis},
	Uuid = {A34674CC-5224-4842-AB57-0E400C42F424},
	Volume = {69},
	Year = {2002},
	url = {papers/Woodbury_JNeurosciRes2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10365}}

@article{Woods:2000,
	Abstract = {The ability of lentiviral vectors to transfer genes into human hematopoietic stem cells was studied, using a human immunodeficiency virus 1 (HIV-1)-derived vector expressing the green fluorescence protein (GFP) downstream of the phosphoglycerate kinase (PGK) promoter and pseudotyped with the G protein of vesicular stomatitis virus (VSV). High-efficiency transduction of human cord blood CD34(+) cells was achieved after overnight incubation with vector particles. Sixteen to 28 percent of individual colony-forming units granulocyte-macrophage (CFU-GM) colonies derived from cord blood CD34(+) cells were positive by polymerase chain reaction (PCR) for the GFP gene. The transduction efficiency of SCID-repopulating cells (SRC) within the cord blood CD34(+) population was assessed by serial transplantation into nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. When 400,000 cord blood CD34(+) cells were transplanted into primary recipients, all primary and secondary recipients contained and expressed the transgene. Over 50\%of CFU-GM colonies derived from the bone marrow of these primary and secondary recipients contained the vector on average as determined by PCR. Transplantation of transduced cells in limiting dilution generated GFP(+) lymphoid and myeloid progeny cells that may have arisen from a single SRC. Inverse PCR analysis was used to amplify vector-chromosomal junctional fragments in colonies derived from SRC and confirmed that the vector was integrated. These results show that lentiviral vectors can efficiently transduce very primitive human hematopoietic progenitor and stem cells. (Blood. 2000;96:3725-3733)},
	Author = {Woods, N. B. and Fahlman, C. and Mikkola, H. and Hamaguchi, I. and Olsson, K. and Zufferey, R. and Jacobsen, S. E. and Trono, D. and Karlsson, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Transduction, Genetic;HIV-1;Mice, Inbred NOD;Humans;Animals;Lentivirus;Mice, SCID;Antigens, CD34;11 Glia;Immunophenotyping;Hematopoietic Stem Cell Transplantation;Genetic Vectors;Hematopoiesis;Cell Lineage;Gene Transfer Techniques;Polymerase Chain Reaction;Mice;Hematopoietic Stem Cells;Fetal Blood;Graft Survival;Research Support, Non-U.S. Gov't},
	Medline = {20541502},
	Month = {12},
	Nlm_Id = {7603509},
	Number = {12},
	Organization = {Department for Molecular Medicine and Gene Therapy, Institute of Laboratory Medicine, Lund University, Lund, Sweden.},
	Pages = {3725-33},
	Pubmed = {11090053},
	Title = {Lentiviral gene transfer into primary and secondary NOD/SCID repopulating cells},
	Uuid = {6059A270-4F8E-4F7A-8EF1-EE5D64B98533},
	Volume = {96},
	Year = {2000}}

@article{Woods:2003,
	Abstract = {Efficient vector transduction of hematopoietic stem cells is a requirement for successful gene therapy of hematologic disorders. We asked whether human umbilical cord blood CD34(+)CD38(lo) nonobese diabetic/severe combined immunodeficiency (NOD/SCID) repopulating cells (SRCs) could be efficiently transduced using lentiviral vectors, with a particular focus on the average number of vector copies integrating into these primitive progenitor cells. Mouse bone marrow was analyzed by fluorescence-activated cell-sorter scanner and by semiquantitative polymerase chain reaction (PCR) to determine the transduction efficiency into SRCs. Lentiviral vector transduction resulted in an average of 22\%(range, 3\%-90\%) of the human cells expressing green fluorescent protein (GFP), however, multiple vector copies were present in human hematopoietic cells, with an average of 5.6 +/- 3.3 (n = 12) copies per transduced cell. To confirm the ability of lentiviral vectors to integrate multiple vector copies into SRCs, linear amplification mediated (LAM)-PCR was used to analyze the integration site profile of a selected mouse showing low-level engraftment and virtually all human cells expressing GFP. Individually picked granulocyte macrophage colony-forming unit colonies derived from the bone marrow of this mouse were analyzed and shown to have the same 5 vector integrants within each colony. Interestingly, one integration site of the 5 that were sequenced in this mouse was located in a known tumor-suppressor gene, BRCA1. Therefore, these findings demonstrate the ability of lentiviral vectors to transduce multiple copies into a subset of NOD/SCID repopulating cells. While this is efficient in terms of transduction and transgene expression, it may increase the risk of insertional mutagenesis.},
	Author = {Woods, Niels-Bjarne B. and Muessig, Arne and Schmidt, Manfred and Flygare, Johan and Olsson, Karin and Salmon, Patrick and Trono, Didier and von Kalle, Christof and Karlsson, Stefan},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Research Support, Non-U.S. Gov't;Mice, Inbred NOD;ADP-ribosyl Cyclase;Colony-Forming Units Assay;Macrophages;Granulocytes;Transfection;Animals;Humans;Stem Cell Transplantation;Lentivirus;Antigens, CD;Mice, SCID;Antigens, CD34;11 Glia;Green Fluorescent Proteins;Genes, Tumor Suppressor;Genetic Vectors;Bone Marrow Cells;Flow Cytometry;Polymerase Chain Reaction;Fetal Blood;Virus Integration;Mice;Luminescent Proteins;Mutagenesis, Insertional},
	Medline = {22446452},
	Month = {2},
	Nlm_Id = {7603509},
	Number = {4},
	Organization = {Department for Molecular Medicine and Gene Therapy, Institute of Laboratory Medicine, Lund University, Sweden.},
	Pages = {1284-9},
	Pii = {2002-07-2238},
	Pubmed = {12393514},
	Title = {Lentiviral vector transduction of NOD/SCID repopulating cells results in multiple vector integrations per transduced cell: risk of insertional mutagenesis},
	Uuid = {3C5A9790-3576-4F2E-9582-67DABA9F5D16},
	Volume = {101},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2002-07-2238}}

@article{Wootton:2005,
	Abstract = {Ecologists would like to explain general patterns observed across multi-species communities, such as species-area and abundance-frequency relationships, in terms of the fundamental processes of birth, death and migration underlying the dynamics of all constituent species. The unified neutral theory of biodiversity and related theories based on these fundamental population processes have successfully recreated general species-abundance patterns without accounting for either the variation among species and individuals or resource-releasing processes such as predation and disturbance, long emphasized in ecological theory. If ecological communities can be described adequately without estimating variation in species and their interactions, our understanding of ecological community organization and the predicted consequences of reduced biodiversity and environmental change would shift markedly. Here, I introduce a strong method to test the neutral theory that combines field parameterization of the underlying population dynamics with a field experiment, and apply it to a rocky intertidal community. Although the observed abundance-frequency distribution of the system follows that predicted by the neutral theory, the neutral theory predicts poorly the field experimental results, indicating an essential role for variation in species interactions.},
	Author = {Wootton, J. Timothy},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1476-4687},
	Journal = {Nature},
	Keywords = {Models, Biological;research support, non-u.s. gov't;Population Dynamics;Species Specificity;Stochastic Processes;Ecology;research support, u.s. gov't, non-p.h.s.;Bivalvia;Biodiversity;Animals;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {0410462},
	Number = {7023},
	Organization = {Department of Ecology and Evolution, The University of Chicago, 1101 East 57th Street, Chicago, Illinois 60637, USA. twootton\@uchicago.edu},
	Pages = {309-12},
	Pii = {nature03211},
	Pubmed = {15662423},
	Title = {Field parameterization and experimental test of the neutral theory of biodiversity},
	Uuid = {B0A39236-8D56-4D63-A97F-0D642B2A4F82},
	Volume = {433},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature03211}}

@article{Wrana:2000,
	Author = {Wrana, J. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Cell},
	Keywords = {Trans-Activators/*genetics/*metabolism;C;Gene Expression Regulation, Developmental/physiology;Animal;DNA-Binding Proteins/*genetics/*metabolism;Signal Transduction/*genetics;04 Adult neurogenesis factors;Bone Morphogenetic Proteins/genetics/metabolism;Transforming Growth Factor beta/genetics/metabolism},
	Number = {2},
	Organization = {Department of Medical Genetics and Microbiology, University of Toronto, Ontario, Canada.},
	Pages = {189-92.},
	Title = {Regulation of Smad activity},
	Uuid = {56C81843-D727-4C80-9975-007F897F2376},
	Volume = {100},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10660041}}

@article{Wu:2000a,
	Abstract = {The twitcher mouse is a murine model of globoid cell leukodystropy, a genetic demyelinating disease caused by a mutation of the galactosylceramidase gene. Demyelination of the central nervous system commences around 20 postnatal days. Using GFP-transgenic mice as donors, the distribution of hematogenous cells after bone marrow transplantation was investigated in the twitcher mice. Bone marrow transplantation was carried out at 8 postnatal days. In twitcher chimeric mice examined before 30 postnatal days, numerous GFP(+) cells were detected in spleen and peripheral nerve but only a few were detected in the liver, lung, and spinal white matter. In contrast, at 35 to 40 postnatal days when demyelination is evident, many GFP(+) cells with ameboid form were detected in the white matter of the spinal cord, brainstem, and cerebrum. Approximately half of these GFP(+) cells were co-labeled with Mac-1. In twitcher chimeric mice examined after 100 postnatal days, the majority of GFP/Mac-1 double-positive cells displayed the morphological features of ramified microglia with fine delicate processes and was distributed diffusely in both gray and white matter. These results suggest that a significant number of donor hematogenous cells are able to infiltrate into the brain parenchyma, repositioning themselves into areas previously occupied by microglia, and to ameliorate lethality.},
	Author = {Wu, Y. P. and McMahon, E. and Kraine, M. R. and Tisch, R. and Meyers, A. and Frelinger, J. and Matsushima, G. K. and Suzuki, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {Tissue Distribution;Animals;Blood Cells;Viscera;Bone Marrow Transplantation;Postoperative Care;Indicators and Reagents;Mice, Transgenic;Reference Values;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Mice, Neurologic Mutants;Research Support, U.S. Gov't, P.H.S.;Tissue Donors;Mice;Central Nervous System;Luminescent Proteins;Peripheral Nerves},
	Medline = {20313103},
	Month = {6},
	Nlm_Id = {0370502},
	Number = {6},
	Organization = {Department of Pathology and Laboratory Medicine, the University of North Carolina, Chapel Hill 27599-7525, USA.},
	Pages = {1849-54},
	Pubmed = {10854208},
	Title = {Distribution and characterization of GFP(+) donor hematogenous cells in Twitcher mice after bone marrow transplantation},
	Uuid = {E4E156CC-1E30-48AB-A65D-6A01CC9C8ED4},
	Volume = {156},
	Year = {2000}}

@article{Wu:2005,
	Abstract = {Macrophages/microglia are implicated in spinal cord injury but their precise role in the process is not clear. Our previous studies have reported that radial glia (RG) possess properties of neural stem cells and remerged after central nervous system (CNS) injury which may play an important role in neural repair and regeneration. In the present study, we examined the expression of ED1 (a specific marker for activated macrophages/microglia) and RG in a spinal cord injury (SCI) model and detected the activation at 1, 4, 8, and 12 weeks in both dorsal funiculus and ventral white matter after SCI. For both ED1-positive cells and RG cells, there was a gradual increase in density and in number from 1 to 4 weeks followed by down-regulation up to 12 weeks after injury. The morphologies of macrophages and radial glia were different. However, some ED1-positive cells were also stained by RG marker. These results suggest that macrophages may have some lineage to radial glial cells.},
	Author = {Wu, and Miyamoto, and Shibuya, and Mori, and Norimatsu, and Janjua, and Itano,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {0045503},
	Organization = {Department of Orthopaedic Surgery, School of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kagawa 761-0793, Japan.},
	Pii = {S0006-8993(05)00789-4},
	Pubmed = {15993386},
	Title = {Co-expression of radial glial marker in macrophages/microglia in rat spinal cord contusion injury model},
	Uuid = {88655040-1933-445E-A22D-9E11FFA00E87},
	Year = {2005},
	url = {papers/Wu_BrainRes2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.brainres.2005.05.054}}

@article{Wu:2007,
	Abstract = {Microglial cells are the resident macrophages that are involved in brain injuries and infections. Recent studies using transcranial two-photon microscopy have shown that ATP and P2Y receptors mediated rapid chemotactic responses of miroglia to local injury. However, the molecular mechanism for microglial chemotaxis toward ATP is still unknown. To address this question, we employed a combination of simultaneous perforated whole-cell recordings and time-lapse confocal imaging in GFP-labeled microglia in acute brain slices from adult mice. We found that ATP-induced rapid chemotaxis is correlated with P2Y receptor associated-outward potassium current in microglia. Activation of both P2Y receptor and its associated potassium channels are required for ATP-induced chemotaxis and baseline motility of microglial cells. The chemotaxis required the activation of phosphoinositide 3-kinase but not mitogen-activated protein kinase pathway. Our results provide strong evidence that P2Y receptor-associated outward potassium channels and the phosphoinositide 3-kinase pathway are important for ATP-induced microglial motility in acute brain slices. (c) 2007 Wiley-Liss, Inc.},
	Author = {Wu, and Vadakkan, and Zhuo,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {11 Glia;24 Pubmed search results 2008},
	Month = {3},
	Nlm_Id = {8806785},
	Organization = {Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.},
	Pubmed = {17357150},
	Title = {ATP-induced chemotaxis of microglial processes requires P2Y receptor-activated initiation of outward potassium currents},
	Uuid = {0A74AFB2-1464-4095-B916-0A024F6CDCDC},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20500}}

@article{Wu:1994,
	Abstract = {The present study describes the ultrastructural localization and labelling pattern of lectin in different microglial cell phenotypes in the postnatal rat brain using the isolectin, GSA I-B4. The nascent round and amoeboid microglial cells (round cells and cells displaying short processes) were labelled at their cytoplasmic membrane and the membrane of the subplasmalemmal vacuoles. In the course of their transformation into ramified forms with age, dense lectin labelling was observed successively at different sites in the differentiating cells. The most striking feature was the staining of the Golgi saccules on the trans face, the trans tubular network and associated vesicles and vacuoles in the 'intermediate' ramified microglia (ramified cells bearing thick and long processes and those with thin and long processes). The vacuoles with accumulated reaction products were closely associated with many microtubules extending into the cytoplasmic processes. At the surface, the lectin-labelled vacuoles and vesicles appeared to fuse with the membrane and their contents communicated with the exterior. In the advanced or most differentiated ramified microglial cells (cells bearing attenuated processes), the lectin staining at all the above mentioned sites became diminished. In conclusion, in the transformation of the round microglia into their ramified derivatives, the glycoconjugates at the cytoplasmic membrane are progressively reduced. It is postulated from this study that the down-regulation of the glycoconjugates of the microglial plasma membrane is due primarily to their internalization during endocytosis. This process would trigger a de novo galactosyl protein synthesis and/or modification at the trans Golgi saccules and trans tubular network probably in an attempt to degrade the internalized membrane glycoproteins or to replenish the consumption of the membrane glycoconjugates.},
	Author = {Wu, C. H. and Wen, C. Y. and Shieh, J. Y. and Ling, E. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {0300-4864},
	Journal = {J Neurocytol},
	Keywords = {G;Organelles;Animals;Aging;Rats;Vacuoles;Brain;Microglia;Cell Membrane;Rats, Wistar;11 Glia;Animals, Newborn;Membrane Glycoproteins;Endocytosis;Microscopy, Electron;24 Pubmed search results 2008;Intracellular Membranes;Lectins;Research Support, Non-U.S. Gov't},
	Medline = {94308820},
	Month = {4},
	Nlm_Id = {0364620},
	Number = {4},
	Organization = {Department of Anatomy, College of Medicine, National Taiwan University, Taipei.},
	Pages = {258-69},
	Pubmed = {8035208},
	Title = {Down-regulation of membrane glycoprotein in amoeboid microglia transforming into ramified microglia in postnatal rat brain},
	Uuid = {11E54057-E1E9-11DA-9DD9-000D9346EC2A},
	Volume = {23},
	Year = {1994}}

@article{Wu:2002,
	Abstract = {Pluripotent or multipotent stem cells isolated from human embryos or adult central nervous system (CNS) may provide new neurons to ameliorate neural disorders. A major obstacle, however, is that the majority of such cells do not differentiate into neurons when grafted into non-neurogenic areas of the adult CNS. Here we report a new in vitro priming procedure that generates a nearly pure population of neurons from fetal human neural stem cells (hNSCs) transplanted into adult rat CNS. Furthermore, the grafted cells differentiated by acquiring a cholinergic phenotype in a region-specific manner. This technology may advance stem cell-based therapy to replace lost neurons in neural injury or neurodegenerative disorders. 1097-6256 Journal Article},
	Author = {Wu, P. and Tarasenko, Y. I. and Gu, Y. and Huang, L. Y. and Coggeshall, R. E. and Yu, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Nat Neurosci},
	Keywords = {Fetus;Heparin/pharmacology;Human;Animals;Cells, Cultured;Rats;Nerve Growth Factors/pharmacology;Laminin/pharmacology;Cell Culture/*methods;Phenotype;L pdf;Neurodegenerative Diseases/*therapy;Choline O-Acetyltransferase/metabolism;17 Transplant Regeneration;Male;Brain Tissue Transplantation/*methods;Stem Cells/*cytology/drug effects/metabolism;Neurons/*cytology/drug effects/metabolism;Support, Non-U.S. Gov't;Graft Survival/drug effects/*physiology;Acetylcholine/metabolism;Stem Cell Transplantation/*methods;Support, U.S. Gov't, P.H.S.;Immunohistochemistry},
	Number = {12},
	Organization = {Department of Anatomy, University of Texas Medical Branch, Galveston, Texas 77555, USA. piwu\@utmb.edu},
	Pages = {1271-8},
	Title = {Region-specific generation of cholinergic neurons from fetal human neural stem cells grafted in adult rat},
	Uuid = {A8B38E9F-5444-403E-B80E-5B4BD4FA2151},
	Volume = {5},
	Year = {2002},
	url = {papers/Wu_NatNeurosci2002}}

@article{Wu:2000,
	Abstract = {Immunocytochemical studies of postmortem human tissue have shown that the neurons at risk for degeneration in Alzheimer's are marked by the ectopic expression of several cell cycle components. The current work investigates the roles that beta-amyloid activated microglia might play in leading neurons to re-express cell cycle components. Stable cultures of E16.5 mouse cortical neurons were exposed to beta-amyloid alone, microglial cells alone, or microglial cells activated by beta-amyloid. Increased cell death was found in response to each of these treatments, however, only the amyloid activated microglial treatment increased the number of neurons that were positive for cell cycle markers such as PCNA or cyclin D and incorporation of BrdU. Double labeling with BrdU and TUNEL techniques verified that the 'dividing' neurons were dying, most likely through an apoptotic mechanism. The identity of the soluble factor(s) elaborated by the microglia remains unknown, but FGF2, a suspected neuronal mitogen, was ruled out. These results further support a model in which microglial activation by beta-amyloid is a key event in the progression in Alzheimer's disease.},
	Author = {Wu, Q. and Combs, C. and Cannady, S. B. and Geldmacher, D. S. and Herrup, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0197-4580},
	Journal = {Neurobiol Aging},
	Keywords = {Human;Animals;Cells, Cultured;Amyloid beta-Protein;Cell Cycle;Apoptosis;Female;Microglia;Kinetics;Culture Media, Conditioned;Not relevant;Mice, Inbred C57BL;11 Glia;Embryo;Male;Cell Line;Support, Non-U.S. Gov't;Cerebral Cortex;Neurons;Support, U.S. Gov't, P.H.S.;Mice;Cell Division},
	Medline = {20574083},
	Nlm_Id = {8100437},
	Number = {6},
	Organization = {Alzheimer Research Laboratory, University Hospitals of Cleveland, Case Western Reserve University, School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.},
	Pages = {797-806},
	Pii = {S0197458000002190},
	Pubmed = {11124423},
	Title = {Beta-amyloid activated microglia induce cell cycling and cell death in cultured cortical neurons},
	Uuid = {83187F85-510C-4806-AC0C-7B0ABFD3AB34},
	Volume = {21},
	Year = {2000},
	url = {papers/Wu_NeurobiolAging2000.pdf}}

@article{Wu:2002a,
	Abstract = {Here we report a novel method of supplying cultured neurosphere cells to the injured spinal cord, by injection of cells into the cerebrospinal fluid (CSF) through the fourth ventricle or cisterna magna. Hippocampus-derived neurosphere cells, isolated from a transgenic rat fetus expressing green fluorescent protein, were transplanted into the CSF of a rat with spinal cord injury. It was found that injected cells were extensively transported by CSF within the subarachnoidal space, and survived as clusters on the pial surface of the spinal cord. The most notable finding was that a large number of injected cells migrated into the lesion site and integrated into the injured spinal cord tissues.},
	Author = {Wu, Sufan and Suzuki, Yoshihisa and Kitada, Masaaki and Kataoka, Kazuya and Kitaura, Miyako and Chou, Hirotomi and Nishimura, Yoshihiko and Ide, Chizuka},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {Fetus;Research Support, Non-U.S. Gov't;Animals;Stem Cell Transplantation;Brain Tissue Transplantation;Rats;Recovery of Function;Tubulin;Fourth Ventricle;Indicators and Reagents;Rats, Sprague-Dawley;Hippocampus;Animals, Genetically Modified;Subarachnoid Space;11 Glia;Green Fluorescent Proteins;Cell Movement;Nerve Regeneration;Spinal Cord Injuries;Pia Mater;Cerebrospinal Fluid;Luminescent Proteins;Immunohistochemistry;Graft Survival;Glial Fibrillary Acidic Protein},
	Medline = {21655590},
	Month = {1},
	Nlm_Id = {7600130},
	Number = {2},
	Organization = {Department of Plastic and Reconstructive Surgery, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8507, Japan.},
	Pages = {81-4},
	Pii = {S0304394001024880},
	Pubmed = {11796191},
	Title = {New method for transplantation of neurosphere cells into injured spinal cord through cerebrospinal fluid in rat},
	Uuid = {ABBC0D1C-EC9A-4E7E-9AAF-647D15BD2480},
	Volume = {318},
	Year = {2002}}

@article{Wu:2001a,
	Abstract = {Human umbilical cord blood provides an alternative source of hematopoietic cells for purposes of transplantation or ex vivo genetic modification. The objective of this study was to evaluate electroporation as a means to introduce foreign genes into human cord blood CD34+ cells and evaluate gene expression in CD34+/CD38(dim) and committed myeloid progenitors (CD33+, CD11b+). CD34+ cells were cultured in X-VIVO 10 supplemented with thrombopoietin, stem cell factor, and Flt-3 ligand. Electroporation efficiency and cell viability measured by flow cytometry using enhanced green fluorescent protein (EGFP) as a reporter indicated 31\%+/- 2\%EGFP+ /CD34+ efficiency and 77\%+/- 3\%viability as determined 48 hours post-electroporation. The addition of allogeneic cord blood plasma increased the efficiency to 44\%+/- 5\%with no effect on viability. Of the total CD34+ cells 48 hours post-electroporation, 20\%were CD38(dim)/EGFP+. CD34+ cells exposed to interleukin-3, GM-CSF and G-CSF for an additional 11 days differentiated into CD33+ and CD11b+ cells, and 9\%+/- 3\%and 8\%+/- 7\%were expressing the reporter gene, respectively. We show that electroporation can be used to introduce foreign genes into early hematopoietic stem cells (CD34+/CD38(dim)), and that the introduced gene is functionally expressed following expansion into committed myeloid progenitors (CD33+, CD11b+) in response to corresponding cytokines. Further investigation is needed to determine the transgene expression in functional terminal cells derived from the genetically modified CD34+ cells, such as T cells and dendritic cells.},
	Author = {Wu, M. H. and Smith, S. L. and Dolan, M. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:43 -0400},
	Issn = {1066-5099},
	Journal = {Stem Cells},
	Keywords = {ADP-ribosyl Cyclase;Humans;Transfection;Plasma;Antigens, Differentiation;NAD+ Nucleosidase;Antigens, CD;Electroporation;Granulocyte Colony-Stimulating Factor;Antigens, CD34;Recombinant Fusion Proteins;Granulocyte-Macrophage Colony-Stimulating Factor;11 Glia;Green Fluorescent Proteins;Interleukin-3;Research Support, U.S. Gov't, P.H.S.;Hematopoietic Stem Cells;Cell Division;Luminescent Proteins;Fetal Blood;Gene Expression},
	Medline = {21570680},
	Nlm_Id = {9304532},
	Number = {6},
	Organization = {Section of Hematology-Oncology, Department of Medicine and Cancer Research Center, University of Chicago, 5841 S. Maryland Ave., Chicago, IL 60637, USA.},
	Pages = {492-9},
	Pubmed = {11713340},
	Title = {High efficiency electroporation of human umbilical cord blood CD34+ hematopoietic precursor cells},
	Uuid = {9EB84240-94A2-4312-884A-F4EE79F08D97},
	Volume = {19},
	Year = {2001}}

@article{Wurmser:2002,
	Abstract = {0028-0836 Comment News},
	Author = {Wurmser, A. E. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Nature},
	Keywords = {EE pdf;Embryo/cytology;Neurons/cytology;Human;Bone Marrow Cells/cytology;*Cell Fusion;08 Aberrant cell cycle;*Cell Differentiation;Animals;Stem Cells/*cytology},
	Number = {6880},
	Pages = {485-7},
	Title = {Stem cells: cell fusion causes confusion},
	Uuid = {41E98EC3-D3AE-11D9-A0E9-000D9346EC2A},
	Volume = {416},
	Year = {2002},
	url = {papers/Wurmser_Nature2002.pdf}}

@article{Wuttke:1972,
	Author = {Wuttke, W. and Michael, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0031-6768},
	Journal = {Pflugers Arch},
	Keywords = {Gonadotropins;Rats;Female;Ovulation;Action Potentials;Animals;24 Pubmed search results 2008;Neurons;Frontal Lobe},
	Medline = {72256430},
	Nlm_Id = {0154720},
	Pages = {Suppl 332:R87},
	Pubmed = {5065871},
	Title = {[Correlation of hypophyseal gonadotropin secretion with neural activity in the medial preoptic region]},
	Uuid = {5BF08662-9C51-4A3B-AAB8-1497CB5B0EF7},
	Volume = {332},
	Year = {1972}}

@article{Xiao:2002,
	Abstract = {Microglia are often considered a type of tissue macrophages analogous Langerhans' cells, while dendritic cells (DC) can be generated in vitro from cultured microglia in the presence of GM-CSF. In this study, we show that TGF-beta 1, in the presence of GM-CSF, promoted the growth and differentiation of glial cell-derived dendritic cells (GC-DC). TGF-beta 1-driven GC-DC exhibited an immature state reflected by low CD11c expression, augmented endocytosis, and reduced antigen presentation. Expression of Fas was inhibited in GM-CSF+TGF-beta 1-supplemented cell cultures and may relate to a long life span of GC-DC treated with GM-CSF+TGF-beta 1. IL-10 and IL-12 mRNA on GC-DC was not affected upon exposure to GM-CSF alone or to GM-CSF+IFN-gamma, GM-CSF+IL-10 or GM-CSF+TGF-beta 1. In sharp contrast, TGF-beta 1, in the presence of GM-CSF, dramatically up-regulated the expression of TNF-alpha and TGF-beta 1 mRNA. These results demonstrate that TGF-beta 1 seems to play a crucial role in the differentiation, functional skewing, and cytokine profile of GC-DC. TGF-beta 1-driven GC-DC awaits further investigation to facilitate a better understanding of the glia-T cell dialog as well as the pathogenesis and immunotherapy of central nervous system inflammatory and degenerative diseases.},
	Author = {Xiao, Bao-Guo G. and Xu, Ling-Yun Y. and Yang, Jian-She S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0889-1591},
	Journal = {Brain Behav Immun},
	Keywords = {Cell Aging;Drug Synergism;Tumor Necrosis Factor;Cell Differentiation;Rats, Inbred Lew;In Vitro;Animals;Rats;Transforming Growth Factor beta;Cells, Cultured;Dendritic Cells;Not relevant;Granulocyte-Macrophage Colony-Stimulating Factor;11 Glia;RNA, Messenger;Support, Non-U.S. Gov't;Cerebral Cortex;Neuroglia;Gene Expression},
	Medline = {22368141},
	Month = {12},
	Nlm_Id = {8800478},
	Notes = {glia culture experiment},
	Number = {6},
	Organization = {Experimental Neurology Unit, Division of Neurology, Karolinska Institute, Huddinge University Hospital, S-141 86 Huddinge, Stockholm, Sweden. bao-guo.xiao\@neurotec.ki.se},
	Pages = {685-97},
	Pii = {S088915910200020X},
	Pubmed = {12480499},
	Title = {TGF-beta 1 synergizes with GM-CSF to promote the generation of glial cell-derived dendriform cells in vitro},
	Uuid = {C3D9DB43-82BD-4F14-B7B6-40F717B1567D},
	Volume = {16},
	Year = {2002},
	url = {papers/Xiao_BrainBehavImmun2002.pdf}}

@article{Xie:2004,
	Abstract = {Chronic glial activation in neurodegenerative diseases contributes to neuronal dysfunction and neuron loss through production of neuroinflammatory molecules. However, the molecular mechanisms, particularly the signal transduction pathways involved in glia-dependent neuron death, are poorly understood. As a first step to address this question, we used a neuron-glia co-culture system that allows diffusion of soluble molecules between glia and neurons to test the potential importance of mitogen-activated protein kinase (MAPK) signaling pathways in the glia-induced neuron death. Activation of glia in co-culture by lipopolysaccharide (LPS) induced apoptotic-like neuron death. The MAPKs tested (p38, JNK, ERK1/2) were activated in both glia and neurons following LPS treatment, suggesting their involvement in both glial activation and neuronal response to diffusible, glia-derived neurotoxic molecules. Inhibitors of p38 and JNK partially blocked neuron death in the LPS-treated co-culture, whereas an ERK1/2 pathway inhibitor did not protect neurons. These results show that p38 and JNK MAPKs, but not ERK1/2 MAPK, are important signal transduction pathways contributing to glia-induced neuron death.},
	Author = {Xie, Zhong and Smith, Carolyn J. and Van Eldik, Linda J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Interferons;Neurodegenerative Diseases;Alpha;Reaction Time;Animals;Cells, Cultured;Lipopolysaccharides;Nitric-Oxide Synthase;MAP Kinase Signaling System;Interleukin-1;Mitochondria;Mice, Inbred C57BL;Membrane Potentials;Gliosis;11 Glia;Cell Communication;Not relevant;Rats, Sprague-Dawley;07 Excitotoxicity Apoptosis;Enzyme Inhibitors;Neuroglia;Cell Death;Rats;Fetus;Microglia;Encephalitis;Mice;Mitogen-Activated Protein Kinases;Coculture;Neurons;Fluorescent Dyes},
	Month = {1},
	Nlm_Id = {8806785},
	Number = {2},
	Organization = {Department of Cell and Molecular Biology, and Drug Discovery Program, Northwestern University Feinberg School of Medicine, 303 E. Chicago Avenue, Chicago, IL 60612, USA.},
	Pages = {170-9},
	Pubmed = {14730710},
	Title = {Activated glia induce neuron death via MAP kinase signaling pathways involving JNK and p38},
	Uuid = {AEC32F78-ABAA-4E73-9BBF-658109EA98C6},
	Volume = {45},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10314}}

@article{Xie:2002,
	Abstract = {Transgenic mice were generated to permit the targeted ablation of cortical preplate cells at the time they are born. In these mice, the 1.3 kb golli promoter of the myelin basic protein gene was used to drive the herpes simplex virus thymidine kinase (TK) transgene in cortical preplate cells. Heterozygous transgenic pairs were bred, and pregnant dams were treated with ganciclovir at embryonic days 11-12 to ablate preplate cells at the time the preplate was forming. This paradigm exposed control (TK-) and experimental (TK+) littermates to exactly the same conditions. Embryological ablation of preplate cells led to an early disruption of the radial glial framework and subplate structure in the developing cortex and dramatically altered the cellular lamination and connectivity of the cortical plate. The disturbed radial glial network contributed to an impaired radial migration of neurons into the cortical plate from the ventricular zone. The cortical plate became dyslaminated, and there was a substantial reduction in short- and long-range cortical projections within the cortex and to subcortical regions. Cell death within the cortical plate and the proliferative zones was substantially increased in the ablated animals. After birth, a cortical lesion developed, which became exacerbated with the secondary onset of hydrocephaly in the second postnatal week. The results underscore the critical importance of the preplate in cortex formation, mediated through its guidance of the formation of radial glial scaffolding, subsequent neuronal migration into the incipient cortical plate, and the final arrangement of its vertical organization and cellular connectivity. 1529-2401 Journal Article},
	Author = {Xie, Y. and Skinner, E. and Landry, C. and Handley, V. and Schonmann, V. and Jacobs, E. and Fisher, R. and Campagnoni, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 12:12:01 -0400},
	Journal = {J Neurosci},
	Keywords = {Nervous System Malformations/chemically induced/genetics/pathology;Cell Death/drug effects/genetics;Ganciclovir/pharmacology;Animals;10 Development;Neurons/cytology/*drug effects;Cell Movement/drug effects;Promoter Regions (Genetics)/genetics;Mice, Transgenic;F pdf;Hydrocephalus/chemically induced/genetics/pathology;Neuroglia/cytology/drug effects;Myelin Basic Proteins/genetics;In Situ Nick-End Labeling;Cerebral Cortex/cytology/drug effects/*embryology;Simplexvirus/genetics;Support, U.S. Gov't, P.H.S.;Thymidine Kinase/biosynthesis/genetics;Mice;Immunohistochemistry;Models, Animal;Bromodeoxyuridine;Embryonic Structures/cytology/drug effects/*embryology},
	Number = {20},
	Organization = {Developmental and Molecular Neuroscience Group, Neuropsychiatric Institute, University of California at Los Angeles, School of Medicine, Los Angeles, California 90024-1759, USA.},
	Pages = {8981-91},
	Title = {Influence of the embryonic preplate on the organization of the cerebral cortex: a targeted ablation model},
	Uuid = {780EC16C-F86C-48CC-AE94-B87EF111C9C5},
	Volume = {22},
	Year = {2002},
	url = {papers/Xie_JNeurosci2002.pdf}}

@article{Xie:2007,
	Abstract = {Centrosome- and microtubule-associated proteins have been shown to be important for maintaining the neural progenitor pool during neocortical development by regulating the mitotic spindle. It remains unclear whether these proteins may control neurogenesis by regulating other microtubule-dependent processes such as nuclear migration. Here, we identify Cep120, a centrosomal protein preferentially expressed in neural progenitors during neocortical development. We demonstrate that silencing Cep120 in the developing neocortex impairs both interkinetic nuclear migration (INM), a characteristic pattern of nuclear movement in neural progenitors, and neural progenitor self-renewal. Furthermore, we show that Cep120 interacts with transforming acidic coiled-coil proteins (TACCs) and that silencing TACCs also causes defects in INM and neural progenitor self-renewal. Our data suggest a critical role for Cep120 and TACCs in both INM and neurogenesis. We propose that sustaining INM may be a mechanism by which microtubule-regulating proteins maintain the neural progenitor pool during neocortical development.},
	Author = {Xie, Zhigang and Moy, Lily Y. and Sanada, Kamon and Zhou, Ying and Buchman, Joshua J. and Tsai, Li-Huei H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {research support, non-u.s. gov't;research support, n.i.h., extramural;24 Pubmed search results 2008},
	Month = {10},
	Nlm_Id = {8809320},
	Number = {1},
	Organization = {Department of Brain and Cognitive Sciences, Picower Institute for Learning and Memory, RIKEN-MIT Neuroscience Research Center, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.},
	Pages = {79-93},
	Pii = {S0896-6273(07)00675-7},
	Pubmed = {17920017},
	Title = {Cep120 and TACCs control interkinetic nuclear migration and the neural progenitor pool},
	Uuid = {F4E6FBA8-7FF2-41BA-B782-C6A4326B6E94},
	Volume = {56},
	Year = {2007},
	url = {papers/Xie_Neuron2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2007.08.026}}

@article{Xu:2004a,
	Abstract = {OBJECTIVE: Arterial injury results in vascular remodeling associated with proliferation and migration of smooth muscle cells (SMCs) and the development of intimal hyperplasia, which is a critical component of restenosis after angioplasty of human coronary arteries and an important feature of atherosclerotic lesions. However, the origin of SMCs and other cells in the development of vascular remodeling is not yet fully understood. METHODS AND RESULTS: We utilized a cuff-induced vascular injury model after transplantation of the bone marrow (BM) from green fluorescent protein (GFP)-transgenic mice. We found that macrophages were major cells recruited to the adventitia of the vascular injury lesion along with SMCs and endothelial cells (ECs). While investigating whether those cells are derived from the donor, we found that most of the macrophages were GFP-positive, and some of the SMCs and ECs were also GFP-positive. Administration of the anti-c-fms antibody resulted in a marked decrease in macrophages and a relative increase of SMCs, while administration of antibodies against the platelet-derived growth factor receptor-beta caused a prominent decrease in SMCs and a relative increase in macrophages. CONCLUSIONS: The current study indicates that BM-derived cells play an important role in vascular injury, and that differentiation of macrophages and SMCs might be dependent on each other.},
	Author = {Xu, Yang and Arai, Hidenori and Zhuge, Xin and Sano, Hideto and Murayama, Toshinori and Yoshimoto, Momoko and Heike, Toshio and Nakahata, Tatsutoshi and Nishikawa, Shin-ichi and Kita, Toru and Yokode, Masayuki},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1524-4636},
	Journal = {Arterioscler Thromb Vasc Biol},
	Keywords = {Cell Differentiation;Wound Healing;Animals;Macrophages;Bone Marrow Transplantation;Endothelial Cells;Receptor, Macrophage Colony-Stimulating Factor;Female;Cell Movement;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Radiation Chimera;Femoral Artery;Bone Marrow Cells;Cell Lineage;Antibodies, Monoclonal;Mice;Stem Cells;Constriction;Receptor, Platelet-Derived Growth Factor beta;Myocytes, Smooth Muscle;Research Support, Non-U.S. Gov't},
	Month = {3},
	Nlm_Id = {9505803},
	Number = {3},
	Organization = {Department of Geriatric Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.},
	Pages = {477-82},
	Pii = {01.ATV.0000118016.94368.35},
	Pubmed = {14739121},
	Title = {Role of bone marrow-derived progenitor cells in cuff-induced vascular injury in mice},
	Uuid = {2471BFD1-25BD-4C5C-B120-333B7744190F},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.ATV.0000118016.94368.35}}

