Mechanisms of excitotoxicity in neurologic diseases.

Abstract

Excitotoxicity refers to neuronal cell death caused by activation of excitatory amino acid receptors. A substantial body of evidence has implicated excitotoxicity as a mechanism of cell death in both acute and chronic neurologic diseases. A major recent advance has been the successful cloning and expression of the N-methyl-D-aspartate (NMDA), non-NMDA, and metabotropic glutamate receptors. The cellular mechanisms responsible for cell death after activation of these receptors are still being clarified. In acute neurologic diseases such as stroke and head trauma, excitotoxicity may be related to excessive glutamate release. In chronic neurodegenerative diseases, however, a slow excitotoxic process is more likely to occur as a consequence of either a receptor abnormality or an impairment of energy metabolism. Recent therapeutic studies have demonstrated the efficacy of non-NMDA receptor antagonists in experimental studies of global ischemia.

• Authors: M F Beal
• Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology (FASEB J) Vol. 6 Issue 15 Pg. 3338-44 (Dec 1992) ISSN: 0892-6638 [Print] United States
• PMID: 1464368 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Neurotoxins
• Receptors, Amino Acid
• Receptors, N-Methyl-D-Aspartate

Topics

• Animals
• Cell Death
• Humans
• Nerve Degeneration
• Nervous System Diseases (etiology, pathology)
• Neurotoxins (metabolism, pharmacology)
• Receptors, Amino Acid (metabolism)
• Receptors, N-Methyl-D-Aspartate (metabolism)