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Biology of Reproduction, Vol 25, 134-142, Copyright © 1981 by Society for the Study of Reproduction
1 Dept. of Physiology, West Virginia University, Morgantown, WV 26506. The contributions of the follicular phase increase in LH and the decrease in progesterone to the
determination of the preovulatory estradiol rise in the ewe were examined by mimicking these
changes, separately or in combination, in seasonally anestrous animals. Prior to this test, each ewe
was pretreated for 15 days with Silastic implants containing progesterone to produce an artificial
luteal phase. The implants were then either removed or left in place, and purified ovine LH was
infused to simulate the progressive increase in mean serum LH concentrations seen during the
follicular phase of the estrous cycle. If LH was not given, the concentration of estradiol remained
low and constant, whether or not progesterone was withdrawn. When LH was infused after progesterone withdrawal (n = 8), a significant increase in serum estradiol from 1 to 5 pg/ml resulted. Four
of these ewes had an LH surge, which induced ovulation and formation of functional corpora lutea.
In these ewes, estradiol fell precipitously within 4 h of the LH peak. In the other four animals, no
LH surge occurred and estradiol remained elevated until the end of the infusion. When a luteal
phase progesterone concentration was maintained, LH infusion produced an elevation in serum
estradiol, but the response was significantly less (P<0.01) than that produced by LH when progesterone was withdrawn. These data suggest that, in the ewe, the follicular phase estradiol rise is driven by the sustained
increase in tonic LH secretion and is terminated by the preovulatory LH surge. The fall in progesterone at luteolysis probably contributes to the estradiol rise in 2 ways: 1) it allows the requisite
increase in tonic LH secretion; and 2) it increases the response of the follicle to this LH increase.
Finally, by demonstrating that the ovary of the anestrous ewe can produce an estradiol rise in
response to a follicular phase increment in LH, these studies provide important support for the
hypothesis that a primary cause of seasonal anestrus is the absence of a sustained rise in tonic
LH secretion.
2 Department of Biochemistry,
The Albany Medical College of Union University,
Albany, New York 12208
3 Dept. of Physiology and Biophysics, University of Kentucky, Lexington, KY 40536.
4 Dept. of Physiology, University of Pittsburgh, Pittsburgh, PA 15261.
5 Reproductive Endocrinology Program, Departments of Pathology, Physiology,
Biological Sciences and Department of Obstetrics and Gynecology,
The University of Michigan, Ann Arbor, Michigan 48109
Note:
ACKNOWLEDGMENTS
We wish to thank Douglas Doop for his help with
the animal experimentation, Barbara Glover for
estradiol measurements, Mark Byrne for preparation
of iodinated hormones used in the assays, Dr. G. D.
Niswender for antisera, and NIAMDD for rat FSH
used in the FSH RIA. The advice of Dr. J. S. Richards
on the preparation of this manuscript is also greatly
appreciated.
This article has been cited by other articles:
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  J. Pielecka, S. D. Quaynor, and S. M. Moenter Androgens Increase Gonadotropin-Releasing Hormone Neuron Firing Activity in Females and Interfere with Progesterone Negative Feedback Endocrinology, March 1, 2006; 147(3): 1474 - 1479. [Abstract] [Full Text] [PDF]
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 T.A. Richter, J.E. Robinson, and N.P. Evans Progesterone Blocks the Estradiol-Stimulated Luteinizing Hormone Surge by Disrupting Activation in Response to a Stimulatory Estradiol Signal in the Ewe Biol Reprod, July 1, 2002; 67(1): 119 - 125. [Abstract] [Full Text] [PDF]
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