Abstract
Different behavioral and biochemical data suggest that ethanol has different effects on central dopaminergic transmission in rat and mouse. We found that ethanol induces an increase of striatal dopamine turnover which does not persist after chronic drinking. Following chronic ethanol treatment, we observed the development of supersensitivity of the striatal dopamine (DA) recognition sites, in terms of an enhanced affinity. We investigated various experimental models to clarify the existence of an enkephalinergic modulation of ethanol effects on the dopaminergic system. We found that in the rat, a pretreatment with naloxone abolishes the striatal DA turnover increase observed after ethanol. DBA 2J mice, which differ from C57 BL/6J and Swiss Albino, by genetically lacking enkephalinergic modulation on dopaminergic activity in the striatum, do not show any change of DA metabolism after acute ethanol. In the rat retina, where we hypothesized a less operant regulation of dopaminergic activity by enkephalins, tolerance does not develop after chronic drinking to the increase in DA turnover as it did in striatum. Our results confirm the importance of the endogenous opioid system in the regulation of the ethanol induced neurochemical and behavioral effects.
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