Department of Biomedical Science, Colorado State University, Fort Collins, Colorado 80523, USA.
Reprod Biol Endocrinol. 2010 May 10;8:40. doi: 10.1186/1477-7827-8-40.
We demonstrated that E2 conjugated to BSA (E2BSA) induces a rapid membrane-initiated inhibition of LH secretion followed hours later by a slight increase in LH secretion. Whether these actions of E2BSA are restricted to the pituitary gland and whether the membrane-initiated pathway of E2BSA contributes to the up-regulation of the number of GnRH receptors during the positive feedback effect of E2 were evaluated here. We have shown that the suppression of LH secretion induced by E2 and E2BSA is the result of a decreased responsiveness of the pituitary gland to GnRH. In this study we further tested the ability of E2BSA to decrease the responsiveness of the pituitary gland to GnRH under the paradigm of the preovulatory surge of LH induced by E2.
For the first experiment GnRH and LH secretions were determined in samples of pituitary portal and jugular blood, respectively, in ewes treated with 12 mg E2BSA. In the second experiment, the number of GnRH receptors was quantified in ewes 12 h after administration of 25 micrograms E2 (the expected time for the increase in the number of GnRH receptors and the positive feedback effect of E2 in LH secretion) or 12 mg E2BSA. In the third experiment, the preovulatory-like surge of LH was characterized in ewes injected with 25 micrograms E2 alone or followed 8 h later (before the beginning of the LH surge) with 60 mg E2BSA.
a) the decrease in LH secretion induced by E2BSA was not accompanied by changes in the pulsatile pattern of GnRH, b) E2BSA increased the number of GnRH receptors, and c) the presence of E2BSA in E2-treated ewes delayed the onset, reduced the length, and decreased the amount of LH released during the preovulatory surge of LH.
a) the rapid suppression of LH secretion induced by E2BSA is mediated only via a direct action on the pituitary gland, b) E2 acting via a membrane-initiated pathway contributes to increase the number of GnRH receptors and, c) administration of E2BSA near the beginning of the pre-ovulatory surge of LH delays and reduces the magnitude of the surge.
我们已经证明，E2 与 BSA 的结合物（E2BSA）会引起 LH 分泌的快速起始膜抑制，随后数小时后 LH 分泌略有增加。E2BSA 的这些作用是否仅限于垂体，以及 E2BSA 的起始膜途径是否有助于在 E2 的正反馈作用期间上调 GnRH 受体的数量，在这里进行了评估。我们已经表明，E2 和 E2BSA 诱导的 LH 分泌抑制是垂体对 GnRH 反应性降低的结果。在这项研究中，我们进一步测试了 E2BSA 在 E2 诱导的 LH 预排卵激增范式下降低垂体对 GnRH 反应性的能力。
在第一个实验中，用 12mg E2BSA 处理绵羊后，分别测定垂体门脉和颈静脉血样中的 GnRH 和 LH 分泌。在第二个实验中，在给予 25μg E2（预计 GnRH 受体数量增加和 E2 对 LH 分泌的正反馈作用的时间）或 12mg E2BSA 后 12 小时，在绵羊中定量 GnRH 受体的数量。在第三个实验中，单独注射 25μg E2 的绵羊或在注射后 8 小时（在 LH 激增开始前）注射 60mg E2BSA 的绵羊中，描述了类似于排卵前的 LH 激增。
a）E2BSA 诱导的 LH 分泌减少并不伴有 GnRH 脉冲模式的变化，b）E2BSA 增加了 GnRH 受体的数量，c）E2BSA 在 E2 处理的绵羊中存在延迟了 LH 预排卵激增的开始，减少了激增的长度，并降低了 LH 的释放量。
a）E2BSA 诱导的 LH 分泌的快速抑制仅通过对垂体的直接作用介导，b）通过起始膜途径作用的 E2 有助于增加 GnRH 受体的数量，c）在 LH 预排卵激增开始时给予 E2BSA 会延迟并减少激增的幅度。
