excitotoxicity

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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 ?
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.
NOX activation is related to NMDA activation and glutamate excitotoxicity.
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.
These compounds represent the only therapy that addresses all aspects of the postulated mechanisms of hearing loss due to noise, including free radical generation, glutamate excitotoxicity, glutathione depletion, mitochondrial injury, and programmed cell death.
ALS is a complex disease in which neurons are subjected to a variety of insults, for example, from genetic mutations, unidentified environmental factors, and glutamate excitotoxicity.
N-methyl-q-aspartate receptors (NMDARs) play a key role in mediating glutamate excitotoxicity because their high calcium permeability (Brennan et al.
TNF alpha can activate the NMDA receptor leading to glutamate excitotoxicity and neuronal degeneration.
Ruxton Pharmaceuticals is focused on developing modulators of glutamate excitotoxicity in the central nervous system.

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