Effects of molsidomine on scopolamine-induced amnesia and hypermotility inthe rat

Nitric oxide (NO) is hypothesized to be a novel intracellular messenger in the central nervous system. Recently, NO involvement in learning and memory processes has been proposed. Compounds that inhibit nitric oxide synthase, the key synthesizing enzyme, may block cognition, while NO donors may faci litate it. The aim of this study was to assess in the rat the effects of th e NO donor molsidomine (2 and 4 mg/kg, i.p.) on memory deficits caused by s copolamine. For this purpose, the object recognition task and the step-thro ugh passive avoidance procedure were chosen. In addition, the effects of mo lsidomine in antagonizing the scopolamine-induced hypermotility were also e xamined. Scopolamine at 0.2 mg/kg (object recognition) and 0.75 mg/kg (pass ive avoidance) disrupted acquisition in both the tasks and induced locomoto r hyperactivity at the dose of 0.2 mg/kg. Molsidomine at either dose revers ed the scopolamine-induced deficits in the object recognition paradigm but did not counteract the hypermotility and the deficits occurred in the passi ve avoidance test. These results suggest that to some extent, the NO donor molsidomine is involved in memory processing. (C) 2001 Elsevier Science B.V . All rights reserved.