@article{Xu:2007,
	Abstract = {The retina contains two distinct populations of monocyte-derived cells: perivascular cells (macrophages) and parenchymal cells (microglia), important in homeostasis, neuroinflammation, degeneration, and injury. The turnover of these cells in the retina and their repopulation in normal physiological conditions have not been clarified. Bone marrow (BM) cells from EGFP-transgenic mice were adoptively transferred into lethally irradiated normal adult C57BL/6 mice. Eight, 14, and 26 weeks later mice were sacrificed and retinal flatmounts were prepared. Retinal microglia were identified by F4/80, CD45, and Iba-1 immunostaining. BrdU was injected into normal mice for 3-14 days and cell proliferation was examined by confocal microscopy of retinal flatmounts. Few (6.15 +/- 2.02 cells/retina) BrdU(+) cells were detected and of these some coexpressed CD11b (1.67 +/- 0.62 cells/retina) or F4/80 (0.57 +/- 0.30 cells/retina). BM-derived EGFP(+) cells were detected by 8-weeks post-transplantation. By 6 months, all retinal myeloid cells were EGFP(+). Consecutively, donor BM-EGFP(+) cells were demonstrated within the: (1) peripheral and juxtapapillary retina, (2) ganglion cell layer, (3) inner and outer plexiform layers, and (4) photoreceptor layer. EGFP(+) cells within the ganglion layer were amoeboid in shape and F4/80(high)CD45(high)Iba-1(high), whereas cells in the inner and outer plexiform layers were ramified and F4/80(low) CD45(low)Iba-1(low). Perivascular macrophages expressed less F4/80, CD45, and Iba-1 compared with parenchymal microglia. Our results suggest that BM-derived monocyte precursor cells are able to migrate across the BRB and replace retinal microglia/macrophages. The complete replacement of retinal microglia/macrophages takes about 6 months. In situ proliferation was predominantly of nonhemopoetic retinal cells.},
	Author = {Xu, Heping and Chen, Mei and Mayer, Eric J. and Forrester, John V. and Dick, Andrew D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Retina;Antigens, CD45;Animals;Macrophages;Bone Marrow Transplantation;Microscopy, Confocal;Microglia;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;research support, non-u.s. gov't;Cell Proliferation;Green Fluorescent Proteins;Antimetabolites;Bone Marrow Cells;Cell Lineage;Antigens, CD11b;Mice;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine;Tissue Fixation},
	Month = {8},
	Nlm_Id = {8806785},
	Number = {11},
	Organization = {Department of Ophthalmology, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK. h.xu\@abdn.ac.uk},
	Pages = {1189-98},
	Pubmed = {17600341},
	Title = {Turnover of resident retinal microglia in the normal adult mouse},
	Uuid = {0D082641-89BF-4841-91FB-11FB3A46AC45},
	Volume = {55},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.20535}}

@article{Xu:1997,
	Abstract = {In the adult CNS, proliferating cells persist only in the olfactory epithelium, olfactory bulb and subventricular zones. The cells of the subventricular zone are believed to constitute the cells in the adult mammalian brain, including the human brain, which can be stimulated to proliferate in response to epidermal growth factor or basic fibroblast growth factor. These cells are of particular interest, as they may be amenable to genetic engineering with markers such as tyrosine hydroxylase, and they may represent a long-term source of modified neurons suitable for transplantation therapy. Recent work by Lois and Alvarez-Buylla, in the mouse, has shown that labelled subventricular zone cells can migrate from the subventricular zone to the olfactory bulb, where they contribute to the granule cell population. In this study we have used an antibody we raised recently against the carboxy- terminal sequence of the vesicular monoamine transporter 2 (also known as the synaptic vesicle monoamine transporter) to detect vesicular monoamine transporter 2-like immunoreactive subventricular zone cells in the rat, and to visualize them as they migrate from the edge of the ventricle, through the olfactory bulb to locate them as differentiated neurons in the granule cell layer of the olfactory bulb. These data show that the subventricular zone cells express a vesicular monoamine transporter 2-like antigen and demonstrate that this protein may be a useful developmental marker for rat neuronal stem cells.},
	Author = {Xu, W. and Emson, P. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuroscience},
	Keywords = {Membrane Glycoproteins/*metabolism;Cerebral Ventricles/metabolism;Neurons/*metabolism;Rats;Stem Cells/*metabolism;Animal;04 Adult neurogenesis factors;Fluorescent Antibody Technique;Support, Non-U.S. Gov't;C abstr},
	Number = {1},
	Organization = {MRC Molecular Neuroscience Group, Babraham Institute, Cambridge, U.K.},
	Pages = {7-10.},
	Title = {Neuronal stem cells express vesicular monoamine transporter 2 immunoreactivity in the adult rat},
	Uuid = {786F4CB5-5115-4AC9-8FCA-812850C6F41D},
	Volume = {76},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8971754}}

@article{Yagi:2005,
	Abstract = {Osteoclasts are bone-resorbing cells that play a pivotal role in bone remodeling. Osteoclasts form large multinuclear giant cells by fusion of mononuclear osteoclasts. How cell fusion is mediated, however, is unclear. We identify the dendritic cell-specific transmembrane protein (DC-STAMP), a putative seven-transmembrane protein, by a DNA subtraction screen between multinuclear osteoclasts and mononuclear macrophages. DC-STAMP is highly expressed in osteoclasts but not in macrophages. DC-STAMP-deficient mice were generated, and osteoclast cell fusion was completely abrogated in homozygotes despite normal expression of osteoclast markers and cytoskeletal structure. As osteoclast multinucleation was restored by retroviral introduction of DC-STAMP, loss of cell fusion was directly attributable to a lack of DC-STAMP. Defects in osteoclast multinucleation reduce bone-resorbing activity, leading to osteopetrosis. Similar to osteoclasts, foreign body giant cell formation by macrophage cell fusion was also completely abrogated in DC-STAMP-deficient mice. We have thus identified an essential regulator of osteoclast and macrophage cell fusion, DC-STAMP, and an essential role of osteoclast multinucleation in bone homeostasis.},
	Author = {Yagi, Mitsuru and Miyamoto, Takeshi and Sawatani, Yumi and Iwamoto, Katsuya and Hosogane, Naobumi and Fujita, Nobuyuki and Morita, Kozo and Ninomiya, Ken and Suzuki, Toru and Miyamoto, Kana and Oike, Yuichi and Takeya, Motohiro and Toyama, Yoshiaki and Suda, Toshio},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0022-1007},
	Journal = {J Exp Med},
	Keywords = {11 Glia},
	Month = {8},
	Nlm_Id = {2985109R},
	Number = {3},
	Organization = {Department of Cell Differentiation, The Sakaguchi Laboratory.},
	Pages = {345-51},
	Pii = {jem.20050645},
	Pubmed = {16061724},
	Title = {DC-STAMP is essential for cell-cell fusion in osteoclasts and foreign body giant cells},
	Uuid = {ABC90DEC-0E1D-4FD9-96CF-B566FFE10320},
	Volume = {202},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1084/jem.20050645}}

@article{Yagi:2004,
	Abstract = {The twitcher mouse is an authentic murine model of a genetic demyelinating disease globoid cell leukodystrophy. Allogeneic bone marrow transplantation (BMT) in twitcher mice resulted in the clinicopathological improvement. Thus, using green fluorescent protein (GFP) transgenic mice as the donor, we investigated the behavior and fate of the donor cells and the possibility of transdifferentiation of the donor cells into neuroglial cells in the chimeric twitcher mice. GFP(+) cells were found throughout the brain, most conspicuous in the areas of demyelination. The donor GFP(+) cells expressed RCA-1, a marker for microglia/macrophages but were never exceed 70\%of the entire population of the RCA-1(+) microglia/macrophages. There was no convincing evidence that GFP(+) donor cells expressed markers for neurons, astrocytes, or oligodendrocytes. We concluded BMT is therapeutic for this model. However, this effect is not mediated by donor cells transdifferentiation in the brain.},
	Author = {Yagi, Takashi and McMahon, Eileen J. and Takikita, Shoichi and Mohri, Ikuko and Matsushima, Glenn K. and Suzuki, Kinuko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0969-9961},
	Journal = {Neurobiol Dis},
	Keywords = {Animals;Bone Marrow Transplantation;Comparative Study;Female;Mice, Transgenic;Liver;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Hematopoietic Stem Cell Transplantation;Male;Mice, Neurologic Mutants;Genotype;Hematopoietic Stem Cells;Mice;Luminescent Proteins;Demyelinating Diseases;Lung},
	Month = {6},
	Nlm_Id = {9500169},
	Number = {1},
	Organization = {Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.},
	Pages = {98-109},
	Pii = {S0969996104000129},
	Pubmed = {15207267},
	Title = {Fate of donor hematopoietic cells in demyelinating mutant mouse, twitcher, following transplantation of GFP+ bone marrow cells},
	Uuid = {BACAB63E-FB57-45CA-BB21-91D0C0A9D1E9},
	Volume = {16},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.nbd.2004.01.002}}

@article{Yagi:1993,
	Abstract = {Mutant mice in which beta-galactosidase gene (lacZ) was inserted into fyn locus were generated by homologous recombination in embryonic stem cells to examine the Fyn expression in the central nervous system. In adult brain, intensive beta-galactosidase activity was observed in olfactory bulb, cerebellum and hippocampus of the limbic system; the subcellular distribution of the activity was apparent not only in cell body but also in neural processes, and homozygous mutant mice live-born displayed an anatomical abnormality in the neural cell layer of the hippocampal formation. In spinal cord it was specifically expressed in dorsal horn, and in brain stem it was more characteristic in the sensory pathway, suggesting roles of Fyn in the sensory nervous network. In the white matter area, it was intense at postnatal day 10 but not detectable in adult, suggesting Fyn's role in myelinization.},
	Author = {Yagi, T. and Shigetani, Y. and Okado, N. and Tokunaga, T. and Ikawa, Y. and Aizawa, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Oncogene},
	Keywords = {Cerebral Cortex/chemistry/cytology/embryology;Olfactory Bulb/chemistry/cytology/embryology;Heterozygote;Nervous System/chemistry/cytology/embryology;Cerebellum/chemistry/cytology/embryology;Proto-Oncogenes/*genetics;Embryo/chemistry/cytology;04 Adult neurogenesis factors;Gene Expression/genetics;Hippocampus/chemistry/cytology/embryology;Base Sequence;In Vitro;*Brain Chemistry;Molecular Sequence Data;Mice, Inbred C57BL;Mice, Mutant Strains;Spinal Cord/chemistry/cytology/embryology;beta-Galactosidase/genetics/metabolism/physiology;Mice, Inbred CBA;In Situ Hybridization, Fluorescence;Mutation;Animal;Blotting, Western;Proto-Oncogene Proteins/*analysis/*genetics/physiology;Mice, Inbred ICR;Mice;Support, Non-U.S. Gov't;Homozygote;Lac Operon/*genetics;C abstr},
	Number = {12},
	Organization = {Laboratory of Molecular Oncology, Tsukuba Life Science Center, Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan.},
	Pages = {3343-51.},
	Title = {Regional localization of Fyn in adult brain; studies with mice in which fyn gene was replaced by lacZ},
	Uuid = {192BCE52-66DA-4E17-8B61-50A73C08D9DF},
	Volume = {8},
	Year = {1993},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8247536}}

@article{Yagita:2002,
	Abstract = {Both nestin and the neural RNA-binding protein Musashi1 (Msi1) are expressed in neural stem cells in the subventricular zone. Neurogenesis in the hippocampus has received much attention, so we evaluated the expression of Msi1 and nestin in the adult rat hippocampus after transient forebrain ischemia. Both Msi1 and nestin were induced in the reactive astrocytes after ischemia, especially in the CA1 region, until 35 days after ischemia. Induction of both molecules suggested that reactive astrocytes might have immature characteristics. In the subgranular zone (SGZ) of the hippocampal dentate gyrus, Msi1-positive cells formed clusters after ischemia. These cells were labeled by bromodeoxyuridine (BrdU) but did not express glial fibrillary acidic protein. In contrast, very few nestin-positive cells were labeled by BrdU. Our results suggest that neuronal progenitor cells in the SGZ expressed Msi1 but not nestin. 22194563 0360-4012 Journal Article},
	Author = {Yagita, Y. and Kitagawa, K. and Sasaki, T. and Miyata, T. and Okano, H. and Hori, M. and Matsumoto, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {J Neurosci Res},
	Keywords = {Rats;D-14;Animal;Glial Fibrillary Acidic Protein/analysis;Rats, Wistar;Nerve Tissue Proteins/analysis/*biosynthesis;Antimetabolites;Intermediate Filament Proteins/analysis/*biosynthesis;Male;Support, Non-U.S. Gov't;06 Adult neurogenesis injury induced;Age Factors;RNA-Binding Proteins/analysis/*biosynthesis;Brain Ischemia/*metabolism;Immunohistochemistry;Biological Markers;Bromodeoxyuridine;Hippocampus/chemistry/*metabolism},
	Number = {6},
	Organization = {Division of Strokology, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita City, Osaka, Japan.},
	Pages = {750-6},
	Pubmed = {12205668},
	Title = {Differential expression of Musashi1 and nestin in the adult rat hippocampus after ischemia},
	Uuid = {15918EE0-FF59-4706-9528-7ADF66CC6F3E},
	Volume = {69},
	Year = {2002},
	url = {papers/Yagita_JNeurosciRes2002}}

@article{Yagita:2001,
	Abstract = {BACKGROUND AND PURPOSE: Recently, there has been great interest in adult neurogenesis. We investigated whether transient forebrain ischemia could influence the proliferation of neuronal progenitor in the subgranular zone (SGZ) of the rat hippocampus and whether aging could influence the neurogenesis after ischemia. METHODS: Male Wistar rats were subjected to 4-vessel occlusion model. We used a bromodeoxyuridine (BrdU) labeling method to identify the postproliferation cells and double-immunostaining with confocal microscopy to determine the cell phenotype. RESULTS: The number of BrdU-positive cells in the SGZ increased approximately 5.7-fold 8 days after ischemia, compared with the control. BrdU-positive cells formed clusters, which suggested that these cells had divided from an original progenitor cell, and expressed Musashi1 (Msi1), a marker of neural stem/progenitor cells. Although astrocytes also expressed Msi1 in the adult brain, Msi1-positive cells that formed clusters in the SGZ did not express glial fibrillary acidic protein, an astrocyte marker. About 70\%of all BrdU-positive cells in the SGZ represented the neuronal phenotype 4 weeks after the BrdU injection. Although proliferation of progenitor cells was stimulated in both young and older animals, aging accelerated the reduction in newborn cells after ischemia. CONCLUSIONS: Our results indicate that ischemic stress stimulated the proliferation of neuronal progenitor cells in the SGZ of both young and old rats but resulted in increased neurogenesis only in young animals. Our findings will be important in developing therapeutic intervention to enhance endogenous neurogenesis after brain injury. 1524-4628 Journal Article},
	Author = {Yagita, Y. and Kitagawa, K. and Ohtsuki, T. and Takasawa, Ki and Miyata, T. and Okano, H. and Hori, M. and Matsumoto, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Stroke},
	Keywords = {Hippocampus/blood supply/*pathology;Prosencephalon/blood supply/pathology;Glial Fibrillary Acidic Protein/biosynthesis;Animals;Rats;Stem Cells/*cytology/metabolism;Mitosis/physiology;Dentate Gyrus/pathology;Nerve Tissue Proteins/biosynthesis;Cell Count;Rats, Wistar;Disease Models, Animal;Male;Support, Non-U.S. Gov't;D abstr;Astrocytes/cytology/metabolism;Cell Division/physiology;06 Adult neurogenesis injury induced;*Aging/physiology;Ischemic Attack, Transient/*pathology;RNA-Binding Proteins/biosynthesis;Neurons/cytology/metabolism;Bromodeoxyuridine},
	Number = {8},
	Organization = {Division of Strokology, Department of Internal Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.},
	Pages = {1890-6},
	Pubmed = {11486122},
	Title = {Neurogenesis by progenitor cells in the ischemic adult rat hippocampus},
	Uuid = {414076D5-EC81-11DA-8605-000D9346EC2A},
	Volume = {32},
	Year = {2001},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11486122}}

@article{Yamada:1998a,
	Abstract = {The glutamate transporter GLT-1 is expressed in astrocytes of the mature brain and spinal cord. In the present study, we examined its expression in the developing mouse spinal cord. By in situ hybridization, 35S-labeled antisense oligonucleotide probes for GLT-1 mRNA consistently labeled the mantle zone/gray matter from embryonic day 11 through the adult stage. However, immunohistochemistry with a specific antibody visualized distinct regional and cellular localizations during the time between the fetal and postnatal stages. At fetal stages, GLT-1 immunoreactivity predominated in the marginal zone/white matter, observed as tiny puncta in cross-sections and as thin fibers in longitudinal sections. The GLT-1-immunopositive structures were also labeled for neuron-specific enolase, a glycolytic enzyme specific to postmitotic neurons and endocrine cells. By electron microscopy, GLT-1 immunoreactivity was detected in axons forming frequent enlargements and was focally localized on a small portion of the axolemma, particularly that facing adjacent axons. At early postnatal stages, GLT-1 disappeared from axons in white matter tracts and, instead, appeared in astrocytic processes surrounding various neuronal elements in the gray matter. Therefore, before switching to astrocytic expression, GLT-1 is transiently expressed in neurons and localized in differentiating axons. Together with our previous finding on the localization of glutamate transporter GLAST in radial glial fibers, GLT-1 and GLAST are thus localized during development on distinct directional cellular elements along which young neurons elongate their axons or move their cell bodies, respectively.},
	Author = {Yamada, K. and Watanabe, M. and Shibata, T. and Nagashima, M. and Tanaka, K. and Inoue, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Neurosci},
	Keywords = {Biological Transport/physiology;ABC Transporters/*analysis;Spinal Cord/*chemistry/embryology/growth &development;Axons/*chemistry;Animal;Antibody Formation;G-need;Mice, Inbred C57BL;11 Glia;Astrocytes/*chemistry;Time Factors;In Situ Hybridization;Support, Non-U.S. Gov't;Mice;Immunohistochemistry;Molecular Sequence Data;Amino Acid Sequence;Neurons/*chemistry/ultrastructure;Nerve Tissue Proteins/*analysis;Fetal Development/physiology},
	Number = {15},
	Organization = {Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan.},
	Pages = {5706-13.},
	Title = {Glutamate transporter GLT-1 is transiently localized on growing axons of the mouse spinal cord before establishing astrocytic expression},
	Uuid = {F1EF68A5-6FCE-430E-B5A2-3E9C56DA4FD1},
	Volume = {18},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9671661}}

@article{Yamada:1998,
	Abstract = {Therapeutic strategies for leukemia are directed to induction of differentiation and apoptosis as well as growth inhibition. One of the key antileukemic agents, 1-beta-D-arabinofuranosylcytosine (ara C), is clinically applied according to these therapeutic aims. However, the molecular effects of 0.1 microg/ml of ara C, a concentration that corresponds to the serum level in leukemic patients on a conventional dose of ara C, have not been well disclosed. Here, we addressed these issues using K562 cells which derived from a blastic crisis of chronic myeloid leukemia. DNA synthesis of treated cells was suppressed from 1-6 h. But, it recovered at 12 h and no further inhibition was observed. The number of cells was not decreased but DNA fragmentation was observed at 72 h. The number of erythroid-differentiated cells also increased to 30\%at 72 h. Along with treatment, no marked alteration of mRNAs for cell cycle-regulating genes was found and the retinoblastoma gene product remained hyperphosphorylated throughout treatment. The expression of mRNAs for apoptosis-regulating genes also remained unchanged, except for slight down-regulation of Bax. c-myc protein was not found later than 48 h, and Max mRNA was downregulated. c-jun was immediately induced, followed by the fluctuated expression level along with treatment. These findings suggest that the 0.1 microg/ml ara C changed the proliferation, differentiation and death of K562 cells in a biphasic manner. In the early phase, DNA synthesis was inhibited without altering the expression of cell cycle regulating-genes. In the latter phase, cell death and erythroid- differentiation occurred in accordance with the down-regulation of c-myc. 0300-8177 Journal Article},
	Author = {Yamada, H. and Horiguchi-Yamada, J. and Nagai, M. and Takahara, S. and Sekikawa, T. and Kawano, T. and Itoh, K. and Fukumi, S. and Iwase, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Mol Cell Biochem},
	Keywords = {Cell Differentiation/drug effects;Human;Benzidines/analysis;Phosphorylation;Comparative Study;Retinoblastoma Protein/metabolism;Genes, myc;Genes, jun;Gene Expression Regulation/drug effects;08 Aberrant cell cycle;DNA Fragmentation/drug effects;Reverse Transcriptase Polymerase Chain Reaction;Cytarabine/*pharmacology/therapeutic use;DNA/biosynthesis;Erythrocytes/*cytology/drug effects;Support, Non-U.S. Gov't;Genes, cdc/genetics;Blotting, Western;Apoptosis/*drug effects/genetics;Cell Cycle/*drug effects;K562 Cells;EE abstr},
	Number = {1-2},
	Organization = {Department of Internal Medicine (IV), Aoto Hospital, Institute of DNA Medicine, The Jikei University School of Medicine, Tokyo, Japan.},
	Pages = {211-20},
	Pubmed = {9788759},
	Title = {Biological effects of a relatively low concentration of 1-beta-D-arabinofuranosylcytosine in K562 cells: alterations of the cell cycle, erythroid-differentiation, and apoptosis},
	Uuid = {089F6BB3-1A1E-483F-B82B-4524936F6F20},
	Volume = {187},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9788759}}

@article{Yamagata:2002,
	Abstract = {A major determinant of specific connectivity in the central nervous system is that synapses made by distinct afferent populations are restricted to particular laminae in their target area. We identify Sidekick (Sdk)-1 and -2, homologous transmembrane immunoglobulin superfamily molecules that mediate homophilic adhesion in vitro and direct laminar targeting of neurites in vivo. sdk-1 and -2 are expressed by nonoverlapping subsets of retinal neurons; each sdk is expressed by presynaptic (amacrine and bipolar) and postsynaptic (ganglion) cells that project to common inner plexiform (synaptic) sublaminae. Sdk proteins are concentrated at synaptic sites, and Sdk-positive synapses are restricted to the 2 (of > or =10) sublaminae to which sdk-expressing cells project. Ectopic expression of Sdk in Sdk-negative cells redirects their processes to a Sdk-positive sublamina. These results implicate Sdks as determinants of lamina-specific synaptic connectivity.},
	Author = {Yamagata, Masahito and Weiner, Joshua A. and Sanes, Joshua R.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Synapses;Retina;research support, u.s. gov't, p.h.s. ;Neural Cell Adhesion Molecules;Cell Adhesion;21 Neurophysiology;Molecular Sequence Data;Eye Proteins;Membrane Proteins;research support, non-u.s. gov't ;Drosophila Proteins;Amacrine Cells;Amino Acid Sequence;Retinal Ganglion Cells;Animals;Chickens;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {0413066},
	Number = {5},
	Organization = {Department of Anatomy and Neurobiology, School of Medicine, Washington University, Saint Louis, MO 63110, USA.},
	Pages = {649-60},
	Pii = {S0092867402009108},
	Pubmed = {12230981},
	Title = {Sidekicks: synaptic adhesion molecules that promote lamina-specific connectivity in the retina},
	Uuid = {CFBAB388-08E2-4128-B869-8F2FCC98CA00},
	Volume = {110},
	Year = {2002}}

@article{Yamashita:1997,
	Abstract = {In adult rodents, proliferating cells in the subventricular zone of lateral ventricle tangentially migrate into the olfactory bulb, where they become the interneurons. The present immunocytochemical analysis revealed that S100A6 (calcyclin), a specific calcium-binding protein of the S100 family, is restrictedly distributed in some astrocytes in the tangential migration pathway of the rat. These results suggest that a particular type of astrocytes containing S100A6 is associated with the tangential migration pathway.},
	Author = {Yamashita, N. and Kosaka, K. and Ilg, E. C. and Schafer, B. W. and Heizmann, C. W. and Kosaka, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Brain Res},
	Keywords = {Microscopy, Confocal;*Cell Movement;G abstr;Rats;Olfactory Bulb/cytology;Calcium-Binding Proteins/*analysis/immunology;Epidermal Growth Factor/analysis/immunology;Rats, Wistar;Cell Communication;11 Glia;Cerebral Ventricles/*cytology;Neurons/*cytology;Animal;Support, Non-U.S. Gov't;Male;Antibodies;Astrocytes/*chemistry/cytology},
	Number = {2},
	Organization = {Department of Anatomy and Neurobiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.},
	Pages = {388-92.},
	Title = {Selective association of S100A6 (calcyclin)-immunoreactive astrocytes with the tangential migration pathway of subventricular zone cells in the rat},
	Uuid = {E2D1779F-CE62-4D69-8355-A3E83A127744},
	Volume = {778},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9459556}}

@article{Yang:2001,
	Abstract = {Alzheimer's disease (AD) is a devastating dementia of late life that is correlated with a region-specific neuronal cell loss. Despite progress in uncovering many of the factors that contribute to the etiology of the disease, the cause of the nerve cell death remains unknown. One promising theory is that the neurons degenerate because they reenter a lethal cell cycle. This theory receives support from immunocytochemical evidence for the reexpression of several cell cycle-related proteins. Direct proof for DNA replication, however, has been lacking. We report here the use of fluorescent in situ hybridization to examine the chromosomal complement of interphase neuronal nuclei in the adult human brain. We demonstrate that a significant fraction of the hippocampal pyramidal and basal forebrain neurons in AD have fully or partially replicated four separate genetic loci on three different chromosomes. Cells in unaffected regions of the AD brain or in the hippocampus of nondemented age-matched controls show no such anomalies. We conclude that the AD neurons complete a nearly full S phase, but because mitosis is not initiated, the cells remain tetraploid. Quantitative analysis indicates that the genetic imbalance persists for many months before the cells die, and we propose that this imbalance is the direct cause of the neuronal loss in Alzheimer's disease. 1529-2401 Journal Article},
	Author = {Yang, Y. and Geldmacher, D. S. and Herrup, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Neurosci},
	Keywords = {Chromosomes;Human;In Situ Hybridization, Fluorescence;Alzheimer Disease/*etiology/*metabolism/pathology;Cyclin B/metabolism;Hippocampus/metabolism/pathology;Cell Nucleus/metabolism/pathology;*DNA Replication;Interphase;Neurons/*metabolism/pathology;Female;EE pdf;Basal Nucleus of Meynert/metabolism/pathology;Male;Aged;Support, Non-U.S. Gov't;Aged, 80 and over;Support, U.S. Gov't, P.H.S.;Polyploidy;Pyramidal Cells/metabolism/pathology;S Phase;Immunohistochemistry;Prosencephalon/metabolism/pathology;Cell Death;Proliferating Cell Nuclear Antigen/metabolism},
	Number = {8},
	Organization = {University Alzheimer Center, Department of Neuroscience, University Hospitals of Cleveland and Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.},
	Pages = {2661-8},
	Pubmed = {11306619},
	Title = {DNA replication precedes neuronal cell death in Alzheimer's disease},
	Uuid = {32528674-D395-11D9-A0E9-000D9346EC2A},
	Volume = {21},
	Year = {2001},
	url = {papers/Yang_JNeurosci2001.pdf},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11306619}}

@article{Yang:2003,
	Abstract = {Recent studies based predominantly on nucleotide hybridization techniques have identified aneuploid neurons and glia in the normal brain. To substantiate these findings and address how neural aneuploidy arises, we examined individual neural progenitor cells (NPCs) undergoing mitosis. Here we report the identification of chromosomal segregation defects in normal NPCs of the mouse cerebral cortex. Immunofluorescence in fixed tissue sections revealed the presence of supernumerary centrosomes and lagging chromosomes among mitotic NPCs. The extent of aneuploidy followed the prevalence of supernumerary centrosomes within distinct cell populations. Real-time imaging of live NPCs revealed lagging chromosomes and multipolar divisions. NPCs undergoing nondisjunction were also observed, along with interphase cells that harbored micronuclei or multiple nuclei, consistent with unbalanced nuclear division. These data independently confirm the presence of aneuploid NPCs and demonstrate the occurrence of mitotic segregation defects in normal cells that can mechanistically account for aneuploidy in the CNS. 1529-2401 Journal Article},
	Author = {Yang, A. H. and Kaushal, D. and Rehen, S. K. and Kriedt, K. and Kingsbury, M. A. and McConnell, M. J. and Chun, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {J Neurosci},
	Keywords = {Karyotyping;EE pdf;Nondisjunction, Genetic;Chromosomes/genetics;*Aneuploidy;Female;08 Aberrant cell cycle;Metaphase/physiology;Mice, Inbred BALB C/genetics;Support, U.S. Gov't, P.H.S.;Mitosis;Chromosome Segregation/*physiology;Support, Non-U.S. Gov't;Animals;Neurons/*cytology/ultrastructure;Stem Cells/*cytology/*metabolism;Mice},
	Number = {32},
	Organization = {Biomedical Sciences, School of Medicine, University of California, San Diego, California 92093, USA.},
	Pages = {10454-62},
	Title = {Chromosome segregation defects contribute to aneuploidy in normal neural progenitor cells},
	Uuid = {0387BBB2-8F56-493C-9584-18F11020AAD2},
	Volume = {23},
	Year = {2003},
	url = {papers/Yang_JNeurosci2003.pdf}}

@article{Yang:2003a,
	Abstract = {Cell cycle events play a major role in the loss of neurons in advanced Alzheimer's disease (AD). It is currently unknown, however, whether the same is true for the neuronal losses in early disease stages. To explore this issue we analyzed brain autopsy material from individuals clinically categorized with mild cognitive impairment (MCI), many if not most of whom will progress to AD. Immunocytochemistry for three cell cycle-related proteins, proliferating cell nuclear antigen, cyclin D, and cyclin B, was performed on sections from hippocampus, basal nucleus of Meynert, and entorhinal cortex. The results obtained from MCI cases were compared with material from individuals diagnosed with AD and those without cognitive impairment. In both hippocampus and basal nucleus, there was a significant percentage of cell cycle immunopositive neurons in the MCI cases. These percentages were similar to those found in the AD cases but significantly higher than non-cognitively impaired controls. In entorhinal cortex, the density of cell cycle-positive neurons was greater in MCI than in AD. However, we observed large variations in the percentages of immunopositive neurons from individual to individual. These findings lend support to the hypothesis that both the mechanism of cell loss (a cell cycle-induced death) and the rate of cell loss (a slow atrophy over several months) are identical at all stages of the AD disease process. The implication of the findings for human clinical trials is discussed. 1529-2401 Journal Article},
	Author = {Yang, Y. and Mufson, E. J. and Herrup, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {J Neurosci},
	Keywords = {Human;Disease Progression;Neurons/chemistry/*pathology;Basal Nucleus of Meynert/chemistry/pathology;Cell Cycle;Entorhinal Cortex/chemistry/pathology;Female;Cell Count;EE pdf;Hippocampus/chemistry/pathology;08 Aberrant cell cycle;Male;Aged;Cyclins/analysis/immunology;Cognition Disorders/diagnosis/pathology;Proliferating Cell Nuclear Antigen/analysis/immunology;Support, U.S. Gov't, P.H.S.;Alzheimer Disease/diagnosis/metabolism/*pathology;Immunohistochemistry;Cyclin B/analysis/immunology;Cell Death},
	Number = {7},
	Organization = {Alzheimer Research Laboratory, University Hospitals of Cleveland and Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106, USA. yxy33\@po.cwru.edu},
	Pages = {2557-63},
	Pubmed = {12684440},
	Title = {Neuronal cell death is preceded by cell cycle events at all stages of Alzheimer's disease},
	Uuid = {B12B6DA0-B177-4D7A-A670-ABED3745017D},
	Volume = {23},
	Year = {2003},
	url = {papers/Yang_JNeurosci2003a.pdf}}

@article{Yang:2005a,
	Abstract = {In ataxia-telangiectasia (A-T), the loss of the ataxia-telangiectasia mutated (ATM) kinase leads to a failure of cell cycle checkpoints and DNA double-strand break detection resulting in cellular radiation sensitivity and a predisposition to cancer. There is also a significant loss of neurons, in particular cerebellar granule and Purkinje cells. Mice homozygous for null alleles of atm reproduce the radiation sensitivity and high-tumor incidence of the human disease but show no significant nerve cell loss. Using immunocytochemistry, we found the re-expression of cell cycle proteins in Purkinje cells and striatal neurons in both human and mouse A-T. In the mouse, we used fluorescent in situ hybridization (FISH) to document that DNA replication accompanies the reappearance of these proteins in at-risk neuronal cells. We also found the presence of significant cell cycle activity in the Purkinje cells of the atm+/- heterozygote mouse. The cell cycle events in mouse cerebellum occur primarily during the third postnatal week by both FISH and immunocytochemistry. Thus, the initiation of this ectopic cell division occurs just as the final stages of Purkinje cell development are being completed. These results suggest that loss of cell cycle control represents a common disease mechanism that underlies the defects in the affected tissues in both human and mouse diseases.},
	Author = {Yang, Yan and Herrup, Karl},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {08 Aberrant cell cycle},
	Month = {3},
	Nlm_Id = {8102140},
	Number = {10},
	Organization = {Department of Neurology, Alzheimer Research Laboratory (E504), Case School of Medicine, Cleveland, Ohio 44106, USA. yan.yang\@case.edu},
	Pages = {2522-9},
	Pii = {25/10/2522},
	Pubmed = {15758161},
	Title = {Loss of neuronal cell cycle control in ataxia-telangiectasia: a unified disease mechanism},
	Uuid = {E3C78D53-F309-48E6-BA22-B7D932D45784},
	Volume = {25},
	Year = {2005},
	url = {papers/Yang_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4946-04.2005}}

@article{Yang:2006c,
	Abstract = {NG2 cells (polydendrocytes) comprise an abundant glial population that is widely and uniformly distributed throughout the developing and mature CNS and are identified by the expression of the NG2 proteoglycan at the cell surface. Although recent electrophysiological studies suggest that they are capable of receiving signals from axon terminals, other studies, based on the finding that the NG2 molecule itself induces growth cone collapse, have led to a widely held speculation that NG2 cells themselves also repel and inhibit growing axons. In this study, we have examined the effects of rat NG2 cells on growing hippocampal and neocortical axons in vitro and in vivo. NG2 cells did not repel growing axons but promoted their growth in vitro, and axonal growth cones formed extensive contacts with NG2 cells both in vitro and in the developing corpus callosum. Punctate immunoreactivity for fibronectin and laminin was found to be colocalized with NG2 on the surface of NG2 cells. Altering the level of cell surface NG2 expression had no effect on the growth-promoting effects of NG2 cells on growing axons. Thus, our study indicates that NG2 cells are not inhibitory to growing axons but provide an adhesive substrate for axonal growth cones and promote their growth even in the presence of elevated levels of the NG2 proteoglycan. These findings suggest a novel role for NG2 cells in facilitating axonal growth during development and regeneration.},
	Author = {Yang, Zhongshu and Suzuki, Ryusuke and Daniels, Stephen B. and Brunquell, Christopher B. and Sala, Christopher J. and Nishiyama, Akiko},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {14},
	Organization = {Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut 06269-3156, USA.},
	Pages = {3829-39},
	Pii = {26/14/3829},
	Pubmed = {16597737},
	Title = {NG2 glial cells provide a favorable substrate for growing axons},
	Uuid = {5489D66D-EF4A-4A0F-983C-44CB369E6DCA},
	Volume = {26},
	Year = {2006},
	url = {papers/Yang_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4247-05.2006}}

@article{Yang:2006,
	Abstract = {Neurogenesis has been described in various regions of the CNS throughout life. We examined the extent of natural cell division and replacement from 7 weeks to 7 months after cervical spinal cord injury in four adult rhesus monkeys. Bromodeoxyuridine (BrdU) injections revealed an increase of >80-fold in the number of newly divided cells in the primate spinal cord after injury, with an average of 725,000 BrdU-labeled cells identified per monkey in the immediate injury zone. By 7 months after injury, 15\%of these new cells expressed mature markers of oligodendrocytes and 12\%expressed mature astrocytic markers. Newly born oligodendrocytes were present in zones of injury-induced demyelination and appeared to ensheath or remyelinate host axons. Thus, cell replacement is an extensive natural compensatory response to injury in the primate spinal cord that contributes to neural repair and is a potential target for therapeutic enhancement.},
	Author = {Yang, Hong and Lu, Paul and McKay, Heather M. and Bernot, Tim and Keirstead, Hans and Steward, Oswald and Gage, Fred H. and Edgerton, V. Reggie and Tuszynski, Mark H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;Spinal Cord Injuries;Macaca mulatta;Neuronal Plasticity;Cell Proliferation;Astrocytes;Cell Division;Nerve Regeneration;Research Support, N.I.H., Extramural;Spinal Cord;Animals;Oligodendroglia;24 Pubmed search results 2008;Male;Neurons},
	Month = {2},
	Nlm_Id = {8102140},
	Number = {8},
	Organization = {Department of Neurosciences, University of California, San Diego, La Jolla, California 92093-0626, USA.},
	Pages = {2157-66},
	Pii = {26/8/2157},
	Pubmed = {16495442},
	Title = {Endogenous neurogenesis replaces oligodendrocytes and astrocytes after primate spinal cord injury},
	Uuid = {A13CC3CF-4414-4A2E-A7BE-D97F9FB78BFF},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4070-05.2005}}

@article{Yang:2004,
	Abstract = {Doublecortin (Dcx) is a microtubule-associated protein expressed by migrating neuroblasts in the embryo and in the adult subventricular zone (SVZ). The adult SVZ contains neuroblasts that migrate in the rostral migratory stream (RMS) to the olfactory bulbs. We have examined the distribution and phenotype of Dcx-positive cells in the adult mouse SVZ and surrounding regions. Chains of Dcx-positive cells in the SVZ were distributed in a tight dorsal population contiguous with the RMS, with a separate ventral population comprised of discontinuous chains. Unexpectedly, Dcx-positive cells were also found outside of the SVZ: dorsally in the corpus callosum, and ventrally in the nucleus accumbens, ventromedial striatum, ventrolateral septum, and bed nucleus of the stria terminalis. Dcx-positive cells outside the SVZ had the morphology of migrating cells, occurred as individual cells or in chain-like clusters, and were more numerous anteriorly. Of the Dcx-positive cells found outside of the SVZ, 47\%expressed the immature neuronal protein class III beta-tubulin, 8\%expressed NeuN, a marker of mature neurons. Dcx-positive cells did not express molecules found in astrocytes, oligodendrocytes, or microglia. Structural and immunoelectron microscopy revealed that cells with the ultrastructural features of neuroblasts in the SVZ were Dcx+, and that clusters of neuroblasts emanated ventrally from the SVZ into the parenchyma. Our results suggest that the distribution of cells comprising the walls of the lateral ventricle are more heterogeneous than was thought previously, that SVZ cells may migrate dorsally and ventrally away from the SVZ, and that some emigrated cells express a neuronal phenotype.},
	Author = {Yang, Helen K. C. and Sundholm-Peters, Nikki L. and Goings, Gwendolyn E. and Walker, Avery S. and Hyland, Kenneth and Szele, Francis G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Mice;Nucleus Accumbens;02 Adult neurogenesis migration;Tissue Distribution;Female;Immunohistochemistry;Stem Cells;Neuropeptides;Lateral Ventricles;Support, U.S. Gov't, P.H.S.;Male;Cell Movement;Animals;Neurons;Microtubule-Associated Proteins},
	Month = {5},
	Nlm_Id = {7600111},
	Number = {3},
	Organization = {Children's Memorial Hospital, Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60614-3394, USA.},
	Pages = {282-95},
	Pubmed = {15079857},
	Title = {Distribution of doublecortin expressing cells near the lateral ventricles in the adult mouse brain},
	Uuid = {2DDD1439-B38A-41FB-A5E9-B8E56C2DCB0B},
	Volume = {76},
	Year = {2004},
	url = {papers/Yang_JNeurosciRes2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.20071}}

