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Endocrinology, doi:10.1210/endo-101-3-818
Endocrinology Vol. 101, No. 3 818-824
Copyright © 1977 by the Endocrine Society.
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The Endocrine Control of Seasonal Reproductive Function in the Ewe: A Marked Change in Response to the Negative Feedback Action of Estradiol on Luteinizing Hormone Secretion1,2

SANDRA J. LEGAN, FRED J. KARSCH and DOUGLAS L. FOSTER

Reproductive Endocrinology Program, Departments of Pathology, Physiology, Biological Sciences, and Obstetrics and Gynecology, The University of Michigan Ann Arbor, Michigan 48109

Abstract

A group of 6 ewes was ovariectomized and treated sc for 20 months with Silastic capsules containing estradiol-17β. Although this treatment maintained serum estradiol concentrations relatively constant at mid-luteal levels (3–5 pg/ml), there was a dramatic seasonal variation in serum LH concentrations. Throughout anestrus, LH levels remained undetectable. At the onset of the breeding season, there was a striking increase in LH concentrations to levels which approached those in untreated ovariectomized ewes. Mean LH concentrations remained high until the beginning of the next anestrous season, when they decreased precipitously to undetectable levels where they remained until the subsequent breeding season. These biannual changes in the negative feedback action of estradiol occurred within 2–3 weeks in each ewe and coincided with the transitions between the breeding season and anestrus in intact ewes. In contrast to the biphasic annual pattern in LH secretion observed in estradiol-treated ovariectomized ewes, there was no major seasonal variation in serum LH concentrations in a group of ovariectomized ewes not treated with estradiol. These findings demonstrate that there is a marked seasonal variation in response of the hypothalamo-hypophyseal axis to the negative feedback action of estradiol, and lead to the formulation of a working hypothesis for the endocrine control of seasonal reproductive function: namely, the occurrence of breeding season or anestrus is governed, at least in part, by the capacity of estradiol to function as a negative feedback hormone.

Footnotes

1 Supported by grants from the NIH (HD-07689, HD-09071, HD-08333) and The University of Michigan.

2 A preliminary report of this study has appeared in Fed Proc 35: 615, 1976.

Received January 13, 1977.




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