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A Previously Undescribed Role for Luteinizing Hormone (LH:hCG) on Follicular Cell Differentiation^*

JAMES J. IRELAND and JOANNE S. RICHARDS

Reproductive Endocrinology Program, Department of Pathology, The University of Michigan Ann Arbor, Michigan 48109

Abstract

Experiments were designed to determine if an ovulatory dose of human CG (hCG) could act on ovarian preantral follicles to modify the ability of FSH to stimulate follicular growth and to increase the number of gonadotropic hormone receptors in granulosa cells. Hypophysectomized, immature rats were primed with 2.0 mg estradiol or vehicle for 3 days. Subsequently, groups of rats received either 2 µg human FSH (hFSH), 5 IU hCG, hFSH followed 12 h later by hCG, or hCG followed 12 h later by hFSH. In estradiol-primed rats hFSH stimulated a transitory increase in granulosa cell LH receptor by 24 h and an 1.5-fold increase in FSH receptor by 12 h. hCG alone had little or no effect. In contrast, hCG followed by hFSH stimulated a dramatic 15-fold increase in LH receptor by 36 h, a 3-fold increase in FSH receptor by 48 h, and marked development of antral follicles. hFSH followed by hCG also resulted in pronounced follicular growth and marked increases in LH and FSH receptors in granulosa cells. Neither estradiol (2.0 mg) nor testosterone (2 mg) mimicked the effects of hCG when administered 12 h after hFSH. Vehicle-primed hypophysectomized rats did not respond to the various gonadotropin treatments. Thus, hCG can act on estradiol-primed preantral follicles to enhance the ability of FSH to stimulate the growth of preovulatory follicles and to induce the appearance of gonadotropin receptors. These effects of hCG are in marked contrast to the known ability of ovulatory doses of LH and hCG to cause luteinization and a loss of LH and FSH receptors in the granulosa cells of antral follicles. Thus, during the final stages of follicular growth before ovulation, LH, as well as FSH, may be capable of acting to stimulate granulosa cell differentiation and an increase in LH receptors. (Endocrinology 102: 1458, 1978)

Footnotes

^* This work was supported by NIH Grants HD-08333 and HD-09110.

NICHHD Postdoctoral Fellow (F32 HD05240-01A1). To whom requests for reprints should be addressed.

Received July 27, 1977.

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