Sleep and Performance Research Center, WWAMI Medical Education Program, Washington State University, Spokane, WA 99210-1495, USA.
J Appl Physiol (1985). 2012 Mar;112(6):1015-22. doi: 10.1152/japplphysiol.01307.2011. Epub 2011 Dec 15.
Interleukin (IL)-1β 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-1β/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-1β. 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-1β, 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.
白细胞介素 (IL)-1β 参与多种脑功能，包括睡眠调节。它通过 IL-1 型受体促进非快速眼动 (NREM) 睡眠。IL-1β/IL-1 受体复合物信号需要衔接蛋白，例如白细胞介素-1 受体脑特异性辅助蛋白 (AcPb)。我们已经克隆并表征了大鼠 AcPb，它与小鼠 AcPb 具有显著的同源性，与 AcP 相比，在大脑中优先表达。此外，大鼠体感皮层 AcPb mRNA 随睡眠倾向在一天中变化，睡眠剥夺后增加，并被 IL-1β 的促睡眠剂量诱导。AcPb 基因敲除小鼠的 NREM 睡眠时间略短，REM 睡眠时间略长。在 AcPb 基因敲除小鼠中，脂多糖（用于诱导 IL-1β）引起的睡眠反应被夸大，这表明在正常小鼠中，炎症介导的睡眠反应被 AcPb 减弱。我们得出结论，AcPb 在对炎症刺激的睡眠反应中起作用，并且可能在生理睡眠调节中起作用。
