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Progesterone Promotes Oocyte Maturation, but Not Ovulation, in Nonhuman Primate Follicles Without a Gonadotropin Surge¹

Oregon National Primate Research Center,³ Beaverton, Oregon 97006 Department of Physiology,⁴ Medical College of Georgia, Augusta, Georgia 30912 Department of Physiology and Pharmacology,⁵ Oregon Health and Science University, Portland, Oregon 97239

During the periovulatory interval, intrafollicular progesterone (P) prevents follicular atresia and promotes ovulation. Whether P influences oocyte quality or maturation and follicle rupture independent of the midcycle gonadotropin surge was examined. Rhesus monkeys underwent controlled ovarian stimulation with recombinant human gonadotropins followed by a) experiment 1: an ovulatory bolus of hCG alone or with a steroid synthesis inhibitor (trilostane, TRL), or TRL + the progestin R5020; or b) no hCG, but rather sesame oil (vehicle), R5020, or dihydrotestosterone (DHT). In experiment 1, the majority of oocytes remained immature (65% ± 20%) by 12 h post-hCG. However, the percentage of degenerating oocytes increased (P < 0.05) with TRL (42% ± 22% vs. 0% controls), but was reduced (P < 0.05) by progestin replacement (15% ± 7%). By 36 h post-hCG, the majority of oocytes in all three groups reached metaphase II (MI). In experiment 2, no evidence of follicle rupture was observed in the vehicle, R5020, or DHT groups. Despite the absence of hCG, a significant (P < 0.05) percentage of oocytes resumed meiosis to metaphase I in R5020- (41 ± 9) and DHT- (36 ± 15) but not vehicle- (4 ± 4) treated animals. Only oocytes from R5020-treated animals continued meiosis in vivo to MII. More (P < 0.05) oocytes fertilized in vitro with R5020 (40%) than with vehicle (20%) or DHT (22%). Thus, P is unable to elicit ovulation in the absence of an ovulatory gonadotropin surge; however, P and/or androgens may prevent oocyte atresia and promote oocyte nuclear maturation in primate follicles.

¹ Supported by NICHD/NIH though cooperative agreement U54 HD18185 as part of the Specialized Cooperative Centers Program in Reproductive Research and National Institute of Health grants 2T32 HDO7133 (S.M.B.), RR00163 (R.L.S.), and HD20869 (R.L.S.).

² Correspondence: Mary B. Zelinski-Wooten, Oregon National Primate Research Center, 505 NW 185th Ave., Beaverton, Oregon 97006. FAX: 503 690 5563; zelinski{at}ohsu.edu

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