1. The Neuroscience Group and the Discipline of Human Physiology, Faculty of Medicine and Health Sciences, University of Newcastle, NSW, 2308, Australia
2. Present address: Division of Neuroscience, John Curtin School of Medical Research, GPO Box 334, Canberra ACT 2601, Australia.

Correspondence to: Pankaj Sah^1,2 Correspondence and requests for materials should be addressed to P.S. (e-mail: Email: Pankaj.Sah@anu.edu.au).

Abstract

Fear conditioning is a paradigm that has been used as a model for emotional learning in animals¹. The cellular correlate of fear conditioning is thought to be associative N -methyl-D-aspartate (NMDA) receptor-dependent synaptic plasticity within the amygdala^{1, 2, 3}. Here we show that glutamatergic synaptic transmission to inhibitory interneurons in the basolateral amygdala is mediated solely by -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. In contrast to AMPA receptors at inputs to pyramidal neurons, these receptors have an inwardly rectifying current–voltage relationship, indicative of a high permeability to calcium⁴,⁵. Tetanic stimulation of inputs to interneurons caused an immediate and sustained increase in the efficacy of these synapses. This potentiation required a rise in postsynaptic calcium, but was independent of NMDA receptor activation. The potentiation of excitatory inputs to interneurons was reflected as an increase in the amplitude of the GABA_A-mediated inhibitory synaptic current in pyramidal neurons. These results demonstrate that excitatory synapses onto interneurons within a fear conditioning circuit show NMDA-receptor independent long-term potentiation. This plasticity might underlie the increased synchronization of activity between neurons in the basolateral amygdala after fear conditioning⁶.