Extracellular studies on the role of N-methyl-D-aspartate receptors in epileptiform activity recorded from the kainic acid-lesioned hippocampus.

Epileptiform bursts of population spikes were evoked in the CA1 region of slices of the hippocampus in which the CA3 region had been previously lesioned with kainic acid. D-2-amino-5-phosphonovalerate (D-APV), a specific N-methyl-D-aspartate (NMDA) antagonist, would markedly reduce the number of spikes in the burst but had no effects on the primary population spike or the amplitude of the field excitatory postsynaptic potential (EPSP). In unlesioned control slices only a single population spike was evoked and D-APV had no effect on this response or the field EPSP. Multiple population spike bursts evoked following application of bicuculline to control slices were much less attenuated by D-APV. The results suggest that activation of NMDA receptors contributes to the production of epileptiform activity in the kainic acid-lesioned hippocampus.