@article{Yang:2006b,
	Abstract = {Neurons and oligodendrocyte progenitors are highly sensitive to perinatal hypoxic-ischemic injury. As accumulating evidence suggests that many insults to the human infant occur in utero, and preventing brain damage to infants in utero will prove difficult, there is strong rationale to pursue regenerative strategies to reduce the morbidity associated with developmental brain injuries. The purpose of this study was to determine whether a hypoxic-ischemic insult stimulates the neural stem/progenitor cells in the subventricular zone to generate new neurons and oligodendrocytes. Hypoxia-ischemia was induced using the Vannucci rat model on postnatal day-6 pups. Injections of 5'-bromo-2'-deoxyuridine to label cells undergoing DNA synthesis after hypoxia-ischemia revealed that there is a robust proliferative response within the subventricular zone of the injured hemisphere that continues for at least 1 week after the hypoxic-ischemic episode. Using the neurosphere assay to quantify the number of neural stem/progenitor cells in the subventricular zone, we find that there are twice as many neural stem/progenitor cells in the affected dorsolateral subventricular zone at 1 week of recovery and that these cells generate larger spheres in response to growth factors compared with controls. Precursors from the injured hemisphere generate three times as many neurons in vitro and more than twice as many oligodendroglia compared with controls. Hypoxia-ischemia also increases neurogenesis in vivo. Doublecortin positive cells with migratory profiles were observed streaming from the ipsilateral subventricular zone to the striatum and neocortex, whereas, few doublecortin positive cells were found in the contralateral hemisphere after hypoxia-ischemia. These observations provide evidence that the somatic neural progenitors of the subventricular zone participate in the production of new brain cells lost after hypoxia-ischemia.},
	Author = {Yang, Z. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {24 Pubmed search results 2008},
	Nlm_Id = {7605074},
	Number = {2},
	Organization = {Department of Neurology and Neurosciences, UMDNJ-New Jersey Medical School, Newark, NJ 07101, USA.},
	Pages = {555-64},
	Pii = {S0306-4522(06)00043-1},
	Pubmed = {16500031},
	Title = {Hypoxia/ischemia expands the regenerative capacity of progenitors in the perinatal subventricular zone},
	Uuid = {7D715258-2FED-4F77-A87D-30A23CA23B7E},
	Volume = {139},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2005.12.059}}

@article{Yang:2000a,
	Abstract = {Spinal cord neuronal restricted progenitor (NRP) cells, when transplanted into the neonatal anterior forebrain subventricular zone, migrate to distinct regions throughout the forebrain including the olfactory bulb, frontal cortex, and occipital cortex but not to the hippocampus. Their migration pattern and differentiation potential is distinct from anterior forebrain subventricular zone NRPs. Irrespective of their final destination, NRP cells do not differentiate into glia. Rather they synthesize neurotransmitters, acquire region-specific phenotypes, and receive synapses from host neurons after transplantation. Spinal cord NRPs express choline acetyl transferase even in regions where host neurons do not express this marker. The restricted distribution of transplanted spinal cord NRP cells and their acquisition of varied region-specific phenotypes suggest that their ultimate fate and phenotype is dictated by a combination of intrinsic properties and extrinsic cues from the host. 0027-8424 Journal Article},
	Author = {Yang, H. and Mujtaba, T. and Venkatraman, G. and Wu, Y. Y. and Rao, M. S. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Olfactory Nerve/*physiology;Cell Differentiation;Animals;Olfactory Bulb/*physiology;10 Development;Neurons/*cytology/physiology;Transfection;Rats;Synapses/*physiology;Glutamic Acid/analysis;Cell Movement;Brain/cytology/*physiology;Prosencephalon/cytology/physiology;Time Factors;Synaptophysin/analysis;*Cell Transplantation;Choline O-Acetyltransferase/analysis;Luminescent Proteins/analysis/genetics;Animals, Newborn;gamma-Aminobutyric Acid/analysis;Stem Cells/*cytology/physiology;Genes, Reporter;Biological Markers;F;Nerve Tissue Proteins/*analysis;Spinal Cord/*cytology},
	Number = {24},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, GA 30322, USA.},
	Pages = {13366-71},
	Pubmed = {11087876},
	Title = {Region-specific differentiation of neural tube-derived neuronal restricted progenitor cells after heterotopic transplantation},
	Uuid = {324EAEFA-BC4E-44F2-9D82-D18EB50F37E5},
	Volume = {97},
	Year = {2000},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11087876}}

@article{Yang:2006a,
	Abstract = {We have developed an efficient method to target lentivirus-mediated gene transduction to a desired cell type. It involves incorporation of antibody and fusogenic protein as two distinct molecules into the lentiviral surface. The fusogen is constructed by modifying viral envelope proteins, so that they lack the ability to bind to their cognate receptor but still retain the ability to trigger pH-dependent membrane fusion. Thus, the specificity of such a lentiviral vector is solely determined by the antibody, which is chosen to recognize a specific surface antigen of the desired cell type. This specific binding then induces endocytosis of the surface antigen, bringing the lentivirus into an endosome. There, the fusogen responds to the low pH environment and mediates membrane fusion, allowing the virus core to enter the cytosol. Using CD20 as a target antigen for human B cells, we have demonstrated that this targeting strategy is effective both in vitro and in intact animals. This methodology is flexible and can be extended to other forms of cell type-specific recognition to mediate targeting. The only requirement is that the antibody (or other binding protein) must be endocytosed after interaction with its cell surface-binding determinant.},
	Author = {Yang, Lili and Bailey, Leslie and Baltimore, David and Wang, Pin},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Transduction, Genetic;Animals;Humans;Lentivirus;Female;15 Retrovirus mechanism;23 Technique;Hydrogen-Ion Concentration;B-Lymphocytes;Recombinant Fusion Proteins;Genetic Vectors;Viral Envelope Proteins;research support, non-u.s. gov't ;Cell Line;Antibodies;Mice, Knockout;Membrane Fusion;Mice;24 Pubmed search results 2008;Antigens, CD20},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {31},
	Organization = {Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.},
	Pages = {11479-84},
	Pii = {0604993103},
	Pubmed = {16864770},
	Title = {Targeting lentiviral vectors to specific cell types in vivo},
	Uuid = {583840C9-A941-4998-93C4-3CD64F3C764D},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0604993103}}

@article{Yang:2005,
	Abstract = {OBJECTIVES: To investigate the mRNA and protein expression of SMN gene in neuron-like cells by inducing MSC to differentiate into neuron-like cells. METHODS: Human MSC (hMSC) were isolated and purified. Human MSC were treated with basic fibroblast growth factor (bFGF) before inducing hMSC to differentiate into neuron-like cells with dimethylsulfoxide (DMSO) and butylated hydroxyanisole (BHA). The expression of NSE, NF, and SMN protein in neuron-like cells were detected by immunohistochemistry. The expression of SMN mRNA were detected with reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Human MSC progressively assumed neuronal morphological characteristics after being induced for 3 hours. Cell bodies had long processe contacting with each other. The neuronal marker of NSE and NF was positive in neuron-like cells. Both hMSC and neuron-like cells expressed the mRNA of SMN gene. Compared with hMSC the latter expressed highly the mRNA of SMN gene and it was significance (P < 0.01). SMN protein was only expressed in neuron-like cells. CONCLUSIONS: Human MSC are able to differentiate into neuron-like cells with expressing the neuronal marker. Neuron-like cells can express highly the mRNA of SMN gene and express SMN protein.},
	Author = {Yang, Xiao-Su S. and Wu, Hai-Xiang X. and Xiao, Bo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0376-2491},
	Journal = {Zhonghua Yi Xue Za Zhi},
	Keywords = {11 Glia},
	Month = {4},
	Nlm_Id = {7511141},
	Notes = {cell fusion, dendrite fusing to microglia or macrophages},
	Number = {16},
	Organization = {Department of Neurology, XiangYa Hospital of Centersouth University. Changsha 410008, China. Email: yanxia\@public.cs.hn.cn.},
	Pages = {1125-8},
	Pubmed = {16029573},
	Title = {[Human mesenchymal stem cells differentiat into neuron-like cells and show SMN protein expression.]},
	Uuid = {4B9391B4-9A09-4018-BF3A-C496BAEA4AF8},
	Volume = {85},
	Year = {2005}}

@article{Yao:2003,
	Abstract = {The fusogenic envelope glycoprotein G of the rhabdovirus vesicular stomatitis virus (VSV) induces membrane fusion at acidic pH. At acidic pH the G protein undergoes a major structural reorganization leading to the fusogenic conformation. However, unlike other viral fusion proteins, the low-pH-induced conformational change of VSV G is completely reversible. As well, the presence of an alpha-helical coiled-coil motif required for fusion by a number of viral and cellular fusion proteins was not predicted in VSV G protein by using a number of algorithms. Results of pH dependence of the thermal stability of G protein as determined by intrinsic Trp fluorescence and circular dichroism (CD) spectroscopy show that the G protein is equally stable at neutral or acidic pH. Destabilization of G structure at neutral pH with either heat or urea did not induce membrane fusion or conformational change(s) leading to membrane fusion. Taken together, these data suggest that the mechanism of VSV G-induced fusion is distinct from the fusion mechanism of fusion proteins that involve a coiled-coil motif.},
	Author = {Yao, Yi and Ghosh, Kakoli and Epand, Raquel F. and Epand, Richard M. and Ghosh, Hara P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0042-6822},
	Journal = {Virology},
	Keywords = {Membrane Glycoproteins;Research Support, Non-U.S. Gov't;Virus Replication;Membrane Fusion;Cell Line;Time Factors;Urea;Heat;Vesicular stomatitis-Indiana virus;15 Retrovirus mechanism;Animals;Hydrogen-Ion Concentration;24 Pubmed search results 2008;Viral Envelope Proteins},
	Medline = {22667914},
	Month = {6},
	Nlm_Id = {0110674},
	Number = {2},
	Organization = {Department of Biochemistry, McMaster University, Hamilton, Ontario, Canada.},
	Pages = {319-32},
	Pii = {S0042682203001466},
	Pubmed = {12781719},
	Title = {Membrane fusion activity of vesicular stomatitis virus glycoprotein G is induced by low pH but not by heat or denaturant},
	Uuid = {2F4C41BA-BD48-4F9F-9FEC-55E6D1BC7FF2},
	Volume = {310},
	Year = {2003},
	url = {papers/Yao_Virology2003.pdf}}

@article{Yasuhara:2006,
	Abstract = {Neural stem cells (NSCs) possess high potencies of self-renewal and neuronal differentiation. We explored here whether transplantation of human NSCs cloned by v-myc gene transfer, HB1.F3 cells, is a feasible therapeutic option for Parkinson's disease. In vivo, green fluorescent protein-labeled HB1.F3 cells (200,000 viable cells in 3 microl of PBS) when stereotaxically transplanted (same-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantly ameliorated parkinsonian behavioral symptoms compared with controls (vehicle, single bolus, or continuous minipump infusion of trophic factor, or killed cell grafts). Such graft-derived functional effects were accompanied by preservation of tyrosine hydroxylase (TH) immunoreactivity along the nigrostriatal pathway. Grafted HB1.F3 cells survived in the lesioned brain with some labeled with neuronal marker mitogen-activated protein 2 and decorated with synaptophysin-positive terminals. Furthermore, endogenous neurogenesis was activated in the subventricular zone of transplanted rats. To further explore the neuroprotective mechanisms underlying HB1.F3 cell transplantation, we performed cell culture studies and found that a modest number of HB1.F3 cells were TH and dopamine and cAMP-regulated phosphoprotein 32 positive, although most cells were nestin positive, suggesting a mixed population of mature and immature cells. Administration of the HB1.F3 supernatant to human derived dopaminergic SH-SY5Y cells and fetal rat ventral mesencephalic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis through Bcl-2 upregulation, which was blocked by anti-stem cell factor antibody alone, the phosphatidylinositol 3-kinase/Akt inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one] alone, or a combination of both. These results suggest that HB1.F3 cell transplantation exerts neuroprotective effects against dopaminergic depletion in vitro and in vivo because of trophic factor secretion and neuronal differentiation.},
	Author = {Yasuhara, Takao and Matsukawa, Noriyuki and Hara, Koichi and Yu, Guolong and Xu, Lin and Maki, Mina and Kim, Seung U. and Borlongan, Cesario V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Brain Tissue Transplantation;research support, non-u.s. gov't;Rats, Sprague-Dawley;Rats;Cell Line;Stem Cells;Corpus Striatum;Parkinson Disease;comparative study;Motor Activity;Animals;Disease Models, Animal;Humans;Stem Cell Transplantation;24 Pubmed search results 2008},
	Month = {11},
	Nlm_Id = {8102140},
	Number = {48},
	Organization = {Department of Neurology, Medical College of Georgia, Augusta, Georgia 30912, USA.},
	Pages = {12497-511},
	Pii = {26/48/12497},
	Pubmed = {17135412},
	Title = {Transplantation of human neural stem cells exerts neuroprotection in a rat model of Parkinson's disease},
	Uuid = {1BF690CB-CB63-4D4F-A942-3A134FBFA55F},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3719-06.2006}}

@article{Yates:2002,
	Abstract = {Patients with mutations of either RAG-1 or RAG-2 genes suffer from severe combined immunodeficiency (SCID) characterized by the lack of T and B lymphocytes. The only curative treatment today consists of hematopoietic stem cell (HSC) transplantation, which is only partially successful in the absence of an HLA genoidentical donor, thus justifying research to find an alternative therapeutic approach. To this end, RAG-2-deficient mice were used to test whether retrovirally mediated ex vivo gene transfer into HSCs could provide long-term correction of the immunologic deficiency. Murine RAG-2-/-Sca-1(+) selected bone marrow cells were transduced with a modified Moloney leukemia virus (MLV)-based MND (myeloproliferative sarcoma virus enhancer, negative control region deleted, dl587rev primer-binding site substituted) retroviral vector containing the RAG-2 cDNA and transplanted into RAG-2-/- sublethally irradiated mice (3Gy). Two months later, T- and B-cell development was achieved in all mice. Diverse repertoire of T cells as well as proliferative capacity in the presence of mitogens, allogeneic cells, and keyhole limpet hemocyanin (KLH) were shown. B-cell function as shown by serum Ig levels and antibody response to a challenge by KLH also developed. Lymphoid subsets and function were shown to be stable over a one-year period without evidence of any detectable toxicity. Noteworthy, a selective advantage for transduced lymphoid cells was evidenced by comparative provirus quantification in lymphoid and myeloid lineages. Altogether, this study demonstrates the efficiency of ex vivo RAG-2 gene transfer in HSCs to correct the immune deficiency of RAG-2-/- mice, constituting a significant step toward clinical application.},
	Author = {Yates, Frank and Malassis-S{\'e}ris, Mich\`{e}le and Stockholm, Daniel and Bouneaud, C{\'e}cile and Larousserie, Fr{\'e}d{\'e}rique and Noguiez-Hellin, Patricia and Danos, Olivier and Kohn, Donald B. and Fischer, Alain and de Villartay, Jean-Pierre P. and Cavazzana-Calvo, Marina},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {T-Lymphocytes;Transduction, Genetic;Animals;DNA-Binding Proteins;Bone Marrow Transplantation;Severe Combined Immunodeficiency;Female;Mice, Inbred C3H;B-Lymphocytes;Mice, Inbred C57BL;Retroviridae;11 Glia;Male;Bone Marrow Cells;Cell Lineage;Gene Therapy;Mice, Knockout;Mice;Virus Integration;Receptors, Antigen, T-Cell;Cell Division;Research Support, Non-U.S. Gov't},
	Medline = {22320963},
	Month = {12},
	Nlm_Id = {7603509},
	Number = {12},
	Organization = {Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale (INSERM) U429, H\^{o}pital Necker-Enfants Malades, Paris, France.},
	Pages = {3942-9},
	Pii = {2002-03-0782},
	Pubmed = {12393742},
	Title = {Gene therapy of RAG-2-/- mice: sustained correction of the immunodeficiency},
	Uuid = {44BDBB6C-0836-4B39-9102-BE8918211341},
	Volume = {100},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1182/blood-2002-03-0782}}

@article{Ye:2007,
	Abstract = {Little is known about how the distinct architectures of dendrites and axons are established. From a genetic screen, we isolated dendritic arbor reduction (dar) mutants with reduced dendritic arbors but normal axons of Drosophila neurons. We identified dar2, dar3, and dar6 genes as the homologs of Sec23, Sar1, and Rab1 of the secretory pathway. In both Drosophila and rodent neurons, defects in Sar1 expression preferentially affected dendritic growth, revealing evolutionarily conserved difference between dendritic and axonal development in the sensitivity to limiting membrane supply from the secretory pathway. Whereas limiting ER-to-Golgi transport resulted in decreased membrane supply from soma to dendrites, membrane supply to axons remained sustained. We also show that dendritic growth is contributed by Golgi outposts, which are found predominantly in dendrites. The distinct dependence between dendritic and axonal growth on the secretory pathway helps to establish different morphology of dendrites and axons.},
	Author = {Ye, Bing and Zhang, Ye and Song, Wei and Younger, Susan H. and Jan, Lily Yeh and Jan, Yuh Nung},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Golgi Apparatus;Exocytosis;Animals;Cells, Cultured;comparative study;Transfection;Neural Pathways;Cell Membrane;Mutation;Hippocampus;Cell Polarity;RNA, Small Interfering;research support, non-u.s. gov't;Axons;Dendrites;Fluorescence Recovery After Photobleaching;Neurons;Drosophila;research support, n.i.h., extramural;24 Pubmed search results 2008;Embryo, Nonmammalian},
	Month = {8},
	Nlm_Id = {0413066},
	Number = {4},
	Organization = {Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, CA 94143, USA.},
	Pages = {717-29},
	Pii = {S0092-8674(07)00836-7},
	Pubmed = {17719548},
	Title = {Growing dendrites and axons differ in their reliance on the secretory pathway},
	Uuid = {73401A63-36CF-4CFD-956F-3E097D7A06ED},
	Volume = {130},
	Year = {2007},
	url = {papers/Ye_Cell2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2007.06.032}}

@article{Yee:2003,
	Abstract = {This paper analyzes the effects of a convulsant and an anticonvulsant manipulation on spontaneous bursts in CA3 pyramidal cells in the in vitro slice preparation under conditions of low (3.3 mM [K(+)](o)) and high (8.5 mM [K(+)](o)) burst probability. When burst probability was low, the anticonvulsant, pentobarbital, produced the anticipated effects: the burst duration decreased and interburst interval increased. However, when burst probability was high, both anticonvulsant and convulsant manipulations decreased the interburst interval and the burst duration. To reconcile these findings, we utilized a model in which CA3 burst duration is limited by activity-dependent depression of CA3 excitatory recurrent collateral synapses and the interburst interval is determined by the time required to recover from this depression. We defined the burst end threshold as the level of synaptic depression at which bursts terminate, and the burst start threshold as the level of synaptic depression at which burst initiation is possible. Synapses were considered to oscillate between these thresholds. When average burst duration and interburst interval data were fit using this model, the paradoxically similar effects of the convulsant and anticonvulsant manipulations could be quantitatively interpreted. The convulsant maneuver decreased both the burst start and end thresholds. The start threshold decreased more than the end threshold, so that the thresholds were closer together. This decreased the time needed to transition from one threshold to the other, i.e., the interburst interval and burst duration. The anticonvulsant manipulation primarily increased the burst end threshold. This also decreased the difference between thresholds, decreasing both interburst interval and burst duration. This model resolves the paradoxical proconvulsant effects of pentobarbital in the CA3 preparation and provides insights into the effects of anticonvulsants on epileptiform discharges in the human EEG.},
	Author = {Yee, Audrey S. and Longacher, J. Mark and Staley, Kevin J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0022-3077},
	Journal = {J Neurophysiol},
	Keywords = {Animals;Rats;Pentobarbital;Acetazolamide;research support, u.s. gov't, p.h.s. ;Epilepsy;Hippocampus;Pyramidal Cells;Rats, Wistar;Organ Culture Techniques;research support, non-u.s. gov't ;Action Potentials;21 Neurophysiology;Picrotoxin;Convulsants;24 Pubmed search results 2008;Models, Neurological;Anticonvulsants},
	Month = {1},
	Nlm_Id = {0375404},
	Number = {1},
	Organization = {Department of Pediatrics, B 182, University of Colorado Health Sciences Center, Denver 80262, USA.},
	Pages = {427-41},
	Pubmed = {12522191},
	Title = {Convulsant and anticonvulsant effects on spontaneous CA3 population bursts},
	Uuid = {A49C6CEA-FBA4-4431-93F7-56B72AB06712},
	Volume = {89},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1152/jn.00594.2002}}

@article{Yeung:1997,
	Abstract = {Tuberous sclerosis (TSC) is an autosomal dominant syndrome that is linked to two genetic loci: TSC1 (9q34) and TSC2 (16p13). Brain manifestations such as cortical tubers and subependymal hamartoma/giant cell astrocytomas are major causes of TSC-related morbidity. In this study, we describe the central nervous system involvement in a unique rodent model of tuberous sclerosis. The Eker rat carries a spontaneous germline mutation of the TSC2 gene and is predisposed to multiple neoplasia. In a series of 45 adult Eker carriers (TSC2 +/-), three types of focal intracranial lesions were found, of which the subependymal and subcortical hamartomas were most prevalent (65\%). There exist remarkable phenotypic similarities between the Eker rat and human subependymal lesions. Our study indicates that the predominant cellular phenotype of the subependymal hamartomas is astroglial and suggests that the neuronal contribution within these lesions is, in part, the result of pre-existing myelinated axons. The hamartomas did not show evidence of loss of the wild-type TSC2 allele; it remains to be determined whether TSC2 inactivation is necessary for their pathogenesis. This genetically-defined rodent model may be useful in elucidating the molecular and developmental basis of the subependymal giant cell astrocytoma in humans.},
	Author = {Yeung, R. S. and Katsetos, C. D. and Klein-Szanto, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0002-9440},
	Journal = {Am J Pathol},
	Keywords = {10 Development;Animals;Astrocytes;Rats;Myelin Basic Proteins;Tubulin;Hamartoma;Tuberous Sclerosis;Rodent Diseases;Neurofilament Proteins;research support, non-u.s. gov't;Brain Diseases;Calcium-Binding Protein, Vitamin D-Dependent;Disease Models, Animal;Rats, Inbred F344;10 genetics malformation;research support, u.s. gov't, p.h.s.;Ependyma;Loss of Heterozygosity;24 Pubmed search results 2008;Immunohistochemistry;Glial Fibrillary Acidic Protein},
	Month = {11},
	Nlm_Id = {0370502},
	Number = {5},
	Organization = {Division of Medical Sciences, Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA. ryeung\@u.washington.edu},
	Pages = {1477-86},
	Pubmed = {9358774},
	Title = {Subependymal astrocytic hamartomas in the Eker rat model of tuberous sclerosis},
	Uuid = {28398DBA-A19A-41E9-AF9C-78592DA9CE3D},
	Volume = {151},
	Year = {1997}}

@article{Yi:2003,
	Abstract = {Macrophage/microglia cells are the principal targets for human immunodeficiency virus type 1 (HIV-1) in the central nervous system (CNS). Prototype HIV-1 isolates from the CNS are macrophage (M)-tropic, non-syncytia-inducing (NSI), and use CCR5 for entry (R5 strains), but whether syncytia-inducing (SI) CXCR4-using X4 strains might play a role in macrophage/microglia infection and neuronal injury is unknown. To explore the range of features among HIV-1 primary isolates from the CNS, the authors analyzed an HIV-1 strain (TYBE) from cerebrospinal fluid of an individual with acquired immunodeficiency syndrome (AIDS) that was unusual because it was SI. Like other CNS isolates, HIV-1/TYBE replicated to high level in primary human macrophages, but, in contrast to CNS prototypes, TYBE used CXCR4 exclusively to infect macrophages. A functional TYBE env clone confirmed the X4 phenotype and displayed a highly charged V3 sequence typical of X4 strains. Supernatant from TYBE-infected primary human macrophages induced apoptosis of neurons. Thus, TYBE represents a novel type of CNS-derived HIV-1 isolate that is CXCR4-restricted yet replicates efficiently in macrophages and induce neuronal injury. These results demonstrate that HIV-1 variants in the CNS may possess a broader range of biological characteristics than generally appreciated, raise the possibility that X4 strains may participate in AIDS neuropathogenesis, and provide a prototype clade B HIV-1 strain that replicates efficiently in primary macrophages through the exclusive use of CXCR4 as a coreceptor.},
	Author = {Yi, Yanjie and Chen, Wei and Frank, Ian and Cutilli, Joann and Singh, Anjali and Starr-Spires, Linda and Sulcove, Jerrold and Kolson, Dennis L. and Collman, Ronald G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {1355-0284},
	Journal = {J Neurovirol},
	Keywords = {Giant Cells;HIV-1;Molecular Sequence Data;Human;AIDS Dementia Complex;Apoptosis;Research Support, U.S. Gov't, P.H.S.;11 Glia;Amino Acid Sequence;Macrophages;Support, U.S. Gov't, P.H.S.;Humans;Receptors, CXCR4;Viral Envelope Proteins;Neurons},
	Medline = {22788971},
	Month = {8},
	Nlm_Id = {9508123},
	Number = {4},
	Organization = {Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.},
	Pages = {432-41},
	Pii = {DENFV4EX0QK78HR5},
	Pubmed = {12907388},
	Title = {An unusual syncytia-inducing human immunodeficiency virus type 1 primary isolate from the central nervous system that is restricted to CXCR4, replicates efficiently in macrophages, and induces neuronal apoptosis},
	Uuid = {917DA5AA-86B9-4800-92AE-A223DC03C9AA},
	Volume = {9},
	Year = {2003}}

@article{Yin:2006,
	Abstract = {The optic nerve, like most mature CNS pathways, does not regenerate after injury. Through unknown mechanisms, however, macrophage activation in the eye stimulates retinal ganglion cells (RGCs) to regenerate long axons beyond the site of optic nerve injury. Here we identify the calcium (Ca(2+))-binding protein oncomodulin as a potent macrophage-derived growth factor for RGCs and other neurons. Oncomodulin binds to rat RGCs with high affinity in a cyclic AMP (cAMP)-dependent manner and stimulates more extensive outgrowth than other known trophic agents. Depletion of oncomodulin from macrophage-conditioned media (MCM) eliminates the axon-promoting activity of MCM. The effects of oncomodulin involve downstream signaling via Ca(2+)/calmodulin kinase and gene transcription. In vivo, oncomodulin released from microspheres promotes regeneration in the mature rat optic nerve. Oncomodulin also stimulates outgrowth from peripheral sensory neurons. Thus, oncomodulin is a new growth factor for neurons of the mature central and peripheral nervous systems.},
	Author = {Yin, Yuqin and Henzl, Michael T. and Lorber, Barbara and Nakazawa, Toru and Thomas, Tommy T. and Jiang, Fan and Langer, Robert and Benowitz, Larry I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {10 Development;11 Glia;10 Structural plasticity;24 Pubmed search results 2008},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Organization = {[1] Department of Neurosurgery and Neurobiology Program, Children's Hospital, 300 Longwood Avenue, Boston, Massachusetts 02115, USA. [2] Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.},
	Pages = {843-52},
	Pii = {nn1701},
	Pubmed = {16699509},
	Title = {Oncomodulin is a macrophage-derived signal for axon regeneration in retinal ganglion cells},
	Uuid = {BD41E2CA-4E98-4F57-8AFD-83A78AA77E90},
	Volume = {9},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1701}}

@article{Ying:2002,
	Abstract = {Recent reports have suggested that mammalian stem cells residing in one tissue may have the capacity to produce differentiated cell types for other tissues and organs 1-9. Here we define a mechanism by which progenitor cells of the central nervous system can give rise to non-neural derivatives. Cells taken from mouse brain were co-cultured with pluripotent embryonic stem cells. Following selection for a transgenic marker carried only by the brain cells, undifferentiated stem cells are recovered in which the brain cell genome has undergone epigenetic reprogramming. However, these cells also carry a transgenic marker and chromosomes derived from the embryonic stem cells. Therefore the altered phenotype does not arise by direct conversion of brain to embryonic stem cell but rather through spontaneous generation of hybrid cells. The tetraploid hybrids exhibit full pluripotent character, including multilineage contribution to chimaeras. We propose that transdetermination consequent to cell fusion 10 could underlie many observations otherwise attributed to an intrinsic plasticity of tissue stem cells 9. 0028-0836 Journal Article},
	Author = {Ying, Q. L. and Nichols, J. and Evans, E. P. and Smith, A. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Nature},
	Keywords = {Drug Resistance/genetics;Animals;Cells, Cultured;Chimera;*Cell Differentiation;Neurons/*cytology;Antigens, Differentiation;Embryo and Fetal Development;EE pdf;Blastocyst/cytology;Female;Mice, Transgenic;Mice, Inbred C57BL;08 Aberrant cell cycle;Male;Embryo/cytology;Stem Cells/*cytology;Cell Line;Support, Non-U.S. Gov't;*Cinnamates;Hygromycin B/*analogs &derivatives/pharmacology;*Cell Fusion;Coculture;Anti-Bacterial Agents/pharmacology;Brain/cytology;Mice;Hybrid Cells/cytology},
	Number = {6880},
	Organization = {Centre for Genome Research, University of Edinburgh, The King's Buildings, West Mains Road, Edinburgh EH9 3JQ, UK.},
	Pages = {545-8},
	Title = {Changing potency by spontaneous fusion},
	Uuid = {96427206-D3B0-11D9-A0E9-000D9346EC2A},
	Volume = {416},
	Year = {2002},
	url = {papers/Ying_Nature2002.pdf}}

@article{Yokoo:2003,
	Abstract = {BACKGROUND: Bone marrow reconstitution using genetically-modified hematopoietic stem cells has been reported to confer resistance to inflammation and prevent renal injury in glomerulonephritis. Although this strategy has potentials for clinical use, taking hematopoietic stem cells from bone marrow is highly stressful for patients. In this regard, umbilical cord blood may be a useful alternative and, therefore, we focused on their suitability as a source of hematopoietic stem cells for transplantation-based therapy for glomerulonephritis. METHODS: CD34+ cells were obtained from human umbilical cord blood, retrovirally transduced with human beta-glucuronidase (HBG) gene, and transplanted into nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice. After confirming the successful chimerism, these mice were treated with lipopolysaccharide (LPS), and local HBG expression in glomeruli was examined using immunohistochemical analysis, HBG bioassay, and Western blot analysis. RESULTS: Clonogenic assay showed that 88.4 +/- 5.9\%burst-forming unit-erythroid (BFU-E), 79.7 +/- 11.4\%in colony-forming unit-macrophage (CFU-M), and 81.1 +/- 14.1\%in colony-forming unit-granulocyte (CFU-G), respectively, possessed the transgene after transfection, suggesting that precommited cells were susceptible to retroviral infection. Flow cytometric analysis revealed that 24.1 +/- 14.5\%of bone marrow cells in these chimera mice expressed human lymphocyte antigen (HLA) 8 weeks after transplantation. Also, clonogenic assay showed that a sustained engraftment of human hematopoietic cells expressed HBG. CD14-positive cells were recruited into the glomeruli upon LPS treatment and they secreted bioactive HBG, suggesting that cord blood-derived CD34+cells may differentiate into monocyte lineage while maintaining the expression of the transgene. CONCLUSION: These data indicate that umbilical cord blood cells can be utilized as a source of hematopoietic stem cells for the transplantation-based therapy of glomerulonephritis.},
	Author = {Yokoo, Takashi and Ohashi, Toya and Utsunomiya, Yasunori and Okamoto, Aikou and Suzuki, Takahide and Shen, Jin Song and Tanaka, Tadao and Kawamura, Tetsuya and Hosoya, Tatsuo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0085-2538},
	Journal = {Kidney Int},
	Keywords = {Glucuronidase;Cell Differentiation;Mice, Inbred NOD;Animals;Monocytes;Humans;Blood Cells;Transfection;Glomerulonephritis;Lipopolysaccharides;Mice, SCID;Antigens, CD34;Retroviridae;Transplantation Chimera;11 Glia;Kidney Glomerulus;Genetic Vectors;Hematopoietic Stem Cell Transplantation;Gene Transfer Techniques;Mice;Fetal Blood;Blood Component Transfusion;Research Support, Non-U.S. Gov't},
	Medline = {22672614},
	Month = {7},
	Nlm_Id = {0323470},
	Number = {1},
	Organization = {Division of Nephrology and Hypertension, Department of Internal Medicine, Institute of DNA Medicine, Jikei University School of Medicine, Tokyo, Japan. tyokoo\@jikei.ac.jp},
	Pages = {102-9},
	Pii = {kid046},
	Pubmed = {12787400},
	Title = {Gene delivery using human cord blood-derived CD34+cells into inflamed glomeruli in NOD/SCID mice},
	Uuid = {A58CB037-8F74-471F-9338-1531EB08B24C},
	Volume = {64},
	Year = {2003}}

@article{Yokota:1993,
	Abstract = {The rate of migration of immature granule cells of the rat olfactory bulb and polarity of cell-organelles in the migrating granule cells were investigated by 3H-thymidine autoradiographic and electron microscopic methods. The time lag in migration between two points was determined by cross-correlation analysis of labeling indices of the two areas. Granule cells were estimated to take 6 days to migrate rostralwardly from the subependymal layer at the anterior wall of the lateral ventricle to the center of the bulb, and an additional 1 to 6 days to migrate radially from the subependymal layer to the granular layer of the bulb. These results showed that the rate of rostralward migration of granule cells was faster than that of their radial migration. Golgi-electron microscopic as well as routine electron microscopic studies on migrating granule cells revealed that centrioles and Golgi apparatus were located at the base of the leading process that possesses a growth cone at its tip. eng Journal Article},
	Author = {Yokota, S. and Kakuta, S. and Ishikawa, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Journal = {Arch Histol Cytol},
	Keywords = {Cell Differentiation;Centrioles/ultrastructure;Rats;Microscopy, Electron;Olfactory Bulb/*cytology/ultrastructure;Thymidine/metabolism;Rats, Wistar;Autoradiography;Animal;*Cell Polarity;I abstr;Golgi Apparatus/ultrastructure;Cell Movement;13 Olfactory bulb anatomy},
	Number = {1},
	Organization = {Department of Anatomy, Toho University School of Medicine, Tokyo, Japan.},
	Pages = {27-36.},
	Title = {Development of granule cells of the rat olfactory bulb: an autoradiographic and electron microscopic study},
	Uuid = {C4860140-8FD2-4FE9-9927-5721D213BB86},
	Volume = {56},
	Year = {1993}}

@article{Yokoyama:2004,
	Abstract = {Microglia are considered the only cell population of mesodermal origin in the brain, although their role is not fully understood. The present study demonstrated that rat primary microglial cells expressed nestin, A2B5, and O4 antigens, which are markers for oligodendrocyte precursor cells. Based on these findings, we investigated whether microglial cells generated neurons or macroglial cells. Purified microglial cells were cultured in the presence of 10\%fetal bovine serum for 3 days, followed by culture in the presence of 70\%serum for 2 days. During the two-step culture, microglial cells became highly proliferative and strongly expressed inhibitor of DNA binding (Id) genes, indicative of dedifferentiation of the cells. The dedifferentiated cells also expressed transcription factors that promote differentiation into neurons or macroglial cells. When the dedifferentiated cells were transferred into serum-free medium on poly-L-lysine-coated substrate, a substantial number of the cells rapidly turned into long process-bearing cells, which expressed microtubule-associated protein 2, synapsin I, neurofilament proteins, glial fibrillary acidic protein, or galactocerebroside. When microglial cells were fluorescently labeled through acetylated low-density lipoprotein (LDL) receptors or by a phagocytosis-dependent mechanism, fluorescence-bearing neurons, astrocytes, or oligodendrocytes were observed. Neurospheres, aggregates of neural stem cells, expressed Musashi 1 and epidermal growth factor receptor, but the microglia-derived cells did not. These results suggest a novel role of microglia as multipotential stem cells to give rise to neurons, astrocytes, or oligodendrocytes.},
	Author = {Yokoyama, Akiko and Yang, Lihua and Itoh, Suzuka and Mori, Kohji and Tanaka, Junya},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Animals;Cell Differentiation;Alpha;Rats;Astrocytes;Not relevant;Rats, Wistar;11 Glia;Microglia;Support, Non-U.S. Gov't;Oligodendroglia;Intermediate Filament Proteins;Neurons;Cells, Cultured},
	Month = {1},
	Nlm_Id = {8806785},
	Notes = {microglia culture experiments immunocytochemistry},
	Number = {1},
	Organization = {Department of Physiology, School of Medicine, Ehime University, Ehime, Japan.},
	Pages = {96-104},
	Pubmed = {14648550},
	Title = {Microglia, a potential source of neurons, astrocytes, and oligodendrocytes},
	Uuid = {5D91C73B-22D2-4ABA-AAA6-6183206CE6DF},
	Volume = {45},
	Year = {2004},
	url = {papers/Yokoyama_Glia2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/glia.10306}}

@article{Yoon:1996,
	Abstract = {Precursor cells found in the subventricular zone (SVZ) of the adult brain can undergo cell division and migrate long distances before differentiating into mature neurons. We have investigated the possibility of introducing genes stably into this population of cells. Replication-defective adenoviruses were injected into the SVZ of the lateral ventricle of adult mice. The adenoviruses carried a cDNA for the LacZ reporter or the human p75 neurotrophin receptor, for which species-specific antibodies are available. Injection of the viruses into the SVZ led to efficient labeling of neuronal precursors. Two months after viral injection, infected cells were detected in the olfactory bulb, a significant distance from the site of injection. Labeled periglomerular and granular neurons with extensive dendritic arborization were found in the olfactory bulb. These results demonstrate that foreign genes can be efficiently introduced into neuronal precursor cells. Furthermore, adenovirus-directed infection can lead to long-term stable gene expression in progenitor cells found in the adult central nervous system.},
	Author = {Yoon, S. O. and Lois, C. and Alvirez, M. and Alvarez-Buylla, A. and Falck-Pedersen, E. and Chao, M. V.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {beta-Galactosidase/biosynthesis;Human;Olfactory Bulb/cytology/physiology;Stereotaxic Techniques;Brain/*physiology;Cytomegalovirus;Neurons/cytology/*physiology;Animal;02 Adult neurogenesis migration;Receptors, Nerve Growth Factor/analysis/*biosynthesis;Genetic Vectors;BB abstr;03 Adult neurogenesis progenitor source;Support, Non-U.S. Gov't;*Gene Transfer Techniques;Cerebral Ventricles/cytology/*physiology;Adenoviridae;Support, U.S. Gov't, P.H.S.;Receptor, Nerve Growth Factor;Mice;Genes, Reporter},
	Number = {21},
	Organization = {Department of Cell Biology, Cornell University Medical College, New York, NY 10021, USA.},
	Pages = {11974-9.},
	Title = {Adenovirus-mediated gene delivery into neuronal precursors of the adult mouse brain},
	Uuid = {48E9994B-CB7D-4813-B9F3-E8DE1FF07C0F},
	Volume = {93},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8876247}}

@article{Yoshihara:1999,
	Abstract = {The wiring patterns among various types of neurons via specific synaptic connections are the basis of functional logic employed by the brain for information processing. This study introduces a powerful method of analyzing the neuronal connectivity patterns by delivering a tracer selectively to specific types of neurons while simultaneously transsynaptically labeling their target neurons. We developed a novel genetic approach introducing cDNA for a plant lectin, wheat germ agglutinin (WGA), as a transgene under the control of specific promoter elements. Using this method, we demonstrate three examples of visualization of specific transsynaptic neural pathways: the mouse cerebellar efferent pathways, the mouse olfactory pathways, and the Drosophila visual pathways. This strategy should greatly facilitate studies on the anatomical and functional organization of the developing and mature nervous system.},
	Author = {Yoshihara, Y. and Mizuno, T. and Nakahira, M. and Kawasaki, M. and Watanabe, Y. and Kagamiyama, H. and Jishage, K. and Ueda, O. and Suzuki, H. and Tabuchi, K. and Sawamoto, K. and Okano, H. and Noda, T. and Mori, K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {Efferent Pathways/physiology;*Diagnostic Imaging;Cells, Cultured;Synapses/*physiology;Wheat Germ Agglutinins/*genetics/metabolism;Animal;*Nervous System Physiology;23 Technique;*Transgenes/genetics;Visual Pathways/physiology;Neural Pathways/physiology;Mice, Transgenic/genetics;Drosophila/genetics;Support, Non-U.S. Gov't;Cerebellum/physiology;Olfactory Pathways/physiology;Mice;Neurons/metabolism;*Genetic Techniques;T},
	Number = {1},
	Organization = {Laboratory for Neurobiology of Synapse, RIKEN Brain Science Institute, Saitama, Japan. yoshihara\@brain.riken.go.jp},
	Pages = {33-41.},
	Title = {A genetic approach to visualization of multisynaptic neural pathways using plant lectin transgene},
	Uuid = {A8647876-282D-4D63-BDAF-51C4F22F57F1},
	Volume = {22},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10027287}}

