The involvement of the N-methyl-D-aspartate (NMDA) receptor in the epileptiform activity induced by 4-aminopyridine (4-AP) was studied in rat amygdala slices using intracellelar recording techniques. Stimulation of the ventral endopyriform nucleus evoked an excitatory postsynaptic potential (EPSP). After exposure to 4-AP (200 μM) the amygdala slices usually exhibited spontaneous and evoked epileptiform activity. The epileptiform events had an average duration of 522 ± 78 ms with a frequency of 0.5-8.5 bursts/min. Superfusion of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a selective non-NMDA receptor antagonist, practially abolished the epileptiform bursting. However, there remained a residual depolarizing component in 13 out of 18 neurons. This CNQX-resistant component was markedly enchanced both in amplitude and duration when extracellular Mg2+ was removed and could be reversibly blocked by the specific NMDA receptor antagonist, DL-2-amino-5-phosphonovaleate (DL-APV). Compared with the CNQX-sensitive component, the APV-sensitive component had a much smaller amplitude shorter duration. These data suggest that the NMDA receptor is likely to play only a minor role, and activation of the NMDA receptor may contribute to but is not required, for the generation of these bursts.
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