Abstract
Young rats prenatally exposed to ethanol exhibit heightened responses to dopaminergie (DA) drugs, altered brain concentrations of dopamine, and its metabolite dihydroxyphenylacetic acid (DOPAC), and transient reductions in DA receptor binding. Adult mice exposed to ethanol prenatally also exhibit increased responses to DA drugs; however, brain concentrations of DA and DOPAC are unaltered. The effects of prenatal ethanol exposure on DA or DOPAC concentrations in young mice or on DA receptor binding in mice of any age are unknown. Therefore, to determine if the different effects of prenatal ethanol exposure on rats and mice are due to age at time of testing or species, we determined its effects on DA concentrations and turnover in young mice under conditions previously reported for adult offspring and on DA D1 and D2 receptor binding in both young and adult offspring. Consistent with our previous report for adult offspring, prenatal ethanol exposure did not alter DA concentrations or turnover. The treatment did, however, diminish periadolescent growth as previously reported and produced a transient increase in DA D1, but not DA D2 receptor binding. DA receptor binding was not altered in adult offspring. Although unrelated to prenatal ethanol exposure, the sexes differed on all of the DA measures. Combined with previous reports, the present study suggests that species rather than age is more likely to account for the different effects of prenatal ethanol exposure on DA systems, and that sex differences in DA systems should be further examined.
Published Version
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