@article{Yoshizawa:2002,
	Abstract = {STEF (Sif- and Tiam1-like exchange factor), a guanine nucleotide exchange factor, was identified as a candidate molecule in regulation of neural development. The STEF gene product specifically activates Rac1, a member of the Rho-like small G proteins. Here we report the detailed examination of the expression profile of the stef gene in the mouse brain. In situ hybridization revealed that the stef gene was expressed in a stage- and region-specific manner in the mouse brain; it was expressed during certain developmental stages in the cerebral cortex, the olfactory bulb, the rostral migratory pathway (RMP) and the hippocampus. In the cerebral cortex, stef transcripts were detected in migrating cells in the intermediate zone as well as neurons in the cortical plate. While the expression in the cerebral cortex was reduced at adult stages, considerable expression was found to be maintained in other regions (RMP, olfactory bulb, hippocampal formation), which are the tissues where neurons continue to undergo morphological remodeling including cellular migration, neurite extension and synapse formation even in adults. Thus, stef gene expression appears to correspond to neuronal morphological changes.},
	Author = {Yoshizawa, M. and Hoshino, M. and Sone, M. and Nabeshima, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Mech Dev},
	Keywords = {04 Adult neurogenesis factors;C abstr},
	Number = {1},
	Organization = {Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, 606-8501, Kyoto, Japan},
	Pages = {65-8.},
	Title = {Expression of stef, an activator of Rac1, correlates with the stages of neuronal morphological development in the mouse brain},
	Uuid = {D440CEAA-82B0-4C61-B2D3-02CF7389C364},
	Volume = {113},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11900975}}

@article{Young:1996,
	Abstract = {The juvenile subventricular zone (SVZ) normally produces oligodendrocytes. To determine whether juvenile SVZ cells are lineage- restricted or whether they remain multipotential, we labeled SVZ cells and characterized their progeny after 1 week in vitro using cell morphology and antigen expression. Heterogeneous clones comprised of retrovirally labeled neurons and astrocytes or astrocytes and oligodendrocytes were observed, as well as homogeneous clones of neurons, astrocytes or oligodendrocytes. Large type-1 astrocyte clones were most common, and mixed oligodendrocyte/type-1-astrocyte clusters represented 15\%of the total clusters. Twenty five percent of the total clusters contained at least 1 immature neuron. Of 128 clones, 6-10\%contained neurons, astrocytes and oligodendrocytes. From these results we conclude that the juvenile SVZ is a mixture of lineage-restricted, bipotential and multipotential neural progenitors. Using Smart Source Parsing},
	Author = {Young, G. M. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Dev Neurosci},
	Keywords = {beta-Galactosidase/biosynthesis;Oligodendroglia/*cytology/physiology;Cell Differentiation;Stem Cells/cytology/*physiology;Cells, Cultured;Rats;Recombinant Proteins/biosynthesis;Animal;02 Adult neurogenesis migration;Rats, Sprague-Dawley;Aging/*physiology;Retroviridae;Genetic Vectors;BB abstr;03 Adult neurogenesis progenitor source;Brain/*cytology/growth &development;Support, U.S. Gov't, P.H.S.;Neurons/cytology/physiology;Nerve Tissue Proteins/analysis/biosynthesis;Biological Markers/analysis},
	Number = {4},
	Organization = {Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey, USA.},
	Pages = {255-65},
	Title = {Persistence of multipotential progenitors in the juvenile rat subventricular zone},
	Uuid = {920D8324-D2CC-4D5A-A6EC-1F4B75AFF6DE},
	Volume = {18},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8911765}}

@article{Young:2007,
	Abstract = {We determined the embryonic origins of adult forebrain subventricular zone (SVZ) stem cells by Cre-lox fate mapping in transgenic mice. We found that all parts of the telencephalic neuroepithelium, including the medial ganglionic eminence and lateral ganglionic eminence (LGE) and the cerebral cortex, contribute multipotent, self-renewing stem cells to the adult SVZ. Descendants of the embryonic LGE and cortex settle in ventral and dorsal aspects of the dorsolateral SVZ, respectively. Both populations contribute new (5-bromo-2'-deoxyuridine-labeled) tyrosine hydroxylase- and calretinin-positive interneurons to the adult olfactory bulb. However, calbindin-positive interneurons in the olfactory glomeruli were generated exclusively by LGE-derived stem cells. Thus, different SVZ stem cells have different embryonic origins, colonize different parts of the SVZ, and generate different neuronal progeny, suggesting that some aspects of embryonic patterning are preserved in the adult SVZ. This could have important implications for the design of endogenous stem cell-based therapies in the future.},
	Author = {Young, Kaylene M. and Fogarty, Matthew and Kessaris, Nicoletta and Richardson, William D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Embryonic Development;Cell Differentiation;research support, non-u.s. gov't;Neuroepithelial Cells;Stem Cells;Mice, Transgenic;comparative study;Olfactory Bulb;Animals;Cell Movement;Cerebral Ventricles;Mice;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {31},
	Organization = {Wolfson Institute for Biomedical Research and Department of Biology, University College London, London WC1E 6BT, United Kingdom.},
	Pages = {8286-96},
	Pii = {27/31/8286},
	Pubmed = {17670975},
	Title = {Subventricular zone stem cells are heterogeneous with respect to their embryonic origins and neurogenic fates in the adult olfactory bulb},
	Uuid = {0D071FE7-CB3C-489A-A706-1349552EA303},
	Volume = {27},
	Year = {2007},
	url = {papers/Young_JNeurosci2007.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0476-07.2007}}

@article{Young:1997,
	Abstract = {Many investigators studying oligodendrocytes in vitro have sought out cell lines because it has been difficult to obtain sufficient numbers of primary oligodendrocytes for study. This paper describes three methodological improvements that facilitate culturing oligodendrocytes. We show that by detaching progenitor cells using papain instead of trypsin the total yield of oligodendrocyte progenitors can be doubled. We also show that papain can be used to subculture differentiated oligodendrocytes. Finally we report that primary O-2A progenitors can be cryo-preserved, reducing the demand upon laboratory personnel to produce and propagate them. 98149537 0165-0270 Journal Article},
	Author = {Young, G. M. and Levison, S. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {J Neurosci Methods},
	Keywords = {Cell Separation/methods;Cell Differentiation;Cell Culture/*methods;G abstr;Culture Media, Conditioned;Comparative Study;Rats;Oligodendroglia/*cytology/metabolism;Cell Count;11 Glia;Animal;Cells, Cultured;Papain;Trypsin;Stem Cells/*cytology/metabolism;Cryopreservation/methods},
	Number = {2},
	Organization = {Department of Neuroscience and Anatomy, College of Medicine, Pennsylvania State University, Hershey 17033, USA.},
	Pages = {163-8},
	Pubmed = {9489893},
	Title = {An improved method for propagating oligodendrocyte progenitors in vitro},
	Uuid = {F92848DA-DF01-4A30-9EC6-39E99BB734BC},
	Volume = {77},
	Year = {1997},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9489893}}

@article{Young:1999,
	Abstract = {The mammalian brain has a high degree of plasticity, with dentate granule cell neurogenesis and glial proliferation stimulated by an enriched environment combining both complex inanimate and social stimulation. Moreover, rodents exposed to an enriched environment both before and after a cerebral insult show improved cognitive performance. One of the most robust associations of environmental enrichment is improved learning and memory in the Morris water maze, a spatial task that mainly involves the hippocampus. Furthermore, clinical evidence showing an association between higher educational attainment and reduced risk of Alzheimer and Parkinson-related dementia indicates that a stimulating environment has positive effects on cerebral health that may provide some resilience to cerebral insults. Here we show that in addition to its effects on neurogenesis, an enriched environment reduces spontaneous apoptotic cell death in the rat hippocampus by 45\%. Moreover, these environmental conditions protect against kainate- induced seizures and excitotoxic injury. The enriched environment induces expression of glial-derived neurotrophic factor and brain- derived neurotrophic factor and increases phosphorylation of the transcription factor cyclic-AMP response element binding protein, indicating that the influence of the environment on spontaneous apoptosis and cerebral resistance to insults may be mediated through transcription factor activation and induction of growth factor expression.},
	Author = {Young, D. and Lawlor, P. A. and Leone, P. and Dragunow, M. and During, M. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Nat Med},
	Keywords = {Brain-Derived Neurotrophic Factor/biosynthesis/genetics;Rats;Phosphorylation;07 Excitotoxicity Apoptosis;RNA, Messenger/isolation &purification;Animal;Rats, Wistar;*Environment;DNA-Binding Protein, Cyclic AMP-Responsive/metabolism;Male;Kainic Acid/*adverse effects;In Situ Hybridization;*Apoptosis;Support, Non-U.S. Gov't;Seizures/chemically induced/*prevention &control;Nerve Tissue Proteins/biosynthesis/genetics;Dentate Gyrus/growth &development/pathology;Hippocampus/growth &development/*pathology;E-7},
	Number = {4},
	Organization = {Department of Molecular Medicine, University of Auckland School of Medicine, New Zealand.},
	Pages = {448-53.},
	Title = {Environmental enrichment inhibits spontaneous apoptosis, prevents seizures and is neuroprotective},
	Uuid = {62EE34B6-24F1-4420-887A-4F87E8B825DD},
	Volume = {5},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10202938}}

@article{Young:2008,
	Abstract = {To facilitate a functional analysis of neuronal connectivity in a mammalian nervous system that is tightly packed with billions of cells, we developed a new technique that uses inducible genetic manipulations in fluorescently labeled single neurons in mice. Our technique, single-neuron labeling with inducible Cre-mediated knockout (SLICK), is achieved by coexpressing a drug-inducible form of Cre recombinase and a fluorescent protein in a small subsets of neurons, thus combining the powerful Cre recombinase system for conditional genetic manipulation with fluorescent labeling of single neurons for imaging. Here, we demonstrate efficient inducible genetic manipulation in several types of neurons using SLICK. Furthermore, we applied SLICK to eliminate synaptic transmission in a small subset of neuromuscular junctions. Our results provide evidence for the long-term stability of inactive neuromuscular synapses in adult animals and demonstrate a Cre-loxP compatible system for dissecting gene functions in single identifiable neurons.},
	Author = {Young, Paul and Qiu, Li and Wang, Dongqing and Zhao, Shengli and Gross, James and Feng, Guoping},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:42:21 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {Estrogen Antagonists;Animals;Ganglia, Spinal;Integrases;Mice, Transgenic;Mice, Inbred C57BL;Green Fluorescent Proteins;research support, non-u.s. gov't;Mice, Knockout;Potassium Channels;Neurons;Tamoxifen;research support, n.i.h., extramural;Mice;Genes, Reporter;Central Nervous System;Gene Expression;24 Pubmed search results 2008;Luminescent Proteins;Nerve Tissue Proteins},
	Month = {6},
	Nlm_Id = {9809671},
	Number = {6},
	Organization = {Department of Neurobiology, Duke University Medical Center, Research Drive, Durham, North Carolina 27710, USA. p.young\@ucc.ie},
	Pages = {721-8},
	Pii = {nn.2118},
	Pubmed = {18454144},
	Title = {Single-neuron labeling with inducible Cre-mediated knockout in transgenic mice},
	Uuid = {6A2E5C55-9787-4E46-983F-753C397B53B6},
	Volume = {11},
	Year = {2008},
	url = {papers/Young_NatNeurosci2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn.2118}}

@article{Youngentob:2001,
	Abstract = {The present study assessed the functional consequences of viral infection with a neurotropic coronavirus, designated MHV OBLV, that specifically targets central olfactory structures. Using standard operant techniques and a 'go, no-go'successive discrimination paradigm, six BALB/c mice were trained to discriminate between the presentation of an air or odor stimulus (three mice for each of the odorants propanol and propyl acetate). Two additional BALB/c mice were trained to discriminate between the presentation of air and the presentation of either vanillin or propionic acid. Following criterion performance, each mouse received an additional 2000 trials of overtraining. At completion of overtraining one mouse from the propanol and propyl acetate groups were allocated as untreated. The remaining six mice were inoculated with 300 microl of the OBLV stock per nostril for a total of 1.5 x 10(6) p.f.u. in 600 microl. Following a 1 month rest, untreated and inoculated animals were again tested on their respective air versus odor discrimination task. Untreated animals immediately performed at criterion levels. In contrast, inoculated animals varied in their capacity to discriminate between air and odorant. Five of the six inoculated mice showed massive disruption of the olfactory bulb, including death of mitral cells; the other was more modestly affected. In addition, the density of innervation of the olfactory mucosa by substance P-containing trigeminal fibers is also affected by inoculation. Those mice that remained anosmic to the training odorants had the most severe reduction in mitral cell number and substance P fiber density among the inoculated animals. 0379-864x Journal Article},
	Author = {Youngentob, S. L. and Schwob, J. E. and Saha, S. and Manglapus, G. and Jubelt, B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Chem Senses},
	Keywords = {Murine hepatitis virus/*metabolism;Substance P/biosynthesis;Benzaldehydes/analysis;Mice, Inbred BALB C;Air;Propionic Acids/analysis;T pdf;Time Factors;Support, U.S. Gov't, P.H.S.;*Administration, Intranasal;*Smell;Animals;Mice;Olfactory Bulb/metabolism/pathology/*virology;23 Technique;Male},
	Number = {8},
	Organization = {Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, NY 13210, USA. youngens\@mail.upstate.edu},
	Pages = {953-63},
	Title = {Functional consequences following infection of the olfactory system by intranasal infusion of the olfactory bulb line variant (OBLV) of mouse hepatitis strain JHM},
	Uuid = {B818E1C1-1A62-4DAC-BB49-6C6111126653},
	Volume = {26},
	Year = {2001},
	url = {papers/Youngentob_ChemSenses2001}}

@article{Yozu:2005,
	Abstract = {The migratory paths of interneurons derived from the ganglionic eminence (GE), and particularly its caudal portion (CGE), remain essentially unknown. To clarify the three-dimensional migration profile of interneurons derived from each part of the GE, we developed a technique involving focal electroporation into a small, defined portion of the telencephalic hemisphere. While the medial GE cells migrated laterally and spread widely throughout the cortex, the majority of the CGE cells migrated caudally toward the caudal-most end of the telencephalon. Time-lapse imaging and an in vivo immunohistochemical study confirmed the existence of a migratory stream depicted by a population of CGE cells directed caudally that eventually reached the hippocampus. Transplantation experiments suggested that the caudal direction of migration of the CGE cells was intrinsically determined as early as embryonic day 13.5. The caudal migratory stream is a novel migratory path for a population of CGE-derived interneurons passing from the subpallium to the hippocampus.},
	Author = {Yozu, Masato and Tabata, Hidenori and Nakajima, Kazunori},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {31},
	Organization = {Department of Anatomy, Keio University School of Medicine, Tokyo 160-8582, Japan.},
	Pages = {7268-77},
	Pii = {25/31/7268},
	Pubmed = {16079409},
	Title = {The caudal migratory stream: a novel migratory stream of interneurons derived from the caudal ganglionic eminence in the developing mouse forebrain},
	Uuid = {41C491CE-4F26-400D-9A8D-91D9E309C440},
	Volume = {25},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2072-05.2005}}

@article{Yu:1976,
	Abstract = {The effect of a thymidine analog, 5-bromodeoxyuridine (BrdU), on the postnatal development of the cerebellum was studied. Rats were injected with 15 mg per 100 gram body weight of BrdU twice a day for 3 consecutive days from the second day after birth, and were killed at 5, 7, 15, 22 and 35 days of age. One hour prior to killing, the rats were given tritiated thymidine. The cerebellar DNA, RNA, protein and cerebroside, and the incorporation of thymidine were measured. BrdU administration caused a markedly retarded growth of the body and the cerebellum. At 35 days of age, the weights of the body and the cerebellum were 42 and 69\%of the controls. Quantitative measurements of cerebellar nucleic acids and isotope uptake correlated well with previous morphological observation, and indicated that the analog caused a transient inhibition of cell formation and possibly destruction of stem cell population of the external granular layer. This inhibitory effect was compensated later by a more rapid DNA deposition and a prolongation of the period of cell proliferation. However, the restitution was incomplete and resulted in a permanent deficit in the final cell number, as reflected by the reduction in the size of the cerebellum of the BrdU-treated rats. 0006-8993 Journal Article},
	Author = {Yu, W. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Brain Res},
	Keywords = {A, T abstr;01 Adult neurogenesis general;Neurons/drug effects;DNA/biosynthesis;Rats;Female;Organ Weight/drug effects;Bromodeoxyuridine/*pharmacology;Animals, Newborn;Support, U.S. Gov't, P.H.S.;Animals;Body Weight/drug effects;Age Factors;Cerebellum/cytology/drug effects/*growth &development;Male},
	Number = {2},
	Pages = {281-91},
	Pubmed = {1000291},
	Title = {The effect of 5-bromodeoxyuridine on the postnatal development of the rat cerebellum: a biochemical study},
	Uuid = {09EE7737-1845-4B49-929A-FD93608980CA},
	Volume = {118},
	Year = {1976},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1000291}}

@article{Yu:2006,
	Abstract = {The mammalian central nervous system is organized by a variety of cells, such as neurons and glial cells, that are generated from a common progenitor, the neural stem cell (NSC). NSCs are defined as undifferentiated neural cells that are characterized by their high proliferative potential while retaining the capacity for self-renewal and multipotency. NSCs and their progeny may be distinguished by the expression of glycoconjugates (e.g., glycoproteins, glycolipids, and proteoglycans). The carbohydrate antigens carried by glycoconjugates are mainly localized on the plasma membrane surface of the cells and they serve as excellent biomarkers for various stages of cellular differentiation. Thus, they have been utilized as ligands for sorting NSCs or their progeny by cell cytometry. Methods have been established for utilizing polysialic acid-neural cell adhesion molecule (PSA-NCAM), stage-specific embryonic antigen-1 (SSEA-1), and gangliosides for cell sorting. Furthermore, glycoconjugates have also been suggested to have a wide range of receptor and signaling functions in NSCs. For example, basic fibroblast growth factor, an important mitogen of NSCs, requires heparan sulfate proteoglycans and glycosylated cystatin C for activity. Notch signaling, which regulates a wide variety of developmental processes in various cells including NSCs, is modulated by the O-fucose glycan modification. In peripheral nervous system (PNS), the human natural killer-1 (HNK-1) antigen regulates the migration of neural crest cells, cell populations containing the stem cells. Thus, glycoconjugates serve not only as marker molecules, but also as functional molecules as well. In the present review, we discuss the expression pattern and possible functions of glycoconjugates in NSCs.},
	Author = {Yu, Robert K. and Yanagisawa, Makoto},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {1871-5273},
	Journal = {CNS Neurol Disord Drug Targets},
	Keywords = {24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {101269155},
	Number = {4},
	Organization = {Program in Developmental Neurobiology, Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, 30912, USA. ryu\@mcg.edu},
	Pages = {415-23},
	Pubmed = {16918393},
	Title = {Glycobiology of neural stem cells},
	Uuid = {13AED705-47C7-4650-885E-CBD32F5C0F4E},
	Volume = {5},
	Year = {2006}}

@article{Yu:2002,
	Abstract = {Duplexes of 21-nt RNAs, known as short-interfering RNAs (siRNAs), efficiently inhibit gene expression by RNA interference (RNAi) when introduced into mammalian cells. We show that siRNAs can be synthesized by in vitro transcription with T7 RNA polymerase, providing an economical alternative to chemical synthesis of siRNAs. By using this method, we show that short hairpin siRNAs can function like siRNA duplexes to inhibit gene expression in a sequence-specific manner. Further, we find that hairpin siRNAs or siRNAs expressed from an RNA polymerase III vector based on the mouse U6 RNA promoter can effectively inhibit gene expression in mammalian cells. U6-driven hairpin siRNAs dramatically reduced the expression of a neuron-specific beta-tubulin protein during the neuronal differentiation of mouse P19 cells, demonstrating that this approach should be useful for studies of differentiation and neurogenesis. We also observe that mismatches within hairpin siRNAs can increase the strand selectivity of a hairpin siRNA, which may reduce self-targeting of vectors expressing siRNAs. Use of hairpin siRNA expression vectors for RNAi should provide a rapid and versatile method for assessing gene function in mammalian cells, and may have applications in gene therapy.},
	Author = {Yu, Jenn-Yah Y. and DeRuiter, Stacy L. and Turner, David L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Research Support, Non-U.S. Gov't;Animals;RNA Polymerase III;RNA;Base Sequence;Transfection;23 Technique;RNA, Small Interfering;Genetic Vectors;Cell Line;Research Support, U.S. Gov't, P.H.S.;Plasmids;Neurons;Tubulin Modulators;23 RNAi;Promoter Regions (Genetics);RNA, Untranslated;24 Pubmed search results 2008;Genes, Reporter;Mice;Immunohistochemistry;Molecular Sequence Data;Transcription, Genetic},
	Medline = {21980630},
	Month = {4},
	Nlm_Id = {7505876},
	Number = {9},
	Organization = {Mental Health Research Institute, Program in Neuroscience, and Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109-0669, USA.},
	Pages = {6047-52},
	Pii = {092143499},
	Pubmed = {11972060},
	Title = {RNA interference by expression of short-interfering RNAs and hairpin RNAs in mammalian cells},
	Uuid = {876A9993-4240-4827-A85B-49EA455F709D},
	Volume = {99},
	Year = {2002},
	url = {papers/Yu_ProcNatlAcadSciUSA2002.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.092143499}}

@article{Yuan:2004,
	Abstract = {Self-renewal of stem cells is critical for tissue repair and maintenance of organ integrity in most mammalian systems. The relative asymmetry between self-renewal and differentiation in balance with apoptosis determines the size and durability of a stem-cell pool. Regulation of the cell cycle is one of the fundamental mechanisms underlying determination of cell fate. Absence of p21(Cip1/Waf1), a late G1-phase cyclin-dependent kinase inhibitor (CKI), has previously been shown to enable cell-cycle entry of haematopoietic stem cells, but leads to premature exhaustion of the stem cells under conditions of stress. We show here that deletion of an early G1-phase CKI, p18(INK4C), results in strikingly improved long-term engraftment, largely by increasing self-renewing divisions of the primitive cells in murine transplant models. Therefore, different CKIs have highly distinct effects on the kinetics of stem cells, possibly because of their active position in the cell cycle, and p18(INK4C) appears to be a strong inhibitor limiting the potential of stem-cell self-renewal in vivo. 1465-7392 Journal Article},
	Author = {Yuan, Y. and Shen, H. and Franklin, D. S. and Scadden, D. T. and Cheng, T.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Nat Cell Biol},
	Keywords = {EE pdf;08 Aberrant cell cycle},
	Number = {5},
	Organization = {University of Pittsburgh Cancer Institute and Department of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh PA 15213, USA.},
	Pages = {436-42},
	Title = {In vivo self-renewing divisions of haematopoietic stem cells are increased in the absence of the early G1-phase inhibitor, p18INK4C},
	Uuid = {C5089314-5E92-4AC1-B8E3-1127D437BF3E},
	Volume = {6},
	Year = {2004},
	url = {papers/Yuan_NatCellBiol2004.pdf}}

@article{Yuan:2003,
	Abstract = {Neurons may die as a normal physiological process during development or as a pathological process in diseases. The best-understood mechanism of neuronal cell death is apoptosis, which is regulated by an evolutionarily conserved cellular pathway that consists of the caspase family, the Bcl-2 family, and the adaptor protein Apaf-1. Apoptosis, however, may not be the only cellular mechanism that regulates neuronal cell death. Neuronal cell death may exhibit morphological features of autophagy or necrosis, which differ from that of the canonical apoptosis. This review evaluates the evidence supporting the existence of alternative mechanisms of neuronal cell death and proposes the possible existence of an evolutionarily conserved pathway of necrosis. 0896-6273 Journal Article Review Review, Tutorial},
	Author = {Yuan, J. and Lipinski, M. and Degterev, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:01 -0400},
	Journal = {Neuron},
	Keywords = {EE pdf;Neurons/*physiology;Human;08 Aberrant cell cycle;Cell Death/physiology;Caspases/physiology;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Animals;Apoptosis/*physiology},
	Number = {2},
	Organization = {Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA. jyuan\@hms.harvard.edu},
	Pages = {401-13},
	Pubmed = {14556717},
	Title = {Diversity in the mechanisms of neuronal cell death},
	Uuid = {28B79997-E8A6-41A9-B045-A39E5E42330F},
	Volume = {40},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14556717}}

@article{Zachary:1997,
	Abstract = {Motor neuron degeneration caused by ts1 MoMuLV occurs by an indirect mechanism and hypothetically appears associated with a two-cell or three-cell pathogenesis hypothesis. The first step in this hypothesis is associated with a small subset of resident microglial cells that serve as the principal target cells for ts1 MoMuLV infection. The second step is likely linked to trophic events, probably mediated by cytokines, that lead to hypertrophy and activation of a substantial number of additional microglial cells (autocrine effect) and adjacent astrocytes (paracrine effect). The third step in this hypothesis appears related to indirect neuronal degeneration mediated by cytotoxins produced by activated microglial cells and astrocytes. In this last step, motor neurons located within these foci of activated microglial cells and astrocytes are 'innocent bystander cells' and degenerate and die due to paracrine effects. The mechanism of motor neuron degeneration is poorly understood but is likely linked to a sequential cascade of trophic factors and cytokines resulting in a final common pathway for motor neuron death involving production of oxidative radicals, excitatory aminoacid neurotransmitter-like substances, prostaglandins, or nitric oxide.},
	Author = {Zachary, J. F. and Baszler, T. V. and French, R. A. and Kelley, K. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {1359-4184},
	Journal = {Mol Psychiatry},
	Keywords = {Nerve Degeneration;Animals;Cells, Cultured;review, tutorial;Tumor Virus Infections;review;Microglia;Not relevant;11 Glia;Spinal Cord;Retroviridae Infections;Animals, Newborn;Moloney murine leukemia virus;Neurons;Motor Neuron Disease;Mice;Cytotoxins;Brain Stem},
	Medline = {97260132},
	Month = {3},
	Nlm_Id = {9607835},
	Number = {2},
	Organization = {College of Veterinary Medicine, University of Illinois, Urbana, USA. zacharyj\@ux1.cso.uiuc.edu},
	Pages = {104-6},
	Pubmed = {9106227},
	Title = {Mouse Moloney leukemia virus infects microglia but not neurons even though it induces motor neuron disease},
	Uuid = {131409D4-B893-43F7-AE16-771C6495460B},
	Volume = {2},
	Year = {1997}}

@article{Zarbalis:2007,
	Abstract = {We report the identification of a hypomorphic mouse allele for Foxc1 (Foxc1(hith)) that survives into adulthood revealing previously unknown roles for Foxc1 in development of the skull and cerebral cortex. This line of mice was recovered in a forward genetic screen using ENU mutagenesis to identify mutants with cortical defects. In the hith allele a missense mutation substitutes a Leu for a conserved Phe at amino acid 107, leading to destabilization of the protein without substantially altering transcriptional activity. Embryonic and postnatal histological analyses indicate that diminished Foxc1 protein expression in all three layers of meningeal cells in Foxc1(hith/hith) mice contributes to the cortical and skull defects in mutant mice and that the prominent phenotypes appear as the meninges differentiate into pia, arachnoid, and dura. Careful analysis of the cortical phenotypes shows that Foxc1(hith/hith) mice display detachment of radial glial endfeet, marginal zone heterotopias, and cortical dyslamination. These abnormalities have some features resembling defects in type 2 (cobblestone) lissencephaly or congenital muscular dystrophies but appear later in corticogenesis because of the delay in breakdown of the basement membrane. Our data reveal that the meninges regulate the development of the skull and cerebral cortex by controlling aspects of the formation of these neighboring structures. Furthermore, we provide evidence that defects in meningeal differentiation can lead to severe cortical dysplasia.},
	Author = {Zarbalis, Konstantinos and Siegenthaler, Julie A. and Choe, Youngshik and May, Scott R. and Peterson, Andrew S. and Pleasure, Samuel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Aging;Cell Differentiation;research support, non-u.s. gov't;Ethylnitrosourea;Forkhead Transcription Factors;Point Mutation;Meninges;research support, n.i.h., extramural;Animals;Mice;Cerebral Cortex;Neurons;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {35},
	Organization = {Department of Neurology, University of California, 1550 Fourth Street, San Francisco, CA 94158, USA.},
	Pages = {14002-7},
	Pii = {0702618104},
	Pubmed = {17715063},
	Title = {Cortical dysplasia and skull defects in mice with a Foxc1 allele reveal the role of meningeal differentiation in regulating cortical development},
	Uuid = {401FE36B-006F-441F-A88C-6DCE644D91EA},
	Volume = {104},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0702618104}}

@article{Zeev-Brann:1998,
	Abstract = {The poor ability of injured central nervous system (CNS) axons to regenerate has been correlated, at least partially, with a limited and suppressed postinjury inflammatory response. A key cell type in the inflammatory process is the macrophage, which can respond in various ways, depending on the conditions of stimulation. The aim of this study is to compare the activities of macrophages or microglia when encountering CNS and peripheral nervous systems (PNS), on the assumption that nerve-related differences in the inflammatory response may have implications for tissue repair and thus for nerve regeneration. Phagocytic activity of macrophages or of isolated brain-derived microglia was enhanced upon their exposure to sciatic (PNS) nerve segments, but inhibited by exposure to optic (CNS) nerve segments. Similarly, nitric oxide production by macrophages or microglia was induced by sciatic nerve segments but not by optic nerve segments. The previously demonstrated presence of a resident inhibitory activity in CNS nerve, could account, at least in part, for the inhibited phagocytic activity of blood-borne macrophages in CNS nerve as well as of microglia resident in the brain. It seems that the CNS microglia are reversibly immunosuppressed by the CNS environment, at least with respect to the activities examined here. It also appears from this study that the weak induction of early healing-related activities of macrophages/microglia in the environment of CNS might explain the subsequent failure of this environment to acquire growth-supportive properties in temporal and spatial synchrony with the needs of regrowing axons.},
	Author = {Zeev-Brann, A. B. and Lazarov-Spiegler, O. and Brenner, T. and Schwartz, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Phagocytosis;Animals;Cells, Cultured;Macrophages;Rats;Transforming Growth Factor beta;Comparative Study;Microglia;Optic Nerve;Sciatic Nerve;Macrophage Activation;Culture Media, Conditioned;Not relevant;Rats, Wistar;11 Glia;Nerve Regeneration;Male;Coculture;Organ Specificity;Central Nervous System;Optic Nerve Injuries;Nitric Oxide;Organ Culture;Inflammation;Peripheral Nerves},
	Medline = {98295560},
	Month = {7},
	Nlm_Id = {8806785},
	Number = {3},
	Organization = {Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel.},
	Pages = {181-90},
	Pii = {10.1002/(SICI)1098-1136(199807)23:3<181::AID-GLIA1>3.0.CO;2-8},
	Pubmed = {9633803},
	Title = {Differential effects of central and peripheral nerves on macrophages and microglia},
	Uuid = {5CDDE5D7-1CD5-43E3-879A-991ACF13AF76},
	Volume = {23},
	Year = {1998}}

@article{Zeringue:2004,
	Abstract = {The techniques evolving from the rapidly developing field of small RNAs promise accessible approaches to dissecting cellular and molecular mechanisms of higher brain function. Here, a current overview of the technology is presented, along with an outline of how these approaches might help neuroscientists to more rapidly uncover the cellular and molecular bases of behavior.},
	Author = {Zeringue, Henry C. and Constantine-Paton, Martha},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0959-4388},
	Journal = {Curr Opin Neurobiol},
	Keywords = {Neurons;RNA, Messenger;RNA, Small Interfering;Models, Animal;24 Pubmed search results 2008;21 Neurophysiology;Nerve Tissue Proteins;RNA Interference;Gene Targeting;Animals;Brain;Humans;review;Genetic Vectors},
	Month = {10},
	Nlm_Id = {9111376},
	Number = {5},
	Organization = {Department of Biology, McGovern Institute for Brain Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.},
	Pages = {654-9},
	Pii = {S0959-4388(04)00123-0},
	Pubmed = {15464901},
	Title = {Post-transcriptional gene silencing in neurons},
	Uuid = {82E249AD-F6E6-4B7C-8210-A763A7FD8534},
	Volume = {14},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2004.08.009}}

@article{Zerlin:2004,
	Abstract = {The subventricular zone (SVZ) of the developing mammalian forebrain gives rise to astrocytes and oligodendrocytes in the neocortex and white matter, and neurons in the olfactory bulb in perinatal life. We have examined the developmental fates and spatial distributions of the descendants of single SVZ cells by infecting them in vivo at postnatal day 0-1 (P0-1) with a retroviral "library". In most cases, individual SVZ cells gave rise to either oligodendrocytes or astrocytes, but some generated both types of glia. Members of glial clones can disperse widely through the gray and white matter. Progenitors continued to divide after stopping migration, generating clusters of related cells. However, the progeny of a single SVZ cell does not differentiate synchronously: individual clones contained both mature and less mature glia after short or long intervals. For example, progenitors that settled in the white matter generated three types of clonal oligodendrocyte clusters: those composed of only myelinating oligodendrocytes, of both myelinating oligodendrocytes and non-myelinating oligodendrocytes, or of only non-myelinating cells of the oligodendrocyte lineage. Thus, some progenitors do not fully differentiate, but remain immature and may continue to cycle well into adult life.},
	Author = {Zerlin, Marielba and Milosevic, Ana and Goldman, James E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {Staining and Labeling;Cell Differentiation;Neuroglia;Rats, Sprague-Dawley;03 Adult neurogenesis progenitor source;Rats;Retroviridae;Stem Cells;11 Glia;Support, U.S. Gov't, P.H.S.;Animals, Newborn;Prosencephalon;Animals;Cell Movement;Cell Lineage},
	Month = {6},
	Nlm_Id = {0372762},
	Number = {1},
	Organization = {Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.},
	Pages = {200-13},
	Pii = {S0012160604001575},
	Pubmed = {15136150},
	Title = {Glial progenitors of the neonatal subventricular zone differentiate asynchronously, leading to spatial dispersion of glial clones and to the persistence of immature glia in the adult mammalian CNS},
	Uuid = {7CB6A8D9-71EE-49C1-BF35-ED4B7653A6D5},
	Volume = {270},
	Year = {2004},
	url = {papers/Zerlin_DevBiol2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ydbio.2004.02.024}}

@article{Zerlin:1995,
	Abstract = {Recent studies using retroviral labeling of subventricular zone (SVZ) progenitors in vivo in neonatal rats have directly demonstrated the generation of both astrocytes and oligodendrocytes from these progenitors. In the present study, we used a recombinant retroviral vector encoding beta-galactosidase, and analyzed brains within the first week after retroviral injection to trace the early routes that SVZ cells take as they migrate into white matter and cortex and characterized the early morphological and antigenic changes that accompanied their differentiation. SVZ cells follow specifically definable migratory routes as they colonize the cortex and subcortical white matter. Glial progenitors do not populate the cortex in a systematic, laminar fashion, as do neuroblasts. The abundance of labeled progenitors in radial arrangements and the close apposition of many immature cells to vimentin+ radial glial processes, suggest that glial progenitors migrate along radial glia. Labeled SVZ cells, which displayed a simple, unipolar or bipolar morphology, lacked detectable vimentin and nestin intermediate filaments. Similarly, beta-galactosidase-positive cells in white matter lacked these filaments. In contrast, labeled, multipolar cells in the cortex, and a few of the immature-appearing cortical cells expressed nestin and vimentin. At these early time points, GFAP was not detected in beta-galactosidase-labeled cells. Multipolar cells in cortex frequently displayed processes extending toward and contacting blood vessels. These observations suggest that the expression of nestin and vimentin occurs after progenitors emigrate from the SVZ and that filament expression and contact with blood vessels represent an early stage of astrocyte differentiation. eng Journal Article},
	Author = {Zerlin, M. and Levison, S. W. and Goldman, J. E.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Journal = {J Neurosci},
	Keywords = {Neurons/*physiology;02 Adult neurogenesis migration;beta-Galactosidase/metabolism;Prosencephalon/cytology/*metabolism;Cerebral Cortex/cytology;Rats;Cell Aging;Cerebral Ventricles/cytology/*metabolism;Intermediate Filament Proteins/*metabolism;Animal;Microglia/physiology;B abstr;Support, U.S. Gov't, P.H.S.;Animals, Newborn;Cell Movement;Morphogenesis},
	Number = {11},
	Organization = {Department of Pathology, Columbia University College of P&S, New York, New York 10032, USA.},
	Pages = {7238-49.},
	Title = {Early patterns of migration, morphogenesis, and intermediate filament expression of subventricular zone cells in the postnatal rat forebrain},
	Uuid = {9B054116-E557-444D-86CF-F2D9BDBEE9A2},
	Volume = {15},
	Year = {1995}}

@article{Zhai:2003,
	Abstract = {Local axon degeneration is a common pathological feature of many neurodegenerative diseases and peripheral neuropathies. While it is believed to operate with an apoptosis-independent molecular program, the underlying molecular mechanisms are largely unknown. In this study, we used the degeneration of transected axons, termed "Wallerian degeneration," as a model to examine the possible involvement of the ubiquitin proteasome system (UPS). Inhibiting UPS activity by both pharmacological and genetic means profoundly delays axon degeneration both in vitro and in vivo. In addition, we found that the fragmentation of microtubules is the earliest detectable change in axons undergoing Wallerian degeneration, which among other degenerative events, can be delayed by proteasome inhibitors. Interestingly, similar to transected axons, degeneration of axons from nerve growth factor (NGF)-deprived sympathetic neurons could also be suppressed by proteasome inhibitors. Our findings suggest a possibility that inhibiting UPS activity may serve to retard axon degeneration in pathological conditions.},
	Author = {Zhai, Qiwei and Wang, Jing and Kim, Anna and Liu, Qing and Watts, Ryan and Hoopfer, Eric and Mitchison, Timothy and Luo, Liqun and He, Zhigang},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Cysteine Proteinase Inhibitors;Wallerian Degeneration;Peptide Fragments;Disease Models, Animal;24 Pubmed search results 2008;Immunohistochemistry;Leupeptins;Chelating Agents;Animals;Cells, Cultured;Research Support, U.S. Gov't, P.H.S.;Egtazic Acid;Cysteine Endopeptidases;Multienzyme Complexes;Calpain;Drug Interactions;Tubulin;Axons;Ubiquitin;Microtubules;Optic Nerve Injuries;Nerve Growth Factor;Comparative Study;Blotting, Western;Proteasome Endopeptidase Complex;Amino Acids;Benzimidazoles;Rats;Time Factors;Endopeptidases;Animals, Newborn;Optic Nerve;Cytoskeleton;Research Support, Non-U.S. Gov't;Ganglia, Sympathetic},
	Medline = {22756941},
	Month = {7},
	Nlm_Id = {8809320},
	Number = {2},
	Organization = {Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.},
	Pages = {217-25},
	Pii = {S089662730300429X},
	Pubmed = {12873380},
	Title = {Involvement of the ubiquitin-proteasome system in the early stages of wallerian degeneration},
	Uuid = {244BA733-28BD-41A1-9F9D-99859A276D75},
	Volume = {39},
	Year = {2003}}

