Homeostatic sleep and body temperature responses to acute sleep deprivation are preserved following chronic sleep restriction in rats

2021 ◽  
Author(s):  
Samuel Deurveilher ◽  
Stephanie M. Shewchuk ◽  
Kazue Semba
Keyword(s):  
Body Temperature ◽  
Sleep Deprivation ◽  
Sleep Restriction ◽  
Acute Sleep Deprivation ◽  
Temperature Responses ◽  
Chronic Sleep

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.

scholarly journals 0270 Somnolence Profiles in Mice Submitted to Acute and Chronic Sleep Deprivation

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A103-A103
Author(s):  
G L Fernandes ◽  
P Araujo ◽  
S Tufik ◽  
M Andersen
Keyword(s):  
Sleep Deprivation ◽  
Individual Variation ◽  
Individual Variability ◽  
Interindividual Variation ◽  
Dark Phase ◽  
Sleep Regulation ◽  
Study Objective ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

Abstract Introduction Sleepiness is a behavioral marker of homeostatic sleep regulation and is related to several negative outcomes with interindividual variation, which may amount to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by acute and chronic sleep deprivation. Thus, the study objective was to investigate the development of sleepiness in sleep deprived mice. Methods C57BL/6J male mice (n=340) were distributed in 5 sleep deprivation groups, 5 sleep rebound groups and 10 control groups. Animals underwent acute total sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had the opportunity to sleep for 1, 2, 3, 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocol, sleep attempts were counted as a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant to sleepiness animals (mean<group average). Frequency of resistant mice was 65%, 56%, 56% and 53% for 3, 6, 9 and 12 hours of acute sleep deprivation, respectively, and 74% in chronic sleep deprivation. 52% of the sleepiness variance might be explained by individual variation during chronic sleep deprivation and 68% of sleepiness variance during acute sleep deprivation was attributed to extended wakefulness. A normal corticosterone zenith was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different degrees of sleepiness in sleep deprived mice were verified. Sleep deprivation per se was the main factor explaining sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support This work was financially supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (#2017/18455-5), Coordenação de Aperfeiçoamento de Pessoal Nível Superior (CAPES) - grant code 001, ConselhoNacional de Desenvolvimento Científico e Tecnológico (CNPq) (#169040/2017–8)and Associação Fundo de Incentivo à Pesquisa (AFIP).

scholarly journals Circadian and sleep/wake-dependent variations in tau phosphorylation are driven by temperature

SLEEP ◽  
2019 ◽  
Vol 43 (4) ◽  
Author(s):  
Isabelle Guisle ◽  
Maud Gratuze ◽  
Séréna Petry ◽  
Françoise Morin ◽  
Rémi Keraudren ◽  
...  
Keyword(s):  
Body Temperature ◽  
Sleep Deprivation ◽  
Tau Protein ◽  
Sleep Disturbances ◽  
Tau Phosphorylation ◽  
Physiological Basis ◽  
Physiological Regulation ◽  
Hyperphosphorylated Tau Protein ◽  
Phosphatase 2A ◽  
Acute Sleep Deprivation

Abstract Study Objectives Aggregates of hyperphosphorylated tau protein are a hallmark of Alzheimer’s disease (AD) and other tauopathies. Sleep disturbances are common in AD patients, and insufficient sleep may be a risk factor for AD. Recent evidence suggests that tau phosphorylation is dysregulated by sleep disturbances in mice. However, the physiological regulation of tau phosphorylation during the sleep–wake cycle is currently unknown. We thus aimed to determine whether tau phosphorylation is regulated by circadian rhythms, inherently linked to the sleep–wake cycle. Methods To answer these questions, we analyzed by Western blotting tau protein and associated kinases and phosphatases in the brains of awake, sleeping, and sleep-deprived B6 mice. We also recorded their temperature. Results We found that tau phosphorylation undergoes sleep-driven circadian variations as it is hyperphosphorylated during sleep but not during acute sleep deprivation. Moreover, we demonstrate that the mechanism behind these changes involves temperature, as tau phosphorylation was inversely correlated with circadian- and sleep deprivation-induced variations in body temperature, and prevented by housing the animals at a warmer temperature. Notably, similar changes in tau phosphorylation were reproduced in neuronal cells exposed to temperatures recorded during the sleep–wake cycle. Our results also suggest that inhibition of protein phosphatase 2A (PP2A) may explain the hyperphosphorylation of tau during sleep-induced hypothermia. Conclusion Taken together, our results demonstrate that tau phosphorylation follows a circadian rhythm driven mostly by body temperature and sleep, and provide the physiological basis for further understanding how sleep deregulation can affect tau and ultimately AD pathology.

