Prenatal cocaine produces dose-dependent suppression of prolactin and growth hormone in neonatal rats.

Pregnant Long-Evans hooded rats were dosed with 5, 10, 20, or 40 mg/kg/d cocaine from GD7 through GD20; pairfed/vehicle-injected, and uninjected controls were included. At birth, representative pups from each litter were killed by decapitation and serum assayed for prolactin and growth hormone via radioimmunoassay. Prolactin levels were significantly reduced on P1 in offspring which had been dosed prenatally with 20 or 40 mg/kg/d, while growth hormone levels were significantly lower than control levels in the 5 and 10 mg/kg/d animals. Pairfed/vehicle controls did not differ from uninjected controls on levels of either hormone. These endocrine changes associated with cocaine dosing may affect subsequent development of the organism.

Behavioral and neuroanatomical sequelae of prenatal naloxone administration in the rat.

Pregnant Long-Evans hooded rats were dosed subcutaneously with 1 or 5 mg/kg/day naloxone hydrochloride, or an equal volume of vehicle, from gestational Day 4 (GD4) through GD19. Offspring were assessed for development of righting reflex, negative geotaxis, and open field activity, and for acquisition of a Warden maze; offspring sacrificed at postnatal Day (PND) 21 were assessed for several parameters of cerebellar, hippocampal, and motor cortical morphology. Five mg/kg/day naloxone accelerated development of negative geotaxis and righting reflex, while 1 mg/kg/day naloxone tended to slow development. Low dose females had significantly more errors than controls on the first day of maze learning. The high dose group had a significantly higher concentration of granule cells in the curvature of the dentate gyrus than controls; other neuroanatomical measures were unaffected by dosing. These findings confirm and extend previous work indicating that prenatal exposure to naloxone may alter neurobehavioral development in the rat.