Prenatal antiandrogen feminizes behavioral but not neurochemical response to estrogen.
In ovariectomized female rats, estrogen activates high levels of female sexual behavior and induces an increase in the number of cholinergic muscarinic binding sites in the medial basal hypothalamus, an area known to regulate this behavior. Male rats normally show low levels of female sexual behavior and no alteration in muscarinic binding in response to estrogen treatment. An experiment was conducted to determine if a prenatal treatment that feminizes the sexual behavior of male rats would also establish the potential for estrogen to increase muscarinic binding in the male hypothalamus. Results indicate that prenatal exposure to the antiandrogen, flutamide, enhanced estrogen-activated female sexual behavior in male rats but failed to reverse the inability of estrogen to increase muscarinic binding in the medial basal hypothalamus.
D000726:Androgen Antagonists / Q000494:pharmacology*; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D004958:Estradiol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005485:Flutamide / Q000494:pharmacology; D008297:Male; D010052:Ovariectomy; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011976:Receptors, Muscarinic / Q000187:drug effects; D012737:Sex Factors; D012726:Sexual Behavior, Animal / Q000187:drug effects*
D000726:Androgen Antagonists; D004967:Estrogens; D011976:Receptors, Muscarinic; D004958:Estradiol; D005485:Flutamide