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*Compound via MeSH
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*ESTRADIOL
*MENOTROPINS
*TESTOSTERONE

Endocrinology, Vol 118, 2225-2234, Copyright © 1986 by Endocrine Society


ARTICLES

Control of gonadotropin secretion in the male during puberty: a decrease in response to steroid inhibitory feedback in the absence of an increase in steroid-independent drive in the sheep

DH Olster and DL Foster

The gonadostat hypothesis, i.e. that a decrease in response to the inhibitory feedback action of gonadal steroids occurs during puberty, was tested in the male lamb. Also investigated was whether a simultaneous steroid-independent rise in gonadotropin secretion could be the underlying mechanism for the reduction in steroid feedback sensitivity during puberty. Sexual maturation in intact Suffolk lambs was characterized by increases in all of the following parameters: Serum FSH and LH and LH pulse frequency (during 4-7 weeks of age), testicular size and testosterone (T) concentrations (during 7-28 weeks of age). Estradiol (E2) levels were elevated at 32 weeks. Motile spermatozoa were produced by 16-18 weeks of age. Castration at 5 weeks of age resulted in a prompt increase in gonadotropin concentrations. LH pulse frequency reached a plateau of approximately 5 pulses/4 h (n = 5) at 7 weeks of age and did not change thereafter. T or E2 replacement suppressed pulsatile LH secretion for several weeks. However, despite maintenance of constant serum T (approximately 1.0 ng/ml) or E2 (3-5 pg/ml) concentrations, LH pulse frequency began to increase after 9 weeks of age, and by 13 weeks, pulsatile secretion was apparent in all steroid-replaced castrated lambs. This was well after LH pulse frequency had ceased to increase in untreated castrated animals. These data support the gonadostat hypothesis for puberty in the male lamb. Furthermore, the temporal dissociation of increasing LH secretion in untreated castrated lambs and steroid-replaced castrated lambs suggests that a steroid-independent increase in gonadotropin secretion is not the mechanism underlying the decrease in responsiveness to steroid negative feedback.


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