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1
Charbord, Jérémie. "Criblage à haut débit d'inhibiteurs du répresseur de transcription REST dans des progénies neurales issues de cellules souches embryonnaires humaines". Thesis, Evry-Val d'Essonne, 2012. http://www.theses.fr/2012EVRY0004.
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Nous avons identifié des inhibiteurs pharmacologiques de REST capables d’augmenter l’expression d’un ensemble de gènes cibles de REST (gènes RE1) neuronaux dans des cellules souches neurales (NSC) issues de cellules souches embryonnaires humaines (HESC). De tels composés ont pour intérêt de constituer un nouveau type d’outil pour étudier la fonction de REST dans la prolifération et la différenciation des NSC normales ou pathologiques et pourraient posséder des propriétés thérapeutiques dans les maladies ou une sur-activation de REST participe ou marque la pathologie cellulaire telles que la maladie de Huntington ou certaines tumeurs du cerveau. L’identification des inhibiteurs de REST a été réalisée grâce à la technologie puissante du criblage à haut débit (HTS). Le succès de cette méthode a reposé sur l’élaboration d’un test cellulaire fonctionnel robuste de l’activité de REST dans les NSC. Un système rapporteur de cette activité a été construit autour d’une cassette d’expression de la Luciferase Renilla placée sous le contrôle d’un promoteur constitutif fort. Plusieurs sites RE1 ont été insérés en amont de cette cassette afin de rendre l’expression de la Luciferase dépendante de l’activité de REST. Nous avons ainsi isolé le compose x5050, un benzimidazole qui entraîne, comme montre par l’étude transcriptomique, la surexpression spécifique des gènes RE1 neuronaux. x5050 ne modifie ni la transcription de REST ni la fixation de REST sur une séquence oligonucléotidique RE1 marquée. En revanche, x5050 entraîne la diminution du niveau de la protéine REST, vraisemblablement en modulant la dégradation de REST par le système ubiquitine-protéasomeOur goal was to identify pharmacological inhibitors of REST that would be able to increase the expression of a set of neuronal gene targets of REST (RE1 genes) in human neural stem cells (NSCS) derived from human embryonic stem cells (HESC). These compounds would at first provide a new type of tool to better understand REST action on proliferation and differentiation in normal or pathological NSCS and could have therapeutical properties for diseases in which an over-activation of REST is implicated in or influences cellular pathology such as huntington’s disease or some brain tumors. Identification of REST inhibitors was performed using the powerful technology of high throughput screening (HTS). Success of this method was based on the set up of a robust functional cell assay of REST activity in NSCS. A reporter system of this activity has been constructed using an expression cassette of the renilla luciferase placed under control of a strong constitutive promoter. Several RE1 sites have been inserted upstream of this cassette to make the expression of Luciferase dependent on REST activity. We have isolated x5050 compound, a benzimidazole which leads to upregulation of RE1 genes as shown by transcriptomic studies. x5050 modified neither rest transcription nor rest fixation on a labeled nucleotidic RE1 sequence. On the contrary, x5050 treatment induced the decrease in rest protein level, probably by modulating REST degradation by the ubiquitin-proteasome system
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Sandberg, Magnus. "Sox proteins and neurogenesis". Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-873-0/.
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Brill, Monika. "Regionalization of adult neurogenesis". Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-101449.
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Aaku-Saraste, E. (Eeva). "A prelude to neurogenesis". Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514253655.
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Abstract
All neurons and macroglial cells of vertebrates derive from the neuroepithelium. Neuroepithelial (NE) cells first proliferate and, after closure of the neural tube, some cells start generating neurons. It is still unclear what triggers differentiation but apparently there is interplay between extrinsic (secreted or transmembrane signals) and intrinsic factors. Diriving from the embryonic ectoderm, the NE cells inherit epithelial characteristics. It has been shown in other developmental systems that epithelial determinants, such as cell-cell contacts and contact to basal laminar components can guide differentiation.
The key epithelial features include cell polarity, and tight junctions. We studied these in the NE at two developmental stages, the neural plate, a proliferative stage and the neural tube, a differentiative stage.
The polarity of membrane proteins in NE cells was studied with polarly budding viruses. Mouse embryos were infected with Fowl plague- and vesicular stomatitis viruses and cultured in a whole embryo culture system. Viral envelope proteins (HA and G-protein) were localized by indirect immunofluorescence and immunoelectron microscopy. HA was polarized in the plate stage neuroepithelial cells, whereas in the tube it was not polarized anymore.
It is also shown by penetrance of apically injected horseradish peroxidase that in the neural plate, NE cells have functional tight junctions. At this stage, they also express occludin, a transmembrane protein of tight junctions, as shown by indirect immunofluorescence. In the neural tube, the paracellular barrier is lost and there is no occludin expression. In contrast, expression of ZO-1, a cytoplasmic protein binding to occiudin, is upregulated.
The downregulation of these epithelial features occurs in all NE cells, irrespective of their mode of division and before any neurons are generated in the NE. The change is initiated already at the plate stage and coincides with the switch from E- to N-cadherin. Later, with birth of neurons, the proliferative cell layer also looses contact to basal lamina. This is probably an important step in the regulation of neurogenesis. Furthermore, lack of apico-basolateral polarity of non-anchored membrane proteins may contribute to the mechanism of rapid neuron generation.
Until now, it has been impossible to distinguish a neuroepithelial cell preparing for neuron generation from the surrounding cells that give rise to two precursor cells. In this study, the immediate neuron precursors are shown to express the antiproliferative gene TIS2 1. Using this new marker and ISH in serial sections, we show that the switch to differentiation is initiated in single NE cells.
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Tosti, Claudia. "NEUROGENESIS IN UTERINE DISORDERS". Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1095599.
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Endometriosis, adenomyosis and uterine fibroids represent benign gynecologic diseases, affecting women of reproductive age associated with chronic pelvic pain, dysmenorrhea, dyspareunia and infertility.
The present knowledge indicates that hormonal function (estrogen and progesterone receptors), immunological and neuroinflammatory factors are critically altered in every of uterine disorders.
The aggressive behaviour of deep infiltrating endometriosis may be explained by the highly decreased apoptosis, by the increased proliferation activity related to oxidative stress and by invasive neurogenic mechanisms and inflammatory patterns that explain its correlation with chronic pelvic pain. Adenomyotic nodules are novel site of protein expression of inflammatory and neurogenic factors, probably involved in the pathogenesis of adenomyosis: endometrial cells invade and proliferate within myometrium, and inflammatory mediators participate to the intense painful symptoms.
The increased expression of neurogenic factors in uterine fibroids and endometrium may contribute to explain the painful stimuli; in addition, NGF hyperexpression, in both fibroids and endometrium, may be associated with infertility. Accordingly, in the future, these neurogenic factors may represent potential therapeutic avenues to treat the fibroid-related symptoms.
In conclusion, our results give new insights into the neurogenic characteristics of uterine disorders showing that endometriosis, adenomyosis and fibroids has distinct molecular patterns.
With further advances in our understanding of uterine disorders, preventive strategies, novel non-surgical diagnostic modalities, and targeted therapeutics hold great promise of becoming realities and help to treat our patients.
The future research may contribute to a better phenotyping of these benign gynaecological diseases in order to give a specific efficient management to each disorder. Basic science approach is necessary to increase pathogenesis knowledge of endometriosis, adenomyosis and uterine fibroids, and new medical treatment, and the clinical and diagnostic approach is necessary for planning an accurate surgical or medical treatment.
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Vaculik, Michael. "Beclin1 Regulates Adult Hippocampal Neurogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32994.