@article{Zhang:2004b,
	Abstract = {OBJECTIVE: Vein graft disease involves neointimal smooth muscle cells, the origins of which are unclear. This study sought to characterize and quantitate vein graft infiltration by cells extrinsic to the graft in a mouse model of vein graft disease. METHODS AND RESULTS: Inferior vena cava-to-carotid artery interposition grafting between C57Bl/6 and congenic beta-galactosidase-expressing ROSA26 mice was performed. Vein grafts were harvested 6 weeks postoperatively and stained with X-gal. More than 60\%of neointimal cells derived from the recipient, and 50\%of these cells expressed smooth muscle alpha-actin. The distribution of donor and recipient-derived cells within this vein graft wall layer was distinctly focal, consistent with focal infiltration and expansion of progenitor cells. When bone marrow transplantation with congenic green fluorescent protein (GFP)-expressing cells was used in vein graft recipients 1 month before surgery, abundant GFP-expressing cells appeared in the media, but not the neointima, of mature grafts. Endothelial cells in mature grafts derived from graft-intrinsic and graft-extrinsic sources and were, in part, of bone marrow origin. CONCLUSIONS: Cells extrinsic to the graft, including bone marrow-derived cells, predominate during vein graft remodeling.},
	Author = {Zhang, Lisheng and Freedman, Neil J. and Brian, Leigh and Peppel, Karsten},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1524-4636},
	Journal = {Arterioscler Thromb Vasc Biol},
	Keywords = {Cell Differentiation;Lac Operon;Cell Survival;Immunoenzyme Techniques;T-Lymphocyte Subsets;Green Fluorescent Proteins;Animals;Myocytes, Smooth Muscle;Genes, Reporter;Cell Movement;Research Support, U.S. Gov't, P.H.S.;Animals, Congenic;Cell Count;Carotid Artery, Common;Bone Marrow Transplantation;Mice, Inbred C57BL;Macrophages;Endothelial Cells;11 Glia;Anastomosis, Surgical;Vena Cava, Inferior;Graft Survival;Radiation Chimera;Cell Lineage;Stem Cells;Tunica Intima;Mice;Research Support, Non-U.S. Gov't;Microscopy, Fluorescence;Mice, Transgenic},
	Month = {3},
	Nlm_Id = {9505803},
	Number = {3},
	Organization = {Duke University Department of Medicine (Cardiology), Duke University Medical Center, Durham, NC 27710, USA.},
	Pages = {470-6},
	Pii = {01.ATV.0000116865.98067.31},
	Pubmed = {14726410},
	Title = {Graft-extrinsic cells predominate in vein graft arterialization},
	Uuid = {4D48D83A-93C1-413A-A1A0-868BF502C8ED},
	Volume = {24},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.ATV.0000116865.98067.31}}

@article{Zhang:2002,
	Abstract = {Gap junctions represent an important mode of intercellular communication. Connexin 45 (Cx45) is a member of the connexin family that forms gap junctions between adjacent cells. In this study, we demonstrate the expression of Cx45 in the olfactory epithelium and olfactory bulb in adult mice. Reverse transcription polymerase chain reaction amplification of total RNA from mouse turbinates and olfactory bulb yielded cDNA fragments partially encoding for Cx45. In situ hybridization using Cx45 cRNA probes revealed that hybridization products were more abundant in the olfactory epithelial layer than in the lamina propria underneath the epithelium. In the olfactory epithelial layer, hybridization signals were relatively intense in a band spreading from the basal cell layer to 4/5 of the distance from the basal cell layer to the apical process. The distribution of cells positive for Cx45 mRNA is largely overlapping with that of cells expressing olfactory marker protein mRNA, indicating that a substantial number of mature olfactory neurons express Cx45 mRNA. In the olfactory bulb, cells with large nuclei in the mitral cell layer, presumably mitral cells, express Cx45 mRNA. Immunoblotting with an antibody recognizing Cx45 revealed a band at approximately 46 kDa in homogenates of mouse turbinates and olfactory bulb. Immunohistochemical studies showed fine immunoreactive puncta in the olfactory epithelium. Immunoreactivity was observed surrounding cell bodies and the proximal processes of mitral cells in the olfactory bulb. The data suggest that Cx45 is a neuronal connexin that is expressed in mature neurons in adult mice. Our study implicates a functional role for Cx45 in the olfactory system deserving future study.},
	Author = {Zhang, C. and Restrepo, D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Brain Res},
	Keywords = {I abstr;13 Olfactory bulb anatomy},
	Number = {1},
	Organization = {Department of Cellular and Structural Biology, Neuroscience Program and the Rocky Mountain Taste and Smell Center, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, 80262, Denver, CO, USA},
	Pages = {37-47.},
	Title = {Expression of connexin 45 in the olfactory system},
	Uuid = {CABB22D7-D44D-4212-A563-DDF919991DE1},
	Volume = {929},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11852029}}

@article{Zhang:2004a,
	Abstract = {Directed migration of oligodendrocyte precursor cells (OPCs) is important for myelin formation and repair but the mechanisms of directional control are poorly understood. Here we have tested the role of polysialic acid-neural cell adhesion molecule (PSA-NCAM) in the directional migration of OPCs towards platelet-derived growth factor (PDGF). Using a Boyden microchemotaxis chamber and the Dunn direct viewing chamber, we show that in concentration gradients of PDGF, PSA-positive OPCs polarize and efficiently migrate towards the source of PDGF (chemotaxis). The loss or inactivation of the polysialic tail of NCAM leads to an altered pattern of OPC migration in response to PDGF gradients. Cells under these conditions, while being polarized and migrating, show no bias of displacement towards the source of PDGF and make random turns. By contrast, directed migration of OPCs towards basic fibroblast growth factor was not affected by the removal of PSA. Moreover, inactivation of PSA does not interfere with the random migration pattern of cells in uniform concentrations of PDGF (chemokinesis). These results suggest that PSA-NCAM is specifically involved in establishing the directionality of OPC migration in response to the concentration gradient of PDGF, but it is not essential for cell motility per se.},
	Author = {Zhang, H. and Vutskits, L. and Calaora, V. and Durbec, P. and Kiss, J. Z.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0021-9533},
	Journal = {J Cell Sci},
	Keywords = {24 Pubmed search results 2008;Platelet-Derived Growth Factor;Cell Differentiation;Research Support, Non-U.S. Gov't;Neural Cell Adhesion Molecule L1;Myelin Sheath;Rats;Pseudopodia;Stem Cells;Cells, Cultured;Oligodendroglia;Chemotaxis;Sialic Acids;Animals},
	Month = {1},
	Nlm_Id = {0052457},
	Number = {Pt 1},
	Organization = {Department of Morphology, University of Geneva Medical School, 1 rue Michel Servet, CH-1211 Geneva 4, Switzerland.},
	Pages = {93-103},
	Pii = {jcs.00827},
	Pubmed = {14627627},
	Title = {A role for the polysialic acid-neural cell adhesion molecule in PDGF-induced chemotaxis of oligodendrocyte precursor cells},
	Uuid = {9C389EE9-CA42-41B6-B565-49C814DDC37C},
	Volume = {117},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/jcs.00827}}

@article{Zhang:2002a,
	Abstract = {Murine sclerodermatous graft-vs-host disease (Scl GVHD) models human scleroderma, with prominent skin thickening, lung fibrosis, and up-regulation of cutaneous collagen mRNA. Fibrosis in Scl GVHD may be driven by infiltrating TGF-beta1-producing mononuclear cells. Here we characterize the origin and types of those cutaneous effector cells, the cytokine and chemokine environments, and the effects of anti-TGF-beta Ab on skin fibrosis, immune cell activation markers, and collagen and cytokine synthesis. Donor cells infiltrating skin in Scl GVHD increase significantly at early time points post-transplantation and are detectable by PCR analysis of Y-chromosome sequences when female mice are transplanted with male cells. Cutaneous monocyte/macrophages and T cells are the most numerous cells in Scl GVHD compared with syngeneic controls. These immune cells up-regulate activation markers (MHC class II I-A(d) molecules and class A scavenger receptors), suggesting Ag presentation by cutaneous macrophages in early fibrosing disease. Early elevated cutaneous mRNA expression of TGF-beta1, but not TGF-beta2 or TGF-beta3, and elevated C-C chemokines macrophage chemoattractant protein-1, macrophage inflammatory protein-1alpha, and RANTES precede subsequent skin and lung fibrosis. Therefore, TGF-beta1-producing donor mononuclear cells may be critical effector cells, and C-C chemokines may play important roles in the initiation of Scl GVHD. Abs to TGF-beta prevent Scl GVHD by effectively blocking the influx of monocyte/macrophages and T cells into skin and by abrogating up-regulation of TGF-beta1, thereby preventing new collagen synthesis. The Scl GVHD model is valuable for testing new interventions in early fibrosing diseases, and chemokines may be new potential targets in scleroderma.},
	Author = {Zhang, Yan and McCormick, Laura L. and Desai, Snehal R. and Wu, Caiyun and Gilliam, Anita C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0022-1767},
	Journal = {J Immunol},
	Keywords = {Macrophage Inflammatory Protein-1;Cell Migration Inhibition;RANTES;Immune Sera;Disease Models, Animal;Male;Antigens, CD45;Up-Regulation;Lymphocyte Activation;Chemokines;Transforming Growth Factor beta;Animals;Research Support, U.S. Gov't, P.H.S.;Cell Movement;Macrophage-1 Antigen;Mice, Inbred BALB C;Bone Marrow Transplantation;Mice, Inbred C57BL;RNA, Messenger;Receptors, Immunologic;Skin;Macrophages;T-Lymphocytes;Graft vs Host Disease;Spleen;Histocompatibility Antigens Class II;Macrophage Activation;Collagen Type I;11 Glia;Receptors, Lipoprotein;Scleroderma, Systemic;Female;Membrane Proteins;Cytokines;Monocytes;Mice;Monocyte Chemoattractant Protein-1;Research Support, Non-U.S. Gov't;Humans},
	Medline = {21881787},
	Month = {3},
	Nlm_Id = {2985117R},
	Number = {6},
	Organization = {Department of Dermatology, Case Western Reserve University/University Hospitals of Cleveland, Cleveland, OH 44106, USA.},
	Pages = {3088-98},
	Pubmed = {11884483},
	Title = {Murine sclerodermatous graft-versus-host disease, a model for human scleroderma: cutaneous cytokines, chemokines, and immune cell activation},
	Uuid = {8C05622D-5959-4E67-BF99-0124B2CAD0AA},
	Volume = {168},
	Year = {2002}}

@article{Zhang:2004c,
	Abstract = {The orientation of mitotic cleavage regulates neurogenesis during neural development. We examined the orientation of mitotic cleavage of dividing progenitor cells in the subventricular zone (SVZ) of adult rats subjected to stroke. In nonstroke rats, 55\%of dividing cells were oriented horizontally, whereas 40\%were oriented vertically. Horizontal and vertical cleavage orientations produce asymmetric and symmetric divisions, respectively. Four days after stroke, the number of dividing cells increased twofold, whereas the proportion of symmetric dividing cells significantly (p <0.01) increased from 40\%before stroke to 60\%. Fourteen days after stroke, the percentage of symmetric dividing cells was 47\%. Stroke-increased numbers of dividing cells in M-phase were confirmed by immuostaining. In nonstroke rats, 37 and 33\%of symmetric and asymmetric dividing cells, respectively, exhibited a neuronal marker (TuJ1). Four days after stroke, rats exhibited a significant (p <0.05) augmentation of the frequency (47\%) of neuronal distribution showing TuJ1 immunoreactivity in cells with symmetric division but not cells with asymmetric division (33\%). Numb immunoreactivity was detected in SVZ cells of nonstroke rats. Stroke did not change Numb distribution. Our data suggest that neurons are produced by both asymmetric and symmetric cell divisions in the adult SVZ, and the transient increases in symmetric division and neuronal differentiation may result in stroke-induced neurogenesis.},
	Author = {Zhang, Ruilan and Zhang, Zhenggang and Zhang, Chunling and Zhang, Li and Robin, Adam and Wang, Ying and Lu, Mei and Chopp, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cerebrovascular Accident;Cell Differentiation;Indicators and Reagents;Rats;Immunohistochemistry;Nerve Tissue Proteins;Stem Cells;Research Support, U.S. Gov't, P.H.S.;Time Factors;Rats, Wistar;06 Adult neurogenesis injury induced;Mitosis;Animals;Bromodeoxyuridine;Cerebral Ventricles;Neurons;Male},
	Month = {6},
	Nlm_Id = {8102140},
	Number = {25},
	Organization = {Department of Neurology, Henry Ford Health Sciences Center, Detroit, Michigan 48202, USA.},
	Pages = {5810-5},
	Pii = {24/25/5810},
	Pubmed = {15215303},
	Title = {Stroke transiently increases subventricular zone cell division from asymmetric to symmetric and increases neuronal differentiation in the adult rat},
	Uuid = {70519FDF-C3FB-47F1-A3A4-27439870B99D},
	Volume = {24},
	Year = {2004},
	url = {papers/Zhang_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1109-04.2004}}

@article{Zhang:1997,
	Abstract = {We have characterized the cellular localization of stem cell factor (SCF) and c-kit receptor (c-kitR) in the adult mouse nervous system in situ and in culture by using immunocytochemistry. We found that SCF is largely confined to the neuronal population in normal brain, whereas c-kitR is expressed by glial cells as well as some neurons. We also found that astroglia at an early stage of culture (7 days in vitro) are strongly SCF positive and weakly c-kitR positive. Microglia in cultures express both SCF and c-kitR, but the immunostaining of SCF is weak and diffuse when microglia are cultured in the presence of colony stimulating factor-1. Northern blot analysis confirmed the expression of mRNAs of c-kit and SCF in cultured neurons, astroglia, and microglia. The addition of recombinant SCF to astroglia in culture upregulates the expression of mRNAs of nerve growth factor, brain derived neurotrophic factor, and ciliary neurotrophic factor. These observations suggest that SCF/c-kitR signaling is involved in neuron-neuron as well as neuron-glia interactions.},
	Author = {Zhang, S. C. and Fedoroff, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Proto-Oncogene Protein c-kit;Animals;Astrocytes;Cells, Cultured;Ganglia, Spinal;Nervous System;Microglia;Mice, Inbred C3H;RNA, Messenger;11 Glia;Spinal Cord;Prosencephalon;Olfactory Bulb;Support, Non-U.S. Gov't;Blotting, Northern;Antibody Specificity;Cerebral Cortex;Neurons;Cerebellum;Mice;Stem Cell Factor;Immunohistochemistry;Brain Stem;Gene Expression;Peripheral Nerves},
	Medline = {97135696},
	Month = {1},
	Nlm_Id = {7600111},
	Number = {1},
	Organization = {Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.},
	Pages = {1-15},
	Pii = {10.1002/(SICI)1097-4547(19970101)47:1<1::AID-JNR1>3.0.CO;2-N},
	Pubmed = {8981233},
	Title = {Cellular localization of stem cell factor and c-kit receptor in the mouse nervous system},
	Uuid = {D1CB18FE-CB7B-42FE-916D-95952C3EFA3B},
	Volume = {47},
	Year = {1997}}

@article{Zhang:2003a,
	Abstract = {Microglia are prominently involved in neural degenerative diseases of the CNS and the retina. In this study, we determined the activation and phagocytotic function of different subtypes of retinal microglial cells at 1 week and 1 month following optic axotomy. Fluorescent DiI crystals were placed at the stumps of the cut optic nerves of Lewis rats to retrolabel retinal ganglion cells. Microglial cells were indirectly labeled as they phagocytosed the dye particles in the dying ganglion cells. OX-42, 5D4, ED1, and OX-6 antibodies were used for immunohistochemical study. The OX-42- and 5D4-positive microglial cells were increased in the inner retinal layers after optic axotomy. The increase of OX-42-positive cells was considerably greater than that of 5D4-positive cells. The 5D4-positive cells were ramified in shape, whereas OX-42-positive cells were ameboid and ovoid. Both 5D4- and OX-42-positive cells phagocytosed dying ganglion cells at 1 week and 1 month after axotomy. Scattered ameboid ED1-positive cells were detected in the normal retina and showed phagocytotic activity at 1 month after optic axotomy. The number of ED1-positive cells in the retina was unchanged after axotomy. In optic axotomy, three types of microglial cells were activated, namely, 5D4-positive ramified cells and OX-42- and ED1-positive ameboid cells. All of them exhibited the phagocytosis of dying ganglion cells. Insofar as the blood-retinal barrier presumably remained intact in optic axotomy, the OX-42- and 5D4-positive cells might derive from resident microglial cells. The ED1-positive cells, presumably recently blood-borne macrophage in the CNS, remained the same number in the axotomized retina.},
	Author = {Zhang, Cheng and Tso, Mark O. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Microscopy, Confocal;Retina;Membrane Glycoproteins;Indoles;Case-Control Studies;Rats;Comparative Study;Time Factors;Not relevant;Cell Count;11 Glia;Microglia;Optic Nerve Injuries;Optic Nerve;Amino Acids;Animals;Axotomy},
	Medline = {22830189},
	Month = {9},
	Nlm_Id = {7600111},
	Number = {6},
	Organization = {Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-9238, USA. czhang1\@jhmi.edu},
	Pages = {840-5},
	Pubmed = {12949910},
	Title = {Characterization of activated retinal microglia following optic axotomy},
	Uuid = {43A6A6A0-44FF-4863-B22E-1F72D80337A8},
	Volume = {73},
	Year = {2003},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.10713}}

@article{Zhang:1994,
	Abstract = {The envelope glycoprotein G of vesicular stomatitis virus induces membrane fusion at low pH. Site-directed mutagenesis of specific amino acids within a segment spanning amino acids 123 to 137 of G protein, which is highly conserved in vesiculoviruses and was previously shown by us to be involved in fusogenic activity (Y. Li, C. Drone, E. Sat, and H. P. Ghosh, J. Virol. 67:4070-4077, 1993), was used to determine the role of this region in low-pH-induced membrane fusion. The mutant glycoproteins expressed in COS cells were assayed for acid-pH-induced cell-cell fusion. Substitution of the variant Pro-123 with Leu had no effect on the fusogenic activity, while substitution of conserved Phe-125 and Asp-137 with Tyr and Asn, respectively, shifted the pH optimum of membrane fusion to a more acidic pH value and decreased the fusion efficiency. The deletion of amino acid residues 124 to 127, 131 to 137, or 124 to 137 produced mutants defective in transport. Mutation of the conserved residues Gly-124 and Pro-127 to Ala and to Gly or Leu, respectively, inhibited cell-cell fusion activity by about 90\%without affecting transport of the mutant proteins to the cell surface, suggesting that these two residues may be present within the fusion peptide and thus may be directly involved in fusion. This highly conserved domain containing neutral amino acids of G protein may therefore represent the putative fusion domain of vesicular stomatitis virus G protein.},
	Author = {Zhang, L. and Ghosh, H. P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Glycoproteins;Research Support, Non-U.S. Gov't;Conserved Sequence;Base Sequence;Sequence Homology, Amino Acid;Biological Transport;Protein Folding;Recombinant Proteins;Vesicular stomatitis-Indiana virus;15 Retrovirus mechanism;Cell Fusion;Glycosylation;Hydrogen-Ion Concentration;Viral Envelope Proteins;Protein Conformation;Membrane Glycoproteins;Cell Compartmentation;Amino Acid Sequence;24 Pubmed search results 2008;Molecular Sequence Data;Structure-Activity Relationship;Mutagenesis, Insertional},
	Medline = {94187058},
	Month = {4},
	Nlm_Id = {0113724},
	Number = {4},
	Organization = {Department of Biochemistry, McMaster University, Hamilton, Ontario, Canada.},
	Pages = {2186-93},
	Pubmed = {8139003},
	Title = {Characterization of the putative fusogenic domain in vesicular stomatitis virus glycoprotein G},
	Uuid = {3C4CE65A-EE2C-11DA-8605-000D9346EC2A},
	Volume = {68},
	Year = {1994}}

@article{Zhang:2003b,
	Abstract = {ts1 is a temperature-sensitive mutant of Moloney murine leukemia virus that induces a rapid spongiform encephalopathy in mice infected as newborns. The pathological features include the formation of ubiquitinated inclusions resembling Lewy bodies. To determine how perturbation of the ubiquitin-proteasome pathway might affect ts1-mediated neurodegeneration, the virus was introduced into transgenic mice in which the assembly of ubiquitin chains was compromised by the expression of dominant-negative mutant ubiquitin. The onset of symptoms was greatly delayed in a transgenic mouse line expressing K48R mutant ubiquitin; no such delay was observed in mice expressing a wild-type ubiquitin transgene or K63R mutant ubiquitin. The extended latency was found to correlate with a delayed increase in viral titers. Pathological findings in K48R transgenic mice at 60 days were found to be similar to those in the other strains at 30 days, suggesting that while delayed, the neurodegenerative process in K48R mice was otherwise similar. These data demonstrate the sensitivity of retroviral replication to the partial disruption of ubiquitin-mediated proteolysis in vivo, a finding that may have therapeutic potential.},
	Author = {Zhang, Mei and Thurig, Sherry and Tsirigotis, Maria and Wong, Paul K. Y. and Reuhl, Kenneth R. and Gray, Douglas A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0022-538X},
	Journal = {J Virol},
	Keywords = {Mutation;Moloney murine leukemia virus;Not relevant;11 Glia;Mice, Transgenic;Support, U.S. Gov't, P.H.S.;Ubiquitin;Mice;Brain;Support, Non-U.S. Gov't;Animals},
	Medline = {22689657},
	Month = {7},
	Nlm_Id = {0113724},
	Number = {13},
	Organization = {Centre for Cancer Therapeutics, Ottawa Regional Cancer Centre, Ottawa, Ontario, Canada K1H 1C4.},
	Pages = {7193-201},
	Pubmed = {12805418},
	Title = {Effects of mutant ubiquitin on ts1 retrovirus-mediated neuropathology},
	Uuid = {93B41BA1-376E-4066-A320-1B0AE3EEF014},
	Volume = {77},
	Year = {2003},
	url = {papers/Zhang_JVirol2003.pdf}}

@article{Zhang:2001b,
	Abstract = {Neuroglia are non-neuronal cells in the nervous system and are involved in virtually every aspect of neural function. Because of the ambiguity of glial function, the definition of glial cells relies chiefly on structural and biochemical characteristics. The use of molecular markers in identifying glial cells along their differentiation pathways is further complicated by recent findings that many of the molecules are also expressed by cells of the neuronal lineage. So, how specific are glial markers and how can a glial cell be defined during development?},
	Author = {Zhang, S. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Nat Rev Neurosci},
	Keywords = {10 Development;F pdf},
	Number = {11},
	Organization = {Su-Chun Zhang is at the Department of Anatomy and the Waisman Center, University of Wisconsin, 1500 Highland Avenue, Madison, Wisconsin 53705, USA.zhang\@waisman.wisc.edu},
	Pages = {840-3.},
	Title = {Defining glial cells during CNS development},
	Uuid = {BC4B8B68-096D-4362-AA06-6AA06336A00B},
	Volume = {2},
	Year = {2001},
	url = {papers/Zhang_NatRevNeurosci2001.pdf}}

@article{Zhang:2001a,
	Abstract = {Progenitor cells in the subventricular zone of the lateral ventricle and in the dentate gyrus of the hippocampus can proliferate throughout the life of the animal. To examine the proliferation and fate of progenitor cells in the subventricular zone and dentate gyrus after focal cerebral ischemia, we measured the temporal and spatial profiles of proliferation of cells and the phenotypic fate of proliferating cells in ischemic brain in a model of embolic middle cerebral artery occlusion in the adult rat. Proliferating cells were labeled by injection of bromodeoxyuridine (BrdU) in a pulse or a cumulative protocol. To determine the temporal profile of proliferating cells, ischemic rats were injected with BrdU every 4 h for 12 h on the day preceding death. Rats were killed 2-14 days after ischemia. We observed significant increases in numbers of proliferating cells in the ipsilateral cortex and subventricular zone 2-14 days with a peak at 7 days after ischemia compared with the control group. To maximize labeling of proliferating cells, a single daily injection of BrdU was administered over a 14-day period starting the day after ischemia. Rats were killed either 2 h or 28 days after the last injection of BrdU. A significant increase in numbers of BrdU immunoreactive cells in the subventricular zone was coincident with a significant increase in numbers of BrdU immunoreactive cells in the olfactory bulb 14 days after ischemia and numbers of BrdU immunoreactive cells did not significantly increase in the dentate gyrus. However, 28 days after the last labeling, the number of BrdU labeled cells decreased by 90\%compared with number at 14 days. Clusters of BrdU labeled cells were present in the cortex distal to the infarction. Numerous cells immunostained for the polysialylated form of the neuronal cell adhesion molecule were detected in the ipsilateral subventricular zone. Only 6\%of BrdU labeled cells exhibited glial fibrillary acidic protein immunoreactivity in the cortex and subcortex and no BrdU labeled cells expressed neuronal protein markers (neural nuclear protein and microtubule associated protein-2). From these data we suggest that focal cerebral ischemia induces transient and regional specific increases in cell proliferation in the ipsilateral hemisphere and that proliferating progenitor cells may exist in the adult cortex.},
	Author = {Zhang, R. L. and Zhang, Z. G. and Zhang, L. and Chopp, M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {Neural Cell Adhesion Molecules;Glial Fibrillary Acidic Protein;Cell Differentiation;Animals;Microtubule-Associated Proteins;Rats;Recovery of Function;Rats, Wistar;Male;Antimetabolites;Nerve Regeneration;Research Support, U.S. Gov't, P.H.S.;Sialic Acids;Cerebral Cortex;Neurons;Brain Ischemia;Age Factors;Cell Division;24 Pubmed search results 2008;Immunohistochemistry;Stem Cells;Bromodeoxyuridine;Lateral Ventricles;Neural Cell Adhesion Molecule L1},
	Medline = {21376613},
	Nlm_Id = {7605074},
	Number = {1},
	Organization = {Department of Neurology, Henri Ford Health Sciences Center, Detroit, MI 48202, USA.},
	Pages = {33-41},
	Pii = {S0306452201001178},
	Pubmed = {11483298},
	Title = {Proliferation and differentiation of progenitor cells in the cortex and the subventricular zone in the adult rat after focal cerebral ischemia},
	Uuid = {7217B296-89E9-4C04-B17A-500BC7A692FF},
	Volume = {105},
	Year = {2001}}

@article{Zhang:2003,
	Abstract = {OBJECTIVE: To investigate the proliferation and differentiation of neural stem cells after cerebral infarction(CI) in adult rats. METHODS: CI animal model was made by ligating the common carotid artery and external carotid artery and inserting a piece of nylon thread into the internal carotid artery among 100 male Wistar rats. Then the rats were randomly divided into 5 groups: group of I day after brain infarction (n = 20), group of 3 days after brain infarction (n = 20), group of 7 days after brain infarction (n = 20), group of 14 days after brain infarction (n = 20), and group of 28 days after brain infarction (n = 20). Twelve rats undergoing sham operation with a piece of nylon thread inserted only into the common carotid artery were used as controls. The rats were killed at different time points and their brains were taken out. The expression of bromodeoxyuridine (BrdU) and Musashil (both used to mark the dividing neural stem cells), and of glial fibrillary acidic protein (GFAP) and neuronal nuclear antigen (NeuN) (both used to mark the differentiating neural stem cells) were determined by immunohistochemistry and immunofluorescence staining. RESULTS: In the normal brain tissues, only a small amount of BrdU(+) cells were found in the hippocampus. One day after CI the number of BrdU(+) cells began to increase in the hippocampus at the CI side (P < 0.05), peaked 7 days after CI with a number 6 times that at the normal side, began to decrease 14 days after, and almost reached normal 28 days after. The number of BrdU(+)/Musashil(+) cells began to increase 1 day after CI (P < 0.05), peaked 7 days after, began to decrease 14 days after, and almost reached normal 28 days after. The number of BrdU(+)/GFAP(+) cells at the CI side remained almost unchanged after CI. The number of BrdU(+)/NeuN(+) cells began to increase 14 days after CI (P < 0.05) and peaked 38 days after. CONCLUSION: Cerebral infarction stimulates the proliferation of inherent neural stem cells and most proliferated neural stem cells differentiate into neurons.},
	Author = {Zhang, Bo and Wang, Ren-zhi Z. and Yao, Yong and Wang, Xin and Li, Gui-lin L. and Dou, Wan-chen C. and Tian, Shi-qiang Q. and Zheng, Tong and Tian, Yu},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0376-2491},
	Journal = {Zhonghua Yi Xue Za Zhi},
	Keywords = {Cell Differentiation;Research Support, Non-U.S. Gov't;Immunohistochemistry;Rats;English Abstract;Cell Division;Cerebral Infarction;Rats, Wistar;Stem Cells;Fluorescent Antibody Technique;Animals;Bromodeoxyuridine;24 Pubmed search results 2008;Male;Neurons},
	Month = {11},
	Nlm_Id = {7511141},
	Number = {22},
	Organization = {Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.},
	Pages = {1975-9},
	Pubmed = {14703433},
	Title = {[Proliferation and differentiation of neural stem cells after cerebral infarction: an experimental study of adult rats]},
	Uuid = {788227EB-7A23-463D-A8F8-8B3D3A094179},
	Volume = {83},
	Year = {2003}}

@article{Zhao:2008,
	Abstract = {The generation of new neurons is sustained throughout adulthood in the mammalian brain due to the proliferation and differentiation of adult neural stem cells. In this review, we discuss the factors that regulate proliferation and fate determination of adult neural stem cells and describe recent studies concerning the integration of newborn neurons into the existing neural circuitry. We further address the potential significance of adult neurogenesis in memory, depression, and neurodegenerative disorders such as Alzheimer's and Parkinson's disease.},
	Author = {Zhao, Chunmei and Deng, Wei and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1097-4172},
	Journal = {Cell},
	Keywords = {Neurons;01 Adult neurogenesis general;Cell Differentiation;research support, non-u.s. gov't;24 Pubmed search results 2008;Stem Cells;research support, n.i.h., extramural;Animals;Brain;Humans;review;Nervous System Diseases},
	Month = {2},
	Nlm_Id = {0413066},
	Number = {4},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.},
	Pages = {645-60},
	Pii = {S0092-8674(08)00134-7},
	Pubmed = {18295581},
	Title = {Mechanisms and functional implications of adult neurogenesis},
	Uuid = {738203B3-7794-4DDA-8CE5-F291210EC140},
	Volume = {132},
	Year = {2008},
	url = {papers/Zhao_Cell2008.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cell.2008.01.033}}

@article{Zhao:2007a,
	Abstract = {The extracellular matrix protein reelin is essential for the proper radial migration of cortical neurons. In reeler mice lacking reelin, there is a malformation of the radial glial scaffold required for granule cell migration. Immunostaining for glial fibrillary acidic protein (GFAP) reveals abundant radial glial cells with long fibers traversing the granular layer in the wild type, but almost exclusively astrocytes in the reeler mutant. With the concept that radial glial cells are precursors of neurons, we hypothesized that the balance between neurogenesis and gliogenesis is altered in the reeler mutant. To this end, adult reeler mutants and their wild-type littermates were injected with bromodeoxyuridine (BrdU), a marker of newly generated cells. When compared to wild-type animals, we found a reduction in the number of BrdU-labeled cells in the adult reeler dentate gyrus. Moreover, whereas there was a dramatic decrease in the number of newly generated granule cells identified by double labeling for BrdU and NeuN, the number of BrdU-labeled, GFAP-positive astrocytes had increased. Decreased neurogenesis in the adult reeler dentate gyrus was confirmed by immunostaining for doublecortin, a marker of newly generated neurons. These results indicate that adult neurogenesis is altered in the reeler dentate gyrus and that newly generated cells preferentially differentiate into astrocytes.},
	Author = {Zhao, Shanting and Chai, Xuejun and Frotscher, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0378-5866},
	Journal = {Dev Neurosci},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Nlm_Id = {7809375},
	Number = {1-2},
	Organization = {Institut fur Anatomie und Zellbiologie, Albert-Ludwigs-Universitat Freiburg, Freiburg, Deutschland.},
	Pages = {84-90},
	Pii = {DNE20070291_2084},
	Pubmed = {17148951},
	Title = {Balance between neurogenesis and gliogenesis in the adult hippocampus: role for reelin},
	Uuid = {DA576DA5-EB10-4FD1-B204-D7881C428AD4},
	Volume = {29},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1159/000096213}}

@article{Zhao:2004a,
	Abstract = {Reelin is required for the proper positioning of neurons in the cerebral cortex. In the reeler mutant lacking reelin, the granule cells of the dentate gyrus fail to form a regular, densely packed cell layer. Recent evidence suggests that this defect is due to the malformation of radial glial processes required for granule cell migration. Here, we show that recombinant reelin in the medium significantly increases the length of GFAP-positive radial glial fibers in slice cultures of reeler hippocampus, but does not rescue either radial glial fiber orientation or granule cell lamination. However, rescue of radial glial fiber orientation and granule cell lamination was achieved when reelin was present in the normotopic position provided by wild-type co-culture, an effect that is blocked by the CR-50 antibody against reelin. These results indicate a dual function of reelin in the dentate gyrus, as a differentiation factor for radial glial cells and as a positional cue for radial fiber orientation and granule cell migration.},
	Author = {Zhao, Shanting and Chai, Xuejun and F{\"o}rster, Eckart and Frotscher, Michael},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0950-1991},
	Journal = {Development},
	Keywords = {Research Support, Non-U.S. Gov't;Extracellular Matrix Proteins;Rats;Dentate Gyrus;Animals;Cell Movement;Cell Adhesion Molecules, Neuronal;Neurons;Mice},
	Month = {10},
	Nlm_Id = {8701744},
	Number = {20},
	Organization = {Institute of Anatomy and Cell Biology, Albert-Ludwigs-Universit{\"a}t Freiburg, Albertstr. 17, 79104 Freiburg, Germany.},
	Pages = {5117-25},
	Pii = {131/20/5117},
	Pubmed = {15459104},
	Title = {Reelin is a positional signal for the lamination of dentate granule cells},
	Uuid = {021B4122-716E-11DA-A383-000D9346EC2A},
	Volume = {131},
	Year = {2004},
	url = {papers/Zhao_Development2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1242/dev.01387}}

@article{Zhao:2004,
	Abstract = {The hippocampus develops from the medial wall of the forming cerebral cortex during embryonic life. Morphogenic signals from the Wnt pathway regulate several events during hippocampal development (Galceran et al.: Development 127:469-482, 2000; Lee et al.: Development 127:457-467, 2000; Zhou et al.: J Neurosci 24:121-126, 2004) and we have previously shown that Wnt receptors from the Frizzled (Fzd) family are expressed in discreet cortical domains during development (Kim et al.: Mech Dev 103:167-172, 2001). We generated transgenic mice using the putative control elements of the Fzd9 gene, normally selectively expressed in the developing and adult hippocampus, driving expression of a marker gene. These mice express LacZ in the brain in the same developmental distribution as endogenous Fzd protein. Postnatally, expression remains strong in the dendritic fields of hippocampal principal cells as well as hippocampal efferent axons. These mice provide a genetic and anatomic tool for analyzing development and reorganization in the hippocampus.},
	Author = {Zhao, Chunjie and Pleasure, Samuel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1526-954X},
	Journal = {Genesis},
	Keywords = {beta-Galactosidase;Animals;Cloning, Molecular;Base Sequence;Mice, Transgenic;Hippocampus;RNA, Messenger;DNA Primers;Peptide Fragments;Research Support, U.S. Gov't, P.H.S.;Cerebral Cortex;Receptors, Neurotransmitter;Promoter Regions (Genetics);Mice;Immunohistochemistry;Molecular Sequence Data;Amino Acid Sequence;Research Support, Non-U.S. Gov't},
	Month = {9},
	Nlm_Id = {100931242},
	Number = {1},
	Organization = {Department of Neurology, Programs in Neuroscience and Developmental Biology, University of California, San Francisco, California, USA.},
	Pages = {32-9},
	Pubmed = {15354291},
	Title = {Frizzled-9 promoter drives expression of transgenes in the medial wall of the cortex and its chief derivative the hippocampus},
	Uuid = {AD8B1299-A3E5-11DA-AB00-000D9346EC2A},
	Volume = {40},
	Year = {2004},
	url = {papers/Zhao_Genesis2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/gene.20058}}

@article{Zhao:1996,
	Abstract = {We used recombinant adenoviruses as a means of expressing exogenous genes in olfactory neurons in vivo. A replication incompetent adenovirus (type 5, Ad5) carrying the reporter gene lacZ, which codes for the enzyme beta-galactosidase (beta-Gal), was applied in solution to the olfactory epithelia of rats. The expression of lacZ was controlled by the cytomegalovirus immediate-early promoter/enhancer. beta-Gal expression was observed 1 day postinfection and was maximal at 3-10 days, although it could be detected for at least 21 days postinfection. Expression patterns were heterogeneous, ranging from a few percent to over 25\%of the cells in different regions of both turbinate and septal epithelium. Staining was stronger in the olfactory versus respiratory epithelia. In olfactory epithelium staining was almost entirely restricted to olfactory neurons. beta-Gal staining was also observed in the olfactory axons so that nerve bundles could be traced to their targets in the glomerular layer of the olfactory bulb. Intense staining of some glomeruli was evident as long as 21 days postinfection. There was no evidence of cell loss or tissue damage due to viral infection. These results demonstrate that it is possible to use recombinant Ad5 for expressing foreign genes in olfactory neurons. This technique could be used in olfactory neurons to increase expression levels of olfactory specific genes, including the odor receptor, putative guidance and growth molecules, or elements of the transduction cascade, in order to elucidate their biological functions in vivo.},
	Author = {Zhao, H. and Otaki, J. M. and Firestein, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {J Neurobiol},
	Keywords = {beta-Galactosidase/metabolism;Rats, Sprague-Dawley;*Adenoviridae;Lac Operon;Rats;Neurons, Afferent/*physiology;Animal;Support, U.S. Gov't, P.H.S.;I abstr;Olfactory Pathways/cytology/*physiology;Histocytochemistry;13 Olfactory bulb anatomy;*Gene Transfer Techniques},
	Number = {4},
	Organization = {Interdepartmental Neuroscience Program, Yale University, New Haven, Connecticut 06510, USA.},
	Pages = {521-30.},
	Title = {Adenovirus-mediated gene transfer in olfactory neurons in vivo},
	Uuid = {65EF9FC7-4A4C-41D0-ACB9-8F7F8DF6D7AC},
	Volume = {30},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=8844515}}

@article{Zhao:2006,
	Abstract = {Adult neurogenesis in the dentate gyrus may contribute to hippocampus-dependent functions, yet little is known about when and how newborn neurons are functional because of limited information about the time course of their connectivity. By using retrovirus-mediated gene transduction, we followed the dendritic and axonal growth of adult-born neurons in the mouse dentate gyrus and identified distinct morphological stages that may indicate different levels of connectivity. Axonal projections of newborn neurons reach the CA3 area 10-11 d after viral infection, 5-6 d before the first spines are formed. Quantitative analyses show that the peak of spine growth occurs during the first 3-4 weeks, but further structural modifications of newborn neurons take place for months. Moreover, the morphological maturation is differentially affected by age and experience, as shown by comparisons between adult and postnatal brains and between housing conditions. Our study reveals the key morphological transitions of newborn granule neurons during their course of maturation.},
	Author = {Zhao, Chunmei and Teng, E. Matthew and Summers, Robert G. and Ming, Guo-Li L. and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {01 Adult neurogenesis general;24 Pubmed search results 2008},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {1},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {3-11},
	Pii = {26/1/3},
	Pubmed = {16399667},
	Title = {Distinct morphological stages of dentate granule neuron maturation in the adult mouse hippocampus},
	Uuid = {BFA769B1-F8D3-479E-A9E6-B378AA68E45A},
	Volume = {26},
	Year = {2006},
	url = {papers/Zhao_JNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3648-05.2006}}

