Ca. Leslie et al., EFFECTS OF PRENATAL COCAINE EXPOSURE UPON POSTNATAL-DEVELOPMENT OF NEOSTRIATAL DOPAMINERGIC FUNCTION, Synapse, 17(3), 1994, pp. 210-215
Pregnant rats were injected twice daily with 20 mg/kg cocaine (or sali
ne) from gestational day 10 to parturition. Brains from offspring were
examined with quantitative receptor autoradiography [D1 receptor (D1R
), D2 receptor (D2R) and dopamine transporter (DAT)] and quantitative
in situ hybridization [D1R mRNA, D2R mRNA, preproenkephalin (PPE) mRNA
] for markers of neostriatal dopaminergic function. Prenatal cocaine e
xposure did not alter postnatal development of striatal D1R sites, but
D1R mRNA levels were reduced by a third at days 14 and 35. D2R sites
were increased over control in lateral striatum by day 6, and remained
elevated through postnatal day 35. Total D2R mRNA was increased over
control in both medial and lateral striatum at 7 and 14 days but was e
qual to control at 35 days. Prenatal cocaine exposure increased DAT de
nsity at postnatal days 1 through 5, but reduced it at days 14 and 35;
PPE mRNA expression was reduced at days 7, 14 and 35. Many of these r
esults are similar to those found in experimental animals and humans f
ollowing cocaine withdrawal. (C) 1994 Wiley-Liss, Inc.