Cellular localization of luteinizing hormone receptor immunoreactivity in the ovaries of immature, gonadotropin-primed and normal cycling rats.

In this study we used two monoclonal antibodies against purified LH receptor (LHR) to localize and quantify LHR in ovarian compartments during follicular development, using gonads from immature, gonadotropin-primed, and normal cycling rats. In early preantral follicles, LHR immunoreactivity (LHRI) was identified in vascular endothelium and subsequently appeared in vascular pericytes. In healthy small antral (200-550-microns) follicles, LHRI continued to be present in thecal pericytes, but not in cells of the theca interna. However, in small antral follicles undergoing atresia, a dramatic decrease in thecal vessel LHRI with a concomitant increase in LHRI in hypertrophied theca was observed. In healthy antral follicles, LHRI of thecal cells was not observed until the cells reached medium (550-microns) size. High LHRI was occasionally observed in macrophage-like cells adjacent to the oocyte of large preantral follicles and among granulosa layers of medium-sized antral follicles. In the membrana granulosa, LHRI first appeared in cumulus cells of medium-sized antral follicles and subsequently spread to the entire granulosa cell population of large (750 microns) antral follicles. Treatment of immature rats with eCG markedly enhanced LHRI in theca and granulosa cells of all antral follicles, while eCG/hCG-treated (pseudopregnant) rats showed lack of LHRI in follicles and interstitial glands, but not in corpora lutea (CL). Within degenerating CL in the cycling ovary, compared to fresh and mature CL, a significant decrease occurred in intracellular LHRI. Our observations indicate that 1) vascular pericytes may play a role in follicular development; 2) LHR expression in granulosa may require an interaction of macrophages, oocytes, and cumulus cells; and 3) thecal hypertrophy accompanied by enhanced LHR expression occurs on follicles undergoing atresia.