Parsons B, Rainbow T C, McEwen B S
Endocrinology. 1984 Oct;115(4):1412-7. doi: 10.1210/endo-115-4-1412.
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.
本研究旨在确定睾酮在发育过程中的雌激素作用是否控制雄性中女性生殖行为的明显不可逆抑制，并导致下丘脑腹内侧核（VMN）产生细胞溶质孕激素受体（CPR）以响应雌激素预处理的能力受到抑制。从怀孕第14天到分娩，定时怀孕的雌性大鼠每天注射芳香化酶抑制剂1,4,6-雄甾三烯-3,17-二酮（ATD；5mg/0.2ml）。子宫内暴露于ATD的雄性在出生后的前10天接受含有ATD的硅胶胶囊。一些未暴露于ATD的窝中的雌性在出生后6-12小时和3天接受苯甲酸雌二醇（EB；10微克）注射。其余未暴露于ATD的幼崽作为对照。幼崽在60-70天进行性腺切除，并在85-90天测试其雌性生殖行为或处死以进行CPR测量。为了引发行为，动物在测试前每天注射EB（15微克，共3天）和一次孕酮（500微克）。为了诱导CPR，动物接受EB但不接受孕酮。与围产期给予ATD的正常雌性和雄性相比，围产期给予EB的雄性和雌性观察到的接受和主动行为明显减少。雄性VMN的CPR含量与围产期给予EB的雌性相似，明显低于围产期给予ATD的正常雌性和雄性。新生儿激素处理未改变其他下丘脑或视前核的CPR含量。这些发现与以下假设一致，即雌激素介导的一个事件是VMN中CPR的诱导，这是激活雌性生殖行为的基础。这种能力显然受到围产期雄性中雌激素介导事件的限制。