@article{Zhao:2005,
	Abstract = {CNS remyelination occurs more rapidly in young adult rats than in old rats. Since the inflammatory response initiated by demyelination is an important trigger for remyelination, we address whether ageing changes in remyelination are associated with changes in the inflammatory response. Using a toxin model of demyelination, where the inflammatory response largely comprises macrophages, we show that there is a delay in both recruitment and activation of OX-42+ and macrophage scavenger receptor B+ macrophages following demyelination in older rats (10-13 months) compared to young rats (8-10 weeks). This difference is associated with a slower onset of increased expression of several chemokine mRNAs. However, many inflammatory cytokines have similar mRNA expression patterns, with the exception of IL-1beta, IL-6 and TNF-alpha, which have prolonged expression in the older animals. Differences in IL-1beta mRNA expression, a cytokine specifically implicated in CNS remyelination, are not reflected in differences in protein expression detected by immunocytochemistry. These data relate the age-associated delay in remyelination efficiency to changes in the macrophage and inflammatory mediator response to demyelination.},
	Author = {Zhao, and Li, and Franklin,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0197-4580},
	Journal = {Neurobiol Aging},
	Keywords = {11 Glia},
	Month = {7},
	Nlm_Id = {8100437},
	Organization = {Cambridge Center for Brain Repair and Neuroregeneration Laboratory, Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, UK.},
	Pii = {S0197-4580(05)00183-1},
	Pubmed = {16051398},
	Title = {Differences in the early inflammatory responses to toxin-induced demyelination are associated with the age-related decline in CNS remyelination},
	Uuid = {730A63EE-E4FF-4C47-AF53-74DD80CADF8A},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neurobiolaging.2005.06.008}}

@article{Zhao:2007,
	Abstract = {Neural progenitor cells (NPCs) in the subventricular zone (SVZ) travel a long distance along the rostral migratory stream (RMS) to give rise to interneurons in the olfactory bulb (OB). Using the multiphoton microscope and time-lapse recording techniques we here report the behavior of NPCs in the RMS under both intact and ischemic conditions in living brain slices. The NPCs were visualized in 3-week-old transgenic mice that carry the reporter gene, green fluorescent protein (GFP), driven by the nestin promoter. Cortical brain ischemia was induced by permanent occlusion of the right common carotid artery and the middle cerebral artery. We observed that the RMS contained two populations of NPCs: nonmigrating cells (bridge cells) and migrating cells. Bridge cells enabled migrating cells to travel and also produced new cells in the RMS. The direction of NPC migration in the RMS was bidirectional in both intact and ischemic conditions. Cortical ischemia impeded NPC travel in the RMS next to the lesion area during the early period of ischemia. Cell-cell contact was a prominent feature affecting NPC translocation and migratory direction. These data suggest that behavior and function of nestin-positive NPCs in the RMS are variable. Cell-cell contacts and microenvironmental changes influence NPC behavior in the RMS. This study may provide insights to help in understanding NPC biology.},
	Author = {Zhao, Li-Ru R. and Nam, Sang Chae},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0304-3940},
	Journal = {Neurosci Lett},
	Keywords = {research support, non-u.s. gov't;24 Pubmed search results 2008},
	Month = {9},
	Nlm_Id = {7600130},
	Number = {2},
	Organization = {Department of Neurology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Avenue, Chicago, IL 60611, USA. lzhao\@lsuhsc.edu},
	Pages = {83-8},
	Pii = {S0304-3940(07)00775-6},
	Pubmed = {17723276},
	Title = {Multiphoton microscope imaging: the behavior of neural progenitor cells in the rostral migratory stream},
	Uuid = {0B54556D-9CF1-481B-842B-4877C6AC091B},
	Volume = {425},
	Year = {2007},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neulet.2007.07.032}}

@article{Zhao:2003,
	Abstract = {New neurons are generated from stem cells in a few regions of the adult mammalian brain. Here we provide evidence for the generation of dopaminergic projection neurons of the type that are lost in Parkinson's disease from stem cells in the adult rodent brain and show that the rate of neurogenesis is increased after a lesion. The number of new neurons generated under physiological conditions in substantia nigra pars compacta was found to be several orders of magnitude smaller than in the granular cell layer of the dentate gyrus of the hippocampus. However, if the rate of neuronal turnover is constant, the entire population of dopaminergic neurons in substantia nigra could be replaced during the lifespan of a mouse. These data indicate that neurogenesis in the adult brain is more widespread than previously thought and may have implications for our understanding of the pathogenesis and treatment of neurodegenerative disorders such as Parkinson's disease. 0027-8424 Journal Article},
	Author = {Zhao, M. and Momma, S. and Delfani, K. and Carlen, M. and Cassidy, R. M. and Johansson, C. B. and Brismar, H. and Shupliakov, O. and Frisen, J. and Janson, A. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Human;Neurons/*metabolism/pathology;Animals;Synapses;Bromodeoxyuridine/pharmacology;Parkinson Disease/pathology;Stem Cells/metabolism;Dopamine Agents/pharmacology;Dopamine/metabolism;Hippocampus/pathology;Apoptosis;1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology;Mice, Inbred C57BL;Microscopy, Fluorescence;Male;Time Factors;01 Adult neurogenesis general;Substantia Nigra/*anatomy &histology/metabolism/*pathology;Antimetabolites/pharmacology;Mice;A pdf},
	Number = {13},
	Organization = {Departments of Neuroscience, Cell and Molecular Biology, Medical Nobel Institute, and Woman and Child Health, Karolinska Institute, SE-171 77 Stockholm, Sweden.},
	Pages = {7925-30},
	Pubmed = {12792021},
	Title = {Evidence for neurogenesis in the adult mammalian substantia nigra},
	Uuid = {973755E6-7347-4515-8D32-C66D3560A57C},
	Volume = {100},
	Year = {2003},
	url = {papers/Zhao_ProcNatlAcadSciUSA2003.pdf}}

@article{Zhao:2003a,
	Abstract = {DNA methylation-mediated epigenetic regulation plays critical roles in regulating mammalian gene expression, but its role in normal brain function is not clear. Methyl-CpG binding protein 1 (MBD1), a member of the methylated DNA-binding protein family, has been shown to bind methylated gene promoters and facilitate transcriptional repression in vitro. Here we report the generation and analysis of MBD1-/- mice. MBD1-/- mice had no detectable developmental defects and appeared healthy throughout life. However, we found that MBD1-/- neural stem cells exhibited reduced neuronal differentiation and increased genomic instability. Furthermore, adult MBD1-/- mice had decreased neurogenesis, impaired spatial learning, and a significant reduction in long-term potentiation in the dentate gyrus of the hippocampus. Our findings indicate that DNA methylation is important in maintaining cellular genomic stability and is crucial for normal neural stem cell and brain functions. 0027-8424 Journal Article},
	Author = {Zhao, X. and Ueba, T. and Christie, B. R. and Barkho, B. and McConnell, M. J. and Nakashima, K. and Lein, E. S. and Eadie, B. D. and Willhoite, A. R. and Muotri, A. R. and Summers, R. G. and Chun, J. and Lee, K. F. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Cell Differentiation;Mice, Knockout;Neurons/cytology;Hippocampus/cytology/*physiology;C pdf;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;*CpG Islands;Support, Non-U.S. Gov't;Animals;DNA-Binding Proteins/*genetics;Mice},
	Number = {11},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.},
	Pages = {6777-82},
	Pubmed = {12748381},
	Title = {Mice lacking methyl-CpG binding protein 1 have deficits in adult neurogenesis and hippocampal function},
	Uuid = {15ED9CF0-E6BA-4963-B858-0ADBE7F7FD6B},
	Volume = {100},
	Year = {2003},
	url = {papers/Zhao_ProcNatlAcadSciUSA2003a.pdf}}

@article{Zharkovsky:2003,
	Abstract = {Administration of ethanol during brain development induces widespread neuronal loss in various structures of the brain. Here, we show that a single administration of ethanol given during the early postnatal period can induce not only neuronal death, but also an increase in proliferation of the progenitor cells in the dentate gyrus of hippocampal formation in rats. Ethanol (1.5 or 3 g/kg, i.p.) administered to 10-day-old rats induced massive neuronal degeneration as evidenced by TUNEL assay in the dentate gyrus. The neuronal death induced by a high dose of ethanol (3 g/kg) was accompanied by an enhanced proliferation of the progenitor cells labeled by bromodeoxyuridine (BrdU, 50 mg/kg, i.p.) in dentate gyrus. One and 3 weeks following ethanol or saline administration, ethanol-treated rats still had significantly more BrdU-labeled cells than control animals. In ethanol-treated rats, a higher proportion of newly born cells acquired the phenotype of immature postmitotic neurons whereas the final differentiation into calbindin-expressing granule cells remained unchanged. The proportion of astroglial cells was also increased in ethanol-treated rats. Thus, ethanol given in high doses not only induces neurodegeneration but also initiates the process of neuro- and gliogenesis, which might be responsible for the neuronal and glial reorganization of the dentate gyrus.},
	Author = {Zharkovsky, Tamara and Kaasik, Allen and Jaako, K{\"u}lli and Zharkovsky, Alexander},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Research Support, Non-U.S. Gov't;Dose-Response Relationship, Drug;Nerve Degeneration;Ethanol;Animals;Rats;Comparative Study;Radiation-Sensitizing Agents;Central Nervous System Depressants;Cell Count;Hippocampus;Rats, Wistar;Animals, Newborn;Sialic Acids;In Situ Nick-End Labeling;Dentate Gyrus;Cell Division;Immunohistochemistry;24 Pubmed search results 2008;Bromodeoxyuridine;Neural Cell Adhesion Molecule L1;DNA Fragmentation;Regeneration},
	Medline = {22718819},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {1-2},
	Organization = {Department of Pharmacology, University of Tartu, 19 Ravila Street, 51014 Tartu, Estonia.},
	Pages = {115-23},
	Pii = {S0006899303027963},
	Pubmed = {12834905},
	Title = {Neurodegeneration and production of the new cells in the dentate gyrus of juvenile rat hippocampus after a single administration of ethanol},
	Uuid = {6F368281-E8FE-45F2-8CC1-CE22B0E4057A},
	Volume = {978},
	Year = {2003}}

@article{Zheng:2000,
	Abstract = {Nucleoside kinases from several species are investigated as "suicide genes" for treatment of malignant tumors by combined gene/chemotherapy. We have recently cloned a multisubstrate deoxyribonucleoside kinase of Drosophila melanogaster (Dm-dNK), and we have shown that the enzyme phosphorylates cytotoxic pyrimidine and purine nucleoside analogs. The broad substrate specificity of the enzyme, as well as its very high catalytic rate, makes it a unique member of the nucleoside kinase enzyme family. In the present study, we evaluated Dm-dNK as a suicide gene by constructing a replication-deficient retroviral vector that expresses the enzyme. The human pancreatic adenocarcinoma cell line MIA PaCa-2 and a thymidine kinase-deficient osteosarcoma cell line were transduced with the recombinant virus. We showed that Dm-dNK can be expressed in human cells, that the enzyme retained its enzymatic activity, and that it is localized in the cell nuclei due to a nuclear localization signal in its C-terminal region. The cells expressing Dm-dNK exhibited increased sensitivity to several cytotoxic nucleoside analogs, such as 1-beta-d-arabinofuranosylcytosine, 1-beta-d-arabinofuranosylthymine, (E)-5-(2-bromovinyl)-2'-deoxyuridine, 2-chloro-2'-deoxyadenosine, and 2',2'-difluorodeoxycytidine. These findings suggest that Dm-dNK may be used as a suicide gene in combined gene/chemotherapy of cancer.},
	Author = {Zheng, X. and Johansson, M. and Karlsson, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0021-9258},
	Journal = {J Biol Chem},
	Keywords = {Inhibitory Concentration 50;Adenocarcinoma;24 Pubmed search results 2008;Drosophila melanogaster;Tumor Cells, Cultured;Thymidine Kinase;Transduction, Genetic;Animals;Cytarabine;Osteosarcoma;Arabinonucleosides;Kinetics;Cladribine;15 Retrovirus mechanism;Promoter Regions (Genetics);Bromodeoxyuridine;Phosphotransferases (Alcohol Group Acceptor);Cell Division;Substrate Specificity;Antimetabolites, Antineoplastic;Retroviridae;Pancreatic Neoplasms;Deoxycytidine;Cell Nucleus;Antineoplastic Agents;Thymidine;Research Support, Non-U.S. Gov't;Antiviral Agents;Humans;Phosphorylation;Catalysis},
	Medline = {20564273},
	Month = {12},
	Nlm_Id = {2985121R},
	Number = {50},
	Organization = {Karolinska Institute, Division of Clinical Virology, Huddinge University Hospital, S-141 86 Stockholm, Sweden.},
	Pages = {39125-9},
	Pii = {M006212200},
	Pubmed = {10993893},
	Title = {Retroviral transduction of cancer cell lines with the gene encoding Drosophila melanogaster multisubstrate deoxyribonucleoside kinase},
	Uuid = {84ADFAD7-4C2E-4AF1-A929-F5A51DE50289},
	Volume = {275},
	Year = {2000},
	Bdsk-Url-1 = {http://dx.doi.org/10.1074/jbc.M006212200}}

@article{Zheng:2006,
	Abstract = {In the rodent hippocampus, the radial glial scaffold consists of radial glial cells (RGCs) and plays important roles in neurogenesis in this area after birth. However, the mechanisms that maintain the radial glial scaffold in the postnatal dentate gyrus (DG) area remain elusive. In the present work, we studied the role of Neuregulin (NRG) in the formation and maintenance of the radial glial scaffold in the hippocampal DG of postnatal rats using slice culture. We found that ErbB4 receptors were expressed in vimentin-positive RGCs in DG of postnatal day 6 (P6) rats. Treatment with NRG and Ab-3, the inhibitor of ErbB4, revealed that in P6 rats exogenous NRG promoted the proliferation of Vimentin-positive RGCs in DG. On the other hand, endogenous NRG was found necessary for maintaining the characteristic morphological and immunohistochemical features of these cells. These results indicated that NRG plays a critical role in the formation and maintenance of the radial glial scaffold in the hippocampal DG of postnatal rats. J. Cell. Physiol. (c) 2006 Wiley-Liss, Inc.},
	Author = {Zheng, and Feng,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0021-9541},
	Journal = {J Cell Physiol},
	Keywords = {10 Development;10 Hippocampus;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {0050222},
	Organization = {Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.},
	Pubmed = {16456862},
	Title = {Neuregulin regulates the formation of radial glial scaffold in hippocampal dentate gyrus of postnatal rats},
	Uuid = {A03D5AFB-8E5E-45CF-B4F8-5170AF77469B},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jcp.20591}}

@article{Zhong:1996,
	Abstract = {During Drosophila neurogenesis, differential segregation of Numb is necessary for daughter cells of asymmetric divisions to adopt distinct fates, at least partly by biasing the Notch-mediated cell-cell interaction. We have isolated a highly conserved mammalian homolog of Drosophila numb, m-numb. During mouse cortical neurogenesis, m-Numb is asymmetrically localized to the apical membrane of dividing ventricular neural progenitors. Depending upon the orientation of the cleavage plane, m-Numb may be distributed into one or both of the daughter cells. When expressed in Drosophila embryos, m-Numb is localized asymmetrically in dividing neural precursors and rescues the numb mutant phenotype. Furthermore, m-Numb can physically interact with mouse Notch1. We propose that some shared molecular mechanisms, both cell-intrinsic and cell-extrinsic, generate asymmetric cell divisions during neurogenesis of vertebrates and invertebrates. 0896-6273 Journal Article},
	Author = {Zhong, W. and Feder, J. N. and Jiang, M. M. and Jan, L. Y. and Jan, Y. N.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Neuron},
	Keywords = {10 Development;Tissue Distribution;Animals;Sequence Homology, Amino Acid;Rats;Mice/*embryology;*Embryo and Fetal Development;Mutation;Membrane Proteins/metabolism;Support, Non-U.S. Gov't;Embryo/metabolism;Cell Membrane/metabolism;Support, U.S. Gov't, P.H.S.;Juvenile Hormones/genetics/*metabolism;Drosophila;Cell Division;Amino Acid Sequence;Molecular Sequence Data;Neurons/metabolism;Receptors, Cell Surface/metabolism;Cerebral Cortex/cytology/*embryology/*metabolism;F},
	Number = {1},
	Organization = {Howard Hughes Medical Institute, University of California, San Francisco 94143-0724, USA.},
	Pages = {43-53},
	Pubmed = {8755477},
	Title = {Asymmetric localization of a mammalian numb homolog during mouse cortical neurogenesis},
	Uuid = {939273D9-778E-4996-8F1F-EAD6CA7D8600},
	Volume = {17},
	Year = {1996},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8755477}}

@article{Zhong:2003,
	Abstract = {A key question in developmental neurobiology is how the diversity of cell types that make up the mature nervous system are generated from a common set of progenitor cells. Drosophila genes governing temporal cell fate determination and asymmetric cell divisions involving numb may represent evolutionarily conserved mechanisms for regulating cell fate diversification in the developing nervous system. 0896-6273 Journal Article Review Review, Tutorial},
	Author = {Zhong, W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Neuron},
	Keywords = {Juvenile Hormones/genetics/metabolism;Cell Differentiation/*physiology;10 Development;Cell Lineage/*physiology;Human;Neurons/*cytology/physiology;Stem Cells/*cytology/physiology;Nervous System/cytology/*embryology;Nerve Tissue Proteins/genetics/metabolism;F;Cell Division/*physiology;Animals;Drosophila melanogaster/cytology/embryology/physiology},
	Number = {1},
	Organization = {Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06511, USA. weimin.zhong\@yale.edu},
	Pages = {11-4},
	Pubmed = {12526768},
	Title = {Diversifying neural cells through order of birth and asymmetry of division},
	Uuid = {AD3DDDB1-3EAF-4790-9F71-0167B7A99133},
	Volume = {37},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12526768}}

@article{Zhou:2002,
	Abstract = {OLIG1 and OLIG2 are basic-helix-loop-helix (bHLH) transcription factors expressed in the pMN domain of the spinal cord, which sequentially generates motoneurons and oligodendrocytes. In Olig1/2 double-mutant mice, motoneurons are largely eliminated, and oligodendrocyte differentiation is abolished. Lineage tracing data suggest that Olig1(-/-)2(-/-) pMN progenitors instead generate V2 interneurons and then astrocytes. This apparent conversion likely reflects independent roles for OLIG1/2 in specifying motoneuron and oligodendrocyte fates. Olig genes therefore couple neuronal and glial subtype specification, unlike proneural bHLH factors that control the neuron versus glia decision. Our results suggest that in the spinal cord, Olig and proneural genes comprise a combinatorial code for the specification of neurons, astrocytes, and oligodendrocytes, the three fundamental cell types of the central nervous system. 0092-8674 Journal Article},
	Author = {Zhou, Q. and Anderson, D. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Cell},
	Keywords = {Nerve Tissue Proteins/*deficiency/genetics/metabolism;Neuroglia/cytology/*metabolism;Transcription Factors/deficiency/genetics/metabolism;Animals;Helix-Loop-Helix Motifs/genetics;Neurons/cytology/*metabolism;Female;Cell Lineage/*physiology;Interneurons/cytology/metabolism;G abstr;11 Glia;Male;Oligodendroglia/cytology/metabolism;Cell Differentiation/*physiology;Stem Cells/cytology/*metabolism;Astrocytes/cytology/metabolism;Rhombencephalon/cytology/embryology/metabolism;Mutation/physiology;Homeodomain Proteins/genetics/metabolism;Spinal Cord/cytology/*embryology/metabolism;Mice, Knockout;Support, U.S. Gov't, P.H.S.;Motor Neurons/cytology/metabolism;Mice},
	Number = {1},
	Organization = {Division of Biology 216-76, California Institute of Technology, Pasadena, CA 91125, USA.},
	Pages = {61-73},
	Pubmed = {11955447},
	Title = {The bHLH transcription factors OLIG2 and OLIG1 couple neuronal and glial subtype specification},
	Uuid = {11B34EA1-6852-4CE8-802E-665D363038E3},
	Volume = {109},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11955447}}

@article{Zhou:2004,
	Abstract = {Mice with mutations in the Wnt coreceptor low-density lipoprotein receptor-related protein-6 (LRP6) have a smaller and severely disorganized dorsal thalamus and lack thalamocortical projections. Using molecular markers, we showed that most dorsal thalamic and epithalamic neurons were missing, and most of the major dorsal thalamic nuclei were not identifiable. However, the ventral thalamus was essentially unaffected, although the dorsal thalamic defect leads to rostral displacement of portions of the ventral thalamus. Analysis of younger embryos showed that epithalamic and dorsal thalamic neurons were not produced at early stages of development, whereas ventral thalamic neurons were still produced. These defects were accompanied by improper formation of the boundary between dorsal and ventral thalamus, the zona limitans interthalamica (ZLI). Furthermore, the expression of an early marker of posterior forebrain development that marks the compartment from the midbrain-hindbrain junction to the ZLI (including the future dorsal thalamus, pretectum, and midbrain) was disrupted, supporting the idea that diencephalic development is abnormal from very early in embryogenesis. This study provides compelling in vivo evidence that thalamic development requires normal activity of the LRP6-mediated canonical Wnt signaling pathway.},
	Author = {Zhou, Cheng-Ji J. and Pinson, Kathleen I. and Pleasure, Samuel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Cytoskeletal Proteins;10 Development;Signal Transduction;Animals;10 Hippocampus;Trans-Activators;Thalamic Nuclei;Diencephalon;Receptors, LDL;Wnt Proteins;LDL-Receptor Related Proteins;Research Support, U.S. Gov't, P.H.S.;Thalamus;Intercellular Signaling Peptides and Proteins;Mice, Knockout;Morphogenesis;Mice;Proto-Oncogene Proteins;beta Catenin;Gestational Age;Research Support, Non-U.S. Gov't},
	Month = {9},
	Nlm_Id = {8102140},
	Number = {35},
	Organization = {Department of Neurology, Program in Neuroscience, University of California, San Francisco 94143-0435, USA.},
	Pages = {7632-9},
	Pii = {24/35/7632},
	Pubmed = {15342729},
	Title = {Severe defects in dorsal thalamic development in low-density lipoprotein receptor-related protein-6 mutants},
	Uuid = {659D0E96-FD90-4552-94ED-516D3D9A8375},
	Volume = {24},
	Year = {2004},
	url = {papers/Zhou_JNeurosci2004a.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.2123-04.2004}}

@article{Zhou:2004a,
	Abstract = {LRP6 mutant mice have generalized defects in the Wnt/beta-catenin signaling pathway because of the crucial function of LRP6 as a Wnt signaling co-receptor (Pinson et al., 2000). We examined the hippocampal phenotype of single LRP6 mutant mice as well as LRP6/Lef1 double mutant mice. LRP6 mutants had reduced production of dentate granule neurons and abnormalities of the radial glial scaffolding in the forming dentate gyrus. These defects were more severe with the addition of a single Lef1 null allele to an LRP6 null background. Pyramidal cell fields were unaffected in the LRP6, Lef1, or double mutants. The dentate defects were accompanied by decreased numbers of mitotic precursors in the migratory pathway to the dentate and in the displaced proliferative zone in the dentate itself. At earlier gestational ages, there was a reduction in the number of dentate granule cell progenitors in the dentate ventricular zone before the emigration of the earliest differentiated granule neurons and precursors to form the dentate anlage.},
	Author = {Zhou, Cheng-Ji J. and Zhao, Chunjie and Pleasure, Samuel J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {10 Development;Signal Transduction;Animals;Transcription Factors;DNA-Binding Proteins;10 Hippocampus;Receptors, LDL;Phenotype;Wnt Proteins;Research Support, U.S. Gov't, P.H.S.;Alleles;Mice, Knockout;Neurons;Lymphoid Enhancer-Binding Factor 1;Neuroglia;Dentate Gyrus;Zebrafish Proteins;Mice;Proto-Oncogene Proteins;Stem Cells;Research Support, Non-U.S. Gov't},
	Month = {1},
	Nlm_Id = {8102140},
	Number = {1},
	Organization = {Department of Neurology, Programs in Neuroscience and Developmental Biology, University of California, San Francisco, California 94143-0435, USA.},
	Pages = {121-6},
	Pii = {24/1/121},
	Pubmed = {14715945},
	Title = {Wnt signaling mutants have decreased dentate granule cell production and radial glial scaffolding abnormalities},
	Uuid = {E0841C8C-7113-11DA-9A4D-000D9346EC2A},
	Volume = {24},
	Year = {2004},
	url = {papers/Zhou_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.4071-03.2004}}

@article{Zhou:1999,
	Abstract = {Chicken ovalbumin upstream promotor-transcription factor I (COUP-TFI), an orphan member of the nuclear receptor superfamily, is highly expressed in the developing nervous systems. In the cerebral cortex of Coup-tfl mutants, cortical layer IV was absent due to excessive cell death, a consequence of the failure of thalamocortical projections. Moreover, subplate neurons underwent improper differentiation and premature cell death during corticogenesis. Our results indicate that the subplate neuron defects lead to the failure of guidance and innervation of thalamocortical projections. Thus, our findings demonstrate a critical role of the subplate in early corticothalamic connectivity and confirm the importance of afferent innervation for the survival of layer IV neurons. These results also substantiate COUP-TFI as an important regulator of neuronal development and differentiation.},
	Author = {Zhou, C. and Qiu, Y. and Pereira, F. A. and Crair, M. C. and Tsai, S. Y. and Tsai, M. J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0896-6273},
	Journal = {Neuron},
	Keywords = {Fluorescent Dyes;Cell Differentiation;Animals;Transcription Factors;DNA-Binding Proteins;Neural Pathways;Axons;Mutation;research support, non-u.s. gov't;Antimetabolites;Male;In Situ Hybridization;COUP Transcription Factor I;Thalamus;Cerebral Cortex;Neurons;research support, u.s. gov't, p.h.s.;Carbocyanines;Mice;24 Pubmed search results 2008;Immunohistochemistry;Bromodeoxyuridine;Cell Death;Receptors, Glucocorticoid},
	Month = {12},
	Nlm_Id = {8809320},
	Number = {4},
	Organization = {Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.},
	Pages = {847-59},
	Pii = {S0896-6273(00)81032-6},
	Pubmed = {10624948},
	Title = {The nuclear orphan receptor COUP-TFI is required for differentiation of subplate neurons and guidance of thalamocortical axons},
	Uuid = {A985017D-B453-44FD-9331-5E20029DBB1B},
	Volume = {24},
	Year = {1999}}

@article{Zhou:2006a,
	Abstract = {To better understand the function of the Wnt pathway in the developing telencephalon, we analyzed neocortical development in low density lipoprotein receptor-related protein (LRP) 6 mutants. LRP6 mutant mice are hypomorphic for the canonical Wnt signaling pathway and have hypoplasia of the developing neocortex. While early telencephalic morphogenesis is largely intact in these mice, probably due to compensation by LRP5, the mutant mice develop a dramatically thinner cortical plate. There is a prominent reduction of neurogenesis leading to a thin cortical plate. Reduced proliferation late in gestation probably also contributes to the hypoplasia. Although there are marked decreases in the numbers of layer 6 and layers 2-4 neurons all laminar identities are generated and there is no evidence of compensatory increases in layer 5 neurons. In addition, LRP6 mutants have partial penetrance of a complex of cortical dysmorphologies resembling those found in patients with developmental forms of epilepsy and mental retardation. These include ventricular and marginal zone heterotopias and cobblestone lissencephaly. This analysis demonstrates that canonical Wnt signaling is required for a diverse array of developmental processes in the neocortex in addition to the previously known roles in regulating precursor proliferation and patterning.},
	Author = {Zhou, and Borello, and Rubenstein, and Pleasure,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:35 -0400},
	Issn = {0306-4522},
	Journal = {Neuroscience},
	Keywords = {24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {7605074},
	Organization = {UCSF Mission Bay, Box 2722, Rock Hall, Department of Neurology, 1550 Fourth Street, Room RH-348D, San Francisco, CA 94143-2722, USA; Department of Psychiatry, Programs in Neuroscience and Developmental Biology, University of California, San Francisco, CA, USA.},
	Pii = {S0306-4522(06)00932-8},
	Pubmed = {16920270},
	Title = {Neuronal production and precursor proliferation defects in the neocortex of mice with loss of function in the canonical Wnt signaling pathway},
	Uuid = {51F17DD5-2712-4910-99F2-ECAA2F563EDB},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuroscience.2006.07.007}}

@article{Zhu:1999,
	Abstract = {0002-9440 Journal Article Review Review, Tutorial},
	Author = {Zhu, X. and Raina, A. K. and Smith, M. A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Am J Pathol},
	Keywords = {Mice, Neurologic Mutants/*genetics;Mutation;*Cell Cycle;Cell Differentiation;Neurodegenerative Diseases/*pathology;Cerebellum/pathology;EE pdf;Neurons/pathology/*physiology;08 Aberrant cell cycle;Cell Death;Animals;Disease Models, Animal;Mice;*Cell Division;Potassium Channels/genetics},
	Number = {2},
	Organization = {Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.},
	Pages = {327-9},
	Pubmed = {10433924},
	Title = {Cell cycle events in neurons. Proliferation or death?},
	Uuid = {590B7AA2-D037-4A94-A082-56521B4E55B6},
	Volume = {155},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10433924}}

@article{Zhu:2003,
	Abstract = {Proliferating cells are hardly detectable in the adult mammalian brain by microscopy of stained sections, but after pre-labeling with radioactive thymidine or 5'-bromo-2-deoxyuridine (BrdU), either marks the nucleus, as do mitosis-related proteins such as Ki67 and PCNA. Engineered virus may also be used to mark proliferating cells. One alternative approach is to use the enzyme ribonucleotide reductase (RNR), expressed by proliferating cells, but not by quiescent ones. A monoclonal antibody against the M1 subunit of RNR was used to visualize proliferating cells in the brains of adult normal rats, rabbits, pigs and sheep. Stem cells were distinctly outlined. In the subgranular layer in the hippocampal dentate gyrus, most RNR immunoreactive cells were bipolar to multipolar, and had a large cell body and long processes. Two different populations of RNR expressing cells were visualized in the subventricular zone in the forebrain, one dominated by small, bipolar cells extending into the rostral migratory stream, while the other was formed by large multipolar cells, adjacent to the ependyma, with processes extending to the lateral ventricle. Furthermore, rare RNR-expressing cells were recognized throughout the brain. The RNR immunoreactive cells were immature, as they did not express any marker characterizing differentiated neurons and glial cells, except for a fraction that co-expressed the gliofibrillary acidic protein. BrdU and RNR were co-localized in proliferating cells in animals pretreated with BrdU. We conclude that RNR immunohistochemistry can accurately visualize proliferating cells, including stem cells, in adult mammalian brains. The occurrence of processes at cell proliferation is elucidated. Further, the advocated approach does not require any pre-labeling, and can be carried out on fixed tissues.},
	Author = {Zhu, Hong and Wang, Zhan-You Y. and Hansson, Hans-Arne A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0006-8993},
	Journal = {Brain Res},
	Keywords = {Rabbits;Protein Subunits;Animals;Rats;Microscopy, Confocal;Radiation-Sensitizing Agents;Comparative Study;Brain;Female;Sheep;Swine;23 Technique;Species Specificity;Calcium-Binding Protein, Vitamin D-Dependent;Neurofilament Proteins;Male;01 Adult neurogenesis general;Ribonucleotide Reductases;Support, Non-U.S. Gov't;Cell Division;Immunohistochemistry;Bromodeoxyuridine;Stem Cells;Biological Markers;Glial Fibrillary Acidic Protein},
	Medline = {22718792},
	Month = {7},
	Nlm_Id = {0045503},
	Number = {2},
	Organization = {Institute of Anatomy and Cell Biology, G{\"o}teborg University, P.O. Box 420, SE 40530 Gothenburg, Sweden.},
	Pages = {180-9},
	Pii = {S0006899303026271},
	Pubmed = {12834878},
	Title = {Visualization of proliferating cells in the adult mammalian brain with the aid of ribonucleotide reductase},
	Uuid = {7D277A51-B07E-4755-9E6D-A3016CD005C2},
	Volume = {977},
	Year = {2003},
	url = {papers/Zhu_BrainRes2003.pdf}}

@article{Zhu:2005,
	Abstract = {Neural stem cells (NSCs) are present not only in the developing nervous systems, but also in the adult human central nervous system (CNS). It is long thought that the subventricular zone of the lateral ventricles and the dentate gyrus of the hippocampus are the main sources of human adult NSCs, which are considered to be a reservoir of new neural cells. Recently adult NSCs with potential neural capacity have been isolated from white matter and inferior prefrontal subcortex in the human brain. Rapid advances in the stem cell biology have raised appealing possibilities of replacing damaged or lost neural cells by transplantation of in vitro-expanded stem cells and/or their neuronal progeny. However, sources of stem cells, large scale expansion, control of the differentiations, and tracking in vivo represent formidable challenges. In this paper we review the characteristics of the adult human NSCs, their potentiality in terms of proliferation and differentiation capabilities, as well as their large scale expansion for clinical needs. This review focuses on the major advances in brain stem cell-based therapy from the clinical perspective, and summarizes our work in clinical phase I-II trials with autologuous transplantation of adult NSCs for patients with open brain trauma. It also describes multiple approaches to monitor adult human NSCs labeled superparamagnetic nanoparticles after transplantation and explores the intriguing possibility of stem cell transplantation.},
	Author = {Zhu, J. and Wu, X. and Zhang, H. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:46 -0400},
	Issn = {1389-4501},
	Journal = {Curr Drug Targets},
	Keywords = {delete_this;24 Pubmed search results 2008},
	Month = {2},
	Nlm_Id = {100960531},
	Number = {1},
	Organization = {Department of Neurosurgery, Fudan University Huashan Hospital, 12 Wulumuqi Zhong Road, Shanghai, 200040, China. jzhu\@fudan.edu.cn.},
	Pages = {97-110},
	Pubmed = {15720217},
	Title = {Adult neural stem cell therapy: expansion in vitro, tracking in vivo and clinical transplantation},
	Uuid = {4F721768-1537-46C7-A1A8-0F146BB9633C},
	Volume = {6},
	Year = {2005}}

@article{Zhu:1999a,
	Abstract = {Formation of the normal mammalian cerebral cortex requires the migration of GABAergic inhibitory interneurons from an extracortical origin, the lateral ganglionic eminence (LGE). Mechanisms guiding the migratory direction of these neurons, or other neurons in the neocortex, are not well understood. We have used an explant assay to study GABAergic neuronal migration and found that the ventricular zone (VZ) of the LGE is repulsive to GABAergic neurons. Furthermore, the secreted protein Slit is a chemorepellent guiding the migratory direction of GABAergic neurons, and blockade of endogenous Slit signaling inhibits the repulsive activity in the VZ. These results have revealed a cellular source of guidance for GABAergic neurons, demonstrated a molecular cue important for cortical development, and suggested a guidance mechanism for the migration of extracortical neurons into the neocortex.},
	Author = {Zhu, Y. and Li, H. and Zhou, L. and Wu, J. Y. and Rao, Y.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Neuron},
	Keywords = {Fetus/cytology;Rats, Sprague-Dawley;Rats;Corpus Striatum/*cytology/embryology;Neurons/chemistry/*cytology;Cell Communication/physiology;Animal;Neocortex/*cytology/embryology;Organ Culture;Cell Movement/*physiology;Support, Non-U.S. Gov't;12 Interneuron development;GABA/*physiology;H},
	Number = {3},
	Organization = {Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.},
	Pages = {473-85.},
	Title = {Cellular and molecular guidance of GABAergic neuronal migration from an extracortical origin to the neocortex},
	Uuid = {D9D42D89-8A34-4A8C-9724-92556AF33CAF},
	Volume = {23},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10433260}}

@article{Ziegelhoeffer:2004,
	Abstract = {Bone marrow-Derived cells have been proposed to form new vessels or at least incorporate into growing vessels in adult organisms under certain physiological and pathological conditions. We investigated whether bone marrow-Derived cells incorporate into vessels using mouse models of hindlimb ischemia (arteriogenesis and angiogenesis) and tumor growth. C57BL/6 wild-type mice were lethally irradiated and transplanted with bone marrow cells from littermates expressing enhanced green fluorescent protein (GFP). At least 6 weeks after bone marrow transplantation, the animals underwent unilateral femoral artery occlusions with or without pretreatment with vascular endothelial growth factor or were subcutaneously implanted with methylcholanthrene-induced fibrosarcoma (BFS-1) cells. Seven and 21 days after surgery, proximal hindlimb muscles with growing collateral arteries and ischemic gastrocnemius muscles as well as grown tumors and various organs were excised for histological analysis. We failed to colocalize GFP signals with endothelial or smooth muscle cell markers. Occasionally, the use of high-power laser scanning confocal microscopy uncovered false-positive results because of overlap of different fluorescent signals from adjacent cells. Nevertheless, we observed accumulations of GFP-positive cells around growing collateral arteries (3-fold increase versus nonoccluded side, P<0.001) and in ischemic distal hindlimbs. These cells were identified as fibroblasts, pericytes, and primarily leukocytes that stained positive for several growth factors and chemokines. Our findings suggest that in the adult organism, bone marrow-Derived cells do not promote vascular growth by incorporating into vessel walls but may function as supporting cells.},
	Author = {Ziegelhoeffer, Tibor and Fernandez, Borja and Kostin, Sawa and Heil, Matthias and Voswinckel, Robert and Helisch, Armin and Schaper, Wolfgang},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {1524-4571},
	Journal = {Circ Res},
	Keywords = {Ischemia;Research Support, Non-U.S. Gov't;Cell Differentiation;Animals;Blood Vessels;Fibrosarcoma;Pericytes;Microscopy, Confocal;Ligation;Neoplasm Transplantation;Fibroblasts;Mice, Transgenic;Mice, Inbred C57BL;11 Glia;Green Fluorescent Proteins;Neovascularization, Physiologic;Radiation Chimera;Femoral Artery;Neovascularization, Pathologic;Bone Marrow Cells;Leukocytes;Organ Specificity;Hindlimb;Mice;Muscle, Smooth, Vascular;Genes, Reporter;Luminescent Proteins;Endothelium, Vascular},
	Month = {2},
	Nlm_Id = {0047103},
	Number = {2},
	Organization = {Max-Planck-Institute for Clinical &Physiological Research, Bad Nauheim, Germany. t.ziegelhoeffer\@kerckhoff.mpg.de},
	Pages = {230-8},
	Pii = {01.RES.0000110419.50982.1C},
	Pubmed = {14656934},
	Title = {Bone marrow-derived cells do not incorporate into the adult growing vasculature},
	Uuid = {0BE91453-FBD2-4D41-8E4B-2F2D5AF921EF},
	Volume = {94},
	Year = {2004},
	Bdsk-Url-1 = {http://dx.doi.org/10.1161/01.RES.0000110419.50982.1C}}

