The role of gonadal steroid receptor activation in the restoration of sociosexual behavior in adult male rats.
This work tested the hypothesis that gonadal steroid receptor activation was necessary for the restoration of several sociosexual behaviors (such as copulatory behavior, partner preference, 50-kHz vocalizations, and scent marking) in testosterone-treated gonadectomized male rats. Gonadal steroid receptors were blocked by systemic administration of the antiandrogen hydroxyflutamide, the antiestrogen RU 58668, or both antagonists simultaneously in a restoration paradigm. Inhibiting androgen receptors with hydroxyflutamide blocked the restoration of male copulatory behavior, partner preference (time spent with a sexually receptive female over a nonreceptive female), 50-kHz ultrasonic vocalizations, and scent marking. On the other hand, we did not find that blocking estrogen receptors with RU 58668 inhibited the restoration of copulatory behavior or partner preference in testosterone-treated gonadectomized male rats, even though the level of brain nuclear estrogen receptor occupation was significantly reduced to the level found in gonadectomized males. However, the restoration of scent marking and 50-kHz vocalizations were impaired by RU 58668. Blocking both nuclear androgen and estrogen receptors with the two antagonists simultaneously did not have a greater inhibitory effect than treatment with each antagonist alone. Therefore, the activation of nuclear estrogen receptors is necessary for the restoration of some, but not all, sociosexual behaviors, which are also androgen receptor-dependent. Besides nuclear estrogen receptors, there are additional, but unknown, targets of estradiol that play a role in mediating copulatory behavior in adult male rats. Moreover, the signals from multiple gonadal steroid signaling pathways converge in the regulation of some sociosexual behaviors in adult male rats.
Vagell
M E
ME
Mount Sinai School of Medicine, City University of New York, New York, New York, 10029-6574, USA.
McGinnis
M Y
MY
D000679:Amygdala / Q000737:chemistry / Q000502:physiology; D059002:Androgen Receptor Antagonists; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D003307:Copulation / Q000502:physiology*; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D004971:Estrus / Q000502:physiology; D005260:Female; D000077267:Fulvestrant; D008297:Male; D009919:Orchiectomy; D009929:Organ Size; D010675:Pheromones / Q000502:physiology; D010902:Pituitary Gland / Q000737:chemistry / Q000502:physiology; D011301:Preoptic Area / Q000737:chemistry / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D011944:Receptors, Androgen / Q000502:physiology*; D011960:Receptors, Estrogen / Q000037:antagonists & inhibitors / Q000502:physiology*; D012543:Scent Glands / Q000502:physiology; D012669:Seminal Vesicles / Q000737:chemistry / Q000502:physiology; D012686:Septal Nuclei / Q000737:chemistry / Q000502:physiology; D012919:Social Behavior; D013739:Testosterone / Q000494:pharmacology; D014828:Vocalization, Animal / Q000502:physiology; D005466:Fluorocarbons
D059002:Androgen Receptor Antagonists; D004958:Estradiol; D004965:Estrogen Antagonists; D000077267:Fulvestrant; D010675:Pheromones; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D013739:Testosterone; C086511:RU 58668; D005466:Fluorocarbons