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Biology of Reproduction, Vol 21, 419-423, Copyright © 1979 by Society for the Study of Reproduction

Synergistic Effects of Prolactin and Estradiol in the Luteotropic Process in the Pregnant Rat: Regulation of Estradiol Receptor by Prolactin

GEULA GIBORI 1, JOANNE S. RICHARDS 2, , and P. LANDIS KEYES 2

1 Department of Physiology and Biophysics, University of Illinois at the Medical Center, Chicago, Illinois 60612
2 Reproductive Endocrinology Program, Department of Pathology, Department of Physiology, The University of Michigan, Ann Arbor, Michigan 48109


Our findings that the direct luteotropic effect of estrogen was dependent on the presence of prolactin or rat placental lactogen have suggested to us that prolactin may control estrogen receptor content in the corpora lutea of pregnant rats. To test this hypothesis, the cytosolic and nuclear contents of estrogen receptor were measured in the corpora lutea of pregnant rats in which endogenous prolactin was removed by 1) hypophysectomy and hysterectomy on Day 9, or 2) treatment with ergocryptine (1 mg/rat) on Day 6. Within 24 h, nuclear content of estrogen receptor in lutea cells dropped by 70% in hypophysectomized-hysterectomized rats and 75% in ergocryptine treated rats, while cytosol content dropped by 40% and 38%, respectively. Estradiol treatment (100 µg/ day) did not prevent the decrease in cytosolic or nuclear receptor, whereas prolactin (250 µg/ day) or serum containing rat placental lactogen did maintain luteal cell cytoplasmic receptor content. Nuclear content of estradiol receptor was maintained in ergocryptine treated rats by administration of prolactin alone. However, estradiol had to be administered with prolactin in hypophysectomized-hysterectomized rats to achieve the same effect, suggesting that after ergocryptine treatment intraluteal concentrations of estrogen were sufficient to affect the translocation of cytosolic receptor to the nucleus.

These studies indicate that the synergistic action of prolactin with estradiol in the luteotropic process in the pregnant rat may involve, in part, prolactin stimulation of luteal receptor for estradiol, a prolactin dependent response not previously reported.

Note:
ACKNOWLEDGMENTS We wish to thank Katherine Kersey and Janet Lee Chien for technical assistance, Dr. Leo E. Reichert, Jr. and the Endocrinology Study Section, NIH, for the ovine prolactin and Ms. K. D. Roskaz, Sandoz Pharmaceuticals, East Hanover, NJ for the gift of 2-Br-agr-ergocryptine (CB-154).

Submitted on February 14, 1979
Accepted on April 16, 1979




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