scholarly journals Unraveling Why We Sleep: Quantitative Analysis Reveals Abrupt Transition from Neural Reorganization to Repair in Early Development

2019 ◽  
Author(s):  
Junyu Cao ◽  
Alexander B. Herman ◽  
Geoffrey B. West ◽  
Gina Poe ◽  
Van M. Savage
Keyword(s):  
Quantitative Analysis ◽  
Rem Sleep ◽  
Brain Size ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Early Ontogeny ◽  
Neural Repair ◽  
Abrupt Transition ◽  
Metabolite Clearance

Sleep serves disparate functions, most notably neural repair, metabolite clearance and circuit reorganization, yet the relative importance of these functions remains hotly debated. Here, we create a novel mechanistic framework for understanding and predicting how sleep changes during ontogeny (why babies sleep twice as long as adults) and across phylogeny (why mice sleep roughly five times that of whales). We use this theory to quantitatively distinguish between sleep used for neural reorganization versus repair. We conduct a comprehensive, quantitative analysis of human sleep using total sleep time, cerebral metabolic rate, brain size, synaptic density, and REM sleep (used here to also refer to Active Sleep in infants and children). Our findings reveal an abrupt transition, between 2 and 3 years of age in humans. Specifically, our results show that differences in sleep across phylogeny and during late ontogeny (after 2 or 3 years in humans) are primarily due to sleep functioning for repair or clearance, while changes in sleep during early ontogeny (before 2 - 3 years in humans) primarily support neural reorganization and learning. Moreover, our analysis shows that neuroplastic reorganization occurs primarily in REM sleep but not in NREM. In accordance with the developmental role of neuroplasticity, the percent of time spent in REM sleep is independent of brain size across species but decreases dramatically as brain size grows through development. Furthermore, the ratio of NREM sleep time to awake time emerges as a new invariant across development. This developmental transition and fundamental shift across ontogeny and phylogeny suggests a complex interplay between developmental and evolutionary constraints on sleep.

scholarly journals Unraveling why we sleep: Quantitative analysis reveals abrupt transition from neural reorganization to repair in early development

2020 ◽  
Vol 6 (38) ◽  
pp. eaba0398 ◽  
Author(s):  
Junyu Cao ◽  
Alexander B. Herman ◽  
Geoffrey B. West ◽  
Gina Poe ◽  
Van M. Savage
Keyword(s):  
Quantitative Analysis ◽  
Early Development ◽  
Rem Sleep ◽  
Early Ontogeny ◽  
Evolutionary Constraints ◽  
Relative Importance ◽  
Complex Interplay ◽  
Neural Repair ◽  
Abrupt Transition ◽  
Metabolite Clearance

Sleep serves disparate functions, most notably neural repair, metabolite clearance and circuit reorganization. Yet the relative importance remains hotly debated. Here, we create a novel mechanistic framework for understanding and predicting how sleep changes during ontogeny and across phylogeny. We use this theory to quantitatively distinguish between sleep used for neural reorganization versus repair. Our findings reveal an abrupt transition, between 2 and 3 years of age in humans. Specifically, our results show that differences in sleep across phylogeny and during late ontogeny (after 2 or 3 years in humans) are primarily due to sleep functioning for repair or clearance, while changes in sleep during early ontogeny (before 2 or 3 years) primarily support neural reorganization and learning. Moreover, our analysis shows that neuroplastic reorganization occurs primarily in REM sleep but not in NREM. This developmental transition suggests a complex interplay between developmental and evolutionary constraints on sleep.

scholarly journals The European starling (Sturnus vulgaris) shows signs of NREM sleep homeostasis but has very little REM sleep and no REM sleep homeostasis

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Spectral Power ◽  
Nrem Sleep ◽  
Sleep Time ◽  
European Starling ◽  
Dark Phase ◽  
Rapid Eye Movement ◽  
Sleep Homeostasis

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.

scholarly journals Electroacupuncture Treatment Normalized Sleep Disturbance in Morphine Withdrawal Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Yi-Jing Li ◽  
Fei Zhong ◽  
Peng Yu ◽  
Ji-Sheng Han ◽  
Cai-Lian Cui ◽  
...  
Keyword(s):  
Sleep Disturbance ◽  
Rem Sleep ◽  
Total Sleep Time ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Morphine Withdrawal ◽  
Opiate Withdrawal ◽  
Important Symptom ◽  
Opiate Addicts ◽  
Retention In Treatment

