Sexual receptivity is induced by the activity of estradiol (the primary estrogen in the body) through complex mechanisms that involve multiple signaling strategies in the brain. Using a rodent model, we have identified specific endogenous opioid circuits in the area of the hypothalamus that are rapidly activated by estradiol to transiently inhibit sexual receptivity, and its behavioral correlate, the lordosis reflex. In turn, progesterone, the other ovarian steroid, acts on these same circuits to reverse the inhibitory action of estradiol and facilitate lordosis. Interestingly, this transient inhibition is critical for the induction of sexual receptivity. We are studying the neurochemistry of these circuits and identifying the specific signaling pathways through which estradiol and progesterone modulate receptive behavior.
