Normal Sleep in Childhood

2021 ◽  
pp. 33-48
Author(s):  
Hovig K. Artinian ◽  
Mary Anne Tablizo ◽  
Manisha Witmans
Keyword(s):  
Eye Movement ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Respiratory Parameters ◽  
Normal Sleep ◽  
Brain Changes ◽  
And Behavior ◽  
Changes Over Time ◽  
The Brain ◽  
Critical Process

Sleep is a critical process in children in that it influences all aspects of physiological functioning, development, and behavior. The two types of sleep, rapid eye movement (REM) sleep and non–rapid eye movement (NREM) sleep, are inherent throughout life; however, the sleep architecture and sleep duration changes over time as the brain changes from the newborn period to adulthood. There are hallmarks related to sleep architectural changes that are specific and unique to the different age ranges. Although the process and neuromodulation of sleep is similar across the life span, there are attributes that are different in children compared to adults. There are also physiological differences in the brain waves and changes in respiratory parameters. This chapter highlights normal sleep in children.

Sleep Disorders

2016 ◽  
pp. 275-296
Author(s):  
Douglas J. Gelb
Keyword(s):  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
The Body ◽  
Rapid Eye Movement ◽  
Cyclic Activity ◽  
Abnormal Behaviors ◽  
The Brain ◽  
Meaningful Stimuli

Sleep consists of a highly patterned sequence of cyclic activity in various regions of the brain; it is not simply a state of temporary unconsciousness. Although the brain is less responsive than normal during sleep, it is not totally unresponsive. In fact, during sleep the brain responds more readily to meaningful stimuli. Rapid eye movement (REM) sleep can be characterized as a period when the brain is active and the body is paralyzed, whereas in nonrapid eye movement (NREM) sleep, the brain is less active but the body can move. Sleep disorders are grouped into three general categories, based on whether patients have trouble staying awake, trouble sleeping, or abnormal behaviors during sleep.

scholarly journals Cortical monitoring of cardiac activity during rapid eye movement sleep: the heartbeat evoked potential in phasic and tonic REM microstates

SLEEP ◽  
2021 ◽  
Author(s):  
Péter Simor ◽  
Tamás Bogdány ◽  
Róbert Bódizs ◽  
Pandelis Perakakis
Keyword(s):  
Eye Movement ◽  
Sensory Processing ◽  
Rem Sleep ◽  
Evoked Potential ◽  
Physiological State ◽  
Cardiac Activity ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Heartbeat Evoked Potential ◽  
The Brain

Abstract Sleep is a fundamental physiological state that facilitates neural recovery during periods of attenuated sensory processing. On the other hand, mammalian sleep is also characterized by the interplay between periods of increased sleep depth and environmental alertness. Whereas the heterogeneity of microstates during non-rapid-eye-movement (NREM) sleep was extensively studied in the last decades, transient microstates during REM sleep received less attention. REM sleep features two distinct microstates: phasic and tonic. Previous studies indicate that sensory processing is largely diminished during phasic REM periods, whereas environmental alertness is partially reinstated when the brain switches into tonic REM sleep. Here, we investigated interoceptive processing as quantified by the heartbeat evoked potential (HEP) during REM microstates. We contrasted the HEPs of phasic and tonic REM periods using two separate databases that included the nighttime polysomnographic recordings of healthy young individuals (N = 20 and N = 19). We find a differential HEP modulation of a late HEP component (after 500 ms post-R-peak) between tonic and phasic REM. Moreover, the late tonic HEP component resembled the HEP found in resting wakefulness. Our results indicate that interoception with respect to cardiac signals is not uniform across REM microstates, and suggest that interoceptive processing is partially reinstated during tonic REM periods. The analyses of the HEP during REM sleep may shed new light on the organization and putative function of REM microstates.