Sleep disturbance is considered as an important symptom of acute and protracted opiate withdrawal. Current results suggest that sleep disturbance may be taken as a predictor of relapse. Appropriate sleep enhancement therapy will be in favor of the retention in treatment for opiate addicts. Our previous studies have shown that electroacupuncture (EA) is effective in suppressing morphine withdrawal syndrome. The aim of the present study is to investigate the effect of 2 and 100 Hz EA on the sleep disturbance during morphine withdrawal. Rats were made dependent on morphine by repeated morphine injections (escalating doses of 5–80 mg kg−1, subcutaneously, twice a day) for 5 days. EA of 2 or 100 Hz was given twice a day for 3 days, starting at 48 h after the last morphine injection. Electroencephalogram and electromyogram were monitored at the end of the first and the last EA treatments, respectively. Results showed that non-rapid eye movement (NREM) sleep, REM sleep and total sleep time decreased dramatically, while the sleep latency prolonged significantly during acute morphine withdrawal. Both 2 and 100 Hz EA produced a significant increase in NREM sleep, REM sleep and total sleep time. It was suggested that EA could be a potential treatment for sleep disturbance during morphine withdrawal.

scholarly journals 0074 Inhibitory Neurons in the Dorsomedial Medulla Promote REM Sleep

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A30-A30
Author(s):  
J Stucynski ◽  
A Schott ◽  
J Baik ◽  
J Hong ◽  
F Weber ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Nrem Sleep ◽  
Inhibitory Neurons ◽  
Brain State ◽  
Sleep Regulation ◽  
Optogenetic Stimulation ◽  
Electrophysiological Recordings ◽  
Stimulation Of

Abstract Introduction The neural circuits controlling rapid eye movement (REM) sleep, and in particular the role of the medulla in regulating this brain state, remains an active area of study. Previous electrophysiological recordings in the dorsomedial medulla (DM) and electrical stimulation experiments suggested an important role of this area in the control of REM sleep. However the identity of the involved neurons and their precise role in REM sleep regulation are still unclear. Methods The properties of DM GAD2 neurons in mice were investigated through stereotaxic injection of CRE-dependent viruses in conjunction with implantation of electrodes for electroencephalogram (EEG) and electromyogram (EMG) recordings and optic fibers. Experiments included in vivo calcium imaging (fiber photometry) across sleep and wake states, optogenetic stimulation of cell bodies, chemogenetic excitation and suppression (DREADDs), and connectivity mapping using viral tracing and optogenetics. Results Imaging the calcium activity of DM GAD2 neurons in vivo indicates that these neurons are most active during REM sleep. Optogenetic stimulation of DM GAD2 neurons reliably triggered transitions into REM sleep from NREM sleep. Consistent with this, chemogenetic activation of DM GAD2 neurons increased the amount of REM sleep while inhibition suppressed its occurrence and enhanced NREM sleep. Anatomical tracing revealed that DM GAD2 neurons project to several areas involved in sleep / wake regulation including the wake-promoting locus coeruleus (LC) and the REM sleep-suppressing ventrolateral periaquaductal gray (vlPAG). Optogenetic activation of axonal projections from DM to LC, and DM to vlPAG was sufficient to induce REM sleep. Conclusion These experiments demonstrate that DM inhibitory neurons expressing GAD2 powerfully promote initiation of REM sleep in mice. These findings further characterize the dorsomedial medulla as a critical structure involved in REM sleep regulation and inform future investigations of the REM sleep circuitry. Support R01 HL149133

scholarly journals The truncated TrkB receptor influences mammalian sleep

2015 ◽  
Vol 308 (3) ◽  
pp. R199-R207 ◽  
Author(s):  
Adam J. Watson ◽  
Kyle Henson ◽  
Susan G. Dorsey ◽  
Marcos G. Frank
Keyword(s):  
Rem Sleep ◽  
Knockout Mice ◽  
Psychiatric Illness ◽  
Sleep Latency ◽  
Sleep Time ◽  
Sleep Regulation ◽  
Trkb Receptor ◽  
Adult Mice ◽  
The Relationship

Brain-derived neurotrophic factor (BDNF) is a neurotrophin hypothesized to play an important role in mammalian sleep expression and regulation. In order to investigate the role of the truncated receptor for BDNF, TrkB.T1, in mammalian sleep, we examined sleep architecture and sleep regulation in adult mice constitutively lacking this receptor. We find that TrkB.T1 knockout mice have increased REM sleep time, reduced REM sleep latency, and reduced sleep continuity. These results demonstrate a novel role for the TrkB.T1 receptor in sleep expression and provide new insights into the relationship between BDNF, psychiatric illness, and sleep.

