The effects of chronic amphetamine treatment on prenatal ethanol-induced changes in dopamine receptor function: electrophysiological findings.

The sensitivity of dopamine (DA) receptors in the mesoaccumbens DA system was investigated with extracellular recording and microiontophoresis techniques in adult rats that received prenatal ethanol exposure and chronic postnatal amphetamine treatment. Pregnant rats were fed with a liquid diet containing 0 or 35% ethanol-derived calories from gestation day 6 to 20. An ad libitum group received laboratory chow and water. Offspring were injected with amphetamine (2 mg/kg/day s.c.) or saline from postnatal day 22 to 10- to 12-months of age. Electrophysiological recording procedures were performed 16 to 24 hr after the last amphetamine injection. A supersensitivity of somatodendritic DA autoreceptors in the ventral tegmental area was observed in animals exposed prenatally to ethanol. This prenatal ethanol exposure-induced supersensitivity was not observed after postnatal amphetamine treatment. In control animals, postnatal amphetamine treatment did not affect the sensitivity of somatodendritic DA autoreceptors. The sensitivity of D-1 DA receptors in the nucleus accumbens was reduced by prenatal ethanol exposure. Postnatal amphetamine treatment reduced D-1 DA receptor sensitivity in control animals, but not in animals exposed prenatally to ethanol. Neither prenatal ethanol treatment nor postnatal amphetamine treatment altered the sensitivity of D-2 DA receptors in the nucleus accumbens. There were no differences between the ad libitum and 0% ethanol-derived calorie groups, indicating undernutrition did not affect DA receptor function. These results show that prenatal ethanol exposure altered DA receptor function in the mesoaccumbens DA system in adult animals. Furthermore, postnatal amphetamine treatment was able to eliminate the supersensitivity of somatodendritic DA autoreceptors in prenatal ethanol-exposed animals.