Basolateral amygdala-nucleus accumbens interactions in mediating glucocorticoid enhancement of memory consolidation

Systemic or intracerebral administration of glucocorticoids enhances memory consolidation in several tasks. Previously, we reported that these effects depend on an intact basolateral nucleus of the amygdala (BLA) and efferent s from the BLA that run through the stria terminalis (ST). The BLA projects directly to the nucleus accumbens (NAc) via this ST pathway. The NAc also receives direct projections from the hippocampus and, therefore, may be a s ite of convergence of BLA and hippocampal influences in modulating memory c onsolidation. In support of this view, we found previously that lesions of either the NAc or the ST also block the memory-modulatory effect of systemi cally administered glucocorticoids. The present experiments examined the ef fects of lesions of the NAc or the ST on the memory-modulatory effects of i ntracerebral glucocorticoids on inhibitory avoidance training. Microinfusio ns of the specific glucocorticoid receptor agonist 11 beta ,17 beta -dihydr oxy-6,21-dimethyl-17 alpha -pregna-4,6-trien-20yn-3-one (RU 28362; 1.0 or 3 .0 ng) into either the BLA or the hippocampus of male Sprague Dawley rats a dministered immediately after training enhanced the 48 hr retention perform ance in a dose-dependent manner. Bilateral lesions of the NAc or the ST alo ne did not affect retention performance but blocked the memory enhancement induced by intra-BLA or intrahippocampal glucocorticoid receptor agonist ad ministration. These findings indicate that the BLA-NAc pathway plays an ess ential role in mediating glucocorticoid effects on memory consolidation and suggest that the BLA interacts with hippocampal effects on memory consolid ation via this pathway.