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BOR - Papers in Press, published online ahead of print March 16, 2005.
Biol Reprod 2005, 10.1095/biolreprod.105.040329
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BIOLOGY OF REPRODUCTION 73, 115–122 (2005)
DOI: 10.1095/biolreprod.105.040329
© 2005 by the Society for the Study of Reproduction, Inc.

A Nongenomic Action of 17ß-Estradiol as the Mechanism Underlying the Acute Suppression of Secretion of Luteinizing Hormone1

J. Alejandro Arreguin-Arevalo , and Terry M. Nett 2 

Department of Biomedical Science, Colorado State University, Fort Collins, Colorado 80523

The objective of the present study was to determine the ability of 17ß-estradiol (E2) and conjugated forms of E2 (E2 conjugated to BSA [E2-BSA] and a novel conjugate, E2 conjugated to a small peptide [E2-PEP]) to prevent the GnRH-induced secretion of LH and to determine the role of estradiol receptors (ERs) and ER subtypes (ER{alpha}, also known as ESR1, and ERß, also known as ESR2) in the mediation of the acute action of E2 in primary cultures of ovine pituitary cells. Preincubation of cells for 15 min with E2, E2-BSA, or E2-PEP prevented the GnRH-induced secretion of LH (P < 0.01). Treatment of cells with nonestrogenic steroid hormones did not affect secretion of LH when given alone, nor did these steroids impair the E2-induced inhibition of LH secretion (P > 0.1). Likewise, treatment of cells with the ER-antagonists tamoxifen, hydroxytamoxifen, or ICI 182 780 did not affect (P > 0.1) secretion of LH when given alone but did prevent (P < 0.01) the inhibition by E2 and the E2-conjugates on GnRH-induced secretion of LH. When cells were treated with subtype-selective ER agonists, the ER{alpha} agonist (propylpyrazole-triol), but not the ERß agonist (diarylpropionitrile), decreased (P < 0.01) the GnRH-induced secretion of LH. In conclusion, the rapidity by which E2 prevented GnRH-induced release of LH in ovine pituitary cells suggests that this inhibition is mediated via a nongenomic action of E2. The inhibition of GnRH-induced secretion of LH proved to be steroid specific and mediated by ERs. It may occur specifically through ER{alpha}. The fact that E2-BSA or E2-PEP mimicked the action of E2 suggests that this effect was mediated by an ER associated with the plasma membrane.

anterior pituitary, estradiol, estradiol receptor, gonadotropin-releasing hormone, luteinizing hormone

1 Supported by a grant from the Colorado State University Agricultural Experiments Station. The academic program of J.A.A.-A. was supported by the National Council for Science and Technology (CONACYT-Mexico) and the National Institute for Research in Forestry, Agriculture, and Livestock (INIFAP-Mexico).

2 Correspondence: Terry M. Nett, Animal Reproduction and Biotechnology Laboratory, Department of Biomedical Science, 3801 W Rampart Rd., Fort Collins, CO 80523-1683. FAX: 970 491 3557; terry.nett{at}colostate.edu




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