The excitation and inhibition of sexual receptivity in female hamsters by progesterone: time and dose relationships, neural localization and mechanisms of action.

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) following EB using both 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 tritiated 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 was found to concentrate 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 also studied. Concurrent P treatment had no effect upon the receptor depletion-replenishment process. It was concluded that P can both facilitate and inhibit estrogen-induced lordosis and that the inhibitory effects of P are not upon estrogen-sensitive cells in the brain.