MONOAMINE TRANSPORTERS AND THE NEUROBEHAVIORAL TERATOLOGY OF COCAINE

Prenatal cocaine exposure has been associated with various postnatal b ehavioral abnormalities in human infants, and also with changes in loc omotor activity, learning deficits, and altered responses to drug chal lenge in nonhuman offspring. Several studies have further demonstrated that cocaine exerts an activating effect on fetal behavior. A variety of mechanisms have been proposed to account for the neurobehavioral t eratogenic effects of developmental cocaine treatment. including inhib ition of fetal brain neurotransmitter uptake and fetal hypoxemia secon dary to constriction of the uteroplacental vascular bed. In support of the hypothesis that cocaine effects may be mediated partly by monoami ne uptake inhibition, we and other investigators have recently demonst rated the presence of functional dopamine (DA), serotonin (5-HT), and norepinephrine (NE) transporters in the fetal rat brain. Transporter-r elated cocaine recognition sites are found in a number of fetal brain areas and could mediate the acute effects of cocaine on these areas as well as developmental changes that are manifested postnatally. For ex ample, DA transporter blockade may underlie the above-mentioned activa tional effects of cocaine on fetal behavior. Time-dependent changes in DA or 5-HT transporter expression produced by prenatal cocaine exposu re could likewise play an important role in some of the behavioral eff ects observed when offspring are tested postnatally. Copyright (C) 199 6 Elsevier Science Inc.