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Relevant bibliographies by topics / Excitotoxicity / Dissertations / Theses

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Dissertations / Theses on the topic 'Excitotoxicity'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Chen, Yongmei. "Excitotoxicity in neurodegenerative disorders." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901225.

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2

Scott, Michael Murray. "Development of in vitro models of NMDA excitotoxicity and assessment of excitotoxicity modulation by neurosteroids." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ36079.pdf.

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3

Giardina, Sarah Filippa 1974. "Neuropharmacology of kainate receptor-mediated excitotoxicity." Monash University, Dept. of Pharmacology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8980.

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4

Soundarapandian, Mangala Meenakshi. "Glutamate Excitotoxicity in Epilepsy and Ischemia." Doctoral diss., University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/3169.

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'Excitotoxicity' represents the excitatory amino acid mediated degeneration of neurons. Glutamate is the major excitatory neurotransmitter in the brain. Glutamate excitotoxicity has been implicated in a number of neurodegenerative disorders like Stroke, Epilepsy, Alzheimer's disease and traumatic brain injury. This neurotoxicity is summed up by the 'glutamate hypothesis' which describes the cause of neuronal cell death as an excessive release of glutamate causing over excitation of the glutamate receptors and subsequent increase in influx of calcium leading to cell death. An effort to countera

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5

Gladbach, Philip Amadeus Wilhelm. "The role of tau in excitotoxicity." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/9557.

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Stroke is a leading cause of death. The majority are ischemic strokes resulting from acute focal brain infarction with sudden and persisting neurological deficits. This primary brain damage is followed by more substantial secondary destruction of surrounding areas (=penumbra). A major pathomechanism underlying penumbra formation is excitotoxicity, which results from over-excitation of glutaminergic synapses involving N-methyl-D-aspartate receptor signaling. Excitotoxicity also contributes to neurodegeneration in Alzheimer’s disease (AD), where the microtubule-associated protein tau deposits in

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6

Zhu, Shanshan. "Factors in glutamate excitotoxicity, inflammation and epilepsy." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/39844.

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Studying the mechanisms underlying glutamate excitotoxicity and inflammatory responses provides hints to the pathology of neurological diseases such as epilepsy. In this dissertation I investigated the expression and function of Krüppel-like factor 4 (KLF4) in glutamate excitotoxicity. I also studied the distribution and the role of progranulin (PGRN) in inflammatory stimulation, in epilepsy and in astrocytes subjected to glutamate excitotoxicity. First, I studied the role of KLF4 and found that NMDA induced KLF4 expression in cultured neurons and in brain slices. Overexpression of KLF4 upregu

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7

Bakshi, Deeksha. "The role of NMDA receptors in excitotoxicity." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/43907.

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NMDA receptors are glutamate-gated cation channels named after their prototypical selective agonist NMDA. The channels occur as multiple subtypes, which are formed from interactions between different receptor subunits. NMDA receptor subunits are classified into three families: NR1, NR2A-D, and NR3A, B. NMDA receptors are implicated in HD pathology. During HD, a subset of medium-sized aspiny interneurons in the striatum that co-localize SST, NPY, and the enzyme NOS are selectively spared. In contrast, medium-sized spiny cells that constitute 80 % of all striatal neurons undergo selective

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8

Jones, Paul A. "Modulation of kainate-induced excitotoxicity in rats." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244361.

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9

Serzysko, Malgorzata. "Endocannabinoids and excitotoxicity: lessons from hypoglossal motoneurons." Doctoral thesis, SISSA, 2015. http://hdl.handle.net/20.500.11767/3908.

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Brainstem hypoglossal motoneurons (HMs) exclusively innervate tongue muscles and are severely damaged in the neurodegenerative disease called amyotrophic lateral sclerosis (ALS). One mechanism leading to such cell death is proposed to be glutamate-mediated excitotoxic stress. HMs are particularly vulnerable to excitotoxicity due to their expression of calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and scarcity of intracellular Ca2+ binding proteins like parvalbumin and calbindin. Indeed, blocking glutamate uptake in medullary slices can l

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10

Tannenberg, Rudi. "Excitotoxicity in Alzheimer disease : a synaptic terminal study /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18741.pdf.

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11

Vladimirov, Andrew A. "Metabolic receptor cross-talk and excitotoxicity in astrocytes." Thesis, University of Bristol, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399955.

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12

Carrier, Raeann Lynn. "Excitotoxicity and bioenergetics in Huntington's disease transgenic neurons." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1213361299.