@article{Zietlow:1999,
	Abstract = {When embryonic dopaminergic neurons are transplanted into the adult brain, approximately 95\%die within a few days. To assess whether microglia activated during transplantation might be responsible for this rapid death, we examined the effect of microglia on rat embryonic dopaminergic neurons in vitro. Conditioned medium from 7-day-old microglia was found to decrease the number of dopamine neurons surviving in primary culture, but activation of the microglia with N-formyl-methionyl-leucyl-phenylalanine (FMLP) or Zymosan A did not increase the toxicity of the conditioned medium. We next tested the effect of coculturing microglia and dopaminergic neurons by placing microglia in semipermeable well inserts over the neuronal cultures. The presence of microglia now increased dopaminergic neuronal survival, microglial activation again having no effect. To increase yet further the possible interactions between microglia and neurons, the mesencephalic cells and microglia were mixed together and placed as a tissue in three-dimensional culture, and here again the presence of microglia increased dopaminergic neuronal survival with no effect of activation. Contact of microglia with the mesencephalic cells therefore converted them from being toxic to dopaminergic neurons to promoting their survival. The change in microglial effect from toxic to protective was caused by soluble molecules secreted by cells in the neuronal cultures, as conditioned medium derived from microglia-neuronal cocultures also had a dopaminergic neuron survival effect, indicating that microglia in cocultures behave differently from microglia removed from neuronal and glial influence. Microglia cocultured with either neurons or astrocytes downregulated inducible nitric oxide synthase (iNOS), indicating a decrease in the production of nitric oxide and possibly other toxic molecules. These findings indicate that in their natural environment, microglia are likely to be beneficial for the survival of embryonic dopaminergic grafts.},
	Author = {Zietlow, R. and Dunnett, S. B. and Fawcett, J. W.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Cell Survival;Pregnancy;Dopamine;Neurotoxins;Animals;Cells, Cultured;Brain Tissue Transplantation;Rats;Neuroprotective Agents;Female;Cell Communication;Rats, Sprague-Dawley;Culture Media, Conditioned;Microglia;Not relevant;Fetal Tissue Transplantation;11 Glia;Nitric-Oxide Synthase;Substantia Nigra;Support, Non-U.S. Gov't;Cerebral Cortex;Neurons;Zymosan;N-Formylmethionine Leucyl-Phenylalanine;Cell Culture;Graft Survival},
	Medline = {99233957},
	Month = {5},
	Nlm_Id = {8918110},
	Number = {5},
	Organization = {MRC Cambridge Centre for Brain Repair, University of Cambridge, UK.},
	Pages = {1657-67},
	Pubmed = {10215919},
	Title = {The effect of microglia on embryonic dopaminergic neuronal survival in vitro: diffusible signals from neurons and glia change microglia from neurotoxic to neuroprotective},
	Uuid = {2F5111C6-B078-4167-9A19-6D55E3BE3D84},
	Volume = {11},
	Year = {1999},
	url = {papers/Zietlow_EurJNeurosci1999.pdf}}

@article{Zigova:1998,
	Abstract = {We have investigated the suitability of a recently identified and characterized population of neuronal progenitor cells for their potential use in the replacement of degenerating or damaged neurons in the mammalian brain. The unique population of neuronal progenitor cells is situated in a well-delineated region of the anterior part of the neonatal subventricular zone (referred to as SVZa). This region can be separated from the remaining proliferative, gliogenic, subventricular zone encircling the lateral ventricles of the forebrain. Because the neurons arising from the highly enriched neurogenic progenitor cell population of the SVZa ordinarily migrate considerable distances and ultimately express the neurotransmitters GABA and dopamine, we have examined whether they could serve as an alternative source of tissue for neural transplantation. SVZa cells from postnatal day 0-2 rats, prelabeled by intraperitoneal injections of the cell proliferation marker BrdU, were implanted into the striatum of adult rats approximately 1 mo after unilateral denervation by 6-OHDA. To examine the spatio-temporal distribution and phenotype of the transplanted SVZa cells, the experimental recipients were perfused at short (less than 1 wk), intermediate (2-3 wk) and long (5 mo) postimplantation times. The host brains were sectioned and stained with an antibody to BrdU and one of several cell-type specific markers to determine the phenotypic characteristics of the transplanted SVZa cells. To identify neurons we used the neuron-specific antibody TuJ1, or antimembrane-associated protein 2 (MAP-2), and anti-GFAP was used to identify astrocytic glia. At all studied intervals the majority of the surviving SVZa cells exhibited a neuronal phenotype. Moreover, morphologically they could be distinguished from the cells of the host striatum because they resembled the intrinsic granule cells of the olfactory bulb, their usual fate. At longer times, a greater number of the transplanted SVZa cells had migrated from their site of implantation, often towards an outlying blood vessel, and the density of cells within the core of the transplant was reduced. Furthermore, there were rarely signs of transplant rejection or a glial scar surrounding the transplant. In the core of the transplant there were low numbers of GFAP-positive cells, indicating that the transplanted SVZa cells, predominantly TuJ1- positive/MAP2-positive, express a neuronal phenotype. Collectively, the propensity of the SVZa cells to express a neuronal phenotype and to survive and integrate in the striatal environment suggest that they may be useful in the reconstruction of the brain following CNS injury or disease.},
	Author = {Zigova, T. and Pencea, V. and Betarbet, R. and Wiegand, S. J. and Alexander, C. and Bakay, R. A. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Issn = {0963-6897},
	Journal = {Cell Transplant},
	Keywords = {Cell Differentiation;Cerebral Ventricles;L abstr;Cell Survival;24 Pubmed search results 2008;Corpus Striatum;Oxidopamine/toxicity;Interneurons;Bromodeoxyuridine/metabolism;Animals;Cerebral Ventricles/cytology;Research Support, U.S. Gov't, P.H.S.;Cell Movement;Brain Tissue Transplantation;Phenotype;Cell Count;Bromodeoxyuridine;Oxidopamine;Olfactory Bulb;Corpus Striatum/drug effects/*pathology/*transplantation;Neurons/metabolism/*pathology;Brain Tissue Transplantation/*pathology/physiology;Support, U.S. Gov't, P.H.S.;Interneurons/cytology;Animal;Rats, Sprague-Dawley;17 Transplant Regeneration;Rats;Olfactory Bulb/cytology;Animals, Newborn;Stem Cells;Support, Non-U.S. Gov't;Research Support, Non-U.S. Gov't;Neurons;Stem Cells/metabolism/*pathology},
	Medline = {98248010},
	Nlm_Id = {9208854},
	Number = {2},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, GA 30322, USA.},
	Pages = {137-56.},
	Pii = {S0963689798000098},
	Pubmed = {9588596},
	Title = {Neuronal progenitor cells of the neonatal subventricular zone differentiate and disperse following transplantation into the adult rat striatum},
	Uuid = {2DAEB83A-1C3E-41DB-9120-3BB46337B65F},
	Volume = {7},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9588596}}

@article{Zigova:1996,
	Abstract = {The cells arising in the anterior part of the subventricular zone (SVZa) migrate along a well-demarcated pathway which lacks radial glial fibers to the olfactory bulb where they differentiate into interneurons of the granule cell layer or glomerular layer (Luskin, 1993, Neuron 11, 173). To analyze the mechanisms underlying this highly directed migration, we have compared the migratory behavior of unmanipulated SVZa-derived cells to that of homotopically transplanted SVZa cells and of heterotopically transplanted telencephalic ventricular zone (VZ) cells that ordinarily migrate in association with radial glial fibers. To identify the phenotype of the SVZa progenitor cells prior to their transplantation, we characterized them in vitro using cell type-specific markers. After 1 day in culture nearly all the SVZa cells were stained with TuJ1, a neuron-specific marker; only an occasional cell exhibited a glial phenotype as judged by the presence of GFAP-immunoreactivity. This indicates that SVZa cells express a neuronal phenotype. To reveal the spatiotemporal distribution of homotopically transplanted neonatal SVZa cells in a host brain, dissociated SVZa cells from Postnatal Day 0 (P0)-P2 animals were labeled with the lipophilic dye PKH26 or the cell proliferation marker BrdU and implanted into the SVZa of host animals of the same age. Within the first week after transplantation there were vast numbers of labeled cells throughout the pathway. Over the next 2 weeks the labeled cells migrated into the overlying cellular layer of the olfactory bulb and began to differentiate, and within 4 weeks the transplanted cells had reached their final positions in the granule cell and glomerular layers of the olfactory bulb in the same proportions as for unmanipulated SVZa-derived cells. While en route to the olfactory bulb the homotopically transplanted cells never strayed from the migratory pathway. In contrast, heterotopically transplanted VZ cells from the embryonic telencephalon did not undergo migration although they did differentiate. These results demonstrate that the homotopically transplanted SVZa-derived cells adopt a mode of migration indistinguishable from that ordinarily utilized by SVZa-derived neurons and that the VZ cells are unable to decipher the same set of guidance cues.},
	Author = {Zigova, T. and Betarbet, R. and Soteres, B. J. and Brock, S. and Bakay, R. A. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0012-1606},
	Journal = {Dev Biol},
	Keywords = {Research Support, Non-U.S. Gov't;Telencephalon;17 Transplant Regeneration;Cell Transplantation;Rats, Sprague-Dawley;Phenotype;Rats;Research Support, U.S. Gov't, P.H.S.;Stem Cells;Cell Survival;Olfactory Bulb;Animals, Newborn;Transplantation, Heterotopic;Cells, Cultured;Animals;Cell Movement;Neurons},
	Medline = {96187867},
	Month = {2},
	Nlm_Id = {0372762},
	Number = {2},
	Organization = {Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.},
	Pages = {459-74},
	Pii = {S0012-1606(96)90040-8},
	Pubmed = {8606005},
	Title = {A comparison of the patterns of migration and the destinations of homotopically transplanted neonatal subventricular zone cells and heterotopically transplanted telencephalic ventricular zone cells},
	Uuid = {FBEBFC97-D067-11DA-8A8C-000D9346EC2A},
	Volume = {173},
	Year = {1996},
	Bdsk-Url-1 = {http://dx.doi.org/10.1006/dbio.1996.0040}}

@article{Zigova:1998a,
	Abstract = {We have previously demonstrated that the most rostral part of the subventricular zone (SVZ) is a source of neuronal progenitor cells whose progeny are destined to become interneurons of the olfactory bulb. To determine whether the number of newly generated neurons in the adult olfactory bulb could be increased by the administration of an exogenous factor, brain-derived neurotrophic factor (BDNF) was infused for 12 days into the right lateral ventricle of adult rat brains. The production of new cells was monitored by either the intraventricular infusion or intraperitoneal injection of the cell proliferation marker BrdU. In both experimental paradigms we observed significantly more BrdU-labeled cells in the olfactory bulbs on the BDNF-infused side than in the olfactory bulb of PBS-infused animals. Analysis of the BDNF- infused brains of animals injected intraperitoneally with BrdU demonstrated a 100\%increase in the number of BrdU-labeled cells in the bulb, the preponderance ( approximately 90\%) of which were double- labeled with a neuron-specific antibody. These results demonstrate that the generation and/or survival of new neurons in the adult brain can be increased substantially by an exogenous factor. Furthermore, the SVZ, and in particular the rostral part, may constitute a reserve pool of progenitor cells available for neuronal replacement in the diseased or damaged brain.},
	Author = {Zigova, T. and Pencea, V. and Wiegand, S. J. and Luskin, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Journal = {Mol Cell Neurosci},
	Keywords = {Olfactory Bulb/cytology/*drug effects;Receptor, Ciliary Neurotrophic Factor;Rats;Stem Cells/cytology/*drug effects;Brain-Derived Neurotrophic Factor/administration &dosage/*pharmacology;Cell Count;Rats, Sprague-Dawley;Animal;Injections, Intraventricular;Bromodeoxyuridine/administration &dosage/pharmacology;Cell Lineage;Receptor Protein-Tyrosine Kinases/biosynthesis/genetics;Support, Non-U.S. Gov't;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Nerve Tissue Proteins/biosynthesis/genetics;C pdf;Injections, Intraperitoneal;Cell Division/drug effects;Receptors, Nerve Growth Factor/biosynthesis/genetics},
	Number = {4},
	Organization = {Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia, 30322, USA.},
	Pages = {234-45.},
	Title = {Intraventricular administration of BDNF increases the number of newly generated neurons in the adult olfactory bulb},
	Uuid = {BAAD845B-B595-42D4-A132-A1170B654016},
	Volume = {11},
	Year = {1998},
	url = {papers/Zigova_MolCellNeurosci1998}}

@article{Zimmer:2004,
	Abstract = {Projection neurons destined for the cortical plate are generated sequentially from the proliferative ventricular and subventricular zones (VZ/SVZ) of the pallium. However, the respective contribution of both proliferative zones to the generation of cortical plate neurons is better established in humans and non-human primates than in rodents. We identified Cux2 as a new marker for murine cortical subpopulations and used it to provide new insights to the development of the mouse cortex. Cux2 is an orthologue of the Drosophila cut gene, which encodes a homeodomain protein involved in neuronal specification. During cortical development Cux2 identifies two subpopulations with different spatial origins, migratory behaviours and phenotypic characteristics: (i) a population of interneurons, which invades the pallium from the subpallium; and (ii) a neuronal population produced in the pallium around embryonic day 11.5, which divides in the SVZ and accumulates in the intermediate zone (IZ). Subsequently, Cux2 is a marker of upper cortical layers. Using different molecular markers and Pax6-deficient mice, we provide data that suggest a relationship between the early-determined Cux2-positive neuronal precursors in the SVZ/IZ and upper layer neurons. This suggests that laminar determination of upper cortical layer neurons occurs during the earliest stages of corticogenesis.},
	Author = {Zimmer, C{\'e}line and Tiveron, Marie-Catherine C. and Bodmer, Rolf and Cremer, Harold},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {1047-3211},
	Journal = {Cereb Cortex},
	Keywords = {Cerebral Cortex;Neurons;Cell Differentiation;Gene Expression Regulation, Developmental;Mice;Research Support, Non-U.S. Gov't;03 Adult neurogenesis progenitor source;Comparative Study;Mice, Inbred BALB C;Mice, Inbred C57BL;Cell Division;Mice, Mutant Strains;Animals;Cerebral Ventricles;Homeodomain Proteins;Mice, Neurologic Mutants;Cell Lineage},
	Month = {12},
	Nlm_Id = {9110718},
	Number = {12},
	Organization = {Developmental Biology Institute of Marseille, NMDA, Campus de Luminy case 907, 13288 Marseille Cedex 9, France.},
	Pages = {1408-20},
	Pii = {bhh102},
	Pubmed = {15238450},
	Title = {Dynamics of Cux2 expression suggests that an early pool of SVZ precursors is fated to become upper cortical layer neurons},
	Uuid = {AB53D074-C3F4-41EC-8759-78298DC14F1C},
	Volume = {14},
	Year = {2004},
	url = {papers/Zimmer_CerebCortex2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1093/cercor/bhh102}}

@article{Zin-Ka-Ieu:1999,
	Abstract = {Previous light microscopical studies have indicated that fibres from the ventrolateral thalamic nucleus (VL) establish direct axo-somatic and axo-dendritic presumed contacts with layers III and V neurones of the intact frontal cortex projecting to the striatum. Additional experiments provided evidence that this thalamo-fronto-striate pathway could be partly reconstructed by transplantation of embryonic frontal tissue into the damaged cortex. The present study was undertaken to validate these results at the ultrastructural level. Several months after the transplantation of fetal frontal tissue into the damaged frontal cortex of newborn rats, a retrograde neurotracer (subunit b of the cholera toxin) was used to label the grafted neurones projecting to the striatum whereas an anterograde neurotracer (Phaseolus vulgaris leuco-agglutinin) was used to label within the transplant, axons and terminations arising from the VL. The same injection procedures were applied to intact adult rats (control). The distribution of retrograde and anterograde labellings within the intact cortex and within the graft was examined at light and electron microscopic levels to identify the synaptic contacts. Our findings showed that labelled contacts were less numerous within the transplant than within the intact cortex but their synaptic organization was similar: asymmetrical synaptic axo-dendritic and axo-somatic contacts. This synaptic articulation is probably supplied by a thalamic excitatory input. These results provide ultrastructural evidence of the capacity of a frontal cortical transplant placed in damaged frontal cortex of newborn rats to help reconstruction of appropriate synaptic integration within the thalamo-fronto-striate system.},
	Author = {Zin-Ka-Ieu, S. and Roger, M. and Arnault, P.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:46 -0400},
	Issn = {0899-0220},
	Journal = {Somatosens Mot Res},
	Keywords = {Cholera Toxin;Phytohemagglutinins;Animals;Synapses;Corpus Striatum;Thalamic Nuclei;Brain Tissue Transplantation;Rats;Neural Pathways;Frontal Lobe;Axons;Rats, Wistar;Fetal Tissue Transplantation;Axonal Transport;Animals, Newborn;Neurons;Immunohistochemistry;Microscopy, Electron;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't},
	Medline = {20095891},
	Nlm_Id = {8904127},
	Number = {4},
	Organization = {CNRS: UMR 6558, D{\'e}partement des Neurosciences, Laboratoire de Neurophysiologie, Universit{\'e} de Poitiers, France.},
	Pages = {338-51},
	Pubmed = {10632030},
	Title = {The thalamo-fronto-striate system: ultrastructural evidence of appropriate synaptic integration of embryonic neurones grafted within the frontal cortex of newborn rats},
	Uuid = {FE62FF2A-73A3-4539-8761-F3961FD5E10D},
	Volume = {16},
	Year = {1999}}

@article{Zitnik:2002,
	Abstract = {0360-4012 Journal Article Review Review, Tutorial},
	Author = {Zitnik, G. and Martin, G. M.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {J Neurosci Res},
	Keywords = {01 Adult neurogenesis general;Aging/pathology/*physiology;Cell Division/physiology;Alzheimer Disease/pathology/physiopathology;Human;Brain/*pathology/physiopathology;Neurodegenerative Diseases/*pathology/physiopathology;A abstr;Stem Cells/pathology;Cell Differentiation/physiology;Support, U.S. Gov't, P.H.S.;Animals;Neurons/*pathology},
	Number = {3},
	Organization = {Department of Pathology, University of Washington, Seattle, Washington 98995, USA.},
	Pages = {258-63},
	Pubmed = {12391584},
	Title = {Age-related decline in neurogenesis: old cells or old environment?},
	Uuid = {0688E827-CDF1-11D9-B244-000D9346EC2A},
	Volume = {70},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12391584}}

@article{Ziv:2006,
	Abstract = {Neurogenesis is known to take place in the adult brain. This work identifies T lymphocytes and microglia as being important to the maintenance of hippocampal neurogenesis and spatial learning abilities in adulthood. Hippocampal neurogenesis induced by an enriched environment was associated with the recruitment of T cells and the activation of microglia. In immune-deficient mice, hippocampal neurogenesis was markedly impaired and could not be enhanced by environmental enrichment, but was restored and boosted by T cells recognizing a specific CNS antigen. CNS-specific T cells were also found to be required for spatial learning and memory and for the expression of brain-derived neurotrophic factor in the dentate gyrus, implying that a common immune-associated mechanism underlies different aspects of hippocampal plasticity and cell renewal in the adult brain.},
	Author = {Ziv, and Ron, and Butovsky, and Landa, and Sudai, and Greenberg, and Cohen, and Kipnis, and Schwartz,},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {1097-6256},
	Journal = {Nat Neurosci},
	Keywords = {01 Adult neurogenesis general;03 Adult neurogenesis progenitor source;11 Glia;04 Adult neurogenesis factors},
	Month = {1},
	Nlm_Id = {9809671},
	Number = {2},
	Organization = {[1] Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel. [2] These authors contributed equally to this work.},
	Pages = {268-75},
	Pii = {nn1629},
	Pubmed = {16415867},
	Title = {Immune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood},
	Uuid = {C2104CDC-1E8A-4037-A673-A94DD0501F5E},
	Volume = {9},
	Year = {2006},
	url = {papers/Ziv_NatNeurosci2006.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nn1629}}

@article{Ziv:2006a,
	Abstract = {The well regulated activities of microglia and T cells specific to central nervous system (CNS) antigens can contribute to the protection of CNS neural cells and their renewal from adult neural stem/progenitor cells (aNPCs). Here we report that T cell-based vaccination of mice with a myelin-derived peptide, when combined with transplantation of aNPCs into the cerebrospinal fluid (CSF), synergistically promoted functional recovery after spinal cord injury. The synergistic effect was correlated with modulation of the nature and intensity of the local T cell and microglial response, expression of brain-derived neurotrophic factor and noggin protein, and appearance of newly formed neurons from endogenous precursor-cell pools. These results substantiate the contention that the local immune response plays a crucial role in recruitment of aNPCs to the lesion site, and suggest that similar immunological manipulations might also serve as a therapeutic means for controlled migration of stem/progenitor cells to other acutely injured CNS sites.},
	Author = {Ziv, Yaniv and Avidan, Hila and Pluchino, Stefano and Martino, Gianvito and Schwartz, Michal},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {T-Lymphocytes;Cell Differentiation;Wound Healing;Myelin Sheath;Animals;Carrier Proteins;Stem Cell Transplantation;Brain-Derived Neurotrophic Factor;Myelin-Associated Glycoprotein;Microglia;Vaccination;Mice, Inbred C57BL;11 Glia;research support, non-u.s. gov't;Green Fluorescent Proteins;Spinal Cord;Spinal Cord Injuries;Neurons;Mice;24 Pubmed search results 2008;Stem Cells},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {35},
	Organization = {*Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.},
	Pages = {13174-9},
	Pii = {0603747103},
	Pubmed = {16938843},
	Title = {Synergy between immune cells and adult neural stem/progenitor cells promotes functional recovery from spinal cord injury},
	Uuid = {145092FB-E6E8-4951-B9A3-2409E5B70B25},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0603747103}}

@article{Zovein:2006,
	Author = {Zovein, Ann C. and Iruela-Arispe, M. Luisa},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0027-8424},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {14 Immune;11 Glia;24 Pubmed search results 2008},
	Month = {8},
	Nlm_Id = {7505876},
	Number = {35},
	Organization = {Department of Molecular, Cell and Developmental Biology and Molecular Biology Institute, University of California, Los Angeles, CA 90095.},
	Pages = {12959-60},
	Pii = {0606018103},
	Pubmed = {16924095},
	Title = {My O'Myeloid, a tale of two lineages},
	Uuid = {61C3A403-07D9-40D8-B199-2880BD7EE426},
	Volume = {103},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0606018103}}

@article{Zuo:1998,
	Abstract = {It was the first time demonstrated by us that the number of newborn neurons was increased after making lesion in forebrain of adult ring dove (Streptopelia risoria) by means of autoradiography and immunohistochemistry. Neurogenesis in the adult avian is restricted to the telencephalon. In doves with bilateral electrolytic lesion of nucleus ectostriatum (E), the mean number of proliferating cells in the lateral ventricular zone (LVZ) and newborn neurons in the forebrain increased by 1.95 times and 2.38 times respectively as compared with that in intact doves. The most remarkable increase of neurogenesis induced by nucleus ectostriatum lesions was found at the anterior- posterior level 3 (L3), where the lesion site was located. These results showed that the electrolytic brain lesion altered the distribution pattern of proliferating cells in the LVZ and resulted in increase of the number of newborn neurons in the non-VZ areas of forebrain. The changes in number and distribution pattern of proliferating cells in LVZ and newborn neurons in forebrain may be dependent on site of lesion. Studies on the relationship between proliferating cells in LVZ and newly generated neurons in non-VZ areas may help to understand the mechanism of brain plasticity and development.},
	Author = {Zuo, M. X.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Cell Res},
	Keywords = {Neurons/*cytology/metabolism;Telencephalon/*cytology/*injuries/metabolism;Microtubule-Associated Proteins/analysis;Comparative Study;Electrodes;Photoperiod;Animal;D-7;Nerve Tissue Proteins/analysis;DNA/biosynthesis;Vocalization, Animal/physiology;Support, Non-U.S. Gov't;tau Proteins/analysis;06 Adult neurogenesis injury induced;Pigeons/*physiology;Cell Division;Immunohistochemistry;Autoradiography;Neostriatum/*cytology},
	Number = {2},
	Organization = {Biology Department, Beijing Normal University, China.},
	Pages = {151-8.},
	Title = {The studies on neurogenesis induced by brain injury in adult ring dove},
	Uuid = {D5C5544E-F9F0-4860-A0CD-F3FF752658A9},
	Volume = {8},
	Year = {1998},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=9669030}}

@article{Zuo:2004,
	Abstract = {To enable vital observation of glia at the neuromuscular junction, transgenic mice were generated that express proteins of the green fluorescent protein family under control of transcriptional regulatory sequences of the human S100B gene. Terminal Schwann cells were imaged repetitively in living animals of one of the transgenic lines to show that, except for extension and retraction of short processes, the glial coverings of the adult neuromuscular synapse are stable. In other lines, subsets of Schwann cells were labeled. The distribution of label suggests that Schwann cells at individual synapses are clonally related, a finding with implications for how these cells might be sorted during postnatal development. Other labeling patterns, some present in unique lines, included astrocytes, microglia, and subsets of cerebellar Bergmann glia, spinal motor neurons, macrophages, and dendritic cells. We show that lines with labeled macrophages can be used to follow the accumulation of these cells at sites of injury.},
	Author = {Zuo, Yi and Lubischer, Jane L. and Kang, Hyuno and Tian, Le and Mikesh, Michelle and Marks, Alexander and Scofield, Virginia L. and Maika, Shan and Newman, Craig and Krieg, Paul and Thompson, Wesley J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {Transgenes;Animals;Humans;Macrophages;Mice, Transgenic;Mice, Inbred C57BL;Recombinant Fusion Proteins;Dendritic Cells;11 Glia;Microscopy, Fluorescence;Green Fluorescent Proteins;Schwann Cells;Cell Line;Receptors, Cholinergic;Neuromuscular Junction;Research Support, U.S. Gov't, P.H.S.;Neuroglia;Neurons;Mice;Luminescent Proteins;Research Support, N.I.H., Extramural;Adipocytes;S100 Proteins;Lens, Crystalline;Langerhans Cells},
	Month = {12},
	Nlm_Id = {8102140},
	Number = {49},
	Organization = {Section of Neurobiology, Institute for Neuroscience, University of Texas, Austin, Texas 78712, USA.},
	Pages = {10999-1009},
	Pii = {24/49/10999},
	Pubmed = {15590915},
	Title = {Fluorescent proteins expressed in mouse transgenic lines mark subsets of glia, neurons, macrophages, and dendritic cells for vital examination},
	Uuid = {3EE0D1DF-FA7C-4985-BFBA-39AC11444B79},
	Volume = {24},
	Year = {2004},
	url = {papers/Zuo_JNeurosci2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.3934-04.2004}}

@article{Zupanc:2003,
	Abstract = {Persistence of radial glia within the adult central nervous system is a widespread phenomenon among fish. Based on a series of studies in the teleost species Apteronotus leptorhynchus, we propose that one function of this persistence is the involvement of radial glia in adult neurogenesis, i.e., the generation and further development of new neurons in the adult central nervous system. In particular, evidence has been obtained for the involvement of radial glia in the guidance of migrating young neurons in both the intact and the regenerating brain; for a possible role as precursor cells from which new neurons arise; and for its role as a source of trophic substances promoting the generation, differentiation, and/or survival of new neurons. These functions contribute not only to the potential of the intact brain to generate new neurons continuously, and of the injured brain to replace damaged cells by newly generated ones, but they also provide an essential part of the cellular substrate of behavioral plasticity. 0894-1491 Journal Article Review Review, Tutorial},
	Author = {Zupanc, G. K. and Clint, S. C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Glia},
	Keywords = {Brain/cytology/*growth &development;01 Adult neurogenesis general;Neuronal Plasticity/physiology;Neurons/*cytology/physiology;Fishes/anatomy &histology/*growth &development;Stem Cells/*cytology/physiology;Neuroglia/*cytology/physiology;Cell Differentiation/physiology;Animals;Nerve Regeneration/physiology;A pdf;Cell Movement/physiology},
	Number = {1},
	Organization = {School of Engineering and Science, International University Bremen, Bremen, Germany. g.zupanc\@iu-bremen.de},
	Pages = {77-86},
	Pubmed = {12761870},
	Title = {Potential role of radial glia in adult neurogenesis of teleost fish},
	Uuid = {3EABF79B-60A5-4AF7-AD0A-12A387FD0D6B},
	Volume = {43},
	Year = {2003},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12761870}}

@article{abd-el-Basset:1995,
	Abstract = {We examined the effect of bacterial wall lipopolysaccharide (LPS), a strong inflammatory agent, on the morphology, cell motility, cytoskeletal organization, and phagocytic activity of microglia in tissue cultures initiated from neopallia of newborn C3H/OuJ mice. Normally, the microglia in our cultures are non-migratory and Mac-1 positive, have ameboid cell morphology, no polarity, many short processes that extend into lamellipodia in opposing directions, and undulating cell membrane projections. When 1-5 micrograms/ml LPS is added to such cultures, some cells acquire polarity by forming a large lamellipodium and begin to migrate. Two hours later migration ceases; the membrane undulations stop; and the cells become non-polar, assume a large, round, flat shape, and gradually develop many microspikes all over the cell body. Those cells that do not transform into large, round, flat cells enlarge and extend numerous lamellipodia in opposing directions. We found that the cytoskeleton of microglia is composed of actin, vimentin-containing intermediate filaments (IF) and microtubules (MT). Vimentin-containing IF and MT form dense networks that radiate into the cell periphery, whereas F-actin is diffusely arranged throughout the cytoplasm. The LPS-treated cells show changes in the organization of the main components of the cytoskeleton. F-actin is reorganized by the formation of bundles underneath and parallel to the cell membrane and other bundles projecting into the cores of the microspikes. The vimentin-containing IF dense network reorganizes into two condensed rings, with fine strands of IF extended between the two rings and the MT networks become less dense and extend throughout the cytoplasm. The LPS treatment potentiates the phagocytic activity of the microglia. However, approximately 30\%of microglia lose the expression of MHC class II antigens.},
	Author = {abd-el-Basset, E. and Fedoroff, S.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0360-4012},
	Journal = {J Neurosci Res},
	Keywords = {Mice, Inbred Strains;24 Pubmed search results 2008;Research Support, Non-U.S. Gov't;Immunohistochemistry;Antigens;Microtubules;Antibodies, Monoclonal;11 Glia;Microglia;Animals, Newborn;Mice;Cells, Cultured;Animals;Actins;Lipopolysaccharides},
	Medline = {95379100},
	Month = {6},
	Nlm_Id = {7600111},
	Number = {2},
	Organization = {Department of Anatomy, College of Medicine, University of Saskatchewan, Saskatoon, Canada.},
	Pages = {222-37},
	Pubmed = {7650758},
	Title = {Effect of bacterial wall lipopolysaccharide (LPS) on morphology, motility, and cytoskeletal organization of microglia in cultures},
	Uuid = {B0EA318C-BAAB-11DA-93EA-000D9346EC2A},
	Volume = {41},
	Year = {1995},
	Bdsk-Url-1 = {http://dx.doi.org/10.1002/jnr.490410210}}

@article{Groot:1992,
	Abstract = {The origin and nature of brain macrophages and microglial cells in the mouse central nervous system (CNS) were investigated. First, the expression and localization of determinants recognized by the different monoclonal antibodies (mAbs) MOMA-1, Mac-1-alpha, and F4/80 (raised against cells of the mononuclear phagocyte system) were immunohistochemically studied in the developing and adult mouse brain. In order to clarify the origin of brain macrophages and microglial cells, we used bacteriophage lambda transgenic mice as donors for bone marrow transplantations in recipient mice of different ages. During ontogeny, numerous MOMA-1-, Mac-1-alpha-, and F4/80-positive blood monocyte-derived brain macrophages (amoeboid microglia) infiltrated the CNS parenchyma. These brain macrophages gradually disappeared from the brain parenchyma at postnatal day 7 (P7). From P17 on, Mac-1-alpha- and F4/80-positive cells were detected within the brain parenchyma with the morphology of resting microglial cells. Transitional forms between brain macrophages and "resting" microglia were not observed in the developing brain. Combined non-radioactive in situ hybridization and immunohistochemistry revealed many MOMA-1-positive bone marrow-derived brain macrophages that were located in the leptomeninges, the ventricles, and occasionally the blood vessel walls. These results show that brain macrophages are of bone marrow origin. Many "resting" microglial cells were detected in the brain, mainly in the white matter. It appeared that about 10\%of these cells displayed the transgenic signal. This result indicates that the majority of "resting" microglial cells are of local, presumably neuroectodermal, origin.},
	Author = {de Groot, C. J. and Huppes, W. and Sminia, T. and Kraal, G. and Dijkstra, C. D.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0894-1491},
	Journal = {Glia},
	Keywords = {Fetus;Research Support, Non-U.S. Gov't;Immune Sera;Animals;Macrophages;Bone Marrow Transplantation;Immunoenzyme Techniques;Brain;Mice, Transgenic;Staining and Labeling;11 Glia;Phagocytes;Embryonic and Fetal Development;Cell Line;Bone Marrow Cells;Animals, Newborn;Antibodies, Monoclonal;Neuroglia;Mice;Nucleic Acid Hybridization},
	Medline = {93100083},
	Nlm_Id = {8806785},
	Number = {4},
	Organization = {Department of Cell Biology, Vrije Universiteit, Amsterdam, The Netherlands.},
	Pages = {301-9},
	Pubmed = {1281462},
	Title = {Determination of the origin and nature of brain macrophages and microglial cells in mouse central nervous system, using non-radioactive in situ hybridization and immunoperoxidase techniques},
	Uuid = {337F068C-B22D-4039-9C92-85FFD4187C98},
	Volume = {6},
	Year = {1992}}

@article{Jong:2005,
	Abstract = {Whenever neurons in the CNS are injured, microglia become activated. In addition to local activation, microglia remote from the primary lesion site are stimulated. Because this so-called secondary activation of microglia is instrumental for long-term changes after neuronal injury, it is important to understand how microglia activity is controlled. The remote activation of microglia implies that the activating signals are transported along neuronal projections. However, the identity of these signals has not yet been identified. It is shown here that glutamate-treated neurons rapidly express and release the chemokine CCL21. We also provide evidence that neuronal CCL21 is packed in vesicles and transported throughout neuronal processes to reach presynaptic structures. Chemotaxis assays show that functional CCL21 is released from endangered neurons and activate microglia via the chemokine receptor CXCR3. Based on these findings, we suggest that neuronal CCL21 is important in directed neuron-microglia signaling and that this communication could account for the remote activation of microglia, far distant from a primary lesion.},
	Author = {de Jong, Eiko K. and Dijkstra, Ineke M. and Hensens, Marjolein and Brouwer, Nieske and van Amerongen, Machteld and Liem, Robert S. B. and Boddeke, Hendrikus W. G. M. and Biber, Knut},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {11 Glia},
	Month = {8},
	Nlm_Id = {8102140},
	Number = {33},
	Organization = {Department of Medical Physiology, University of Groningen, 9713 AV Groningen, The Netherlands.},
	Pages = {7548-57},
	Pii = {25/33/7548},
	Pubmed = {16107642},
	Title = {Vesicle-mediated transport and release of CCL21 in endangered neurons: a possible explanation for microglia activation remote from a primary lesion},
	Uuid = {AC74FB10-C9CE-4F1B-94D5-75E0084EAF92},
	Volume = {25},
	Year = {2005},
	url = {papers/Jong_JNeurosci2005.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1019-05.2005}}

@article{Rio:2002,
	Abstract = {Severed adult CNS axons can extend over long distances when a permissive 'milieu', such as grafted Schwann cells or ensheathing cells, is provided. Moreover, functional blocking of endogenous inhibitory factors, such as Nogo-A or proteoglycans, enhances the regeneration of axotomized neurons. Here we examine whether guidance cues available during the development of axonal pathways could also potentiate the regeneration of lesioned adult circuits. The Cajal-Retzius cells in the hippocampus are transient pioneer neurons that guide entorhino-hippocampal afferents to their target layers. By using an in vitro model of axotomy of the entorhino-hippocampal pathway we show that Cajal-Retzius cells triggered the regeneration of the axotomized entorhino-hippocampal pathway. Furthermore, the regrowth induced by Cajal-Retzius cells was robust and its pattern was indistinguishable from that of the unlesioned entorhino-hippocampal pathway. Thus, regenerating axons regrew in a layer-specific fashion towards the appropriate target layers, making synaptic contacts with target pyramidal neurons. Interestingly, the ability of lesioned entorhinal axons to regrow was maintained for at least 9 days after axotomy. These results show that the growth-promoting cells controlling the development of neural circuits will be a relevant approach to promoting the regeneration of lesioned adult CNS pathways.},
	Author = {del R{\'\i}o, Jos{\'e} A. and Sol{\'e}, Marta and Borrell, V{\'\i}ctor and Mart{\'\i}nez, Albert and Soriano, Eduardo},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Research Support, Non-U.S. Gov't;Presynaptic Terminals;Lysine;Animals;Coculture Techniques;Aging;Neuronal Plasticity;Neural Pathways;Cell Communication;Entorhinal Cortex;Hippocampus;Pyramidal Cells;Organ Culture Techniques;Nerve Regeneration;Animals, Newborn;Mice, Inbred Strains;Axotomy;Body Patterning;Mice;24 Pubmed search results 2008;Microscopy, Electron;Stem Cells;Cues;Growth Cones;Growth Substances},
	Medline = {22095224},
	Month = {6},
	Nlm_Id = {8918110},
	Number = {12},
	Organization = {Department of Cell Biology, Faculty of Biology, and Neuroscience Research Center (CERN), University of Barcelona, Diagonal 645, 08028 Barcelona, Spain. jario\@porthos.bio.ub.es},
	Pages = {1881-90},
	Pii = {2027},
	Pubmed = {12099894},
	Title = {Involvement of Cajal-Retzius cells in robust and layer-specific regeneration of the entorhino-hippocampal pathways},
	Uuid = {D21EEB28-BCD7-445C-AC14-A1D4393DF0CE},
	Volume = {15},
	Year = {2002}}

@article{Portes:1998,
	Abstract = {X-SCLH/LIS syndrome is a neuronal migration disorder with disruption of the six-layered neocortex. It consists of subcortical laminar heterotopia (SCLH, band heterotopia, or double cortex) in females and lissencephaly (LIS) in males, leading to epilepsy and cognitive impairment. We report the characterization of a novel CNS gene encoding a 40 kDa predicted protein that we named Doublecortin and the identification of mutations in four unrelated X-SCLH/LIS cases. The predicted protein shares significant homology with the N-terminal segment of a protein containing a protein kinase domain at its C-terminal part. This novel gene is highly expressed during brain development, mainly in fetal neurons including precursors. The complete disorganization observed in lissencephaly and heterotopia thus seems to reflect a failure of early events associated with neuron dispersion.},
	Author = {des Portes, V. and Pinard, J. M. and Billuart, P. and Vinet, M. C. and Koulakoff, A. and Carri{\'e}, A. and Gelot, A. and Dupuis, E. and Motte, J. and Berwald-Netter, Y. and Catala, M. and Kahn, A. and Beldjord, C. and Chelly, J.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:39 -0400},
	Issn = {0092-8674},
	Journal = {Cell},
	Keywords = {Epilepsy;24 Pubmed search results 2008;Male;Cerebral Cortex;Peptides;10 Development;Transcription, Genetic;Base Sequence;Cell Movement;X Chromosome;Central Nervous System;Sex Chromosome Aberrations;Gene Expression;Molecular Sequence Data;Child, Preschool;Sequence Tagged Sites;Microtubule-Associated Proteins;Chromosomes, Artificial, Yeast;Chromosome Mapping;Mutation;Neuropeptides;Adolescent;Amino Acid Sequence;Pedigree;Female;Family Health;Syndrome;DNA, Complementary;research support, non-u.s. gov't;Genes;Humans;Neurons;10 genetics malformation;Sequence Homology, Amino Acid},
	Month = {1},
	Nlm_Id = {0413066},
	Number = {1},
	Organization = {INSERM U129-ICGM, Facult{\'e} de M{\'e}decine Cochin, Paris, France.},
	Pages = {51-61},
	Pubmed = {9489699},
	Title = {A novel CNS gene required for neuronal migration and involved in X-linked subcortical laminar heterotopia and lissencephaly syndrome},
	Uuid = {B90CA395-BE10-41AF-A4F8-FEC9FB0CAC6A},
	Volume = {92},
	Year = {1998}}

