State-specific Effects of Sevoflurane Anesthesia on Sleep Homeostasis

Background Prolonged propofol administration does not result in signs of sleep deprivation, and propofol anesthesia appears to satisfy the homeostatic need for both rapid eye movement (REM) and non-REM (NREM) sleep. In the current study, the effects of sevoflurane on recovery from total sleep deprivation were investigated. Methods Ten male rats were instrumented for electrophysiologic recordings under three conditions: (1) 36-h ad libitum sleep; (2) 12-h sleep deprivation followed by 24-h ad libitum sleep; and (3) 12-h sleep deprivation, followed by 6-h sevoflurane exposure, followed by 18-h ad libitum sleep. The percentage of waking, NREM sleep, and REM sleep, as well as NREM sleep δ power, were calculated and compared for all three conditions. Results Total sleep deprivation resulted in significantly increased NREM and REM sleep for 12-h postdeprivation. Sevoflurane exposure after deprivation eliminated the homeostatic increase in NREM sleep and produced a significant decrease in the NREM sleep δ power during the postanesthetic period, indicating a complete recovery from the effects of deprivation. However, sevoflurane did not affect the time course of REM sleep recovery, which required 12 h after deprivation and anesthetic exposure. Conclusion Unlike propofol, sevoflurane anesthesia has differential effects on NREM and REM sleep homeostasis. These data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.

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The European starling (Sturnus vulgaris) shows signs of NREM sleep homeostasis but has very little REM sleep and no REM sleep homeostasis

SLEEP ◽

10.1093/sleep/zsz311 ◽

2019 ◽

Vol 43 (6) ◽

Cited By ~ 4

Author(s):

Sjoerd J van Hasselt ◽

Maria Rusche ◽

Alexei L Vyssotski ◽

Simon Verhulst ◽

Niels C Rattenborg ◽

...

Keyword(s):

Sleep Deprivation ◽

Eye Movement ◽

Rem Sleep ◽

Spectral Power ◽

Nrem Sleep ◽

Sleep Time ◽

European Starling ◽

Dark Phase ◽

Rapid Eye Movement ◽

Sleep Homeostasis

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.

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Total sleep deprivation in the rat transiently abolishes the delta amplitude response to darkness: implications for the mechanism of the “negative delta rebound”

Journal of Neurophysiology ◽

10.1152/jn.1993.70.6.2695 ◽

1993 ◽

Vol 70 (6) ◽

pp. 2695-2699 ◽

Cited By ~ 13

Author(s):

I. Feinberg ◽

I. G. Campbell

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Nrem Sleep ◽

Sleep Research ◽

Amplitude Response ◽

Total Sleep Deprivation ◽

Sleep Physiology ◽

Total Failure ◽

Delta Sleep ◽

Homeostatic Model

1. The homeostatic model of delta sleep has provided a useful framework for basic sleep research. This model is based on the relation of delta EEG to the duration of prior waking in man, a relation highlighted by the marked increase (rebound) in the delta EEG of nonrapid eye movement (NREM) sleep that follows total sleep deprivation (TSD). The generality of this model is severely challenged by the response to TSD in the rat. In the 12-h light period (LP) that immediately follows TSD, the rat shows a massive increase in REM sleep but only a modest increase in NREM delta EEG. Although this initial delta increase does not nearly compensate for the delta lost during deprivation, the rat then exhibits a depressed rate of delta production (the “negative delta rebound”). This robust and reproducible reaction worsens the delta deficit. 2. Using rats with chronic electrode implantations, we deprived them of all sleep for 24 h by handling them gently when they became inactive. We found that the negative delta rebound entails a transient, near-total failure of delta amplitude to increase normally in response to the onset of darkness. This loss of the rat's EEG response to darkness suggests a disruption of basic sleep physiology and raises the possibility that the negative rebound is also a pathological response. 3. We hypothesize that the negative rebound is maladaptive, and is caused by the massive increase in REM sleep that precedes it; this hypothesis can be tested experimentally.(ABSTRACT TRUNCATED AT 250 WORDS)

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332 Non-REM EEG Spectral Power at Baseline and After Total Sleep Deprivation in Individuals with Sleep-Onset Insomnia

SLEEP ◽

10.1093/sleep/zsab072.331 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A133-A133

Author(s):

