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

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”.

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Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽

10.1093/sleep/zsab106 ◽

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.

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EEG delta power and auditory arousal in rested and sleep-deprived rabbits

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.272.2.r648 ◽

1997 ◽

Vol 272 (2) ◽

pp. R648-R655 ◽

Cited By ~ 4

Author(s):

M. R. Opp ◽

L. A. Toth ◽

E. A. Tolley

Keyword(s):

Slow Wave ◽

Slow Wave Sleep ◽

Rabbit Model ◽

Stimulus Presentation ◽

Wave Activity ◽

Slow Wave Activity ◽

Auditory Stimuli ◽

Delta Power ◽

Postural Changes ◽

Behavioral Responsiveness

Slow-wave activity in the electroencephalogram is thought to reflect the depth or intensity of sleep. This hypothesis is primarily derived from studies of rats or humans. However, some characteristics of sleep of rabbits differ from those of rats or humans. To determine whether slow-wave activity (power density in the delta frequency band of 0.5-5.0 Hz) correlates with arousability in rabbits, we presented auditory stimuli (72-90 dB) to control or sleep-deprived animals during slow-wave sleep. The resulting behavioral responses, defined by changes in eye state and body posture, and the latency to return to sleep were used as measures of arousability. Behavioral responsiveness to auditory stimuli increased with increasing stimulus intensity in both control and sleep-deprived animals. Overall, however, sleep-deprived animals exhibited fewer postural changes and eye openings than did control rabbits. Sleep-deprived rabbits also more rapidly returned to sleep after the stimulus presentation than did control animals. Latency to return to sleep was correlated with delta power before stimulus presentation, but behavioral responsiveness was not. These data suggest that, in this rabbit model, delta power may not be predictive of behavioral arousability but may reflect sleep propensity.

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

Scientific Reports ◽

10.1038/s41598-019-54790-y ◽

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.

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Heightened Delta Power during Slow-Wave-Sleep in Patients with Rett Syndrome Associated with Poor Sleep Efficiency

PLoS ONE ◽

10.1371/journal.pone.0138113 ◽

2015 ◽

Vol 10 (10) ◽

pp. e0138113 ◽

Cited By ~ 8

Author(s):

Simon Ammanuel ◽

Wesley C. Chan ◽

Daniel A. Adler ◽

Balaji M. Lakshamanan ◽

Siddharth S. Gupta ◽

...

Keyword(s):

Rett Syndrome ◽

Slow Wave ◽

Slow Wave Sleep ◽

Sleep Efficiency ◽

Poor Sleep ◽

Delta Power

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

SLEEP ◽

10.5665/sleep.4656 ◽

2015 ◽

Vol 38 (5) ◽

pp. 685-697 ◽

Cited By ~ 13

Author(s):

Richard Stephenson ◽

Aimee M. Caron ◽

Svetlana Famina

Keyword(s):

Sleep Restriction ◽

Delta Power ◽

Chronic Sleep

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0869 Slow Wave Sleep Is Associated With Decreased Risk Of Gestational Diabetes Mellitus

SLEEP ◽

10.1093/sleep/zsaa056.865 ◽

2020 ◽

Vol 43 (Supplement_1) ◽

pp. A331-A331

Author(s):

B Izci Balserak ◽

U Bronas ◽

B Prasad ◽

K Shah ◽

A Steffen ◽

...

Keyword(s):

Diabetes Mellitus ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Slow Wave ◽

