McNeilly A S, Crawford J L, Taragnat C, Nicol L, McNeilly J R
MRC Human Reproductive Sciences Unit, University of Edinburgh Centre for Reproductive Biology, The Chancellor's Building, New Royal Infirmary, 49 Little France Crescent, Old Dalkeith Road, Edinburgh EH16 4SB, UK.
Reprod Suppl. 2003;61:463-76.
While the role of oestradiol and progesterone in the control of GnRH pulsatile secretion and generation of the preovulatory GnRH surge to induce release of the LH surge has been fully investigated, less attention has been given to changes in the pituitary gland that may sensitize gonadotrophs to switch from pulsatile release to surge release of LH, in particular. Furthermore, in the follicular phase while pulsatile secretion of LH is maximal, FSH secretion is reduced, yet both hormones are produced by the same gonadotrophs. The mechanisms whereby this differential release can occur are still unclear. The main regulator of FSH secretion is through the negative feedback effects of oestradiol and inhibin, which directly affect FSHbeta mRNA content and subsequent synthesis of FSH. FSH is then released predominantly via a constitutive pathway and the amount released is closely related to the rate of synthesis. In contrast, while basal LH secretion occurs via a constitutive pathway, the principal release of LH through pulsatile secretion is through the regulated pathway with GnRH stimulating the release of pre-synthesized LH contained in storage granules without significant changes in LHbeta mRNA. Secretogranin II (SgII) is associated with LH in these electron-dense storage granules and LH-SgII granules appear to be the principal form of granule released in response to GnRH through the regulated pathway. At the time of the preovulatory LH surge, granule movement to the gonadotrope cell membrane abutting a capillary, polarization, appears to play an important part in the priming mechanism for release of LH during the preovulatory LH surge in response to the GnRH surge. As there appears to be limited or no gonadotroph cell division in the adult pituitary gland, each gonadotroph passes through this synthesis and secretion pathway repeatedly through successive oestrous cycles. Packaging of LH and FSH into different secretory granules within the same cell is thus pivotal for the differential secretion of these gonadotrophins.
虽然雌二醇和孕酮在控制促性腺激素释放激素（GnRH）脉冲式分泌以及诱导排卵前GnRH峰以引发促黄体生成素（LH）峰释放方面的作用已得到充分研究，但人们对垂体的变化关注较少，尤其是这些变化可能使促性腺细胞从LH的脉冲式释放转变为峰式释放。此外，在卵泡期，LH的脉冲式分泌达到最大值时，促卵泡生成素（FSH）分泌减少，但这两种激素均由相同的促性腺细胞产生。这种差异释放发生的机制仍不清楚。FSH分泌的主要调节因子是雌二醇和抑制素的负反馈作用，它们直接影响FSHβ mRNA含量及随后FSH的合成。然后，FSH主要通过组成性途径释放，释放量与合成速率密切相关。相比之下，虽然基础LH分泌通过组成性途径发生，但LH通过脉冲式分泌的主要释放是通过调节性途径，即GnRH刺激储存颗粒中预先合成的LH释放，而LHβ mRNA无显著变化。分泌粒蛋白II（SgII）与这些电子致密储存颗粒中的LH相关，LH - SgII颗粒似乎是通过调节性途径响应GnRH释放的主要颗粒形式。在排卵前LH峰出现时，颗粒向与毛细血管相邻的促性腺细胞细胞膜移动、极化，这似乎在排卵前LH峰期间响应GnRH峰时LH释放的启动机制中起重要作用。由于成年垂体中促性腺细胞分裂似乎有限或不存在，每个促性腺细胞在连续的发情周期中反复经历这种合成和分泌途径。因此，将LH和FSH包装到同一细胞内不同的分泌颗粒中对于这些促性腺激素的差异分泌至关重要。
