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Introduction: Previous studies have indicated that stress levels of glucocorticoid hormones induce impairment of long term memory retrieval, but the underlying mechanisms (genomic or non-genomic) are not clear. To clarify this issue, we investigated the involvement of brain corticosteroid receptors and protein synthesis in the glucocorticoid-induced impairment of memory retrieval. Methods: 140 young rats were trained in the water maze (WM) task with six trials per day for six consecutive days. Retention of the spatial training was assessed 24 h after the last training session with a 60-s probe trial. Experiments included intraventricular injections of anisomycin ( 187.5 or 450 µg/5µl) , a specific protein synthesis inhibitor or specific antagonists for mineralocorticoid receptors (MR, 37.5, 75, 150 µg/5ul) or glucocorticoids receptors (GR, 75 or 150 µg/5ul) before corticosterone administration (1 mg/kg) shortly before retention testing. Results: The results showed that administration of anisomycin did not change the corticosterone response. Administration of the MR, but not GR, antagonist blocked the corticosterone-induced response. Conclusion: These findings provide evidence for the view that glucocorticoids impair memory retrieval through non-genomic mechanisms involving an interaction with central MRs.

Keywords: Glucocorticoids, Mineralocorticoid receptor, Glucocorticoid receptor, Spironolactone, RU 38486, Anisomycin, Memory retrieval, Water Maze

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