excitotoxicity

(redirected from Glutamate-induced neurotoxicity)

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 ?
Pyrroloquinoline quinone against glutamate-induced neurotoxicity in cultured neural stem and progenitor cells.
Pyrroloquinoline quinine protects rat brain cortex against acute glutamate-induced neurotoxicity.
javanica has high antioxidant properties via scavenging ROS [sup][13] and has been known to protect primary cultured rat cortical cells from glutamate-induced neurotoxicity.
Aripiprazole inhibits glutamate-induced neurotoxicity and, in contrast to haloperidol, increases BDNF, glycogen synthase kinase (GSK)-1[beta], and the anti-apoptotic protein Bc1-2.
These finding may explain the neuroprotective mechanism of minocycline in models of global and focal cerebral ischemia, the R6/2 model of Huntington's disease, as well as glutamate-induced neurotoxicity in mixed neuronal/ glial cultures (9).
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.
9]-THC and the synthetic non-psychotropic cannabinoid, cannabidiol, both protect against glutamate-induced neurotoxicity but not via the CB1 receptor.
javanica displayed neuroprotective activity against glutamate-induced neurotoxicity in primary cultured rat cortical cells.
officinalis fruits against glutamate-induced neurotoxicity in HT22 hippocampal cells.

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