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Mellor, Robert. "Neurochemical studies on cultured glial cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300038.
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Sinclair, Michael S. "Modulation of Peripheral Taste Function by Glial-like Taste Cells." Scholarly Repository, 2012. http://scholarlyrepository.miami.edu/oa_dissertations/715.
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Taste is detected by cells of taste buds in the oral cavity. Mammalian taste buds contain three types of cells: receptor, presynaptic, and glial-like. Of these three, glial-like cells are the least studied. Their only known function is that they clear neurotransmitters from the extracellular space. The present work describes two previously undocumented properties of glial-like cells. First, Oxytocin receptor (OXTR) mRNA was detected by RT-PCR in taste tissue of mice. In the taste buds of Oxtr-YFP knockin mice, YFP was seen in glial-like taste cells and other cells immediately outside the taste bud, but no other cells in oral epithelium. Oxytocin (OXT) elicited Ca2+ responses from cells that resemble glial-like taste cells (by criteria including gene expression and lack of excitability). The EC50 for OXT in these cells was 33 nM, and responses saturated at 1 µM. 500 nM L-371,257 (an OXTR antagonist) significantly inhihited the responses to OXT. In a semi-intact preparation of lingual slices, OXT did not alter bitter tastant-evoked Ca2+ responses. Further, in behavioral studies, OXT (10 mg/kg i.p.) did not alter the responses of mice to aversive salty (NaCl), bitter (quinine), or sour (citric acid) solutions. In contrast, OXT (0.1 mg/kg i.p.) significantly decreased taste behavioral responses to low-to-intermediate concentrations of sucrose. My data suggest that OXT may modulate sweet taste sensitivity in vivo by acting on glial-like cells in taste buds. Second, Renal Outer Medullary K channel (ROMK) mRNA was also detected by RT-PCR in taste buds . Immunostaining revealed that ROMK is localized to the apical tips of glial-like taste cells. In the kidney, ROMK, apically localized in nephron epithelium facilitates a unidirectional flow (i.e. excretion) of K+. I suggest that, analogous to glia in the central nervous system, glial-like taste cells homeostatically redistribute extracellular [K+ ] within taste buds to maintain their sensitivity. The results of this study reveal that glial-like taste cells resemble nervous system glia in more ways than simply clearing neurotransmitters. They may also modulate the sensory output of the taste bud and buffer the extracellular [K+]. A more active role for glial-like cells in the functioning of the taste bud should be investigated.
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Jarjour, Andrew A. "Netrin and netrin receptor function in glial motility and myelination." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102513.
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Netrin-1 and its receptors play crucial roles during embryogenesis, guiding axon and neuronal cell migration. Here, roles of netrins and their receptors in glial function were investigated. In the embryonic spinal cord, netrin-1 expressed at the ventral midline orients axon extension. Spinal oligodendrocyte precursor (OP) cells are born close to, and migrate away from, the ventral midline. We find that OPs express DCC and UNC5 netrin receptors and, in an in vitro microchemotaxis assay, are repelled by a netrin-1 gradient. In the absence of netrin-1 or DCC function in vivo, fewer OPs migrate from the ventral to the dorsal embryonic spinal cord, consistent with netrin-1 acting as a repellent guidance cue for these cells.In the adult CNS, oligodendrocytes continue to express DCC and UNC5 receptors, and upregulate netrin-1 expression. Our findings indicate that netrin-1 and its receptors are localized to paranodal axo-glial junctions, specialized cell-cell adhesions between non-compact myelin loops and axons. In myelinating cerebellar slice cultures derived from neonatal DCC-/- and netrin-1-/- mice, paranodes develop and mature normally but later become disorganized, resulting in loss of domain segregation at the nodal region. These data suggest that netrin-1 and DCC are essential for the maintenance of paranodal junctions, and may be indicative of a wider role in mediating cell-cell contacts in the adult.
Netrin-1, DCC, and UNC5 homologues have also been identified as putative tumor suppressors, and their expression is downregulated in many cancers, including glial tumors. In our studies, netrins were found to act as autocrine factors that restrain human glioblastoma cell migration, slowing cell movement and inhibiting the formation of focal contacts associated with lamellipodial protrusion and membrane extension. DCC and UNC5 homologues have previously been proposed to inhibit tumorigenesis by inducing cell death when unbound by netrin. However, we found no evidence of increased cell death in the absence of netrin function in oligodendrocyte precursors, oligodendrocytes or glioma cells. Instead, we find that netrins act as long-range guidance cues during glial precursor migration during development, while acting at short distances to stabilize cell-cell and cell-matrix interactions of mature glia and glial tumor cells, maintaining tissue organization and preventing inappropriate cell motility.
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Niemiec, Aurore. "Relevance of glial release in mouse retinal development and function." Strasbourg, 2009. http://www.theses.fr/2009STRA6287.
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Le système nerveux central (SNC) est principalement composé de neurones, et de cellules gliales. Parmi celles-ci l'on distingue les microglies, les oligodendrocytes et les astrocytes, ces derniers représentant à eux seuls plus de 50% du nombre total de cellules du cerveau. Longtemps considérées comme un vulgaire tissu de soutien, de nombreuses études ont mis en évidence un rôle beaucoup plus actif des cellules gliales dans le fonctionnement du système nerveux. En plus de maintenir l'homéostasie extracellulaire, d'assurer l'apport énergétique aux neurones et de permettre la formation/migration/différentiation des neurones au cours du développement du SNC il est apparu au cours de ces dernières décennies qu'un dialogue entre neurones et glies existe et que celles-ci peuvent moduler la neurotransmission. Durant ma thèse j'ai étudié certains aspects de ce dialogue entre neurones et cellules gliales. En effet leurs interactions sont depuis peu considérées comme déterminantes dans certains processus neurodégénératifs. L'influence des cellules gliales sur les neurones tient notamment aux molécules qu'elles sécrètent comme les facteurs trophiques, les lipoprotéines ou encore comme certaines molécules dont la libération semble être régulée comme la D-sérine. Notre équipe a montré précédemment que le cholestérol d'origine gliale était un facteur nécessaire pour la différentiation dendritique neuronale et la formation de synapses efficaces dans des cellules ganglionnaires de la rétine in vitro. Mon projet de thèse visait ainsi à étudier le rôle de deux types de sécrétion gliale dans la maturation et le fonctionnement du SNC à un niveau plus intégré, à savoir d'une part la sécrétion de cholestérol via les lipoprotéines et d'autre part la sécrétion régulée impliquant les SNAREs.
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Ingersoll, Sarah. "The role of complement anaphylatoxins in CNS pathology and glial cell function." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/823.
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Demyelination in the CNS is known to involve several immune effector mechanisms, including complement proteins. For this dissertation project the central hypothesis that C3 and downstream effector complement proteins exacerbate demyelination through activation of glial cells was tested. To investigate the role of C3 and downstream complement proteins in demyelination and remyelination pathology in vivo we utilized the cuprizone model. We used C3 knockout mice (C3-/-), which are lacking the central C3 protein and subsequently all downstream complement effector proteins, and transgenic mice expressing C3a or C5a under the control of the glial GFAP promoter. Interestingly, we found no changes in demyelination or remyelination pathology between C3-/- and control mice. However, C3a and C5a transgenic mice had exacerbated demyelination and slightly delayed remyelination in the corpus callosum compared to WT mice. Transgenic mice had increased cellularity in the corpus callosum due to increased activation and/or migration of microglia. There was also evidence of T cells in the corpus callosum during demyelination in C5a transgenic mice, suggesting C5a may modulate BBB permeability. During early remyelination oligodendrocytes migrated to the corpus callosum in higher numbers in C3a and C5a transgenic mice, thus enabling these mice to remyelinate as effectively as WT mice by the end of the ten week study.
To determine the effects of anaphylatoxins on individual glial subsets, we created murine recombinant C3a and C5a proteins. We found that the MAPK pathway proteins JNK1 and ERK1/2 were activated in glia upon stimulation with recombinant anaphylatoxin proteins. When microglia and mixed glial cultures were stimulated with C3a and/or C5a, we observed an increase in the production of proinflammatory cytokines and chemokines. In contrast, anaphylatoxin-treated primary astrocytes had suppressed cytokine and chemokine production compared to untreated astrocytes. In vitro, primary microglia and astrocytes did not significantly migrate in response to stimulation with C3a or C5a proteins, suggesting migration may not be a primary anaphylatoxin-mediated function in the CNS. Overall, our findings show that anaphylatoxin production in the brain plays a negative proinflammatory role during demyelination and that anaphylatoxin proteins can activate individual subsets of glia, initiating the production of inflammatory mediators.
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Rabah, Yasmine. "Satellite glial cell-proprioceptor interactions in dorsal root ganglia Characterization of transgenic mouse lines for selectively targeting glial cells in dorsal root ganglia Satellite glial cells modulate proprioceptive neuron function." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB208.
