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Showing 1 to 20 of 54 for “"excitotoxic"”.

  1. Excitotoxic mechanisms in Huntington's disease

    Thesis (Ph. D.)--Massachusetts Institute of Technology, Whitaker College of Health Sciences and Technology, 1992.

    mit Repository record for Excitotoxic mechanisms in Huntington's disease (opens in a new tab)

  2. Excitotoxic Injury Mechanisms in Central White Matter

    … injury is controversial. Glutamate-mediated excitotoxicity is now recognised as a crucial event in the development of ischemic WM pathology. This thesis investigates the potential mechanisms of glutamate release in central WM and examines the hypothesis that NMDA receptor over-activation …

    plymouth Repository record for Excitotoxic Injury Mechanisms in Central White Matter (opens in a new tab)

  3. Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration

    <p>Excitotoxicity is an important and frequently observed neurodegenerative process. Excitotoxicity mediates brain damage in a range of diseases and conditions including stroke, and is triggered by excessive stimulation of glutamatergic synapses. In spite of extensive studies, the molecular …

    cuny Repository record for Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration (opens in a new tab)

  4. Misregulation of Iron Handling Proteins in Excitotoxic Brain Injury

    The increased iron has been implicated as a major generator of reactive oxygen species (ROS), which can cause neuronal death in neurodegenerative diseases. The present study was also carried out to elucidate the expression of iron handling proteins such as divalent metal transporter-1 (DMT1) …

    nus Repository record for Misregulation of Iron Handling Proteins in Excitotoxic Brain Injury (opens in a new tab)

  5. The GluK4 Kainate Receptor Subunit Regulates Mood, Memory and Excitotoxic Neurodegeneration

    … indicate that GluK4 is a key mediator of excitotoxic neurodegeneration: GluK4 knockout mice showed robust neuroprotection in the Cornu Ammonis 3 (CA3) region of the hippocampus following intrahippocampal injection of kainate, a potent excitotoxin, and widespread neuroprotection throughout …

    rockefeller Repository record for The GluK4 Kainate Receptor Subunit Regulates Mood, Memory and Excitotoxic Neurodegeneration (opens in a new tab)

  6. The Role of Transcription Factors in Regulating Adult Neurogenesis after Excitotoxic Brain Injury

    While compensatory striatal neurogenesis is well documented in many injury models, cells of the correct lineage for endogenous repair are not always regenerated. To understand why, the molecular profile of subventricular zone (SVZ)-derived neural progenitor cells (NPCs), and their response to …

    auckland-ms Repository record for The Role of Transcription Factors in Regulating Adult Neurogenesis after Excitotoxic Brain Injury (opens in a new tab)

  7. Neuroprotective effects of overexpression of the inhibitor of apoptosis proteins in the quinolinic acid model of excitotoxic injury.

    Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder which results in the selective loss of the medium spiny neurons in the striatum. The neuropathological and behavioural deficits of HD can be modeled in rats by injection of the NMDA receptor agonist quinolinic acid (2,3 …

    ottawa-retro Repository record for Neuroprotective effects of overexpression of the inhibitor of apoptosis proteins in the quinolinic acid model of excitotoxic injury. (opens in a new tab)

  8. Non-canonical Activation of CREB/crh-1 Mediates Neuroprotection in a <i>Caenorhabditis elegans</i> Model of Excitotoxic Necrosis

    <p>Excitotoxicity, which is a major cause of neurodegeneration in brain ischemia, can also activate neuroprotective pathways. A frequently suggested neuroprotective cascade involves the activation of the transcription factor CREB by its phosphorylation, but on its own this mode of CREB activation …

    cuny-grad Repository record for Non-canonical Activation of CREB/crh-1 Mediates Neuroprotection in a <i>Caenorhabditis elegans</i> Model of Excitotoxic Necrosis (opens in a new tab)

  9. The mGluR2/3 Agonist LY397268 Improves Morphometric and Behavioral Outcomes in R6/2 Huntington's Disease Mice

    … pathology of Huntington's Disease (HD) is the excitotoxic injury to the striatum. Continual exposure of ionotropic NMDA receptors to glutamate from the cortex can be excitotoxic in HD and leave striatal neurons vulnerable to damage. Activation of presynaptic mGluR2/3 by an agonist dampens …

    tenn-hsc Repository record for The mGluR2/3 Agonist LY397268 Improves Morphometric and Behavioral Outcomes in R6/2 Huntington's Disease Mice (opens in a new tab)

  10. Rapid neuronal responses during spreading neurotoxic and neuroprotective network activity

    … receptors that trigger neuronal cell death (excitotoxicity). In this study, we have used dissociated hippocampal neurons cultured on coverslips and within novel microfluidic devices to study neuronal responses, both functional and morphological, to prolonged exposure to glutamate.<br/><br/>We …

    dundee Repository record for Rapid neuronal responses during spreading neurotoxic and neuroprotective network activity (opens in a new tab)

