excitotoxicity

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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 ?
The patent mentions cannabidiol's ability as an antiepileptic, to lower intraocular pressure in the treatment of glaucoma, lack of toxicity or serious side effects in large acute doses, its neuroprotectant properties, its ability to prevent neurotoxicity mediated by NMDA, AMPA, or kainate receptors; its ability to attenuate glutamate toxicity, its ability to protect against cellular damage, its ability to protect brains from ischemic damage, its anxiolytic effect, and its superior antioxidant activity which can be used in the prophylaxis and treatment of oxidation associated diseases.
Additional potential neuroprotective effects of curcumin and/or the curcuminoids include as an antidepressant; protection against aluminium induced neurotoxicity, ethanol-induced brain damage, sodium-arsenite toxicity, 3-nitorpropionic acid-induced toxicity, MPTP toxicity, traumatic brain injury, lead induced neurotoxicity, glutamate toxicity and brain focel ischemia; memory improvement by HIV glycoprotein; anti aging; reversal of amyloid pathology and ethanol induced neurotoxicity; and restoration of the synaptic plasticity.
Glutamate is known to cause neuronal cell death via both glutamate receptor-mediated excitotoxicity and reactive oxygen species-mediated oxidative glutamate toxicity (Satoh et al.
Glutamate toxicity is a new mechanism of beta cell destruction not previously known, Drs.
Considered an initiator (8) Table 2: Comparison Between Contributing Factors and Initiators in ALS and MCS ALS MCS Glutamate Toxicity Glutamate Toxicity Oxidative Stress Stress: Physical, Psychological, Emotional Trauma Mitochondrial Dysfunction Mitochondrial Dysfunction Autoimmune Disease Infectious Disease Viral, Bacterial, Parasitic, Fungal Infection Toxic Chemical Exposure Toxic Chemical Exposure Exposure to Heavy Metals Heavy Metal Toxicity Calcium and Magnesium Deficiency Nutrient Deficiencies Carbohydrate Metabolism Dysfunction Growth Factor Deficiency Hormone Disruption
NMDA receptor-mediated glutamate toxicity of cultured cerebellar, cortical and mesen-cephalic neurons: Neuroprotective properties of amantadine and memantine.
com) announces updates to their Glutamate Toxicity research database.
Glutamate is known to cause neuronal cell death through both glutamate receptor-mediated excitotoxicity and reactive oxygen species (ROS)-mediated oxidative glutamate toxicity (Satoh et al.
Zinc is an important modifier of glutamate toxicity, a neurotransmitter linked to cell death in ALS patients.
Dodecylglycerol provides partial protection against glutamate toxicity in neuronal cultures derived from different regions of the embryonic rat brain.
In the next step of the experiment, BI-6C9 (an inhibitor of the pro-apoptotic BH-3 protein BID) was used to prevent glutamate toxicity in HT-22 cells.
Previously, Guilford scientists reported that in a tissue culture model of ALS, NAALADase inhibitors could protect against chronic glutamate toxicity.

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