Altered patterns of sleep and behavioral adaptability in NPAS2-defficient mice
Altered patterns of sleep and behavioral adaptability in NPAS2-defficient mice
复制标题
DOI：
10.1126/science.1082795
复制
发表时间：
2003-07-18
期刊：
影响因子：
56.9
通讯作者：
McKnight, SL
中科院分区：
文献类型：
--
作者：
Dudley, CA;Erbel-Sieler, C;McKnight, SL
动物的行为是同步的24小时光：暗（LD）周期的调节程序，产生昼夜波动的基因表达在整个身体。在哺乳动物中，转录因子CLOCK控制大脑视交叉上核的昼夜节律振荡;其副产物神经元PAS结构域蛋白2（NPAS 2）在其他前脑部位执行类似的功能。为了研究NPAS 2在昼夜节律行为表现中的作用，我们研究了NPAS 2缺陷小鼠的自发活动、睡眠模式和对光照和限制性食物驱动的夹带的适应性。我们的研究结果表明，NPAS 2在维持正常LD和喂养条件下的昼夜节律行为中起着实质性的作用，并且NPAS 2对食物限制的适应性至关重要。
Animal behavior is synchronized to the 24-hour light:dark (LD) cycle by regulatory programs that produce circadian fluctuations in gene expression throughout the body. In mammals, the transcription factor CLOCK controls circadian oscillation in the suprachiasmatic nucleus of the brain; its paralog, neuronal PAS domain protein 2 (NPAS2), performs a similar function in other forebrain sites. To investigate the role of NPAS2 in behavioral manifestations of circadian rhythm, we studied locomotor activity, sleep patterns, and adaptability to both light- and restricted food-driven entrainment in NPAS2-deficient mice. Our results indicate that NPAS2 plays a substantive role in maintaining circadian behaviors in normal LD and feeding conditions and that NPAS2 is critical for adaptability to food restriction.