Systems mediating acute glucocorticoid effects on memory consolidation and retrieval

It is well established that glucocorticoid hormones, secreted by the adrenal cortex after a stressful event, influence cognitive performance. This article reviews recent findings from this laboratory on the acute effects of glucocorticoids in rats on specific memory phases, i.e., memory consolidation and memory retrieval. Posttraining activation of glucocorticoid-sensitive pathways involving glucocorticoid receptors (GRs) enhances memory consolidation in a dose-dependent manner. Glucocorticoid influences on memory consolidation depend on noradrenergic activation of the basolateral complex of the amygdala (BLA) and interactions of the BLA with other brain regions. By contrast, memory retrieval processes are usually impaired with high circulating levels of glucocorticoids or following infusions of GR agonists into the hippocampus. Although the BLA does not appear to be a site of glucocorticoid action in influencing memory retrieval, an intact BLA is required for enabling glucocorticoid effects on memory retrieval. The BLA appears to be a key structure in a memory-modulatory system that regulates, in concert with other brain regions, stress and glucocorticoid effects on both memory consolidation and memory retrieval.