Out with the old and in with the new: Synaptic mechanisms of extinction in the amygdala

Abstract

Considerable research indicates that long-term synaptic plasticity in the amygdala underlies the acquisition of emotional memories, including those learned during Pavlovian fear conditioning. Much less is known about the synaptic mechanisms involved in other forms of associative learning, including extinction, that update fear memories. Extinction learning might reverse conditioning-related changes (e.g., depotentiation) or induce plasticity at inhibitory synapses (e.g., long-term potentiation) to suppress conditioned fear responses. Either mechanism must account for fear recovery phenomena after extinction, as well as savings of extinction after fear recovery. This article is part of a Special Issue entitled SI: Brain and Memory.

Keywords: Depotentiation; Extinction; Fear conditioning; Interneuron; Learning; Long-term potentiation; Memory.

Figure 1. Synaptic mechanisms of conditioning and extinction

Conditioning (tan panel) is associated with long-term potentiation (LTP) at excitatory synapses from afferents carrying conditioned stimulus (CS) information that terminate on principal neurons (PN) in the basolateral amygdala [LTP (principal)]. Extinction (green panel) might result from a number of synaptic plasticity mechanisms including 1) depotentiation or long-term depression of previously potentiated PN synapses, 2) induction of LTP at CS afferents on interneurons (LTP-IN), or 3) LTP of inhibitory synaptic transmission (‘inhibitory’ LTP). Blue circles indicate the target synapses undergoing the forms of plasticity indicated above each microcircuit.