Dissertations / Theses on the topic 'Astrocytes'
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Contreras-Sesvold, Carmen Sesvold Carmen Contreras. "Reactive astrocytes : phenotypic and functional characteristics and astrocytes as neural stem cells /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/ContrerasSesvold2006.pdf.
Full textFeresten, Abigail Helms. "Astrocytes in psychotic disorder." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45435.
Full textJai-Yoon, Sul. "Calcium signalling in astrocytes." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391921.
Full textŠkovierova, H., S. Mahmood, E. Blahovcova, J. Strnadel, J. Sopkova, and E. Halašova. "Homocystene and human astrocytes." Thesis, Сумський державний університет, 2016. http://essuir.sumdu.edu.ua/handle/123456789/44950.
Full textJames, L. R. "Calcium signal transduction in astrocytes." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.605022.
Full textCambray-Deakin, M. "Astrocytes : targets for neuroactive substances." Thesis, Open University, 1985. http://oro.open.ac.uk/56910/.
Full textCahoy, John David. "Genomic analysis of highly purified astrocytes reveals in vivo astrocyte gene expression : a new resource for understanding astrocyte development and function /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Full textMhyre, Andrew James. "Mechanisms of estrogen signaling in astrocytes /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/6266.
Full textSiushansian, Ramin. "Vitamin C transport by cerebral astrocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21315.pdf.
Full textBlaszczyk, Lucie. "Etude des cellules astrocytaires et microgliales thalamiques dans un modèle de douleur neuropathique chez le rat." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0081/document.
Full textChronic pain is an incapacitating and long lasting pathology mainly characterized by threesymptoms: allodynia (a non painful stimulus is perceived as painful), hyperalgesia (a painfulstimulus is perceived as more painful) and ambulatory pains. When chronic pain is due to alesion or dysfunction of nervous system it is called neuropathic pain. In both patients and animalmodels of neuropathic pain, researchers found that thalamic neurons are hyperexcitable. Glialcells, astrocytes and microglia, are strong synaptic partners involved in synaptic transmissionand plasticity and therefore could be involved in this phenomenon. Indeed, these cells canmodify their phenotype when nervous system is damaged. They become reactive: theirmorphology is hypertrophied, mRNA and protein expression of iba-1 (ionized binding-adaptormolecule 1) and CD11b/c (cluster of differentiation 11b/c) for microglia and GFAP (glialfibrillary acidic protein) and S100β (S100 calcium binding protein β) for astrocytes is increased.They could also release pro-inflammatory molecules. All of these could contribute to generate oramplify the thalamic neuronal hyperexcitability.In my PhD work I studied thalamic astrocytes and microglia in a rat neuropathic pain model ofL5-L6 spinal nerves ligation (SNL). Mechanical allodynia and hyperalgesia were characterizedwith von Frey filament test and ambulatory pain with dynamic weight bearing apparatus. mRNAexpression of glial markers were studied with qRT-PCR technique on thalamic punches andlaser-microdissected nuclei. Neurochemical expressions of iba-1, CD11b/c, cathepsin S, GFAPand S100β markers were quantified using an immunohistofluorescence approach to count thenumber of immunopositive cells and surface stained by these markers. All these experimentswere done at D14 and D28 after surgery.At D14, SNL animals develop mechanical allodynia and hyperalgesia as well as ambulatory pain..For these animals, thalamic microglial cells showed signs of reactivity with the increase mRNAexpression of CTSS and CX3CR1, fractalkine receptor, well known markers involved in spinalneuronal hyperexcitability under neuropathic pain conditions. In addition, the number ofimmunopositive cells for the glial markers is decreased in SNL animals. At D28, the neuropathicpain symptoms are still present. Furthermore, thalamic microglial reactivity found at D14 withqRT-PCRm method is still present with the increased mRNA expression of fractalkine (CX3CL1),partner of CTSS/CX3CR1/CX3CL1 pathway. The decreased neurochemical expression of glialmarkers found at D14 was transient as I didn’t find this result at D28. However, thalamicastrocytic reactivity was found at D28 in SNL animals.So, this work reveal a new glial process at thalamic level in this SNL model of neuropathic pain :an early decreased expression of glial markers and then a later thalamic astrocytic reactivityconcomitant with signs of thalamic microglial reactivity. Numerous studies are required toexplore the role of such novel ambivalent glial alterations in the context of neuropathic pain
Chen, Xiaoqian. "The identification of 14-3-3[gamma] in astrocytes and its mechanism in protecting astrocytes from ischemia /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20CHEN.
