Hines M, Alsum P, Roy M, Gorski R A, Goy R W
Wisconsin Regional Primate Research Center, University of Wisconsin, Madison 53715.
Horm Behav. 1987 Sep;21(3):402-17. doi: 10.1016/0018-506x(87)90024-9.
We administered the synthetic estrogen, diethylstilbestrol (DES), or the antiestrogen, tamoxifen, to pregnant guinea pigs and observed the consequences for sexual differentiation of their female offspring. Hormones were administered during the period when treatment of fetuses with testosterone influences the development of sex-related traits (approximately Days 30 to 65 of gestation). Ovarian function, masculine and feminine sexual behavior, and the structure of a sexually dimorphic neural region in the preoptic area were assessed in adulthood in hormone-exposed animals and in oil-treated and untreated controls. Prenatal exposure to DES dipropionate (DESDP) caused masculinization and defeminization. DESDP-treated females mounted more than control females, both without hormonal stimulation and when given testosterone propionate (TP) as adults. The sexually dimorphic neural region was also masculinized in these females. In regard to defeminization, they showed delayed vaginal opening, impaired progesterone (P) production, an absence of corpora lutea, and impaired lordosis and mounting responses to estradiol benzoate (EB) and P. Prenatal treatment with tamoxifen produced a complicated pattern of results. Tamoxifen-exposed females evidenced less masculine-typical behavior, showing diminished mounting without hormonal stimulation and in response to TP. However, they also showed delayed vaginal opening, enhanced P production, and impaired mounting in response to EB and P. Their lordosis behavior and the volume of the sexually dimorphic neural region were unaffected. These results suggest that estrogens play a substantial role in sexual differentiation in the guinea pig. High levels of estrogen promote masculine-typical development, and unusually low levels may impair some aspects of both masculine-typical and feminine-typical development.
我们给怀孕的豚鼠注射合成雌激素己烯雌酚（DES）或抗雌激素他莫昔芬，并观察其对雌性后代性分化的影响。在睾酮处理胎儿会影响与性别相关特征发育的时期（大约在妊娠第30至65天）给予激素。在成年期对接受激素处理的动物以及接受油处理和未处理的对照动物的卵巢功能、雄性和雌性性行为以及视前区性二态神经区域的结构进行评估。产前暴露于己烯雌酚二丙酸酯（DESDP）会导致雄性化和去雌性化。经DESDP处理的雌性在没有激素刺激以及成年后给予丙酸睾酮（TP）时，骑跨行为比对照雌性更多。这些雌性的性二态神经区域也出现了雄性化。在去雌性化方面，它们表现出阴道开口延迟、孕酮（P）分泌受损、无黄体形成，以及对苯甲酸雌二醇（EB）和P的弓背行为及骑跨反应受损。产前用他莫昔芬处理产生了复杂的结果模式。暴露于他莫昔芬的雌性表现出较少的雄性典型行为，在没有激素刺激以及对TP的反应中骑跨行为减少。然而，它们也表现出阴道开口延迟、P分泌增加，以及对EB和P的骑跨行为受损。它们的弓背行为和性二态神经区域的体积未受影响。这些结果表明，雌激素在豚鼠的性分化中起重要作用。高水平的雌激素促进雄性典型发育，而异常低水平的雌激素可能会损害雄性典型和雌性典型发育的某些方面。
