[Experimental models of alcoholism]

Ethanol causes behavioral effects in rats and mice similar to those observed in humans. Moreover, by selective breeding, lines of rats or mice have been obtained that prefer ethanol solution to water and vice versa (ethanol-preferring and ethanol-avoiding animals). Recent studies suggest that ethanol stimulates GABA receptor-mediated opening of the chloride channels in neuronal membranes, and that some behavioral responses to ethanol, such as its sedative and anxiolytic effects, are mediated by central GABA receptors. Recently, we have shown that ethanol suppresses the firing of neurons in the pars reticulata of the substantia nigra, which exert an inhibitory control over dopaminergic neurons. Escaping from inhibitory control, the latter neurons are stimulated by ethanol. Dopaminergic neurons especially sensitive to ethanol are those of the meso-cortico-limbic system, belonging to the "pleasure centers" of the brain. In addiction, it has been shown that ethanol stimulates dopamine metabolism in different brain areas, but more effectively so in ethanol-preferring than in ethanol-avoiding rats. Finally, voluntary ethanol intake modifies dopamine metabolism in different brain areas.