Tumor necrosis factor (TNF) is a well characterized sleep-regulatory substance. To study receptor mechanisms for the sleep-promoting effects of TNF, sleep patterns were determined in control and TNF 55 kDa receptor knock-out (TNFR-KO) mice with a B6 x 129 background after intraperitoneal injections of saline or murine TNFalpha. The TNFR-KO mice had significantly less baseline sleep than the controls. TNFalpha dose-dependently increased non-rapid eye movement sleep (NREMS) in the controls but did not influence sleep in TNFR-KO mice. Although TNFR-KO mice failed to respond to TNFalpha, they had an increase in NREMS and a decrease in rapid eye movement sleep after interleukin-1beta treatment. These results indicate that TNFalpha affects sleep via the 55 kDa receptor and provide further evidence that TNFalpha is involved in physiological sleep regulation. Current results also extend the list of species to mice in which TNFalpha and interleukin-1beta are somnogenic.

译文

肿瘤坏死因子(TNF)是一种特征良好的睡眠调节物质。为了研究TNF促进睡眠的受体机制,在腹膜内注射盐水或鼠TNFalpha后,在B6 x 129背景的对照组和TNF 55kDa受体敲除(TNFR-KO)小鼠中确定睡眠模式。 TNFR-KO小鼠的基线睡眠明显少于对照组。 TNFalpha剂量依赖性地增加了对照组的非快速眼动睡眠(NREMS),但不影响TNFR-KO小鼠的睡眠。尽管TNFR-KO小鼠对TNFα无效,但在白介素1β治疗后,它们的NREMS升高且眼球快速睡眠减少。这些结果表明TNFα通过55kDa受体影响睡眠,并提供进一步的证据证明TNFα参与生理性睡眠调节。目前的结果也将TNFα和白细胞介素-1β具有催眠作用的小鼠扩大了物种种类。

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