Rapid eye movement (REM) sleep homeostatic regulatory processes in the rat: Changes in the sleep–wake stages and electroencephalographic power spectra

Shea, Jessica; Mochizuki, Takatoshi; Sagvaag, V.; Aspevik, T.; Bjørkum, Alvhild Alette; Datta, Subimal

doi:10.1016/j.brainres.2008.03.062

Cited by 45 publications

(50 citation statements)

References 56 publications

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“…Stress increased REM sleep (p ＜0.005), but RGE unfortunately did affect these changes REM sleep. Our results are consistent with ginseng's effects in ameliorating stress-related sleep disorders, particularly by changing the balance of NREM and REM sleep (Bjorvatn et al, 1998;Shea et al, 2008). These results suggest that RGE may be useful for treatment of stress-related disorders.…”

Section: Discussionsupporting

confidence: 86%

Anti-Stress Effects of Ginsenoside Rg₃-Standardized Ginseng Extract in Restraint Stressed Animals

Kim¹,

Jo²,

Park³

et al. 2010

Biomolecules and Therapeutics

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-We tested whether ginsenosides Rg3-standardized ginseng extract (RGE) has anti-stress effects in restraint-stressed animals. RGE increased time spent in the open arms and open arm entries in the elevated plus-maze test. In addition, RGE blocked the reduction of center zone distance and stereotypes behaviors in the open-field test. RGE also increased head dips in stressed mice, indicating anxiolytic-like effects. Stress decreased movement distance and duration, burrowing, and rearing frequency but increased face washing and grooming. RGE significantly reversed burrowing and rearing activity in stressed mice. In addition, we measured sleep architecture in restraint stressed rats using EEG recorder. Stress increased rapid eye movement (REM) sleep, but total sleep and non-rapid eye movement (NREM) sleep were not changed. RGE did not affect sleep architecture in stressed rats. These behavioral experiments suggest that RGE has anti-stress effects in restraint-stressed animal models.

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Section: Discussionsupporting

confidence: 86%

Anti-Stress Effects of Ginsenoside Rg₃-Standardized Ginseng Extract in Restraint Stressed Animals

Kim¹,

Jo²,

Park³

et al. 2010

Biomolecules and Therapeutics

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“…12 and this study) along with other measures of REM sleep behavior, such as higher REM sleep episode number and shortened REM sleep latency (12). This pattern is different from that observed in acute sleep deprivation in which REM sleep rebound positively correlates with sleep pressure (9,10). In CSR, daily accumulation of REM sleep loss [∼1.5 h/d (11)] did not lead to progressive increasing REM sleep rebound.…”

Section: Discussionmentioning

confidence: 59%

“…REM sleep shows strong homeostatic regulation; acute losses are compensated by rebounds proportional to the lost amount of REM sleep (9,10). However, recent studies using the CSR paradigm, which better resembles common human sleep loss (11,12), revealed limitations of this mechanism, demonstrating that after the first day of sleep loss, REM sleep rebound settles on a persistent elevated level and does not show a progressive increase over days as REM sleep debt keeps accumulating.…”

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confidence: 99%

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation

Kim

Kocsis

Hwang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Homeostatic rebound in rapid eye movement (REM) sleep normally occurs after acute sleep deprivation, but REM sleep rebound settles on a persistently elevated level despite continued accumulation of REM sleep debt during chronic sleep restriction (CSR). Using highdensity EEG in mice, we studied how this pattern of global regulation is implemented in cortical regions with different functions and network architectures. We found that across all areas, slow oscillations repeated the behavioral pattern of persistent enhancement during CSR, whereas high-frequency oscillations showed progressive increases. This pattern followed a common rule despite marked topographic differences. The findings suggest that REM sleep slow oscillations may translate top-down homeostatic control to widely separated brain regions whereas fast oscillations synchronizing local neuronal ensembles escape this global command. These patterns of EEG oscillation changes are interpreted to reconcile two prevailing theories of the function of sleep, synaptic homeostasis and sleep dependent memory consolidation. There has been substantial recent progress in understanding the neuronal mechanisms of two seemingly unrelated but, more likely, complementary functions of sleep. The first, conceptualized as the synaptic homeostasis theory (1), produced experimental evidence for a global downscaling of synaptic strength during sleep to offset the unsustainable upscaling associated with neuronal activation during the preceding period of wakefulness (2). The second line of research keeps accumulating data to support an active role of sleep in offline memory processing (3) and argues that certain synapses not only escape global downscaling in sleep but instead are potentiated; firing rate and synchrony in select neuronal ensembles representing newly acquired and deemed relevant information are increased. The mechanisms of how these two proposed functions of sleep are reconciled on the network or ensemble level are poorly understood.From the very beginning, both processes were linked to specific oscillatory patterns of neuronal activity. The synaptic homeostasis hypothesis, and sleep homeostatic regulation in general, was correlated with EEG delta power (4) and memory consolidation was associated with episodic fast oscillations during non-REM (NREM) sleep (5). Recent evidence from network level investigations concur. On the one hand, different measures of homeostatic downscaling on the neuronal level (synaptic depotentiation, decrease in firing rate, decreased synchrony, etc.) were shown to correlate with the global decrease in delta power (6). On the other hand, reactivation of memory traces primarily occur during spindle-ripple events (7) and requires the temporal organization provided by local fast oscillations for coordination of firing within local neuronal ensembles.Slow and fast oscillations, respectively, support global and local processing, not only in NREM sleep but also in any brain state, in general. Slow oscillations (delta, theta, alpha, beta1) all...

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“…S8B). In previous studies (37,38) an increased ratio SWA to alpha/theta during REM sleep was suggested to reflect the buildup of REM pressure, but during our SR experiment this ratio either did not change (frontal and occipital cortex) or increased, but not progressively (parietal cortex). Large increases in REM sleep were also present after SR and as a result, almost all REM sleep lost during SR was recovered by the end of the second post-SR day (Fig.…”

Section: ) (C) 4smentioning

confidence: 61%

Sleep homeostasis in the rat is preserved during chronic sleep restriction

Leemburg

Vyazovskiy

Olcese

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

144

147

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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...

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Rapid eye movement (REM) sleep homeostatic regulatory processes in the rat: Changes in the sleep–wake stages and electroencephalographic power spectra

Cited by 45 publications

References 56 publications

Anti-Stress Effects of Ginsenoside Rg₃-Standardized Ginseng Extract in Restraint Stressed Animals

Anti-Stress Effects of Ginsenoside Rg₃-Standardized Ginseng Extract in Restraint Stressed Animals

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation

Sleep homeostasis in the rat is preserved during chronic sleep restriction

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Rapid eye movement (REM) sleep homeostatic regulatory processes in the rat: Changes in the sleep–wake stages and electroencephalographic power spectra

Cited by 45 publications

References 56 publications

Anti-Stress Effects of Ginsenoside Rg3-Standardized Ginseng Extract in Restraint Stressed Animals

Anti-Stress Effects of Ginsenoside Rg3-Standardized Ginseng Extract in Restraint Stressed Animals

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation

Sleep homeostasis in the rat is preserved during chronic sleep restriction

Contact Info

Product

Resources

About

Anti-Stress Effects of Ginsenoside Rg₃-Standardized Ginseng Extract in Restraint Stressed Animals

Anti-Stress Effects of Ginsenoside Rg₃-Standardized Ginseng Extract in Restraint Stressed Animals