4.5 Article

Brain-specific interleukin-1 receptor accessory protein in sleep regulation

期刊

JOURNAL OF APPLIED PHYSIOLOGY
卷 112, 期 6, 页码 1015-1022

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.01307.2011

关键词

brain-specific accessory protein knockout; interleukin-1; lipopolysaccharide; immune response; cytokines; growth hormone-releasing hormone

资金

  1. National Institutes of Health [NS-025378, NS-031453, HD-036520]

向作者/读者索取更多资源

Taishi P, Davis CJ, Bayomy O, Zielinski MR, Liao F, Clinton JM, Smith DE, Krueger JM. Brain-specific interleukin-1 receptor accessory protein in sleep regulation. J Appl Physiol 112: 1015-1022, 2012. First published December 15, 2011; doi: 10.1152/japplphysiol.01307.2011.-Interleukin (IL)-1 beta is involved in several brain functions, including sleep regulation. It promotes non-rapid eye movement (NREM) sleep via the IL-1 type I receptor. IL-1 beta/IL-1 receptor complex signaling requires adaptor proteins, e. g., the IL-1 receptor brain-specific accessory protein (AcPb). We have cloned and characterized rat AcPb, which shares substantial homologies with mouse AcPb and, compared with AcP, is preferentially expressed in the brain. Furthermore, rat somatosensory cortex AcPb mRNA varied across the day with sleep propensity, increased after sleep deprivation, and was induced by somnogenic doses of IL-1 beta. Duration of NREM sleep was slightly shorter and duration of REM sleep was slightly longer in AcPb knockout than wild-type mice. In response to lipopolysaccharide, which is used to induce IL-1 beta, sleep responses were exaggerated in AcPb knockout mice, suggesting that, in normal mice, inflammation-mediated sleep responses are attenuated by AcPb. We conclude that AcPb has a role in sleep responses to inflammatory stimuli and, possibly, in physiological sleep regulation.

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