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13

Bordiga, Pierrick. "Caractérisation des mécanismes de réparation synaptique de l'oreille interne." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0625.

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Les connexions entre les cellules sensorielles et les neurones primaires de l’oreille interne, appelées synapses sont essentielles à l’encodage et la transmission des informations auditives et vestibulaires vers le cerveau. C’est aussi une zone extrêmement exposée et fragile qui semble impliquée dans de nombreuses atteintes de l’audition et de l’équilibration, mais également au cours du vieillissement. Des récupérations spontanées de l’audition et de l’équilibre ont été observées suite à ces différentes atteintes chez l’Homme. Dans le cadre de ma thèse, j’ai étudié d’une part, comment des atte

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14

Rogers, Derek Charles. "The effects of neuroprotective agents on in vitro and in vivo models of neurotoxicity." Thesis, University of Hertfordshire, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283890.

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15

Smith, Andrew John. "Excitotoxicity, oxidative stress and neuroprotection in cerebellar granule neurones." Thesis, Connect to e-thesis, 2008. http://theses.gla.ac.uk/305/.

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16

Olivieri, Dario. "New Spinal cord models: Characterization of Excitotoxicity and Neuroprotection." Doctoral thesis, SISSA, 2015. http://hdl.handle.net/20.500.11767/3892.

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Group III metabotropic glutamate receptors (mGluR III) are known to decrease glutamate release and to play an important role in controlling pain as documented in neuropathic pain models. Much less is known about their potential neuroprotective effect against excitotoxicity that is considered important for damage onset of spinal cord injury. Using rat spinal cord organotypic slices model, we investigated if mGluR III receptor activation might contrast excitotoxic cell death evoked by kainic acid (0.1 mM) applied for 1h and followed by wash for further 24h. The specific agonist of mGluR III rece

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17

Brun-Salabert, Anne-Sophie. "Développement préclinique de sondes fluorées utilisées dans l'imagerie moléculaire des pathologies neurodégénératives." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30371/document.

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Les mécanismes physiopathologiques liés aux maladies neurodégénératives restent encore largement méconnus. Deux processus semblent être particulièrement en cause dans les phénomènes de neurodégénérescence : la neurotoxicité par afflux massif de calcium due à une activation excessive des récepteurs NMDA (GluN) et la neurotoxicité par déstabilisation du cytosquelette du neurone par le biais de la phosphorylation anormale de la protéine tau. L'imagerie moléculaire par le biais de la tomographie par émission de positons (TEP) et de radiotraceurs, en étudiant les mécanismes moléculaires in vivo, pe

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18

Vaur, Pauline Magda Marie. "Caractérisation des effets protecteurs du NAD+ et du Nicotinamide Riboside lors de la dégénérescence axonale dans le système nerveux central : Implications dans les processus neurodégénératifs." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066594/document.

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Les maladies neurodégénératives se caractérisent par une déconnexion synaptique et une dégénérescence des axones (DA) précoces, menant à la mort spécifique d’une population neuronale. Les niveaux intracellulaires de NAD+, co-facteur essentiel dans le maintien de l’intégrité axonale, sont fortement diminués lors de ces pathologies. L’augmentation des taux de NAD+ est ainsi une stratégie thérapeutique dans la prévention de ces maladies. La capacité du nicotinamide riboside (NR) à retarder la DA dans le système nerveux périphérique (SNP) ainsi que la récente mise en évidence d'une conversion extr

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19

Miller, Brandon Andrew. "The effects of excitotoxicity and microglial activation on oligodendrocyte survival." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1177537595.

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20

Mizielinska, Sarah. "Rapid neuronal responses to glutamate-induced excitotoxicity and morphological change." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521697.

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21

Tan, Hiang Khoon. "Investigating the effects of TIMPs on excitotoxicity and neurite regeneration." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247230.

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22

Zou, Shenglong. "Crosstalk between somatostatin receptor subtypes and cannabinoid receptor 1 in excitotoxicity." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/64231.

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23

Miranda, Allan F. "Modulation of quinolinic acid-induced excitotoxicity by endogenous kynurenine pathway intermediates." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq22484.pdf.

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24

Murphy, Michael Paul. "Interactions between excitotoxicity and lysosomal inhibition, implications for Alzheimer's disease pathogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ35262.pdf.

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25

Evans, Gary Lee. "The induction of long-term potentiation attenuates kainic acid-induced excitotoxicity." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/777.

