STEROID PRIMING PROMOTES OXYTOCIN-INDUCED NOREPINEPHRINE RELEASE IN THE VENTROMEDIAL HYPOTHALAMUS OF FEMALE RATS

In vivo microdialysis was used to detect norepinephrine (NE) release in the ventromedial hypothalamus of estradiol (E2)- or E2 plus progesterone (P)-treated female rats injected with 1.0 IU of oxytocin (OXY). Dialysates were collected before and after OXY administration on 3 consecutive days and analyzed for NE content by high performance liquid chromatography with electrochemical detection. After the last sample was collected on day 1, animals were injected with 3 mug E2 benzoate or oil. On day 3, E2-primed animals received 200 mug of P and control females received oil prior to OXY administration. OXY administration did not induce NE release on day 1. When OXY was administered to animals that received E2 approximately 20 h earlier, increased release of NE was not consistently seen. In contrast, E2-primed animals that received P on day 3 displayed significant increases in the release of NE after OXY administration compared to their own basal levels and to NE levels in control animals. To distinguish whether E2 priming is sufficient to promote OXY-induced release of NE without the addition of P, NE content of VMH dialysates in a second group of animals was examined following exposure to vehicle or E2 alone. When OXY was administered 24 or 48 h after estrogen priming, only 1 of 4 E2-primed females had modestly elevated dialysate NE levels. To evaluate the interactions between OXY and NE in the regulation of reproductive behavior, lordosis responses were observed in hormone-primed female rats receiving systemic injections of OXY, the alpha1-adrenoceptor antagonist prazosin, or both OXY and prazosin. OXY enhanced lordosis behavior in females primed with subthreshold doses of E2 and P. Prazosin abolished lordosis behavior in rats primed with behaviorally effective doses of E2 and P and significantly inhibited lordosis in steroid-primed females given OXY. These data suggest that after priming with both E2 and P together, but not with E2 alone, OXY may facilitate lordosis behavior through activation of NE transmission.