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Blockade of Neonatal Activation of the Pituitary-Testicular Axis: Effect on Peripubertal Luteinizing Hormone and Testosterone Secretion and on Testicular Development in Male Monkeys^*

Department of Physiology, Morehouse School of Medicine (D.R.M.) Atlanta, Georgia 30310
Yerkes Regional Primate Research Center (K.G.G., K.W.), and the Department of Psychology, Emory University (K.W.) Atlanta, Georgia 30322
Departments of Biochemistry and Medicine, Medical Research Service, Veterans Administration Medical Center (D.C.C.) Decatur, Georgia 30033

Address all correspondence and requests for reprints to: David R. Mann, Ph.D., Department of Physiology, Morehouse School of Medicine, 720 Westview Drive SW, Atlanta, Georgia 30310.

The objective of this study was to examine the effect of blockade of neonatal activation of the pituitary-testicular axis, using a GnRH agonist, on sexual development in male rhesus monkeys. Monkeys were treated with either a GnRH agonist (10 µg/day; n = 8) or vehicle (n = 9) for 112 days using osmotic minipumps beginning at 10–13 days of age. In control monkeys serum LH and testosterone concentrations during the first 3 postnatal months were similar to those in adults; they then declined to very low levels. GnRH agonist administration caused an immediate and precipitous decline in serum LH and testosterone concentrations to very low levels, and both remained low throughout the rest of the agonist administration period. Neither group had any significant elevation in serum LH or testosterone concentrations during the next 2 yr. In the control monkeys serum LH and testosterone began to rise during the third year, with a rapid increase occurring during the fall coincident with the breeding season. This peripubertal rise of LH and testosterone secretion was associated with rapid enlargement of the testes and the appearance of sperm in ejaculates. The monkeys who had received GnRH agonist had subnormal serum LH and testosterone increases, and testicular enlargement was also attenuated compared to that in the control animals during the third year of life. Semen samples were recovered from only 50% of the GnRH agonist-treated monkeys during this period, and the sperm count per ejaculate was suppressed. The serum LH responses of the GnRH agonist-treated monkeys to an iv bolus dose of GnRH (5 µg/kg BW) during the third year were normal. These results suggest that the induction of reversible hypogonadotropin-hypogonadism in neonatal male monkeys alters subsequent testicular development and peripubertal endocrine changes. Thus, neonatal activation of the pituitary-testicular axis may be a critical developmental event in the process of sexual development in male primates.

^* This work was supported by NIH Grants RR-08248 (via cofunding from the NIMH), RR-00165, and HD-23295; NSF Grant BNS 86-07295; and USAID Grant DAN-5053-G-SS-5018-00.

Received August 25, 1988.

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