Monoamines, estrogen and female sexual behavior in the golden hamster

Abstract

In the golden hamster drugs which inhibit monoaminergic function (includingp-chlorophenylalanine (PCPA), methysergide and?-methyl-p-tyrosine (?-MPT) facilitated lordosis in ovarietomized female hamsters as a function of the duration of estradiol benzoate (EB) priming. ?-MPT (200 mg/kg), methysergide (6 mg/animal) or PCPA (150 or 360 mg/kg) potentiated lordosis if 6 days of EB priming preceded drug treatment. However, if female hamsters were primed with EB for only 2 days, ?-MPT and methysergide were ineffective. PCPA (360 mg/kg) was less effective after 2 days of EB than after 6 days of EB priming. ?-MPT produced a three-fold elevation in progesterone levels in ovariectomized females but methysergide and PCPA did not influence serum progesterone. PCPA (360 mg/kg) facilitated lordosis in adrenalectomized, ovariectomized females, eliminating the possibility that adrenal progesterone is essential for the behavioral effects of the drug. Luteinizing hormone-releasing hormone levels in the preoptic/anterior hypothalamic area and the medial basal hypothalamus were also not significantly altered at 1 h after PCPA injection. Pimozide (1.5 mg/kg) and pimozide (1.5 mg/kg) and amphetamine (2.5 mg/kg) did not potentiate lordosis in ovariectomized hamsters after either 2 or 6 days of EB priming. Pargyline, a monoamine oxidase inhibitor, inhibited female sexual behavior in females in estrogen alone-induced estrus. Lordosis in the female rat is more readily elicited both by drugs and estrogen. It is proposed with regard to female sexual behavior that species differences in estrogen sensitivity may underlie apparent differences in drug sensitivity.