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Les neurones propriocepteurs sont nécessaires au contrôle du mouvement et à la locomotion. Ils connectent les fuseaux musculaires et les tendons aux motoneurones de la moelle épinière pour informer le système nerveux central de l’état d’élongation et de contraction des muscles. Leurs corps cellulaires sont localisés dans les ganglions rachidiens dorsaux (GRD), où ils sont intimement entourés de cellules gliales GFAP-positives appelées cellules satellites gliales (CSG). Comme les astrocytes du système nerveux central, les CSG expriment à leur surface des récepteurs couplés aux protéines Gq (Gq RCPG) qui peuvent être activés par les neurotransmetteurs libérés par les corps cellulaires de neurones sensoriels du GRD. Les corps cellulaires des neurones sensoriels expriment aussi un certain nombre de récepteurs et transmetteurs. Ces caractéristiques, ainsi que la proximité physique entre les CSG et les neurones sensoriels a permis d’émettre l’hypothèse que les deux types cellulaires sont capables de communiquer. De récentes données de la littérature suggèrent que les CSG et les neurones sensoriels responsables de la détection de la douleur sont capables de dialoguer. Cependant, à notre connaissance, aucune donnée n’a permis jusqu’à présent de démontrer une interaction entre les CSG et les neurones propriocepteurs. Dans cette étude, nous avons émis l’hypothèse que l’activation des Gq RCPG des CSG permet la modulation de l’activité des propriocepteurs. Pour tester cette hypothèse, nous avons utilisé des approches techniques complémentaires (imagerie calcique bi-photonique, immunohistochimie, biochimie et analyses comportementales) combinées à un outil chemogénétique puissant basé sur la technologie DREADD afin d’activer sélectivement la voie de signalisation Gq RCPG dans les CSG. Nous avons démontré dans une préparation de GRD intacte que les CSG sont capables de moduler l’activité des propriocepteurs via une signalisation purinergique. Pour tester la pertinence de cette communication, nous avons réalisé des expériences de comportement sensorimoteur et mis en évidence que l’activation des cellules gliales GFAP-positives induit des déficits sensorimoteurs. Déterminer si la modulation des propriocepteurs par les CSG affecte la transmission sensorimotrice a de profondes implications pour la compréhension du système sensorimoteur et de ses dérèglementsProprioceptive neurons (one’s own neurons) are necessary for controlling motor control and locomotion. They arise from muscle spindles and tendons and synapse onto ventral horn motoneurons to deliver information about the length and contraction of muscles. Proprioceptor somata reside within the dorsal root ganglia (DRG) and are tightly enwrapped in a thin sheath of GFAP-expressing glial cells, called satellite glial cells (SGCs). Interestingly, SGCs express a number of Gq protein- coupled receptors (Gq GPCRs), which can be activated by neurotransmitters released by sensory neuron somata. Sensory neuron somata also express a number of receptors and transmitters. Both the expression of receptors and the close contact between SGCs and sensory neurons led to the hypothesis that these two cell types communicate. There is emerging evidence that SGCs and nociceptive sensory neuron (pain-sensing neurons) somata can communicate. Furthermore, to date, there is no study conducted on SGC-proprioceptor interaction. We hypothesized that SGC Gq GPCR signaling induces the release of neuroactive molecules from SGCs, leading to the modulation of proprioceptor activity. The main goal of this project has been to test this hypothesis using complementary technical approaches (2-photon Ca2+ imaging, immunohistochemistry, biochemistry and behavior) combined with a powerful chemogenetic DREADD-based tool to activate SGC Gq GPCR activity. We have demonstrated ex vivo that SGCs modulate proprioceptive neuron activity through a purinergic pathway. In order to test the physiological relevance of this discovery in vivo, we performed sensorimotor behavioral experiments and have shown that activating GFAP-expressing glial cells induces sensorimotor deficits. Determining whether SGC-induced proprioceptor activity has profound implications in the understanding of sensorimotor functions in health and diseases
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Murphy, John Anthony. "The protein kinase C of glia." Thesis, University of York, 1989. http://etheses.whiterose.ac.uk/9762/.
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Wunderlich, Kirsten A. [Verfasser], and Eberhart [Akademischer Betreuer] Zrenner. "Novel Findings about the Role of Glial Cells in Retinal Function, Disease, and Therapy / Kirsten A. Wunderlich ; Betreuer: Eberhart Zrenner." Tübingen : Universitätsbibliothek Tübingen, 2016. http://d-nb.info/1197694161/34.
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Littrell, Ofelia Meagan. "NIGROSTRIATAL DOPAMINE-NEURON FUNCTION FROM NEUROTROPHIC-LIKE PEPTIDE TREATMENT AND NEUROTROPHIC FACTOR DEPLETION." UKnowledge, 2011. http://uknowledge.uky.edu/neurobio_etds/1.
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Trophic factors have shown great promise in their potential to treat neurological disease. In particular, glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent neurotrophic factor for midbrain dopamine (DA) neurons in the substantia nigra (SN), which lose function in Parkinson’s disease (PD). GDNF progressed to phase II clinical trials, which did not meet proposed endpoints. The large size and binding characteristics of GDNF have been suspected to contribute to some of the shortcomings of GDNF related to delivery to target brain regions. Smaller peptides derived from GDNF (Dopamine-Neuron Stimulating Peptides – DNSPs) have been recently investigated and appear to demonstrate trophic-like effects comparable to GDNF. In the described studies, a time course study was conducted to determine in vivo DA-release characteristics 1-, 2- and 4- weeks after peptide treatment. These studies determined the effects on DA terminals within striatal sub-regions using microelectrodes. A heterogeneous effect on striatal sub-regions was apparent with the maximum effect in the dorsal striatum – corresponding to terminals originating from the SN.
Dysregulation of GDNF or GDNF signaling is believed to contribute to motor dysfunction in aging and PD. Thus, it is hypothesized that GDNF is necessary for the maintenance and function of neurons. To extend this line of investigation, in vivo functional measures (DA-release and -uptake) and behavioral and cellular alterations were investigated in a transgenic mouse model (Gdnf+/-) with reduced GDNF protein levels. The described studies determined that both DA-uptake and -release properties were altered in middle-aged Gdnf+/- mice with only modest reductions in DA neurochemical levels. GDNF levels in Gdnf+/- mice were restored to levels comparable to wild-type (WT) counterparts by treatment with GDNF. GDNF protein supplementation led to enhanced motor behavior and increased markers for DA neurons in the SN of Gdnf+/- mice. Gdnf+/- mice appeared to show a heightened sensitivity to GDNF treatment compared to WT counterparts.
Overall, this body of work examines novel synthetic peptides with potential to enhance DA-neuron function and expands upon the current understanding of GDNF’s role in the nigrostriatal pathway.
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Altas, Bekir [Verfasser], Nils [Akademischer Betreuer] Brose, Judith [Gutachter] Stegmüller, and Dirk [Gutachter] Goerlich. "Roles of the Nedd4 Family E3 Ligases in Glial Function and Nerve Cell Development / Bekir Altas ; Gutachter: Judith Stegmüller, Dirk Goerlich ; Betreuer: Nils Brose." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1131875710/34.
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Latzer, Pauline [Verfasser], Carsten [Gutachter] Theiss, and Schlegel [Gutachter] Uwe. "Influence of bevacizumab on the morphology, the function and the molecular signaling of neurons and glial cells in the central nervous system / Pauline Latzer ; Gutachter: Carsten Theiss, Schlegel Uwe." Bochum : Ruhr-Universität Bochum, 2016. http://d-nb.info/1123283095/34.
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Lee, Hui-kwan Rebecca, and 李曉鈞. "Differential effects of glial cell line-derived neurotrophic factor and neurturin on NG108-15 cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B27771362.
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Menjot, de Champfleur Nicolas. "La voie ventrale sémantique du langage : une étude de connectivite anatomique, de connectivite fonctionnelle et de sa plasticité périopératoire." Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON1T012/document.