Full textIncludes bibliographical references (leaves 180-202). Also available in electronic version. Access restricted to campus users.
Carney, Karen. "Caractérisation Protéomique Des Prolongements Astrocytaires au Cours de la Plasticité Synaptique." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0270/document.
Full textAstrocytes are the most abundant cell type in the brain and mediate a myriad offunctions, including neurogenesis, ion homeostasis, metabolic support, clearance oftoxic substances and responses to brain injuries. Alterations in astrocyte functionhave been linked with neurological disorders such as epilepsy, depression, dementiaand schizophrenia, and thus the continued study of astrocytic contributions tosynaptic function are of clinical and societal relevance. In this thesis I have evaluatedthe potential utility of several preparations for the assessment of astrocyte proteinsinvolved in the regulation of synaptic plasticity, and employed the most suitable ofthese preparations to measure regulation in astrocyte protein levels in models ofsynaptic plasticity. I have characterized several preparations that can be used toevaluate astrocyte contributions to synaptic plasticity and identified numerousastrocyte-enriched proteins regulated by synaptic plasticity that can be targeted infuture studies to elaborate upon the mechanisms of action of astrocytes in bothphysiological and pathological contexts
Morgan, Sarah V. "Tight junction protein expression in human astrocytes." Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/14403/.
Full textO'Brien, Emma Rosemary. "The role of astrocytes in brain metastasis." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:60efc7bd-4f00-4e84-a964-c4ef55009dfb.
Full textSupattapone, Surachai. "The effects of endothelin on rat astrocytes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279908.
Full textNash, Besma. "The dual role of astrocytes in myelination." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/2378/.
Full textHashemian, Sanazalsadat. "Interaction between nerve fiber formation and astrocytes." Doctoral thesis, Umeå universitet, Histologi med cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-88366.
Full textMead, Carole. "Studies of toxic responses in cultured astrocytes." Thesis, University of Salford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244928.
Full textMarschinke, Franziska. "From dopamine nerve fiber formation to astrocytes." Doctoral thesis, Umeå : Department of Integrative Medical Biology, Section for Histology and Cell Biology, Umeå University, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-20615.
Full textCHIACCHIARETTA, MARTINA. "Impact of graphene nanosheets on primary astrocytes." Doctoral thesis, Università degli studi di Genova, 2018. http://hdl.handle.net/11567/929833.
Full textTsang, Yuen Ting. "Expression of brain-derived neurotrophic factor in reactive astrocytes provides neuroprotection to SH-SY5Y cells against six-hydroxydopamine toxicity invitro." HKBU Institutional Repository, 2012. https://repository.hkbu.edu.hk/etd_ra/1392.
Full textSmith, Maria Civita. "MAPPING ASTROCYTE DEVELOPMENT IN THE DORSAL CORTEX OF THE MOUSE BRAIN." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1373039738.
Full textNadkarni, Suhita. "Dynamics of Dressed Neurons: Modeling the Neural-Glial Circuit and Exploring its Normal and Pathological Implications." Ohio : Ohio University, 2005. http://www.ohiolink.edu/etd/view.cgi?ohiou1125689320.
Full textLe, Douce Juliette. "Altération métabolique et déficit synaptique dans la maladie d'Alzheimer : rôle de la PHGDH astrocytaire." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066552/document.
