excitotoxin


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excitotoxin

(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.

ex·ci′to·tox′ic (ĭk-sī′tə-tŏk′sĭk) adj.

excitotoxin

(ĕk-sī″tō-tŏks′ĭn)
A neurotransmitter (e.g., glutamate or aspartate) that can cause brain cell injury or death if its action is unabated. Brain damage is mediated by excitotoxins during prolonged seizure activity and stroke.
References in periodicals archive ?
16) Lithium's ability to stimulate neural stem cell production may prove to be of significant benefit in individuals recovering from spinal cord injury and neurological injuries caused by severe trauma (TBI, traumatic brain injury), dietary and environmental excitotoxins (mercury, aspartame, monosodium glutamate), and substance abuse.
Brain cells that are low in magnesium are particularly sensitive to the damaging effects of excitotoxins like aspartame.
Increased lipid peroxidation during kindling is independent of iron salts and excitotoxin.
Because APM is an excitotoxin, it stimulates the brain to destruction.
What all of these diseases have in common is a slow destruction of brain cells that are specifically sensitive to excitotoxin damage.
Martin's group recently reported that they were able to produce the Huntington's pattern of neuronal destruction by injecting the excitotoxin quinolinic acid into rat brains.
Renewal of an NIH grant of $749,000 to allow the completion of pre-clinical work on a series of glial excitotoxin release inhibitors.
Quinolinic acid induced brain neurotransmitter deficits; modulation by endogenous excitotoxin antagonists.
Inducing hypothermia by lowering the patient's core temperature acts to reduce secondary brain injury by suppressing excitotoxin and free-radical reactions, stabilizing cell membranes, reducing intracellular acidosis, and reducing abnormal electrical activity (Kabon, Bacher, & Spiss, 2003).
AMEX:QSC) announced today that the National Institutes of Health (NIH) notified Questcor of the renewal of an SBIR grant for further research on its series of glial excitotoxin release inhibitors (GERI) compounds.
A number of serious neurological conditions cite reduced membrane fluidity as part of the disease process involved in modulation of NMDA (glutamate) receptors, acting to control excitotoxin damage.
The animals were treated with kainic acid, an excitotoxin known to induce recurrent seizures, and either EUK-134 or saline.