Sleep and Cytokines
Sleep and Cytokines
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DOI：
10.1016/j.jsmc.2007.03.003
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发表时间：
2007-06-01
影响因子：
2.8
通讯作者：
Churchill, Lynn
中科院分区：
文献类型：
--
作者：
Krueger, James M.;Rector, David M.;Churchill, Lynn
IL 1和TNF是特征性的SRS，形成睡眠稳态的一部分。它们的释放通过ATP被神经元活动增强。IL 1和TNF激活核因子kappa B、腺苷和NO下游机制。因此，睡眠稳态与大脑代谢和血液流动密切相关。我们对细胞因子睡眠机制的了解导致了这样一种观点，即睡眠是神经网络启动的局部特性，例如，在皮质柱内。皮质柱在功能状态之间振荡;皮质柱的睡眠样状态由TNF促进。由于TNF参与谷氨酸能AMPA受体表达和突触缩放机制，细胞因子睡眠机制为睡眠提供突触连接功能的假设提供了额外的支持。
IL1 and TNF are well-characterized SRSs, forming part of the sleep homeostat. Their release is enhanced by neuronal activity via ATP. IL1 and TNF activate nuclear factor kappa B, adenosine, and NO downstream mechanisms. The sleep homeostat is thus closely linked to cerebral metabolism and blood flow. Our knowledge of cytokine sleep mechanisms led to a view that sleep is a local property of neural networks being initiated, eg, within cortical columns. Cortical columns oscillate between functional states; the sleep-like state of cortical columns is promoted by TNF. Because TNF is involved in glutamanergic AMPA receptor expression and in synaptic scaling mechanisms, cytokine sleep mechanisms provide additional support for the hypothesis that sleep serves a synaptic-connectivity function.