EXTENSIVE EVIDENCES INDICATE THAT GLUCOCORTICOID HORMONES, SECRETED BY THE ADRENAL CORTEX AFTER A STRESSFUL EVENT, INFLUENCE COGNITIVE FUNCTIONS. THIS ARTICLE REVIEWS OUR RECENT FINDINGS ON THE EFFECTS OF GLUCOCORTICOIDS IN RATS ON SPECIFIC MEMORY PHASES, I.E., MEMORY CONSOLIDATION, MEMORY RETRIEVAL, MEMORY RECONSOLIDATION, AND MEMORY EXTINCTION. …

Previous findings indicate that stress and GLUCOCORTICOIDS impair retrieval of previously acquired information in both animal and human subjects. Acute exposure to stressful stimuli and also administration corticosterone shortly before retention testing were shown to impair retrieval of spatial and contextual memories in rats. Similarly, acute administration of cortisone impairs retrieval of hippocampal dependent free recall of previously learned words in humans. However, the underlying mechanisms of GLUCOCORTICOIDS effects on memory retrieval are not known. In this article, we focus on our recent findings in GLUCOCORTICOIDS effects on memory retrieval processes. In a series of experiments, we have shown that the impairing effects of GLUCOCORTICOIDS on memory mainly mediate through non-genomic mechanisms which may involve an interaction with membrane receptors and several neurotransmitters in the brain.

Ample evidences indicate that glucocorticoid hormones, secreted by the adrenal cortex after a stressful event, influence cognitive performance. This article reviews our recent findings on the effects of GLUCOCORTICOIDS in rats on specific memory phases, i.e., memory consolidation, memory retrieval and memory reconsolidation. The effects of GLUCOCORTICOIDS on memory process mediate via glucocorticoid receptors (GR) and mineralcorticoid receptors (MR). Post-training administration of synthetic glucocorticoid or glucocorticoid agonist enhances memory consolidation in a dose-dependent manner. This effect depends on integrity of basolateral amygdala and cholinergic system and NMDA receptors. Conversely, memory retrieval is impaired under high levels of GLUCOCORTICOIDS. These effects usually appear too fast and mediate through non-genomic mechanisms as well as genomic ones. Finally, peripheral and central administrations of GR and MR antagonists impair memory reconsolidation after memory activation. These findings show that GLUCOCORTICOIDS differentially affect specific phases of memory process. Functional significance of these differential effects will be discussed.