哺乳动物卵母细胞减数分裂恢复的诱导

促使哺乳动物卵母细胞减数分裂恢复的机制尚不十分清楚。有腔卵泡中发育充分的卵母细胞被减数分裂抑制因子阻滞在生发泡（GV）期，环一磷酸腺苷（cAMP)是研究得最为清楚的减数分裂抑制因子。然而，其它因子也参与了卵母细胞减数分裂的阻滞。虽然排卵前的促黄体素（LH）峰诱导卵母细胞减数分裂恢复已成定论，但是参与该事件的各种过程非常复杂，因而还没有完全确定。目前，有两种主要但并不互相排斥的假说。第一种假说认为，LH对颗粒细胞的刺激作用终止减数分裂抑制因子流向卵母细胞，从而使卵母细胞膈离这些抑制因子并进而促使减数分裂恢复，第二种假设认为LH刺激颗粒细胞产生一种减数分裂诱导信号，该信号进而克服或者破坏减数分裂抑制因子的作用。权衡这两种假说，目前的证据倾向于支持阳性信号假说，而且最近的研究暗示，该种阳性信号的产生发生在颗粒细胞中LH诱导的cAMP水平上升和MAPK激酶激活之后。

INDUCTION OF MEIOTIC RESUMPTION IN MAMMALIAN OOCYTES

The mechanisms that promote the resumption of meiosis in mammalian oocytes remain poorly understood. Fully-grown oocytes within antral follicles are maintained at the germinal vesicle (GV) stage by meiosis-arresting factors. Cyclic AMP (cAMP) is the best-characterized meiosis-arresting factor; yet, other factors almost certainly also participate. The induction of oocyte meiotic resumption by the preovulatory luteinizing hormone (LH) surge is well established, however the processes involved are complex and inadequately defined. Two hypotheses prevail, though they are not mutually exclusive. The first hypothesis is that LH stimulation of granulosa cells terminates the flow of meiosis-arresting factors to the oocyte, thus depriving the oocyte of these factors and promoting the resumption of meiosis. The second hypothesis is that LH stimulates the generation of a meiosis-inducing signal by the granulosa cells that overcomes or destroys the meiosis-arresting factor(s). On balance, current evidence favors the positive signal hypothesis. Moreover, recent studies suggest that this signal is probably generated downstream of LH-induced elevation of granulosa cell cAMP and the activation of mitogen-activated kinases (MAPK) in the granulosa cells.