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La conception classique de l'organisation des réseaux cérébraux participant au langage décrit deux zones corticales, l'une frontale (Broca), l'autre temporale intervenant respectivement dans la production et la compréhension du langage, unies par un faisceau de substance blanche: le faisceau longitudinal supérieur. L'imagerie par résonance magnétique d'activation (IRMf) a rendu possible la visualisation de zones d'activation corticales, et l'imagerie en tenseur de diffusion avec la tractographie celle des faisceaux de substance blanche. Ces données nouvelles permettent de repenser l'organisation corticale et sous-corticale du langage. L'ensemble des travaux en imagerie d'activation étaye l'hypothèse d'une dissociation dorso-ventrale du traitement du langage. Les zones de traitement de l'information phonétique étant dorsales, et les centres impliqués dans le traitement sémantique plus ventraux. Imagerie d'activation, imagerie du tenseur de diffusion, stimulations corticales et sous-corticales ont permis d'aboutir à un modèle de réseau du langage impliquant une voie dorsale, essentiellement phonologique et une voie ventrale, sémantique présentant deux composantes. La première est directe, par le faisceau fronto-occipital inférieur connectant les aires temporales postérieures à la région orbito-frontale. La seconde est une voie indirecte qui connecte successivement la région occipito-temporale au pôle temporal par l'intermédiaire du faisceau longitudinal inférieur puis le pôle temporal aux aires basifrontales par le faisceau unciné. Cette dernière voie est compensée après résection ou lors des stimulations per-opératoires, suggérant la possibilité de réseaux de suppléance parallèles et bilatéraux. Dans cette vision d'une voie ventrale sémantique bilatérale, notre travail a pour objet par l'utilisation de l'imagerie fonctionnelle d'activation, d'une part, et de l'imagerie en tenseur de diffusion d'autre part, 1) de vérifier le nombre de faisceaux qui sous-tendent cette voie et en particulier de la part attribuable au faisceau longitudinal moyen; 2) de caractériser les réorganisations de la connectivité fonctionnelle du réseau du langage après une chirurgie de tumeur gliale hémisphérique gauche. Dans la première partie de ce travail, après avoir rappelé la filiation phylogénétique de l'homme et du primate non-humain, en insistant sur les dissemblances qui existent dans leur anatomie corticale et sous-corticale, nous exposons comment ces données ont permis d'aboutir à la découverte du faisceau longitudinal moyen chez l'homme. Nous confirmons la visibilité en imagerie du tenseur de diffusion de ce faisceau et nous précisons ses rapports avec les différents faisceaux de substance blanche constitutifs des voies ventrales et dorsales du langage. Enfin nous discutons ces données tractographiques à la lumière de la dissection et discutons du rôle présumé du faisceau dans le langage. Dans un deuxième temps, nous présentons les concepts de connectivité anatomique, fonctionnelle et effective. Puis nous appliquons un outil d'analyse de la connectivité fonctionnelle à des données périopératoires en tâches de fluence afin de réaliser une cartographie de la plasticité périopératoire de la composante sémantique du langage. Les résultats de cette deuxième étude suggèrent un recrutement de l'hémisphère ipsilatéral à la lésion au décours de la chirurgie. Enfin, nous évoquons la possibilité d'induire une désynchronisation (i.e. une altération de la connectivité) du réseau du mode par défaut par une stimulation peropératoire de la partie postérieure du faisceau cingulaire, induisant une sensation de dépersonnalisation, ces résultats suggérant qu'une des fonctions du noeud le plus postérieur du réseau soit de maintenir un état de conscience du monde extérieurAccording to classical conception of the anatomo-functional organization of language, there are two main cortical areas: a frontal area (Broca) and a temporal one (Wernicke) respectively involved in language production and comprehension. Functional magnetic resonance Imaging (fMRI) reveals cortical areas of activation and diffusion tensor imaging-based tractography (DTI) makes feasible the visualization of white-matter tracts in the human brain. On the basis of these techniques, a new conception of language cortical and sub-cortical organization arose, supporting the hypothesis that language processing network is dissociated in an dorso-ventral way. Dorsal areas of the brain being devoted to phonologic processing and its ventral areas to semantic processing of speech. Different techniques such as fMRI, DTI, intraoperative cortical and subcortical mapping made possible to describe two pathways involved in the language network: a dorsal stream and a ventral stream respectively involved in phonologic and semantic processing. As the dorsal route is composed of a unique pathway, the superior longitudinal fasciculus, the ventral stream appears to be composed of two different pathways. First a direct pathway, the inferior occipitofrontal fasciculus, connecting the posterior temporal areas to the orbitofrontal region. The second one, an indirect pathway, the inferior longitudinal fasciculus links the posterior occipitotemporal to the temporal pole, then relayed by the uncinate fasciculus connecting the temporal pole to the basifrontal areas. According to these observations the aim of our work is In the present work, we aim (1) to confirm that the MdLF is constantly found in control subjects and that it can be delineated from the other fiber tracts that constitute language pathways, (2) to characterize the reorganization of language network's functional connectivity follmowing surgical removal of left hemisphere low grade gliomas. In this study, we confirmed that the MdLF is constantly found in healthy volunteers and we clearly delineate the MdLF from the other fascicles that constitute language pathways, especially the ventral pathway. Considering language plasticity, our findings suggest that in the postoperative period, brain plasticity occurs with an ipsilateral recrutment and increased fonctional connectivity in the left hemisphere. Finally, we report a collaborative work observing that intraoperative electrostimulations of the white matter underlying the left posterior cingulate, while performing a naming task, systematically induced an unresponsive state for few seconds in relationship with a dream-like state. This result provides direct evidence that connectivity underlying the posterior node of the default mode network permits maintained consciousness of the external world
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Cheung, Giselle [Verfasser]. "Properties and functions of glial cells in the developing and injured brains / Giselle Cheung." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1023261537/34.
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Charlton-Perkins, Mark. "Control of Drosophila Eye Specification, Patterning and Function by the Transcription Factors prospero and Pax2." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406819630.
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Böttcher, Chotima [Verfasser]. "Elucidation of neuronal and glial cell phenotypes and functions utilizing mass spectrometry techniques / Chotima Böttcher." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1202042309/34.
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Spielman, Lindsay Joy. "Metabolic hormones and physical activity as regulators of brain glial cell functions and neuroimmune status." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/60304.
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Alzheimer’s disease (AD), the most prevalent form of dementia worldwide, is characterized by several cellular hallmarks including chronic neuroinflammation. Glial cells, the immune and support cells of the brain, become activated in response to pathological formations in the AD brain and neuroinflammation occurs as a result. Persistent activation of glial cells can result in chronic neuroinflammation, which can be damaging to brain tissue. The goal of my PhD research project was to elucidate the cellular mechanisms by which certain non-neuronal factors increase the risk of developing AD, such that new treatment options for AD might be identified. My research focused on two risk factors for developing AD: type 2 diabetes mellitus (T2DM) and sedentary (SED) lifestyles. The overarching hypothesis of my thesis is that the metabolic hormone dysregulation as well as reduced physical activity, contribute to AD pathogenesis through neuroimmune mechanisms. I focused on three specific hypotheses: 1) insulin, a metabolic hormone that has reduced functionality in T2DM, regulates the neuroinflammatory response of glia; 2) the incretin hormones glucagon like peptide (GLP)-1 and glucose dependent insulinotropic polypeptide (GIP), which also become dysregulated in T2DM, control several aspects of glial cell function; and 3) physical activity (PA) has an impact on the neuroimmune status of the brain, which is regulated in a monocyte chemoattractant protein (MCP)-1-dependent manner. Using in vitro cell culture techniques, I demonstrate that glial cells express the insulin receptors. I show that insulin could have anti- inflammatory properties in the brain and may protect against glia-mediated neurotoxicity, while GLP-1 and GIP exhibit anti-apoptotic, antioxidant and trophic effects on glial cells. Utilizing in vivo murine studies, I demonstrate that PA can modify glial cell activation and regulate the expression of immune cytokines in the brain. Additionally, I reveal that the neuroimmune status-modifying activity of PA relies partially on MCP-1. I have discovered that insulin, GLP-1, GIP and PA regulate specific aspects of neuroinflammation. Therefore, targeting neuroinflammation may represent viable AD treatment options, which should be explored in future clinical studies.Irving K. Barber School of Arts and Sciences (Okanagan)
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Bay, Virginia Elisabeth. "Expression and function of inward rectifying potassium channels in CNS glia." Thesis, University of Portsmouth, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511201.
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Stacey, Stephanie. "Notch signaling promotes functional diversity among Drosophila Longitudinal Glia." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86934.
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Reciprocal interactions between neurons and glia are essential for the development and maintenance of neural circuits. The many functions of glial cells and the intrinsic and extrinsic factors that regulate their diversity and functional specification are not well understood. An important challenge is to understand how neurons contribute to glial subtype differentiation and how glial subtypes serve neuronal function. My thesis work has identified a number of Drosophila glial subtype specific genes whose expression is regulated by neuron glial interactions through the Notch (N) signaling pathway. I found that N signaling positively regulated the expression of two subtype specific genes and negatively regulated the expression of four subtype specific genes. Additionally, the expression of these six genes was dependent upon the glycosyltransferase Fringe (Fng) which sensitizes the N receptor to activation by its ligand Delta (Dl). I determined that the subtype specific glial glutamate transporter, Excitatory amino acid transporter 1 (Eaat1), was expressed in an anterior subtype of the longitudinal glia (LG). Through the generation of Eaat1 mutants, I found that the LG were important for larval locomotion. My data supports an acute role for Eaat1 during larval locomotion rather than a developmental requirement. Dorsal motor neuron output was impaired in Eaat1 mutants suggesting that the anterior LG regulate CNS glutamatergic transmission important for dorsal motor neuron function. My work describes functional diversity among subtypes of glia whose differentiation is influenced by neuron-glial communication via Dl-N signaling.Les interactions réciproques entre neurones et cellules gliales sont essentielles pour le développement et l'entretien des circuits neuronaux. Les nombreuses fonctions des cellules gliales ainsi que les facteurs intrinsèques et extrinsèques qui régissent leurs diversités et spécifications fonctionnelles ne sont pas bien compris. Un défi important est de comprendre comment les neurones contribuent à la différenciation des sous-types gliaux et comment ces sous-types servent la fonction neuronale. Mon travail de thèse a identifié un certain nombre de gènes spécifique à certains sous-types gliaux chez la Drosophile dont l'expression est régulée par des interactions neurones gliales à travers la voie de signalisation Notch (N). Mes travaux m'ont permis d'identifier six gènes exprimés de façon spécifique dans certains sous-types gliaux et dont l'expression est régulé par la voie de signalisation N. Notamment l'expression de ces six gènes dépend de la glycoslytransferase Fringe (Fng), qui sensibilise les récepteurs N à l'activation par son ligand Delta (Dl). J'ai observe que Eaat1, un transporteur du glutamate, était seulement exprime dans les cellules gliales longitudinales antérieures (LG). Grâce à la génération de mutants Eaat1, j'ai trouvé que les cellules LG sont importantes pour la locomotion larvaire. Mes données favorise un rôle aigu pour Eaat1 pour la locomotion larvaire plutôt qu'une exigence lors du développement. Chez les mutants Eaat1 l'activité des neurones moteurs est altérée suggérant que les LG antérieure régulent les transmissions glutamatergique du système nerveux central importante pour la fonction des neurones moteur dorsale. Mon travail décrit la diversité fonctionnelle des sous-types gliaux dont la différenciation est influencée via des interactions neurones gliales grâce à la voie de signalisationjDl-N.
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Bayatti, Nadhim. "Modulation of growth factor function by additional extracellular signals in CNS neurones and glia." Ulm : Universität Ulm, Medizinische Fakultät, 2001. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB9802368.
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Bustos, Bustos Alvaro Enrique [Verfasser]. "Comparative functional analysis of factors controlling glial differentiation in Drosophila and mouse / Alvaro Enrique Bustos Bustos." Mainz : Universitätsbibliothek Mainz, 2015. http://d-nb.info/1068941057/34.
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Armstrong, Victoria Diane. "Functional changes in neurons and glia following amphetamine-induced behavior sensitization." CSUSB ScholarWorks, 2003. https://scholarworks.lib.csusb.edu/etd-project/2168.
