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首页> 外文期刊>Chronobiology international >The aging suprachiasmatic nucleus and cytokines: Functional, molecular, and cellular changes in rodents
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The aging suprachiasmatic nucleus and cytokines: Functional, molecular, and cellular changes in rodents

机译：老化的视交叉上核和细胞因子：啮齿动物的功能，分子和细胞变化

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The aging process brings about a switch to a low- grade chronic inflammatory condition in the periphery and brain, a condition which may prime brain cells, including those of the hypothalamic suprachiasmatic nucleus (SCN). Little information is available, however, on the responses of the SCN to neuroinflammation and immune-related challenges, and such responses have not been hitherto investigated during aging. We here provide an overview of these issues and summarize data we obtained in the study of the SCN of young and aged mice. In particular, we analyzed: i) the electrophysiological properties of the SCN core (the retino-recipient region) in tissue slices; ii) expression and dayight variation of transcripts encoding the receptors for the cytokines interferon-gamma and tumor necrosis factor-alpha, as well as the expression of transcripts encoding the proteins "suppressors of cytokine signaling" SOCS1 and SOCS3, by means of quantitative real-time polymerase chain reaction; levels of mRNAs were correlated with neuronal activation, revealed by Fos induction, elicited in the SCN by intracerebroventricular injections of a mixture of interferon-gamma and tumor necrosis factor-alpha during the daytime and nighttime; and iii) response of astrocytes and microglia in the SCN to the same paradigm of cytokine administration. Marked changes of all the above-mentioned parameters were found in the aged SCN, indicating that the circadian pacemaker is a target of the aging process. In addition, the findings indicate that neurons and glial cells of the biological clock are sensitive to inflammatory signals, and that the response to such signals is altered during senescence.
机译：衰老过程导致周围和大脑向低度的慢性炎症状态转变，该状态可能引发脑细胞，包括下丘脑上视交叉上核（SCN）。但是，关于SCN对神经炎症和免疫相关挑战的反应的信息很少，并且迄今为止尚未在衰老过程中研究这种反应。我们在这里提供了这些问题的概述，并总结了我们在研究年轻和老年小鼠的SCN中获得的数据。特别地，我们分析了：i）组织切片中SCN核心（视网膜-受体区域）的电生理特性; ii）通过定量分析，编码细胞因子干扰素-γ和肿瘤坏死因子-α受体的转录本的表达和昼夜变化，以及编码“细胞因子信号抑制剂” SOCS1和SOCS3的转录本的表达实时聚合酶链反应;在白天和晚上，通过脑室内注射干扰素-γ和肿瘤坏死因子-α的混合物在SCN中引起的Fos诱导揭示了mRNA的水平与神经元激活相关。 iii）SCN中星形胶质细胞和小胶质细胞对相同的细胞因子给药方式的反应。在老化的SCN中发现所有上述参数都有明显变化，这表明昼夜节律起搏器是老化过程的目标。另外，该发现表明生物钟的神经元和神经胶质细胞对炎症信号敏感，并且在衰老过程中对此类信号的反应发生了改变。

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