Figure 1.

The estradiol induction of sexual receptivity in the female rat is indicated by lordosis behavior. The CNS regulation of this global response to hormonal and sensory input is regulated by a diffuse circuit that extends from the limbic system to the spinal cord. Within this lordosis regulating circuit, estradiol acts rapidly through estradiol membrane signaling (EMS) to release neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus (ARH), which activates β-endorphin (β-END) projection neurons that extend to the medial preoptic nucleus (MPN). The MPN is an important integrative node receiving accessory olfactory and limbic input. β-END activates MOR, producing a transient inhibition of the MPN which is relieved by progesterone in the cycling female. The MPN MOR neurons in turn project to the ventromedial nucleus of the hypothalamus (VMH), the final common output of the hypothalamus. The EMS and resulting transient inhibition is necessary for the full expression of lordosis behavior in the rat. In addition to its VMH efferents, the MPN sends a GABAergic inhibitory projection to the VTA. Estrogen inhibition of the MPN contributes to dopaminergic activation of the nucleus accumbens, which both regulates sexual motivation and mediates the rewarding consequences of sexual behavior. Estradiol's actions on the combined circuits serve to initiate sexual motivation in the male's presence, modulate the expression of sexual behavior to tactile stimulation provided by the mounting male, and to feed forward, increasing the efficiency of future copulatory interactions in a way that presumably increases reproductive success.