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Stimulation of Pituitary-Testicular Function with Gonadotropin-Releasing Hormone in Fetal and Infant Monkeys^*

ILPO T. HUHTANIEM^,, DONALD R. KORITNIK, CAROL C. KORENBROT, STEWART MENNIN^,, DALLAS B. FOSTER and ROBERT B. JAFFE

Reproductive Endocrinology Center, Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Francisco, California 94143

Abstract

To assess the integrity of the pituitary-gonadal axis in the perinatal period and infancy, fetal and infant male monkeys (n = 22) were challenged with synthetic hypothalamic gonadotropin-releasing hormone (GnRH) between 130 days of gestation and 1 yr after birth. LH and testosterone responses were measured. Intravenous administration of either 10 or 50 µg GnRH to catheterized fetuses in utero resulted in a mean LH increase of 857 ± 494% (SEM) and a mean testosterone increase of 69 ± 28% above basal levels. During the 4 days after delivery, 3–10 µg (10–20 µg/kg) GnRH stimulated similar rises in LH (592 ± 201%) and testosterone (93 ± 23%). From 18–89 days of age, a dose of 10–20 µg/kg resulted in a mean LH response of 862 ± 116% and the greatest testosterone response (371 ± 101%). After 3 months of age, LH and testosterone responses to the same dose of GnRH declined (174 ± 86% and 133 ± 37%, respectively, for ages 102–218 days; 16 ± 11% and 44 ± 30%, respectively, for ages 286–392 days). In other monkeys, sc injections of GnRH in slow release form (500 µg every 2 weeks) produced high testosterone levels (6–10 ng/ml) until 65–80 days of age. No stimulation was seen after this time. It is concluded that, in the perinatal period, the male monkey pituitary-gonadal axis responds to GnRH. After birth, the pituitary-gonadal axis reaches peak responsiveness to GnRH between 2 weeks and 3 months of age. Thereafter, this increased responsiveness declines regardless of whether the infant is exposed repetitively to GnRH. These findings correlate well with changes seen in pituitary and gonadal function in the human male infant.

Footnotes

^* This work was supported in part by NIH Grant HD-08478 and a grant from the Rockefeller Foundation. Portions of these studies were presented at 24th Annual Meeting of the Society for Gynecologic Investigation, Tucson, AZ, March 1977.

Postdoctoral Fellow in Reproductive Endocrinology.

Supported by NIH International Research Fellowship F05-TW 2243.

Supported by NICHD Fellowship HD-01001.

To whom requests for reprints should be addressed.

Received October 27, 1978.