Full textAn early alteration of both cerebral glucose metabolism and synaptic activity has been consistently described in Alzheimer's disease (AD) patients. Metabolism of glucose via glycolysis and the citric acid cycle produces ATP that is essential for synaptic activity and plasticity. In the brain, glucose is predominantly processed glycolytically into astrocytes and not by neurons. Beyond ATP production, a major function of aerobic glycolysis is to provide precursors to support macromolecular synthesis. L-serine, generated from glucose through diversion of the glycolytic intermediate 3-phosphoglycerate (3PG) into the phosphorylated pathway, is only produced in astrocytes by 3-phosphoglycerate dehydrogenase (PHGDH), selectively expressed in those glial cells. L-serine is the precursor of D-serine, the main co-agonist of synaptic NMDAR, required for synaptic activity and plasticity. We used 3xTg-AD mice, which develop a progressive pathology, to investigate whether a defective production of L-/D-serine contributes to early synaptic deficits in AD. We found that 3xTg-AD mice display early in vivo alterations of glucose metabolism, synaptic deficits (LTP) in the CA1 region and also lower concentration of L-serine. The local expression of PHGDH was significantly altered. Exogenous D-serine completely rescued LTP in 3xTg-AD mice. These data support the hypothesis that a deficit of L-serine synthesis by astrocytes likely mediated by a decreased glycolytic flux may be responsible for the synaptic alteration mediated by NMDAR in the hippocampus of 3xTg-AD mice
Syed, Nasser. "Arginine vasopressin and somatostatin receptors in rat astrocytes." [Ames, Iowa : Iowa State University], 2006.
Find full textSmall, Lorne N. (Lorne Neil). "The composition of inclusions specific to Gomori astrocytes." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22805.
Full textCookson, Mark R. "Studies of activation and toxicity in cultured astrocytes." Thesis, University of Salford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308094.
Full textVladimirov, Andrew A. "Metabolic receptor cross-talk and excitotoxicity in astrocytes." Thesis, University of Bristol, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399955.
Full textMartin-Biran, Magali. "Etude par spectroscopie de RMN du métabolisme des neurones et des astrocytes en culture primaire." Bordeaux 2, 1994. http://www.theses.fr/1994BOR28314.
Full textIn order to investigate the cellular compartmentation of the central nervous system, we first defined the metabolic properties of neurons and astrocytes in homogenous primary culture. The metabolic fate of [1-13C]glucose in cerebellar neurons and astrocytes, as well as in cortical astrocytes, was characterized by NMR spectroscopy. The astrocytes, contrary to neurons, synthesized glutamine. The maturation of the glutamine synthesis pathway was delayed in cerebellar astrocytes, as compared to cortical astrocytes. The fluxes involved in exogenous glucose utilization were quantified. The results demonstrated that if neurons used exclusively glucose as carbon source to fuel the Krebs cycle, the carbon sources for astrocytes were diversified (glucose, exogenous amino acids, endogenous carbon sources). In the same way, the pyruvate carboxylase activity was of minor importance in neurons, that implied the need for these cells of exogenous carbon substrates. We evidenced that alanine and citrate were also synthesized by astrocytes and exported to their extracellular medium. These metabolites may play a role as carbon and/or nitrogen shuttles betwen neurons and astrocytes. 31P NMR data showed similar energy charges in cerebellar neurons, astrocytes and in the cerebellum. Differences in the content of metabolites linked to membrane metabolism were observed. The postnatal development of the cerebellum was studied using 31P and 1H NMR spectroscopy. A large content of acetate was evidenced at birth, that decreased during the first postnatal days whereas the NAA content increased
Abjean, Laurene. "Les astrocytes réactifs, des partenaires anti-agrégants dans la maladie de Huntington : identification des mécanismes impliqués dans le dialogue neurone-astrocyte." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS088.
