Special Issue "Sleep and Brain Development"

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A special issue of Brain Sciences (ISSN 2076-3425).

Deadline for manuscript submissions: closed (30 October 2015)

Special Issue Editor

Guest Editor
Prof Dr. Marcos G. Frank

Washington State University-Spokane, Sleep and Performance Research Center College of Medical Sciences, Pharmaceutical and Biomedical Sciences Building 213, 412 E Spokane Falls Blvd., Spokane, WA 99202, USA
Website | E-Mail
Phone: +1 509 368 6747
Fax: +1 509 368 6766
Interests: neural development; sleep; synaptic plasticity; glia

Special Issue Information

Dear Colleagues,

The function of sleep is an enduring biological mystery. This mystery only deepens when we look back in ontogenetic time. Across a wide variety of animal species, sleep amounts are maximal during early development. This abundance of sleep coincides with periods of heightened brain growth and plasticity. This suggests that one function of sleep may be to promote normal brain maturation. This intuitive idea, however, has been minimally explored. A more complete understanding of sleep ontogenesis and the impact of normal and abnormal sleep on the developing brain is needed.

The current special issue will feature articles that address how sleep and sleep regulation change during development, and the interactions between sleep, brain maturation and plasticity, and behavior.

Dr. Marcos G. Frank
Guest Editor

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 600 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Keywords

  • ontogenesis
  • synaptic plasticity
  • sleep
  • neural development
  • infants
  • children
  • adolescence
  • fetal

Published Papers (9 papers)

