• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Sleep rhythmicity and homeostasis in mice with targeted disruption of mPeriod genes.
【24h】

Sleep rhythmicity and homeostasis in mice with targeted disruption of mPeriod genes.

机译：靶向干扰mPeriod基因的小鼠的睡眠节律和体内平衡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In mammals, sleep is regulated by circadian and homeostatic mechanisms. The circadian component, residing in the suprachiasmatic nucleus (SCN), regulates the timing of sleep, whereas homeostatic factors determine the amount of sleep. It is believed that these two processes regulating sleep are independent because sleep amount is unchanged after SCN lesions. However, because such lesions necessarily damage neuronal connectivity, it is preferable to investigate this question in a genetic model that overcomes the confounding influence of circadian rhythmicity. Mice with disruption of both mouse Period genes (mPer)1 and mPer2 have a robust diurnal sleep-wake rhythm in an entrained light-dark cycle but lose rhythmicity in a free-run condition. Here, we examine the role of the mPer genes on the rhythmic and homeostatic regulation of sleep. In entrained conditions, when averaged over the 24-h period, there were no significant differences in waking, slow-wave sleep (SWS), or rapid eye movement (REM) sleep between mPer1, mPer2, mPer3, mPer1-mPer2 double-mutant, and wild-type mice. The mice were then kept awake for 6 h (light period 6-12), and the mPer mutants exhibited increased sleep drive, indicating an intact sleep homeostatic response in the absence of the mPer genes. In free-run conditions (constant darkness), the mPer1-mPer2 double mutants became arrhythmic, but they continued to maintain their sleep levels even after 36 days in free-running conditions. Although mPer1 and mPer2 represent key elements of the molecular clock in the SCN, they are not required for homeostatic regulation of the daily amounts of waking, SWS, or REM sleep.
机译：在哺乳动物中，睡眠由昼夜节律和体内平衡机制调节。昼夜节律成分位于上交叉眼上核（SCN）中，可调节睡眠时间，而稳态因素可决定睡眠量。据信，调节睡眠的这两个过程是独立的，因为SCN损伤后睡眠量没有改变。但是，由于此类损伤必定会破坏神经元的连通性，因此最好在克服了昼夜节律性混杂影响的遗传模型中研究此问题。小鼠Period基因（mPer）1和mPer2均被破坏的小鼠在暗夜周期中具有强大的昼夜睡眠节律，但在自由奔跑条件下失去节律。在这里，我们检查了mPer基因在睡眠的节律和体内平衡调节中的作用。在夹带条件下，如果在24小时内取平均值，则mPer1，mPer2，mPer3，mPer1-mPer2双突变体在清醒，慢波睡眠（SWS）或快速眼动（REM）睡眠方面没有显着差异和野生型小鼠。然后将小鼠保持清醒6小时（光照期6-12），并且mPer突变体表现出增强的睡眠驱动力，表明在不存在mPer基因的情况下完整的睡眠体内稳态反应。在自由运行条件下（恒定的黑暗），mPer1-mPer2双重突变体出现了心律失常，但即使在自由运行条件下运行36天后，它们仍继续保持睡眠水平。尽管mPer1和mPer2代表SCN中分子时钟的关键元素，但对于每天的清醒，SWS或REM睡眠量的体内平衡调节并不需要它们。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号