Sleep is homeostatically regulated in all animal species that have been carefully studied so far. The best characterized marker of sleep homeostasis is slow wave activity (SWA), the EEG power between 0.5 and 4 Hz during nonrapid eye movement (NREM) sleep. SWA reflects the accumulation of sleep pressure as a function of duration and/or intensity of prior wake: it increases after spontaneous wake and short-term (3-24 h) sleep deprivation and decreases during sleep. However, recent evidence suggests that during chronic sleep restriction (SR) sleep may be regulated by both allostatic and homeostatic mechanisms. Here, we performed continuous, almost completely artifact-free EEG recordings from frontal, parietal, and occipital cortex in freely moving rats (n = 11) during and after 5 d of SR. During SR, rats were allowed to sleep during the first 4 h of the light period (4S + ) but not during the following 20 h (20S − ). During the daily 20S− most sleep was prevented, whereas the number of short (<20 s) sleep attempts increased. Low-frequency EEG power (1-6 Hz) in both sleep and wake also increased during 20S − , most notably in the occipital cortex. In all animals NREM SWA increased above baseline levels during the 4S + periods and in post-SR recovery. The SWA increase was more pronounced in frontal cortex, and its magnitude was determined by the efficiency of SR. Analysis of cumulative slow wave energy demonstrated that the loss of SWA during SR was compensated by the end of the second recovery day. Thus, the homeostatic regulation of sleep is preserved under conditions of chronic SR.cortex | EEG | slow wave activity | slow wave energy | theta activity S leep is homeostatically regulated in all mammalian and nonmammalian species that have been carefully studied so far: in general, the longer an animal stays awake, the longer and/or deeper it sleeps (1-4). The best characterized marker of sleep pressure in mammals and birds is slow wave activity (SWA), defined as the electroencephalogram (EEG) power between 0.5 and 4 Hz during nonrapid eye movement (NREM) sleep. SWA peaks at sleep onset and decreases with time spent asleep (3). Staying awake from ∼3 to ∼24 h results in progressively higher SWA levels at sleep onset, and naps during the day reduce SWA the following night (3). Slow waves reflect the synchronous firing of large groups of cortical neurons coordinated by an underlying slow oscillation, the fundamental cellular phenomenon of NREM sleep (5). Increasing evidence suggests that slow waves can mediate some of sleep's beneficial effects, from the prevention of cognitive impairment to memory consolidation (6-9). Thus, SWA may be more than just an epiphenomenon of NREM sleep and may be related to its functions.Numerous studies have shown that SWA increases after periods of spontaneous wake or following a few hours of sleep deprivation (10-12). However, fewer experiments have measured SWA after >1 d of sleep deprivation or after several days of sleep restriction (SR), during which sleep is only allowed for a few hou...

No abstract

Electroencephalography (EEG) changes across vigilance states have been observed after ischemic stroke in patients and experimental stroke models, but their relation to functional recovery remains unclear. Here, we evaluate motor function, as measured by single pellet reaching (SPR), as well as local EEG changes in nonrapid eye movement (NREM), rapid eye movement (REM), and wakefulness during a 30 day recovery period after middle cerebral artery occlusion or sham surgery in rats. Small cortical infarcts resulted in poor SPR performance and induced widespread changes in EEG spectra in the ipsilesional hemisphere in all vigilance states, without causing major changes in sleep-wake architecture. Ipsilesional 1-4 Hz power was increased after stroke, whereas power in higher frequencies was reduced, resulting in a steeper slope of the power spectrum. Microelectrode array analysis of ipsilesional M1 showed that these spectral changes were present on the microelectrode level throughout M1 and were not related to increased synchronization between electrodes. Spectrum slope was significantly correlated with poststroke motor function and may thus be a useful readout of recovery-related plasticity.