Downs S M, Eppig J J
Jackson Laboratory, Bar Harbor, ME 04609.
Tokai J Exp Clin Med. 1986 Dec;11(6):463-9.
Meiotic arrest of mammalian oocytes within ovarian follicles is maintained by a specific factor(s) within the follicle. There is strong evidence that cAMP plays an important role in the control of meiosis. Purines have also been implicated in the maintenance of meiotic arrest in vivo. Hypoxanthine and/or adenosine have been identified in pig and mouse follicular fluid and exert a meiosis-arresting action on mouse oocytes in culture. While adenosine apparently need not be metabolized to exert its action on oocyte maturation, the action of hypoxanthine is apparently due to the production of guanyl and/or xanthyl compounds by the oocyte-cumulus cell complex. The inosine monophosphate dehydrogenase inhibitors, mycophenolic acid and bredinin, induced maturation in cumulus cell-enclosed oocytes maintained in meiotic arrest by hypoxanthine. Hypoxanthine and adenosine are not toxic to oocytes, because oocytes undergo normal fertilization and pre- and post-implantation development following exposure to these molecules in vitro. It is not known how gonadotropins stimulate the resumption of meiosis within the follicle, but there are several possibilities: (1) the intrafollicular level of an oocyte maturation inhibitor is decreased; (2) the oocyte is uncoupled from surrounding follicle cells; (3) an inhibitory molecule is secreted or metabolized by the oocyte; and/or (4) a positive stimulus is produced by the follicle that overrides the presence of inhibitory molecules. Preliminary evidence suggests that cumulus cells may produce a positive stimulus that induces the maturation of cultured cumulus cell-enclosed oocytes. Whether germinal vesicle breakdown in vivo results from a positive induction, a loss of inhibitory input, or a combination of these two mechanisms remains to be determined.
哺乳动物卵泡内卵母细胞的减数分裂阻滞由卵泡内的特定因子维持。有强有力的证据表明,环磷酸腺苷(cAMP)在减数分裂的控制中起重要作用。嘌呤也与体内减数分裂阻滞的维持有关。次黄嘌呤和/或腺苷已在猪和小鼠的卵泡液中被鉴定出来,并对培养中的小鼠卵母细胞发挥减数分裂阻滞作用。虽然腺苷显然无需代谢即可对卵母细胞成熟发挥作用,但次黄嘌呤的作用显然是由于卵母细胞-卵丘细胞复合体产生了鸟苷和/或黄苷化合物。肌苷单磷酸脱氢酶抑制剂霉酚酸和布累迪宁可诱导由次黄嘌呤维持减数分裂阻滞的卵丘细胞包裹的卵母细胞成熟。次黄嘌呤和腺苷对卵母细胞无毒,因为卵母细胞在体外接触这些分子后能正常受精并进行植入前和植入后发育。目前尚不清楚促性腺激素如何刺激卵泡内减数分裂的恢复,但有几种可能性:(1)卵母细胞成熟抑制剂的卵泡内水平降低;(2)卵母细胞与周围卵泡细胞解偶联;(3)卵母细胞分泌或代谢一种抑制性分子;和/或(4)卵泡产生一种积极刺激,从而克服抑制性分子的存在。初步证据表明,卵丘细胞可能产生一种积极刺激,诱导培养的卵丘细胞包裹的卵母细胞成熟。体内生发泡破裂是由积极诱导、抑制性输入丧失还是这两种机制的结合导致,仍有待确定。