In male rats, copulatory behavior depends on estrogen-responsive neurons located in brain areas known to be crucial for mating. Blocking the aromatization of testosterone (T) to estradiol (E<sub>2</sub>) either throughout the brain or within the medial preoptic area (MPO) reduces mating, whereas E<sub>2</sub> treatment of either the MPO or the medial amygdala (MEA) maintains sexual behavior. The effects of T aromatization in the MEA have received less attention; therefore, 2 studies were done to further elucidate the effects of E<sub>2</sub> in the MEA. In experiment 1, gonadally intact male rats that showed robust mating behavior were administered chronic fadrozole, a nonsteroidal aromatase inhibitor, to the MEA to stop the conversion of T to E<sub>2</sub> and then paired with receptive females. Infusion of fadrozole to the MEA significantly lowered mating behavior in experimental males compared to vehicle-infused control males. To further investigate the mechanism by which E<sub>2</sub> acts in the MEA, in experiment 2, E<sub>2</sub> conjugated to bovine serum albumin (BSA-E<sub>2</sub>: a complex of E<sub>2 </sub>and a large protein that does not cross the plasma membrane, thereby restricting the action of E<sub>2</sub> to cell-surface signaling) was chronically administered bilaterally to the MEA of castrated, dihydrotestosterone-treated males. This treatment did not maintain mating behavior. These studies show that E<sub>2</sub> acts in the MEA to promote male sexual behavior and suggest an intercellular mechanism of E<sub>2</sub> action.