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.

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 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.

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.

scholarly journals 0188 Mood Disorders Moderate the Relationship Between Sleep Quality and Leadership Development for U.S. Army Officer Candidates During ROTC Advanced Camp

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A74-A74
Author(s):  
J Choynowski ◽  
M Pirner ◽  
C Mickelson ◽  
J Mantua ◽  
W J Sowden ◽  
...  
Keyword(s):  
College Students ◽  
Sleep Quality ◽  
Mood Disorders ◽  
Process Model ◽  
The United States ◽  
Anxiety And Depression ◽  
Poor Sleep ◽  
Medicine Research ◽  
The Us ◽  
Rotc Cadets

Abstract Introduction U.S. Army Reserve Officer Training Corps (ROTC) Cadets are college students training to be Army Officers. During a month-long capstone course (Advanced Camp), Cadets are rated on their leadership ability. Little work has been done to determine predictors of leadership ability at Advanced Camp. This study examined the effect of poor sleep and mood disorders -- two prevalent factors among college students -- on leadership ability. Methods Metrics on leadership, sleep quality, anxiety, and depression, were assessed in 159 ROTC Cadets (22.06±2.49 years; 23.90%female) at Days 1 (Baseline), 14 (Mid), and 29 (Post) of Advanced Camp. Leadership ratings were determined by ROTC Instructors over the course of Advanced Camp (1–5 score; higher score indicates poorer leadership). Predictors were the Pittsburgh Sleep Quality Index, Generalized Anxiety Disorder-7, and Patient Health Questionnaire-9. The relationships between the predictors and leadership scores were tested using linear regression. The interaction between mood disorders and sleep quality on leadership was tested using SPSS Process (Model 1). Results Poorer sleep quality at the Post time point (reflecting the prior 2 weeks of sleep) predicted poorer leadership (B=.05,p=.03), while sleep quality from Baseline (B=.03,p=.14) and Mid (B=.01,p=.67) did not. Higher anxiety and depression scores from all time points predicted poorer leadership (p-values<.03). There was an interaction: higher anxiety and high depression predicted poorer leadership only in the context of poor sleep quality (not good or average sleep quality) [anxiety: R2=.04,F(1,159)=6.04,p=.02; interaction: R2=.03,F(1,155)=5.30,p=.02]. Conclusion The current study identified a relationship between sleep quality and leadership ratings in ROTC cadets. This relationship was moderated by anxiety and depression. ROTC instructors should encourage ROTC Cadets to take advantage of sleep opportunities at Advanced Camp in order to maximize leadership potential. Support Support for this study came from the Military Operational Medicine Research Program (MOMRP) of the United States Army Medical Research and Development Command (USAMRDC). Disclaimer: The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Army or of the US

scholarly journals The two-process model of sleep regulation: a reappraisal

2016 ◽  
Vol 25 (2) ◽  
pp. 131-143 ◽  
Author(s):  
Alexander A. Borbély ◽  
Serge Daan ◽  
Anna Wirz-Justice ◽  
Tom Deboer
Keyword(s):  
Process Model ◽  
Sleep Regulation

Sleep regulation in rats: effects of sleep deprivation, light, and circadian phase

1986 ◽  
Vol 251 (6) ◽  
pp. R1037-R1044 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave Sleep ◽  
Rest Period ◽  
Activity Period ◽  
Base Line ◽  
Sleep Regulation ◽  
Continuous Darkness ◽  
Circadian Phase ◽  
Sleep Homeostasis ◽  
Pentobarbital Sodium Anesthesia

Sleep states and electroencephalographic (EEG) parameters were determined in unrestrained rats that had been implanted with electrodes under deep pentobarbital sodium anesthesia. Two base-line days with a light-dark cycle (LD) and 2 days under continuous darkness (DD) were followed by 24 h of sleep deprivation (SD) ending in the middle of the circadian activity period and by 2 recovery days in DD. In the base-line LD rest period, the amount of rapid-eye-movement sleep (REMS) and the EEG amplitude of non-REMS (NREMS) were lower than in the corresponding DD period. SD caused an immediate enhancement of REMS, NREMS, the slow-wave sleep (SWS) fraction of NREMS, and NREMS EEG amplitude. Although REMS, NREMS, and SWS showed a second peak at habitual light onset, they did not exceed base line. Subsequently, all parameters exhibited a marked negative rebound. We conclude that REMS and the EEG amplitude of NREMS are suppressed by light, amplitude and frequency parameters of NREMS are differently affected by light as well as by SD, and the short duration of the SD-induced increase of SWS may reflect a circadian influence on sleep homeostasis.

