In its pattern of sensitivity to anticonvulsants, kainic acid (KA) showed little resemblance to pentylenetetrazol (PTZ), 3-mercaptopropionic acid (3-MP), bicuculline, picrotoxin or bemegride. That KA may have an action on the gamma-aminobutyrate system is suggested by the following: it is strongly antagonized by aminooxyacetic acid; ethosuximide is ineffective against KA as it is against 3-MP; and a subconvulsive dose of KA potentiated 3-MP but not PTZ. However, 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 also slightly potentiated bicuculline, but not other convulsants tested; it slightly antagonized PTZ. Nuciferine potentiated all except PTZ and bemegride. The failure of these 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.