• M-H Qiu, M C Chen, and J Lu.
• State Key Laboratory of Medical Neurobiology and Department of Neurobiology, School of Basic Medical Science, Fudan University, Shanghai 200032, China; Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston 02115, USA. Electronic address: mhqiu@shmu.edu.cn.
• Neuroscience. 2015 Jun 25;297:211-8.

AbstractThe 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 (100mg/kg) to rats, producing a dissociated state with slow-wave cortical electroencephalogram (EEG) but waking behavior (e.g. locomotion). Atropine injections during the light period produced 6h of slow-wave cortical EEG but also subcortical arousal. Afterward, 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.Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

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