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Neß, Julia Verfasser], Sascha [Akademischer Betreuer] Weggen, and Dieter [Akademischer Betreuer] [Willbold. "Expression and functional analysis of progranulin (GRN) in glial brain tumors / Julia Neß. Gutachter: Sascha Weggen ; Dieter Willbold." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2012. http://d-nb.info/1024161013/34.
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Tawil, Nabil Jean. "Identification of integrins on the central nervous system glia and their function in cell-substratum contacts." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70365.
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The rat integrin $ alpha sb1$ subunit was purified, its N-terminal sequence and its full cDNA sequence were obtained. The $ alpha sb1$ subunit is found complexed with the $ beta sb1$ subunit forming a heterodimer that mediates the adhesion of type-1 astrocytes to laminin and collagen. Cultured type-1 astrocytes also express other functional integrins from the $ beta sb1$ and $ beta sb3$ subclasses. Type-2 astrocytes and oligodendrocytes express different arrays of $ beta sb1$ and $ beta sb3$ integrins suggesting that CNS glia interact differentially with the extracellular matrix. Integrins on type-1 astrocytes are localized either to focal contacts or point contacts. In well spread astrocytes, most integrins are concentrated in focal contacts. This thesis presents the first evidence that integrins in point contacts are functional mediating the adhesion and spreading of type-1 astrocytes. Unlike integrins in focal contacts, integrins in point contacts rarely colocalize with actin or vinculin and instead they codistribute with clathrin. These point contacts are also seen on the cell body and growth cones of dorsal root ganglion neurons (Wilson and Carbonetto, unpublished data) suggesting that point contacts are common cell-substratum contacts for neural and non-neural cells.
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Bayatti, Nadhim [Verfasser]. "Modulation of growth factor function by additional extracellular signals in CNS neurones and glia / Nadhim Bayatti." Ulm : Universität Ulm. Medizinische Fakultät, 2002. http://d-nb.info/1015325025/34.
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Leoni, Giampaolo. "Characterisation of NG2-GLIA and an immunoablation approach to study their functions in the C.N.S." Thesis, University of Portsmouth, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494140.
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An abundant population of glial cells in the central nervous system (CNS) is identified by the specific expression of the NG2 chondroitin sulphate proteoglycan (CSPG) and are termed NG. NG2-slia are phenotypically distinct from astrocytes, oligodendrocytes, ependyma and microglia, and represent a fifth major type of glia in the brain. Generally, NG2-glia have been considered to be oligodendrocyte progenitor cells (OPCs), but there is evidence that NG2-glia possess neural stem cell-like properties, being able to generate oligodendrocytes, astrocytes and neurons. In addition, NG2-glia respond to different types of brain injury by a rapid and extensive proliferation, or gliosis, and contribute to the axon growth inhibitory glial scar and regeneration of oligodendrocytes. A notable feature of NG2-glia is that they have complex multibranched process fields that form multiple glutamatergic synaptic contacts with neurons. So far, the function of NG2-glial glutamatergic 'synapses' is unresolved. The overall aim of this thesis was to test the hypothesis that NG2-glia may be important for the stabilization and integrity of synapses, and that glutamate released at these synapses may regulate the proliferation and differentiation capacity of NG2-glia.
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Yang, Xin. "Evaluation of neurochemical and functional effects of glial cell-derived neurotrophic factor gene delivery using a tetracycline-regulatable adeno-associated viral vector." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209984.
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Gene transfer to the brain is a promising therapeutic strategy for a variety of neurodegenerative disorders including Parkinson‟s disease (PD). PD is the second most common neurodegenerative disease. Although many drugs have been developed and introduced into the market to provide symptomatic treatment, there is still no cure for PD. Glial cell line-derived neurotrophic factor (GDNF) is a potent survival factor for injured nigrostriatal dopamine neurons and is currently being evaluated as a potential treatment for PD. Gene therapy allows localized, long-term and stable transgene expression after a single intervention to obtain a therapeutic effect. Regulatable promoters for transgene expression furthermore allow optimizing GDNF concentration to avoid undesirable biological activity and clinical side effects. In the first part of the study, an autoregulatory tetracycline-inducible recombinant adeno-associated viral vector (rAAV-pTetbidiON) utilizing the rtTAM2 reverse tetracycline transactivator (rAAV-rtTAM2) was used to conditionally express the human GDNF cDNA. Eight weeks after a single intrastriatal injection of the rAAV-rtTAM2-GDNF vector encapsidated into AAV serotype 1 capsids (rAAV2/1), the GDNF protein level was respectively 15 fold higherand undistinguishable from the endogenous level in doxycycline(Dox) treated and untreated animals. However, a residual GDNF expression in the uninduced animals was evidenced by a sensitive immunohistochemical staining. As compared to rAAV2/1-rtTAM2-GDNF, the rAAV2/1-rtTAM2-WPRE-GDNF vector harboring a woodchuck hepatitis post-transcriptional regulatory element, which increases and stabilizes the transgene transcript, expressed a similar concentration of GDNF in the induced state but a basal level ~2.5-fold higher than the endogenous striatal level. However, the distribution of GDNF in the striatum in induced state was more widespread using the rAAV2/1-rtTAM2-WPRE-GDNF vector as compared to rAAV2/1-rtTAM2- GDNF. As a proof for biological activity, for both vectors, downregulation of tyrosine hydroxylase (TH) was evidenced in dopaminergic terminals of Dox-treated but not untreated animals. In the second part of my study, functional (behavioural) and neurochemical changes mediated by delayed intrastriatal GDNF gene delivery in the partial Parkinson‟s disease rat model were investigated. The rAAV2/1-rtTAM2-WPRE-GDNF vector (3.5 108 viral genomes) was administered unilaterally in the rat striatum 5 weeks after intrastriatal injection of 6-hydroxydopamine (6-OHDA) which produces a partial and progressive lesion of the nigro-striatal dopaminergic pathway. Rats were treated with Dox or untreated from the day of vector injection until sacrifice at 4 or 14 weeks (continuous treatment). A sub-group was Dox-treated for 7 weeks (temporary treatment) then untreated until 14 weeks. In the absence of Dox, the GDNF tissue concentration was found to be equivalent to the endogenous level in 6-OHDA-lesioned rats. In the presence of Dox, it was ~10-fold higher. Dox-dependent behavioral improvements were demonstrated 4 weeks post-vector injection. At later time points, spontaneous partial recovery was observed in all rats, but no further improvement was found in Dox-treated animals. Moreover GDNF gene delivery only transiently improved dopaminergic function. Over the long term, TH was more abundant, but not functional, and the increase was lost when GDNF gene expression was switched off. The third part of my study consisted in the evaluation of the respective dose-range of therapeutical and undesirable effects of GDNF. Functional effects appeared after delivery of 3.5 108 viral particles which produced 200-300 pg/mg protein of GDNF in the lesioned rat striatum (see above). In order to evaluate the viral dose producing undesirable effects, we compared two different doses of vector: 3.5x108 and 4.4x109 viral genome. In the low dose group, the GDNF concentration in the striatum was ~300 pg/mg protein in the Dox-treated animals and equivalent to the endogenous level in untreated animals (~20 pg/mg protein). In contrast, in the high dose group, GDNF levels reached ~1200 pg/mg protein in induced animals but up to ~300 pg/mg protein in uniduced animals. In the low dose group, Dox-dependent downregulation of TH but no asymetrical behaviour was evidenced. In the high dose group, TH downregulation was observed in both Dox+ and Dox-rats. In addition, amphetamine-induced rotational behaviour was evidenced in Dox+ but not in Dox-rats. These data suggest that low doses of virus are sufficient to induce therapeutically-relevant but not undesirable functional effects of GDNF. Nevertheless,a neurochemical effect of GDNF (TH down-regulation) did appear at low dose. In order to understand the GDNF-induced motor asymmetry, we investigated the anatomical pattern of TH down regulation in striatum. Strikingly, there was a greater loss of TH labeling in striosomes than in the surrounding matrix. Receptors which are known to be differentially expressed in the striosomes i.e. µ-opioid receptor(MOR-1) and N-methyl-D-aspartic acid (NMDA) receptor 1 (NR1) as compared to the matrix were analyzed in the high-dose group of animals. MOR-1 was not affected by GDNF gene delivery. In contrast, NR1 was down regulated. The potential relationship between TH and NR1 down-regulation as well as other previously described neurochemical effects of GDNF (as enhancement of DA release and metabolism, of DA neurons excitability or of TH phosphorylation) and behavioural asymmetry remains to be clarified. As summary, our data suggest that behavioural and neurochemical effects of striatal delivery of GDNF can be controlled by Dox by using the autoregulatory rAAV2/1-TetON- GDNF vector, provided the dose range of gene delivery is carefully adjusted.Doctorat en Sciences biomédicales et pharmaceutiques
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Hughes, Lucinda Jane. "Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/412035.
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Biomedical SciencesPh.D.
