EFFECTS OF FELBAMATE ON VERATRIDINE-STIMULATED AND K-STIMULATED RELEASE OF GLUTAMATE FROM MOUSE CORTEX()

Felbamate is a novel anticonvulsant which may modulate the strychnine- insensitive glycine site of the N-methyl-D-aspartate (NMDA) receptor c omplex. This study examined the effect of felbamate and 5,7-dichloroky nurenic acid on veratridine (20 mu M)- and K+ (60 mM)-stimulated relea se of amino acids in mouse cortical slices. Felbamate significantly de creased veratridine-induced release of glutamate at 400 mu M and 800 m u M but had no effect on K+-stimulated release. 5,7-Dichlorokynurenic acid had no effect on amino-acid release in concentrations up to 200 m u M. The inhibitory effect of felbamate on veratridine-induced release of glutamate may be due to inactivation of voltage-sensitive Na+ chan nels.