The ovarian steroids estradiol (E(2)) and progesterone (P) act on target neurons in the hypothalamus and preoptic area to coordinate the expression of female reproductive behaviors with the timing of the preovulatory luteinizing hormone (LH) surge. This chapter will summarize evidence that E(2) and P facilitation of the receptive component of female reproductive behavior, lordosis, involves changes in both the expression of and intracellular signal transduction pathways engaged by alpha(1)-adrenergic receptors in the hypothalamus and preoptic area. The alpha(1)-adrenoceptors are thought to mediate the facilitatory effects of the catecholamine neurotransmitter norepinephrine on both lordosis behavior and LH release. E(2) first induces the expression of the alpha(1B)-adrenergic receptor subtype in the hypothalamus and preoptic area. P then acts in an E(2)-dependent manner to promote linkage of hypothalamic alpha(1)-adrenoceptors to an intracellular signaling pathway involving nitric oxide and cyclic GMP. This chapter will also describe recent findings that implicate brain insulin-like growth factor-I (IGF-I) receptors as obligatory co-mediators of hormonal regulation of hypothalamic alpha(1)-adrenoceptors and female neuroendocrine function. Additional studies suggest that E(2) and IGF-I facilitate lordosis behavior by activating kinases traditionally associated with growth factor signal transduction (mitogen-activated protein kinases and phosphatidlyinositol-3-kinases). These molecular events are proposed to help coordinate the timing of ovulation with the expression of sexual receptivity, thereby maximizing reproductive success.