scholarly journals Differential modulation of NREM sleep regulation and EEG topography by chronic sleep restriction in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bowon Kim ◽  
Eunjin Hwang ◽  
Robert E. Strecker ◽  
Jee Hyun Choi ◽  
Youngsoo Kim
Keyword(s):  
Nrem Sleep ◽  
Brain Regions ◽  
Sleep Eeg ◽  
Sleep Restriction ◽  
Electrode Arrays ◽  
Sleep Regulation ◽  
Amplitude Analysis ◽  
Delta Power ◽  
Eeg Topography ◽  
Chronic Sleep

AbstractCompensatory elevation in NREM sleep EEG delta power has been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indicator. However, recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progressively increased despite of accumulated sleep loss over days. In addition, there has been little progress in understanding how sleep EEG in different brain regions responds to CSR. Using novel high-density EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day for 5 consecutive days, we performed an extensive analysis of topographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of individual slow waves. As previously reported in our analysis of REM sleep responses, we found different patterns of changes: (i) progressive decrease in NREM sleep duration and consolidation, (ii) persistent enhancement in NREM delta power especially in the frontal and parietal regions, and (iii) progressive increases in individual slow wave slope and frontal fast oscillation power. These results suggest that multiple sleep-wake regulatory systems exist in a brain region-specific manner, which can be modulated independently, especially in the CSR condition.

Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Animal Studies ◽  
Sleep Restriction ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Sleep Homeostasis ◽  
High Prevalence ◽  
Homeostatic Response ◽  
Chronic Sleep

Abstract The high prevalence of chronic sleep restriction in adolescents underscores the importance of understanding how adolescent sleep is regulated under such conditions. One component of sleep regulation is a homeostatic process: if sleep is restricted, then sleep intensity increases. Our knowledge of this process is primarily informed by total sleep deprivation studies and has been incorporated in mathematical models of human sleep regulation. Several animal studies, however, suggest that adaptation occurs in chronic sleep restriction conditions, showing an attenuated or even decreased homeostatic response. We investigated the homeostatic response of adolescents to different sleep opportunities. Thirty-four participants were allocated to one of three groups with 5, 7.5 or 10 h of sleep opportunity per night for 5 nights. Each group underwent a protocol of 9 nights designed to mimic a school week between 2 weekends: 2 baseline nights (10 h sleep opportunity), 5 condition nights (5, 7.5 or 10 h), and two recovery nights (10 h). Measures of sleep homeostasis (slow-wave activity and slow-wave energy) were calculated from frontal and central EEG derivations and compared to predictions derived from simulations of the homeostatic process of the two-process model of sleep regulation. Only minor differences were found between empirical data and model predictions, indicating that sleep homeostasis is preserved under chronic sleep restriction in adolescents. These findings improve our understanding of effects of repetitive short sleep in adolescents.

scholarly journals 0327 NREM Sleep EEG in Typically Developing and Drug-Naïve ADHD Adolescents: Data from a Longitudinal Study

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A124-A124
Author(s):  
T Basishvili ◽  
M Eliozishvili ◽  
T Oniani ◽  
T Tchintcharauli ◽  
I Sakhelashvili ◽  
...  
Keyword(s):  
Longitudinal Study ◽  
Nrem Sleep ◽  
Sleep Eeg ◽  
Brain Maturation ◽  
Adhd Group ◽  
Typically Developing ◽  
Eeg Activity ◽  
Theta Power ◽  
Delta Power ◽  
Drug Naïve

Abstract Introduction Structural MRI studies suggest delayed brain maturation in children with attention deficit hyperactivity disorder (ADHD). The steep adolescent decline in sleep slow wave EEG activity provides an opportunity to investigate brain electrophysiological evidence for this maturational delay. Most ADHD sleep EEG studies have been cross-sectional. Here we present data from an ongoing longitudinal study of the maturational trajectories of sleep EEG in drug-naïve ADHD and typically developing adolescents. Methods Nine children diagnosed with ADHD (combined subtype, DSM-V criteria, mean age 12.39±0.61 years), and nine typically developing controls (12.07±0.35 years) were recruited. Subjects underwent an adaptation night and all night polysomnography twice yearly at the Laboratory. Sleep EEG was analyzed using fast Fourier transform. NREM delta and theta EEG activity were compared across first two recordings. Results Group effects (ADHD vs. control) on all night delta and theta energy, and delta power were not significant (p>0.2 for all). All night theta power was lower (p=0.035) for the ADHD group, and all night NREM sleep duration trended (p=0.060) toward being lower for the ADHD group. Controlling for sleep duration differences by examining only the first 5 h of NREM sleep showed no group effect on delta power (p=0.77) and a trend toward lower theta power (p=0.057) for the ADHD group. Conclusion At age 12 to 13 years, NREM sleep delta EEG did not differ between ADHD and control subjects. Theta power, which declines at a younger age than delta, was lower in control subjects. The two recordings thus far differ only by 6 months. The entire study will provide 5 semiannual recordings and allow us to determine if the higher theta power in the ADHD group will hold and if delta power will be greater as well, and thus provide electrophysiological support for the delayed brain maturation suggested by MRI findings. Support Shota Rustaveli National Science Foundation Grant FR17_94; Subjects Recruitment Support - Mental Health Service in Tbilisi “Kamara”.

