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 ?
Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage.
The role of excitotoxicity in neurological disease.
Mitochondrial membrane potential and glutamate excitotoxicity in cultured cerebellar granule cells.
11) research on disease mechanisms on the cellular or subcellular level (oxidative stress, excitotoxicity, apoptosis) from neurotoxic exposures; and
Recently, we showed that carnosine protects against NMDA-induced excitotoxicity in differentiated PC12 cells through a histaminergic pathway.
Depression is most likely involved in the regulation of hypothalamic-pituitary-adrenal (HPA) axis, monoamine neurotransmitters, excitotoxicity, hippocampal neurons and neurotrophic factors.
The Guam cycad toxin methylazoxymethanol damages neuronal DNA and modulates tau mRNA expression and excitotoxicity.
Excitotoxicity, oxidative stress, endothelial dysfunction, and inflammation.
Additional impressive effects of progesterone in traumatic brain injury include its ability to control excitotoxicity,14,15 or heightened responsiveness of injured brain cells that may cause seizure activity, and its ability to help restore the damaged blood-brain barrier16 that normally protects against intrusion of unwanted substances into brain tissue.
Estrogens attenuate and cortisone exacerbates excitotoxicity, oxidative injury and amyloid [beta]-peptide toxicity in hippocampal neurons.
These findings suggest that BB supplementation may protect against neuro-degeneration and cognitive impairment mediated by excitotoxicity and oxidative stress.
Glutamate receptor-mediated excitotoxicity is accompanied by oxidative stress (Jhamandas et al.