Department of Dairy Science, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
Biol Reprod. 2013 Jun 27;88(6):165. doi: 10.1095/biolreprod.112.107342. Print 2013 Jun.
Mechanisms regulating gonadotropin surges and gonadotropin requirements for follicle emergence and selection were studied in heifers. Experiment 1 evaluated whether follicular inhibins regulate the preovulatory luteinizing hormone (LH)/follicle-stimulating hormone (FSH) surges elicited by gonadotropin-releasing hormone (GnRH) injection (Hour = 0) and the subsequent periovulatory FSH surge. Treatments included control (n = 6), steroid-depleted bovine follicular fluid (bFF) at Hour -4 (n = 6), and bFF at Hour 6 (n = 6). Gonadotropins in blood were assessed hourly from Hours -6 to 36, and follicle growth tracked by ultrasound. Consistent with inhibin independence, bFF at Hour -4 did not impact the GnRH-induced preovulatory FSH surge, whereas treatment at Hour 6 delayed onset of the periovulatory FSH surge and impeded growth of a new follicular wave. Experiment 2 examined GnRH and estradiol (E2) regulation of the periovulatory FSH surge. Treatment groups were control (n = 8), GnRH-receptor antagonist (GnRHr-ant, n = 8), and E2 + GnRHr-ant (n = 4). GnRHr-ant (acyline) did not reduce the concentrations of FSH during the periovulatory surge and early follicle development (<7.0 mm) was unaffected, although subsequent growth of a dominant follicle (>8.0 mm) was prevented by GnRHr-ant. Addition of E2 delayed both the onset of the periovulatory FSH surge and emergence of a follicular wave. Failure to select a dominant follicle in the GnRHr-ant group was associated with reduced concentrations of LH but not FSH. Maximum diameter of F1 in controls (13.3 ± 0.5 mm) was greater than in both GnRHr-ant (7.7 ± 0.3 mm) and E2 + GnRHr-ant (6.7 ± 0.8 mm) groups. Results indicated that the periovulatory FSH surge stems from removal of negative stimuli (follicular E2 and inhibin), but is independent of GnRH stimulation. Emergence and early growth of follicles (until about 8 mm) requires the periovulatory FSH surge but not LH pulses. However, follicular deviation and late-stage growth of a single dominant follicle requires GnRH-dependent LH pulses.
本研究旨在探讨调节促性腺激素激增和促性腺激素需求以促进卵泡出现和选择的机制。实验 1 评估了卵泡抑制素是否调节由促性腺激素释放激素 (GnRH) 注射引起的促黄体生成素 (LH)/促卵泡激素 (FSH) 预排卵激增 (Hour = 0) 和随后的促排卵 FSH 激增。处理包括对照 (n = 6)、卵泡期牛卵泡液 (bFF) 去类固醇处理组 (Hour -4,n = 6) 和 bFF 处理组 (Hour 6,n = 6)。从 Hour -6 到 Hour 36 每小时评估血液中的促性腺激素,通过超声监测卵泡生长情况。与抑制素无关,Hour -4 的 bFF 并不影响 GnRH 诱导的促排卵 FSH 激增,而 Hour 6 的处理则延迟了促排卵 FSH 激增的开始,并阻碍了新的卵泡波的生长。实验 2 研究了 GnRH 和雌二醇 (E2) 对促排卵 FSH 激增的调节。处理组为对照组 (n = 8)、 GnRH 受体拮抗剂 (GnRHr-ant,n = 8) 和 E2 + GnRHr-ant (n = 4)。GnRHr-ant (acyline) 并未降低促排卵激增期间的 FSH 浓度,并且早期卵泡发育 (<7.0 mm) 不受影响,尽管 GnRHr-ant 阻止了优势卵泡 (>8.0 mm) 的随后生长。E2 的添加延迟了促排卵 FSH 激增和卵泡波的出现。在 GnRHr-ant 组中未能选择优势卵泡与 LH 浓度降低有关,但 FSH 浓度没有降低。对照组中 F1 的最大直径 (13.3 ± 0.5 mm) 大于 GnRHr-ant 组 (7.7 ± 0.3 mm) 和 E2 + GnRHr-ant 组 (6.7 ± 0.8 mm)。结果表明,促排卵 FSH 激增源于消除负性刺激 (卵泡 E2 和抑制素),但与 GnRH 刺激无关。卵泡的出现和早期生长 (直到约 8mm) 需要促排卵 FSH 激增,但不需要 LH 脉冲。然而,卵泡的偏离和单个优势卵泡的晚期生长需要 GnRH 依赖的 LH 脉冲。