EFFECT OF LUTEINIZING-HORMONE-RELEASING HORMONE ON THE PITUITARY-GONADAL AXIS IN FETAL AND INFANT RHESUS-MONKEYS

The response of the pituitary-gonadal axis to synthetic LHRH was investigated in fetal (gestational age, 150–159 days), infant (6 months old), and prepubertal (18 months old) rhesus monkeys. In the fetal studies, saline or 80 μg LHRH was adminstered in utero through a cannula placed in the femoral vein. Blood pressure was stable in both fetus and mother throughout each experiment. Immunoreactive serum LH was significantly elevated over control samples in fetal males (n = 3) and females (n = 8) and in infant (n = 6) and prepubertal females (n = 6) after LHRH administration; infant males (n = 4) showed no response. Prepubertal males were not studied. There was no change in LH levels in the maternal circulation after LHRH was given to the fetus, nor was there any change in LH levels in agematched fetuses given saline. Although LH levels were quantitatively different when measured by bioassay and immunoassay, both assays showed an increase in LH after LHRH adminstration. Serum titers of 17β-estradiol (E2) and testosterone (T) were not affected by LHRH-induced LH release in fetal, infant, or prepubertal females. In male fetuses, serum E2 levels were unaffected, but serum T increased an average of more than 300% after LHRH administration. There was neither an LH nor a T response in infant males given LHRH. No change in serum concentrations of E2or T was observed in either fetuses or infants given saline. These data demonstrate that female fetuses, infants, and prepubertal individuals and male fetuses can release LH in response to LHRH. With regard to T or E2secretion, neither near-term fetal nor 6-month-old infant ovaries are as responsive to elevations in serum LH as are fetal testes. © 1979 by The Endocrine Society.