The Hippo signaling pathway was first discovered in Drosophila melanogaster and is involved in organ size control by regulating cell proliferation and apoptosis. This well conserved pathway is activated by various signal inputs, including cell-cell contact, mechanotransduction, and G-protein coupled receptors, with signals converging on the downstream effector protein Yap and its homologue Taz, which are transcriptional co-activators. When the Hippo pathway is activated, Yap/Taz are phosphorylated, leading to cytoplasmic retention and degradation, and diminishing their transcriptional activity. Yap has also been recently implicated as a potential oncogene, as it is upregulated and transcriptionally active in several tumor types. Furthermore, inhibiting Yap activity in various cancer models has been shown to revert cancer cells to a normal phenotype. Although the role of Yap has been described in several organ systems, there is a paucity of information about the function of Yap in the central nervous system. I investigated the function of Yap/Taz in the murine cerebellum to determine its significance during normal development and a potential role for Yap/Taz in medulloblastoma, a tumor that arises in the cerebellum. In Chapter 2, I describe the expression pattern of Yap from embryonic through adult stages in mice, and demonstrate the functional significance of Yap/Taz in different cell populations using conditional knockout mouse models. I show that Yap plays a significant role in cell fate determination as well as in cerebellar foliation: Yap is highly expressed in the ventricular zone and is required for the proper formation of ependymal cells, and is also strongly expressed in Bergmann glia (BG) during early developmental stages, where Yap, together with Taz, plays a significant role in cerebellar foliation. Furthermore, Yap/Taz-deficient BG exhibit migrational defects, as their cell bodies can be found mislocalized to the molecular layer (ML), rather than remaining tightly associated with Purkinje Cells (PCs) in the PC layer. BG support the health of PCs, and severely defective BG positioning eventually leads to a loss of PCs. However, although Yap is highly expressed in granule neuron progenitors (GNPs) during the rapid postnatal expansion stage, it does not appear to play a major role in proliferation of these cells as conditionally knocking-out Yap/Taz in GNPs does not alter their proliferative capacity. Our observations demonstrate that in the cerebellum, Yap has a novel function in glia that is required for the development of normal foliation and organization, but plays a minimal role in GNP proliferation. Importantly, I also show that the reduction of sphingosine-1-phosphate G-protein-coupled receptor (S1P1) signal transduction activates the upstream kinase Lats with concomitant increases of phosphorylated Yap as well as a reduction of the known Yap target connective tissue growth factor (CTGF). This study identifies a novel function of Yap/Taz in cerebellar glia that is required for the development of normal foliation and laminar organization with sphingosine-1-phosphate (S1P) signaling as a potential extracellular cue regulating Yap activity during cerebellar development. In Chapter 3, I present further support for the finding that Yap/Taz are not required for GNP proliferation in vivo by discussing the failure of Yap/Taz loss to rescue the Sonic-hedgehog (Shh) mediated medulloblastoma phenotype, in which GNPs are considered to be the tumor cell of origin. Furthermore, I provide evidence suggestive of a tumor suppressive function of Yap/Taz in the cerebellum. Together, previously unknown functions of Yap in the developing and malignant cerebellum are described, providing a foundation for future studies of Yap in the central nervous system (CNS).
Temple University--Theses
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Padovani-Claudio, Dolly Ann. "FUNCTIONAL ANALYSES OF THE CHEMOKINE RECEPTOR CXCR2 IN THE NORMAL AND DEMYELINATED ADULT CENTRAL NERVOUS SYSTEM." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1152193193.
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Timmermann, Aline [Verfasser]. "Functional impact of Kir4.1 channels in hippocampal NG2 glia on neuronal plasticity and behavior / Aline Timmermann." Bonn : Universitäts- und Landesbibliothek Bonn, 2020. http://d-nb.info/1219140368/34.
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Müller, Jochen [Verfasser]. "Two glial cell types make structural and functional contact to the calyx of Held in the mouse medial nucleus of the trapezoid body / Jochen Müller." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1027306357/34.
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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.
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Thomaty, Sandie. "Influence des processus inflammatoires sur la neuroplasticité et sur les récupérations fonctionnelles après lésion spinale chez le rat adulte." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM4772.
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Les lésions spinales conduisent à des altérations majeures des fonctions sensorimotrices. Les récupérations fonctionnelles consécutives à ces atteintes sont très limitées, notamment en raison des capacités réduites de réparation des tissus endommagés dans le SNC. En outre, ces récupérations dépendent notamment de plusieurs processus cellulaires tels que l'activation astrogliale qui conduit à la formation de la cicatrice gliale, ou encore l'inflammation dont les cellules microgliales et les mastocytes sont les effecteurs les plus précoces. Cette inflammation est connue pour exacerber les dommages tissulaires et restreindre les possibilités de récupération. Cependant, des études récentes chez l'animal et chez l'Homme montrent que l'inflammation pourrait également avoir des effets favorisant les processus de récupération. Le but de cette thèse était de mieux comprendre les liens qui existent entre neuroinflammation, neuroplasticité et récupérations fonctionnelles après lésion spinale. L’objectif expérimental visait à examiner les réactivités microgliales, mastocytaires et astrocytaires post-lésionnelles, en parallèle avec des restaurations fonctionnelles. Dans ce contexte nous nous sommes plus particulièrement intéressés à l'influence d'une cytokine pro-inflammatoire, le Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) sur ces processus inflammatoires et la plasticité fonctionnelle après une hémisection C4-C5 chez le rat adulte. L’ensemble de nos travaux suggère que le GM-CSF pourrait agir par l’intermédiaire de plusieurs événements cellulaires et moléculaires, en favorisant des phénomènes de plasticité adaptatifs et la récupération partielle de fonctions altéréesSpinal cord injuries are mostly of traumatic origin and result in major sensorimotor deficits. Postlesion functional recovery is limited, especially because of the reduced capacity of repairing damaged tissues. Moreover, this recovery depends specifically on several cellular processes such as astroglial activation conducting to glial scar formation, or inflammation for which microglial and mast cells are the earliest effectors. This inflammation is known to exacerbate tissue damages and restrain the capacity to recover. However, recent studies in animals and humans show that inflammation may also have beneficial aeffects on recovery processes. The studies conducted during my doctoral research were intended to better understand the links between neuroinflammation, neuroplasticity and functional recovery following spinal cord injury. We aimed at examining microglial, mast cells and astroglial reactivities after the injury, in relation with functional recovery of somatosensory and motor functions. In this context, we were particularly interested in the influence of Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) on inflammatory and plasticity mechanisms after a C4-C5 hemisection in the adult rat. Our doctoral research suggests that GM-CSF could act through several cellular and molecular events promoting adaptive plasticity phenomena underlying partial recovery of impaired functions
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Schneider, Sarah [Verfasser], and Leda [Akademischer Betreuer] Dimou. "Proliferating NG2-glia and their functional importance in the healthy and injured brain / Sarah Schneider. Betreuer: Leda Dimou." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1084582775/34.
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Krill, Jennifer. "Neuroprotection during Acute Hyperthermic Stress| Role of the PKG Pathway in Neurons and Glia in the Protection of Neural Function in Drosophila melanogaster." Thesis, Florida Atlantic University, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10809769.
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The human brain functions within a narrow range of temperatures and variations outside of this range incur cellular damage and death and, ultimately, death of the organism. Other organisms, like the poikilotherm Drosophila melanogaster, have adapted mechanisms to maintain brain function over wide ranges in temperature and, if exposed to high temperatures where brain function is no longer supported, these animals enter a protective coma to promote survival of the organism once the acute temperature stress is alleviated.
This research characterized the role of different neuronal cell types, including glia, in the protection of brain function during acute hyperthermia, specifically looking at two protective pathways: the heat shock protein (HSP) pathway and the cGMP-dependent protein kinase G (PKG) pathway. Whole animal behavioral assays were used in combination with tissue-specific genetic manipulation of protective pathways to determine the specific cell types sufficient to confer protection of neuronal function during acute hyperthermia. Using the neuromuscular junction (NMJ) preparation, calcium imaging techniques were combined with pharmacological and genetic manipulations to test the hypothesis that alterations in ion channel conductance via endogenous mechanisms regulating the cellular response to high temperature stress alter neuronal function.
Expression of foraging RNAi to inhibit PKG expression in neurons or glia demonstrated protection of function during acute hyperthermia measured behaviorally through the extension of locomotor function. This extension of function with the tissue-specific inhibition of PKG was also confirmed at the cellular level using the genetically encoded calcium indicator (GECI), GCaMP3, to image calcium dynamics at the NMJ, where preparations expressing foraging RNAi could continue to elicit changes in calcium dynamics in response to stimulation. Over the course of this study, the mechanism underlying a novel glial calcium wave in the peripheral nervous system was characterized in order to elucidate glia’s role in the protection of neuronal function during acute hyperthermia.
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Xiu, Jin. "Distribution and function of nicotinic acetylcholine receptors in glia cells and neurons with focus on the neuroprotective mechanisms of cholesterol-lowering drugs in Alzheimer's disease /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-758-8/.
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Yu, Diana Xuan. "Towards functional regeneration of the central nervous system glial calcium signaling in reactive gliosis and the therapeutic potential of bone marrow-derived mesenchymal stem cells for retinal degenerative diseases /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3320122.
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Thesis (Ph. D.)--University of California, San Diego, 2008.Title from first page of PDF file (viewed Sept. 11, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 147-180).
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Marcand-Sauvant, Julie. "Impact d'une neuroinflammation transitoire ou chronique à bas bruit sur le fonctionnement neuronal." Thesis, Bordeaux 2, 2010. http://www.theses.fr/2010BOR21755/document.
