The estradiol-induced inhibition of lordosis is mediated by µ-opioid receptors (MOR) that respond to morphine and the endogenous neuropeptide β-endorphin. In the arcuate nucleus of the hypothalamus, estradiol treatment causes synaptic release of neuropeptide Y onto POMC neurons that project to the medial preoptic nucleus and release β-endorphin to activate MOR. We study the activity of this lordosis-regulating circuit by monitoring the phenomenon of MOR receptor internalization that follows the activation of a G protein-coupled receptor (GPCR) by its endogenous ligand.
