Abstract

Two experiments were conducted to test the hypothesis that progesterone (P 4) acts to induce a preovulatory rise of luteinizing hormone (LH) by initiating a true positive feedback interaction between P 4 and LH. In each experiment, ten hens were stereotaxically implanted with a third ventricle cannula. Aminoglutethimide phosphate (AGP), an inhibitor of steroidogenesis, was administered (200 mg iv) to hens at 10 and 6 hr (Experiment 1) and 10 and 7 hr (Experiment 2) before an expected C 1 ovulation. A 20-μg injection of P 4 ( n = 5) or the vehicle ( n = 5) was made intraventricularly at 6 hr (Experiment 1) or 7 hr (Experiment 2) before the expected ovulation. Blood samples were taken via branchial vein cannula at regular intervals after the injection. In Experiment 1, four of five P 4-treated hens ovulated, and no atretic follicles were found in any of the five P 4-treated hens, including the one which did not ovulate. Ovulations were always accompanied by preovulatory LH peaks. By comparison, none of the vehicle-injected animals ovulated and in four of five hens the largest follicle was determined to be atretic. No ovulations occurred in Experiment 2 for either the P 4- or vehicle-injected hens. Atresia of the largest follicle occurred in all five hens in the P 4-treated group and four of five hens of the vehicle-treated group. The difference in results between Experiment 1 and Experiment 2 can be explained assuming that the steroidogenesis-inhibiting action of the initial AGP injection in Experiment 1 (at 10 hr before ovulation) had diminished prior to the second AGP treatment (at 6 h before ovulation). In both Experiments 1 and 2, intraventricular P 4 injection caused a significant ( P < 0.001 for Experiment 1; P < 0.03 for Experiment 2) rise in plasma P 4 within 10 min after injection due to leakage of P 4 from the third ventricle into the systemic circulation. Nevertheless, in the absence of any steroid feedback from the ovary (Experiment 2), the small rise in LH induced by the P 4 injection was not potentiated, and no preovulatory surge of LH occurred. These results support the hypothesis that a positive feedback interaction between P 4 and LH, in contrast to a stimulatory effect of P 4, is necessary for the preovulatory LH surge and ovulation.

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