Visser Jenny A, Durlinger Alexandra L L, Peters Isolde J J, van den Heuvel Edwin R, Rose Ursula M, Kramer Piet, de Jong Frank H, Themmen Axel P N
Department of Internal Medicine, Erasmus MC, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.
Endocrinology. 2007 May;148(5):2301-8. doi: 10.1210/en.2006-1265. Epub 2007 Jan 25.
Anti-Müllerian hormone (AMH) plays an important role in folliculogenesis. AMH null mice display an increased recruitment of primordial follicles. Nevertheless, these mice do not have proportionally more preovulatory follicles. Therefore, AMH null mice provide an interesting genetic model to study the regulation of species-specific number of preovulatory follicles. We studied the follicle pool throughout the estrous cycle at 4 months of age. Analysis of the follicle pool revealed that AMH null mice have an increased and earlier cyclic recruitment of growing follicles despite a blunted FSH surge at estrus. However, FSH levels at estrus were apparently too low to support growth to the preovulatory stage because an increased level of atresia was observed, which neutralized the increased cyclic recruitment. When AMH null mice were subjected to a superovulation scheme, the rise in FSH levels resulted in the rescue of the recruited cohort of growing follicles. Analysis of the follicle pool also revealed that the increased recruitment of primordial follicles in AMH null mice was neutralized by an increased loss of follicles during the transition from small preantral to large preantral follicle. This major loss of follicles was not completely reflected by a corresponding augmentation of atresia but did correspond with an increased number of oocyte remnants observed in AMH null mice. We conclude that a combination of increased oocyte degeneration and increased follicular atresia neutralizes the increased initial and cyclic recruitment in AMH null mice to a normal number of preovulatory follicles.
抗苗勒管激素（AMH）在卵泡发生过程中发挥着重要作用。AMH基因敲除小鼠的原始卵泡募集增加。然而，这些小鼠的排卵前卵泡数量并未相应增加。因此，AMH基因敲除小鼠为研究排卵前卵泡的物种特异性数量调控提供了一个有趣的遗传模型。我们研究了4月龄小鼠在整个发情周期中的卵泡库。对卵泡库的分析表明，尽管发情期促卵泡生成素（FSH）峰值减弱，但AMH基因敲除小鼠生长卵泡的周期性募集增加且提前。然而，发情期的FSH水平明显过低，无法支持卵泡生长至排卵前阶段，因为观察到闭锁增加，抵消了周期性募集的增加。当对AMH基因敲除小鼠进行超排卵方案时，FSH水平的升高导致募集的生长卵泡群得到挽救。对卵泡库的分析还表明，AMH基因敲除小鼠原始卵泡募集的增加被从小的腔前卵泡向大的腔前卵泡转变过程中卵泡损失的增加所抵消。这种卵泡的大量损失并未完全反映在相应增加的闭锁上，但确实与AMH基因敲除小鼠中观察到的卵母细胞残余数量增加相对应。我们得出结论，卵母细胞退化增加和卵泡闭锁增加共同作用，将AMH基因敲除小鼠中初始和周期性募集增加的卵泡数量抵消至正常的排卵前卵泡数量。