Full textHuntington’s disease (HD) is a hereditary neurodegenerative disease caused by an expansion of CAG codons in the Huntingtin gene. It is characterized by the death of striatal neurons and the presence of mutant Huntingtin (mHtt) aggregates. In pathological conditions, as in HD, astrocytes change and become reactive. Astrocyte reactivity is characterized by morphological and significant transcriptomic changes. Astrocytes are essential for the proper functioning of neurons but the functional changes associated with reactivity are still unclear.To better understand the roles played by reactive astrocytes in HD, we took advantage of our recently developed viral vectors that infect selectively astrocytes in vivo and either block or induce reactivity, through manipulation of the JAK2-STAT3 pathway. We used these vectors in two complementary mouse models of HD and found that reactive astrocytes decrease the number and the size of mHtt aggregates that mainly form in neurons. Reduced mHtt aggregation was associated with improvement of neuronal alterations observed in our mouse models of HD. A genome-wide transcriptomic analysis was performed on acutely sorted reactive astrocytes and revealed an enrichment in genes linked to proteolysis. Lysosomal and proteosomal activities were also increased in reactive astrocytes in HD mice. Moreover, we show that reactive astrocytes degrade more efficiently their own mHtt aggregates, suggesting that these cells could siphon mHtt away from neurons. Alternatively, several chaperones were induced in reactive astrocytes. In particular, the co-chaperone DNAJB1/Hsp40 was upregulated in reactive astrocytes and was present in exosomal fraction from HD mouse striatum. Loss and gain of function experiments suggest that this chaperone is involved in the beneficial effects of reactive astrocytes on mHtt aggregation and neuronal status. Therefore, reactive astrocytes could release anti-aggregation proteins that could promote mHtt clearance in neurons.Overall, our data show that astrocytes, by becoming reactive in HD, develop a protective response that involves complex bidirectional signaling with neurons to reduce mHtt aggregation
Moreno, García Álvaro. "Endocannabinoid modulation of astroglial cells in multiple sclerosis." Electronic Thesis or Diss., Bordeaux, 2022. http://www.theses.fr/2022BORD0171.
Full textMultiple sclerosis (MS) is an immune-mediated, chronic inflammatory disease of the central nervous system and a leading cause of disability in young adults. It is well-established that astrocyte activation drives chronic inflammation and neurodegeneration in the experimental autoimmune encephalomyelitis (EAE) model of MS and in vivo modulation of astrocyte signaling exhibits beneficial effects during disease progression. It is thus envisaged that the identification of factors driving pathogenic astrocyte activity in MS will contribute to the development of novel and more successful treatment strategies. In this context, a neurotoxic population of neurotoxic reactive astrocytes induced by activated microglia that contributes to the death of neurons and oligodendrocytes has been recently identified in MS.Astrocytes present complex and tightly controlled Ca2+ dynamics which are fundamental to intracellular signaling and intercellular communication. Activity-dependent Ca2+ signals in astrocyte regulate directly the biological functions of these cells and affect the integration and processing of synaptic information, modulating synaptic transmission, plasticity and behavior. Indeed, astrocytes respond with cytosolic Ca2+ elevations to a wide variety of neurotransmitters released by neurons and subsequently release a plethora of neuroactive molecules, called gliotransmitters, which comprise glutamate, ATP, D-serine and GABA. Reactive astrocytes displaying deregulated Ca2+ signaling have been found in several neurological disorders. However, astrocyte Ca2+ dynamics have not been investigated in the context of MS.Astrocytes and microglia are modulated by endocannabinoids and participate in the biosynthesis and metabolism of these compounds. However, the role of neuroglial cells as targets and mediators of endocannabinoid signaling in MS remains poorly understood. (Endo)cannabinoids acting through cannabinoid type 1 receptors (CB1Rs) exert symptom control in MS. These beneficial effects are mainly mediated by the activation of neuronal CB1Rs that engage protection from glutamate excitotoxicity. On the other hand, CB1Rs expressed in astrocytes induce intracellular Ca2+ elevations that promote glutamate release. This mechanism underlies working memory impairment by acute cannabinoids in rodents and may contribute to excitotoxic events in neurodegenerative conditions such as MS.In this work, we have addressed several objectives aimed at deciphering the role of the endocannabinoid system in modulating astrocytes during MS. In the EAE model of chronic MS we have 1) investigated the temporal dynamics of endocannabinoid signaling deregulation in reactive astrocytes, 2) characterized changes in astrocyte Ca2+ signaling and 3) examined the role of astroglial CB1Rs during autoimmune demyelination using conditional mutant mice. Our results show that astrocyte activation during EAE involves early transcriptional alterations affecting endocannabinoid signaling associated molecules. Secondly, we have identifies CB1Rs as crucial regulators of astrocytic Ca2+ dynamics in the mouse cortex in vivo and uncover aberrant Ca2+ signaling in MS. Lastly, we unveil that astrocyte CB1Rs exacerbate neurological disability and neuroinflammation during EAE pointing out to a previously unexpected role of the ECS in the pathophysiology of myelin. These data broaden current knowledge on the mechanisms involved in benefits/side effects of currently available MS treatments targeting CB1Rs and pave the way for the development of novel, more efficacious endocannabinoid system-modulating drugs to treat MS
Eraso, Pichot Abel. "Adaptive regulation of calcium excitability and energy metabolism by CREB-dependent transcription in astrocytes: study of the mechanisms governing astrocyte plasticity." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/664170.