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Adult neurogenesis is a process that produces neurons in the adult brain and garners potential for the development of novel therapeutic interventions to combat neurodegenerative and other brain related diseases. With the hope of increasing neurogenesis, active investigations are defining the cellular and molecular mechanisms that regulate adult neural precursor cell (NPC) survival, and thus maintain neurogenesis. Recently, autophagy, an intracellular recycling pathway, has been implicated in regulating adult NPCs in embryonic knockout mice models. Whether autophagy has a similar effect within the adult and how autophagy regulates development of adult NPC remains unknown. Here, we investigate the role of Beclin1, a gene responsible for autophagy induction, in adult hippocampal NPC function in mice. Retroviral-mediated removal of Beclin1 from proliferating adult NPCs in vivo led to a reduction in the survival of adult-born neurons. In addition, Beclin1 was removed specifically from nestin-expressing adult neural stem- and progenitor-cells through the development of a Beclin1 nestin-inducible knockout mouse. Beclin1 nKO mice had a reduction in NPC proliferation and development, and overall fewer adult-generated neurons. Together, these findings reveal Beclin1 is required for adult hippocampal neurogenesis through regulating the proliferation and survival of the NPCs, in the absence of changing NPC fate.
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Dhaliwal, Jagroop. "Regulators of Adult Hippocampal Neurogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35712.
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One mechanism of plasticity within the adult mammalian brain is the dynamic process of adult neurogenesis that is functionally important in physiological and pathological conditions. During this process, neurons develop from adult neural stem cells (NSCs) via intermediate neural progenitors (NPCs) through several processes including proliferation, survival, differentiation, migration and integration. Despite neurogenesis during development sharing these same processes, there is growing evidence highlighting unique mechanisms that regulate adult versus embryonic neurogenesis.
The studies in this thesis test the cell-intrinsic function of genes that have defined roles in embryonic neurogenesis and undefined roles in adult hippocampal neurogenesis using a combination of transgenic inducible mice and in vivo retroviral techniques. The first study examines the microtubule associated protein Doublecortin (DCX), which is transiently expressed by NPCs and is critical for neuronal migration. Our results show that, in the context of adult hippocampal neurogenesis, DCX is not required for the survival or differentiation of the NPCs within the subgranular zone (SGZ). The second study examines the functional role of the autophagy-associated gene 5 (Atg5) which is critical for embryonic neurogenesis and survival. Our findings demonstrate that the intracellular recycling process of autophagy is active throughout maturation of adult hippocampal NPCs and that ablation of Atg5 produces a drastic reduction in NPC survival, without altering the neuronal fate of these cells. The third study examines the requirement of the familial-Alzheimer’s disease associated genes, presenilin 1 and presenilin 2 (PS1 & PS2), which are critical for embryonic NSC maintenance and differentiation. Similar to the findings with DCX, our results demonstrate that presenilins are dispensable for adult neurogenesis. Altogether, these studies add to the growing evidence suggesting differences in the regulation of adult versus embryonic neurogenesis, and highlight autophagy as a novel regulator of survival for adult generated granule neurons in the hippocampus.
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Teutenberg, Kevin. "Glucose, glucose transporters and neurogenesis". Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/28026.
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Since the pioneering work of Altman in the late 60's, much has been learned about the generation of neurons in the adult brains of several species, including mice, rats, and humans. An underlying assumption is that these newborn neurons acquire their energy, in the form of glucose, in a similar manner to mature neurons: via glucose transporters. Using BRDU and double immunohistochemistry, we investigated the relationship between hippocampal neurogenesis and glucose transporters, as well as monocarboxylate transporters. Unexpectedly, the results suggest that newborn neurons do not acquire their energy via the major glucose transporters (1, 3, 4, and 8), nor via either monocarboxylate transporter tested (1 and 2). Future studies will have to resolve whether lesser known glucose transporters carry this function or if other mechanisms are used to provide metabolic energy to newborn neurons.
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Wright, Rupert. "Engineering surfaces to control neurogenesis". Thesis, Keele University, 2015. http://eprints.keele.ac.uk/2350/.
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Producing therapeutic neural cell populations in vitro to treat neurodegenerative diseases is a key aim of regenerative medicine. Various protocols have been developed to produce a wide range of neural cell types in vitro, but the protocols are labour and resource intensive. Lower costs will take the cell therapy closer to clinical adoption. Cell-material interactions can be used to control cellular processes and behaviours in the place of expensive reagents. The thesis went about developing superior materials to culture neurons in vitro by using simple surface parameters. By using simple surfaces findings could be leveraged by incorporation in to other materials, and protocols to culture neurons. We have investigated the responses of primary neural tissue derived from rat ventral mesencephalon (VM), interacting with a range of surface chemical functionalities and net molecular properties by using silanes. Specific substrate functionality leads to higher ratios of neurons, longer neurites and neurosphere spreading capacity. All of these characteristics indicate a high neuro-regenerative capacity. Next it became important to optimize the amine functionalised surface with the addition of secondary amines in to the surface. The rational of adding secondary amines to the surface would produce functionalities which have a closer resemblance to biological molecules. The biomimicry in the surfaces provides extra scope for selective surface interactions to provide more control over neural cell culture which could steer protocols away from the use of expensive surfaces which are coated in extra cellular matrix molecules such as laminin. Controlling differentiation with surfaces has long been an aim in regenerative medicine to deliver productive production protocols. It has been shown that surfaces can induce differentiation of stem cells; however there is little control where stem cells and adult cells are simultaneously cultured. To achieve controlled differentiation of neural stem cells a surface gradient of amine polymer lengths, and polymer densities. That is in contrast to the surfaces used in previous chapters which had homogeneous presentations of surface chemistries.
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Lyons, David Anthony. "Neurogenesis in the zebrafish hindbrain". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407357.
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Howell, Owain W. "Neuropeptide Y modulates hippocampal neurogenesis". Thesis, University of Southampton, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403849.
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Rooney, Alasdair Grant. "Matrix signalling and hippocampal neurogenesis". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33168.
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The adult mammalian brain harbours at least two germinal - or neurogenic - niches in which new neurons are born throughout life. These neurogenic niches comprise the subependymal zone which lines the ventricular system, and the subgranular zone in the hippocampal dentate gyrus. Post-natal hippocampal neurogenesis was in fact first identified experimentally in the 1960s. However perhaps due partly to aforementioned institutionalised belief and partly to a lack of accessible experimental tools, the phenomenon of hippocampal neurogenesis was widely recognised by the scientific community only shortly before the millennium. Consequent study has established that adult hippocampal neurogenesis has been conserved through millions of years of evolution in nearly every mammalian species studied to date. Importantly, post-mortem studies and radioisotope carbon dating techniques suggest that it also occurs in humans. A great deal of this research has focused on understanding the inner workings of the cells that undergo the transformation to become new adult-born neurons. By contrast, relatively little is known about the potential regulatory role of the surrounding extracellular microenvironment. This might be useful to know in light of much evidence that the extracellular matrix is a key regulator of developmental neurogenesis. This thesis describes my study of whether extracellular matrix regulates hippocampal neurogenesis.
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Tata, M. A. J. "Vascular regulation of embryonic neurogenesis". Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1531030/.
