Involvement of a basolateral amygdala complex-nucleus accumbens pathway in glucocorticoid-induced modulation of memory consolidation.

Systemic or intracerebral administration of glucocorticoids modulates memory consolidation in several tasks. Previously, we have shown that these memory-modulatory effects depend on an intact basolateral complex of the amygdala (BLC) and efferents from the BLC that run through the stria terminalis. It is currently unknown, however, what BLC efferent structures mediate these effects. The present experiments were designed to determine whether the nucleus accumbens (NA), which receives BLC efferents through the stria terminalis and is involved in several BLC-dependent behaviours, is involved in glucocorticoid-induced modulation of memory consolidation. In experiment 1, rats with bilateral sham or N-methyl-D-aspartate (NMDA)-induced lesions of the NA were trained on a one-trial, footshock-motivated inhibitory avoidance task, and given immediate post-training injections of either the synthetic glucocorticoid dexamethasone (0.3 or 1.0 mg/kg, s.c.) or vehicle. Testing 48 h later revealed that dexamethasone significantly enhanced retention in sham-lesioned rats but that the enhancing effect was blocked in NA-lesioned rats. An asymmetrical, or crossed-lesion design was employed in experiment 2. Rats with a unilateral NMDA-induced lesion of the BLC and a unilateral lesion of either the ipsilateral or contralateral NA were trained as in experiment 1. Testing 48 h later revealed that dexamethasone enhanced retention in ipsilaterally lesioned rats, but that this effect was blocked in contralaterally lesioned rats. These findings indicate that an intact BLC-NA pathway is critical for the enhancing effects of glucocorticoids on memory consolidation, and are consistent with the view that the BLC regulates memory consolidation in other brain regions.