Progesterone-induced sequential inhibition of copulatory behavior in hysterectomized rats: Relationship to neural cytoplasmic progestin receptors

Abstract

The inhibitory effects of progesterone on the copulatory behavior and on neural cytoplasmic progestin receptors were examined in ovariectomized (DV) and ovariectomized-hysterectomized (OH) rats. Ovariectomized and OH rats were given 2.0 μg of estradiol benzoate (EB) followed 24 hr later by 0.1, 0.5, 0.1 or 2.0 mg of progesterone (P) and were tested for lordosis 6 hr later (30 hr). Twenty four hr after the first P treatment, all animals received 0.5 mg of P and were tested again (54 hr). The initial doses of 1.0 and 2.0 mg of P significantly reduced lordosis quotients in response to the subsequent P treatment in OV animals but only the 2.0 mg dose of P effectively suppressed lordosis in OH animals. In order to determine whether the priming dose of EB influences the inhibitory effects of progesterone, OV and OH rats were injected with 1.0 μg of EB followed by 1.0 mg of P, or 6.0 μg of EB followed by 2.0 mg of P and were tested for receptivity under the same schedule. Treatment with 1.0 μg of EB permitted, and 6.0 μg of EB prevented sequential inhibition of sexual behavior by progesterone in both OV and OH rats. Hypothalamic cytoplasmic progestin ([ 3H]R5020) receptors were then measured 48 hr after EB injection in OV or OH rats given the same treatments with EB and P. Hypothalamic progestin receptors were significantly lower in OV animals given 2.0 μg of EB followed by 1.0 or 2.0 mg of P than oil-treated controls, but only the 2.0 mg dose of P significantly reduced receptors in OH rats. The 1.0 mg dose of P significantly depleted hypothalamic progestin receptors in OV and OH animals given just 1.0 μg EB. The result of these experiments indicate a close correlation between the progesterone-induced inhibition of copulatory behavior and the ability of the steroid to deplete its own receptors and suggest that the higher dose of progesterone required to inhibit receptivity in OH animals may be due to the enhanced induction of hypothalamic progestin receptors by EB following hysterectomy. The latter finding is consistant with the generally increased effectiveness of estradiol in OH rats.