It has been suggested that ethanol may interact with the central nicotinic 
acetylcholine receptor, thus providing a basis for the often observed high 
consumption of both ethanol and nicotine. In the present in vivo microdialysis 
study, ethanol (2.5 g/kg) moderately increased dopamine overflow in the rat 
nucleus accumbens. The central nicotinic acetylcholine receptor antagonist 
mecamylamine totally counteracted this effect in a dose (1.0 mg/kg) that did not 
alter dopamine overflow per se. Ethanol also increased the overflow of 
dihydroxyphenylacetic acid and homovanillic acid, but this effect was not 
altered by mecamylamine (1.0 mg/kg). Furthermore, the ethanol-induced 
enhancement of 3,4-dihydroxyphenylalanine accumulation in the mesolimbic 
dopamine terminal area after NSD 1015 (an inhibitor of l-aromatic amino acid 
decarboxylase) was completely antagonized by mecamylamine in doses (3.0 and 6.0 
mg/kg) that exerted no effects per se. Neither ethanol nor mecamylamine changed 
the catecholamine synthesis rate in the striatum or the cerebral cortex. These 
results provide further evidence that ethanol-induced activation of the 
mesolimbic dopamine system (increased dopamine synthesis and release) may be 
mediated via stimulation of central nicotinic acetylcholine receptors. It is 
suggested that antagonists of central nicotinic acetylcholine receptors may be 
useful in the treatment of alcoholism.