Organizational effects of testosterone via aromatization on feminine reproductive behavior and neural progestin receptors in rat brain.
The present studies were undertaken to determine whether estrogenic actions of testosterone during development govern the apparently irreversible suppression of feminine reproductive behavior in the male and lead to a suppression of the capacity of the ventromedial nucleus (VMN) of the hypothalamus to produce cytosol progestin receptors (CPRs) in response to estrogen priming. Timed-pregnant female rats received daily injections of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD; 5 mg/0.2 ml) from the 14th day of pregnancy until parturition. Males exposed to ATD in utero received Silastic capsules containing ATD for the first 10 days of life. Some females from litters not exposed to ATD received injections of estradiol benzoate (EB; 10 micrograms) 6-12 h and 3 days after birth. The remaining pups not exposed to ATD served as controls. Pups were gonadectomized on days 60-70 and were tested for feminine reproductive behavior or killed for CPR measurements on days 85-90. To elicit behavior, animals received daily injections of EB (15 micrograms for 3 days) and one injection of progesterone (500 micrograms) 4 h before testing. To induce CPRs, animals received EB but not progesterone. Significantly less receptive and proceptive behavior was observed in males and females given perinatal EB than in normal females and males given perinatal ATD. The CPR content of the VMN in males was similar to that in females given perinatal EB and significantly less than that in normal females and males given perinatal ATD. Neonatal hormonal manipulation did not alter the CPR content of other hypothalamic or preoptic nuclei. These findings are consistent with the hypothesis that one event mediated by estradiol which underlies activation of feminine reproductive behavior is the induction of CPRs in the VMN. This capacity is apparently restricted by estrogen-mediated events in males during the perinatal period.
D000733:Androstatrienes / Q000494:pharmacology; D000818:Animals; D001141:Aromatase / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D009474:Neurons / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D011980:Receptors, Progesterone / Q000378:metabolism*; D012098:Reproduction; D012726:Sexual Behavior, Animal; D013739:Testosterone / Q000502:physiology*; D014697:Ventromedial Hypothalamic Nucleus / Q000502:physiology*
D000733:Androstatrienes; D011980:Receptors, Progesterone; C011658:androsta-1,4,6-triene-3,17-dione; D013739:Testosterone; D004958:Estradiol; D010088:Oxidoreductases; D001141:Aromatase