Abstract
Stimulation of cAMP production by luteinizing hormone (LH) or follicle stimulating hormone (FSH) is markedly reduced when whole prepubertal rat ovaries (from 23-24 day old rats) are preincubated for 2-3 hours with the homologous hormone, or when the rats are injected with the homologous hormone 2-3 hours before excision of the ovary. Full responsiveness to LH or FSH, respectively, is restored 8-12 hours after the injection of the homologous hormone. When the prepubertal ovary is in-cubated in the presence of gonadotrophins together with puromycin or cycloheximide, the effects of both LH and FSH on cAMP formation are drastically prolonged, demonstrating that inhibitors of protein synthesis can inhibit the development of refractoriness. Preovulatory follicles of the rat ovary show decreased sensitivity to LH stimulation in vitro when extirpated 3-6 hours after the endogenous LH-FSH surge (evening follicles), as compared to the stimulation of the cAMP system seen in follicles extirpated before the gonadotrophin surge (morning follicles). However, granulosa cells isolated from evening follicles did not show refractoriness to LH-stimulation: LH markedly stimulated cAMP production in these cells. Addition of follicular fluid (approximately 1%) to the isolated granulosa cells inhibited LH stimulation of the cAMP system. Development of refractoriness to LH was also studied in corpora lutea from pregnant mare serum gonadotrophin (PMSG) injected immature rats. In vitro addition of LH to three and five day old corpora lutea markedly stimulated the production of cAMP. When LH or human chorionic gonadotrophin (HCG) was injected 2-4 hours before excision of the corpora lutea, LH stimulation in vitro was markedly reduced. Full responsiveness to LH in vitro was regained 12-24 hours after injection of LH. The duration of refractoriness to LH was much longer after injection of HCG: full responsiveness was not seen until 4-6 days after its administration.
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