Homeostatic regulation of sleep in arrhythmic Siberian hamsters

2004 ◽  
Vol 287 (1) ◽  
pp. R104-R111 ◽  
Author(s):  
Jennie E. Larkin ◽  
Tohei Yokogawa ◽  
H. Craig Heller ◽  
Paul Franken ◽  
Norman F. Ruby
Keyword(s):  
Constant Darkness ◽  
Sleep Regulation ◽  
Light Phase ◽  
Compensatory Response ◽  
Recovery Sleep ◽  
Siberian Hamsters ◽  
Novel Approach ◽  
Sleep Homeostasis ◽  
Circadian Organization ◽  
Simple Phase

Sleep is regulated by independent yet interacting circadian and homeostatic processes. The present study used a novel approach to study sleep homeostasis in the absence of circadian influences by exposing Siberian hamsters to a simple phase delay of the photocycle to make them arrhythmic. Because these hamsters lacked any circadian organization, their sleep homeostasis could be studied in the absence of circadian interactions. Control animals retained circadian rhythmicity after the phase shift and re-entrained to the phase-shifted photocycle. These animals displayed robust daily sleep-wake rhythms with consolidated sleep during the light phase beginning about 1 h after light onset. This marked sleep-wake pattern was circadian in that it persisted in constant darkness. The distribution of sleep in the arrhythmic hamsters over 24 h was similar to that in the light phase of rhythmic animals. Therefore, daily sleep amounts were higher in arrhythmic animals compared with rhythmic ones. During 2- and 6-h sleep deprivations (SD), it was more difficult to keep arrhythmic hamsters awake than it was for rhythmic hamsters. Because the arrhythmic animals obtained more non-rapid eye movement sleep (NREMS) during the SD, they showed a diminished compensatory response in NREMS EEG slow-wave activity during recovery sleep. When amounts of sleep during the SD were taken into account, there were no differences in sleep homeostasis between experimental and control hamsters. Thus loss of circadian control did not alter the homeostatic response to SD. This supports the view that circadian and homeostatic influences on sleep regulation are independent processes.

scholarly journals An Asymmetrical Hypothesis for the NREM-REM Sleep Alternation—What Is the NREM-REM Cycle?

2021 ◽  
Vol 15 ◽  
Author(s):  
Olivier Le Bon
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Refractory Period ◽  
High Variability ◽  
Oscillator Model ◽  
Rapid Eye Movement ◽  
Sleep Regulation ◽  
Short Term ◽  
Sleep Episode ◽  
Sleep Homeostasis

Since the discovery of rapid eye movement (REM) sleep (Aserinsky and Kleitman, 1953), sleep has been described as a succession of cycles of non-REM (NREM) and REM sleep episodes. The hypothesis of short-term REM sleep homeostasis, which is currently the basis of most credible theories on sleep regulation, is built upon a positive correlation between the duration of a REM sleep episode and the duration of the interval until the next REM sleep episode (inter-REM interval): the duration of REM sleep would therefore predict the duration of this interval. However, the high variability of inter-REM intervals, especially in polyphasic sleep, argues against a simple oscillator model. A new “asymmetrical” hypothesis is presented here, where REM sleep episodes only determine the duration of a proportional post-REM refractory period (PRRP), during which REM sleep is forbidden and the only remaining options are isolated NREM episodes or waking. After the PRRP, all three options are available again (NREM, REM, and Wake). I will explain why I think this hypothesis also calls into question the notion of NREM-REM sleep cycles.

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