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Abstract
The role played by the inhibitory transmitters, GABA, glycine and taurine, and by excitatory (aspartate/glutamate) antagonists in mediating anticonvulsant action will be documented. This study provides examples of one anticonvulsant compound that affects glycine metabolism (milacemide), and another that affects aspartate metabolism (beta-methylene-aspartate). Beta-Methylene-aspartate, a selective inhibitor of glutamate-aspartate transaminase activity, protects against sound-induced seizures in audiogenic DBA/2 mice, with an ED50 value of 1.9 mumoles (icv; clonic phase). Forebrain and cerebellar aspartate, glutamate and GABA levels are reduced by 15-30% following the administration of beta-methylene-aspartate. Milacemide, a glycinamide derivative with experimental and clinical anticonvulsant activity, is ineffective against sound-induced seizures in DBA/2 mice. Following the ip administration of milacemide (100 mg/kg; 3 hours) there were significant increases in rat brain glycine levels in the cerebellum (+137%), cortex (+45%) and hippocampus (+59%).
Published Version
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