scholarly journals Behavioral Sleep-Wake Homeostasis and EEG Delta Power Are Decoupled By Chronic Sleep Restriction in the Rat

SLEEP ◽  
2015 ◽  
Vol 38 (5) ◽  
pp. 685-697 ◽  
Author(s):  
Richard Stephenson ◽  
Aimee M. Caron ◽  
Svetlana Famina
Keyword(s):  
Sleep Restriction ◽  
Delta Power ◽  
Chronic Sleep

scholarly journals 0324 Effect of Sleep Restriction on Sleep Electroencephalogram Waveforms in Adolescents

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A123-A123
Author(s):  
I G Campbell ◽  
A Cruz Basilio ◽  
Z Y Zhang ◽  
N Darchia ◽  
I Feinberg
Keyword(s):  
Total Sleep Time ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Sleep Restriction ◽  
Sleep Spindles ◽  
Alpha Power ◽  
The Past ◽  
Delta Power ◽  
Eeg Power ◽  
Eeg Recordings

Abstract Introduction Over the past 18 years, our laboratory has been carrying out longitudinal studies of sleep and sleep need across adolescence. Our current study uses a dose-response design to examine daytime performance and sleep EEG after varied sleep durations. Here we present results for 1-30 Hz EEG power in NREM and REM sleep. Methods Home EEG recording in children 10-16 years old (N=77, mean age = 13.2). Adhering to their habitual rise time participants kept an assigned TIB schedule of 7, 8.5, or 10 hours for four consecutive nights. Participants completed all three conditions each year of the 3 year study. EEG recordings from the fourth night of each condition were scored and analyzed with FFT. Results Reducing TIB from 10 to 7 hours effectively decreased total sleep time (TST) from an average of 531 min to an average of 407 min. Decreasing TIB (from 10 to 7 h) produced a small increase (4.6%, p=0.0004) in delta (1-4 Hz) power and a larger decrease (9.0%, p=0.0032) in alpha (8-11 Hz) power in the first 5 h of NREM sleep. In REM periods 2 and 3, the same TIB reduction also increased (12.1%, p<0.0001) delta power and decreased (14.2%, p<0.0001) alpha power. Decreasing TIB reduced (11%, p<0.0001) sigma (11-15 Hz) power in the first 5h of NREM sleep and reduced (28%, p<0.0001) all night NREM sigma energy. Conclusion Reducing TST changes EEG power in several frequency bands. The increase in NREM delta power, expected from homeostatic models, may be too small to be biologically significant. The larger loss of sigma power may be of greater consequence. Sigma frequency activity is an indicator of sleep spindles which have been affected in aging, learning, memory and psychopathology. The sigma response to sleep restriction could be used to study these relations. Support PHS grant R01 HL116490 supported this work.

scholarly journals 0280 Change in Sleep Depth Across the Night as a Measure of Sleep Adequacy

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A106-A106
Author(s):  
P K Schweitzer ◽  
K Griffin ◽  
M Younes ◽  
J K Walsh
Keyword(s):  
Spectral Power ◽  
Secondary Analysis ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Sleep Restriction ◽  
Continuous Measure ◽  
Delta Power ◽  
Sleep Depth ◽  
Sleep Adequacy ◽  
The Individual