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Neural progenitor cells (NPCs) in the embryonic nervous system generate a large number and variety of neurons in a process known as neurogenesis. NPCs reside in a regulatory ‘niche’ that provides an extensive array of diverse signals, and loss of any one of these signals can deplete the pool of NPCs and therefore impair neural development. These niche signals are most commonly studied in the forebrain, where a complex array of cell divisions yields a set of diverse NPCs. In contrast, little is known on the role of niche signals in regulating the behaviour of NPCs in the hindbrain, the evolutionary oldest part of the brain that is essential for many vital bodily functions. In the adult brain, blood vessels and the vascular growth factor VEGF-A regulate the behaviour of neural stem cells (NSC). However, it is not known whether either also regulates hindbrain neurogenesis. For my PhD research, I have used the mouse embryo hindbrain as a model to examine the role of blood vessels and VEGF-A receptors in developmental neurogenesis. My studies have revealed that NPCs divide most actively during a period of extensive blood vessel growth in the hindbrain, that hindbrain NPCs reside within a well-vascularised germinal zone (GZ) and that they make physical contact with the GZ vasculature. To establish whether VEGF-A receptors or hindbrain blood vessels regulate the behaviour of hindbrain NPCs, I have analysed mouse embryos lacking the neurovascular cell surface receptor NRP1 in either the neural or endothelial lineages. I found that NRP1 regulates the proliferative behaviour of hindbrain NPCs through its role in promoting GZ vascularisation, but not as a receptor for VEGF-A in NPCs. I have further shown that GZ vasculature sustains the size of the NPC pool through the period of hindbrain neurogenesis and may do so by limiting the expression of pro-differentiation signals to set the pace of neurogenesis. Even though blood vessels are best know for their role in tissue oxygenation, my results also show that NRP1-dependent GZ vasculature does not regulate hindbrain NPC behaviour through its role in oxygenating the neuroepithelium. In conclusion, my results identify an essential role for blood vessels in regulating NPC behaviour in the embryonic hindbrain and have increased our understanding of the regulatory niche that orchestrates developmental neurogenesis.
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Attardo, Alessio. "Novel in vivo imaging approaches to study embryonic and adult neurogenesis in the mouse". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1169813208146-70320.
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Neurogenesis is the process of generation of neurons during embryonic development and adulthood. The focus of this doctoral work is the study of the cell biological aspects of neurogenesis and the mechanisms regulating the switch of neural stem cells from proliferation to differentiation. During embryonic development neurogenic divisions occur at the apical or basal side of the pseudostratified epithelium that forms the wall of the neural tube, the neuroepithelium. Apical asymmetric neurogenic divisions (AP) give rise to a neuron and a progenitor cell, while basal symmetric neurogenic divisions (BP) give rise to two neurons. The first part of this thesis is focused on the study of some cell biological aspects of BPs. We first validated the use of the Tis21-GFP knock in mouse line, previously generated in our laboratory. We found that the totality of neurogenic progenitors is marked by the expression of a nuclear GFP. We calculated the abundance of BPs overtime since the onset of neurogenesis showing that BPs overcome APs over development. We studied the loss of apical contact of the basal dividing cells. We found that both neurogenic and non-neurogenic basally dividing progenitors miss the apical contact; which is lost prior mitosis. We generated and characterized a second mouse line, the Tubb3-GFP line expressing a plasma membrane-localized GFP in neurons. These two lines were crossed to obtain a new line (TisTubb-GFP) allowing detection of neurogenic divisions and tracking daughter cells. Using this model: (i) we imaged symmetric neurogenic divisions of BPs, identifying daughter cells as neurons, during imaging; (ii) we compared the kinetics of betaIII-tubulin-GFP appearance after apical or basal mitosis, showing that daughters of BPs express betaIII-tubulin-GFP faster than daughters coming from apical divisions; (iii) we imaged neuronal migration and localization of the Golgi apparatus. Neurogenesis in the adult is confined to two specific regions in the telencephalon: the sub ependymal zone, lining the ventricle, and dentate gyrus of the hippocampus. The second part of this thesis focuses on the adult neurogenic progenitors lineage. Tis21-GFP expression was found and characterized in the two adult neurogenic regions from early postnatal to adulthood. Using a panel of markers for the adult neurogenic cell lineage and confocal imaging, we characterized Tis21-GFP expression, in the dentate gyrus. Tis21-GFP is first expressed in the neurogenic subpopulation of doublecortin positive cells. Tis21-GFP is inherited by the neurons and eventually degraded. Moreover, our data suggest that mitotic Tis21-GFP cells are an indicator of the levels of neurogenesis more accurate than doublecortin positive cells, in the early postnatal mouse. (Anlage Quick time movies 77,88 MB)
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Attardo, Alessio. "Novel in vivo imaging approaches to study embryonic and adult neurogenesis in the mouse". Doctoral thesis, Technische Universität Dresden, 2006. https://tud.qucosa.de/id/qucosa%3A25037.
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Neurogenesis is the process of generation of neurons during embryonic development and adulthood. The focus of this doctoral work is the study of the cell biological aspects of neurogenesis and the mechanisms regulating the switch of neural stem cells from proliferation to differentiation. During embryonic development neurogenic divisions occur at the apical or basal side of the pseudostratified epithelium that forms the wall of the neural tube, the neuroepithelium. Apical asymmetric neurogenic divisions (AP) give rise to a neuron and a progenitor cell, while basal symmetric neurogenic divisions (BP) give rise to two neurons. The first part of this thesis is focused on the study of some cell biological aspects of BPs. We first validated the use of the Tis21-GFP knock in mouse line, previously generated in our laboratory. We found that the totality of neurogenic progenitors is marked by the expression of a nuclear GFP. We calculated the abundance of BPs overtime since the onset of neurogenesis showing that BPs overcome APs over development. We studied the loss of apical contact of the basal dividing cells. We found that both neurogenic and non-neurogenic basally dividing progenitors miss the apical contact; which is lost prior mitosis. We generated and characterized a second mouse line, the Tubb3-GFP line expressing a plasma membrane-localized GFP in neurons. These two lines were crossed to obtain a new line (TisTubb-GFP) allowing detection of neurogenic divisions and tracking daughter cells. Using this model: (i) we imaged symmetric neurogenic divisions of BPs, identifying daughter cells as neurons, during imaging; (ii) we compared the kinetics of betaIII-tubulin-GFP appearance after apical or basal mitosis, showing that daughters of BPs express betaIII-tubulin-GFP faster than daughters coming from apical divisions; (iii) we imaged neuronal migration and localization of the Golgi apparatus. Neurogenesis in the adult is confined to two specific regions in the telencephalon: the sub ependymal zone, lining the ventricle, and dentate gyrus of the hippocampus. The second part of this thesis focuses on the adult neurogenic progenitors lineage. Tis21-GFP expression was found and characterized in the two adult neurogenic regions from early postnatal to adulthood. Using a panel of markers for the adult neurogenic cell lineage and confocal imaging, we characterized Tis21-GFP expression, in the dentate gyrus. Tis21-GFP is first expressed in the neurogenic subpopulation of doublecortin positive cells. Tis21-GFP is inherited by the neurons and eventually degraded. Moreover, our data suggest that mitotic Tis21-GFP cells are an indicator of the levels of neurogenesis more accurate than doublecortin positive cells, in the early postnatal mouse. (Anlage Quick time movies 77,88 MB)
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Kaslin, Jan, i Michael Brand. "Cerebellar Development and Neurogenesis in Zebrafish". Springer, 2013. https://tud.qucosa.de/id/qucosa%3A33555.
