USE-DEPENDENT MODIFICATION OF A SLOW NMDA RECEPTOR-MEDIATED SYNAPTIC POTENTIAL IN RAT AMYGDALAR SLICES

A single stimulus applied to the endopyriform nucleus evoked in 35 of the 101 basolateral amygdaloid (BLA) neurons a slow excitatory postsynaptic potential (s-EPSP) of varying latencies. The s-EPSP could be graded by changing the stimulus intensity and, on reaching the threshold, triggered action potentials. At stimulus intensity just subthreshold for evoking a spike, the s-EPSP has an average amplitude of 16.3 +/- 1.4 mV, a time to peak of 25.7 +/- 3.8 ms, and a duration of 124 +/- 14 ms. The s-EPSP was reversibly blocked by DL-2-amino-5-phosphonovaleate (DL-APV) or ketamine, indicating its mediation through N-methyl-D-aspartate (NMDA) receptor activation. However, the s-EPSP was not able to follow stimulus frequency of 1 Hz, suggesting that APV-sensitive s-EPSP is probably generated by a polysynaptic pathway. The s-EPSP was greatly enhanced by synaptic stimulation in the presence of bicuculline or in Mg+ +-free solution leading to the genesis of paroxysmal depolarizing shift (PDS). The s-EPSP can undergo robust long-term potentiation (LTP) following tetanic stimulation. These results suggest that the NMDA receptor-mediated s-EPSP may play an important role in epileptogenesis and synaptic plasticity in the amygdala.