scholarly journals Prolonged Exposure to Social Stress Impairs Homeostatic Sleep Regulation

2021 ◽  
Vol 15 ◽  
Author(s):  
Basma Radwan ◽  
Alvaro Yanez Touzet ◽  
Soaad Hammami ◽  
Dipesh Chaudhury
Keyword(s):  
Chronic Stress ◽  
Social Stress ◽  
Process Model ◽  
Prolonged Exposure ◽  
Temporal Correlation ◽  
Nrem Sleep ◽  
Adaptation To Stress ◽  
Sleep Regulation ◽  
Regulatory Pathways ◽  
Sleep Homeostasis

Stress and sleep are tightly regulated as a result of the substantial overlap in neurotransmitter signaling and regulatory pathways between the neural centers that modulate mood and sleep-wake cycle. The chronicity of the stressor and variability in coping with it are major determinants of the psychiatric outcomes and subsequent effect on sleep. The regulation of sleep is mediated by the interaction of a homeostatic and a circadian process according to the two-process model. Chronic stress induces stress-related disorders which are associated with deficient sleep homeostasis. However, little is known about how chronic stress affects sleep homeostasis and whether the differences in adaptation to stress distinctively influence sleep. Therefore, we assessed sleep homeostasis in C57BL6/J mice following exposure to 15-d of chronic social defeat stress. We implemented wake:sleep ratio as a behavioral correlate of sleep pressure. Both stress-resilient and stress-susceptible mice displayed deficient sleep homeostasis in post-stress baseline sleep. This was due to poor temporal correlation between frontal slow wave activity (SWA) power and sleep pressure in the dark/active phase. Moreover, the buildup rate of sleep pressure in the dark was lower in susceptible mice in comparison to stress-naïve mice. Additionally, 4-h SD in the dark caused a deficient sleep recovery response in susceptible mice characterized by non-rapid eye movement (NREM) sleep loss. Our findings provide evidence of deficient homeostatic sleep process (S) in baseline sleep in stress-exposed mice, while impaired sleep recovery following a mild enforced wakefulness experienced during the dark was only detected in stress-susceptible mice. This alludes to the differential homeostatic adaptation to stress between susceptible and resilient mice and its effect on sleep regulation.

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.

Circadian Rhythms and Homeostatic Mechanisms for Sleep Regulation

2021 ◽  
pp. 65-86
Author(s):  
Cassie J. Hilditch ◽  
Erin E. Flynn-Evans
Keyword(s):  
Circadian Rhythm ◽  
Circadian Rhythms ◽  
Process Model ◽  
Modern Society ◽  
Current Evidence ◽  
Sleep Regulation ◽  
Sleep Homeostasis ◽  
Short And Long Term ◽  
Homeostatic Mechanisms

This chapter examines circadian rhythms and homeostatic mechanisms for sleep regulation. It reviews the current evidence describing the two-process model of sleep regulation and how to assess disruption to either of these sleep drives. This chapter also reviews the role of the photic and non-photic resetting of the circadian rhythm and describes how some aspects of modern society can cause sleep and circadian disruption. Further, this chapter describes how misalignment between the circadian rhythm and sleep homeostasis, such as occurs during jet lag and shift-work, can lead to sleep disruption. The short- and long-term consequences of circadian misalignment are also reviewed.

scholarly journals Glymphatic Dysfunction: A Bridge Between Sleep Disturbance and Mood Disorders

2021 ◽  
Vol 12 ◽  
Author(s):  
Tao Yan ◽  
Yuefeng Qiu ◽  
Xinfeng Yu ◽  
Linglin Yang
Keyword(s):  
Sleep Disturbance ◽  
Mood Disorders ◽  
Process Model ◽  
Water Channel ◽  
Sleep Regulation ◽  
Sleep Homeostasis ◽  
Close Relationship ◽  
Mechanism Of Interaction ◽  
Glymphatic Pathway ◽  
Dynamic Fluctuation

Mounting evidence demonstrates a close relationship between sleep disturbance and mood disorders, including major depression disorder (MDD) and bipolar disorder (BD). According to the classical two-process model of sleep regulation, circadian rhythms driven by the light–dark cycle, and sleep homeostasis modulated by the sleep–wake cycle are disrupted in mood disorders. However, the exact mechanism of interaction between sleep and mood disorders remains unclear. Recent discovery of the glymphatic system and its dynamic fluctuation with sleep provide a plausible explanation. The diurnal variation of the glymphatic circulation is dependent on the astrocytic activity and polarization of water channel protein aquaporin-4 (AQP4). Both animal and human studies have reported suppressed glymphatic transport, abnormal astrocytes, and depolarized AQP4 in mood disorders. In this study, the “glymphatic dysfunction” hypothesis which suggests that the dysfunctional glymphatic pathway serves as a bridge between sleep disturbance and mood disorders is proposed.

scholarly journals Bright morning light advances the human circadian system without affecting NREM sleep homeostasis