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Cerebellar organization and function have been studied in numerous species of fish. Fish models such as goldfish and weakly electric fish have led to important findings about the cerebellar architecture, cerebellar circuit physiology and brain evolution. However, most of the studied fish models are not well suited for developmental and genetic studies of the cerebellum. The rapid transparent ex utero development in zebrafish allows direct access and precise visualization of all the major events in cerebellar development. The superficial position of the cerebellar primordium and cerebellum further facilitates in vivo imaging of cerebellar structures and developmental events at single cell resolution. Furthermore, zebrafish is amenable to high-throughput screening techniques and forward genetics because of its fecundity and easy keeping. Forward genetics screens in zebrafish have resulted in several isolated cerebellar mutants and substantially contributed to the understanding of the genetic networks involved in hindbrain development (Bae et al. 2009; Brand et al. 1996). Recent developments in genetic tools, including the use of site specific recombinases, efficient transgenesis, inducible gene expression systems, and the targeted genome lesioning technologies TALEN and Cas9/CRISPR has opened up new avenues to manipulate and edit the genome of zebrafish (Hans et al. 2009; Scott 2009; Housden et al. 2016; Li et al. 2016)}. These tools enable the use of genome-wide genetic approaches, such as enhancer/exon traps and cell specific temporal control of gene expression in zebrafish. Several seminal papers have used these technologies to successfully elucidate mechanisms involved in the morphogenesis, neurogenesis and cell migration in the cerebellum (Bae et al. 2009; Chaplin et al. ; Hans et al. 2009; Volkmann et al. ; Volkmann et al. 2008). In addition, the use of genetically encoded sensors and probes that allows detection and manipulation of neuronal activity using optical methods have open up new means to study the physiology and function of the cerebellum (Simmich et al. 2012; Matsui et al. 2014). Taken together, these features have allowed zebrafish to emerge as a complete model for studies of molecular, cellular and physiological mechanisms involved in cerebellar development and function at both cell and circuit level.
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Zhang, Yifei. "Fred Regulatory Network in Drosophila Neurogenesis". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1332015401.
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Overall, Rupert. "Modelling genetic networks involved in the activity-dependent modulation of adult neurogenesis". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-164782.
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Die Bildung neuen Nervenzellen im erwachsenen Gehirn—adulte Neurogenese—ist bei Säugetieren auf spezifische Regionen beschränkt. Eine der beiden bekannten ist der Hippokampus, eine Gehirnstruktur, die eine wichtige Rolle beim Lernen sowie der Gedächtnisbildung spielt. Ein Reservoir von neuralen Stammzellen befindet sich in der subgranulären Zone des hippokampalen Gyrus dentatus. Diese Zellen teilen sich fortwährend und bilden neue Nervenzellen. Die Regulation adulter hippokampaler Neurogenese wird sowohl von der Umgebung beeinflusst als auch von mehreren Genen gesteuert. In der vorliegenden Arbeit wurden mittels Hochdurchsatz- Genexpressionsverfahren die an der Neurogenese beteiligten Gene identifiziert und ihr Zusammenspiel untersucht. Anhand von genetischen, umgebungsbedingten und zeitlichen Angaben und Variationen wurde ein vielseitiger Datensatz erstellt, der einen multidimensionalen Blick auf den proliferativen Phänotyp verschafft. Netzwerke aus Gen-Gen und Gen-Phänotyp Interaktionen wurden beschrieben und in einer mehrschichtigen Ressource zusammengefasst. Ein Kern-Netzwerk bestehend aus immerwiederkehrenden Modulen aus verschiedenen Ebenen wurde anhand von Proliferation als Keim-Phänotyp identifiziert. Aus diesem Kern-Netzwerk sind neue Gene und ihre Interaktionen hervorgegangen, die potentiell bei der Regulierung adulter Neurogenesis beteiligt sindNeurogenesis, the production of new neurons, is restricted in the adult brain of mammals to only a few regions. One of these sites of adult neurogenesis is the hippocampus, a structure essential for many types of learning. A pool of stem cells is maintained in the subgranular zone of the hippocampal dentate gyrus which proliferate and can differentiate into new neurons, astrocytes and oligodendroctytes. Regulation of adult hippocampal neurogenesis occurs in response to en- vironmental stimuli and is under the control of many genes. This work employs high-throughput gene expression technologies to identify these genes and their interactions with each other and the neurogenesis phenotype. Harnessing variation from genetic, environmental and temporal sources, a multi-faceted dataset has been generated which offers a multidimensional view of the neural precursor proliferation phenotype. Networks of gene-gene and gene-phenotype interac- tions have been described and merged into a multilayer resource. A core subnetwork derived from modules recurring in the different layers has been identified using the proliferation phenotype as a seed. This subnetwork has suggested novel genes and interactions potentially involved in the regulation of adult hippocampal neurogenesis
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Wells, Layne. "Investigating Neurogenesis as a Veritable Epigenetic Endophenotype for Alzheimer's Disease". Scholarship @ Claremont, 2019. https://scholarship.claremont.edu/scripps_theses/1232.
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Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by progressive amyloid plaque aggregation, neurofibrillary tangles, and cortical tissue death. As the prevalence of AD is projected to climb in coming years, there is a vested interest in identifying endophenotypes by which to improve diagnostics and direct clinical interventions. The risk for complex disorders, such as AD, is influenced by multiple genetic, environmental, and lifestyle factors. Significant strides have been made in identifying genetic variants linked to AD through the genome-wide association study (GWAS). It has been estimated in more recent years, however, that GWAS-identified variants account for limited AD heritability, suggesting the role of non-sequence genetic mechanisms, such as epigenetic moderators. By influencing gene expression, epigenetic markers have been linked to age- associated decline through modulation of chromatin architecture and global genome instability, though such mechanisms are also involved with a number of normal biological processes, including neurogenesis. As the strategies of clinical genetics shift to include a heavier focus on epigenetic contributors, altered adult neurogenesis presents itself as a strong candidate for an endophenotype of AD development. This thesis proposes that, due to neuropathological dysfunction of epigenetic mechanisms in AD, new generations of neurons fail to proliferate, differentiate, and mature correctly, resulting in the larger loss of neurons and cognitive deficits characteristic to neurodegenerative disease. The plasticity of the epigenome and the role of epigenetic factors as mediators of the genome and the environment make such alterations attractive in AD research and implies the potential for therapeutic interventions. The present review submits neurogenesis as a viable target of epigenetic research in AD, highlights shared loci between neurogenesis and AD in the epigenome, and considers the promises and limitations of the neurogenic endophenotype.
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Crews, Leslie Anne. "Molecular regulators of neurogenesis in Alzheimer's disease". Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3398251.
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Thesis (Ph. D.)--University of California, San Diego, 2010.Title from first page of PDF file (viewed May 6, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (leaves 196-218).
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Fargas, Madriles Laura 1989. "Morphogenetic mechanisms in zebrafish inner ear neurogenesis". Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/397795.
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L’orella interna dels vertebrats és una estructura altament organitzada i complexa on cadascun dels específics tipus cel•lulars és generat a dominis concrets. Per aquest motiu, l’especificació cel•lular i la seva organització espaciotemporal està lligada a la morfogènesis de tot l’òrgan. En aquest projecte analitzen en detall la regulació espaciotemporal durant la formació dels dominis sensorial i neurogènic de l’orella interna i la relació entre els gens proneurals i la via de senyalització de Notch. Diferents estudis han mostrat l’expressió dels gens proneurals i l’especificació dels progenitors neuronals. No obstant, la dinàmica de la neurogènesis i els comportaments cel•lulars involucrats en aquest procés romanen desconeguts. Per aquest motiu, analitzem en detall la formació del domini neurogènic. Mitjançant una quantificació dinàmica de l’expressió del gen proneural juntament amb l’anàlisi 4D dels comportaments cel•lulars, revelem el mecanisme d’iniciació del procés de neurogènesis òtica, el qual depèn de la dinàmica cel•lular i de la senyalització de FGF.The vertebrate inner ear is a highly ordered and complex structure, in which specialized cell types originate at distinct but specific domains. Therefore, patterning and cell fate specification must be coupled with morphogenesis of the entire organ. In this work we analyze in detail the spatiotemporal regulation of the formation of the inner ear sensory and neurogenic domains and the relation of proneural genes and Notch signaling. Although several studies have reported the expression of proneural genes and specification of neuronal progenitors, the dynamics of neurogenesis and cell behaviors involved in this process are still elusive. Moreover, we focus in more detail on the formation of the neurogenic domain. We perform a dynamic quantification of proneural gene expression combined with a 4D analysis of cell behaviors, and unveil the mechanisms of initiation of otic neurogenesis, which relies on both cell dynamics and FGF pathway.