Eye movements modulate interoceptive processing during rapid eye movement sleep: the heartbeat evoked potential in phasic and tonic REM microstates

2020 ◽  
Author(s):  
Péter Simor ◽  
Bogdány Tamás ◽  
Robert Bodizs ◽  
Pandelis Perakakis
Keyword(s):  
Eye Movement ◽  
Sensory Processing ◽  
Rem Sleep ◽  
Evoked Potential ◽  
Physiological State ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Heartbeat Evoked Potential ◽  
The Brain

Sleep is a fundamental physiological state that facilitates neural recovery during periods of attenuated sensory processing. On the other hand, mammalian sleep is also characterized by the interplay between periods of increased sleep depth and environmental alertness. Whereas the heterogeneity of microstates during non-rapid-eye-movement (NREM) sleep was extensively studied in the last decades, transient microstates during REM sleep received less attention. REM sleep features two distinct microstates: phasic and tonic. Previous studies indicate that sensory processing is largely diminished during phasic REM periods, whereas environmental alertness is partially reinstated when the brain switches into tonic REM sleep. Here, we investigated interoceptive processing as quantified by the heartbeat evoked potential (HEP) during REM microstates. We contrasted the HEPs of phasic and tonic REM periods using two separate databases that included the nighttime polysomnographic recordings of healthy young individuals (N = 20 and N = 19). We find a differential HEP modulation of a late HEP component (after 500 ms post-R-peak) between tonic and phasic REM. Moreover, the late tonic HEP component resembled the HEP found in resting wakefulness. Our results indicate that interoception with respect to cardiac signals is not uniform across REM microstates, and suggest that interoceptive processing is partially reinstated during tonic REM periods. The analyses of the HEP during REM sleep may shed new light on the organization and putative function of REM microstates.

scholarly journals Microglia modulate stable wakefulness via the thalamic reticular nucleus in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hanxiao Liu ◽  
Xinxing Wang ◽  
Lu Chen ◽  
Liang Chen ◽  
Stella E. Tsirka ◽  
...  
Keyword(s):  
Diurnal Variation ◽  
Eye Movement ◽  
Nrem Sleep ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Rapid Eye Movement ◽  
Metabolomic Analysis ◽  
The Brain ◽  
Ceramide Production ◽  
Brain Homeostasis

AbstractMicroglia are important for brain homeostasis and immunity, but their role in regulating vigilance remains unclear. We employed genetic, physiological, and metabolomic methods to examine microglial involvement in the regulation of wakefulness and sleep. Microglial depletion decreased stable nighttime wakefulness in mice by increasing transitions between wakefulness and non-rapid eye movement (NREM) sleep. Metabolomic analysis revealed that the sleep-wake behavior closely correlated with diurnal variation of the brain ceramide, which disappeared in microglia-depleted mice. Ceramide preferentially influenced microglia in the thalamic reticular nucleus (TRN), and local depletion of TRN microglia produced similar impaired wakefulness. Chemogenetic manipulations of anterior TRN neurons showed that they regulated transitions between wakefulness and NREM sleep. Their firing capacity was suppressed by both microglial depletion and added ceramide. In microglia-depleted mice, activating anterior TRN neurons or inhibiting ceramide production both restored stable wakefulness. These findings demonstrate that microglia can modulate stable wakefulness through anterior TRN neurons via ceramide signaling.

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.

Spontaneous sleep and homeostatic sleep regulation in ghrelin knockout mice

2007 ◽  
Vol 293 (1) ◽  
pp. R510-R517 ◽  
Author(s):  
Éva Szentirmai ◽  
Levente Kapás ◽  
Yuxiang Sun ◽  
Roy G. Smith ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Diurnal Rhythms ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Compensatory Mechanisms ◽  
Regulatory Circuit ◽  
Normal Sleep ◽  
The Brain

