Jhaveri K A, Ramkumar V, Trammell R A, Toth L A
Dept. of Pharmacology, SIU School of Medicine, P.O. Box 19629, Springfield, IL 62794-9629, USA.
Am J Physiol Regul Integr Comp Physiol. 2006 Nov;291(5):R1516-26. doi: 10.1152/ajpregu.00262.2006. Epub 2006 Jun 22.
The dimeric transcription factor nuclear factor-kappaB (NF-kappaB) regulates several endogenous sleep-modulatory substances and thereby serves as a pivotal mediator of sleep-wake homeostasis. To further define the role of NF-kappaB in sleep regulation, we monitored sleep and temperature in mice that lack the p50 subunit of NF-kappaB [p50 knockout (KO) mice]. Compared with the control B6129PF2/J strain, p50 KO mice spend more time in slow-wave sleep (SWS) and rapid eye movement sleep (REMS) under normal conditions and show enhanced homeostatic recovery of sleep after sleep loss. p50 KO mice also show increased SWS and reduced REMS and temperature after the administration of lipopolysaccharide, yet they are behaviorally less responsive to challenge with influenza virus. These data support a role for NF-kappaB, and, in particular, for the p50 subunit, in the regulation of sleep in healthy mice and in mice experiencing immune challenge.
二聚体转录因子核因子-κB（NF-κB）调节多种内源性睡眠调节物质，因此是睡眠-觉醒稳态的关键调节因子。为了进一步明确NF-κB在睡眠调节中的作用，我们监测了缺乏NF-κB p50亚基的小鼠（p50基因敲除KO小鼠）的睡眠和体温。与对照B6129PF2/J品系相比，p50 KO小鼠在正常条件下在慢波睡眠（SWS）和快速眼动睡眠（REMS）中花费的时间更多，并且在睡眠剥夺后显示出更强的睡眠稳态恢复能力。给予脂多糖后，p50 KO小鼠的SWS增加，REMS和体温降低，但它们对流感病毒攻击的行为反应较弱。这些数据支持NF-κB，特别是p50亚基在健康小鼠和经历免疫攻击的小鼠的睡眠调节中发挥作用。