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L’état fébrile et le vieillissement normal sont deux processus physiologiques conduisant à un déséquilibre hydrominéral de l'organisme. Ce déséquilibre se traduit par une déshydratation sévère qui peut être aggravée par des conditions climatiques comme nous l'avons vu durant l'été 2003. Dans les deux cas, fièvre et vieillissement, l'organisme répond par une stimulation du système hypothalamo-neurohypophysaire conduisant à l’augmentation de la libération de vasopressine ou hormone antidiurétique, qui pourrait prévenir une déshydratation possiblement critique. Cependant, les modalités d’activation des neurones vasopressinergiques (AVP) dans ces conditions restent inconnues.Le but des recherches réalisées dans cette thèse, a été de déterminer les mécanismes cellulaires et moléculaires responsables de l’activation des neurones vasopressinergiques (AVP) lors d’une réponse inflammatoire et au cours du vieillissement.Nous avons pu démontrer dans la première partie de ce travail que lors d’un épisode inflammatoire (mimé par une injection de lypopolysaccharide LPS) l’activité des neurones AVP est rapidement augmentée et cette activation est soutenue pendant plus de six heures. De plus, cette activation n’est pas due à un effet potentiel secondaire du LPS sur l'osmolarité plasmatique ou la pression artérielle. L’activation précoce des neurones AVP par le LPS semble être soutenue par l’IL-6 (qui mime les effets du LPS), puisque l’activation par le LPS est bloquée par une injection préalable d’anticorps anti-IL-6.Dans la seconde partie de ce travail, nous avons pu montrer le traitement chronique d’IGF-I chez le rat âgé permet de restaurer une fonction urinaire comparable à celle observée chez l’adulte, en agissant vraisemblablement directement sur les neurones AVP puisque le taux plasmatique d’AVP chez les rats âgés traités par l’IGF-I revient à des valeurs normales, i.e., équivalente à celle de rats adultes. Cette hypothèse est confortée par le fait que (i) les neurones AVP expriment le récepteur de l’IGF-I et qu’il n’y a pas de différence dans l’expression de ces récepteurs entre rats âgés et adultes, et (ii) les neurones AVP sont inhibés par l’IGF-I.Enfin, dans la dernière partie de ce travail, nous avons pu montrer que lors du vieillissement, les neurones AVP sont activés, ce qui se traduit par un taux plasmatique d’AVP élevé et un taux d’apeline très faible. De même, les astrocytes sont activés et ne présentent plus de plasticité morphofonctionelle. La microglie, en état d’alerte, ne semble pas jouer un rôle prépondérant dans cette suractivation neuronale et astrocytaire. De plus, cette suractivation neuronale est palliée par un traitement central par un anticorps anti-IL-6 ou un inhibiteur non sélectif des canaux TRPV. Cependant, un traitement central par un anticorps anti-IL-6 n’affecte pas l’expression des TRPV2 dans le noyau supra-optique (NSO). En conclusion générale, il apparait que :1/ L’IL-1 n’est pas le chef d’orchestre de tous les processus inflammatoires. En effet, dans le NSO, l’activation des neurones AVP est soutenue par l’IL-62/ La balance pro- / anti-inflammatoire est un élément importante du dysfonctionnement neuronal. Cependant, le facteur critique du dysfonctionnement des neurones AVP n’est pas la production excessive de facteurs inflammatoires mais l’insuffisante production compensatoire de facteurs anti-inflammatoires.3/ lors du vieillissement, la neuroinflammation responsable du dysfonctionnement des neurones AVP peut être qualifiée de type « chronique à bas bruit », processus dans lequel (i) la microglie, en alerte, voit sa réactivité décuplée lors d'une sollicitation inflammatoire supplémentaire; (ii) le cross-talk astrocytes-neurones est figé dans une configuration d'hyperactivité, semblable à celle observée à l'âge adulte en condition de stimulation physiologique soutenue (comme lors d'une déshydratation), mais qui empêche toute réponse appropriée du réseau à toute demande physiologique supplémentaire, quelle soit transitoire (comme la réponse à une injection aigüe de LPS ou de NaCl 9%) ou soutenue (déshydratation de 48h).Cependant, les données de la littérature montrent le rôle majeur de la microglie dans d'autres types de neuroinflammation dites à « haut bruit », et dont les effets délétères - qui vont du dysfonctionnement neuronal à la neuro-dégénérescence – trouvent leur origine dans la surexpression de molécules microgliales telles l'IL-1 ou le TNF. Pour tenter de comprendre les mécanismes cellulaires et moléculaires impliqués dans un tel dysfonctionnement et pour caractériser la nature du dysfonctionnement neuronal, nous avons mis au point un modèle pharmacologique de neuroinflammation à haut bruit, en injectant directement dans les NSO de l'IL-1. Nos données préliminaires montrent que le dysfonctionnement neuronal ainsi que les mécanismes cellulaires et moléculaires à l’origine de ce dysfonctionnement diffèrent de ceux observés lors du vieillissement : la microglie est activée et surexprime de nombreuses molécules inflammatoires, probablement à l’origine du dysfonctionnement neuronal (absence de pattern phasique, même lors d’une stimulation osmotique), puisque les astrocytes ne semblent pas être affectés. L’absence de pattern phasique à l’origine du faible taux d’AVP plasmatique traduit une perturbation des propriétés électrophysiologiques intrinsèques sous-tendant ce pattern phasique (récepteurs ; canaux ioniques) et/ou des afférences excitatrices (Glu ; ACh ; Na) ou inhibitrices (GABA) modulant cette activité phasiqueThe fever and normal aging are two physiological processes leading to water and mineral imbalance in the body. This imbalance results in severe dehydration which can be aggravated by climatic conditions as we saw during the summer of 2003. In both cases, fever and age, the body responds by stimulating the hypothalamic-neurohypophysial system leading to increased release of vasopressin or antidiuretic hormone, which could possibly prevent dehydration criticism. However, the modalities of activation of vasopressinergic neurons (AVP) in these conditions remain unknown. The aim of the research done in this thesis was to determine the cellular and molecular mechanisms responsible for the activation of vasopressinergic neurons (AVP) during an inflammatory response and during aging. We showed ,in the first part of this work, that during an inflammatory episode (mimicked by an injection of lypopolysaccharide LPS) the activity of AVP neurons is rapidly increased and this activation is sustained for more than six hours. Moreover, this activation is not due to a potential secondary effect of LPS on plasma osmolarity and blood pressure. The early activation of AVP neurons by LPS seems to be supported by IL-6 (which mimics the effects of LPS), since activation by LPS is blocked by prior injection of anti-IL-6. In the second part of this work, we showed chronic treatment of IGF-I in old rats can restore bladder function similar to that observed in adults, presumably by acting directly on neurons AVP as the rate plasma AVP in aged rats treated with IGF-I returned to normal values, ie, equivalent to that of adult rats. This hypothesis is supported by the fact that (i) AVP neurons express the receptor for IGF-I and there is no difference in the expression of these receptors between adult and aged rats, and (ii) AVP neurons are inhibited by IGF-I. Finally, in the latter part of this work, we showed that during aging, the AVP neurons are activated, which results in increased serum AVP level and a very low rate of apelin. Similarly, astrocytes are activated and show more morphofunctional plasticity. Microglia does not seem to play a role in neuronal and astrocytic overactivation. Moreover, this neuronal overactivation is overcome by a central processing by an anti-IL-6 or a nonselective TRPV channels. However, an icv treatment by an anti-IL-6 does not affect the expression of TRPV2 in the supraoptic nucleus (SON). In general conclusion, it appears that: 1 / IL-1 is not the conductor of all inflammatory processes. Indeed, in the NSO, the activation of AVP neurons is sustained by IL-6 2 / the balance of pro-/ anti-inflammatory is significant in neuronal dysfunction. However, the critical factor in the dysfunction of AVP neurons is not the excessive production of inflammatory factors, but the insufficient production of compensatory anti-inflammatory factors. 3 / during aging, neuroinflammation responsible for the dysfunction of AVP neurons can be classified as type "chronic and low-grade" process in which (i) microglia, in alert, saw its reactivity increased tenfold during inflammatory additional solicitation; (ii) cross-talk astrocyte-neuron is stuck in a pattern of hyperactivity, similar to that observed in adulthood under conditions of sustained physiological arousal (such as in dehydration), but that would prevent the proper response network to any additional physiological demand, which is transient (as the response to acute injection of LPS or NaCl 9%) or sustained (48 h dehydration). However, literature data show the important role of microglia in other types of neuroinflammation called "high grade", and whose deleterious effects - ranging from neuronal dysfunction to neurodegeneration - are rooted in Microglial overexpression of molecules such as IL-1 or TNF . In an attempt to understand the cellular and molecular mechanisms involved in such dysfunction and to characterize the nature of neuronal dysfunction, we have developed a pharmacological model of neuroinflammation high grade by injecting IL-1 directly into the SON. Our preliminary data show that neuronal dysfunction and the cellular and molecular mechanisms behind this dysfunction differ from those observed during aging: activated microglia overexpressing many inflammatory molecules, probably at the origin of neuronal dysfunction ( absence of phasic pattern, even during osmotic stimulation), since astrocytes do not appear to be affected. The absence of phasic pattern causing the low plasma AVP reflects a disturbance of intrinsic electrophysiological properties underlying the phasic pattern (receptors, ion channels) and / or afferent excitatory (Glu, ACh, Na) or inhibitory (GABA) modulating the phasic activity
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Tomba, Caterina. "Primary brain cells in in vitro controlled microenvironments : single cell behaviors for collective functions." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENY039/document.
