EFFECTS OF ANTICONVULSANTS AND GLUTAMATE ANTAGONISTS ON THE CONVULSIVE ACTION OF KAINIC ACID

  • 1 January 1980
    • journal article
    • research article
    • Vol. 243  (1) , 56-65
Abstract
In its pattern of sensitivity to anticonvulsants in mice, kainic acid (KA) showed little resemblance to pentylenetetrazol (PTZ), 3-mercaptopropionic acid (3-MP), bicuculline, picrotoxin or bemegride. KA may have an action on the .gamma.-aminobutyrate system. It is strongly antagonized by aminooxyacetic acid. Ethosuximide is ineffective against KA as it is against 3-MP. A subconvulsive dose of KA potentiated 3-MP but not PTZ. KA is to some extent comparable to PTZ in that it is antagonized by trimethadione, phenobarbital and chlordiazepoxide more effectively than is 3-MP. The convulsive action of KA is potentiated by the glutamate antagonists l-glutamate diethyl ester (GDEE) and l-nuciferine. GDEE slightly potentiated bicuculline, but not other convulsants tested; it slightly antagonized PTZ. Nuciferine potentiated all except PTZ and bemegride. The failure of the agents to antagonize KA-induced seizures is consistent with the view that KA and glutamate act at separate excitatory receptor sites. The potentiation might possibly be due to a blocking of glutamergic activation of neurons that are inhibitory.