Ethanol (EtOH) abouse in pregnancy is known to produce serious damage of internal organs of the fetus, a condition in humans that is classified as "fetal alcohol syndrome". Cadmium (Cd), a heavy metal pollutant of the environment, represents another toxin that produces retarded fetal growth and teratogenic effects. The developing brain is particularly sensitive to both toxins, being affected morphologically and neurochemically. Prenatal EtOH and Cd have been found to reduce endogenous dopamine (DA) levels and turnover in brain. To test whether reactivity of central DA receptors might be altered by prenatal EtOH and Cd, administered separately or jointly, rats were given 10% (v/v) EtOH and/or Cd (5 or 50 ppm) in their drinking water. Male offispring were tested at 3 months for behavioral effects known to be induced by agonists acting at different subtypes of DA receptors. A dose-effect curve demonstrated that SKF 38393-induced oral activity, primarily a DA D!-associated event, was not substantially altered in these rats. However, the dose-effect curve for quinpirole-induced yawning activity, primarily a DA D2/D3-associated event was reduced in the EtOH-exposed rats. This effect of EtOH was prevented by Cd, which alone had little effect on yawning activity. These findings indicate that prenatal EtOH exposure produces a diminished reactivity of receptors of the DA D2/D3 complex and that Cd prevents this effect of EtOH.
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