Intra-hippocampal microinjections of anisomycin did not block glucocorticoid-induced impairment of memory retrieval in rats: An evidence for non-genomic effects of glucocorticoids

Previous findings indicated that intra-cerebral as well as systemic injections of glucocorticoid hormones shortly before retention testing induce impairment of long-term memory retrieval, but the underlying mechanisms (genomic or non-genomic) are not known. To clarify this issue, we investigated the involvement of protein synthesis in the hippocampus in glucocorticoid-induced impairment of memory retrieval. Young rats carrying bilateral cannulae aimed at the hippocampus were trained in a water maze (MWM) 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. Corticosterone (1 mg/kg) was injected 30 min before retention testing with or without prior bilateral intra-hippocampal injections of anisomycin (80 or 160 μg/μl per site) as an inhibitor of protein synthesis. The control animals received vehicle or saline solutions. The results show that corticosterone-induced impairment of memory retrieval was not blocked by intra-hippocampal infusions of anisomycin. Our data suggest that corticosterone influences memory retrieval via a protein independent mechanism and provide evidence for rapid actions (non-genomic) of glucocorticoids on memory retrieval.