The Effects of Gonadectomy and Testosterone Treatment on Luteinizing Hormone Secretion in Fetal Rhesus Monkeys*

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Abstract
Experiments were carried out to examine the roles of the gonads and testosterone in the regulation of LH secretion in fetal rhesus monkeys (Macaca mulatto). Male and female fetuses were gonadectomized near midgestation, and the effects on concentrations of plasma LH were determined. Approximately 3 weeks after gonadectomy, LH concentrations in fetal males (n = 7) had risen from 4.24 ± 1.01 μg/ml (mean ± SE) to 46.33 ± 7.92 μg/ml (P < 0.001). Mean LH concentrations in female fetuses (n = 6) before and after gonadectomy were 18.97 ± 2.80 and 22.90 ± 3.95 μg/ml, respectively (P > 0.2). Sham gonadectomy of fetal males (n = 2) had no effect on LH concentrations. Thus, castration results in a dramatic increase in LH levels in male fetuses, but is without effect in females. To determine if testosterone is the primary testicular factor responsible for the inhibition of LH secretion in fetal males and if the hypothalamic-hypophyseal apparatus of the fetal female is sensitive to the negative feedback actions of testosterone, male and female fetuses were given iv infusions of testosterone (25–50 μg/h) approximately 3 weeks after gonadectomy. Paradoxically, testosterone treatment suppressed circulating LH levels in female fetuses (n = 4), but not in males (n = 4). Saline infusion into three gonadectomized fetuses (two males and one female) had no effect on LH levels. These data provide direct evidence for a functional negative feedback relationship between the testes and the hypothalamicpituitary axis in male rhesus fetuses and demonstrate the lack of involvement of the secretions of the fetal ovaries in the regulation of LH secretion in females. The fact that testosterone treatment suppressed LH secretion in gonadectomized females but not in males suggests that there are sex differences in the gonadotropin regulatory mechanism which are either independent of the steroidogenic capability of the gonads or result from prior exposure to gonadal secretions. The data further suggest that either testosterone is not the primary testicular factor suppressing LH secretion in fetal males or gonadectomy of fetal males causes changes in the hypothalamic-pituitary apparatus that render it insensitive to the negative feedback actions of testosterone.

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