excitotoxicity


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Related to excitotoxicity: excitotoxins

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 ?
2000) Homocysteine elicits a DNA damage response in neurons that promotes apoptosis and hypersensitivity to excitotoxicity.
Recovery of structure and function of inner ear afferent synapses following kainic acid excitotoxicity.
Nicotine is neuroprotective against glutamate excitotoxicity and it also inhibits apoptosis.
Among these are inflammation, oxidative stress, excitotoxicity, toxic exposure, and mitochondrial dysfunction.
According to research published in the journal Phytotherapy Research, it reduces oxidative stress in the brain, neuroinflammation, and excitotoxicity.
Also, cytokines and chemokines produced by macrophages/microglia and activated astrocytes (TNF-[alpha], IL-6, GM-CSF, IL-10) which induce neuronal damage mediated by oxidative stress, excitotoxicity and distress of cellular defense mechanisms (heat-shock proteins--HSP, chaperones and ubiquitin-proteasome system) with consequent apoptosis.
Several theories related to the etiopathogenesis of ALS have been proposed, including oxidative stress, mitochondrial dysfunction, excitotoxicity defective axonal transport, and abnormal protein aggregation; however the true etiopathogenesis is not known with certainty (3).
sup][28] Glutamate excitotoxicity was observed to be related to neuronal apoptosis and necrosis after hypothermic circulatory arrest.
These are so powerful that they can actually prevent excessive blood coagulation, remove toxins, stop or block excitotoxicity (which disturbs brain balance and health).
14),(15),(16) As this was found to correlate with glutamatergic excitotoxicity of the withdrawal state, it was put forth as a possible mechanism mediating the symptoms of alcohol withdrawal (17) The oxidative stress parameters showed correlation with the severity of withdrawal state.
In vitro studies have indicated a relationship between Hcy and DNA damage, apoptosis, excitotoxicity, and oxidative stress, which are of great importance in neurodegeneration [21, 22].
In ischemic injury, oxidative stress is mainly triggered by glutamatergic excitotoxicity as a result of the activation of numerous calcium-dependent enzymes (especially neuronal nitric oxide synthase (nNOS)) that produce excessive amounts of oxygen and other reactive species.