excitotoxicity

(redirected from Glutamate-induced neurotoxicity)
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excitotoxicity

(ek-sī'tō-tok-sis'i-tē),
Neuronal death resulting from increased intracellular glutamate; neuronal ischemia leads to ATP loss and depolarization, with glutamate release from synapses, and subsequent overstimulation leading to sodium and calcium ion gate porosity.

excitotoxicity

Neurology Neuronal injury caused by excessive release of excitatory neurotransmitters–glutamate and aspartate causing damage to nerve and glial cells, which occurs in diverse neurologic diseases that may be acute–eg hypoglycemia, seizures, stroke, or trauma or chronic neurodegenerative disease–eg AIDS-dementia complex, amyotrophic lateral sclerosis, Huntington's disease, and possibly Alzheimer's disease

excitotoxicity

exaggerated and continuous stimulation by a neurotransmitter, especially in those neuronal systems which use glutamate as the transmitter.
References in periodicals archive ?
platyphylla bark and platyphylloside against glutamate-induced neurotoxicity in HT22 hippocampal cells were evaluated (Table 1).
Attenuation of glutamate-induced neurotoxicity in chronically ethanol-exposed cerebellar granule cells by NMDA receptor antagonists and ganglioside GM l.
officinalis fruits against glutamate-induced neurotoxicity in HT22 hippocampal cells.
officinalis fruits revealed that n-BuOH soluble fraction showed high protective activity against glutamate-induced neurotoxicity in HT22 hippocampal cells (data not shown).
The neuroprotective activity of compounds 1-5 against glutamate-induced neurotoxicity in HT22 hippocampal cells was measured.
amurensis against glutamate-induced neurotoxicity (Fig.
Of these components, (+)-ampelopsin A, [gamma]-2-viniferin, and trans-[epsilon]-viniferin protected against glutamate-induced neurotoxicity in cultured cortical neurons.
amurensis on transient focal ischemia-induced brain damage using a MCAO/reperfusion model in rats as well as glutamate-induced neurotoxicity in cultured cortical neurons.
2])- and glutamate-induced neurotoxicity in embryonic rat forebrain neuronal cells (FBNC).
Similarly, head injuries and exposure to pesticides or organophosphates also may induce the generation of oxygen-derived free radicals that can damage neuronal cells or result in glutamate-induced neurotoxicity (Zivin and Choi, 1991; Hall and McCall, 1994).

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