Full textAn increasing body of evidence suggests that astrocytes participate in higher-brain functions, controlling from synaptic transmission to global brain waves and learning and memory processes. Different mechanisms have been proposed to mediate these astrocyte-dependent processes, astrocytic lactate release and calcium-dependent gliotransmission being the main known effectors. The existence of control of brain functions by astrocytes suggests that astrocytes may shape brain functions in response to experience as much as neurons, thus constituting the phenomenon of astrocyte plasticity. In neurons, the transcription factor CREB is the best known coordinator of synaptic and intrinsic plasticity. The fact that, in astrocytes, CREB activation is also activity-dependent, positions CREB as an ideal target to promote plasticity-related changes in astrocytes, too. In this thesis, we have analyzed the effect of the activation of CREB-dependent transcription in astrocytes, specifically regarding calcium signals and metabolism. We have demonstrated that activation of CREB-dependent transcription reduces cytosolic calcium events via mitochondria and increases in lactate release, which may have impact on synaptic transmission. An important contribution of the study is the molecular analysis of astrocytic mitochondria, which has revealed that astrocytes may use fuels other than glucose such as fatty acids to meet basic energy metabolic demands. Taken together, our results establish astrocytic CREB as a hub in astrocyte-plasticity and shed light on the interplay between plasticity and energy metabolism in astrocytes; these findings constitute a conceptual and mechanistic advance in the knowledge of astrocytic biology and how these cells may control learning and memory.
Blum, Andrew E. "G Protein-Coupled Receptor Regulation of ATP release from Astrocytes." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1264192022.
Full textStephan, Jonathan Verfasser], Christine R. [Akademischer Betreuer] Rose, and Dieter [Akademischer Betreuer] [Willbold. "Mechanisms of ammonium-induced depolarization of astrocytes in situ." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2011. http://d-nb.info/1015363687/34.
Full textWrzos, Claudia. "The role of astrocytes for oligodendrocyte death and remyelination." Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2012. http://hdl.handle.net/11858/00-1735-0000-000D-F1F4-E.
Full textHirst, Warren David. "Serotonin receptors on astrocytes in vitro and in vivo." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336284.
Full textHernandez, Ernesto. "MORPHOLOGICAL ANALYSIS OF LARVAL DROSOPHILA ASTROCYTES IN THE VNC." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/613064.
Full textStone, Rebecca. "Glutathione release from astrocytes; characterization and implications for neurodegeneration." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395567.
Full textGee, James Michael. "Genetic tools for imaging intracellular calcium dynamics in astrocytes." Thesis, The University of Utah, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10193205.
Full textNew evidence afforded by advanced live-tissue imaging techniques indicates that astrocytes, the predominant glial cell subtype, play a far more active role in synaptic physiology than was previously appreciated. Evolved iterations of genetically encoded calcium indicators, primarily the GCaMP variants, have enabled high spatiotemporal resolution detection of intracellular activity, but are limited by few options for gene transfection and expression. The goal of this dissertation work was to develop novel GCaMP-based tools for straightforward optical interrogation of astrocytic activity in rodent models of neuropathology.
A Polr2a-targeted, Cre-dependent, CAG-driven, GCaMP5G-expressing reporter mouse line was constructed and designated “PC-G5-tdT”. Detection of positive cells was facilitated by an IRES-tdTomato tag. PC-G5-tdT proved effective in diverse developmental contexts and reported intracellular calcium dynamics in somas and fine processes of astrocytes, microglia and neurons. Electrophysiological and behavioral analyses failed to detect a detrimental impact of GCaMP5G expression on nervous system performance. In acute brain slices prepared from a model of endotoxemia-induced neuroinflammation, a stereotyped sequence of astrocytic intrinsic activity was observed over the acute phase. At early time points, frequent somatic and distal process transients were observed but progressively declined with process event frequency lagging behind the soma.
