Abstract

A single or repeated administration of nicotine in mice produced hyperactivity and conditioned place preference (CPP). Postsynaptic dopamine (DA) receptor supersensitivity was also developed in nicotine-induced CPP mice. The hyperactivity induced by nicotine was evidenced by measuring the enhanced ambulatory activity using a tilting-type ambulometer. CPP effects were evaluated assessing the increased time spent by the mice to nicotine and the inhibition of CPP by the decreased time spent by the mice in the nonpreferred compartment. Postsynaptic DA receptor supersensitivity was evidenced by the enhanced response in ambulatory activity to the apomorphine, a DA receptor agonist. Administration of ginseng total saponin (GTS) prior to and during the nicotine treatment in mice inhibited not only nicotine-induced hyperactivity and CPP but also postsynaptic DA receptor supersensitivity in nicotine-induced CPP mice. These results suggest that inhibition by GTS of the nicotine-induced hyperactivity and CPP may be closely related with the inhibition of dopaminergic activation induced by nicotine and that the development of nicotine-induced CPP may be associated with the enhanced DA receptor supersensitivity. From these results, it is presumed that GTS may be useful for the prevention and therapy of these adverse actions of nicotine.

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