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Research

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Open AccessArticle Topography of Slow Sigma Power during Sleep is Associated with Processing Speed in Preschool Children
Brain Sci. 2015, 5(4), 494-508; doi:10.3390/brainsci5040494
Received: 3 August 2015 / Revised: 23 October 2015 / Accepted: 29 October 2015 / Published: 4 November 2015
Cited by 5 | PDF Full-text (1577 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Cognitive development is influenced by maturational changes in processing speed, a construct reflecting the rapidity of executing cognitive operations. Although cognitive ability and processing speed are linked to spindles and sigma power in the sleep electroencephalogram (EEG), little is known about such associations
[...] Read more.
Cognitive development is influenced by maturational changes in processing speed, a construct reflecting the rapidity of executing cognitive operations. Although cognitive ability and processing speed are linked to spindles and sigma power in the sleep electroencephalogram (EEG), little is known about such associations in early childhood, a time of major neuronal refinement. We calculated EEG power for slow (10–13 Hz) and fast (13.25–17 Hz) sigma power from all-night high-density electroencephalography (EEG) in a cross-sectional sample of healthy preschool children (n = 10, 4.3 ± 1.0 years). Processing speed was assessed as simple reaction time. On average, reaction time was 1409 ± 251 ms; slow sigma power was 4.0 ± 1.5 μV2; and fast sigma power was 0.9 ± 0.2 μV2. Both slow and fast sigma power predominated over central areas. Only slow sigma power was correlated with processing speed in a large parietal electrode cluster (p < 0.05, r ranging from −0.6 to −0.8), such that greater power predicted faster reaction time. Our findings indicate regional correlates between sigma power and processing speed that are specific to early childhood and provide novel insights into the neurobiological features of the EEG that may underlie developing cognitive abilities. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessArticle Caffeine Consuming Children and Adolescents Show Altered Sleep Behavior and Deep Sleep
Brain Sci. 2015, 5(4), 441-455; doi:10.3390/brainsci5040441
Received: 10 August 2015 / Revised: 28 September 2015 / Accepted: 7 October 2015 / Published: 15 October 2015
Cited by 2 | PDF Full-text (384 KB) | HTML Full-text | XML Full-text
Abstract
Caffeine is the most commonly ingested psychoactive drug worldwide with increasing consumption rates among young individuals. While caffeine leads to decreased sleep quality in adults, studies investigating how caffeine consumption affects children’s and adolescents’ sleep remain scarce. We explored the effects of regular
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Caffeine is the most commonly ingested psychoactive drug worldwide with increasing consumption rates among young individuals. While caffeine leads to decreased sleep quality in adults, studies investigating how caffeine consumption affects children’s and adolescents’ sleep remain scarce. We explored the effects of regular caffeine consumption on sleep behavior and the sleep electroencephalogram (EEG) in children and adolescents (10–16 years). While later habitual bedtimes (Caffeine 23:14 ± 11.4, Controls 22:17 ± 15.4) and less time in bed were found in caffeine consumers compared to the control group (Caffeine 08:10 ± 13.3, Controls 09:03 ± 16.1), morning tiredness was unaffected. Furthermore, caffeine consumers exhibited reduced sleep EEG slow-wave activity (SWA, 1–4.5 Hz) at the beginning of the night compared to controls (20% ± 9% average reduction across all electrodes and subjects). Comparable reductions were found for alpha activity (8.25–9.75 Hz). These effects, however, disappeared in the morning hours. Our findings suggest that caffeine consumption in adolescents may lead to later bedtimes and reduced SWA, a well-established marker of sleep depth. Because deep sleep is involved in recovery processes during sleep, further research is needed to understand whether a caffeine-induced loss of sleep depth interacts with neuronal network refinement processes that occur during the sensitive period of adolescent development. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessArticle Larval Population Density Alters Adult Sleep in Wild-Type Drosophila melanogaster but Not in Amnesiac Mutant Flies
Brain Sci. 2014, 4(3), 453-470; doi:10.3390/brainsci4030453
Received: 29 May 2014 / Revised: 27 June 2014 / Accepted: 28 June 2014 / Published: 11 August 2014
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Abstract
Sleep has many important biological functions, but how sleep is regulated remains poorly understood. In humans, social isolation and other stressors early in life can disrupt adult sleep. In fruit flies housed at different population densities during early adulthood, social enrichment was shown
[...] Read more.
Sleep has many important biological functions, but how sleep is regulated remains poorly understood. In humans, social isolation and other stressors early in life can disrupt adult sleep. In fruit flies housed at different population densities during early adulthood, social enrichment was shown to increase subsequent sleep, but it is unknown if population density during early development can also influence adult sleep. To answer this question, we maintained Drosophila larvae at a range of population densities throughout larval development, kept them isolated during early adulthood, and then tested their sleep patterns. Our findings reveal that flies that had been isolated as larvae had more fragmented sleep than those that had been raised at higher population densities. This effect was more prominent in females than in males. Larval population density did not affect sleep in female flies that were mutant for amnesiac, which has been shown to be required for normal memory consolidation, adult sleep regulation, and brain development. In contrast, larval population density effects on sleep persisted in female flies lacking the olfactory receptor or83b, suggesting that olfactory signals are not required for the effects of larval population density on adult sleep. These findings show that population density during early development can alter sleep behavior in adulthood, suggesting that genetic and/or structural changes are induced by this developmental manipulation that persist through metamorphosis. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessArticle Development of Brain EEG Connectivity across Early Childhood: Does Sleep Play a Role?
Brain Sci. 2013, 3(4), 1445-1460; doi:10.3390/brainsci3041445
Received: 4 September 2013 / Revised: 21 October 2013 / Accepted: 29 October 2013 / Published: 12 November 2013
Cited by 8 | PDF Full-text (628 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Sleep has beneficial effects on brain function and learning, which are reflected in plastic changes in the cortex. Early childhood is a time of rapid maturation in fundamental skills—e.g., language, cognitive control, working memory—that are predictive of future functioning. Little is currently known
[...] Read more.
Sleep has beneficial effects on brain function and learning, which are reflected in plastic changes in the cortex. Early childhood is a time of rapid maturation in fundamental skills—e.g., language, cognitive control, working memory—that are predictive of future functioning. Little is currently known about the interactions between sleep and brain maturation during this developmental period. We propose coherent electroencephalogram (EEG) activity during sleep may provide unique insight into maturational processes of functional brain connectivity. Longitudinal sleep EEG assessments were performed in eight healthy subjects at ages 2, 3 and 5 years. Sleep EEG coherence increased across development in a region- and frequency-specific manner. Moreover, although connectivity primarily decreased intra-hemispherically across a night of sleep, an inter-hemispheric overnight increase occurred in the frequency range of slow waves (0.8–2 Hz), theta (4.8–7.8 Hz) and sleep spindles (10–14 Hz), with connectivity changes of up to 20% across a night of sleep. These findings indicate sleep EEG coherence reflects processes of brain maturation—i.e., programmed unfolding of neuronal networks—and moreover, sleep-related alterations of brain connectivity during the sensitive maturational window of early childhood. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessArticle Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
Brain Sci. 2013, 3(1), 318-343; doi:10.3390/brainsci3010318
Received: 30 December 2012 / Revised: 30 January 2013 / Accepted: 27 February 2013 / Published: 19 March 2013
Cited by 9 | PDF Full-text (3820 KB) | HTML Full-text | XML Full-text
Abstract
Sleep changes were studied in mice (n = 59) from early adolescence to adulthood (postnatal days P19–111). REM sleep declined steeply in early adolescence, while total sleep remained constant and NREM sleep increased slightly. Four hours of sleep deprivation starting at light
[...] Read more.
Sleep changes were studied in mice (n = 59) from early adolescence to adulthood (postnatal days P19–111). REM sleep declined steeply in early adolescence, while total sleep remained constant and NREM sleep increased slightly. Four hours of sleep deprivation starting at light onset were performed from ages P26 through adulthood (>P60). Following this acute sleep deprivation all mice slept longer and with more consolidated sleep bouts, while NREM slow wave activity (SWA) showed high interindividual variability in the younger groups, and increased consistently only after P42. Three parameters together explained up to 67% of the variance in SWA rebound in frontal cortex, including weight-adjusted age and increase in alpha power during sleep deprivation, both of which positively correlated with the SWA response. The third, and strongest predictor was the SWA decline during the light phase in baseline: mice with high peak SWA at light onset, resulting in a large SWA decline, were more likely to show no SWA rebound after sleep deprivation, a result that was also confirmed in parietal cortex. During baseline, however, SWA showed the same homeostatic changes in adolescents and adults, declining in the course of sleep and increasing across periods of spontaneous wake. Thus, we hypothesize that, in young adolescent mice, a ceiling effect and not the immaturity of the cellular mechanisms underlying sleep homeostasis may prevent the SWA rebound when wake is extended beyond its physiological duration. Full article
(This article belongs to the Special Issue Sleep and Brain Development)

