Hormone Ontogeny in the Ovine Fetus. VI. Dopaminergic Regulation of Prolactin Secretion*

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Abstract
The concentration of plasma PRL in the ovine fetus is low in midgestation, rises to high concentrations in late gestation, and remains elevated in the early neonatal period. To investigate the development of the dopaminergic regulation of PRL secretion in the ovine fetus and neonate, we infused, after a 2-h control period, the dopaminergic agonist apomorphine (40 or 100 μg/kg, iv over 1 h) or bromergocryptine (1-mg iv bolus) into chronically catheterized ovine fetuses (term gestation, 147 days) and neonatal lambs. Apomorphine at both dosages caused significant (P < 0.01) suppression of PRL concentrations in both the fetuses (118–136 days of age) (40 μg/kg, n = 3; 100 μg/kg, n = 4) and neonatal lambs (40 μg/kg, n = 4; 100 μg/kg, n = 4). The degree of suppression in the neonatal lamb was greater (P < 0.01) than that in the fetus. Similarly, bromergocryptine lowered PRL concentrations in three fetuses (122, 126, and 127 days of age) and one neonate. To assess the presence of tonic dopaminergic regulation of PRL secretion, we administered haloperidol (1-mg iv bolus) to 11 fetuses (92–140 days of age) and 5 neonates. In all but the youngest fetus, haloperidol caused an elevation of plasma PRL concentration. In fetuses with low basal concentrations (n = 4, 106–122 days of age), PRL rose from less than 2 to 4.6 ± 0.6 ng/ ml (P < 0.01) after haloperidol; in fetuses with basal PRL greater than 10 ng/ml (n = 6,113–140 days of age), the mean concentration of PRL increased (P < 0.05) from 32.8 ± 5.9 to 88.2 ± 18.6 ng/ml, and in 5 neonates it increased from 20.1 ± 6.1 to 175.5 ± 26.7 ng/ml (P < 0.005). The response to haloperidol in the neonate was greater (P < 0.05) that that in the late gestation fetus. These observations provide evidence for dopaminergic inhibition of PRL release by 106 days. This mechanism is operative before the rapid rise in PRL concentration in fetal plasma between 110–120 days gestation, suggesting that the high perinatal concentration of PRL is not due to the lack of maturation of dopaminergic control.