Bursting discharges in disinhibited amygdala slices: the role of excitatory amino acid receptors.

The involvement of N-methyl-D-aspartate (NMDA) and non-NMDA receptors in the epileptiform activity, induced by bicuculline, was studied in slices of amygdala in the rat, using intracellular recording techniques. Stimulation of the ventral endopyriform nucleus evoked an excitatory postsynaptic potential (EPSP). After exposure to bicuculline (20 microM), the same stimulus evoked burst firing. Occasionally, spontaneous bursts similar in waveform to synaptically triggered bursts also occurred in disinhibited slices. Superfusion of DL-2-amino-5-phosphonovalerate (DL-APV, 50 microM) or 3-((+)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acids (CPP, 10 microM), rapidly blocked the late component of the paroxysmal depolarizing shift. The spontaneous and evoked bursts were never completely abolished in the presence of DL-APV or CPP. These results suggest that NMDA receptors may contribute to but are not required for the generation of these bursts. In contrast, application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) largely abolished the bursts, indicating that activation of non-NMDA receptors is of primary importance in this model of epilepsy.