Ghrelin is well known for its feeding and growth hormone-releasing actions. It may also be involved in sleep regulation; intracerebroventricular administration and hypothalamic microinjections of ghrelin stimulate wakefulness in rats. Hypothalamic ghrelin, together with neuropeptide Y and orexin form a food intake-regulatory circuit. We hypothesized that this circuit also promotes arousal. To further investigate the role of ghrelin in the regulation of sleep-wakefulness, we characterized spontaneous and homeostatic sleep regulation in ghrelin knockout (KO) and wild-type (WT) mice. Both groups of mice exhibited similar diurnal rhythms with more sleep and less wakefulness during the light period. In ghrelin KO mice, spontaneous wakefulness and rapid-eye-movement sleep (REMS) were slightly elevated, and non-rapid-eye-movement sleep (NREMS) was reduced. KO mice had more fragmented NREMS than WT mice, as indicated by the shorter and greater number of NREMS episodes. Six hours of sleep deprivation induced rebound increases in NREMS and REMS and biphasic changes in electroencephalographic slow-wave activity (EEG SWA) in both genotypes. Ghrelin KO mice recovered from NREMS and REMS loss faster, and the delayed reduction in EEG SWA, occurring after sleep loss-enhanced increases in EEG SWA, was shorter-lasting compared with WT mice. These findings suggest that the basic sleep-wake regulatory mechanisms in ghrelin KO mice are not impaired and they are able to mount adequate rebound sleep in response to a homeostatic challenge. It is possible that redundancy in the arousal systems of the brain or activation of compensatory mechanisms during development allow for normal sleep-wake regulation in ghrelin KO mice.

Interleukin 1β enhances non-rapid eye movement sleep and increases c-Fos protein expression in the median preoptic nucleus of the hypothalamus

2005 ◽  
Vol 288 (4) ◽  
pp. R998-R1005 ◽  
Author(s):  
F. C. Baker ◽  
S. Shah ◽  
D. Stewart ◽  
C. Angara ◽  
H. Gong ◽  
...  
Keyword(s):  
Eye Movement ◽  
Active Sites ◽  
Nrem Sleep ◽  
Interleukin 1Β ◽  
Rapid Eye Movement ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Fos Protein ◽  
The Brain ◽  
Threshold Amount

Interleukin 1β (IL-1) is a key mediator of the acute phase response in an infected host and acts centrally to coordinate responses to an immune challenge, such as fever and increased non-rapid eye movement (NREM) sleep. The preoptic area (POA) is a primary sleep regulatory center in the brain: the ventrolateral POA (VLPO) and median preoptic nucleus (MnPN) each contain high numbers of c-Fos protein immunoreactive (IR) neurons after sleep but not after waking. We hypothesized that IL-1 mediates increased NREM sleep through activation of these sleep-active sites. Rats injected intracerebroventricularly with IL-1 (10 ng) at dark onset spent significantly more time in NREM sleep 4–5 h after injection. This increase in NREM sleep was associated with increased numbers of Fos-IR neurons in the MnPN, but not in the VLPO. Fos IR in the rostral MnPN was significantly increased 2 h post IL-1 injection, although the percentage of NREM sleep in the preceding 2 h was the same as controls. Fos IR was also increased in the extended VLPO 2 h postinjection. Finally, Fos IR in the MnPN did not differ significantly between IL-1 and vehicle-treated rats that had been sleep deprived for 2 h postinjection, but it was increased in VLPO core. Taken together, these results suggest that Fos IR in the MnPN after IL-1 is not independent of behavioral state and may require some threshold amount of sleep for its expression. Our results support a hypothesis that IL-1 enhances NREM sleep, in part, through activation of neurons in the MnPN of the hypothalamus.

scholarly journals Region-specific and state-dependent astrocyte Ca2+ dynamics during the sleep-wake cycle in mice

2020 ◽  
Author(s):  
Tomomi Tsunematsu ◽  
Shuzo Sakata ◽  
Tomomi Sanagi ◽  
Kenji F. Tanaka ◽  
Ko Matsui
Keyword(s):  
Eye Movement ◽  
Neural Activity ◽  
Brain Region ◽  
Principal Component ◽  
Nrem Sleep ◽  
Brain Regions ◽  
Rapid Eye Movement ◽  
State Dependent ◽  
Instinctive Behavior ◽  
The Brain

