ESTROGEN REGULATION OF NORADRENERGIC SIGNALING IN THE HYPOTHALAMUS

Hypothalamic circuits utilizing the monoamine neurotransmitter norepin ephrine (NE) may be key elements upon which the ovarian steroids estra diol (E2) and progesterone (P) act to regulate female reproductive beh avior. Recent studies have focused on the modulation of hypothalamic N E release by E2 and P treatments that facilitate sexual behavior. Brai n microdialysis studies suggest that oxytocin, a neuropeptide known to enhance lordosis when infused into the ventromedial hypothalamus (VMH ) of E2 + P-primed females, modulates NE release in the VMH. Systemic administration of oxytocin reliably enhances extracellular NE levels i n the VMH of animals primed with moderate doses of both E2 and P. Thus , ovarian steroids may facilitate female sexual behavior in part by pr omoting oxytocin-induced NE release in the VMH. Studies examining the release of H-3-NE from superfused hypothalamic slices indicate that es trogen treatment also facilitates NE neurotransmission by attenuating alpha2-adrenergic receptor-mediated inhibition of NE release. Hypothal amic alpha2-adrenergic receptors are not downregulated by estrogen, su ggesting that brain adrenoceptor function can be modulated by E2 indep endent of changes in receptor density. A model is proposed wherein E2 and P enhance hypothalamic NE release, leading to increased excitabili ty of VMH neuronal activity and the expression of lordosis behavior.