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Reevaluation of the Role of Progesterone in Stimulating Sexual Receptivity in Estrogen-Treated Gilts¹

U.S. Department of Agriculture², Clay Center, NE 68933

Abstract

Three studies were conducted to examine the role of progesterone in stimulating sexual receptivity in estrogen-treated, ovariectomized gilts. Progesterone was administered either before, simultaneously with, or 48 h after estrogen. In each study, gilts were treated with either a sub-optimal or an optimal dosage of estradiol benzoate (EB). Progesterone treatment (600 µg·kg BW^–1 · injection^–1) on alternate days for a total of four injections produced serum concentrations of progesterone that were maximal at 9.4 ng/ml and remained greater than 1 ng/ml for 15 d. Estradiol benzoate was administered 22 d after the first of these progesterone injections. When progesterone was administered concurrently with or 48 h after EB, the dosage was 100 µg/kg BW and produced a maximal serum progesterone concentration of 1.8 ng/ml 4 h after treatment. Gilts were placed in an evaluation pen with a boar for 5 min on d 3 and 4 after EB treatment. Traits of interest were total number of mounts by the boar, mounts before the gilt showed the immobilization response, proportion of gilts that showed the immobilization response, and latency from entry of the gilt into the evaluation pen until the immobilization response. In none of the three studies did progesterone improve any of the traits of interest. In each study the immobilization response was observed in a higher proportion of gilts treated with the optimal than in those treated with the suboptimal dosage of EB. Latency from entry of gilts into the evaluation pen until the immobilization response was less on d 4 than on d 3 after EB in all studies. Observations from the present studies indicate that progesterone has no facilitative effect on the stimulatory action of estrogen in expression of sexual receptivity in gilts. Thus, defeminization of sexual receptivity in male pigs apparently does not involve modification of progesterone-sensitive neural processes.

¹ I thank J. Dague, S. Prager, A. Hultine and L. Parnell for their technical assistance. Cooperation of the Nebraska Agr. Exp. Sta., Univ. of Nebraska, Lincoln, is acknowledged.

² Agricultural Research Service, Roman L. Hruska U.S. Meat Animal Research Center. Mention of trade names or companies does not constitute an implied warranty or endorsement by the USDA or the author.