Several rat models of human neuropathology provide systems for researching basic mechanisms of disease. Unfortunately, transgenic rat technologies are immature and viral-based methods are hampered by side effects. In utero electroporation (IUE) is a proven method for transfecting astrocytes and neurons without major drawbacks. A toolset of IUE plasmids carrying CAG-driven, subcellular compartment-targeted GCaMP variants with optional cytosolic tdTomato co-expression was constructed. Stable expression was accomplished via random genomic integration of the reporter cassette through a binary plasmid system derived from the piggyBac transposon. Preparation- and age-specific patterns of activity were readily detected in astrocytes and neurons. In particular, organotypic slice culture astrocytes exhibited frequent global intrinsic transients whereas activity was restricted to distal astrocytic processes in acute brain slices prepared from older animals.
This work has already stimulated progress in the field of glial cell physiology. Future application of these tools will advance our understanding of glial-neuronal interaction and possibly inform development of improved disease modification strategies.
Briens, Aurélien. "Contrôle du système d'activation du plasminogène par les astrocytes." Caen, 2014. http://www.theses.fr/2014CAEN3144.
Full textActivation of plasminogen into plasmin by tissue-type Plasminogen Activator (tPA) initiates fibrinolysis in the vasculature. But enzymes of this system are also found in the brain parenchyma, where they are involved in physiological processes such as synaptic plasticity and in pathological processes such as excitotoxic neuronal death, notably by potentiating glutamatergic signaling. So there must be brain mechanisms regulating the plasminogen activation system. Astrocytes are glial cells cooperating with neurons to control synaptic transmission and plasticity, blood-brain barrier integrity or neurotoxicity. The work carried out in this thesis helped to highlight that astrocytes play a crucial role in the regulation of the effects of plasminogen activation system actors. Thus, a tPA recycling process mediated by astrocytes and inhibited by glutamate provides control of tPA pro-excitotoxic effects. Furthermore, astrocytes represent the first cell type responsible for the clearance of brain plasminogen and plasmin through a mechanism of uptake, a mechanism potentiated by extracellular plasmin activity. Hence, astrocytes can integrate information from the extracellular medium to match the levels of the members of the plasminogen activation system and provide an optimal environment to neurons
Tournier, Cathy. "Regulation des map kinases dans les astrocytes de rat." Paris 11, 1996. http://www.theses.fr/1996PA11T007.
Full textKhan, Dilaware [Verfasser]. "The Relationship between Astrocytes, Inflammation and Epileptogenesis / Dilaware Khan." Bonn : Universitäts- und Landesbibliothek Bonn, 2017. http://d-nb.info/1140525824/34.
Full textReyes, Reno Cervo. "The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/reyes.pdf.
Full textPROVENZANO, FRANCESCA. "Mesenchymal stem cell-derived exosomes and exosome-shuttled miRNAs ameliorate the reactive and neurotoxic phenotype of mouse SOD1G93A astrocytes and human-derived SOD1A4V astrocytes." Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/996729.
Full textHamel, Rodolphe. "Biologie du virus zika dans les cellules cutanées et les astrocytes." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT003.
Full textThe Zika virus (ZIKV) was first isolated from non-human primates the late 1940s. This emerging arbovirus has recently been under the spotlight due to a rapid world pandemic. Belonging to the Flaviviridae family, this flavivirus is transmitted by Aedes’ genus mosquitoes. Historically low pathogenic, a new major concern is the possible association of ZIKV with diverse of neurological complications, including the development of microcephaly and Guillain-Barré syndrome, particularly in newborns of infected mothers. In addition, there is currently no vaccine or specific treatment to cure the disease, so the main preventive measures to fight the spreading of the virus are to prevent mosquitoes’ bites and to plan an effective vector control. A better understanding of the biology of the virus, from the entry in the body, especially at the skin level, to the molecular mechanisms of viral replication, is therefore necessary.Using different molecular and cellular strategies, we investigated the tropism of the virus, identified cell surface receptors and determined the cell’s responses to the infection. Our work also permitted to identify a potential mechanism by which ZIKV evades the host immune system to facilitated his own replication. We also have undertaken original work on a molecular mechanism increasing the pathogenicity of flavivirus. A better knowledge of this mechanism may lead to the identification of potential therapeutic targets. Finally, considering the neuronal tropism of the ZIKV, we studied the immune response of human astrocytes, a very important cell population in the central nervous system, playing a major role in the mechanisms of neurogenesis during the fetus’ brain development
Ghezali, Grégory. "Control of synaptic transmission by astroglial connexin 30 : molecular basis, activity-dependence and physiological implication." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066423/document.
