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Vol. 53, Issue 3, 564-572, March 1998

Ca2+-Independent Excitotoxic Neurodegeneration in Isolated Retina, an Intact Neural Net: A Role for Clminus and Inhibitory Transmitters

Quan Chen, John W. Olney, Peter D. Lukasiewicz, Todd Almli, and Carmelo Romano

Departments of Ophthalmology and Visual Sciences (Q.C., P.D.L., C.R.), Psychiatry (Q.C., J.W.O., T.A.), and Anatomy and Neurobiology (P.D.L., C.R.), Washington University School of Medicine, St. Louis, Missouri 63110

Rapidly triggered excitotoxic cell death is widely thought to be due to excessive influx of extracellular Ca2+, primarily through the N-methyl-D-aspartate subtype of glutamate receptor. By devising conditions that permit the maintenance of isolated retina in the absence of Ca2+, it has become technically feasible to test the dependence of excitotoxic neurodegeneration in this intact neural system on extracellular Ca2+. Using biochemical, Ca2+ imaging, and electrophysiological techniques, we found that (1) rapidly triggered excitotoxic cell death in this system occurs independently of both extracellular Ca2+ and increases in intracellular Ca2+; (2) this cell death is highly dependent on extracellular Cl-; and (3) lethal Cl- entry occurs by multiple paths, but a significant fraction occurs through pathologically activated gamma -aminobutyric acid and glycine receptors. These results emphasize the importance of Ca2+-independent mechanisms and the role that local transmitter circuitry plays in excitotoxic cell death.

Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics


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Copyright © 1998 by the American Society for Pharmacology and Experimental Therapeutics