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The Journal of Neuroscience, October 1, 2001, 21(19):7455-7462
Oxidative Glutamate Toxicity Can Be a Component of the Excitotoxicity Cascade
David Schubert and Dana Piasecki Cellular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037
Along with ionotropic and metabotropic glutamate receptors, the cystine/glutamate antiporter x
may play a critical role in CNS pathology. High levels of extracellular glutamate inhibit the import of cystine, resulting in the depletion of glutathione and a form of cell injury called oxidative glutamate toxicity. Here we show that a portion of the cell death associated with NMDA receptor-initiated excitotoxicity can be caused by oxidative glutamate toxicity. In primary mouse cortical neurons the cell death resulting from the short-term application of 10 µM glutamate can be divided into NMDA and NMDA receptor-independent phases. The NMDA receptor-independent component is associated with high extracellular glutamate and is inhibited by a variety of reagents that block oxidative glutamate toxicity. These results suggest that oxidative glutamate toxicity toward neurons lacking functional NMDA receptors can be a component of the excitotoxicity-initiated cell death pathway. Key words: excitotoxicity; brain; death; nerve; non-NMDA; oxidative stress
Copyright © 2001 Society for Neuroscience 0270-6474/01/21197455-08$05.00/0
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