Behavioral, pharmacological, and neurochemical studies indicate that prenatal ethanol exposure can alter dopamine (DA) systems of developing rats. In addition, some of the behavioral changes described for prenatal-ethanol-exposed rats and mice (e.g., reduced responding for food and other rewards) as well as their response to various psychoactive drugs (e.g., amphetamines, methylphenidate, haloperidol) suggest that the DA system changes might extend into adulthood. Neurochemical studies on the effects of prenatal ethanol on DA systems of adults have not been reported for either species. The present study provides a neurochemical assessment of prenatal ethanol effects on DA systems of fully mature mice. Compared to chow and sucrose controls, adult offspring of mice fed a diet containing 25% ethanol derived calories had preadolescent growth deficits as observed in previous studies which also showed long-term behavioral deficits. Prenatal ethanol exposure in the present study, however, did not alter the concentration of DA or dihydroxyphenylacetic acid (DOPAC) nor the progressive decline in the concentration of these compounds in either striatum or nucleus accumbens of mature mice at intervals after synthesis inhibition by alpha-methyl-DL-p-tyrosine. Thus, the present study provides no neurochemical confirmation of altered DA systems resulting from prenatal ethanol exposure under conditions previously observed to alter adult behavior.