title: Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval.
abstract: It is well established that glucocorticoid hormones, secreted by the adrenal cortex after a stressful event, influence cognitive performance. Some studies have found glucocorticoid-induced memory enhancement. However, many studies have reported impairing effects of glucocorticoids on memory function. This paper 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. The evidence suggests that the consequences of glucocorticoid activation on cognition depend largely on the different memory phases investigated. Posttraining activation of glucocorticoid-sensitive pathways involving glucocorticoid receptors enhances memory consolidation in a pattern highly similar to that previously described for adrenal catecholamines. Also, similar to catecholamine effects on memory consolidation, glucocorticoid influences on memory consolidation depend on noradrenergic activation of the basolateral complex of the amygdala and interactions with other brain regions. By contrast, memory retrieval processes are usually impaired with high circulating levels of glucocorticoids or following infusions of glucocorticoid receptor agonists into the hippocampus. The hypothesis is proposed that these apparently dual effects of glucocorticoids on memory consolidation and memory retrieval might be related and that the basolateral complex of the amygdala is 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.
authors.affiliation: Center for the Neurobiology of Learning, Department of Neurobiology and Behavior, University of Caliornia, Irvine 92697-3800, USA. broozend@uci.edu
authors.forename: Benno
authors.initials: B
authors.lastname: Roozendaal
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000679:Amygdala / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000494:pharmacology*; D003345:Corticosterone / Q000008:administration & dosage / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects; D006801:Humans; D007267:Injections; D008568:Memory / Q000187:drug effects*; D051379:Mice; D009638:Norepinephrine / Q000378:metabolism*; D011930:Reaction Time / Q000187:drug effects; D011965:Receptors, Glucocorticoid / Q000187:drug effects; D013315:Stress, Psychological / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D011965:Receptors, Glucocorticoid; D003345:Corticosterone; D009638:Norepinephrine