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

2002 ◽  
Vol 35 (5) ◽  
pp. 599-604 ◽  
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

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

1993 ◽  
Vol 70 (6) ◽  
pp. 2695-2699 ◽  
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)

Homeostasis of REM Sleep After Total and Selective Sleep Deprivation in the Rat

2000 ◽  
Vol 84 (5) ◽  
pp. 2699-2702 ◽  
Author(s):  
Adrián Ocampo-Garcés ◽  
Enrique Molina ◽  
Alberto Rodríguez ◽  
Ennio A. Vivaldi
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Rapid Eye Movement ◽  
Homeostatic Regulation ◽  
Rem Sleep Deprivation ◽  
Total Sleep Deprivation ◽  
Final Value ◽  
Median Amount

During specific rapid eye movement (REM) sleep deprivation its homeostatic regulation is expressed by progressively more frequent attempts to enter REM and by a compensatory rebound after the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be differentially related to non-REM (NREM) and wakefulness. This problem bears direct implications on the issue of the function of REM and its relation to NREM. We compared three protocols that combined REM-specific and total sleep deprivation so that animals underwent similar 3-h REM deprivations but different concomitant NREM deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours. Deprivation periods started at hour 6 after lights on. Twenty-two chronically implanted rats were recorded. The median amount of REM during all three protocols was ∼1 min. The deficits of median amount of NREM in minutes within the 3-h deprivation periods as compared with their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%), 25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among protocols. Attempted transitions to REM showed a rising trend during REM deprivations reaching a final value that did not differ significantly among the three protocols. These results support the hypothesis that the build up of REM pressure and its subsequent rebound is primarily related to REM absence independent of the presence of NREM.

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

SLEEP ◽  
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

scholarly journals State-specific Effects of Sevoflurane Anesthesia on Sleep Homeostasis

2011 ◽  
Vol 114 (2) ◽  
pp. 302-310 ◽  
Author(s):  
Dinesh Pal ◽  
William J. Lipinski ◽  
Amanda J. Walker ◽  
Ashley M. Turner ◽  
George A. Mashour
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Time Course ◽  
Nrem Sleep ◽  
Complete Recovery ◽  
Male Rats ◽  
Sevoflurane Anesthesia ◽  
Total Sleep Deprivation ◽  
Sleep Homeostasis ◽  
Ad Libitum

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.

scholarly journals Critical Role of CA1 Nicotinic Receptors on Memory Acquisition Deficit Under Induction of Total Sleep Deprivation and REM Sleep Deprivation

2018 ◽  
Vol 5 (1) ◽  
pp. 11-20
Author(s):  
Bibi-Zahra Javad-Moosavi ◽  
Gholamhassan Vaezi ◽  
Mohammad Nasehi ◽  
Seyed-Ali Haeri-Rouhani ◽  
Mohammad-Reza Zarrindast
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Nicotinic Receptors ◽  
Critical Role ◽  
Rem Sleep Deprivation ◽  
Total Sleep Deprivation ◽  
Memory Acquisition

scholarly journals Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Response Speed ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Neurobehavioral Deficits ◽  
Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

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