Nordeen E J, Yahr P
J Neurosci. 1983 May;3(5):933-41. doi: 10.1523/JNEUROSCI.03-05-00933.1983.
Gonadal steroids masculinize and defeminize neuroendocrine development, including behavior. Defeminization makes males less sensitive than females to estrogen for showing female sexual behavior and cyclic gonadotropin secretion. Masculinization makes males more sensitive than females to estrogen for showing male sexual behavior. Thus masculinization and defeminization produce opposite effects on estrogen sensitivity. To study the relationship between estrogen sensitivity and estrogen binding, we studied sex differences in estrogen binding to hypothalamic cell nuclei on a regional and temporal basis. We measured the amount of estradiol (E2) bound to cell nuclei in the preoptic area (POA), mediobasal hypothalamus (MBH), corticomedial amygdala, and cortex of gonadectomized male and female rats 30 and 60 min after [3H]E2 was injected intravenously. In the MBH, males consistently bound less E2 than females did. In the POA, males bound less E2 than females after 60 min, but they bound more E2 than females after 30 min. Decreased estrogen binding in the MBH may underlie defeminized sexual behavior. Similarly, decreased estrogen binding in the POA at 60 min may be a correlate of defeminized gonadotropin secretion, whereas increased estrogen binding in the POA at 30 min may be a correlate of masculinized sexual behavior. To test the hypothesis that decreased estrogen binding in the MBH and POA are correlates of defeminization, we measured E2 binding at 60 min in female rats in which masculinization and defeminization were manipulated independently. Defeminization decreased E2 binding to cell nuclei in both the POA and MBH to the level seen in males at this time point. Masculinization had no effect at this time point. The data suggest that sex differences in E2 binding to hypothalamic cell nuclei correlate reliably with sex differences in estrogen sensitivity even though masculinization and defeminization produce opposing effects on these parameters.
性腺类固醇使神经内分泌发育男性化并消除其女性化特征，包括行为。消除女性化特征使雄性对雌激素的敏感性低于雌性，从而表现出雌性性行为和周期性促性腺激素分泌。男性化使雄性对雌激素的敏感性高于雌性，从而表现出雄性性行为。因此，男性化和消除女性化特征对雌激素敏感性产生相反的影响。为了研究雌激素敏感性与雌激素结合之间的关系，我们在区域和时间基础上研究了雌激素与下丘脑细胞核结合的性别差异。我们测量了静脉注射[3H]雌二醇（E2）后30分钟和60分钟，去势雄性和雌性大鼠视前区（POA）、下丘脑内侧基底部（MBH）、皮质内侧杏仁核和皮质中与细胞核结合的雌二醇（E2）量。在MBH中，雄性始终比雌性结合的E2少。在POA中，60分钟后雄性结合的E2比雌性少，但30分钟后雄性结合的E2比雌性多。MBH中雌激素结合减少可能是性行为女性化特征消除的基础。同样，60分钟时POA中雌激素结合减少可能与促性腺激素分泌的女性化特征消除相关，而30分钟时POA中雌激素结合增加可能与性行为男性化相关。为了检验MBH和POA中雌激素结合减少与女性化特征消除相关的假设，我们测量了在雄性化和女性化特征被独立操纵的雌性大鼠中60分钟时的E2结合情况。女性化特征消除使POA和MBH中与细胞核结合的E2减少到此时雄性中的水平。在这个时间点，雄性化没有影响。数据表明，E2与下丘脑细胞核结合的性别差异与雌激素敏感性的性别差异可靠相关，尽管男性化和女性化特征消除对这些参数产生相反的影响。
