Oestradiol decreases melanin-concentrating hormone (MCH) and MCH receptor expression in the hypothalamus of female rats.

Oestradiol decreases melanin-concentrating hormone (MCH) and MCH receptor expression in the hypothalamus of female rats.
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DOI:
10.1111/jne.12032
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发表时间:
2013-06
影响因子:
3.2
通讯作者:
Eckel LA
Eckel LA
中科院分区:
医学3区
文献类型:
--
作者:
Santollo J;Eckel LA

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以前的研究表明,雌二醇(E_2)可以减少黑色素浓缩激素(MCH)的促食欲作用。在这里,我们研究了E2的这种作用是否通过其降低MCH或其受体(MCHR1)的表达而起作用。采用免疫细胞化学和Western blotting方法,检测雌鼠下丘脑中的MCH免疫反应神经元或MCHR1蛋白含量是否减少。我们发现,与其他周期的大鼠相比,OVX大鼠在急性E2处理后,MCH和MCHR1蛋白的表达均降低,而发情前期大鼠的排卵期循环E2水平则升高。为了确定MCH/MCHR1蛋白表达的这些变化是否可能是由E2‘S直接调节MCH和MCHR1基因转录的能力所介导的,我们用实时荧光定量RT-PCR方法检测了E2对下丘脑神经元细胞系MCH和MCHR1mRNA表达的影响。我们还检测了雌激素受体α(ER-α)和促性腺激素释放激素受体(Mch)在雌性大鼠下丘脑是否共表达。雌二醇组在体外不降低Mch和MCHR1mRNA的表达,也没有发现Mch和ERα共表达的下丘脑神经元。我们的结论是,雌激素依赖的下丘脑MCH/MCHR1蛋白表达的减少介导了E2‘S减少MCH诱导的摄食的能力。然而,目前的发现表明,E2可能通过与其他为MCH和MCHR1神经元提供传入输入的神经系统相互作用,间接地发挥这些作用。
Previous studies have shown that oestradiol (E2) decreases the orexigenic effect of melanin-concentrating hormone (MCH). Here, we examined whether this action of E2 is mediated by its ability to decrease the expression of MCH or its receptor (MCHR1). Using immunocytochemistry and Western blotting, we examined whether E2 decreases MCH-immunoreactive neurones or MCHR1 protein content in the hypothalamus of female rats. We found that both MCH and MCHR1 protein expression was decreased by acute E2 treatment in OVX rats, and by the peri-ovulatory increase in circulating E2 in pro-oestrous rats, relative to rats at other cycle stages. To determine whether these changes in MCH/MCHR1 protein expression may be mediated by E2’s ability to directly regulate the transcription of MCH and MCHR1 genes, the effect of E2 treatment on MCH and MCHR1 mRNA expression in a neuronal hypothalamic cell line was examined using real time RT-PCR. We also determined whether MCH and oestrogen receptor alpha (ERα) are co-expressed in the hypothalamus of female rats. E2 treatment did not decrease MCH or MCHR1 mRNA expression in vitro, and no hypothalamic neurones were identified that co-expressed MCH and ERα. We conclude that E2-dependent decreases in hypothalamic MCH/MCHR1 protein expression mediate E2’s ability to decrease MCH-induced feeding. The current findings suggest, however, that E2 exerts these actions indirectly, likely though interactions with other neuronal systems that provide afferent input to MCH and MCHR1 neurones.
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