Abstract Introduction It is well known that sleep becomes lighter towards the end of the night reflecting the reduction in homeostatic sleep pressure. We hypothesized that more adequate nocturnal sleep (i.e. sufficient quantity and quality for the individual) would result in a greater reduction in sleep depth across the night and would be reflected in decreased next-day sleep tendency. Methods In a secondary analysis of data from a study in which sleep depth was altered by sleep restriction combined with either placebo or gaboxadol (a delta-promoting drug) we correlated change across the night in two measures of sleep depth with next-day Multiple Sleep Latency Test (MSLT) latencies. Forty-one healthy subjects underwent 8 consecutive sleep studies; two baseline, four sleep restriction (5 hours) and two recovery nights. MSLT was performed following each baseline night and the last two restriction nights. Sleep depth in the first and last hours of NREM sleep was determined by two methods 1) Log delta spectral power; 2) The odds-ratio-product (ORP), a recently introduced continuous measure of sleep depth. The difference between initial and final values was calculated (ΔDelta, ΔORP). Post-restriction MSLT latency was correlated with baseline MSLT latency, ΔDelta, ΔORP, log delta power and ORP in the last hour, lost total sleep time and lost REM time. Results ΔDelta was -0.27 ±0.13 and ΔORP was 0.17 ±0.13, both changes reflecting lightening of sleep across the night. In both univariate and multivariate analysis only baseline MSLT latency (p &lt 0.001) and ΔORP (p &lt 0.01) were significantly and positively correlated with post-restriction MSLT latency. Conclusion The reduction in sleep depth across the night as measured by ORP, but not by delta power, is significantly correlated with reduced objective sleepiness following sleep restriction. ΔORP may be a useful index that reflects sleep adequacy during the night. Support None

112 Chronic sleep restriction disrupts slow-wave sleep homeostatic regulation and damages monoaminergic structures in the rat brain

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A46-A46
Author(s):  
Mikhail Guzeev ◽  
Nikita Kurmazov ◽  
Valentina Simonova ◽  
Daria Belan ◽  
Ksenia Lapshina ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Cognitive Disorders ◽  
Emotional Behavior ◽  
Sleep Restriction ◽  
High Tech ◽  
Integrative Physiology ◽  
Delta Power ◽  
Monoaminergic Structures ◽  
Chronic Sleep

Abstract Introduction The neurophysiological mechanisms underlying long-term neurological and cognitive disorders associated with chronic sleep restriction (CSR) are not fully understood. Here we evaluated how the sleep-wake cycle changes during and after a period of sleep restriction in rats, and whether CSR results in neurodegeneration in monoaminergic brain structures. Methods For CSR, 7-8-month-old Wistar rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 5 days on the orbital shaker. Telemetric sleep recordings were made before, during, and after CSR. Neurodegeneration in brain monoaminergic structures was assessed immunohistochemically. Results During SD, wakefulness comprised 85% of the total registration time; the remaining time was represented by drowsiness with low EEG delta power. Rapid eye movement sleep (REMS) was absent. During CSR, slow-wave sleep (SWS) and REMS were reduced by 62% and 57%. Total SWS time during SO periods increased on the first CSR day, but decreased to the baseline by the fifth CSR day. SWS EEG delta power (a measure of sleep intensity) decreased gradually from the first to the fifth CSR day. REMS total time remained elevated during all SO periods. During the first recovery day after CSR, SWS did not change, but REMS increased by 30%. No changes in total sleep time were found on the second recovery day but sleep intensity was decreased. In 14 days after CSR, all sleep parameters returned to the baseline. We revealed a loss of 24% of noradrenergic locus coeruleus neurons, 29% and 17% of dopaminergic neurons in the substantia nigra, the ventral tegmental area as well as in their striatal terminals. Conclusion We consider CSR as a damaging factor leading to a gradual suppression of homeostatic mechanisms governing sleep recovery. CSR can provoke neurodegeneration in monoaminergic structures involved in the regulation of emotional behavior, sleep, and autonomic functions. Support (if any) Ministry of Science and Higher Education of the Russian Federation grant (No. 075-15-2020-916 dated November 13, 2020) for the establishment and development of the Pavlovsky Center “Integrative Physiology for Medicine, High-Tech Healthcare and Stress Resilience Technologies”.

Topography of EEG Dynamics After Sleep Deprivation in Mice

2000 ◽  
Vol 84 (4) ◽  
pp. 1888-1893 ◽  
Author(s):  
Reto Huber ◽  
Tom Deboer ◽  
Irene Tobler
Keyword(s):  
Sleep Deprivation ◽  
Time Constant ◽  
Frequency Band ◽  
Regional Differences ◽  
Process Model ◽  
Nrem Sleep ◽  
Occipital Cortex ◽  
Brain Regions ◽  
Prior History ◽  
Sleep Regulation

