6-hydroxydopamine lesions enhance progesterone-facilitated lordosis of rats and hamsters, independent of effects on motor behavior.
Ovariectomized female rats received two intraventricular injections of 200 microgram of 6-hydroxydopamine (6-OHDA), a treatment which produced 66% depletion of telencephalic norepinephrine and 53% depletion of telencephalic dopamine. Compared to vehicle-injected controls, 6-OHDA-treated animals showed increased lordosis scores when treated with ovarian hormones. This effect was potentiated by additional treatment with 100 mg/kg alpha-methyl-p-tyrosine (AMT), a catecholamine synthesis inhibitor. Besides showing increased frequency and intensity of lordosis, animals treated with both 6-OHDA and AMT retained the lordotic posture significantly longer after the male dismounted than animals given either treatment alone or vehicle controls. The enhancement of lordosis following CA depletion was not prevented by a series of dexamethasone treatments which caused a marked suppression in adrenal steroid (corticosterone) levels. This suggests that normal adrenal function is not a prerequisite for the observed enhancements. It was concluded that the lordotic response is inhibited by the activity of a catecholamine system. Soliciting behavior (hop-darting) was not enhanced by any treatment, suggesting that catecholamine activity has an inhibitory influence on the stop component of sexual behavior, but not on the whole copulatory pattern.