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Biology of Reproduction, Vol 24, 1056-1060, Copyright © 1981 by Society for the Study of Reproduction
1 Reproductive Physiology,
Oregon Regional Primate Research Center,
Beaverton, Oregon 97006 To understand further the testicular components of feedback control of gonadotropins in
primates, we studied feedback regulation in six cryptorchid (CO) and three sham-operated (control) rhesus monkeys (Macaca mulatta) that were castrated (Day 0) 420 days after the initial
operation. Gonadotropins [luteinizing hormone (LH) and follicle stimulating hormone (FSH)],
testosterone (T), and estradiol-17
3 (E2) were quantified by radioimmunoassay in serum collected
daily from Days 1 to 21, 33 to 40, and 48 to 55. Serum was collected on alternate days from Day
59 to Day 97. After castration CO and control monkeys were treated identically: T and E2 in
Silastic capsule implants from Day 0 to Day 58, T only from Day 59 to Day 80, and no treatment
after Day 80. Serum concentrations of T fluctuated between 5 and 10 ng/ml, and E2 fluctuated
between 25 and 60 µg/ml during treatment. Each animal received a single s.c. injection of estradiol
benzoate (EB), 42 µg/kg BW, on Days 1 to 3, 16, 35, and 50 to establish the onset of "positive
feedback" responses to estrogen with time after castration. None of the animals released LH or
FSH in response to EB given on Days 1 to 3. By Day 16, all CO animals released LH and FSH in
response to EB, but none of the control monkeys responded. A similar difference in LH levels
between CO and control monkeys was found on Day 35. Finally, on Day 50 the amount of LH
released in response to EB in one of these control animals was similar to the amount release in CO
animals. Treatment with T plus E2 maintained basal LH at precastration levels for 58 days when
E2 was removed. Serum LH gradually rose to postcastration levels thereafter. Baseline FSH, on the
other hand, was significantly elevated on Day 16 in serum from CO animals only. These data
suggest that cryptorchidism in nonhuman primates affects responsiveness of the hypothalamic-pituitary axis to feedback control by steroids. Furthermore, our data appear relevant to the enigma
of the inability of estrogen to affect gonadotropin release when the testes are present, i.e., they
suggest that a substance (or substances) produced by the germinal epithelia is responsible for this
blockade of estrogen action.
Note:
ACKNOWLEDGMENTS
The work described in this article, Publication No.
1141 of the Oregon Regional Primate Research
Center, was supported by NIH Grants RR-00163 and
HD-11982.
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