Luteal cell receptor content for prolactin (PRL) and luteinizing hormone (LH): regulation by LH and PRL.
Luteal cell receptor content for prolactin (PRL) and luteinizing hormone (LH): regulation by LH and PRL.
复制标题
催乳素 (PRL) 和黄体生成素 (LH) 的黄体细胞受体含量：LH 和 PRL 的调节。
作者：
Joanne S. Richards;Julie J. Williams
通过测定 LH 和 PRL 调节这些激素的黄体细胞受体含量和增加孕酮产生的能力，检查 LH 和 PRL 在颗粒细胞分化为黄体细胞过程中的作用。通过用雌二醇、hFSH 和 oLH 连续治疗，在未成熟垂体切除的雌性大鼠中诱导排卵前卵泡和黄体。大窦卵泡颗粒细胞中LH受体含量较高。施用 LH 导致 LH 受体在 24 小时内显着下降，并在 96 小时内保持低水平。相反，在 LH 刺激后 48 小时内，颗粒细胞中 PRL 受体的含量逐渐增加，并且在完全黄素化的细胞中在 96 小时时仍保持较高水平。 PRL 受体的这种增加似乎在功能上与黄体细胞对 PRL 的反应能力有关。当 LH 后给予 PRL 4 天时，黄体细胞黄体酮的产生和 LH 受体含量在 48 小时后而不是之前逐渐增加。由于这些变化是在没有 LH 的情况下发生的，因此 LH 受体的增加似乎是 PRL 诱导的孕酮产生增加的结果，但不是其必要条件。如果每日注射 PRL 在 LH 诱导黄体化后延迟 72 或 96 小时，则观察到 PRL 的黄体溶解作用而不是促黄体作用。由于 PRL 受体在 72 小时和 96 小时仍保持升高，因此细胞内机制而非受体含量似乎影响黄体细胞对 PRL 的反应。
The effect of LH and PRL during the differentiation of granulosa cells to luteal cells was examined by determining the ability of LH and PRL to regulate luteal cell receptor content for these hormones and to increase production of progesterone. Preovulatory follicles and corpora lutea were hormonally induced in immature hypophysectomized female rats by sequential treatment with estradiol, hFSH and oLH. The content of receptor for LH was high in granulosa cells of large antral follicles. Administration of LH caused receptor for LH to decrease markedly within 24 h and to remain low for 96 h. In contrast, granulosa cell content of receptor for PRL increased progressively for 48 h following LH stimulation and remained elevated in fully luteinized cells at 96 h. This increase in PRL receptor appears to be functionally related to the ability of luteal cells to respond to PRL. When PRL was given for 4 days after LH, both luteal cell progesterone production and LH receptor content increased progressively after, but not before, 48 h. Since these changes occurred in the absence of LH, the increase in LH receptor appears to be a consequence of, but not a requirement for, the PRL-induced increase in progesterone production. If daily injections of PRL were delayed for 72 or 96 h following LH induction of lutenization, luteolytic rather than luteotropic effects of PRL were observed. Since receptor for PRL remained elevated at 72 and 96 h, intracellular mechanisms and not receptor content, appear to be effecting the response of luteal cell to PRL.