scholarly journals The relationship between fasting-induced torpor, sleep and wakefulness in the laboratory mouse

2020 ◽  
Author(s):  
Yi G. Huang ◽  
Sarah J. Flaherty ◽  
Carina A. Pothecary ◽  
Russell G. Foster ◽  
Stuart N. Peirson ◽  
...  
Keyword(s):  
Body Temperature ◽  
Rem Sleep ◽  
Brain Activity ◽  
Mammalian Species ◽  
Laboratory Mouse ◽  
Nrem Sleep ◽  
Early Ontogeny ◽  
State Classification ◽  
The Relationship ◽  
Electroencephalogram Eeg

AbstractTorpor is a regulated reversible state of metabolic suppression used by many mammalian species to conserve energy. Although torpor has been studied extensively in terms of general physiology, metabolism and neuroendocrinology, the effects of hypometabolism and associated hypothermia on brain activity and states of vigilance have received little attention. Here we performed continuous monitoring of electroencephalogram (EEG), electromyogram (EMG) and peripheral body temperature in adult, male C57BL/6 mice over consecutive days of scheduled restricted feeding. All animals showed prominent bouts of hypothermia that became progressively deeper and longer as fasting progressed. EEG and EMG were markedly affected by hypothermia, although the typical electrophysiological signatures of NREM sleep, REM sleep and wakefulness allowed us to perform vigilance-state classification in all cases. Invariably, hypothermia bouts were initiated from a state indistinguishable from NREM sleep, with EEG power decreasing gradually in parallel with decreasing body temperature. Furthermore, during deep hypothermia REM sleep was largely abolished, but we observed brief and intense bursts of muscle activity, which resembled the regular motor discharges seen during early ontogeny associated with immature sleep patterns. We conclude that torpor and sleep are electrophysiologically on a continuum, and that, in order for torpor to occur, mice need to first transition through euthermic sleep.

scholarly journals The maturational trajectories of NREM and REM sleep durations differ across adolescence on both school-night and extended sleep

2012 ◽  
Vol 302 (5) ◽  
pp. R533-R540 ◽  
Author(s):  
Irwin Feinberg ◽  
Nicole M. Davis ◽  
Evan de Bie ◽  
Kevin J. Grimm ◽  
Ian G. Campbell
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Brain Activity ◽  
Physiological Role ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Rapid Eye Movement ◽  
Time In Bed ◽  
Ultimate Explanation ◽  
Brain Changes

We recorded sleep electroencephalogram longitudinally across ages 9–18 yr in subjects sleeping at home. Recordings were made twice yearly on 4 consecutive nights: 2 nights with the subjects maintaining their ongoing school-night schedules, and 2 nights with time in bed extended to 12 h. As expected, school-night total sleep time declined with age. This decline was entirely produced by decreasing non-rapid eye movement (NREM) sleep. Rapid eye movement (REM) sleep durations increased slightly but significantly. NREM and REM sleep durations also exhibited different age trajectories when sleep was extended. Both durations exceeded those on school-night schedules. However, the elevated NREM duration did not change with age, whereas REM durations increased significantly. We interpret the adolescent decline in school-night NREM duration in relation to our hypothesis that NREM sleep reverses changes produced in plastic brain systems during waking. The “substrate” produced during waking declines across adolescence, because synaptic elimination decreases the intensity (metabolic rate) of waking brain activity. Declining substrate reduces both NREM intensity (i.e., delta power) and NREM duration. The absence of a decline in REM sleep duration on school-night sleep and its age-dependent increase in extended sleep pose new challenges to understanding its physiological role. Whatever their ultimate explanation, these robust findings demonstrate that the two physiological states of human sleep respond differently to the maturational brain changes of adolescence. Understanding these differences should shed new light on both brain development and the functions of sleep.

Genetic Evidence for a Role of CREB in Sustained Cortical Arousal

2003 ◽  
Vol 90 (2) ◽  
pp. 1152-1159 ◽  
Author(s):  
Laurel A. Graves ◽  
Kevin Hellman ◽  
Sigrid Veasey ◽  
Julie A. Blendy ◽  
Allan I. Pack ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Nrem Sleep ◽  
Genetic Alterations ◽  
Memory Storage ◽  
Cortical Arousal ◽  
Element Binding Protein ◽  
Cyclic Amp Response Element ◽  
Phosphorylated Creb ◽  
Activity Dependent

