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在底鳉卵泡周期中卵母细胞对血清素调节的敏感性。

Oocyte sensitivity to serotonergic regulation during the follicular cycle of the teleost Fundulus heteroclitus.

作者信息

Cerdà J, Subhedar N, Reich G, Wallace R A, Selman K

机构信息

The Whitney Laboratory, University of Florida, St. Augustine 32086, USA.

出版信息

Biol Reprod. 1998 Jul;59(1):53-61. doi: 10.1095/biolreprod59.1.53.

Abstract

In the teleost Fundulus heteroclitus, serotonin (5-HT) reversibly inhibits oocyte maturation induced in vitro by the maturation-inducing steroid (MIS) 17,20beta-dihydroxy-4-pregnen-3-one (17,20betaP). The 5-HT inhibition of 17,20betaP-induced meiotic maturation was examined in ovarian follicles at different developmental stages or isolated at different times during the follicular cycle. Steroid treatment of late vitellogenic and early maturing follicles (1.2- to 1.7-mm diameter) promoted oocyte maturation in a size-dependent manner, and this maturation was inhibited by 5-HT in follicles of < 1.6- to 1.7-mm diameter. Thus, the 5-HT inhibition progressively decreased as follicles developed the ability to mature in the absence of 17,20betaP. The effectiveness of 5-HT to increase follicular cAMP remained similar within the same developmental stages, indicating that the reduction of 5-HT inhibitory action was not related to the competence of 5-HT to activate inhibitory signals in the oocyte. During the follicular cycle, fully grown follicles (1.3- to 1.4-mm diameter) showed a decreased maturational competence in response to gonadotropin or MIS stimulation after the follicular recruitment into maturation and spawning occurred, which coincided with an increase of the effectiveness of 5-HT at inhibiting 17,20betaP-induced maturation. In further experiments, preincubation of follicles with hCG was found to reduce 5-HT inhibitory action, but when follicles were incubated with either hCG in the presence of a steroidogenesis inhibitor or estradiol-17beta (E2), the 5-HT inhibition was unaffected. These findings suggest that 5-HT inhibition of the MIS-induced meiotic maturation is not under direct gonadotropin or E2 regulation but that it might be regulated in vivo by changes in the competence of the oocytes to undergo oocyte maturation after MIS stimulation.

摘要

在硬骨鱼底鳉中,血清素(5-羟色胺,5-HT)可逆转由成熟诱导类固醇(MIS)17,20β-二羟基-4-孕烯-3-酮(17,20βP)体外诱导的卵母细胞成熟。在不同发育阶段的卵巢卵泡中,或在卵泡周期的不同时间分离出的卵泡中,研究了5-HT对17,20βP诱导的减数分裂成熟的抑制作用。对晚期卵黄生成期和早熟卵泡(直径1.2至1.7毫米)进行类固醇处理,以大小依赖的方式促进卵母细胞成熟,而在直径小于1.6至1.7毫米的卵泡中,这种成熟受到5-HT的抑制。因此,随着卵泡在没有17,20βP的情况下发展出成熟能力,5-HT的抑制作用逐渐减弱。在相同的发育阶段,5-HT增加卵泡环磷酸腺苷(cAMP)的有效性保持相似,这表明5-HT抑制作用的降低与5-HT激活卵母细胞中抑制信号的能力无关。在卵泡周期中,在卵泡募集进入成熟和产卵后,对促性腺激素或MIS刺激有反应的完全成熟卵泡(直径1.3至1.4毫米)表现出成熟能力下降,这与5-HT抑制17,20βP诱导的成熟的有效性增加相吻合。在进一步的实验中,发现用促性腺激素释放激素(hCG)预孵育卵泡可降低5-HT的抑制作用,但当卵泡在存在类固醇生成抑制剂或17β-雌二醇(E2)的情况下与hCG一起孵育时,5-HT的抑制作用不受影响。这些发现表明,5-HT对MIS诱导的减数分裂成熟的抑制作用不受直接的促性腺激素或E2调节,但可能在体内通过MIS刺激后卵母细胞进行卵母细胞成熟的能力变化来调节。

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