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Alspector, Emily Bitler Elizabeth. "The relationship between neurogenesis and pain behavior". Diss., Connect to the thesis, 2008. http://hdl.handle.net/10066/1325.
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Mayor, Olivier. "Lineage analysis of neurogenesis in mouse chimera". Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59410.
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To investigate the lineage relationships that are postulated to underlie the origins of phenotypically different neurons, Thy-1.1 $ leftrightarrow$ Thy-1.2 and hNF-L $ leftrightarrow$ +/+ mouse chimeras were examined for the distribution of the two neuron genotypes. Throughout the nervous system, a finely variegated pattern of mosaicism was always observed and, in each chimera, similar genotype proportions were found in all analysed neuronal populations of the peripheral and central nervous system. These findings require that the chimera neuroectoderm was a homogeneous mix of the two genotypes and that different neuronal phenotypes do not arise clonally from a small number of prespecified progenitors. Rather it would seem that all progenitors contribute daughter cells to all of the neuronal subpopulations at each level of the neuroaxis.
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Zaben, Malik J. "Vasoactive Intestinal Peptide : Control of Hippocampal Neurogenesis". Thesis, University of Southampton, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509485.
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Borders, Aaron S. "THE ROLE OF MACROPHAGES IN OLFACTORY NEUROGENESIS". UKnowledge, 2007. http://uknowledge.uky.edu/physiology_etds/15.
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Olfactory sensory neurons (OSNs) undergo continual degeneration and replacement throughout life, a cycle that can be synchronized experimentally by performing olfactory bulbectomy (OBX). OBX induces apoptosis of mature OSNs, which is followed by an increase in the proliferation of progenitor basal cells. Macrophages, functionally diverse immune effector cells, phagocytose the apoptotic OSNs and regulate the proliferation of basal cells. This provides an advantageous environment to study how macrophages regulate neuronal death, proliferation, and replacement.
The purpose of this dissertation was to identify the cellular and molecular mechanisms by which macrophages regulate the degeneration/proliferation cycle of OSNs. Macrophages were selectively depleted using liposome-encapsulated clodronate (Lip-C). Intranasal and intravenous administration of Lip-C decreased the number of macrophages in the OE of sham and OBX mice by 38% and 35%, respectively, compared to mice treated with empty liposomes (Lip-O). Macrophage depletion significantly decreased OE thickness (22% and 21%, p<0.05), the number of mature OSNs (1.2- and 1.9-fold, p<0.05), and basal cell proliferation (7.6- and 3.8-fold, p<0.05) in sham and OBX mice, respectively, compared to Lip-O mice. Additionally, at 48 h following OBX, OSN apoptosis increased significantly (p<0.05) in the OE of Lip-C mice compared to Lip-O mice.
A microarray analysis was performed to identify the genomic changes underlying the cellular changes associated with macrophage depletion. There were 4,024 genes with either a significant interaction between group (Lip-C vs. Lip-O) and treatment (OBX vs. sham) or a significant main effect. There were a number of significantly regulated immune response and cytoskeletal genes, and genes encoding neurogenesis regulators and growth factors, most of which were expressed at lower levels in Lip-C mice compared to Lip-O mice. Sdf1, the ligand for the chemokine receptor Cxcr4 involved in leukocyte trafficking, axon guidance, and cell migration, was localized to macrophages on the protein level. Additionally, the microarray expression pattern of Hdgf, a growth factor that promotes neuronal survival and proliferation, was validated on the protein level using immunohistochemistry. HDGF appeared to be localized to basal cells and OSNs where it could act as a proliferative or survival factor whose expression is regulated in part by macrophages.
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Jafari, Mehrnoosh. "Disease-associated modulation of adult hippocampal neurogenesis". Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-174174.
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Adult neurogenesis has been the focus of over 1500 articles in the past 10 years. Evidence for the continuous production of new neurons in the adult brain has raised hopes for new therapeutic approaches. On the other hand, the generation of new neurons is modulated in several neurological diseases and disorders, suggesting the involvement of the adult neurogenesis in their pathogenesis. Therefore, a better understanding of the disease-associated modulation of adult neurogenesis is essential for determining the most effective therapeutic strategy.
The purpose of this doctoral project was to investigate long-term adult hippocampal neurogenesis changes in two disease models. BrdU labeling in combination with various cellular markers, and genetic fate-mapping approach were used to reach this goal.
In the first experiment, the impact of the BeAN strain of the Theiler’s virus on hippocampal cell proliferation and neuronal progenitors was evaluated in two mouse strains which differ in the disease course. It was shown that Theiler’s murine encephalomyelitis virus can exert delayed effects on the hippocampal neurogenesis with long-term changes evident 90 days following the infection. The hippocampal changes proved to depend on strain susceptibility and might have been affected by microglial cells.
In the second experiment, hippocampal neurogenesis was analyzed based on genetic fate mapping of transgenic animals in the amygdala-kindling model of epilepsy. The number of new granule neurons added to the dentate gyrus was increased in kindled animals. A prior seizure history proved to be sufficient to induce a long-term net effect on neuron addition and an ongoing occurrence of seizures did not further increase the number of new neurons. Hypertrophic astrocytes were observed in the kindled animals suggesting that seizures result in structural changes of astrocytes that could be detected long after the termination of the insults.
The results of the experiments indicated the importance of methodological considerations in chronic studies of neurogenesis.
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Choi, Minee. "Adult neurogenesis and dopamine in neurodegenerative diseases". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607778.
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Cenci, Caterina. "Regulation of segment-specific neurogenesis in Drosophila". Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446838/.
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Following Drosophila embryogenesis, the morphology of the central nervous system (CNS) becomes dramatically remodelled to reflect the different locomotive and sensory requirements of the adult relative to the larva. The late embryonic onset of segment-to-segment differences in the number and mitotic capacity of neural stem cell-like precursors (termed neuroblasts: NBs) is critical to this resculpting process. My studies address the roles of homeodomain and other transcription factors in regulating thoracic and abdominal-specific patterns of neurogenesis, focusing on one embryonic and one larval example. In the embryo, dividing NBs sequentially express a temporal series of transcription factors required to link birth-order to neuronal identity. The study of a group of neurons expressing the early NB-sublineage determinant Hunchback in a thorax-specific pattern (termed the THBs) was initiated. I developed a lineage- labelling method to show that the THB-producing NBs appear to undergo a delay in their sub-lineage transition from Hunchback-positive to negative status, relative to most other NBs. Importantly, gene skipping in the canonical transcription factor series is also observed. Genetic analysis reveals that this thorax-specific pattern of neurogenesis requires homothorax but surprisingly not the thoracic Hox genes. However, in the abdomen, the Hox genes Ultrabithorax and abdominalA are required to suppress the THB phenotype. In the larva, clonal analysis and CNS-specific mutants were used to test several candidate factors potentially regulating NB divisions. This approach identified critical roles for Polycomb group genes and the transcription factor Grainyhead (Grh). I find that Grh, previously implicated as the ultimate NB-sublineage determinant in the embryo, has a differential effect on larval neurogenesis in the thorax versus the abdomen. Individual grh NB lineages in the thorax are smaller than wild type and stop dividing prematurely whereas those in the abdomen are larger and divide for an abnormally long period. Underlying the latter effect is an inability to respond to the normal NB-apoptosis inducing burst of the Hox protein AbdominalA. Thus, these studies identify Grh as a context-factor for Hox function in the larval NBs, linking late but not early AbdominalA expression with NB-apoptosis.
