Bronson F H
Endocrinology. 1981 Feb;108(2):506-16. doi: 10.1210/endo-108-2-506.
These experiments queried the potential for developmental change in the positive and negative feedback sensitivities of LH secretion to estradiol. Serum LH levels were compared in juvenile, peripubertal, and adult female mice after ovariectomy and challenge with a variety of 4-day steroid treatments. Since male stimuli accelerate the attainment of puberty in this species, comparisons also were made between age- and weight-matched groups of pre- vs. postpubertal females, obtained by housing them in either the presence or absence of males. The following conclusions were derived from eight experiments. 1) Progressively more estradiol is required to suppress the postovariectomy rise in serum LH as the female mouse develops the juvenile stage to full adulthood. 2) This slow, progressive change is due in part to a steadily increasing capacity to secrete LH when unhindered by any negative feedback regulation by the ovary; it is not due to developmental changes in estradiol metabolism. 3) The LH surging mechanism is functional and already coupled to its circadian oscillator in the juvenile mouse, but surges of adult magnitude could not be induced with exogenous steroid until the peripubertal period. 4) The estradiol requirements for preovulatory LH surging change markedly after the peripubertal stage of development; a wide range of temporal changes in blood estradiol levels will elicit LH surging in the adult mouse, but the immature female requires a rigid pattern of change involving only a narrow range of blood levels of this steroid. 5) Exposure of peripubertal females to male stimuli alters neither their negative feedback sensitivity to estradiol nor their estrogen requirements for LH surging. These conclusions are integrated into two working models that focus first on the estrogen requirements for LH surging in the adult mouse, and second on the maturation of this process and the attainment of pubertal ovulation. (Endocrinology 108: 506, 1981)
这些实验探究了促黄体生成素（LH）分泌对雌二醇的正反馈和负反馈敏感性发生发育变化的可能性。对幼年、青春期前后及成年雌性小鼠进行卵巢切除，并给予多种为期4天的类固醇处理进行刺激后，比较了它们的血清LH水平。由于雄性刺激会加速该物种青春期的到来，因此还对青春期前和青春期后年龄及体重匹配的雌性小鼠组进行了比较，这些小鼠分别饲养在有或没有雄性的环境中。八项实验得出了以下结论。1）随着雌性小鼠从幼年阶段发育到成年，抑制卵巢切除术后血清LH升高所需的雌二醇量逐渐增加。2）这种缓慢的、渐进性的变化部分归因于在不受卵巢任何负反馈调节阻碍时，分泌LH的能力稳步增强；这并非由于雌二醇代谢的发育变化。3）LH激增机制在幼年小鼠中是有功能的，并且已经与其昼夜节律振荡器相耦合，但直到青春期前后阶段，外源性类固醇才能诱导出成年水平的激增。4）发育到青春期前后阶段后，排卵前LH激增所需的雌二醇量发生了显著变化；成年小鼠中，血液雌二醇水平的广泛时间变化会引发LH激增，但未成熟雌性小鼠需要严格的变化模式，且仅涉及该类固醇的窄范围血液水平。5）青春期前后的雌性小鼠暴露于雄性刺激下，既不会改变它们对雌二醇的负反馈敏感性，也不会改变它们LH激增所需的雌激素量。这些结论被整合到两个工作模型中，第一个模型关注成年小鼠LH激增所需的雌激素，第二个模型关注这一过程的成熟以及青春期排卵的实现。（《内分泌学》108: 506, 1981）
