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 integrated hypothalamic output is modified by inputs from the periaquaductal gray, and the vestibular complex on its way to the motoneurons mediating lordosis behavior. The EMS that mediates this activation of the circuit requires the transactivation on metabotropic glutamate receptor-1a (mGluR1a), which leads to the phosphorylation of PKCθ and the release of NPY and activation of the Y1 receptor on β-END projection cells. The EMS and resulting transient inhibition is necessary for the full expression of lordosis behavior in the rat.