Rem Sleep ◽

Slow Wave Sleep ◽

Apnea Hypopnea Index ◽

Relative Power ◽

Delta Power ◽

Obstructive Sleep

Abstract Introduction Pregnancy is associated with disrupted slow-wave sleep (SWS) and a high prevalence of sleep disordered breathing (SDB), which may further exacerbate the decrease of deep sleep. Reduced slow wave sleep may impair glucose homeostasis, contributing to Gestational Diabetes Mellitus (GDM). Studies investigating EEG markers of deep and light sleep, and their associations with SDB and GDM are lacking. In this study, we measured associations of EEG Delta-power with objective SDB measures assessed in late-pregnancy to determine if changes in these bands are associated with GDM risk. Methods 74 women (24-36 weeks pregnancy) underwent overnight polysomnography. Spectral profiles for Delta relative power were created for NREM and REM sleep after removing epochs with movements or muscle artifacts. The association of Delta power with SDB, assessed by the Apnea Hypopnea-Index (AHI) and AHI-based SDB severity (none, mild, moderate, severe) was tested by multivariate linear regression including demographic variables with bivariate correlations (p<0.2) versus Delta-power. Conditional-regression was used to explore relationships between Delta-power and GDM, controlling for covariates. Results Obstructive Sleep Apnea (OSA, AHI>5) was present in 14% of subjects (8 GDM-cases and 3 controls). In bivariate analyses, AHI, AHI-severity categories and OSA were associated with Delta-power in NREM (all p<0.2) and AHI was associated with Delta relative-power in REM (p=0.18). However, these associations did not remain significant after adjusting for covariates. Delta relative-power in NREM was significantly associated with decreased risk of GDM (OR:0.50, 95%CI-0.25,0.91), but, in REM sleep, was not associated with GDM risk (OR:1.25, 95%CI-0.79,1.97). Conclusion These analyses failed to demonstrate an association between OSA or OSA severity and EEG Delta power. However, lower levels of SWS, characterized by low Delta power were associated with increased GDM risk. Support NIH-R00-NR013187

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Slow Wave Sleep Enhancement with Gaboxadol Reduces Daytime Sleepiness During Sleep Restriction

SLEEP ◽

10.1093/sleep/31.5.659 ◽

2008 ◽

Vol 31 (5) ◽

pp. 659-672 ◽

Cited By ~ 33

Author(s):

James K. Walsh ◽

Ellen Snyder ◽

Janine Hall ◽

Angela C. Randazzo ◽

Kara Griffin ◽

...

Keyword(s):

Slow Wave ◽

Daytime Sleepiness ◽

Slow Wave Sleep ◽

Sleep Restriction

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Dysfunctional Overnight Memory Consolidation in Patients with Schizophrenia in Comparison to Healthy Controls: Disturbed Slow-Wave Sleep as Contributing Factor?

Neuropsychobiology ◽

10.1159/000517858 ◽

2021 ◽

pp. 1-12

Author(s):

Sara Lena Weinhold ◽

Julia Lechinger ◽

Jasper Ittel ◽

Romina Ritzenhoff ◽

Henning Johannes Drews ◽

...

Keyword(s):

Linear Relationship ◽

Slow Wave ◽

Memory Consolidation ◽

Slow Wave Sleep ◽

Declarative Memory ◽

Sleep Spindles ◽

Sleep Spindle ◽

Delta Power ◽

Sleep Parameters ◽

Spindle Power

Introduction: Memory deficiency has been shown in schizophrenia patients, but results on the role of sleep parameters in overnight consolidation of associative verbal memory are still missing. Therefore, the aim of our study was to elucidate underlying processes of impaired sleep-related consolidation of associative word pairs in schizophrenia including standard sleep parameters as well as sleep spindle counts and spectral analysis. Methods: Eighteen stably medicated schizophrenia patients and 24 healthy age-matched controls performed an associative declarative memory task before and after polysomnographic recordings. Part of the participants expected verbal associative memory testing in the morning, while the others did not. Furthermore, participants filled in self-rating questionnaires of schizophrenia-typical experiences (Eppendorf Schizophrenia Inventory [ESI] and Psychotic Symptom Rating Scale). Results: Schizophrenia patients performed worse in verbal declarative memory in the evening as well as in overnight consolidation (morning compared to evening performance). While duration of slow-wave sleep was nearly comparable between groups, schizophrenia patients showed lower sleep spindle count, reduced delta power during slow-wave sleep, and reduced spindle power during the slow oscillation (SO) up-state. In healthy but not in schizophrenia patients, a linear relationship between overnight memory consolidation and slow-wave sleep duration as well as delta power was evident. No significant effect with respect to the expectation of memory retrieval was evident in our data. Additionally, we observed a negative linear relationship between total number of sleep spindles and ESI score in healthy participants. Discussion/Conclusion: As expected, schizophrenia patients showed deficient overnight verbal declarative memory consolidation as compared to healthy controls. Reduced sleep spindles, delta power, and spindle power during the SO up-state may link sleep and memory deficiency in schizophrenia. Additionally, the absence of a linear relationship between sleep-related memory consolidation and slow-wave sleep as well as delta power suggests further functional impairments in schizophrenia. Note that this conclusion is based on observational data. Future studies should investigate if stimulation of delta waves during sleep could improve memory performance and thereby quality of life in schizophrenia.

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00678.2011 ◽

2012 ◽

Vol 302 (12) ◽

pp. R1411-R1425 ◽

Cited By ~ 18

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.

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