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The activation of N-methyl-D-aspartate glutamate receptors (NMDARs) is required for the long term potentiation (LTP) and long term depression (LTD) of excitatory synaptic transmission at hippocampal CA1 synapses, and plays an important role in learning and memory. In addition, it is accepted that the over-activation of NMDARs leads to the neurotoxicity associated with stroke and other neurodegenerative disorders. Thus, the NMDAR provides a logical starting point to investigate a possible relationship between synaptic plasticity and the cell-signalling pathways which ultimately determine neur

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26

Tortarolo, Massimo. "Role of excitotoxicity in the degeneration of motor neurones in ALS." Thesis, Open University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412382.

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27

Urenjak, Jutta A., and Tihomir P. Obrenovitch. "Accumulation of quinolinic acid with euro-inflammation: does it mean excitotoxicity?" Thesis, Kluwer Academic, Plenum Publishers, New York, 2003. http://hdl.handle.net/10454/2833.

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28

Houlihan, Patrick Ryan. "The role of mitochondrial restructuring in neuronal calcium homeostasis and excitotoxicity." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/2522.

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Mitochondrial Ca2+ buffering is an important physiological modulator of neuronal signaling and bioenergetics, but this propensity toward Ca2+ regulation proves pathological during excitotoxic insult. Specifically, excessive mitochondrial Ca2+ uptake is a key component of glutamate toxicity within the penumbra surrounding the ischemic core following stroke. This mitochondrial toxicity and Ca2+ dyshomeostasis may be visualized in real time as delayed calcium deregulation (DCD). DCD is a predictor of neuronal, excitoxic death

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29

Berry, Jennifer Nicole. "TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_theses/72.

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Excitotoxicity is the overexcitation of neurons due to the excessive activation of excitatory amino acid receptors and is thought to be involved in many neurodegenerative states. The manner in which the neuron breaks down during excitotoxicity is still unclear. The current study used the organotypic hippocampal slice culture model to examine the time-dependent loss of the synaptic vesicular protein synaptophysin and the loss of N-methyl-D-aspartate (NMDA) receptor NR1 subunit availability following an excitotoxic insult (20 μM NMDA) to provide a better understanding of the topographical nature

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30

Li, Shuxin. "Excitotoxicity and sodium(+)-dependent glutamate transport in spinal cord white matter injury." Thesis, University of Ottawa (Canada), 2000. http://hdl.handle.net/10393/9231.

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Spinal cord injury (SCI) is a devastating condition, with much of the clinical disability resulting from disruption of ascending and descending white matter tracts. Recent reports suggest that a component of axonal dysfunction during SCI involves glutamate-mediated white matter damage, but the cellular targets of excitotoxicity and the precise mechanisms of glutamate release from non-synaptic white matter are not understood. In the present study, using combined techniques including electrophysiology, pharmacology, immunohistochemistry and confocal microscopy, we demonstrate that myelinated axo

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31

Li, Shuxin. "Excitotoxicity and Na§+-dependent glutamate transport in spinal cord white matter injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0015/NQ58289.pdf.

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32

Utan, Aneli <1974&gt. "Effects of cannabidiol and cannabis extracts in models of convulsion and excitotoxicity." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/824/1/Tesi_Utan_Aneli.pdf.

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33

Utan, Aneli <1974&gt. "Effects of cannabidiol and cannabis extracts in models of convulsion and excitotoxicity." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/824/.

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34

Lo, Edmund. "The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/233.

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Stroke is a pathological condition that causes extensive brain damage. During ischemic stroke, an excess of the excitatory neurotransmitter glutamate exerts many deleterious effects, which leads to cellular damage and cell death, a phenomenon appropriately termed excitotoxicity. Among the events triggered is the activation of the enzyme calpain, a protease whose action is dependent on the intracellular concentration of calcium, which is known to be elevated during excitotoxicity. In this thesis, I hypothesize that neuroprotective drugs can be better accumulated into stroke-affected regions by

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35

Karmarkar, Sumedha. "MECHANISMS OF NEUROPROTECTION IN SCN2.2 CELLS." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/476.

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As the major excitatory neurotransmitter, glutamate (Glu) is physiologically important in brain function. Excessive Glu release, however, is a critical underlying pathological mechanism in neurodegenerative disease, especially stroke. Strategies to protect neurons from cell death under these conditions are scarce; in part because of incomplete understanding of inherent neuroprotective mechanisms. The suprachiasmatic nucleus (SCN) is a region of the brain that exhibits endogenous resistance to Glu excitotoxicity. A previous study demonstrated that SCN2.2 cells (an immortalized SCN cell line) we

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36

Tsai, Wang Wei Vicky. "The role of group I metabotropic glutamate receptors in neuronal excitotoxicity in Alzheimer's disease /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18689.pdf.