Myles Finlay ◽

Devon Hansen ◽

Lillian Skeiky ◽

Hans Van Dongen

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Spectral Power ◽

Sleep Onset ◽

Sleep Eeg ◽

Alpha Power ◽

Healthy Controls ◽

Total Sleep Deprivation ◽

Delta Power ◽

Sleep Homeostasis

Abstract Introduction The baseline non-REM sleep EEG of individuals with insomnia has been found to display increased spectral power at frequencies >14Hz, which may reflect hyperarousal. There is some evidence in this population of reduced slow wave activity after total sleep deprivation (TSD), potentially indicating altered sleep homeostasis. We investigated non-REM sleep EEG spectra at baseline and after TSD in individuals with sleep-onset insomnia. Methods 10 individuals with sleep-onset insomnia and 5 healthy controls (ages 22-40y, 11 females) completed a 5-day laboratory study with an adaptation night, baseline night, assignment to 38h TSD (n=5 insomnia, n=5 control) or equivalent non-TSD control (n=5 insomnia), and recovery night. Sleep periods were 10h (22:00-08:00) with digital polysomnography (250Hz; Nihon Kohden). Following artifact rejection, 5s subepochs of the non-REM (stages N2, N3) sleep EEG (C3-M2 derivation) in baseline and recovery nights were subjected to spectral analysis. Spectra (0.2Hz bins) were averaged over subepochs in 30s epochs. Repeated-measures ANOVA compared baseline spectra between insomnia and controls, and baseline-recovery difference spectra between TSD insomnia, non-TSD insomnia, and TSD controls. Results Average non-REM sleep amount was 5.9 at baseline, increasing by 1.1h after TSD, with no differences between groups (p≥0.20). At baseline, the insomnia group showed increased power in theta/alpha (~4–12Hz), reaching significance in the lower spindle range, compared to controls (p<0.05). As anticipated, no differences emerged between baseline and recovery nights in the non-TSD insomnia group. However, the TSD insomnia group showed increased delta (~1–3Hz) and theta/alpha (~6–10Hz) power (p<0.05) during recovery. Healthy controls showed expected power increases in delta and lower spindle range, and decreases in upper spindle range (~14–15Hz), after TSD (p<0.05). Conclusion Compared to healthy controls, individuals with sleep-onset insomnia showed increased non-REM sleep EEG power in the theta/alpha bands and low spindle frequency range, with further significant increases in theta/alpha in addition to delta power following TSD, despite small sample size. The increase in delta power following TSD was equivalent to that in healthy controls, suggesting no sleep homeostasis abnormality. Whether the elevated theta/alpha power may be related to hyperarousal is unclear. Support (if any) ONR grant N00014-13-C-0063

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Sleep after arousal from hibernation is not homeostatically regulated

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.2.r522 ◽

1999 ◽

Vol 276 (2) ◽

pp. R522-R529 ◽

Cited By ~ 10

Author(s):

Jennie E. Larkin ◽

H. Craig Heller

Keyword(s):

Sleep Deprivation ◽

Brain Function ◽

Extended Period ◽

Nrem Sleep ◽

Wave Activity ◽

Ground Squirrels ◽

Recovery Sleep ◽

Sleep Homeostasis ◽

Homeostatic Response ◽

Periodic Arousals

Electroencephalographic slow-wave activity (SWA) in non-rapid eye movement (NREM) sleep is directly related to prior sleep/wake history, with high levels of SWA following extended periods of wake. Therefore, SWA has been thought to reflect the level of accumulated sleep need. The discovery that euthermic intervals between hibernation bouts are spent primarily in sleep and that this sleep is characterized by high and monotonically declining SWA has led to speculation that sleep homeostasis may play a fundamental role in the regulation of the timing of bouts of hibernation and periodic arousals to euthermia. It was proposed that because the SWA profile seen after arousal from hibernation is strikingly similar to what is seen in nonhibernating mammals after extended periods of wakefulness, that hibernating mammals may arouse from hibernation with significant accumulated sleep need. This sleep need may accumulate during hibernation because the low brain temperatures during hibernation may not be compatible with sleep restorative processes. In the present study, golden-mantled ground squirrels were sleep deprived during the first 4 h of interbout euthermia by injection of caffeine (20 mg/kg ip). We predicted that if the SWA peaks after bouts of hibernation reflected a homeostatic response to an accumulated sleep need, sleep deprivation should simply have displaced and possibly augmented the SWA to subsequent recovery sleep. Instead we found that after caffeine-induced sleep deprivation of animals just aroused from hibernation, the anticipated high SWA typical of recovery sleep did not occur. Similar results were found in a study that induced sleep deprivation by gentle handling (19). These findings indicate that the SWA peak immediately after hibernation does not represent homeostatic regulation of NREM sleep, as it normally does after prolonged wakefulness during euthermia, but instead may reflect some other neurological process in the recovery of brain function from an extended period at low temperature.

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Neurobiology of REM Sleep, NREM Sleep Homeostasis, and Gamma Band Oscillations

Sleep Disorders Medicine ◽

10.1007/978-1-4939-6578-6_5 ◽

2017 ◽

pp. 55-77 ◽

Cited By ~ 4

Author(s):

James T. McKenna ◽

Mark R. Zielinski ◽

Robert W. McCarley

Keyword(s):

Rem Sleep ◽

Nrem Sleep ◽

Gamma Band ◽

Sleep Homeostasis ◽

Gamma Band Oscillations

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Sawtooth waves during REM sleep after administration of haloperidol combined with total sleep deprivation in healthy young subjects

Brazilian Journal of Medical and Biological Research ◽

10.1590/s0100-879x2002000500013 ◽

2002 ◽

Vol 35 (5) ◽

pp. 599-604 ◽

Cited By ~ 2

Author(s):

L.R. Pinto Jr. ◽

C.A. Peres ◽

R.H. Russo ◽

A.J. Remesar-Lopez ◽

S. Tufik

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Total Sleep Deprivation ◽

Young Subjects

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Pharmacological Modulation of Sleep Homeostasis in Rat: Novel Effects of an mGluR2/3 Antagonist

SLEEP ◽

10.1093/sleep/zsz123 ◽

2019 ◽

Vol 42 (9) ◽

Author(s):

Nicola Hanley ◽

Jerome Paulissen ◽

Brian J Eastwood ◽

Gary Gilmour ◽

Sally Loomis ◽

...

