CONICET | Buscador de Institutos y Recursos Humanos

In the United States approximately 10?15% of women consume alcohol (ethanol) during pregnancy. Even low amounts of ethanol consumption during pregnancy can elicit long-term consequences. Prenatal experience with as few as 3 drinks has been associated with increase problem drinking in adulthood. Such effects are corroborated in rodents; however, the underlying neural adaptations contributing to this effect are not clear. In the current set of experiments, we investigated whether changes in ethanol responding following prenatal ethanol exposure involved kappa opioid receptor activation and expression. Sprague-Dawley rats were prenatally exposed to low levels of alcohol (1.0 g/kg) during late gestation (gestational day 17-20: GD17-20) via intragastric intubation of pregnant dams. Following birth, ethanol intake, kappa and mu opioid-induced place conditioning, and kappa opioid receptor expression in mesolimbic brain regions was assessed in infant rats (postnatal day 14-15: PD14-15) that were offspring of dams given ethanol, vehicle, or untreated, during pregnancy. Animals exposed to prenatal alcohol drank more alcohol later in life and exhibited significant changes in the kappa opioid system. While control subjects found kappa opioid activation aversive, animals exposed to ethanol prenatally exhibited either no aversion or appetitive responding. Further analysis revealed that synaptosomal kappa opioid receptor expression was significantly decreased in brain areas implicated in responding to ethanol. Overall, this data suggests that prenatal ethanol affects kappa opioid function and expression and that these changes may be involved in increased drinking later in life.