Intrahippocampal nicotine in alcohol drinking rats--effects on lever-press response

We have previously shown differences on learning processes between alcohol drinking and non-alcohol drinking rats. Underlying these effects, functional differences in the septo-hippocampal pathway were hypothesized. We have performed a dose-response study for intrahippocampal nicotine (CA1) on acquisition and extinction of the lever-press response and antagonization test by co-administration of mecamylamine. Results show that the administration of nicotine in CAI region has a detrimental dose-dependent effect on acquisition in alcohol drinkers, with a dose of 10 nM being the most disruptive. In the controls, only doses of 10 and 20 nM had detrimental effect. The effect of nicotine (10 nM) was partially (alcoholics) or fully (controls) antagonized by mecamylamine co-administration (30 nM). Summarizing, the alcohol groups showed a dose-response curve for nicotine shifted leftwards, and a partial antagonism of these effects by mecamylamine; these effects may be consequence of the functional sensitization of the nicotinic responsivity in the CAI region which were produced by the chronic alcohol.