This review focuses on the interaction of estrogen with the cholecystokinin (CCK) and endogenous opioid peptide systems in the medial preoptic nucleus, and how these interactions result in alterations of a stereotypic female reproductive behavior--lordosis. The medial preoptic nucleus is an integral part of a circuit controlling lordosis that extends from the limbic system through the hypothalamus. Estrogen alters the integration of sensory information in the circuit that results in the display of sexually receptive behavior. Estrogen determines the activity of CCK and endogenous opioid peptide systems through regulation of expression, release and interaction with specific receptors. Studies of each system individually have indicated that they are pivotal to the expression of lordosis. Recent studies demonstrate an estrogen-dependent interaction between endogenous opioid and CCK systems that control reproductive behavior.