Abstract
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.
- © 1987 by the American Academy of Neurology
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