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首页> 外文期刊>Life sciences >Regulation of inhibin/activin subunits and follistatin mRNA expression in the rat pituitary at early estrus.
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Regulation of inhibin/activin subunits and follistatin mRNA expression in the rat pituitary at early estrus.

机译：发情早期大鼠垂体中抑制素/激活素亚基和卵泡抑素mRNA表达的调节。

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摘要

In the rat pituitary, activin stimulates whereas inhibin prevents FSH synthesis and secretion. Besides, the activin binding protein follistatin neutralizes the action of activin. The control of the FSH secondary surge at early estrus is not completely understood. To investigate the regulation of the inhibin/activin alpha-, betaA- and betaB-subunits and follistatin mRNA expression in the pituitary during the time of the FSH secondary surge, cyclic rats treated with LHRH antagonist (ANT) and ovine LH (oLH), progesterone (P), the anti-steroid RU486, adrenalectomy (ADX) or ADX plus corticosterone (B), were killed at early estrus. The serum concentrations of FSH were measured and the mRNA levels of the above mentioned transcripts were analysed and quantitated by using RNase protection assays. ANT abolished the FSH secondary surge and increased mRNA for alpha- and betaA-subunits and follistatin, but reduced that for betaB-subunit. Both oLH and P reversed these effects. RU486 blocked the effect of oLH on FSH levels and prevented the reduction in the mRNA for follistatin. ADX in ANT+oLH-treated rats reduced the serum FSH concentrations, enhanced mRNA for betaA- and betaB-subunits and, similar to RU486, blocked the drop in follistatin mRNA. Finally, replacement of B in ADX animals reversed these effects. These results demonstrate that, in the cyclic rat, the preovulatory secretion of LH and the surges of P and B on proestrus regulate the synthesis of inhibin/activin subunits and follistatin mRNA in the rat pituitary at early estrus, probably by reducing inhibin and follistatin and increasing activin. Moreover, these effects of LH, P and B at the pituitary level, together with the decrease in the amount of inhibin coming from the ovary, might be responsible for the occurrence of the FSH secondary surge.
机译：在大鼠垂体中，激活素刺激而抑制素阻止FSH合成和分泌。此外，激活素结合蛋白卵泡抑素中和了激活素的作用。 FSH早期发情时继发性潮气的控制尚不完全清楚。为了研究FSH继发性潮气，LHRH拮抗剂（ANT）和绵羊LH（oLH）治疗的周期大鼠垂体抑制素/激活素α-，betaA-和betaB-亚基和卵泡抑素mRNA表达的调节，黄体酮（P），抗类固醇RU486，肾上腺切除术（ADX）或ADX加皮质酮（B）在发情早期被杀死。测量了FSH的血清浓度，并使用RNA酶保护测定法分析和定量了上述转录本的mRNA水平。 ANT取消了FSH继发性激增，并增加了α和βA亚基和卵泡抑素的mRNA表达，但减少了betaB亚基的mRNA表达。 oLH和P都可以逆转这些影响。 RU486阻断了oLH对FSH水平的影响，并阻止了卵泡抑素mRNA的降低。 ANT + oLH处理的大鼠中的ADX降低了血清FSH浓度，增强了betaA和betaB亚基的mRNA，并且类似于RU486，阻止了卵泡抑素mRNA的下降。最后，在ADX动物中替换B可逆转这些影响。这些结果表明，在循环大鼠中，LH的排卵前分泌以及前期P和B的激增可能通过减少体内抑制素和卵泡抑素的含量来调节发情早期大鼠垂体中抑制素/激活素亚基和卵泡抑素mRNA的合成。增加激活素。此外，LH，P和B在垂体水平的这些作用以及来自卵巢的抑制素的减少可能是FSH继发性潮涌的发生原因。

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