Several recent results show that sleep and sleep regulation are not only global phenomena encompassing the entire brain, but have local features. It is well established that slow-wave activity [SWA; mean electroencephalographic (EEG) power density in the 0.75–4.0 Hz band] in non–rapid eye movement (NREM) sleep is a function of the prior history of sleep and wakefulness. SWA is thought to reflect the homeostatic component of the two-process model of sleep regulation. According to this model, originally formulated for the rat and later extended to human sleep, the timing and structure of sleep are determined by the interaction of a homeostatic Process S and a circadian process. Our aim was to investigate the dynamics of SWA in the EEG of two brain regions (frontal and occipital cortex) after sleep deprivation (SD) in two of the mice strains most often used in gene targeting. C57BL/6J ( n = 9) and 129/Ola ( n = 8) were recorded during a 24-h baseline day, 6-h SD, and 18-h recovery. Both derivations showed a significant increase in SWA in NREM sleep after SD in both strains. In the first hour of recovery, SWA was enhanced more in the frontal derivation than in the occipital derivation and showed a faster decline. This difference resulted in a lower value for the time constant for the decrease of SWA in the frontal derivation (frontal: 10.9 ± 2.1 and 6.8 ± 0.9 h in Ola and C57, respectively; occipital: 16.6 ± 2.1 and 14.1 ± 1.5 h; P < 0.02; for each of the strains; paired t-test). Neither time constant differed significantly between the strains. The subdivision of SWA into a slower and faster band (0.75–2.5 Hz and 2.75–4.0 Hz) further highlighted regional differences in the effect of SD. The lower frequency band had a higher initial value in the frontal derivation than in the occipital derivation in both strains. Moreover, in the higher frequency band a prominent reversal took place so that power in the frontal derivation fell below the occipital values in both strains. Thus our results indicate that there may be differences in the brain in the effects of SD on SWA in mice, suggesting regional differences in the dynamics of the homeostatic component of sleep regulation. The data support the hypothesis that sleep has local, use- or waking-dependent features that are reflected in the EEG, as has been shown for humans and the laboratory rat.

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

2012 ◽  
Vol 302 (12) ◽  
pp. R1411-R1425 ◽  
Author(s):  
S. Deurveilher ◽  
B. Rusak ◽  
K. Semba
Keyword(s):  
Eye Movement ◽  
Recovery Period ◽  
Sleep Time ◽  
Time Of Day ◽  
Male Rats ◽  
Sleep Restriction ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Delta Power ◽  
Chronic Sleep

To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.

029 Median preoptic dual control over sleep regulation

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A13-A14
Author(s):  
Natalia Machado ◽  
William Todd ◽  
Clifford Saper
Keyword(s):  
Nrem Sleep ◽  
Underlying Mechanism ◽  
Brain Regions ◽  
Sleep Cycle ◽  
Sleep Regulation ◽  
Sleep Behavior ◽  
Sleep Homeostasis ◽  
Psychological Stressor ◽  
Sleep Control

Abstract Introduction Previous studies suggest that the median preoptic nucleus (MnPO) plays an important role in regulating the wake-sleep cycle and in particular homeostatic sleep drive. However, the precise cellular phenotypes, targets and central mechanisms by which the MnPO neurons regulate the wake-sleep cycle remain unknown. Both glutamatergic (Vglut2+) and GABAergic (Vgat+) MnPO neurons innervate brain regions implicated in sleep promotion and maintenance, suggesting that both cell types may participate on sleep control. Methods In this study, we used two genetically-targeted approaches associated with electroencephalographic (EEG) and electromyographic (EMG) recordings in Vgat-IRES-cre and Vglut2-IRES-cre mice to investigate the role of the MnPOVgat and MnPOVglut2 neurons in modulating wake-sleep behavior. Results First, using a chemogenetic approach, we found that activation of MnPOVgat neurons reduced the latency for the first NREM sleep episode, produced an increase in NREM sleep and reduced wakefulness. Then, to test the role of MnPOVgat and MnPOVglut2 neurons in regulating sleep homeostasis, we recorded EEG and EMG responses in mice that had the Vgat+ or Vglut2+ neurons deleted from the MnPO. After deletion of MnPOVgat neurons, mice showed a reduction of NREM sleep and an increase in wakefulness during the light phase. Deletion of MnPOVgat neurons also reduced sleep recovery after 4 hours of sleep deprivation (SD). On the other hand, deletion of the MnPOVglut2 neurons did not change the wake-sleep cycle during the 24h baseline condition, but prevented the sleep recovery immediately after SD. To understand the underlying mechanism in preventing sleep recovery in both MnPOVglut2- and MnPOVgat-deleted mice groups, we exposed these animals to a psychological stress protocol. In response to a psychological stressor, mice with deletion of glutamatergic, but not GABAergic MnPO neurons, had an exacerbation of the stress-induced insomnia. Conclusion Our results suggest that both neuron populations differentially participate in wake-sleep control, with MnPOVgat neurons being critically involved in sleep homeostasis, and MnPOVglut2 neurons promoting sleep during allostatic (stressful) challenges. Support (if any) NIH Grants NS085477, NS072337, HL095491 and Sleep Research Society Foundation (Award 026-JP-20).

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.

Sign in / Sign up

Export Citation Format

Share Document