  11. Glutamate Excitotoxicty Activates a Novel Calcium Permeable Ion Channel in Cultured Hippocampal Neurons

    Glutamate excitotoxicity is the predominant mechanism implicated in neuronal cell death associated with neurological disorders such as stroke, epilepsy, traumatic brain injury and ALS. Excessive stimulation of NMDA subtypes of glutamate receptors leads to protracted intracellular calcium elevations …

    vcu Repository record for Glutamate Excitotoxicty Activates a Novel Calcium Permeable Ion Channel in Cultured Hippocampal Neurons (opens in a new tab)

  12. Investigating the Roles of DAPK, p53/CEP-1, and Mitochondrial Damage in Necrotic Neurodegeneration in C. elegans

    … Most of the damage is attributed to excitotoxicity, where an accumulation of the neurotransmitter glutamate in the synapse overstimulates postsynaptic neurons and ultimately leads to cell death (largely by necrosis). Stroke treatments are often ineffective, due to the delay between …

    cuny Repository record for Investigating the Roles of DAPK, p53/CEP-1, and Mitochondrial Damage in Necrotic Neurodegeneration in C. elegans (opens in a new tab)

  13. Pre-clinical Targets for Ischemic Brain Injury

    … glutamate release during ischemia, causing excitotoxic injury to oligodendrocytes, resulting in demyelination. Glutamate receptor antagonists have been trialled in stroke patients but fall short due to adverse side effects from high dose preparations. Stroke is largely a disease of ageing, …

    plymouth Repository record for Pre-clinical Targets for Ischemic Brain Injury (opens in a new tab)

  14. Neuroprotection from the huntingtin-repressed transcriptional coactivator PGC-1α

    … which is neuroprotective against oxidative and excitotoxic stress in vitro whereas extrasynaptic NMDAR expression is increased in HD. Excessive NMDAR activity, specifically through extrasynaptic rather than synaptic NMDARs, leads to excitotoxic death in neurons and its regulation has been …

    edinburgh Repository record for Neuroprotection from the huntingtin-repressed transcriptional coactivator PGC-1α (opens in a new tab)

  15. Amygdalar Modulation of the Medial Geniculate Nucleus and Cingulate Cortex in Discriminative Avoidance Training

    … late dTIA in A29. As hypothesized, LA nuclear excitotoxic lesions decreased dTIA in A29. Moreover, A29 theta-like neuronal activity was weaker in these subjects. Not in accord with the hypothesis, LA nuclear lesions impaired the early developing dTIA in A24. Thus, the LA nucleus may contribute …

    uiuc Repository record for Amygdalar Modulation of the Medial Geniculate Nucleus and Cingulate Cortex in Discriminative Avoidance Training (opens in a new tab)

  16. Age-Dependent Effects Of Chronic GABAA Receptor Blockade In Barrel Cortex

    … in the developing rat cortex are vulnerable to excitotoxic effects. To test whether these GABAA receptors might serve to protect neurons from excessive excitatory input, polymer implants containing the GABAA receptor antagonist bicuculline were placed over barrel cortex for a 4-day period in …

    unt Repository record for Age-Dependent Effects Of Chronic GABAA Receptor Blockade In Barrel Cortex (opens in a new tab)

  17. Mechanisms Mediating Adaptive Presynaptic Muting Induction

    … as occurs during stroke or seizure, is known as excitotoxicity. One method utilized by neurons for reducing excitotoxicity within an overly activated neuronal network is to arrest excitatory neurotransmitter release from presynaptic terminals. The mechanisms responsible for inducing this …

    wustl Repository record for Mechanisms Mediating Adaptive Presynaptic Muting Induction (opens in a new tab)

  18. Role of glutamate in lead-induced toxicity: protection by N-acetylcysteine amide (NACA), a novel thiol antioxidant

    … cell damage include glutamatergic component (excitotoxic cell damage arising from impaired clearance of the released glutamate), interference with calcium-mediated cellular processes, and activation of protein kinase C (PKC) resulting in oxidative stress. Chelation therapy has been a choice to …

    must-thes Repository record for Role of glutamate in lead-induced toxicity: protection by N-acetylcysteine amide (NACA), a novel thiol antioxidant (opens in a new tab)

  19. Influence of Prion Protein Expression on Function of Excitatory Amino Acid Transporters in Mouse Primary Astrocytes

    … astrocytes at alleviating L-glutamate-mediated excitotoxic damage in both WT and PrP KO neuronal cultures. Thus, in this model, PrP KO astrocytes exerted a functional influence on neuronal survival and may therefore influence regulation of glutamatergic neurotransmission in vivo.

    montana-tech Repository record for Influence of Prion Protein Expression on Function of Excitatory Amino Acid Transporters in Mouse Primary Astrocytes (opens in a new tab)

  20. Influence of Prion Protein Expression on Function of Excitatory Amino Acid Transporters in Mouse Primary Astrocytes

    … astrocytes at alleviating L-glutamate-mediated excitotoxic damage in both WT and PrP KO neuronal cultures. Thus, in this model, PrP KO astrocytes exerted a functional influence on neuronal survival and may therefore influence regulation of glutamatergic neurotransmission in vivo.

    montana Repository record for Influence of Prion Protein Expression on Function of Excitatory Amino Acid Transporters in Mouse Primary Astrocytes (opens in a new tab)

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