The cyclic AMP-response element binding protein (CREB) is an activity-dependent transcription factor important for synaptic plasticity and memory storage. Levels of phosphorylated CREB within the cortex are higher in waking than in sleep, suggesting that CREB plays a role in sleep/wake regulation in mammals. We tested the hypothesis that CREB is critical for sleep/wake regulation by examining behavioral state parameters in mice lacking the α and Δ isoforms of CREB. Over 24 h, time spent awake was significantly decreased in CREB αΔ mutant mice by approximately 100 min, and time spent in nonrapid eye movement sleep (NREM) sleep was increased correspondingly. Wake and REM sleep periods were shorter in CREB αΔ mice, and CREB αΔ mice had decreased levels of θ-activity during wake and REM sleep, consistent with an impairment in the ability to maintain an activated electroencephalogram. These results suggest that the CREB protein contributes to the mechanisms by which wakefulness is maintained and demonstrate that specific genetic alterations in species as diverse as Drosophila and mice produce similar phenotypes in arousal and wakefulness.

Sleep in the lesser mouse-deer (Tragulus kanchil)

SLEEP ◽  
2021 ◽  
Author(s):  
Oleg I Lyamin ◽  
Jerome M Siegel ◽  
Evgeny A Nazarenko ◽  
Viatcheslav V Rozhnov
Keyword(s):  
Rem Sleep ◽  
National Park ◽  
Adult Mouse ◽  
Average Duration ◽  
Total Sleep Time ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Average Maximum ◽  
Herbivorous Animal ◽  
Environmental Temperatures

Abstract The mouse-deer or chevrotains are the smallest of the ungulates and ruminants. They are characterized by a number of traits which are considered plesiomorphic for the Artiodactyla order. The objective of this study was to examine sleep in the lesser mouse-deer (Tragulus kanchil), which is the smallest in this group (body mass <2.2 kg). Electroencephalogram, nuchal electromyogram, electrooculogram and body acceleration were recorded in 4 adult mouse-deer females using a telemetry system in Bu Gia Map National Park in Vietnam. The mouse-deer spent on average 49.7±3.0% of 24-h in NREM sleep. REM sleep occupied 1.7±0.3% of 24-h or 3.2±0.5% of total sleep time. The average duration of REM sleep episodes was 2.0±0.2 min, the average maximum was 5.1±1.1 min, and the longest episodes lasted 8 min. NREM sleep occurred in sternal recumbency with the head heals above the ground while 64.7+6.4% of REM sleep occurred with the head resting on the ground. The eyes were open throughout most of the NREM sleep period. The mouse-deer displayed polyphasic sleep and crepuscular peaks in activity (04:00-06:00 and 18:00-19:00). The largest amounts of NREM occurred in the morning (06:00-09:00) and the smallest before dusk (at 04:00-06:00). REM sleep occurred throughout most of the daylight hours (08:00-16:00) and in the first half of the night (19:00-02:00). We suggest that the pattern and timing of sleep in the lesser mouse-deer is adapted to the survival of a small herbivorous animal, subject to predation, living in high environmental temperatures in tropical forest undergrowth.

scholarly journals An ether stressor increases REM sleep in rats: possible role of prolactin

2000 ◽  
Vol 279 (5) ◽  
pp. R1590-R1598 ◽  
Author(s):  
B. Bodosi ◽  
F. Obál ◽  
J. Gardi ◽  
J. Komlódi ◽  
J. Fang ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Intracerebroventricular Administration ◽  
Light Onset ◽  
Hypophysectomized Rats ◽  
Sleep Alterations ◽  
Stimulation Of

Sleep alterations after a 1-min exposure to ether vapor were studied in rats to determine if this stressor increases rapid eye-movement (REM) sleep as does an immobilization stressor. Ether exposure before light onset or dark onset was followed by significant increases in REM sleep starting ∼3–4 h later and lasting for several hours. Non-REM (NREM) sleep and electroencephalographic slow-wave activity during NREM sleep were not altered. Exposure to ether vapor elicited prolactin (Prl) secretion. REM sleep was not promoted after ether exposure in hypophysectomized rats. If the hypophysectomy was partial and the rats secreted Prl after ether exposure, then increases in REM sleep were observed. Intracerebroventricular administration of an antiserum to Prl decreased spontaneous REM sleep and inhibited ether exposure-induced REM sleep. The results indicate that a brief exposure to ether vapor is followed by increases in REM sleep if the Prl response associated with stress is unimpaired. This suggests that Prl, which is a previously documented REM sleep-promoting hormone, may contribute to the stimulation of REM sleep after ether exposure.

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