Role of excitotoxicity in human neurological disease.
An increasing body of evidence has implicated excitoxicity as a mechanism of neuronal death in both acute and chronic neurological diseases. A major recent advance has been the successful cloning and expression of the non-NMDA, NMDA, and metabotropic glutamate receptors. The cellular mechanisms responsible for cell death following activation of these receptors are still being clarified. A recent advance in conceptualizing excitotoxicity is the notion that a slow excitotoxic process may occur as a consequence of either a receptor abnormality or an impairment of energy metabolism. It is possible that such a mechanism may occur in neurodegenerative illnesses. Recent therapeutic studies have focused on glycine site antagonists and on the efficacy of non-NMDA antagonists in ischemia.
Beal
M F
MF
Massachusetts General Hospital, Boston.
D000596:Amino Acids / Q000502:physiology*; D000818:Animals; D003001:Cloning, Molecular; D006801:Humans; D009422:Nervous System Diseases / Q000503:physiopathology*; D017459:Receptors, Amino Acid / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000096:biosynthesis*
D000596:Amino Acids; D017459:Receptors, Amino Acid; D016194:Receptors, N-Methyl-D-Aspartate