excitotoxicity

(redirected from Glutamate excitotoxicity)

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 ?
Nasrallah said, are impairment of antiapoptotic signaling, glutamate excitotoxicity, hypercortisolemia, and gamma-aminobutyric acid hypofunction.
This antibiotic has been studied extensively as an adjunctive treatment in schizophrenia and has proven to have several neuroprotective effects including anti-inflammatory, anti-oxidant, and anti-apoptotic, and reduces glutamate excitotoxicity.
The protective effects of L-theanine have been shown in animal models for at least the first three of these disorders, suggesting that regular L-theanine supplementation might be important in fending off these tragic conditions by opposing the destructive effects of long-term glutamate excitotoxicity.
Lithium protection against glutamate excitotoxicity in rat cerebral cortical neurons: involvement of NMDA receptor inhibition possibly by decreasing NR2B tyrosine phosphorylation.
Glutamate excitotoxicity is the pathological process by which neuronal cells are damaged or killed by excess glutamate receptor activation.
Effects of vitamin E in preserving mitochondrial membrane potential of astrocytes after glutamate excitotoxicity
Glutamate excitotoxicity and oxidative stress have been suggested as one of the important pathophysiological mechanisms in glaucomatous neurodegeneration [74, 75].
N-methyl-D-aspartate receptors (NMDARs) play a key role in mediating glutamate excitotoxicity because their high calcium permeability (Hardingham and Bading 2003).
The glutamate generated from pyruvate can produce glutamate excitotoxicity and neuronal degeneration.
During their study, the researchers discovered a common variant in the GRM7 gene, which the research team believes may be associated with susceptibility to glutamate excitotoxicity and hearing loss.
Viral-induced spinal motor neuron death is non-cellautonomous and involves glutamate excitotoxicity.
Studies have indicated that glutamate excitotoxicity occurs in the cochlea under pathologic conditions, such as noise trauma and ischemia.

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