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Griffiths, Dean Stuart. "Molecular characterisation of embryonic stem cell neurogenesis". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/13958.
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One of the biggest challenges currently facing ES cell biology is to understand the mechanisms involved in the differentiation of ES cells to specific lineages. Pure populations of a specific cell lineage cannot be achieved without selection, such as fluorescence activated cell sorting (FACS), immunopanning or growing cells in a selective environment following genetic manipulation. However, such techniques do not address why ES cells do and do not differentiate to particular lineages and cell types. To achieve greater understanding of the mechanism of neuronal differentiation from ES cells, an ES cell line was generated with eGFP driven by the neuronal specific gene tau. Tau is expressed exclusively in all neurons from the earliest stages of neuronal commitment, we find that a neural differentiation of this line results in eGFP expressing neurons. Using FACS, a pure population of neurons can be obtained from a heterogeneous population of differentiated cells. Neuronal differentiation can be quantified either by fluorescent microscopy or flow cytometry. These ES cells have been used to analyse the effect that density and the addition of exogenous factors have on neuronal differentiation, a transcriptome analysis experiment was performed by microarray analysis. Genes already known to be important during mammalian neural development were analysed for their involvement in ES cell neurogenesis. This comparison revealed a strong correlation between events of ES cells differentiation and normal embryonic development. The microarray analysis of ES cell neurogenesis also identified genes with an expression profile suggestive of a role in ES cell neurogenesis and development of the murine nervous system.
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Hashemi, H. M. "The regulation of spinal neurogenesis by PTPγ". Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1400391/.
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RPTPs have striking patterns of expression within the neural tube; raising interesting questions as to their role in the development of this structure. PTPγ expression is initially observed in the first born neurons and this expression domain progressively expands to the lateral motor columns and intermediate zone of differentiating neurons. Short hairpin encoding RNAi constructs were generated against PTPγ, which effectively knocked down this gene in vitro and in ovo. Analysis of silenced embryos through neuronal markers presented a range of phenotypes. The most striking was a dorsoventral truncation of the neural tube arising from a loss of LIM-HD expressing cells not observed among controls. During the onset of neurogenesis, a loss of Lim1/2/3, Islet1/2, and Mnr2/Hb9 positive cells was observed. At later stages, Islet1/2 cells showed no such sustained effect essentially recovering. A further heterotopic phenotype was observed with mislocated neurons located ectopically in the ventricular lumen, that were Islet1/2 and Nkx2.2 positive but never Lim1/2/3. The targeted regions showed a significant decrease in apoptosis suggesting newly born neurons were dying before reaching their pool specific domains. A reduction in the proliferative capacity in the ependymal zone demonstrated by Histone3 activity. Over expression of PTPγ showed a similar reduction in LIM-HD expression however no overall change in S-Phase was observed yet cells at M Phase were reduced with no apoptosis detected through Caspase3 activity. The data suggests PTPγ silencing may result in a failure of Lim1/2/3 cells to reach their final destinations and acquire LIM-HD identities, implicating this gene in the development of inter and motor neuron populations. Preliminary RNAi experiments against PTPσ show a reduction in LIM-HD fated cells and a triggering of the apoptosis programme along with a reduction in number of mitotically active cells. This is consistent with a potential role for PTPs during neurogenesis and the birth of the first neuronal populations in the neural tube.
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Hakim, Marziah. "Neurogenesis and neuroplasticity following olfactory fear conditioning". Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/157474/1/Marziah_Hakim_Thesis.pdf.
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This dissertation focused on determining the neurocircuitry of olfactory fear conditioning in order to further understand the microanatomy of post-traumatic stress disorder and contribute towards the refinement of therapeutic innovations. The study determined that different subnuclei of the amygdala were involved in olfactory fear memory and that recollection of such memories enhanced neuroplasticity and increased the number of new born neurons and astrocytes in the brain regions associated with olfaction and memory processing. This study concluded that following olfactory fear conditioning, newborn neurons may undergo long term potentiation, which may support their survival up to 14 days after birth.
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Sturesson, André. "Exercise-induced adult hippocampal neurogenesis and the effect of exercise and adult hippocampal neurogenesis on spatial learning and memory". Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-15918.
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It was long believed within the scientific community that the adult brain was unable to generate new neurons. In the end of the 1990s the consensus changed and it is since believed that the adult brain can and does generate new neurons after birth, a process referred to as adult neurogenesis. Adult neurogenesis takes place in two places in the adult brain: the subventricular zone (SVZ) in close proximity to the olfactory bulb and the subgranular zone (SGZ) in the hippocampus. The level of adult hippocampal neurogenesis (AHN) can be upregulated and one part of the aim was to examine the effect of voluntary chronic aerobic exercise (VCAE) on AHN. It is clear that voluntary chronic aerobic exercise reliably increases AHN. Still, the function of these new brain cells is under debate. Spatial learning and memory are among the main abilities that have been focused on. The other part of the aim was to examine the effect of VCAE and AHN on spatial learning and memory. The reviewed literature suggests that both AHN and spatial learning and memory increase together from VCAE, although it does not show causation, that an increase of AHN from VCAE causally effects spatial learning and memory. More studies are needed to investigate if a causal relationship exists.
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MELIS, VALENTINA MARIA. "Effetto della separazione materna sulla plasticità dei neuroni nell’ippocampo delle mamme e della prole". Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266624.
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Neuronal plasticity is the capability of neurons to change the structure, function and organization of neurons in response to new experiences. Behavioral studies in rodents, have shown that changes in the environment, in different periods of life, can lead to profound and lasting effects on neuronal plasticity as reflected by increased vulnerability or resilience to stress. Post-natal stress, such as maternal separation, have a deep impact not only for the offspring, but also for mothers, and lead to neuroendocrine, behavioral and structural changes in the brain. Neuroplasticity was evaluated both in mothers and offspring. Mothers were killed 21 days after delivery the day of the weaning and we analized density and morphology of dendritic spines and arborization of the dendritic tree in granule cells of hippocampus. Another goal of our study is to verify on the offspring, if stress induced by insufficient maternal care in the first 15 days of life increases the vulnerability to chronic stress conditions in adulthood. In this research, we used two experimental protocols of maternal separation, a) one group of pups was separated from their mothers for 15 min (short maternal separation), b) pups from the second group were separated for 3h (long maternal separation), every day from the 3rd to day 15th after birth respectively. The weaning day half of the rats belonging to the different groups was isolated for 60 days, while another group was isolated for 30 days then re-grouped for another 30 days. The results obtained were compared with those of rats never separated from their mothers (control), but subjected or not to social isolation. After sacrifice of offspring, we studied the density and morphology of dendritic spines, the arborization of dendritic tree and neurogenesis in the hippocampus. The results obtained in mothers showed that maternal separation reduced dendritic arborization in granule cells of hippocampus, and density of hippocampal dendritic spines is decreased in mothers after maternal separation. The results obtained in the offspring showed that social isolation induced a reduction of the arborization of the dendritic tree, variation of morphology and a reduction of the density of the dendritic spines, and a decrease of neurogenesis in animals not separated from the mother and in the separated ones. In rats subjected to re-group after 30 days of social isolation stress, the morphology and density of dendritic spines, arborization of the dendritic tree and the neurogenesis were completely reverted when compared to animals that have never been separated from their mothers (controls). In contrast, in animals subjected to maternal separation for 3 h, the social enrichment (re-grouped) failed to revert the effects of social isolation stress. In rats exposed to maternal separation for 15 min, social isolation for 60 days did not induce any change in the parameters studied. These results demonstrate that in the offspring, a short maternal separation of the animals in the first 15 days of life increase resilience to chronic stress during adult life. These data suggest that, in the offspring, high maternal care that result from a short maternal separation, increase resilience to chronic
stress during adulthood. On the contrary, a lower maternal care as a consequence of a long maternal separation, reduce resilience and increase vulnerability to chronic stress, impairs neuronal plasticity and effect cognitive functions and emotional state. These results show that maternal separation during early post-natal period, have a negative effects on neuronal plasticity, both in mothers and offspring
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Cooper-Kuhn, Christiana Marie. "Regulation of neurogenesis in the adult mammalian brain". [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968783007.
