The Excitation and Inhibition of Sexual Receptivity in Female Hamsters by Progesterone: Time and Dose Relationships, Neural Localization and Mechanisms of Action

Abstract

Ovariectomized hamsters were administered estradiol benzoate (EB) and 44 h later, progesterone (P). Lordosis behavior was induced. When an additional dose of P was given up to 24 h prior to or 24 h after the EB, EB-P facilitation of lordosis was inhibited. Additional hamsters were given varying doses of P (25-200 .mu.g) following EB using excitatory and inhibitory paradigms. Inhibition of EB-induced lordosis was effected with a lower dose of P than was the facilitation of EB induced lordosis by P. Hamsters were also given intracerebral implants of P using excitatory and inhibitory paradigms. No excitatory loci were found. Inhibition of EB-induced lordosis was effected by implants in the posterior hypothalamus and anterior mesencephalon, but not by diencephalic implants. Other hamsters were administered 3H-estradiol (E2) plus P prior to, concurrent with or shortly after the E2. P had no effect upon the accumulation of E2 by any brain sites, although E2 concentrated to a greater degree in the diencephalon than in the mesencephalon or cortex. The estrogen-induced depletion and replenishment of hypothalamic cytosol estrogen receptors was studied. Concurrent P treatment had no effect upon the receptor depletion-replenishment process. P can facilitate and inhibit estrogen-induced lordosis, and the inhibitory effects of P are not upon estrogen-sensitive cells in the brain.