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Du fait de sa complexité, le fonctionnement du cerveau est exploré par des méthodes très diverses, telles que la neurophysiologie et les neurosciences cognitives, et à des échelles variées, allant de l'observation de l'organe dans son ensemble jusqu'aux molécules impliquées dans les processus biologiques. Ici, nous proposons une étude à l'échelle cellulaire qui s'intéresse à deux briques élémentaires du cerveau : les neurones et les cellules gliales. L'approche choisie est la biophysique, de part les outils utilisés et les questions abordées sous l'angle de la physique. L'originalité de ce travail est d'utiliser des cellules primaires du cerveau dans un souci de proximité avec l'in vivo, au sein de systèmes in vitro dont la structure chimique et physique est contrôlé à l'échelle micrométrique. Utilisant les outils de la microélectronique pour un contrôle robuste des paramètres physico-chimiques de l'environnement cellulaire, ce travail s'intéresse à deux aspects de la biologie du cerveau : la polarisation neuronale, et la sensibilité des cellules gliales aux propriétés mécaniques de leur environnement. A noter que ces deux questions sont étroitement imbriquées lors de la réparation d'une lésion. La première est cruciale pour la directionalité de la transmission de signaux électriques et chimiques et se traduit par une rupture de symétrie dans la morphologie du neurone. La seconde intervient dans les mécanismes de recolonisation des lésions, dont les propriétés mécaniques sont altérées., Les études quantitatives menées au cours de cette thèse portent essentiellement sur la phénoménologie de la croissance de ces deux types de cellules et leur réponse à des contraintes géométriques ou mécaniques. L'objectif in fine est d'élucider quelques mécanismes moléculaires associés aux modifications de la structure cellulaire et donc du cytosquelette. Un des résultats significatifs de ce travail est le contrôle de la polarisation neuronale par le simple contrôle de la morphologie cellulaire. Ce résultat ouvre la possibilité de développer des architectures neuronales contrôlées in vitro à l'échelle de la cellule individuelleThe complex structure of the brain is explored by various methods, such as neurophysiology and cognitive neuroscience. This exploration occurs at different scales, from the observation of this organ as a whole entity to molecules involved in biological processes. Here, we propose a study at the cellular scale that focuses on two building elements of brain: neurons and glial cells. Our approach reachs biophysics field for two main reasons: tools that are used and the physical approach to the issues. The originality of our work is to keep close to the in vivo by using primary brain cells in in vitro systems, where chemical and physical environments are controled at micrometric scale. Microelectronic tools are employed to provide a reliable control of the physical and chemical cellular environment. This work focuses on two aspects of brain cell biology: neuronal polarization and glial cell sensitivity to mechanical properties of their environment. As an example, these two issues are involved in injured brains. The first is crucial for the directionality of the transmission of electrical and chemical signals and is associated to a break of symmetry in neuron morphology. The second occurs in recolonization mechanisms of lesions, whose mechanical properties are impaired. During this thesis, quantitative studies are performed on these two cell types, focusing on their growth and their response to geometrical and mechanical constraints. The final aim is to elucidate some molecular mechanisms underlying changes of the cellular structure, and therefore of the cytoskeleton. A significant outcome of this work is the control of the neuronal polarization by a simple control of cell morphology. This result opens the possibility to develop controlled neural architectures in vitro with a single cell precision
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Nicola, Fabrício do Couto. "Efeito neuroprotetor do transplante de células-tronco mesenquimais derivadas de dente decíduo humano em ratos Wistar submetidos à lesão medular." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/170284.
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A lesão medular (LM) é uma patologia incapacitante que resulta em déficits sensoriais e motores. No Brasil, a incidência anual é de 30 novos casos de lesão medular a cada 1 milhão de indivíduos e, infelizmente, a LM permanece sem um tratamento eficaz. Células-tronco derivadas do dente decíduo humano estão entre as potenciais fontes de células-tronco para transplante após a lesão medular, cujo objetivo é de promover a proteção ou a recuperação da lesão na medula espinal. Buscou-se nesta tese avaliar os efeitos do transplante, uma hora após a lesão, das células tronco de dente decíduo humano (SHED) no período agudo, subagudo e crônico sobre a neuroproteção, proteção tecidual e recuperação funcional em ratos Wistar submetidos à lesão medular por contusão. Os principais objetivos foram: a) investigar os efeitos do transplante das SHED sobre a recuperação funcional, volume da lesão e morte neuronal; b) verificar os efeitos do transplante sobre as células progenitoras, formação da cicatriz glial e modificações astrocitárias após o modelo de contusão medular Observou-se a melhora na recuperação funcional, redução do volume da lesão e morte neuronal na medula espinal dos animais que receberam o transplante de SHED após a lesão medular. As SHED aumentam o número de células precursoras na medula espinal, no período subagudo, reduzem a expressão da proteína fibrilar glial ácida (GFAP) e aumentam a expressão do canal retificador de influxo de potássio 4.1, ambas proteínas astrocitárias. Concluímos que o transplante de células-tronco derivadas do dente decíduo humano após a lesão medular promove a recuperação funcional a partir do efeito neuroprotetor iniciado na fase aguda, confirmado pelo maior número de neurônios motores presentes seis semanas após a contusão. As SHED são capazes de aumentar o número de células precursoras e de produzir modificações astrocitárias na medula espinal de ratos lesados na fase subaguda, reduzindo a formação da cicatriz glial.Spinal cord injury (SCI) is a disabling condition that results in sensory and motor deficits. The estimated annual incidence in Brazil is of 30 new cases of spinal cord injury per 1 million of individuals; unfortunately SCI remains without an effective treatment. Stem cells from human exfoliated deciduous teeth (SHED) are one among potential sources of stem cells for transplantation after spinal cord injury in order to promote protection or tissue and functional recovery after spinal cord injury. The aim of this Thesis was to evaluate the effects of stem cells from human exfoliated deciduous teeth (SHED) transplantation, one hour after lesion, in the acute, subacute and chronic phases on neuroprotection, tissue protection and functional recovery in Wistar rats submitted to spinal cord injury by contusion The main goals were: a) to investigate the effects of SHED transplantation on functional recovery, lesion volume, and neuronal death; b) to verify the effects of the transplantation on the progenitor cells number, glial scar formation and astrocytic modifications after spinal cord contusion. Improvement of functional recovery, reduction of lesion volume and neuronal death were observed in the spinal cord of animals submitted to spinal cord injury and SHED transplantation. SHEDs increased the number of precursor cells in the spinal cord in the subacute period, reduced the expression of glial fibrillary acidic protein (GFAP) and increased the expression of the potassium influx rectifier channel 4.1, both astrocyte proteins. We conclude that transplantation of stem cells from human exfoliated deciduous teeth after spinal cord injury promotes functional recovery from the neuroprotection effect, which starts in the acute phase and is confirmed six weeks after the contusion with a higher number of motor neurons in the ventral horn of spinal cord. SHEDs are able to increase the number of precursor cells and produce astrocyte modifications in the spinal cord of injured rats in the subacute phase, reducing glial scar formation.
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Rosa, Adriane Ribeiro. "Marcadores biológicos e nível de funcionalidade em pacientes bipolares." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2007. http://hdl.handle.net/10183/10328.
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Alterações em estruturas específicas do SNC, em particular, no sistema fronto-límbico, assim como a diminuição das células neuronais e gliais parece estar envolvida com a fisiopatologia do Transtorno do Humor Bipolar (THB). A glia exerce um importante papel no SNC, entre os quais, a produção de neurotrofinas, em especial, o Fator de Crescimento Neurotrófico derivado de Células da Glia (GDNF). Um marcado aumento dos níveis séricos de GDNF em pacientes deprimidos (F= 42.31; p=0.004; one-way ANOVA) e maníacos (F= 42.31; p=0.001; one-way ANOVA) foi demonstrado neste estudo, sugerindo um possível envolvimento desta neurotrofina com o THB. Por outro lado, alterações nos fatores neurotróficos afetam os mecanismos de plasticidade sináptica, podendo contribuir para as deficiências cognitivas apresentadas pelos pacientes. Deficiências cognitivas, em especial, as falhas de memória são descritas, as quais influenciam a funcionalidade destes indivíduos, principalmente a nível ocupacional e social. As altas taxas de disfuncionalidade apresentadas pelos pacientes e a falta de padronização dos instrumentos usados nos estudos para avaliar funcionalidade, nos levaram ao desenvolvimento de uma escala. A Escala Breve de Funcionalidade (FAST) é um instrumento de rápida e fácil aplicação desenvolvida para usar em psiquiatria, em especial, paciente com THB. A FAST avalia objetivamente seis áreas específicas da funcionalidade, tais como autonomia, trabalho, cognição, relacionamentos interpessoais, finanças e lazer. A validação da escala foi realizada através de testes psicométricos, tais como: consistência interna (alfa de Cronbach’s igual a 0.909), validade concorrente comparada com a GAF (r=-0.903; p<0.001), test-retest (0.98; p<0.01), validade em detectar diferenças entre episódios agudos (maníacos: 40.44±9.15 e deprimidos 43.21±13.34) e períodos de remissão (18.55±13.19; F=35.43; p<0.001) e análise fatorial. Os resultados obtidos foram muito positivos, tornando o instrumento válido e prontamente disponível para o uso na prática clínica e investigação. Palavras-chave: transtorno do humor bipolar, GDNF, glia, neurotrofinas, funcionalidade, disfuncionalidade, escalas de funcionalidade.Alterations in specific structures of CNS, in particular, fronto-lymbic system, and a reduction of neurons and glial cells appear to be involved in the pathophysiology of bipolar disorder. Glial cells have an important role in the CNS, for example, the production of neurotrophins, especially, Glial Cell Line-derived Neurotrophic Factor (GDNF). In this study, we showed a marked increased in the serum levels of GDNF in depressive (F= 42.31; p=0.004; one-way ANOVA) and manic bipolar patients (F= 42.31; p=0.001; one-way ANOVA), which suggested that GDNF could be involved in the physiopathology of bipolar disorder. On the other hand, alterations in the neurotrophic factors hinder synaptic plasticity mechanisms, may result in cognitive impairment in bipolar patients. In particular, memory difficulties have been reported here, and these difficulties influence occupational and social functioning in these subjects. High rates of functional impairment showed by bipolar patients and a lack of standardization of the instruments available to assess functioning in the studies motivated us to development the scale. The Functioning Assessment Short test (FAST) is a rapid instrument and easy to apply developed to use in psychiatry, especially, bipolar patients. It assesses six specific domains of functioning, such as autonomy, occupational functioning, cognitive functioning, financial issues and leisure time. The validation of FAST was performed by psychometric tests such as internal consistency (Cronbach’s alpha: 0.909), concurrent validity compared to the GAF (r=-0.903; p<0.001), validity as a discriminative measure to detect the difference between euthymic (18.55; F=23.59; p<0.001) and acute patients (manic: 38.50; depressive: 42.38; mixed: 43.21), factorial analysis and test-retest reliability (0.953; p<0.01). The FAST scale showed strong psychometric properties and it is now available for use in both clinical practice and investigation settings.
