Department of Physiology and Neurobiology, The University of Connecticut, Storrs, Connecticut 06269, USA.
J Neuroendocrinol. 1990 Dec 1;2(6):883-8. doi: 10.1111/j.1365-2826.1990.tb00655.x.
Abstract The object of this study was to examine ovarian regulation of pulsatile luteinizing hormone (LH) secretion during early gestation. This was done primarily by analyzing pulsatile LH release in rats that were either sham ovariectomized (OVX) on Day 7 of pregnancy, implanted with empty Silastic capsules, and bled on Day 8, or OVX on Day 7, immediately implanted with Silastic capsules producing plasma levels of estradiol and/or progesterone characteristic of Day 7 to 8 of pregnancy, and bled on Day 8. In addition, the role of progesterone in regulating pulsatile LH secretion was also examined by administration of the progesterone receptor antagonist, RU486, on Day 7 and examining pulsatile LH release on Day 8 of pregnancy. OVX caused a marked increase in LH pulse amplitude and frequency within 24 h. Replacement with physiological plasma levels of estradiol or progesterone alone had no suppressive effect on this OVX-induced increase in pulsatile LH secretion. Restoration of physiological plasma levels of both estradiol and progesterone returned LH pulse amplitude to values seen in sham OVX controls, and prevented the OVX-induced increase in LH pulse frequency. The group mean LH pulse frequency tended to be less in estradiol + progesterone-treated rats than in sham OVX controls, but this difference was not statistically significant. RU486 blocked uterine progesterone receptors as evidenced by endometrial hemorrhaging. In agreement with the OVX + steroid replacement data, RU486 administration also resulted in increases in LH pulse amplitude and frequency. These data demonstrate that the frequency and amplitude of LH pulses on Day 8 of gestation are held in check by negative feedback signals coming from the ovary. Neither steroid alone exerts any suppressive influence over pulsatile LH secretion during early gestation, but both steroids acting together exert a prominent negative feedback regulation on the pulsatile LH release process.
摘要 本研究旨在探讨卵巢在妊娠早期对促黄体生成素（LH）脉冲分泌的调节作用。主要通过分析妊娠第 7 天行假卵巢切除术（OVX）、植入空白硅酮胶囊并于第 8 天采血的大鼠，以及妊娠第 7 天行 OVX 术、即刻植入产生与妊娠第 7 至 8 天相似的雌二醇和/或孕酮水平的硅酮胶囊，并于第 8 天采血的大鼠的 LH 脉冲释放情况来研究这一问题。此外，还通过在妊娠第 7 天给予孕激素受体拮抗剂 RU486，并在妊娠第 8 天检测 LH 脉冲释放情况，研究了孕激素在调节 LH 脉冲分泌中的作用。OVX 术后 24 小时内，LH 脉冲振幅和频率明显增加。单独补充生理血浆水平的雌二醇或孕酮对 OVX 诱导的 LH 脉冲分泌增加没有抑制作用。恢复生理血浆水平的雌二醇和孕酮使 LH 脉冲振幅恢复到假 OVX 对照组的水平，并防止 OVX 诱导的 LH 脉冲频率增加。与假 OVX 对照组相比，雌二醇+孕酮处理组的 LH 脉冲频率趋于降低，但差异无统计学意义。RU486 阻断了子宫内膜的孕激素受体，表现为子宫内膜出血。与 OVX+类固醇替代数据一致，RU486 给药也导致 LH 脉冲振幅和频率增加。这些数据表明，妊娠第 8 天 LH 脉冲的频率和振幅受到来自卵巢的负反馈信号的控制。单独的类固醇都不能对妊娠早期的 LH 脉冲分泌产生抑制作用，但两者共同作用对 LH 脉冲释放过程产生明显的负反馈调节作用。
