Prenatal ethanol diminishes reactivity of presumed dopamine D3 receptors in rats

Ethanol abuse in pregnancy is known to produce serious damage to the developing central nervous system of mammalian species. As with several other classes of nerves, the ontogenetic influence of ethanol on dopamine (DA) nerves is long-lived. To test whether reactivity of DA receptors might be altered by prenatal ethanol administration, rats were given 10% (v/v) ethanol in their drinking water, starting 10 days before mating and continuing to the end of pregnancy. Male offspring were tested at 3 months for behavioral effects known to be induced by DA agonists acting at specific subtypes of DA receptors. The oral activity dose-effect curve for SKF 38393, a DA D1 agonist, was not altered from control. However, quinpirole-induced yawning behavior, reputedly a DA D3-associated event, was markedly impaired in the male rats that had been exposed in utero to ethanol. These findings indicate that prenatal ethanol exposure may predominately produce diminished reactivity of the DA D3, but not DA D1 subtype of DA receptor.