Effects of melatonin on estrogen receptor expression in the forebrain of outbred (Lak.LVG) golden hamsters.
Effects of melatonin on estrogen receptor expression in the forebrain of outbred (Lak.LVG) golden hamsters.
复制标题
褪黑激素对远交（Lak.LVG）金仓鼠前脑雌激素受体表达的影响。
DOI：
10.1016/s0006-8993(96)00969-9
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发表时间：
1996
期刊：
影响因子：
2.9
通讯作者：
Harlan,RE
中科院分区：
文献类型：
--
作者：
Hill,SM;Spriggs,LL;Lawson,NO;Harlan,RE
研究表明，松果体通过其荷尔蒙褪黑激素，在季节性繁殖的动物中诱导雄性和雌性生殖系统的退化。褪黑素对下丘脑和垂体功能都有直接的抑制作用，这两个功能对雌二醇的反馈作用也非常敏感。由于褪黑素可以调节其他组织中雌激素受体(ER)的表达，因此采用免疫细胞化学和核糖核酸酶保护分析的方法，研究了每天下午晚些时候注射褪黑素12周对Lak.LVG金黄地鼠下丘脑ER蛋白和mRNA水平的影响。褪黑素对内侧视前区(MPOA)和终纹床核(BNST)的ER免疫反应活性显著降低，而下丘脑其他表达ER的区域，如下丘脑前部，变化较小。褪黑素使正常动物和去卵巢动物的下丘脑ER基因表达均下降了25%。在完整的、骑自行车的雌性仓鼠中，褪黑素治疗后子宫重量显著减轻。这些结果表明，褪黑素通过调节MPOA和BNST神经元中的ER水平，从而影响类固醇反馈机制，从而在金黄地鼠中发挥抗生殖作用。
Studies have shown that the pineal gland via its hormone, melatonin, induces the involution of male and female reproductive systems in seasonally reproducing animals. Melatonin has direct inhibitory effects on both hypothalamic and pituitary functions, which are also exquisitely sensitive to the feedback effects of estradiol. Since melatonin can modulate estrogen receptor (ER) expression in other tissues, immunocytochemical and ribonuclease protection analyses were used to examine the effects of 12 weeks of daily late afternoon injections of melatonin on ER protein and mRNA levels in the hypothalamus of Lak.LVG golden hamsters. Significant decreases in ER-immunoreactivity were noted in the medial preoptic area (MPOA) and bed nucleus of the stria terminalis (BNST) in response to melatonin, while other hypothalamic areas which express ER, e.g. the anterior hypothalamus, showed less dramatic changes. Hypothalamic ER mRNA was decreased in response to melatonin in both intact and ovariectomized animals by 25%. In intact, cycling female hamsters, there was a significant reduction in uterine weight after melatonin treatment. These results suggest that melatonin exerts its anti-reproductive effects in hamsters by modulating ER levels in neurons of the MPOA and BNST, thereby influencing steroid feedback mechanisms.