Basolateral amygdala lesions block the memory-enhancing effect of 8-Br-cAMP infused into the entorhinal cortex of rats after training.

There is extensive evidence suggesting that the basolateral nucleus of the amygdala plays a critical role in modulating memory consolidation processes in other brain regions. The present experiments examined interactions between the basolateral amygdala and the entorhinal cortex in modulating memory consolidation for inhibitory avoidance training. Several studies have reported that activation of the second messenger system adenosine 3',5'-cyclic monophosphate (cAMP) in several brain regions enhances memory and induces long-term plasticity. In the present experiments, a unilateral infusion of the cAMP analogue, 8-Br-cAMP (0.25 or 1.25 microg in 0.5 microL), administered into the entorhinal cortex of male Sprague-Dawley rats immediately after training, enhanced 48-h retention. An N-methyl-d-aspartate-induced lesion of the ipsilateral basolateral amygdala did not impair retention, but blocked the memory-enhancing effect of 8-Br-cAMP (infused into the entorhinal cortex) post-training. A lesion of the contralateral basolateral amygdala did not block the 8-Br-cAMP-induced retention enhancement. These findings indicate that an intact basolateral amygdala is essential for modulation of memory consolidation involving the entorhinal cortex, and are consistent with evidence that the basolateral amygdala regulates memory consolidation mediated by other brain regions.