Abstract
Reversible inactivation of the basolateral amygdala (BLA) disrupts the acquisition and expression of conditioned defeat (CD), an ethological model of conditioned fear, suggesting that the BLA may be a critical component of the neural circuit mediating behavioral plasticity associated with the experience of social defeat. We have also shown that this effect is N-methyl-d-aspartic acid (NMDA) receptor-dependent, because infusion of d,l-2-amino-5-phosphovalerate (APV) into the BLA also impairs the acquisition of CD. APV is a non-selective NMDA antagonist, however, thus it disrupts the entire heteromeric receptor complex, making it difficult to distinguish the relative contributions of either the NR2A or NR2B receptor subtypes on the acquisition of CD. There is ample evidence, however, that the NR2B subunit of the NMDA receptor in the amygdala is critical for mediating long-term potentiation and plasticity related to fear learning. The purpose of the present experiment was to determine whether infusion of ifenprodil, a selective antagonist of the NR2B subunit, into the BLA would block the acquisition (but not expression) of CD. In Experiment 1, infusion of ifenprodil immediately before defeat training significantly decreased submissive behaviors and restored territorial aggression when hamsters were later paired with a non-aggressive intruder (NAI). Conversely, infusion of ifenprodil immediately before CD testing failed to inhibit the expression of submissive behaviors in previously defeated hamsters. These results support the hypothesis that the BLA is a critical site for the plasticity underlying social defeat-induced changes in behavior.