@article{Eitzen:1998,
	Abstract = {Recent in vitro experiments suggest that neurotoxicity of the prion protein is dependent on the presence of microglia. We have studied 11 cases of Creutzfeldt-Jakob disease (CJD) using immunocytochemistry in combination with computerized image analysis to clarify the relationship between spongiform change and microglial activation. MHC class II-positive microglia were almost exclusively confined to cortical gray matter where the neuropil area occupied by these cells exceeded that of controls more than 350-fold. In cortical regions with a bimodal distribution of spongiform degeneration, the presence of class II-positive microglia correlated well with the presence of vacuolation in layer V, but significantly less with spongiform change in layers II and III. In areas where spongiform degeneration affected the entire depth of the cortex, activated microglia were predominantly located in the inner one-half of the cortex or were evenly distributed throughout all cortical laminae. Here, microglia exhibited atypical, tortuous cell processes and occasionally intracytoplasmic vacuoles, suggesting that microglia themselves may become a disease target. Taken together, our results provide indirect evidence against an early causative involvement of microglia in the development of spongiform change. At later stages, however, diseased microglia could produce harmful factors which mediate both astrogliosis and neuronal injury.},
	Author = {v Eitzen, U. and Egensperger, R. and K{\"o}sel, S. and Grasbon-Frodl, E. M. and Imai, Y. and Bise, K. and Kohsaka, S. and Mehraein, P. and Graeber, M. B.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:30 -0400},
	Issn = {0022-3069},
	Journal = {J Neuropathol Exp Neurol},
	Keywords = {Creutzfeldt-Jakob Syndrome;DNA-Binding Proteins;Research Support, Non-U.S. Gov't;Aged;Calcium-Binding Proteins;Image Processing, Computer-Assisted;Female;Aged, 80 and over;Histocompatibility Antigens Class II;Immunochemistry;Middle Aged;Microglia;11 Glia;Humans;Brain;Male;case reports},
	Medline = {98260844},
	Month = {3},
	Nlm_Id = {2985192R},
	Number = {3},
	Organization = {Institute of Neuropathology, Reference Center for Neurodegenerative Disorders, Ludwig-Maximilians-University, Munich, Germany.},
	Pages = {246-56},
	Pubmed = {9600217},
	Title = {Microglia and the development of spongiform change in Creutzfeldt-Jakob disease},
	Uuid = {2B96B203-C2B8-4146-8761-F3DAD8C3AE70},
	Volume = {57},
	Year = {1998}}

@article{Furth:1979,
	Abstract = {In this study human mononuclear phagocytes from the bone marrow (promonocytes and monocytes), peripheral blood monocytes, and tissue macrophages from the skin and the peritoneal cavity were studied with respect to their morphological, cytochemical, and functional characteristics, cell surface receptors, and 3H-thymidine incorporation in vitro. The results show similarities between mononuclear phagocytes of the three body compartments with respect to esterase staining, the presence of peroxidase-positive granules, the presence of IgG and C receptors, and pinocytic and phagocytic activity. Promonocytes are the most immature mononuclear phagocytes identified in human bone marrow, and since about 80\%of these cells incorporate 3H-thymidine, they are actively dividing cells. Monocytes, whether in bone marrow or the peripheral blood, and both skin and peritoneal macrophages label minimally with 3H-thymidine and thus are nondividing cells. Since the characteristics of mononuclear phagocytes in man and mouse do not diverge greatly, it is probable that the cell sequence based on in vitro and in vivo 3H-thymidine labeling studies in the mouse holds for man as well. The successive stages of development of the human mononuclear phagocyte cell line will then be as follows: monoblasts (not yet characterized in man) divide to form promonocytes, and these cells in turn divide and give rise to monocytes that do not divide further; they leave the bone marrow, circulate in the peripheral blood, and finally become macrophages in the various tissues.},
	Author = {van Furth, R. and Raeburn, J. A. and van Zwet, T. L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0006-4971},
	Journal = {Blood},
	Keywords = {Monocytes;Binding Sites;Phagocytes;Ascitic Fluid;Bone Marrow Cells;11 Glia;Endocytosis;Macrophages;Skin;Humans;Mitosis},
	Medline = {79210039},
	Month = {8},
	Nlm_Id = {7603509},
	Number = {2},
	Pages = {485-500},
	Pubmed = {454850},
	Title = {Characteristics of human mononuclear phagocytes},
	Uuid = {502624DF-82A9-4C9B-A618-1828DC298965},
	Volume = {54},
	Year = {1979}}

@article{Praag:1999,
	Abstract = {Exposure to an enriched environment increases neurogenesis in the dentate gyrus of adult rodents. Environmental enrichment, however, typically consists of many components, such as expanded learning opportunities, increased social interaction, more physical activity and larger housing. We attempted to separate components by assigning adult mice to various conditions: water-maze learning (learner), swim-time- yoked control (swimmer), voluntary wheel running (runner), and enriched (enriched) and standard housing (control) groups. Neither maze training nor yoked swimming had any effect on bromodeoxyuridine (BrdU)-positive cell number. However, running doubled the number of surviving newborn cells, in amounts similar to enrichment conditions. Our findings demonstrate that voluntary exercise is sufficient for enhanced neurogenesis in the adult mouse dentate gyrus.},
	Author = {van Praag, H. and Kempermann, G. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Journal = {Nat Neurosci},
	Keywords = {A-8a;01 Adult neurogenesis general;Cell Division/physiology;Swimming/physiology;Cell Survival/physiology;Female;Mice, Inbred C57BL;Maze Learning/physiology;Animal;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Bromodeoxyuridine;Mice;Dentate Gyrus/*cytology/*growth &development;Running/*physiology},
	Number = {3},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, California 92037, USA.},
	Pages = {266-70.},
	Title = {Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus},
	Uuid = {517DF153-60AE-416A-A481-2515D22791FC},
	Volume = {2},
	Year = {1999},
	url = {papers/Praag_NatNeurosci1999.pdf}}

@article{Praag:2002,
	Abstract = {There is extensive evidence indicating that new neurons are generated in the dentate gyrus of the adult mammalian hippocampus, a region of the brain that is important for learning and memory. However, it is not known whether these new neurons become functional, as the methods used to study adult neurogenesis are limited to fixed tissue. We use here a retroviral vector expressing green fluorescent protein that only labels dividing cells, and that can be visualized in live hippocampal slices. We report that newly generated cells in the adult mouse hippocampus have neuronal morphology and can display passive membrane properties, action potentials and functional synaptic inputs similar to those found in mature dentate granule cells. Our findings demonstrate that newly generated cells mature into functional neurons in the adult mammalian brain.},
	Author = {van Praag, Henriette and Schinder, Alejandro F. and Christie, Brian R. and Toni, Nicolas and Palmer, Theo D. and Gage, Fred H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0028-0836},
	Journal = {Nature},
	Keywords = {Aging;Synapses;Cell Differentiation;Luminescent Proteins;Research Support, Non-U.S. Gov't;Female;Dentate Gyrus;Mice, Inbred C57BL;Research Support, U.S. Gov't, P.H.S.;Neural Pathways;Cell Division;Green Fluorescent Proteins;Mice;Animals;Membrane Potentials;Neurons;Genetic Vectors},
	Medline = {21864715},
	Month = {2},
	Nlm_Id = {0410462},
	Number = {6875},
	Organization = {Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. vanpraag\@salk.edu},
	Pages = {1030-4},
	Pii = {4151030a},
	Pubmed = {11875571},
	Title = {Functional neurogenesis in the adult hippocampus},
	Uuid = {FBEBE53E-D067-11DA-8A8C-000D9346EC2A},
	Volume = {415},
	Year = {2002},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/4151030a}}

@article{Praag:1999a,
	Abstract = {Running increases neurogenesis in the dentate gyrus of the hippocampus, a brain structure that is important for memory function. Consequently, spatial learning and long-term potentiation (LTP) were tested in groups of mice housed either with a running wheel (runners) or under standard conditions (controls). Mice were injected with bromodeoxyuridine to label dividing cells and trained in the Morris water maze. LTP was studied in the dentate gyrus and area CA1 in hippocampal slices from these mice. Running improved water maze performance, increased bromodeoxyuridine-positive cell numbers, and selectively enhanced dentate gyrus LTP. Our results indicate that physical activity can regulate hippocampal neurogenesis, synaptic plasticity, and learning.},
	Author = {van Praag, H. and Christie, B. R. and Sejnowski, T. J. and Gage, F. H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {Proc Natl Acad Sci U S A},
	Keywords = {Learning/*physiology;Long-Term Potentiation/*physiology;Immunohistochemistry;Female;*Physical Conditioning, Animal;Mice, Inbred C57BL;Animal;04 Adult neurogenesis factors;Support, U.S. Gov't, P.H.S.;Support, Non-U.S. Gov't;Mice;Dentate Gyrus/*cytology/physiology;C abstr},
	Number = {23},
	Organization = {Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.},
	Pages = {13427-31.},
	Title = {Running enhances neurogenesis, learning, and long-term potentiation in mice},
	Uuid = {2EBE2001-1D62-46E6-A64F-80FC108DA9AF},
	Volume = {96},
	Year = {1999},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=10557337%20http://www.pnas.org/cgi/content/full/96/23/13427%20http://www.pnas.org/cgi/content/abstract/96/23/13427}}

@article{Rooijen:1997,
	Abstract = {Macrophages play an important role in host defense reactions, for example, by phagocytosis of particulate materials. This process also results in the rapid removal of targeting devices such as liposomes and adenovirus vectors and of non-autologous grafted cells and materials. Another aspect of macrophage function is their production and secretion of proinflammatory cytokines. Transient and organ-specific suppression of macrophage function by liposome-mediated manipulation has been shown to improve the efficacy of drug and gene targeting and to reduce the symptoms of inflammatory reactions.},
	Author = {van Rooijen, N. and Bakker, J. and Sanders, A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0167-7799},
	Journal = {Trends Biotechnol},
	Keywords = {Organ Specificity;Gene Transfer Techniques;23 Technique;Biotechnology;Liposomes;Inflammation;Drug Carriers;Graft Survival;11 Glia;In Vitro;Macrophages;review, tutorial;Humans;Animals;24 Pubmed search results 2008;Mice;review},
	Medline = {97304689},
	Month = {5},
	Nlm_Id = {8310903},
	Number = {5},
	Organization = {Department of Cell Biology and Immunology, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands. N.van\_Rooijen.cell\@med.vu.nl},
	Pages = {178-85},
	Pii = {S0167779997010196},
	Pubmed = {9161052},
	Title = {Transient suppression of macrophage functions by liposome-encapsulated drugs},
	Uuid = {A2A8DEF6-CED0-11D9-B244-000D9346EC2A},
	Volume = {15},
	Year = {1997},
	url = {papers/Rooijen_TrendsBiotechnol1997.pdf}}

@article{Vliet:2005,
	Abstract = {PURPOSE: Overexpression of multidrug transporters may play a role in the development of pharmacoresistance by decreasing extracellular drug levels in the brain. However, it is not known whether overexpression is due to an initial insult or evolves more gradually because of recurrent spontaneous seizures. In the present study, we investigated the expression of different multidrug transporters during epileptogenesis in the rat. In addition, we determined whether these transporters affected phenytoin (PHT) distribution in the brain. METHODS: Expression of multidrug resistance-associated proteins MRP1 and MRP2 and breast cancer-resistance protein (BCRP) was examined after electrically induced status epilepticus (SE) by immunocytochemistry and Western blot analysis. Brain/blood PHT levels were determined by high-performance liquid chromatography (HPLC) analysis in the presence and absence of the MRP inhibitor probenecid. RESULTS: Shortly after SE, MRP1, MRP2, and BCRP were upregulated in astrocytes within several limbic structures, including hippocampus. In chronic epileptic rats, these proteins were overexpressed in the parahippocampal cortex, specifically in blood vessels and astrocytes surrounding these vessels. Overexpression was related to the occurrence of SE and was present mainly in rats with a high seizure frequency. Brain PHT levels were significantly lower in epileptic rats compared with control rats, but pharmacologic inhibition of MRPs increased the PHT levels. CONCLUSIONS: Overexpression of MRP and BCRP was induced by SE as well as recurrent seizures. Moreover, overexpression was associated with lower PHT levels in the brain, which was reversed through inhibition of MRPs. These data suggest that administration of antiepileptic drugs in combination with specific inhibitors for multidrug transporters may be a promising therapeutic strategy in pharmacoresistant patients.},
	Author = {van Vliet, Erwin A. and Redeker, Sandra and Aronica, Eleonora and Edelbroek, Peter M. and Gorter, Jan A.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0013-9580},
	Journal = {Epilepsia},
	Keywords = {Anticonvulsants;Electric Stimulation;Tissue Distribution;Humans;Animals;Rats;Neoplasm Proteins;07 Excitotoxicity Apoptosis;Brain;Epilepsy;Rats, Sprague-Dawley;ATP-Binding Cassette Transporters;Probenecid;Chronic Disease;Male;Phenytoin;Multidrug Resistance-Associated Proteins;Status Epilepticus;Drug Resistance, Multiple;Membrane Transport Proteins;24 Pubmed search results 2008;Recurrence;Research Support, Non-U.S. Gov't},
	Month = {10},
	Nlm_Id = {2983306R},
	Number = {10},
	Organization = {Epilepsy Institute of the Netherlands (SEIN), Heemstede, the Netherlands.},
	Pages = {1569-80},
	Pii = {EPI250},
	Pubmed = {16190927},
	Title = {Expression of multidrug transporters MRP1, MRP2, and BCRP shortly after status epilepticus, during the latent period, and in chronic epileptic rats},
	Uuid = {AF896A2B-C856-4E33-828A-4E2F323763A2},
	Volume = {46},
	Year = {2005},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1528-1167.2005.00250.x}}

@article{Eijnde:1999,
	Abstract = {Apoptosis is a critical cellular event during several stages of neuronal development. Recently, we have shown that biotinylated annexin V detects apoptosis in vivo in various cell lineages of a wide range of species by binding to phosphatidylserines that are exposed at the outer leaflet of the plasma membrane. In the present study, we tested the specificity by which annexin V binds apoptotic neurons, and subsequently investigated developmental cell death in the central and peripheral nervous system of early mouse embryos at both the cellular and histological level, and compared the phagocytic clearance of apoptotic neurons with that of apoptotic mesodermal cells. Our data indicate: (i) that biotinylated annexin V can be used as a sensitive marker that detects apoptotic neurons, including their extensions at an early stage during development; (ii) that apoptosis plays an important part during early morphogenesis of the central nervous system, and during early quantitative matching of brain-derived neurotrophic factor and neurotrophic factor 3 responsive postmitotic large clear neurons in the peripheral ganglia with their projection areas; and (iii) that apoptotic neurons are removed by a process that differs from classical phagocytosis of non-neuronal tissues.},
	Author = {van den Eijnde, S. M. and Lips, J. and Boshart, L. and Vermeij-Keers, C. and Marani, E. and Reutelingsperger, C. P. and De Zeeuw, C. I.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Annexin V;Phagocytosis;Animals;Rats;Ganglia, Spinal;Apoptosis;Optic Nerve;Neurites;Rats, Wistar;Not relevant;11 Glia;Animals, Newborn;Support, Non-U.S. Gov't;Neurons;Cerebellum;Mice;Trigeminal Nerve;Microscopy, Electron},
	Medline = {99171961},
	Month = {2},
	Nlm_Id = {8918110},
	Number = {2},
	Organization = {MGC Department of Clinical Genetics, Institute of Plastic Surgery, Erasmus University Medical School, Rotterdam, The Netherlands. vandeneijnde\@ikg.fgg.eur.nl},
	Pages = {712-24},
	Pubmed = {10051772},
	Title = {Spatiotemporal distribution of dying neurons during early mouse development},
	Uuid = {38E772A8-68A5-4B0D-8987-1B89AA882CE0},
	Volume = {11},
	Year = {1999},
	url = {papers/Eijnde_EurJNeurosci1999.pdf}}

@article{Pol:2003,
	Abstract = {Olfactory ensheathing cells (OECs) have considerable potential for facilitating axonal growth across regions of spinal cord and brain injury but in this context have been studied primarily in static images of fixed tissue from the olfactory system or after transplantation. In the present work, we studied the behavior of live OECs, and their interactions with neurons, Schwann cells, and astrocytes by using cells that express the reporter gene coding for green fluorescent protein (GFP); the work is based on combinations of fluorescence, phase contrast, digital time lapse imaging, and P75 immunocytochemical identification. Cultures, explants, and regions of olfactory system slices rich in OECs enhanced axonal growth of cerebellar granule cells or hippocampal neurons; axons grew parallel to the long axis of fusiform OECs. Neuron cell bodies and axons preferred OECs over artificial substrates. Axons and neuron cell bodies can take active or passive roles in extension and migration on underlying motile OECs and move from one OEC to another. Axon extension was facilitated to a similar degree by OECs and Schwann cells, whereas astrocytes were more likely to integrate with existing OECs than with Schwann cells. OECs showed a dramatic ability to rapidly change shape, size, and direction of migration and to undergo mitosis. Mitosis was characterized by a quick retraction of all processes, thereby forming a sphere that divided into spherical daughter cells within minutes. Progeny OECs might take on the parental or a non-parental morphotype, with both daughter cells showing robust expression of GFP. Together these OEC data demonstrated a substantial plasticity and capability for relatively rapid changes in structure and support the view that OECs have multiple attributes favorable for enhancing axonal extension and neuronal migration after central nervous system injury. 0021-9967 Journal Article},
	Author = {van den Pol, A. N. and Santarelli, J. G.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Journal = {J Comp Neurol},
	Keywords = {Microscopy, Video;Animals;Astrocytes/*cytology;Cell Communication/*physiology;Neurons/*cytology;Neuronal Plasticity/physiology;Mitosis/physiology;Cerebellum/cytology;L pdf;Mice, Transgenic;17 Transplant Regeneration;Olfactory Pathways/*cytology;Cell Division/physiology;Support, U.S. Gov't, P.H.S.;Cell Movement/physiology;Mice;Cell Adhesion/physiology;Organ Culture;Luminescent Proteins/genetics;Indicators and Reagents/metabolism;Schwann Cells/*cytology},
	Number = {2},
	Organization = {Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06520, USA. anthony.vandenpol\@yale.edu},
	Pages = {175-94},
	Title = {Olfactory ensheathing cells: time lapse imaging of cellular interactions, axonal support, rapid morphologic shifts, and mitosis},
	Uuid = {55B1EB8E-0C01-4D3E-95CA-34A50F2DB45C},
	Volume = {458},
	Year = {2003},
	url = {papers/Pol_JCompNeurol2003}}

@article{Pol:2002,
	Abstract = {A new recombinant vesicular stomatitis virus (rVSV) that expresses green fluorescent protein (GFP) on the cytoplasmic domain of the VSV glycoprotein (G protein) was used in the mouse as a model for studying brain infections by a member of the Mononegavirales order that can cause permanent changes in behavior. After nasal administration, virus moved down the olfactory nerve, first to periglomerular cells, then past the mitral cell layer to granule cells, and finally to the subventricular zone. Eight days postinoculation, rVSV was eliminated from the olfactory bulb. Little sign of infection could be found outside the olfactory system, suggesting that anterograde or retrograde axonal transport of rVSV was an unlikely mechanism for movement of rVSV out of the bulb. When administered intracerebrally by microinjection, rVSV spread rapidly within the brain, with strong infection at the site of injection and at some specific periventricular regions of the brain, including the dorsal raphe, locus coeruleus, and midline thalamus; the ventricular system may play a key role in rapid rVSV dispersion within the brain. Thus, the lack of VSV movement out of the olfactory system was not due to the absence of potential for infections in other brain regions. In cultures of both mouse and human central nervous system (CNS) cells, rVSV inoculations resulted in productive infection, expression of the G-GFP fusion protein in the dendritic and somatic plasma membrane, and death of all neurons and glia, as detected by ethidium homodimer nuclear staining. Although considered a neurotropic virus, rVSV also infected heart, skin, and kidney cells in dispersed cultures. rVSV showed a preference for immature neurons in vitro, as shown by enhanced viral infection in developing hippocampal cultures and in the outer granule cell layer in slices of developing cerebellum. Together, these data suggest a relative affinity of rVSV for some neuronal types in the CNS, adding to our understanding of the long-lasting changes in rodent behavior found after transient VSV infection. 0022-538x Journal Article},
	Author = {van den Pol, A. N. and Dalton, K. P. and Rose, J. K.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 13:57:02 -0400},
	Journal = {J Virol},
	Keywords = {Hamsters;Human;Animals;Cells, Cultured;J;Vesicular stomatitis-Indiana virus/genetics/*physiology/ultrastructure;15 Retrovirus mechanism;Neurons/cytology/*virology;Brain/cytology/*virology;Olfactory Bulb/virology;Time Factors;Olfactory Nerve/virology;Cell Line;Administration, Intranasal;Dendrites/virology;Recombination, Genetic;Support, U.S. Gov't, Non-P.H.S.;Support, U.S. Gov't, P.H.S.;Mice;Genes, Reporter;Cell Death;Luminescent Proteins/genetics;Gene Expression;Transgenes},
	Number = {3},
	Organization = {Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06520, USA. anthony.vandenpol\@yale.edu},
	Pages = {1309-27},
	Pubmed = {11773406},
	Title = {Relative neurotropism of a recombinant rhabdovirus expressing a green fluorescent envelope glycoprotein},
	Uuid = {46BC1FC4-F857-4510-8E5D-736FFD59F590},
	Volume = {76},
	Year = {2002},
	Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11773406}}

@article{Gucht:2001,
	Abstract = {In this immunocytochemical study, we examined the expression profile of neurofilament protein in the cat visual system. We have used SMI-32, a monoclonal antibody that recognizes a nonphosphorylated epitope on the medium- and high-molecular-weight subunits of neurofilament proteins. This antibody labels primarily the cell body and dendrites of pyramidal neurons in cortical layers III, V, and VI. Neurofilament protein-immunoreactive neurons were prominent in 20 visual cortical areas (areas 17, 18, 19, 20a, 20b, 21a, 21b, and 7; posteromedial lateral, posterolateral lateral, anteromedial lateral, anterolateral lateral, dorsal lateral, ventral lateral, and posterior suprasylvian areas; anterior ectosylvian, the splenial, the cingulate, and insular visual areas; and the anterolateral gyrus area). In addition, we have also found strong immunopositive cells in the A laminae of the dorsal part of the lateral geniculate nucleus (dLGN) and in the medial interlaminar nucleus, but no immunoreactive cells were present in the parvocellular C (1-3) laminae of the dLGN, in the ventral part of the LGN and in the perigeniculate nucleus. This SMI-32 antibody against neurofilament protein revealed a characteristic pattern of immunostaining in each visual area. The size, shape, intensity, and density of neurofilament protein-immunoreactive neurons and their dendritic arborization differed substantially across all visual areas. Moreover, it was also obvious that several visual areas showed differences in laminar distribution and that such profiles may be used to delineate various cortical areas. Therefore, the expression of neurofilament protein can be used as a specific marker to define areal patterns and topographic boundaries in the cat visual system.},
	Author = {van der Gucht, E. and Vandesande, F. and Arckens, L.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:31 -0400},
	Issn = {0021-9967},
	Journal = {J Comp Neurol},
	Keywords = {Visual Cortex;Cell Size;Visual Perception;Research Support, Non-U.S. Gov't;Dendrites;Cats;Immunohistochemistry;Geniculate Bodies;Antibodies, Monoclonal;Neurofilament Proteins;Pyramidal Cells;Antibody Specificity;Animals;Visual Pathways;23 Technique},
	Medline = {21611547},
	Month = {12},
	Nlm_Id = {0406041},
	Number = {4},
	Organization = {Laboratory of Neuroendocrinology and Immunological Biotechnology, Katholieke Universiteit Leuven, Naamsestraat 59, B-3000 Leuven, Belgium.},
	Pages = {345-68},
	Pii = {10.1002/cne.1416},
	Pubmed = {11745654},
	Title = {Neurofilament protein: a selective marker for the architectonic parcellation of the visual cortex in adult cat brain},
	Uuid = {FC814231-D31C-11D9-A0E9-000D9346EC2A},
	Volume = {441},
	Year = {2001}}

@article{Bernhardi:2001,
	Abstract = {Astrocytes and microglia are closely associated with amyloid plaques in Alzheimer's disease (AD). Microglia constitute the first barrier surrounding plaques, although they seem to be unable to remove them efficiently. We evaluated the reaction of microglial cells from neonatal rats and mice to plaque mimetics. The C-terminal part of the amyloid precursor protein (APP) or amyloid peptide (A beta) was immobilized to either 60-microm or 2.8-microm beads and incubated with microglial cells. Beads of 60 microm, having approximately the size of senile plaques, were not phagocytosed, in contrast to 2.8-microm beads, which were phagocytosed by microglia but not by astrocytes. Once taken up by the cells, proteins immobilized to the beads were degraded rapidly, as confirmed by mass spectrometry and immunofluorescence with an antibody against beta-amyloid. On the other hand, no protein degradation was observed with 60-microm beads. Also, probably as a reaction to its incapability to phagocytose the beads, glia organized around the beads and started to proliferate. Cell proliferation was more pronounced when the beads contained the A beta epitope compared with the beads with an inert surface. This in vitro effect could be exploited to set up a screening assay for compounds that ameliorate the adverse reaction of microglia supposed to contribute to the pathogenesis of AD.},
	Author = {von Bernhardi, R. and Ram{\'\i}rez, G. and Matile, H. and D{\"o}beli, H.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:27 -0400},
	Issn = {0953-816X},
	Journal = {Eur J Neurosci},
	Keywords = {Amyloid beta-Protein;Endopeptidases;Indicators and Reagents;Neuroglia;Research Support, Non-U.S. Gov't;Spectrum Analysis, Mass;11 Glia;Amyloid beta-Protein Precursor;Endocytosis;Microspheres;Cells, Cultured;Humans;Cloning, Molecular;Fluorescent Antibody Technique;Nitrites},
	Medline = {21479369},
	Month = {9},
	Nlm_Id = {8918110},
	Number = {6},
	Organization = {Faculty of Medicine, Universidad de los Andes, San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile. rvonb\@uandes.cl},
	Pages = {946-56},
	Pii = {ejn1715},
	Pubmed = {11595033},
	Title = {Immobilized amyloid precursor protein constructs: a tool for the in vitro screening of glial cell reactivity},
	Uuid = {783F6750-A63B-4397-8240-BE8700850E37},
	Volume = {14},
	Year = {2001}}

@article{Holst:2006,
	Abstract = {Neural stem cells have been documented in both the developing and the mature adult CNSs of mammals. This cell population holds a considerable promise for therapeutical applications in a wide array of CNS diseases. Therefore, universally applicable strategies for the purification of this population to further its cell biological characterization are sought. Here, we report that the unique chondroitin sulfate epitope recognized by the monoclonal antibody 473HD is surface expressed on actively cycling, multipotent progenitor cells of the developing telencephalon with radial glia-like properties. When used for immunopanning, the antibody enriched at least threefold for neural stem/progenitor cells characterized by the ability to self-renew as neurospheres that generated all major neural lineages in differentiation assays. In contrast, the 473HD-depleted cell fraction was mostly devoid of neurosphere-forming cells. The isolation of 473HD-positive adult multipotent progenitors from the subependymal zone of the lateral ventricle wall revealed a substantial overlap with the known adult neural stem cell marker LewisX. When the chondroitin sulfates were removed from immunoselected 473HD-positive neural stem/progenitor cell surfaces by chondroitinase ABC treatment or perturbed by the monoclonal antibody 473HD that recognizes the unique DSD-1 chondroitin sulfate epitope, the generation of neurospheres was significantly reduced. Thus, the 473HD epitope could not only be used for the isolation of multipotent neural progenitors during forebrain development as well as from the adult neurogenic niche but may also constitute a functionally important entity of the neural stem cell niche.},
	Author = {von Holst, Alexander and Sirko, Swetlana and Faissner, Andreas},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2011-09-12 11:19:36 -0400},
	Issn = {1529-2401},
	Journal = {J Neurosci},
	Keywords = {24 Pubmed search results 2008},
	Month = {4},
	Nlm_Id = {8102140},
	Number = {15},
	Organization = {Cell Morphology and Molecular Neurobiology, Faculty of Biology, Ruhr-University Bochum, D-44780 Bochum, Germany.},
	Pages = {4082-94},
	Pii = {26/15/4082},
	Pubmed = {16611825},
	Title = {The unique 473HD-Chondroitinsulfate epitope is expressed by radial glia and involved in neural precursor cell proliferation},
	Uuid = {9447A27D-1611-4392-8C4D-099B1868DCD0},
	Volume = {26},
	Year = {2006},
	Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.0422-06.2006}}

@article{Zahn:1997,
	Abstract = {Activation of microglial cells in neurological diseases involves proliferation and the induction of phagocytic and cytotoxic properties. We studied the effects of four different cytokines on microglial phagocytosis of latex beads to gain further insights into the signals modulating different aspects of microglial activity. Granulocyte/macrophage colony stimulating factor and tumor necrosis factor-alpha enhanced microglial phagocytic activity as measured by flow cytometry. A phagocytosis inhibiting effect was observed after preincubation with transforming growth factor-beta1 and interleukin-4. In conclusion, the activating and deactivating cytokines differentially regulate microglial phagocytic activity in vitro and might also play an important role in vivo in modulating microglial activation to keep the balance between the protective, defensive and destructive, chronic inflammatory properties of microglia.},
	Author = {von Zahn, J. and M{\"o}ller, T. and Kettenmann, H. and Nolte, C.},
	Date-Added = {2009-03-25 19:34:04 -0400},
	Date-Modified = {2009-03-25 19:55:45 -0400},
	Issn = {0959-4965},
	Journal = {Neuroreport},
	Keywords = {Cells, Cultured;Flow Cytometry;Research Support, Non-U.S. Gov't;Interleukin-4;Cytokines;Inflammation;Granulocyte-Macrophage Colony-Stimulating Factor;Tumor Necrosis Factor-alpha;Microglia;Transforming Growth Factor beta;11 Glia;Microspheres;Mice;Animals;Phagocytosis;Mice, Inbred Strains;Lipopolysaccharides},
	Medline = {98122286},
	Month = {12},
	Nlm_Id = {9100935},
	Number = {18},
	Organization = {University Hospital Benjamin Franklin, Berlin, Germany.},
	Pages = {3851-6},
	Pubmed = {9462454},
	Title = {Microglial phagocytosis is modulated by pro- and anti-inflammatory cytokines},
	Uuid = {908194C7-E3B0-4DBC-9B0A-405906B234E7},
	Volume = {8},
	Year = {1997}}

@article{Mez:2017,
	Abstract = {Importance: Players of American football may be at increased risk of long-term neurological conditions, particularly chronic traumatic encephalopathy (CTE).
Objective: To determine the neuropathological and clinical features of deceased football players with CTE.
Design, Setting, and Participants: Case series of 202 football players whose brains were donated for research. Neuropathological evaluations and retrospective telephone clinical assessments (including head trauma history) with informants were performed blinded. Online questionnaires ascertained athletic and military history.
Exposures: Participation in American football at any level of play.
Main Outcomes and Measures: Neuropathological diagnoses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichotomized into mild [stages I and II] and severe [stages III and IV]); informant-reported athletic history and, for players who died in 2014 or later, clinical presentation, including behavior, mood, and cognitive symptoms and dementia.
Results: Among 202 deceased former football players (median age at death, 66 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; median age at death, 67 years [interquartile range, 52-77 years]; mean years of football participation, 15.1 [SD, 5.2]), including 0 of 2 pre-high school, 3 of 14 high school (21%), 48 of 53 college (91%), 9 of 14 semiprofessional (64%), 7 of 8 Canadian Football League (88%), and 110 of 111 National Football League (99%) players. Neuropathological severity of CTE was distributed across the highest level of play, with all 3 former high school players having mild pathology and the majority of former college (27 [56%]), semiprofessional (5 [56%]), and professional (101 [86%]) players having severe pathology. Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms, and 9 (33%) had signs of dementia. Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms, and 71 (85%) had signs of dementia.
Conclusions and Relevance: In a convenience sample of deceased football players who donated their brains for research, a high proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior participation in football.},
	Author = {Mez, Jesse and Daneshvar, Daniel H and Kiernan, Patrick T and Abdolmohammadi, Bobak and Alvarez, Victor E and Huber, Bertrand R and Alosco, Michael L and Solomon, Todd M and Nowinski, Christopher J and McHale, Lisa and Cormier, Kerry A and Kubilus, Caroline A and Martin, Brett M and Murphy, Lauren and Baugh, Christine M and Montenigro, Phillip H and Chaisson, Christine E and Tripodis, Yorghos and Kowall, Neil W and Weuve, Jennifer and McClean, Michael D and Cantu, Robert C and Goldstein, Lee E and Katz, Douglas I and Stern, Robert A and Stein, Thor D and McKee, Ann C},
	Date-Added = {2018-01-16 23:13:03 +0000},
	Date-Modified = {2018-01-16 23:13:03 +0000},
	Doi = {10.1001/jama.2017.8334},
	Journal = {JAMA},
	Journal-Full = {JAMA},
	Mesh = {Adult; Aged; Athletes; Athletic Injuries; Brain; Brain Concussion; Cause of Death; Chronic Traumatic Encephalopathy; Cognition Disorders; Football; Humans; Male; Mental Disorders; Middle Aged; Severity of Illness Index; Substance-Related Disorders; United States; tau Proteins},
	Month = {07},
	Number = {4},
	Pages = {360-370},
	pmid = {28742910},
	Pst = {ppublish},
	Title = {Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football},
	Volume = {318},
	Year = {2017},
	url = {papers/Mez_JAMA2017.pdf}}

@article{McKee:2014,
	Abstract = {The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable. Physical activity reduces the risk for cardiovascular disease, type 2 diabetes, hypertension, obesity, and stroke, and produces beneficial effects on cholesterol levels, antioxidant systems, inflammation, and vascular function. Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration. Nonetheless, the play of sports is associated with risks, including a risk for mild TBI (mTBI) and, rarely, catastrophic traumatic injury and death. There is also growing awareness that repetitive mTBIs, such as concussion and subconcussion, can occasionally produce persistent cognitive, behavioral, and psychiatric problems as well as lead to the development of a neurodegeneration, chronic traumatic encephalopathy (CTE). In this review, we summarize the beneficial aspects of sports participation on psychological, emotional, physical and cognitive health, and specifically analyze some of the less common adverse neuropathological outcomes, including concussion, second-impact syndrome, juvenile head trauma syndrome, catastrophic sudden death, and CTE. CTE is a latent neurodegeneration clinically associated with behavioral changes, executive dysfunction and cognitive impairments, and pathologically characterized by frontal and temporal lobe atrophy, neuronal and axonal loss, and abnormal deposits of paired helical filament (PHF)-tau and 43 kDa TAR deoxyribonucleic acid (DNA)-binding protein (TDP-43). CTE often occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including motor neuron disease (CTE-MND). Although the incidence and prevalence of CTE are not known, CTE has been reported most frequently in American football players and boxers. Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball.},
	Author = {McKee, Ann C and Daneshvar, Daniel H and Alvarez, Victor E and Stein, Thor D},
	Date-Added = {2018-01-16 23:12:43 +0000},
	Date-Modified = {2018-01-16 23:12:43 +0000},
	Doi = {10.1007/s00401-013-1230-6},
	Journal = {Acta Neuropathol},
	Journal-Full = {Acta neuropathologica},
	Mesh = {Animals; Athletic Injuries; Brain; Brain Injuries; Cognition; Humans; Sports},
	Month = {Jan},
	Number = {1},
	Pages = {29-51},
	Pmc = {PMC4255282},
	pmid = {24366527},
	Pst = {ppublish},
	Title = {The neuropathology of sport},
	Volume = {127},
	Year = {2014},
	url = {papers/McKee_ActaNeuropathol2014.pdf}}

@article{Iverson:2004,
	Abstract = {PRIMARY OBJECTIVE: To examine the possibility that athletes with multiple concussions show cumulative effects of injury.
METHODS AND PROCEDURES: Amateur athletes with a history of three or more concussions were carefully matched (gender, age, education and sport) with athletes with no prior concussions. All completed a computerized neuropsychological test battery at preseason (ImPACT) and then within 5 days of sustaining a concussion (mean = 1.7 days).
MAIN OUTCOMES AND RESULTS: There were differences between groups in symptom reporting and memory performance. At baseline (i.e. preseason), athletes with multiple concussions reported more symptoms than athletes with no history of concussion. At approximately 2 days post-injury, athletes with multiple concussions scored significantly lower on memory testing than athletes with a single concussion. Athletes with multiple concussions were 7.7 times more likely to demonstrate a major drop in memory perfomance than athletes with no previous concussions.
CONCLUSIONS: This study provides preliminary evidence to suggest that athletes with multiple concussions might have cumulative effects.},
	Author = {Iverson, Grant L and Gaetz, Michael and Lovell, Mark R and Collins, Michael W},
	Date-Added = {2018-01-16 22:39:33 +0000},
	Date-Modified = {2018-01-16 22:39:33 +0000},
	Doi = {10.1080/02699050310001617352},
	Journal = {Brain Inj},
	Journal-Full = {Brain injury},
	Mesh = {Adolescent; Amnesia; Analysis of Variance; Athletic Injuries; Brain Concussion; Cumulative Trauma Disorders; Humans; Male; Memory; Neuropsychological Tests; Post-Concussion Syndrome; Psychomotor Performance; Reaction Time},
	Month = {May},
	Number = {5},
	Pages = {433-43},
	pmid = {15195792},
	Pst = {ppublish},
	Title = {Cumulative effects of concussion in amateur athletes},
	Volume = {18},
	Year = {2004},
	url = {papers/Iverson_BrainInj2004.pdf},
	Bdsk-Url-1 = {http://dx.doi.org/10.1080/02699050310001617352}}

@article{Itzhaki:2016,
	Author = {Itzhaki, Ruth F and Lathe, Richard and Balin, Brian J and Ball, Melvyn J and Bearer, Elaine L and Braak, Heiko and Bullido, Maria J and Carter, Chris and Clerici, Mario and Cosby, S Louise and Del Tredici, Kelly and Field, Hugh and Fulop, Tamas and Grassi, Claudio and Griffin, W Sue T and Haas, J{\"u}rgen and Hudson, Alan P and Kamer, Angela R and Kell, Douglas B and Licastro, Federico and Letenneur, Luc and L{\"o}vheim, Hugo and Mancuso, Roberta and Miklossy, Judith and Otth, Carola and Palamara, Anna Teresa and Perry, George and Preston, Christopher and Pretorius, Etheresia and Strandberg, Timo and Tabet, Naji and Taylor-Robinson, Simon D and Whittum-Hudson, Judith A},
	Date-Added = {2018-07-16 21:29:57 +0000},
	Date-Modified = {2018-07-16 21:29:57 +0000},
	Doi = {10.3233/JAD-160152},
	Journal = {J Alzheimers Dis},
	Journal-Full = {Journal of Alzheimer's disease : JAD},
	Mesh = {Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Communicable Diseases; Humans; Microbiota},
	Number = {4},
	Pages = {979-84},
	Pmc = {PMC5457904},
	pmid = {26967229},
	Pst = {ppublish},
	Title = {Microbes and Alzheimer's Disease},
	Volume = {51},
	Year = {2016},
	url = {papers/Itzhaki_JAlzheimersDis2016.pdf}}

