Effects of estrogen in the male rat medial amygdala: infusion of an aromatase inhibitor lowers mating and bovine serum albumin-conjugated estradiol implants do not promote mating.

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(2)) either throughout the brain or within the medial preoptic area (MPO) reduces mating, whereas E(2) 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(2) 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(2) 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(2) acts in the MEA, in experiment 2, E(2) conjugated to bovine serum albumin (BSA-E(2): a complex of E(2 )and a large protein that does not cross the plasma membrane, thereby restricting the action of E(2) 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(2) acts in the MEA to promote male sexual behavior and suggest an intercellular mechanism of E(2) action.