Keyword(s):

Eye Movement ◽

Functional Capacity ◽

Rem Sleep ◽

Critical Role ◽

Nrem Sleep ◽

Rapid Eye Movement ◽

Negative Consequences ◽

Promoting Effect ◽

Two Phase ◽

Sleep Homeostasis

Abstract Increasing vigilance without incurring the negative consequences of extended wakefulness such as daytime sleepiness and cognitive impairment is a major challenge in treating many sleep disorders. The present work compares two closely related mGluR2/3 antagonists LY3020371 and LY341495 with two well-known wake-promoting compounds caffeine and d-amphetamine. Sleep homeostasis properties were explored in male Wistar rats by manipulating levels of wakefulness via (1) physiological sleep restriction (SR), (2) pharmacological action, or (3) a combination of these. A two-phase nonlinear mixed-effects model combining a quadratic and exponential function at an empirically estimated join point allowed the quantification of wake-promoting properties and any subsequent sleep rebound. A simple response latency task (SRLT) following SR assessed functional capacity of sleep-restricted animals treated with our test compounds. Caffeine and d-amphetamine increased wakefulness with a subsequent full recovery of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep and were unable to fully reverse SR-induced impairments in SRLT. In contrast, LY3020371 increased wakefulness with no subsequent elevation of NREM sleep, delta power, delta energy, or sleep bout length and count, yet REM sleep recovered above baseline levels. Prior sleep pressure obtained using an SR protocol had no impact on the wake-promoting effect of LY3020371 and NREM sleep rebound remained blocked. Furthermore, LY341495 increased functional capacity across SRLT measures following SR. These results establish the critical role of glutamate in sleep homeostasis and support the existence of independent mechanisms for NREM and REM sleep homeostasis.

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NREM delta stimulation following MK-801 is a response of sleep systems

Journal of Neurophysiology ◽

10.1152/jn.1996.76.6.3714 ◽

1996 ◽

Vol 76 (6) ◽

pp. 3714-3720 ◽

Cited By ~ 27

Author(s):

I. G. Campbell ◽

I. Feinberg

Keyword(s):

Sleep Deprivation ◽

Eye Movement ◽

Time Course ◽

Sleep Onset ◽

Nrem Sleep ◽

Rapid Eye Movement ◽

Mk 801 ◽

Regulatory Systems ◽

Sleep Centers ◽

Electroencephalogram Eeg

1. We have previously shown that noncompetitive blockade of the N-methyl-D-aspartate (NMDA)-gated cation channel with ketamine or Dizocilpine maleate (MK-801) increases the intensity of non-rapid-eye-movement (NREM) delta during subsequent sleep. This delta increase [measured as integrated amplitude (IA) in 1- to 4-Hz electroencephalogram (EEG)] occurs in the 12-h period following intraperitoneal injection. However, the 12 h after drug injection is also the period in which these drugs induce neurotoxic changes, raising the possibility that the increased delta represents toxic EEG slowing rather than an increase in the physiological delta waves of NREM sleep. 2. We hypothesized that the time course of delta stimulation could be separated from the time course of neurotoxicity. We tested this hypothesis by injecting 0.3 mg/kg MK-801 at the start of the dark period (DP) and depriving rats of sleep until the onset of the light period (LP) 12 h later. 3. There were two control groups: one received MK-801 at the start of the DP with no further manipulation, and the second received a saline injection at DP onset followed by 12 h of sleep deprivation. The dependent variable was the amount of delta IA in the LP, whose onset was 12 h after MK-801 injection. Total IA in the LP was significantly greater in rats that received MK-801 followed by sleep deprivation than in rats that received sleep deprivation alone or MK-801 alone. 4. This finding indicates that delta stimulation by MK-801 is maintained over 12 h of waking, indicating that the delta increase is not due to toxic EEG slowing or persisting MK-801. Instead, NMDA channel blockade by MK-801 increases the homeostatic need for delta or else directly alters sleep regulatory systems. We speculate that these effects are mediated by hypothalamic sleep centers through control of neuroendocrine pulses that produce both NREM and rapid-eye-movement sleep. 5. Imposing a period of waking between drug administration and sleep onset may prove a generally useful strategy for determining whether a drug affects the homeostatic need for sleep or acutely stimulates sleep systems. This strategy can also help distinguish between toxic and physiological increases in delta EEG.

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