Enhancement of NMDA receptor-mediated synaptic potential evoked in rat medial-amygdala neuron following olfactory bulbectomy.

Synaptic potentials evoked in the medial amygdala (m-AMG) neurons were studied in in vitro slice preparations obtained from normal and olfactory bulbectomized rats. Local stimulation induced a sequence of responses: a fast EPSP, a fast IPSP and a slow EPSP. The fast EPSP was suppressed by kynurenic acid (KYN) at a concentration of 1 mM but not by 3-[(+-)-2-carboxypiperazin-4-yl-]-propyl-1-phosphonic acid (CPP) at concentrations up to 20 microM. The slow EPSP was reversibly blocked by both KYN (1 mM) and CPP (5-10 microM). Addition of bicuculline methiodide (50 microM) to the bath suppressed the fast IPSP and augmented both the fast and slow IPSPs leading to burst discharges. In a small population of m-AMG neurons, the slow EPSP was followed by a slow IPSP. The slow IPSP was suppressed by phaclofen (500 microM) but not by bicuculline methiodide (up to 100 microM). In slice preparations obtained from olfactory bulbectomized rats, local stimulation evoked burst discharges, which were similar to those observed when bicuculline methiodide was applied to slice preparations obtained from normal rats. These results suggest that GABAA receptor mediating fast IPSP and N-methyl-D-aspartate (NMDA) receptors mediating slow EPSP regulate activities of m-AMG neurons and that the enhancement of NMDA receptor mediating slow EPSP is responsible for the hyperexcitability of m-AMG neurons following olfactory bulbectomy.