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Biology of Reproduction, Vol 24, 747-759, Copyright © 1981 by Society for the Study of Reproduction
1 Department of Reproductive Medicine,
University of California, San Diego,
La Jolla, California 92093 The role of gonadotropin releasing hormone (GnRH) and its antagonist, [D-pGlu1, D-Phe2-DTrp3,6] GnRH, in the direct regulation of ovarian functions was studied in vivo and in vitro.
Immature hypophysectomized rats were treated twice daily with FSH in the presence or absence of
30 µg GnRH or 500 µg antagonist or both. GnRH inhibited FSH stimulation of ovarian weight as
well as LH receptor content and aromatase activity in the ovarian granulosa cells. In contrast,
concomitant treatment with the antagonist blocked the inhibitory effect of GnRH. In cultured
granulosa cells, GnRH treatment resulted in time-dependent inhibition of FSH-induced increase in
estrogen and progesterone production, whereas addition of the antagonist to these cells reversed
the inhibitory effect of GnRH in a time-related manner. Priming with FSH for 2 days in vitro
induced functional PRL and LH receptors. Subsequent treatment with PRL for 2 days stimulated
progesterone production and LH receptor content of these cells in vitro. PRL stimulation of LH
receptor and progesterone production was inhibited by GnRH, whereas concomitant treatment
with the antagonist blocked the GnRH inhibition. The GnRH inhibition of PRL-stimulated progesterone production was time-dependent and the addition of the antagonist to cells treated with PRL
and GnRH reversed the GnRH inhibition in a time-related manner. LH treatment of FSH-primed
granulosa cells stimulated both estrogen and progesterone production, whereas GnRH inhibited the
LH-stimulated steroidogenesis. In contrast, concomitant treatment with the antagonist blocked the
GnRH inhibition of the LH effect. Furthermore, the antagonist blocked the GnRH inhibition of
cholera toxin-induced estrogen and progesterone production in cultured granulosa cells. These results demonstrate the direct inhibitory effect of GnRH upon ovarian functions maintained by FSH, LH, PRL, and cholera toxin and the ability of a GnRH antagonist to block the
GnRH inhibition in a time- and dose-related manner.
Note:
ACKNOWLEDGMENTS
We thank Dr. N. C. Ling (Salk Institute, CA) for
providing GnRH and the GnRH antagonist, Dr. H.
Papkoff (University of California, San Francisco, CA)
for purified ovine LH and FSH, the National Pituitary
Agency, NIAMDD, for ovine FSH, LH, and PRL
preparations, and the Center for Population Research,
NICHHD for purified hCG. We thank Ms. Carol Yoza
for typing the manuscript.
This article has been cited by other articles:
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  G. Irusta, F. Parborell, and M. Tesone Inhibition of cytochrome P-450 C17 enzyme by a GnRH agonist in ovarian follicles from gonadotropin-stimulated rats Am J Physiol Endocrinol Metab, May 1, 2007; 292(5): E1456 - E1464. [Abstract] [Full Text] [PDF]
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G. Irusta, F. Parborell, M. Peluffo, P. R. Manna, S. I. Gonzalez-Calvar, R. Calandra, D. M. Stocco, and M. Tesone Steroidogenic Acute Regulatory Protein in Ovarian Follicles of Gonadotropin-Stimulated Rats Is Regulated by a Gonadotropin-Releasing Hormone Agonist Biol Reprod, May 1, 2003; 68(5): 1577 - 1583. [Abstract] [Full Text] [PDF]
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F. Parborell, A. Pecci, O. Gonzalez, A. Vitale, and M. Tesone Effects of a Gonadotropin-Releasing Hormone Agonist on Rat Ovarian Follicle Apoptosis: Regulation by Epidermal Growth Factor and the Expression of Bcl-2-Related Genes Biol Reprod, August 1, 2002; 67(2): 481 - 486. [Abstract] [Full Text] [PDF]
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