Involvement of a basolateral amygdala complex-nucleus accumbens pathway inglucocorticoid-induced modulation of memory consolidation

Systemic or intracerebral administration of glucocorticoids modulates memor y consolidation in several tasks. Previously, we have shown that these memo ry-modulatory effects depend on an intact basolateral complex of the amygda la (BLC) and efferents from the BLC that run through the stria terminalis. It is currently unknown, however, what BLC efferent structures mediate thes e effects. The present experiments were designed to determine whether the n ucleus accumbens (NA), which receives BLC efferents through the stria termi nalis and is involved in several BLC-dependent behaviours, is involved in g lucocorticoid-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 avoidanc e task, and given immediate post-training injections of either the syntheti c 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-lesione d rats. An asymmetrical, or crossed-lesion design was employed in experimen t 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 ex periment 1. Testing 48 h later revealed that dexamethasone enhanced retenti on in ipsilaterally lesioned rats, but that this effect was blocked in cont ralaterally lesioned rats. These findings indicate that an intact BLC-NA pa thway is critical for the enhancing effects of glucocorticoids on memory co nsolidation, and are consistent with the view that the BLC regulates memory consolidation in other brain regions.