Cortical neuronal activity does not regulate sleep homeostasis.
Cortical neuronal activity does not regulate sleep homeostasis.
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皮质神经元活动不调节睡眠稳态。
DOI：
10.1016/j.neuroscience.2015.03.070
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发表时间：
2015-06-25
期刊：
影响因子：
3.3
通讯作者：
Lu J
中科院分区：
文献类型：
--
作者：
Qiu MH;Chen MC;Lu J
睡眠稳态的神经基础尚不清楚，但皮质和皮质下结构都被认为参与睡眠调节。为了测试皮层或皮层下区域先前的神经元活动是否会导致睡眠反弹，我们对大鼠全身给予阿托品（100 mg/kg），产生一种具有慢波皮层EEG但具有清醒行为（例如：运动）。在光照期间注射阿托品会产生6小时的慢波皮层脑电图，但也会产生皮层下唤醒。之后，与基线日的同一时期相比，大鼠的非快速眼动（NREM）睡眠显着增加。与全身性阿托品产生的行为和皮层EEG状态一致，c-Fos表达在皮层中低，但在多个皮层下唤醒系统中高。这些数据表明，皮层下的唤醒和行为足以驱动睡眠稳态，而类似睡眠的皮层活动模式不足以满足睡眠稳态。
The neural substrate of sleep homeostasis is unclear, but both cortical and subcortical structures are thought to be involved in sleep regulation. To test whether prior neuronal activity in the cortex or in subcortical regions drives sleep rebound, we systemically administered atropine (100 mg/kg) to rats, producing a dissociated state with slow-wave cortical EEG but waking behavior (eg. locomotion). Atropine injections during the light period produced six hours of slow-wave cortical EEG but also subcortical arousal. Afterwards, rats showed a significant increase in non-rapid eye movement (NREM) sleep, compared to the same period on a baseline day. Consistent with the behavioral and cortical EEG state produced by systemic atropine, c-Fos expression was low in the cortex but high in multiple subcortical arousal systems. These data suggest that subcortical arousal and behavior are sufficient to drive sleep homeostasis, while a sleep-like pattern of cortical activity is not sufficient to satisfy sleep homeostasis.