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
References in periodicals archive ?
[sup][27] This indicates that NCX3 has a close relationship with neuronal degeneration, which is caused by excitotoxicity.
The CREB family of transcription factors is activated by phosphorylation; they promote neuronal survival, protecting neurons from excitotoxicity and apoptosis by regulating the transcription of pro-survival factors (Lonze and Ginty 2002; Mantamadiotis et al.
Blockade of cannabinoid CB(1) receptor function protects against in vivo disseminating brain damage following NMDA-induced excitotoxicity. J Neurochem 2002; 82: 154-158.
CAPs-exposed males have increased levels of the major excitatory neurotransmitter GLU in the hippocampus, a sign of excitotoxicity in that region.
Glutamate mediated excitotoxicity is one of the common mechanisms of neuronal death in neurodegenerative diseases like Alzheimer's disease [1, 2].
Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases.
Glutamate accumulation and excessive stimulation of its receptors induce potent excitotoxicity in the CNS (Fundytus 2001).
Also involved (whether as a trigger or a consequence is not known) is the phenomenon of excitotoxicity: excess levels of the neurotransmitter glutamate acting via NMDA receptors damage mitochondria.
The NMDA receptor/ion channel complex: a drug target for modulating synaptic plasticity and excitotoxicity. Current Pharmaceutical Design, 13, 3185-3194.
Nicholls, "Mitochondria, calcium regulation, and acute glutamate excitotoxicity in cultured cerebellar granule cells," Journal of Neurochemistry, vol.
The glutamate excitotoxicity hypothesis of brain injury after cerebral ischemia may not be proven, but the process likely occurs after SAH, especially in patients who develop focal ischemia due to delayed angiographic vasospasm or other complications or those with reduced cerebral perfusion pressure from brain swelling and edema.