Abstract
Plasticity elicited by fear conditioning (FC) is thought to support the storage of aversive associative memories. Although work over the past decade has revealed FC-induced plasticity beyond canonical sites in the basolateral complex of the amygdala (BLA), it is not known whether modifications across distributed circuits make equivalent or distinct contributions to aversive memory. Here, we review evidence demonstrating that experience-dependent synaptic plasticity in the central nucleus of the amygdala (CeA) has a circumscribed role in memory expression per se, guiding the selection of defensive programs in response to acquired threats. We argue that the CeA may be a key example of a broader phenomenon by which synaptic plasticity at specific nodes of a distributed network makes a complementary contribution to distinct memory processes.