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

TY - JOUR

T1 - The excitation and inhibition of sexual receptivity in female hamsters by progesterone

T2 - Time and dose relationships, neural localization and mechanisms of action

AU - Debold, Joseph F.

AU - Martin, Joseph V.

AU - Whalen, Richard E.

PY - 1976/12

Y1 - 1976/12

N2 - 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 μg) following EB using both excitatory and inhibitory paradigms. Inhibition oi 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.

AB - 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 μg) following EB using both excitatory and inhibitory paradigms. Inhibition oi 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.

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U2 - 10.1210/endo-99-6-1519

DO - 10.1210/endo-99-6-1519

M3 - Article

C2 - 1001252

SN - 0013-7227

VL - 99

SP - 1519

EP - 1527

JO - Endocrinology

JF - Endocrinology

IS - 6

ER -