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37

Oberländer, Kristin [Verfasser], and Hilmar [Akademischer Betreuer] Bading. "Neuronal activity-dependent gene expression in learning and excitotoxicity / Kristin Oberländer ; Betreuer: Hilmar Bading." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/117978216X/34.

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38

Tischbein, Maeve. "FUS and Excitotoxicity Cross Paths in ALS: New Insights into Cellular Stress and Disease." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/990.

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Amyotrophic lateral sclerosis (ALS) is an incurable and fatal neurodegenerative disease characterized by motor neuron loss. Although pathological mutations exist in >15 genes, the mechanism(s) underlying ALS are unknown. FUS is one such gene and encodes the nuclear RNA-binding protein (RBP), fused in sarcoma (FUS), which actively shuttles between the nucleus and cytoplasm. Intriguingly, nearly half of the ALS mutations identified in FUS cause this protein to mislocalize, suggesting that FUS localization is relevant to disease. Here, we found that excitotoxicity, a neuronal stress caused by abe

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39

Sharrett-Field, Lynda. "SOMATIC INJURY PRECEDES DISTAL ATROPHY FOLLOWING EXCITOTOXIC HIPPOCAMPAL INSULT." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_theses/70.

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Excitotoxicity can lead to increases in intracellular Na+ and Ca2+ concentrations via the glutamatergic NMDA receptors, which can lead to cell death. Detailing the time-dependent degradation of neuronal components in response to excitotoxic challenge may help elucidate the sequence in which these signaling pathways are initiated and further, associate these pathways with topographic cellular demise. Using organotypic hippocampal slice culture technique, tissue from neonatal rat pups was exposed to NMDA, APV, or co-exposed for 24, 72 or 120 hours. Fluorescent microscopy of propidium iodide (PI)

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40

Samson, Andrew James. "Rapid neuronal responses during spreading neurotoxic and neuroprotective network activity." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/8c797952-eda1-4c03-a38a-15c2679e984f.

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Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system, playing critical roles in basal synaptic transmission and the molecular correlates of learning and memory, long-term potentiation and long-term depression. However, glutamate is also neurotoxic during prolonged exposure and the dysfunction of the glutamatergic system has been implicated in most neurological disorders, including stroke and epilepsy, and in certain neurodegenerative diseases, including Alzheimer’s disease. In these conditions, an increased concentration of extracellular glutamate causes a

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41

Akins, Mark S. "The Role of the Neuronal gap Junction Protein Connexin36 in Kainic Acid Induced Hippocampal Excitotoxicity." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30392.

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Kainic acid induced excitotoxicity causes pyramidal cell death in the CA3a/b region of the hippocampus. Electrical synapses, gap junctional communication, and single membrane channels in non-junctional membranes (hemichannels) composed of connexin36 (Cx36) have been implicated in both seizure propagation and the spread of excitotoxic cell death. In rats, Cx36 protein is expressed by pyramidal neurons. Localization of protein in mouse, however, is highly controversial. Expression is reported to be restricted to hippocampal interneurons yet the same excitotoxic mechanisms (electrical and metabol

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42

Cuthill, Daniel. "Involvement of excitotoxicity or oxidative stress in the pathophysiology of white and grey matter injury." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414444.

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43

Ting, Ka Ka Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Quinolinic acid and its effect on the astrocyte with relevance to the pathogenesis of Alzheimer??s disease." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41288.

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There is evidence that the excitotoxin quinolinic acid (QUIN) synthesized through the kynurenine pathway (KP) by activated microglia may play a role in the pathogenesis of several major neuroinflammatory diseases and more particularly in Alzheimer??s disease (AD). The hypothesis of this project is QUIN affects the function and morphology of astrocytes. In this study I used human foetal astrocytes stimulated with AD associated cytokines including IFN-gamma, TNF-alpha, TGF-alpha and different concentrations of QUIN ranging from low physiological to high excitotoxic concentrations. I found that Q

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44

Puddifoot, Clare Anne. "Neuroprotection from the huntingtin-repressed transcriptional coactivator PGC-1α". Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8055.

