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Inhibition and Synchronization of Basal Amygdala Principal Neuron Spiking by Parvalbumin-Positive Interneurons

The Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia

Submitted 3 July 2007; accepted in final form 22 August 2007

Using mice that express enhance green fluorescent protein (EGFP) under the control of the parvalbumin promoter, we made paired recordings from interneurons and principal neurons in the basal amygdala. In synaptically connected pairs, we show that single action potentials in a parvalbumin expressing interneuron can inhibit spiking in the synaptically connected principal neuron. When principal neurons were provided with suprathreshold oscillatory drive via a somatic patch pipette, action potentials in the interneuron inhibited spiking in principal neurons only when the interneuron spike occurred shortly before excitation reached threshold in the principal neuron. Moreover, after this spike inhibition, there was a rebound excitation in the principal neurons that was seen as an increased probability of firing on the cycle after inhibition. These results illustrate the major role of local inhibition in the basal amygdala. We propose that these interneurons in the basal amygdala provide a potent inhibition that acts to inhibit firing of principal neurons during cortically driven oscillations.