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Suppression of Follicle-Stimulating Hormone-Dependent Folliculogenesis during the Primate Ovarian Cycle

Pregnancy Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205
Department of Physiology, Arizona Health Sciences Center Tucson, Arizona 85742
Department of Physiology, University of Maryland Baltimore, Maryland 21202

Address requests for reprints to: Dr. Gary D. Hodgen, Pregnancy Research Branch, Building 18, Room 101, National Institutes of Health, Bethesda, Maryland 20205.

That timely recruitment and selection of the dominant follicle and normal corpus luteum function in the primate ovarian cycle reflect changes in serum FSH levels is well known. Further, in the presence of the dominant follicle, the responsiveness of other follicles to gonadotropic stimulation is transiently attenuated. Thus, the principal question emerged: Does the preovulatory (dominant) follicle maintain its preeminence by actively suppressing the response of other follicles to FSH/LH stimulation during its tenure or, alternatively, does the preovulatory follicle maintain dominance passively by retaining unique responsiveness to gonadotropins in the late follicular phase?

To answer this question, charcoal-extracted porcine follicular fluid (pFF; 5–10 ml) was administered to 23 cycling rhesus monkeys: group I received pFF on cycle days 1–5, group II received pFF on cycle days 6–12, and group III received pFF for 3 consecutive days beginning the day after serum estradiol levels first exceeded 100 pg/ml. Sera were collected daily beginning with the onset of menses and analyzed for LH, FSH, estradiol, and progesterone levels by RIA. When pFF was administered throughout the early (group I) or late (group II) follicular phase of the menstrual cycle, serum FSH concentrations were suppressed (P <0.05) within 24 h and remained subnormal until 1–2 days after discontinuation of therapy. Concurrently, serum estradiol levels were reduced (P < 0.05) during and immediately after pFF administration in both groups. Throughout, LH levels seemed unaffected by pFF administration. In the periovulatory interval (group III), pFF administration was followed by the rapid reduction of circulating FSH and estradiol levels as well as delays in (n = 3) or failure of (n = 4) final follicular maturation leading to ovulation. Thus, in group I, recruitment and selection of the preovulatory follicle were deferred until the restoration of FSH and estradiol to pretreatment levels after the cessation of pFF treatment. In group II, pFF apparently caused the already derived dominant follicle to undergo atresia, followed by recruitment and selection of a new dominant follicle after recovery of serum FSH and estradiol to pretreatment levels. Indeed, the interval during which new and ongoing folliculogenesis were suppressed corresponded directly to the interval of pFF treatment.

The findings reported here favor the interpretation that the dominant follicle requires continued FSH support even in the immediate preovulatory interval.

Received June 12, 1980.