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The transcriptional coactivator PPARgamma coactivator 1alpha (PGC-1α) is a regulator of mitochondrial biogenesis and function and is decreased in the striatum of patients with Huntington’s Disease (HD). HD is an autosomal dominant neurological disorder caused by a polyglutamine repeat in the huntingtin protein which leads to degeneration of striatal and cortical tissues. PGC-1α undergoes targeted downregulation by mutant huntingtin protein (mtHtt) and PGC-1α knockout mice have striatal lesions similar to HD transgenic mice. Exogenous PGC-1α partially reverses the toxic effects of mutant huntin

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45

Nascimento, Paula Hespanholo 1984. "Padrão de distribuição e localização de expressão das proteínas VILIP-1, receptor sensor de cálcio e receptor metabotrópico do glutamato 1 em tecidos de pacientes com epilepsia do lobo temporal." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310395.

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Orientador: Lília Freira Rodrigues de Souza Li<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-20T19:22:58Z (GMT). No. of bitstreams: 1 Nascimento_PaulaHespanholo_M.pdf: 1475049 bytes, checksum: f1ec759ca189c1e3404667fb1ce01abc (MD5) Previous issue date: 2012<br>Resumo: A esclerose hipocampal está associada à epilepsia de lobo temporal medial (ELT) e causa expressão alterada de receptores tais como o Receptor Metabotrópico de Glutamato (mGluR1). Contudo, ainda há controvérsias se sua expressão está aumentada

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46

MAZZA, Roberta. "Neurotensin as Modulator of Glutamatergic Signalling: Relevance in Neurodegenerative Diseases." Doctoral thesis, Università degli studi di Ferrara, 2009. http://hdl.handle.net/11392/2389146.

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Rationale: Neurotensin (NT) is a tridecapeptide widely distributed in mammalian brain, where acts as a neurotransmitter or neuromodulator of classical neurotransmitters, mainly through the activation of its receptor NTS1. Several in vitro and in vivo studies have demonstrated the existence of close interactions between NT and dopamine (DA) systems both in limbic and striatal brain regions (Nemeroff CB., 1985; Binder EB., 2001; Caceda R., 2006). Because of the involvement of an over-activation of DA system in the development of neurological disorders such as schizophrenia, psychosis and dyskine

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47

Fan, Jing. "Signaling pathways involved in enhanced NMDA receptor-dependent excitotoxicity in a mouse model of Huntington disease." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38094.

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Huntington disease (HD) is an inherited neurodegenerative disease lacking effective treatment, characterized by involuntary movements, psychiatric disorders, and cognitive symptoms. Pathology shows prominent degeneration of γ-aminobutyric acid (GABA)-ergic medium-sized spiny neurons (MSNs) of the striatum and certain cortical layers (Vonsattel and DiFiglia, 1998). HD is caused by a dominant mutation in the HD gene that leads to >35 glutamine repeats (polyQ) near the N-terminus of the protein huntingtin (htt) (The Huntington’s Disease Collaborative Research Group, 1993). Increasing evidence sug

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48

Vasiljevic, Alexandre. "Caractérisation des fonctions neuroprotectives des interfaces sang-cerveau au cours du développement normal, dans les tumeurs périventriculaires et dans un modèle d’excitotoxicité périnatale." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1328/document.

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Les interfaces sang-cerveau comme la barrière hémato-encéphalique (BHE), les plexus choroïdes (PC) ou les organes circumventriculaires (OCV), constituent des barrières physiologiques nécessaires au fonctionnement du système nerveux central. Ces barrières sont à la fois « physiques », constituées de jonctions serrées, et « enzymatiques ». Longtemps considérées comme immatures chez le fœtus, ces barrières sont en réalité présentes précocement au cours du développement. Leurs caractéristiques et leurs propriétés restent peu connues chez l'homme. Nos travaux montrent que les PC expriment, précocem

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49

Isom, Amanda M. "The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1407407111.

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50

McKay, Sean. "Probing spatial and subunit-dependent signalling by the NMDA receptor." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/14225.

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NMDARs are ligand-gated cation channels which are activated by the neurotransmitter glutamate. NMDARs are essential in coupling electrical activity to biochemical signalling as a consequence of their high Ca2+ permeability. This Ca2+ influx acts as a secondary messenger to mediate neurodevelopment, synaptic plasticity, neuroprotection and neurodegeneration. The biological outcome of NMDAR activation is determined by a complicated interrelationship between the concentration of Ca2+ influx, NMDAR location (synaptic vs. extrasynaptic) as well as the subtype of the GluN2 subunit. Despite the recog

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