Sexual responses of the male rat medial preoptic area and medial amygdala to estrogen I: site specific suppression of estrogen receptor alpha.

Male rat copulation is mediated by estrogen-sensitive neurons in the medial preoptic area (MPO) and medial amygdala (MEA); however, the mechanisms through which estradiol (E(2)) acts are not fully understood. We hypothesized that E(2) acts through estrogen receptor α (ERα) in the MPO and MEA to promote male mating behavior. Antisense oligodeoxynucleotides (AS-ODN) complementary to ERα mRNA were bilaterally infused via minipumps into either brain area to block the synthesis of ERα, which we predicted would reduce mating.

Epididymal fat is necessary for spermatogenesis, but not testosterone production or copulatory behavior.

Surgical removal of the epididymal white adipose tissue (EWAT) depot (lipectomy; EWATx) in laboratory rats or mice decreases spermatogenesis, but this phenomenal finding has not been investigated in depth. Specifically, detailed histology, neuroendocrine profiles, copulatory behavior, lipectomy of other WAT depots, rescue by autologous EWAT transplants, or tests whether this EWATx effect is due to disruption of testes innervation occurring during EWATx have not been performed. Therefore, in the first study, we performed EWATx in male Syrian hamsters and attempted to rescue spermatogenesis by transplanting the removed EWAT to the animal's subcutaneous dorsum, removed comparable or larger amounts of non-gonadal WAT [inguinal WAT (IWAT)] and conducted mating behavior tests.

Implants of estradiol conjugated to bovine serum albumin in the male rat medial preoptic area promote copulatory behavior.

The expression of mating behavior in male rats is dependent on estrogen-responsive neurons in the medial preoptic area (MPO). Previous reports showed that mating is attenuated if the aromatization of testosterone to estradiol (E2) is blocked in the MPO and that mating is maintained by MPO E2 implants. However, the mechanisms by which E2 exerts its action are not fully understood.

Gonadal steroid receptors colocalize with central nervous system neurons projecting to the rat prostate gland.

Mating-induced Fos-immunoreactive (-ir) cells are colocalized with androgen receptors (AR), estrogen receptors (ER), or both in limbic and hypothalamic areas known to mediate male rat mating behavior. A steroid-responsive neural network might govern copulatory behavior in male laboratory rats that is analogous to the network described in female rats that governs the lordosis response. This hypothesized network in males may synchronize and coordinate sexual behavioral responses with physiological responses of the genitals and the internal organs of reproduction.

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.

Estradiol in the male rat amygdala facilitates mounting but not ejaculation.

Mating activates estrogen sensitive neurons in several regions of male rat brain, including the medial amygdala (MEA). Infusion of the aromatase inhibitor, Fadrozole, into the MEA reduced mating, presumably by inhibiting conversion of testosterone (T) to estradiol (E(2)). We investigated whether administering E(2) locally into the amygdala (AMG) would maintain sexual behavior in male rats given systemic Fadrozole to eliminate E(2) elsewhere in the brain.