The contribution of non-NMDA and NMDA receptors to graded bursting activity in the CA1 region of the hippocampus in a chronic model of epilepsy.

The selective excitatory amino acid receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 2-amino-5-phosphonovalerate (D-APV), have been used to investigate the identity of the receptors involved in evoked epileptiform bursting activity in the chronic kainic acid lesioned hippocampus. Comparisons have been made with the acute bursting activity induced by bicuculline. Presented data suggest there are two possible mechanisms contributing to epileptiform bursting activity in the kainic acid lesioned hippocampus. One of these is probably a product of disinhibition, and generates a predominantly non-NMDA receptor mediated burst which is blocked by CNQX (2 microM). The second synaptic mechanism involves a major (or total) contribution by NMDA receptors to the epileptiform burst, and is blocked by D-APV (10 microM).