Gap junction amplification in rat ovarian granulosa cells. I. A direct response to follicle-stimulating hormone.
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abstract
The ability of follicle-stimulating hormone (FSH), the estrogens, estradiol-17 and diethylstilbestrol, and the estrogen antagonists, clomiphene and enclomiphene citrate to affect the growth and internalization of hypophysectomized rat granulosa cell gap junction membranes was compared in ovarian follicles assigned to one of four follicle size classes (60-149, 150-249, 250-319, and 320-450 m diameter). In the absence of exogenous hormone stimulation, atresia prevents follicle growth beyond 320 m in diameter but surface gap junction membrane increases throughout this early follicle growth. Internalization of gap junction membrane is first detected at the 150- to 249-m follicle stage and also increases with follicle size. Therefore, growth and turnover of gap junction membrane occur at a basal rate in the absence of gonadotropin or steroid hormone stimulation. Estrogen and estrogen antagonist injections result in no significant differences in the amount of surface or internalized junction membrane in the three smallest follicle size classes when compared to the untreated hypophysectomized animals. However, estrogen but not estrogen antagonists rescues growing follicles from atresia and permits their further growth into the 320- to 450-m follicle size class. As a result of the additional follicle growth, both surface and internalized junction membrane increase beyond that seen in the largest follicles from hypophysectomized animals. In contrast to other treatments, FSH stimulation promotes amplification of gap junction membrane in all size classes and, like estrogen, rescues follicles from atresia and promotes their entry into the 320- to 450-m follicle size class. Surface gap junction membrane is amplified two- to fourfold over other treatments in the first three follicle size classes, but reaches maximal levels in the 250- to 319-m follicles. The internalized junction membrane which first appears in the 150- to 249-m size class is dramatically increased over other treatments in the 250- to 319- and 320- to 450-m size classes. These studies indicate that exogenous estrogen stimulation promotes gap junction growth indirectly by sustaining the basal rate of junction synthesis in follicles rescued from atresia. In contrast, exogenous FSH stimulation directly amplifies the developmental sequence of gap junction growth and turnover. During early follicle growth, FSH stimulation preferentially promotes increases in surface gap junctions while internalization of surface junctions is increased during later follicle growth. 1982.
