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Effect of anticonvulsant drugs on glutamate neurotoxicity in cortical cell culture

Department of Neurology, Stanford University Medical Center, Stanford. CA.

Pretreatment with anticonvulsants partially protects animals against the brain damage induced by intraparenchymal injection of kainate, an analogue of the neurotransmitter glutamate. In murine cortical cell culture, high concentrations of phenobarbital, diazepam, phenytoin, or GABA itself did not prevent glutamate-induced neuronal loss. Addition of a glutamate receptor antagonist (gamma-D-glutamyl glycine) did reduce glutamate neurotoxicity. The in vivo protective effect of anticonvulsant drugs against the toxicity of excitatory amino acids must be indirect.

Address correspondence and reprint requests to Dr. Choi, Department of Neurology, Stanford University Medical Center, Stanford, CA 94305.

Supported by grants BRSG RR5353 and NS21628 from the NIH, grants from the Wills and Hereditary Disease Foundations and a Hartford Fellowship (to D.W.C.) from the John A. Hartford Foundation.

Received February 20, 1986. Accepted for publication June 6, 1986