scholarly journals Insomnia as a predisposing factor for medical conditions

2021 ◽  
Vol 68 (1) ◽  
pp. 31-33
Author(s):  
Ana Maria Alexandra Stanescu ◽  
◽  
Oana Nicolescu ◽  
Alexandru Mihai Stefanescu ◽  
Gabriela Carmen Obilisteanu ◽  
...  
Keyword(s):  
Public Health ◽  
Sleep Deprivation ◽  
Brain Function ◽  
Public Health Problem ◽  
Disease Development ◽  
Predisposing Factor ◽  
Lack Of Sleep ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep

An essential aspect of human health is sleep. Sleep, among others, interacts with the immune system, plays a role in restoring the body's energy, healing and brain function. Insomnia is often noticed in medical practice, is considered a public health problem. Acute sleep deprivation can alter cognitive performance, and chronic sleep deprivation can lead to disease development. Lack of sleep affects all major systems in the human body, and the major changes that occur in chronic insomnia have been associated with many conditions such as type 2 diabetes, cardiovascular disease, asthma, thyroid disease and gastroesophageal reflux disease.

Acute sleep deprivation elevates brain and body temperature in rats

2020 ◽  
Author(s):  
Lal Chandra Vishwakarma ◽  
Binney Sharma ◽  
Vishwajeet Singh ◽  
Ashok Kumar Jaryal ◽  
Hruda Nanda Mallick
Keyword(s):  
Body Temperature ◽  
Sleep Deprivation ◽  
Acute Sleep Deprivation

MCH levels in the CSF, brain preproMCH and MCHR1 gene expression during paradoxical sleep deprivation, sleep rebound and chronic sleep restriction

Peptides ◽  
2015 ◽  
Vol 74 ◽  
pp. 9-15 ◽  
Author(s):  
Ana Luiza Dias Abdo Agamme ◽  
Bruno Frederico Aguilar Calegare ◽  
Leandro Fernandes ◽  
Alicia Costa ◽  
Patricia Lagos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Paradoxical Sleep ◽  
Sleep Restriction ◽  
Paradoxical Sleep Deprivation ◽  
Chronic Sleep

scholarly journals Sleeping Disorders as a Symptom of Depression

2021 ◽  
Vol 04 (07) ◽  
Author(s):  
Lalitpat Suthisripok ◽  
Keyword(s):  
Sleep Deprivation ◽  
Seasonal Affective Disorder ◽  
Major Depressive ◽  
Sleeping Disorders ◽  
Effective Care ◽  
Bidirectional Relationship ◽  
Acute Sleep Deprivation ◽  
Almost All ◽  
Sleeping Disorder ◽  
Chronic Sleep

Recently, people pay less attention to their sleep since there are a lot of stimulants to keep them awake more than sleeping. According to many reports, the results have shown that many are facing a serious condition, which is sleeping disorder. This condition is related to sleep and affects the ability to sleep well on a regular basis. It is a serious problem that if left untreated, the condition can lead to many more severe problems. There is a significant correlation between sleeping disorder and depression which is called “bidirectional relationship”. The studies show that sleeping disorders are a “symptom” of almost all types of depression such as Major Depressive Disorder, Bipolar Disorder, Seasonal Affective Disorder and so forth. On the other hand, depression itself can also be a cause of sleeping disorders. In addition, the studies show chronic sleep deprivation can cause the changes in Serotonin, which is the brain’s neurotransmitter, and will have a chance to lead to depression greater than acute sleep deprivation. As a result, people should raise awareness in sleeping and usually examine their sleep. To have less chance of depression, a person requires a healthy sleep period and effective care.

scholarly journals 0151 COMPARISON OF THE EFFECTS OF ACUTE TOTAL SLEEP DEPRIVATION, CHRONIC SLEEP RESTRICTION AND RECOVERY SLEEP ON POSITIVE AFFECT

SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A56-A57
Author(s):  
E Hennecke ◽  
D Lange ◽  
J Fronczek ◽  
A Bauer ◽  
D Aeschbach ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Positive Affect ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Recovery Sleep ◽  
Chronic Sleep

scholarly journals The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment

2020 ◽  
Author(s):  
Séverine Lamon ◽  
Aimee Morabito ◽  
Emily Arentson-Lantz ◽  
Olivia Knowles ◽  
Grace Elizabeth Vincent ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Sleep Deprivation ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Metabolic Dysfunction ◽  
Skeletal Muscle Protein ◽  
Skeletal Muscle Protein Synthesis ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep

AbstractChronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N=13; 7 male, 6 female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross-over design. Anabolic and catabolic hormonal profiles, skeletal muscle fractional synthesis rate and markers of muscle protein degradation were assessed across the following day. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015 vs. DEP: 0.059 ± 0.014 %•h-1, p=0.040). In addition, it increased plasma cortisol by 21% (p=0.030) and decreased plasma testosterone, but not IGF-1, by 22% (p=0.029). A single night of total sleep deprivation is sufficient to induce anabolic resistance and a pro-catabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation.

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