Full textPerisynaptic astrocytes are active partners of neurons in cerebral information processing. A key property of astrocytes is to express high levels of the gap junction forming proteins, the connexins (Cxs). Strikingly, astroglial Cx30 was suggested early on to be involved in cognitive processes; however, its specific role in neurophysiology has yet been unexplored. We recently reveal that Cx30, through an unconventional non-channel function, controls hippocampal glutamatergic synaptic strength and plasticity by directly setting synaptic glutamate levels through astroglial glutamate clearance. Yet the cellular and molecular mechanisms involved in such control, its dynamic regulation by activity and its impact in vivo in a physiological context were unknown. To answer these questions, I demonstrated during my PhD that: 1) Cx30 drives the morphological maturation of hippocampal astrocytes via the modulation of a laminin signaling pathway regulating cell polarization; 2) Cx30 expression, perisynaptic localization and functions are modulated by neuronal activity; 3) Cx30-mediated control of astrocyte synapse coverage in the supraoptic nucleus of the hypothalamus sets basal plasmatic level of the neurohormone oxytocin and hence promotes appropriate oxytocin-based social abilities. Taken together, these data shed new light on astroglial Cxs activity-dependent regulations and roles in the postnatal development of neuroglial networks, as well as in astrocyte-synapse structural interactions mediating behavioral processes
Lefevre, Yan. "Rôle de la glie dans la douleur chronique d'origine cancéreuse chez le rat." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22090/document.
Full textThe present work has investigated the role of glia upon pain symptoms in a well established peripheral neuropathic pain model and a bone cancer pain model. The neuropathic pain model was obtained by right L5-L6 spinal nerve ligation in male Wistar rats. Bone cancer pain was induced by injecting MRMT-1 rat mammary gland carcinoma cells into the right tibia of Sprague-Dawley female rats. Mechanical allodynia and hyperalgesia were quantified using von Frey hairs and ambulatory incapacitance using dynamic weight bearing. Drugs were administered either acutely or chronically using osmotic pumps, through intrathecal catheters chronically implanted in experimental animals. Using von Frey hair stimuli, we found that transient inhibition of glia metabolism by intrathecal injection of fluorocitrate was ineffective in both models. In both models, pain symptoms required spinal NMDA receptor activation. Intrathecal administration of a single dose of D-aminoacid oxidase, which degrades D-serine, a co-agonist of NMDA receptors, reduced mechanical allodynia and hyperalgesia in neuropathic rats and allodynia in cancer rats. The effect of chronic fluoroacetate in neuropathic rats was reversed by acutely administered intrathecal D-serine, which had only a slight effect in cancer rats. None of these compounds altered the functional disability shown by neuropathic or cancer animals and measured by the dynamic weight bearing apparatus. These results show that neuropathic pain and cancer pains depend upon D-serine co-activation of spinal NMDA receptors but only neuropathic pain requires functional spinal cord glia in the rat. Glia may thus play different roles in the development and maintenance of chronic pain in these two situations
Ma, Meihui. "Interactions of human immunodeficiency virus type 1 proteins with astrocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23632.pdf.
Full textLi, Lizhen. "The role of reactive astrocytes in brain ischemia and neurotrauma /." Göteborg : Institute of Neuroscience and Physiology, Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/772.
Full textSabri, Farideh. "Astrocytes during HIV infection of the brain : relevance for neuropathogenesis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4536-5/.
Full text