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Dove, Hilary Livia. "Neurogenesis in the millipede Glomeris marginata (Myriapoda: Diplopoda)". [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970030126.
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Andersson, Annika. "Studies on neurogenesis in the adult human brain". Thesis, Södertörn University College, School of Life Sciences, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-3646.
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Many studies on neurogenesis in adult dentate gyrus (DG) have been performed on rodents and other mammalian species, but only a few on adult human DG. This study is focusing on neurogenesis in adult human DG. To characterize the birth of cells in DG, the expression of the cell proliferation marker Ki67 was examined using immunohistochemistry. Ki67-positive labelling was indeed observed in the granular cell layer and the molecular layer of dentate gyrus and in the hilus of hippocampus, as well as in the subgranular zone (SGZ). The Ki67 positive nuclei could be divided into three groups, based on their morphology and position, suggesting that one of the groups represents neuronal precursors. Fewer Ki67 positive cells were seen in aged subjects and in subjects with an alcohol abuse. When comparing the Ki67 positive cells and the amount of blood vessels as determined by anti factor VIII, no systematic pattern could be discerned. To identify possible stem/progenitor cells in DG a co-labelling with nestin and glial fibrillary acid protein was carried out. Co-labelling was found in the SGZ, but most of the filaments were positive for just one of the two antibodies. Antibodies to detect immature/mature neurons were also used to investigate adult human neurogenesis in DG. The immature marker βIII-tubulin showed a weak expression. The other two immature markers (PSA-NCAM and DCX) used did not work, probably since they were not cross-reacting against human tissue. In summary, this study shows that new cells are continuously formed in the adult human hippocampus, but at a slower pace compared to the rat, and that some of these new cells may represent neuronal precursors.
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Rhodes, Christopher. "Epigenetic Repression in the Context of Adult Neurogenesis". Thesis, The University of Texas at San Antonio, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10686193.
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Neural stem progenitor cells (NSPCs) in the mammalian brain contribute to life-long neurogenesis and brain health. Adult mammalian neurogenesis primarily occurs in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the dentate gyrus. Epigenetic repression is a crucial regulator of cell fate specification during adult neurogenesis. How epigenetic repression impacts adult neurogenesis and how epigenetic dysregulation may impact neoplasia or tumorigenesis remains poorly understood. Examination of epigenetic regulation in the adult mammalian brain is complicated by the heterogeneous nature of neurogenic niches and by the highly orchestrated fate specification processes within neural stem progenitor cells involving myriad intrinsic and extrinsic factors. To overcome these challenges, we utilized a cross-species approach. To model histone modifications as they exist in vivo for epigenetic profiling, we isolated neural stem progenitor cells from the adult SVZ and SGZ of non-human primate baboon brains. To determine cellular and molecular changes within the adult SVZ and SGZ following loss of epigenetic repression, we utilized multiple mouse models, including conditional Ezh2 and Suv4-20h1 knockouts. To model the non-cell type specific effects common to small molecule screening and brain chemotherapeutic agents, induction of conditional knockout utilized a recombinant Cre protein. Finally, to model epigenetic mechanisms during SVZ-associated glioblastoma (GBM) tumorigenesis, we conducted comparative analysis between healthy NSPCs and GBM specimens from humans. The convergence of baboon, mouse and human models of adult neurogenesis revealed that epigenetic repression is a critical mechanism regulating proper neural cell fate and that epigenetic dysregulation may be a driver of GBM.
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Ringuette, Randy. "The Role of Signaling Pathway Integration in Neurogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35108.
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Proper central nervous system development is critical for survival and depends on complex intracellular and extracellular signaling to regulate neural progenitor cell growth and differentiation; however, the mechanisms that mediate molecular crosstalk between pathways during neurogenesis are not fully understood. Here, we explored the integration of the Hedgehog (Hh) signaling pathway with the two critical developmental pathways, Receptor Tyrosine Kinase (RTK) and Notch signaling, in the growth and maintenance of neural progenitors in the developing neuroretina. We found combined and sustained RTK and Hh signaling was sufficient to establish long-term retinal progenitor cell (RPC) cultures and these cells maintained neurogenic and gliogenic, but not retinogenic, competence in vitro and in vivo. In addition, we identified crosstalk between Notch and Hh signaling, where Notch is required for Hh-mediated proliferation and Gli protein accumulation, and gain-of-function of Notch is sufficient to extend the window of Hh responsiveness in a subset of Müller glia. Both Hh-RPC monolayer establishment and Notch mediated Hh-responsiveness required Gli2. Taken together, we identified molecular cross-communication between the Hh pathway and two major pathways, Notch and RTK, during retinogenesis, advancing our understanding of mechanisms that influence Hh to control neural progenitor growth.
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Carlén, Marie. "Adult neurogenesis : from stem cell to functional neuron /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-367-1/.
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Melvin, Neal, i University of Lethbridge Faculty of Arts and Science. "Differential neurogenesis in the adult rat dentate gyrus". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/727.
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Adult neurogenesis is a fundamental feature of mammalian nervous systems.
Curiously, neurogenesis in the dentate gyrus is typically regarded as homogenous. This
thesis challenges that view, and reports the discovery and characterization of a novel
region of the dentate gyrus that consistently lacks basal neurogenesis. We demonstrate
that this area, referred to as the neurogenically quiescent zone, represents approximately
1.5% of the total volume of the dentate gyrus, and that its location is invariant among
animals. This region contains several critical cell types and molecular factors that are
known to be critical to the neurogenic niche, including stem cells. We also present data
that attempt to conceptualize the existence of this region in the context of early agerelated
declines in neurogenesis. Finally, we demonstrate that, under some behavioural
conditions, neurogenesis can be induced in this region, suggesting that, under basal
conditions, it may simply lack the presence of pro-neurogenic factors.xvi, 125 leaves : ill. ; 29 cm. --
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Labban, Margaret. "The effects of perinatal hypoxia on hippocampal neurogenesis /". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101594.
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Schizophrenia (SCZ) is believed to be a neurodevelopmental disorder resulting from genetic and environmental factors. Obstetric complications, particularly fetal hypoxia, seem to be a risk factor for SCZ. The hippocampus is highly sensitive to ischemic episodes, and there is substantial evidence for hippocampal malfunction in SCZ. Thus, utilizing a rat model of global anoxia (15 min and 21 min) during Cesarean-section birth (C-section), hippocampal proliferation was examined in the dentate gyrus and CAI region at postnatal day 21 and day 60. Incorporation of 5-bromo-2-deoxyuridine (BrdU) was used as a marker of cell proliferation. Rats were sacrificed 2 hours after BrdU injection to quantify cell proliferation, or 4 weeks after BrdU injection to quantify survival of newly proliferating cells and to identify if these cells express a neuronal phenotype. Only rats that had undergone 15 minutes of hypoxia during C-section birth compared to C-sectioned controls, showed a significant increase in cell proliferation in the dentate gyrus on postnatal day 21. Thus perinatal hypoxia can have lasting effects on the hippocampus that depend on the duration of the hypoxic insult.
