Oral pretreatment with aldosterone or corticosterone blocked the memory-enhancing effects of the calcium antagonist nimodipine, the ACE inhibitor captopril, the NMDA blocker CGP 37,849, and the glycine antagonist strychnine in a passive-avoidance test in mice. The memory-disturbing effects of phenobarbitone, diazepam, CGP 37,849 and scopolamine were not influenced by the hormonal pretreatment. These findings could indicate the involvement of a steroid-sensitive mechanism in drug-induced improvement of memory. In the light of clinical observations showing elevated cortisol levels in Alzheimer patients, the results might also explain why only a limited number of these patients respond to therapy with memory enhancers.
The retention performance of mice in a passive-avoidance task was facilitated by low doses (0.3 mg/kg) of the competitive NMDA-receptor blocker CGP 37849, but impaired by high doses (30 mg/kg). The facilitatory effect was selectively suppressed by elevation of the plasma levels of aldosterone or corticosterone, or by blockade of steroid biosynthesis or the mineralocorticoid receptors. The impairment of memory, on the other hand, was not steroid sensitive. Accordingly, the data are in line with the hypothesis that drug induced memory facilitation is dependent on steroid sensitive processes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.