Baum M J, de Greef W J, Kloet G A, Schretlen P J
J Comp Physiol Psychol. 1979 Apr;93(2):278-94. doi: 10.1037/h0077558.
Daily administration of estradiol benzoate stimulated significantly less lordotic behavior in rats during the second half of pregnancy than in ovariectomized females that received subcutaneous progesterone implants, pituitary grafts that raised plasma prolactin, or both treatments combined. Following an initial facilitation of receptivity, females with progesterone implants showed only moderate reductions in lordosis quotients over 3 test days. The capacity of plasma from pregnant rats to bind estradiol was found to increase significantly during the second half of pregnancy. However, daily administration to pregnant rats of a synthetic estrogen, R 2858, which is not bound by plasma protein, was no more effective than estradiol benzoate in stimulating receptive behavior. Administration of estradiol benzoate also stimulated significantly lower levels of sexual behavior in pregnant females than in females in which pseudopregnancy had been prolonged by previous hysterectomy or induction of uterine decidualization. These findings suggest that some endocrine factor other than progesterone, prolactin, or estradiol-binding protein is primarily responsible for the potent suppression of behavioral responsiveness to estrogen which occurs in pregnant rats. It is suggested that 5 alpha-reduced androgens may cause these behavioral effects.
在妊娠后半期，每日给大鼠注射苯甲酸雌二醇所激发的脊柱前凸行为，显著少于接受皮下植入孕酮的去卵巢雌性大鼠、移植垂体以提高血浆催乳素水平的大鼠，或同时接受这两种处理的大鼠。在最初的性接受能力增强之后，植入孕酮的雌性大鼠在3个测试日内的脊柱前凸商数仅出现中度下降。研究发现，妊娠大鼠血浆结合雌二醇的能力在妊娠后半期显著增加。然而，每日给妊娠大鼠注射一种不与血浆蛋白结合的合成雌激素R 2858，在激发性接受行为方面并不比苯甲酸雌二醇更有效。与通过先前子宫切除术或诱导子宫蜕膜化而延长假孕的雌性大鼠相比，给妊娠雌性大鼠注射苯甲酸雌二醇所激发的性行为水平也显著更低。这些发现表明，除了孕酮、催乳素或雌二醇结合蛋白之外，某些内分泌因子是导致妊娠大鼠对雌激素的行为反应性受到强烈抑制的主要原因。有人提出，5α-还原雄激素可能导致这些行为效应。
