NICOTINE REVERSES SCOPOLAMINE-INDUCED IMPAIRMENT OF PERFORMANCE IN PASSIVE-AVOIDANCE TASK IN RATS THROUGH ITS ACTION ON THE DOPAMINERGIC NEURONAL SYSTEM

Interest has recently focused on tobacco and/or nicotine in relation t o senile dementia of the Alzheimer type because the population of pati ents with this disease among tobacco smokers is significantly smaller than in nonsmokers. We investigated whether, in relation to the dopami nergic neuronal system, nicotine was effective in ameliorating the imp airment of performance in passive avoidance tasks in rats induced by s copolamine, an inhibitor of muscarinic acetylcholine receptors. Scopol amine and nicotine were coadministered to rats 30 min before the acqui sition trial. Some rats received scopolamine alone; they showed much s horter step-through latency (STL) than the control group in the retent ion test. Nicotine significantly prolonged the decreased STL induced b y scopolamine. The effects of nicotine were inhibited by the preadmini stration of mecamylamine, SCH 23390, and (-)sulpiride, which are nicot inic acetylcholine, D-1, and D-2 receptor antagonists, respectively. T hese results suggest that nicotine, by activating the nicotinic acetyl cholinergic and dopaminergic neuronal systems, ameliorates the impairm ent of performance in the passive avoidance task induced by a muscarin ic acetylcholine receptor blocker.