1989 ◽  
Vol 256 (1) ◽  
pp. R106-R111 ◽  
Author(s):  
D. J. Dijk ◽  
D. G. Beersma ◽  
S. Daan ◽  
A. J. Lewy
Keyword(s):  
Rem Sleep ◽  
Process Model ◽  
Sleep Onset ◽  
Light Condition ◽  
Bright Light ◽  
Circadian Pacemaker ◽  
Sleep Regulation ◽  
Plasma Melatonin ◽  
Sleep Homeostasis ◽  
Dim Light

Eight male subjects were exposed to either bright light or dim light between 0600 and 0900 h for 3 consecutive days each. Relative to the dim light condition, the bright light treatment advanced the evening rise in plasma melatonin and the time of sleep termination (sleep onset was held constant) for an average approximately 1 h. The magnitude of the advance of the plasma melatonin rise was dependent on its phase in dim light. The reduction in sleep duration was at the expense of rapid-eye-movement (REM) sleep. Spectral analysis of the sleep electroencephalogram (EEG) revealed that the advance of the circadian pacemaker did not affect EEG power densities between 0.25 and 15.0 Hz during either non-REM or REM sleep. The data show that shifting the human circadian pacemaker by 1 h does not affect non-REM sleep homeostasis. These findings are in accordance with the predictions of the two-process model of sleep regulation.

Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

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.

scholarly journals Reassessing the validity of slow-wave dynamics as a proxy for NREM sleep homeostasis

2019 ◽  
Author(s):  
Jeffrey Hubbard ◽  
Thomas C. Gent ◽  
Marieke M. B. Hoekstra ◽  
Yann Emmenegger ◽  
Valerie Mongrain ◽  
...  
Keyword(s):  
Slow Wave ◽  
Muscle Tone ◽  
Nrem Sleep ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Wave Dynamics ◽  
Sleep Homeostasis ◽  
Human Experiments ◽  
And Function ◽  
Initial Power

AbstractSleep-wake driven changes in NREM sleep (NREMS) EEG delta (δ: ∼0.75-4.5Hz) power are widely used as proxy for a sleep homeostatic process. We noted frequency increases in δ-waves in sleep-deprived (SD) mice, prompting us to re-evaluate how slow-wave characteristics relate to prior sleep-wake history. We discovered two types of δ-waves; one responding to SD with high initial power and fast, discontinuous decay (δ2: ∼2.5-3.5Hz) and another unrelated to time-spent-awake with slow, linear decays (δ1: ∼0.75-1.75Hz). Human experiments confirmed this δ-band heterogeneity. Similar to SD, silencing of centromedial thalamus neurons boosted δ2-waves, specifically. δ2-dynamics paralleled that of temperature, muscle tone, heart-rate, and neuronal UP/DOWN state lengths, all reverting to characteristic NREMS levels within the first recovery hour. Thus, prolonged waking seems to necessitate a physiological recalibration before typical NREMS can be reinstated. These short-lasting δ2-dynamics challenge accepted models of sleep regulation and function based on the merged δ-band as sleep-need proxy.

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).

Sleep after arousal from hibernation is not homeostatically regulated

1999 ◽  
Vol 276 (2) ◽  
pp. R522-R529 ◽  
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.

Vigilance states, EEG spectra, and cortical temperature in the guinea pig

1993 ◽  
Vol 264 (6) ◽  
pp. R1125-R1132 ◽  
Author(s):  
I. Tobler ◽  
P. Franken ◽  
K. Jaggi
Keyword(s):  
Guinea Pig ◽  
Rem Sleep ◽  
Guinea Pigs ◽  
Process Model ◽  
Dark Period ◽  
Nrem Sleep ◽  
Light Period ◽  
Recording Time ◽  
Cortical Temperature ◽  
Eeg Power

Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) were obtained in nine guinea pigs for 24 h in a 12:12-h light-dark (LD 12:12) schedule. Sleep was markedly polyphasic and fragmented and amounted to 32% of recording time, which is a low value compared with sleep in other rodents. There was 6.8% more sleep in the light period than in the dark period. EEG power density in non-rapid eye movement (NREM) sleep showed no significant temporal trend within the light or the dark period. The homeostatic aspects of sleep regulation, as proposed in the two-process model, can account for the slow-wave activity (SWA) pattern also in the guinea pig: The small 24-h amplitude of the sleep-wakefulness pattern resulted in a small, 12% decline of SWA within the light period. In contrast to more distinctly nocturnal rodents, SWA in the dark period was not higher than in the light period. TCRT showed no difference between the light and the dark period. TCRT in REM sleep and waking was higher than TCRT in NREM sleep. TCRT increased after the transition from NREM sleep to either REM sleep or waking, and decreased in the last minute before the transition and after the transition from waking to NREM sleep. Motor activity measured in six animals for 11 days in constant darkness showed no apparent rhythm in three animals and a significant circadian rhythm in three others. Our data support the notion that guinea pigs exhibit only a weak circadian rest-activity rhythm.

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