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Nangla, Jyoti. "The study of neurogenesis in the rodent telencephalon". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325881.
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Bandpey, Zhale. "Biphasic regulation of hippocampal neurogenesis by adrenal steroids". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608250.
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Leung, Wai-hin, i 梁瑋軒. "Neurogenesis in animal model of systemic lupus erythematosus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209497.
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Systemic Lupus Erythematosus (SLE) is an autoimmune disease which is characterized by high level of autoantibody detected in the body. This disease is female predominant with a male to female ratio 1: 9. SLE could cause damage to different organ systems and central nervous system is one of them. Patients diagnosed with SLE could suffer from psychiatric problems like cognitive dysfunction, depression and anxiety.
Neurogenesis refers to the process by which new neurons are generated. Although it has been widely reported that neurogenesis could be enhanced under pathological conditions such as stroke, Huntington’s disease and epilepsy, study focusing on the relationship between neurogenesis and SLE remains limited.
In the present study, by using NZB/W F1 mice as the animal model of SLE, we could demonstrate that there was dramatic increase of neuronal precursor cells at the corpus callosum after the onset of SLE symptoms. Meanwhile, as IBA-1 positive cells and GFAP positive cells also increased significantly there, this suggested inflammation has taken place. I hypothesized there were upregulation of immunological factors after the onset of SLE symptoms and those factors were responsible for the neurogenesis. In my in vitro study, cytokine- interferon gamma (IFN gamma) has been shown to promote neuronal progenitor cells (NPCs) to differentiate into neuronal linage but it did not obviously affect the cell proliferation and migration. For the other cytokine and chemokines, including interleukin-10 (IL-10), interleukin-8 (IL-8), macrophage-derived chemokine (MDC), stromal cell-derived factor 1 alpha (SDF-1alpha) and thymus and activation regulated chemokine (TARC), all of them had no effect on NPC proliferation and differentiation.
As far as we know, this is the first study to report SLE could enhance neurogenesis. Concerning the role of inflammation and IFN gamma on the neurogenesis in our case, it should be worth for further investigation, which will benefit future development of novel treatment targeting psychiatric symptoms in SLE.published_or_final_version
Anatomy
Master
Master of Philosophy
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Abu-Elmagd, Muhammad. "cSox3 expression and neurogenesis in the epibranchial placodes". Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367680.
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Biffar, Lucia. "Early neurogenesis in the flour beetle Tribolium castaneum". Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8406.
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Insects exhibit considerable variety in their morphology and can be found in many diverse habitats. Despite these variations, early neurogenesis seems to be conserved in insects. In all species investigated to date it begins with the formation of neural stem cells (neuroblasts), which establish a distinct internal layer and produce a fixed number of neurons and glial cells. The neuronal cells then form a characteristic rope ladder-like axonal scaffold. However, it is evident that the composition or identity of the individual neurons must have changed during insect evolution to allow for variations in neuronal networks. This raises questions regarding which developmental steps have been changed and the manner in which they have been modified. In order to address these questions, early neurogenesis was analysed in the flour beetle Tribolium castaneum and the results were compared to the well-studied fruit fly Drosophila melanogaster. Initially a map of trunk neuroblasts in T. castaneum was established, which revealed a high degree of conservation in the arrangement of individual neuroblasts compared to D. melanogaster. However, a comparison of the expression patterns of genes that confer regional identity to neuroblasts showed considerable variations. Significant differences in the expression patterns of the segment polarity gene wingless and the columnar gene ventral nerve cord defective (vnd) were found. Furthermore, the impact these changes in neuroblast identity have on the composition and identity of their respective progeny was analysed. As a result changes in the number of Even-skipped and Tailup expressing neurons in T. castaneum embryos were found, with three-fold more Tailup expressing neurons compared to D. melanogaster. To further analyse the role of the neuroblast identity gene vnd in the formation of Even-skipped positive neurons, RNAi gene silencing studies were performed, resulting in the loss of neurons and changes in neuronal migration pattern. In summary, the results demonstrate that evolutionary changes in neuronal networks result from changes in neuroblast identity, which in turn have an impact on the composition of neuronal lineages.
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Krishnan, Vaishnavi M. "Characterisation of dephrin reverse signaling during Drosophila neurogenesis". Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614714.
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Ozen, Ilknur. "Neurogenin2, a molecular marker of postnatal hippocampal neurogenesis". Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612424.
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Patel, Kaushal S. "Post-TBI Hippocampal Neurogenesis in Different TBI Models". VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4134.
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Traumatic brain injury (TBI) leads to short-term and long-term consequences that can cause many different life-long disorders. Studies of TBI have generally focused on the acute stage; however, it is now becoming important to investigate chronic responses following TBI as clinical reports of dementia and cognitive impairments have been linked to a history of TBI. Recent data have established that cognitive function is associated with hippocampal neurogenesis. Chronic injury induced changes in the brain may affect this endogenous process. Chronic responses following TBI include cell death pathways and inflammatory responses that are persistent in the brain for months to years after injury. In this study we investigate the chronic consequences of TBI on adult neurogenesis and the possible involvement of chronic-inflammation in regulating adult neurogenesis. We used two popular TBI animal models, Control Cortical Impact (CCI) and Lateral Fluid Percussion Injury (LFPI) models, to examine focal and diffuse injury responses respectively. Adult rats received CCI, LFPI, or sham injury and were sacrificed at either 15 days or 3 months after injury to examine either subacute or chronic TBI-induced responses respectively. We found no change in levels of proliferation activity at both time points in both TBI models compared to sham animals. Using Doublecortin immunolabeling we found an enhanced generation of new neurons at 15 days after injury and by 3 months this activity was significantly reduced in both TBI models compared to sham animals. We also found persistent inflammation in the injured brains at both time points. Morphological assessment showed that LFPI model of TBI causes shrinkage of the ipsilateral hippocampus. Our results show that moderate TBI induced hippocampal neurogenesis in both models at the early time post-injury. However, at chronic stage, reduced hippocampal neurogenesis is observed in both models and this is accompanied by chronic inflammation. These results suggest that persistent inflammatory responses maybe detrimental to normal neurogenic activity, leading to cognitive impairment and neurodegeneration in long-term TBI survivors.
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Chen, Yanshuang. "The Effect of Inorganic Nanostructured Materials on Neurogenesis". Master's thesis, Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/421454.
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BioengineeringM.S.
Damage and/or loss of functional neurons can lead to detrimental cognitive and paralyzing effects in humans. Prime examples of such negative situations are well documented in patients with Parkinson's and Alzheimer's disease. In recent years, the utilization of neural stem cells and their derivation into neurons have been the focus of many research endeavors. The main reason for this is because neural stem cells are multi-potent and can differentiate into neurons, astrocytes, and oligodendrocytes. The research that will be detailed in this thesis involves the potential use of inorganic nanostructured materials to efficiently deliver bioactive molecules (i.e., retinoic acid, kinase inhibitors) to cells that can modulate the differentiation potential of certain cells into neurons. Specifically, PC12 (derived from rat pheochromocytoma) cells, as a neural model, was treated with select nanostructured materials with and without neuron inducers (molecules and ions) and the results were analyzed via biochemical assays and live-cell fluorescence microscopy. This thesis will include an in depth look into the cytocompatibility of the tested nanostructured materials that include silica nanoparticles, titanate nanotube microspheres, and carbon microparticles.
Temple University--Theses