The role of nitric oxide synthases in the sleep responses to tumor necrosis factor-α
The role of nitric oxide synthases in the sleep responses to tumor necrosis factor-α
复制标题
DOI：
10.1016/j.bbi.2003.12.002
复制
发表时间：
2004-07-01
影响因子：
15.1
通讯作者：
Krueger, JM
中科院分区：
文献类型：
--
作者：
Chen, LC;Taishi, P;Krueger, JM
众所周知，肿瘤坏死因子- α (TNFalpha)和白细胞介素-1 β (il -1 β)等细胞因子参与生理性睡眠调节，但其下游致睡机制仍未得到充分研究。一氧化氮（NO）是一些tnf α作用的效应分子。神经元型一氧化氮合酶（nNOS）和诱导型一氧化氮合酶（iNOS）基因敲除（KO）小鼠的睡眠与各自的对照组不同。在本研究中，我们使用iNOS和nNOS KO小鼠及其相应的野生型对照，验证了NO介导tnfalpha诱导睡眠的假设。全身给药TNFalpha在注射后的头4小时内增加了两个对照株和NOS KO小鼠的非快速眼动睡眠（NREMS），但没有增加NREMS。nNOS对照组的快速眼动睡眠（REMS）受到TNFalpha的抑制，而其他品系则没有。结果表明，TNFa在一定程度上通过nNOS影响睡眠。(C) 2004爱思唯尔公司版权所有。
It is well established that cytokines such as tumor necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) are involved in physiological sleep regulation, yet their downstream somnogenic mechanisms remain largely uninvestigated. Nitric oxide (NO) is an effector molecule for some TNFalpha actions. Neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) gene knockout (KO) mice sleep differently than their respective controls. In this study, we tested the hypothesis that NO mediates TNFalpha-induced sleep using iNOS and nNOS KO mice and their corresponding wild-type controls. Systemic administration of TNFalpha increased non-rapid eye movement sleep (NREMS) in the two control strains and in the NOS KO mice during the first 4h post-injection but failed to increase NREMS in nNOS KO mice. Rapid eye movement sleep (REMS) was suppressed by TNFalpha in nNOS controls but not in the other strains examined. The results suggest that TNFa affects sleep, in part, through nNOS. (C) 2004 Elsevier Inc. All rights reserved.