AbstractNeural activity is diverse, and varies depending on brain regions and sleep/wakefulness states. However, whether astrocyte activity differs between sleep/wakefulness states, and whether there are differences in astrocyte activity among brain regions remain poorly understood. In this study, we recorded astrocyte intracellular calcium (Ca2+) concentrations of mice during sleep/wakefulness states in the cortex, hippocampus, hypothalamus, cerebellum, and pons using fiber photometry. For this purpose, male transgenic mice in which their astrocytes specifically express the genetically encoded ratiometric Ca2+ sensor YCnano50 were used. We demonstrated that Ca2+ levels in astrocytes significantly decrease during Rapid Eye Movement (REM) sleep and increase after the onset of wakefulness. In contrast, differences in Ca2+ levels during non-Rapid Eye Movement (NREM) sleep were observed among different brain regions, and no significant decrease was observed in the hypothalamus and pons. Further analyses focusing on the transition between sleep/wakefulness states and correlation analysis with episode duration of REM showed that Ca2+ dynamics differed among brain regions, suggesting the existence of several clusters. To quantify region-specific Ca2+ dynamics, principal component analysis was performed to uncover three clusters; i.e., the first comprised the cortex and hippocampus, the second comprised the cerebellum, and the third comprised the hypothalamus and pons. Our study demonstrated that astrocyte Ca2+ levels change substantially according to sleep/wakefulness states. These changes were generally consistent, unlike neural activity. However, we also clarified that Ca2+ dynamics varies depending on the brain region, implying that astrocytes may play various physiological roles in sleep.Significance statementSleep is an instinctive behavior of many organisms. In the previous five decades, the mechanism of the neural circuits controlling sleep/wakefulness states and the neural activities associated with sleep/wakefulness states in various brain regions have been elucidated. However, whether astrocytes, which are a type of glial cell, change their activity during different sleep/wakefulness states is poorly understood. Here, we demonstrated that dynamic changes in intracellular Ca2+ concentrations occur in the cortex, hippocampus, hypothalamus, cerebellum, and pons of genetically modified mice during natural sleep. Further analyses demonstrated that Ca2+ dynamics slightly differ among different brain regions, implying that the physiological roles of astrocytes in sleep/wakefulness might vary depending on the brain region.

What Is a Dream?

2020 ◽  
pp. 1-12
Author(s):  
Sue Llewellyn
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Sleep Cycle ◽  
Rapid Eye Movement ◽  
Fixed Sequence ◽  
The World ◽  
The Brain ◽  
Light Sleep

Dreaming happens during sleep. When we aren’t interacting with the world, our minds turn inwards. We dream. These dreams differ. Rapid eye movement (REM) dreams are visual, vivid, bizarre, emotional, and highly associative with embodied narratives, whereas non-rapid eye movement (NREM) dreams tend to be shorter and more thought-like. During REM dreams, the brain is as active, or even more active, than it is during wakefulness. In some dreams, during REM sleep, the dreamer is lucid—they become aware they are dreaming and can, sometimes control the dream content. These different types of dream happen at different times in the sleep cycle. Across the night, we experience NREM sleep (including light sleep and deep sleep) and REM sleep in a fixed sequence. The night isn’t a uniform period of rest. This introductory chapter explains these basic issues about sleep and dreams.

scholarly journals Control of Sleep and Wakefulness

2012 ◽  
Vol 92 (3) ◽  
pp. 1087-1187 ◽  
Author(s):  
Ritchie E. Brown ◽  
Radhika Basheer ◽  
James T. McKenna ◽  
Robert E. Strecker ◽  
Robert W. McCarley
Keyword(s):  
Brain Stem ◽  
Eye Movement ◽  
Rem Sleep ◽  
Emotional Reactivity ◽  
Low Voltage ◽  
Nrem Sleep ◽  
Gabaergic Neurons ◽  
Cortical Activation ◽  
Rapid Eye Movement ◽  
The Brain

This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.

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