excitotoxin

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Related to Excitotoxicity: excitotoxins

ex·ci·to·tox·in

 (ĭk-sī′tə-tŏk′sĭn)
n.
Any of a group of neurologically active compounds, including glutamate and aspartame, that in high concentrations have detrimental excitatory effects on the central nervous system and may cause injury to nerve cells.

[excit(atory) + toxin.]

ex·ci′to·tox′ic (ĭk-sī′tə-tŏk′sĭk) adj.
References in periodicals archive ?
Excitotoxicity as a common mechanism for fetal neuronal injury with hypoxia and intrauterine inflammation.
While CGA and quinic acid had no protective effect against glutamate-induced cell death, caffeic acid and ferulic acid significantly protected neurons from excitotoxicity.
Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression A prominent role in neuroprotection against excitotoxicity.
Nasrallah said, are impairment of antiapoptotic signaling, glutamate excitotoxicity, hypercortisolemia, and gamma-aminobutyric acid hypofunction.
A large part of its wide-ranging action lies in its inhibition of the phosphorylating enzyme glycogen synthase kinase-3 (GSK3), (30,31) thereby protecting brain cells from a wide range of assaults, including oxidative stress, DNA damage, impairment of mitochondrial function, and excitotoxicity.
Additionally, chronic maternal hyperhomocysteinemia may impair brain development and consequently the cognitive functions of the fetuses by the increase of neuronal vulnerability to excitotoxicity, oxidative stress and apoptosis [14,15].
Taurine crosses the blood-brain barrier and is implicated in inhibitory neurotransmission, long-term potentiation (LTP) in striatum and hippocampus, membrane stabilization, adipose tissue regulation, possible obesity prevention, calcium homeostasis, protection against glutamate excitotoxicity, and epileptic seizure prevention in humans (Wu and Prentice 2010).
Metabolic injury can be caused by reactive oxygen species accumulation [6-8], cochlear ischemia followed by reperfusion injury [9], and excitotoxicity of auditory neurons induced by excessive release of the cochlear afferent neurotransmitter [10].
The presence of recombinant human ApoE [epsilon]2 in primary mixed neuronal-glial cell cultures partially protected against oxidative injury by reducing secondary glutamate excitotoxicity (23).
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.
NMDArs play crucial roles in neuroplasticity, memory formation, and learning, and their dysfunction has been associated with excitotoxicity leading to nerve cell death, schizophrenia, epilepsy, and dementia (Dalmau et al.