[Chronic treatment with nicotine enhances the sensitivity of dopamine autoreceptors that modulate dopamine release from the rat striatum].

This study was undertaken to investigate the effect of chronic nicotine treatment on electrically evoked dopamine (DA) release from striatal slices and locomotor activity in rats under the influence of DA autoreceptor agonists and antagonist. Nicotine was supplied chronically by Alzet osmotic minipump for two weeks. B-HT920 and quinpirole decreased and (-)-sulpiride increased the evoked DA release from striatal slices. The B-HT920 and quinpirole-induced decrease and the (-)-sulpiride-induced increase in evoked DA release were enhanced by chronic treatment with nicotine. Nicotine itself has little effect on the evoked DA release. B-HT920 and quinpirole decreased and (-)-sulpiride, methamphetamine and apomorphine increased the locomotor activity in the rat. The B-HT920 and quinpirole-induced decrease and the (-)-sulpiride-induced increase in locomotor activity were enhanced by chronic treatment with nicotine. On the other hand, the methamphetamine and apomorphine-induced increase in locomotor activity were unaltered by chronic treatment with nicotine. Chronic nicotine treatment itself has no effect on locomotor activity. These data indicate that chronic treatment with nicotine caused a supersensitivity in presynaptic DA autoreceptors that modulate DA release from DA terminals in the rat striatum, and no change in the function of postsynaptic DA receptors.