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Karus, Michael [Verfasser], Andreas [Gutachter] Faissner, Michael [Gutachter] Hollmann, and James W. [Gutachter] Fawcett. "Regulatory functions of the neural extracellular matrix for the maturation of the spinal cord radial glia and its progeny / Michael Karus ; Gutachter: Andreas Faissner, Michael Hollmann, James W. Fawcett ; International Graduate School of Neuroscience." Bochum : Ruhr-Universität Bochum, 2011. http://d-nb.info/1226426271/34.
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Thompson, Garth John. "Neural basis and behavioral effects of dynamic resting state functional magnetic resonance imaging as defined by sliding window correlation and quasi-periodic patterns." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/49083.
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While task-based functional magnetic resonance imaging (fMRI) has helped us understand the functional role of many regions in the human brain, many diseases and complex behaviors defy explanation. Alternatively, if no task is performed, the fMRI signal between distant, anatomically connected, brain regions is similar over time. These correlations in “resting state” fMRI have been strongly linked to behavior and disease. Previous work primarily calculated correlation in entire fMRI runs of six minutes or more, making understanding the neural underpinnings of these fluctuations difficult. Recently, coordinated dynamic activity on shorter time scales has been observed in resting state fMRI: correlation calculated in comparatively short sliding windows and quasi-periodic (periodic but not constantly active) spatiotemporal patterns. However, little relevance to behavior or underlying neural activity has been demonstrated. This dissertation addresses this problem, first by using 12.3 second windows to demonstrate a behavior-fMRI relationship previously only observed in entire fMRI runs. Second, simultaneous recording of fMRI and electrical signals from the brains of anesthetized rats is used to demonstrate that both types of dynamic activity have strong correlates in electrophysiology. Very slow neural signals correspond to the quasi-periodic patterns, supporting the idea that low-frequency activity organizes large scale information transfer in the brain. This work both validates the use of dynamic analysis of resting state fMRI, and provides a starting point for the investigation of the systemic basis of many neuropsychiatric diseases.
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Ma, Chun-Ta, and 馬駿達. "The function of zebrafish arnt2 gene in glial cell development." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/23753963820804533983.
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碩士國立臺灣海洋大學
生物科技研究所
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During embryogenesis,the processes of cell differentiation, organogenesis and response to environmental stimulation are all controlled by various gene regulation system. The bHLH-PAS protein family play important roles in vertebrate development 、xenobiotic metabolism and hormone signal transduction. In the bHLH-PAS mediated pathway, ARNT can dimerize with AHR 、HIF and SIM to regulate variety gene. It was shown that repression of arnt2 gene caused severe defect in neuron development. Previously,it was shown that blacking arnt2 translation resulted in sever defect of glial cell development. In here, we use two different arnt2 morpholino (MO2) to verify the function of arnt2 on glial cell development if appear that. the two new arnt2 morpholino blacked gilal cell development including olgodendrocyte、astrocyte、shwann cell and radil glial cell differention like previous arnt2 morpholino did. we have also confirned that arnt2 knockdown inhibited mbp expression and suppress myelin sheath formation.
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Szöke, Katalin. "Function of glial cells in the inhibitory synaptic transmission of the respiratory network." Doctoral thesis, 2005. http://hdl.handle.net/11858/00-1735-0000-0006-B5E4-B.
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Rodrigues, DAVID. "GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTOR MODULATES STRUCTURE AND FUNCTION OF POSTNATAL MYENTERIC NEURONS." Thesis, 2008. http://hdl.handle.net/1974/1396.
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The enteric nervous system (ENS) continues its development after birth, with formation of ganglia and functional synapses; plasticity is also demonstrated in significant axon growth that occurs after experimental colitis in the adult colon. However, little is known about factors in the postnatal intestine that influence and regulate these processes. Therefore we tested the effects of known neurotrophins, NGF, NT-3, BDNF and GDNF on neonatal rat myenteric neurons. Cocultures were developed by isolating the myenteric plexus and surrounding muscular wall from neonatal rats, and effects of exogenous treatment of neurotrophins were analyzed using immunocytochemistry and image analysis. Western blotting and immunocytochemistry were performed to detect implicated neurotrophins and their receptors in the postnatal intestine. Functional aspects of effects of implicated neurotrophins were assessed by [3H]choline uptake and acetylcholine release in myenteric neurons. Last, TNBS-colitis was induced in adult rats to determine changes in GDNF secretion during the course of the disease. Application of 100ng/mL GDNF to a neonatal intestinal coculture containing neurons, glia and smooth muscle cells produced a 91.5% (p≤0.05) increase in axons. GDNF induced morphological changes in the structure and organization of neurons and axons; the incidence of neurons present in ganglia increased by 11.2% (p≤0.05), with a 32.9% (p≤0.05) increase in aggregated axons. Western blotting and immunocytochemistry confirmed intestinal smooth muscle as the major source of GDNF and demonstrated the presence of the GDNF receptor complex, GFRα1 and RET in the myenteric plexus. Choline uptake significantly increased at 50, 100 and 150ng/ml doses of GDNF, whereas stimulated ACh release increased only at 100 and 150ng/ml doses. In TNBS-colitis, a decrease in 35kD GDNF at days 1 and 6 post-induction of inflammation was observed, with a concomitant increase in 15kD GDNF. We conclude that GDNF, produced by intestinal smooth muscle, is a key factor influencing development of the postnatal myenteric neuron and may play a role in ENS-restructuring post-inflammation.Thesis (Master, Physiology) -- Queen's University, 2008-09-03 13:27:23.042
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Altas, Bekir. "Roles of the Nedd4 Family E3 Ligases in Glial Function and Nerve Cell Development." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-0023-3E3B-D.
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Szőke, Katalin [Verfasser]. "Function of glial cells in the inhibitory synaptic transmission of the respiratory network / submitted by Katalin Szőke." 2006. http://d-nb.info/982006802/34.
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Murthy, Smrithi. "Role of CG9650 in Neuronal Development And Function of Drosophila Melanogaster." Thesis, 2016. http://etd.iisc.ernet.in/handle/2005/2696.
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The nervous system is the most complex system in an organism. Functioning of the nervous system requires proper formation of neural cells, as well as accurate connectivity and signaling among them. While the major events that occur during these processes are known, the finer details are yet to be understood. Hence, an attempt was made to look for novel genes that could be involved in them. The focus of the present study is on CG9650, a gene that was uncovered in a misexpression screen, as a possible player in neuronal development in Drosophila melanogaster.
The first chapter of the thesis reviews existing knowledge about neuronal development and function. The first section of this chapter explains in brief the formation and specification of neural stem cells, and their differentiation to neurons and glia. Sections 2 and 3 describe neuronal connectivity and signaling with respect to axon growth, synapse formation, function and plasticity. A comparison of invertebrate and vertebrate neuronal development is provided in section 4 of this chapter. This part also explains the use of Drosophila as a model for neuronal development and function.
Chapter 2 describes the expression pattern of CG9650, which was characterized to gain insights into the possible role it plays during Drosophila neurogenesis.CG9650 is expressed in multiple cell types in the nervous system at the embryonic stage. Some of the cell sub-types have been identified from their morphology and position. Expression was restricted to neurons in the larval stage (except in the optic lobe, where it was expressed in precursors also), and continued in the pupal stage. No expression was seen in adults (except in the optic lobe). CG9650 has a putative DNA binding region, which bears homology to the mouse proteins CTIP1 and CTIP2, implying that CG9650 is possibly a transcription factor.
In order to understand the function of CG9650, the protein was knocked down panneuronally. The resultant animals showed locomotor defects at both larval and adult stages, which have been described in chapter 3. Knock down larvae showed reduced displacement and speed of movement. The number of peristaltic cycles was also reduced in these animals but the cycle period was normal. In adults, movement was uncoordinated and righting reflex was lost, resulting in inability to walk, climb or fly. These results imply a defect in neuronal signaling. Sensory perception was unaffected in these animals. Stage specific knockdown of CG9650 indicated that the requirement for this protein is primarily during the larval stage. All CG9650-expressing neurons in the ventral nerve cord were glutamatergic, implying that its role in controlling locomotor activity is likely through glutamatergic circuits.
Following up on these observations, signaling at the neuromuscular junction was assessed in CG9650 knock down animals. Chapter 4 discusses the signaling defects seen on CG9650 knock down, and the possible role of this protein. Electrophysiological recordings from Dorsal Longitudinal Muscles showed reduced and irregular neuronal firing in the knock down animals. These animals also had reduced bouton and active zone numbers. Moreover, overexpression of BRP, an active zone protein, rescued the locomotor defects caused by knock down of CG9650.
Chapter 5 reports the effect of over expression of CG9650. Pan-neural over expression of CG9650 resulted in embryos with severe axon scaffolding defects, as well as aberrant neuronal and glial pattern. However, the incorrectly positioned glial cells in these embryos did not express CG9650, indicating that their aberrant positioning was probably due to incorrect signaling from the neurons.
In conclusion, this study reports the requirement for CG9650, a hitherto unknown protein, in locomotor activity and signaling, thus ascribing for it a role in neuronal development and function of Drosophila melanogaster.
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Tsung-YingHo and 何宗穎. "Study functions of a specific glial cell type and genes involved in Drosophila glial cell development." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/91252809305892133020.
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