Review

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Open AccessReview Neural Basis of Brain Dysfunction Produced by Early Sleep Problems
Brain Sci. 2016, 6(1), 5; doi:10.3390/brainsci6010005
Received: 9 October 2015 / Revised: 18 January 2016 / Accepted: 21 January 2016 / Published: 29 January 2016
Cited by 3 | PDF Full-text (2204 KB) | HTML Full-text | XML Full-text
Abstract
There is a wealth of evidence that disrupted sleep and circadian rhythms, which are common in modern society even during the early stages of life, have unfavorable effects on brain function. Altered brain function can cause problem behaviors later in life, such as
[...] Read more.
There is a wealth of evidence that disrupted sleep and circadian rhythms, which are common in modern society even during the early stages of life, have unfavorable effects on brain function. Altered brain function can cause problem behaviors later in life, such as truancy from or dropping out of school, quitting employment, and committing suicide. In this review, we discuss findings from several large cohort studies together with recent results of a cohort study using the marshmallow test, which was first introduced in the 1960s. This test assessed the ability of four-year-olds to delay gratification and showed how this ability correlated with success later in life. The role of the serotonergic system in sleep and how this role changes with age are also discussed. The serotonergic system is involved in reward processing and interactions with the dorsal striatum, ventral striatum, and the prefrontal cortex are thought to comprise the neural basis for behavioral patterns that are affected by the quantity, quality, and timing of sleep early in life. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessReview Pedunculopontine Gamma Band Activity and Development
Brain Sci. 2015, 5(4), 546-567; doi:10.3390/brainsci5040546
Received: 29 October 2015 / Revised: 20 November 2015 / Accepted: 23 November 2015 / Published: 3 December 2015
PDF Full-text (1434 KB) | HTML Full-text | XML Full-text
Abstract
This review highlights the most important discovery in the reticular activating system in the last 10 years, the manifestation of gamma band activity in cells of the reticular activating system (RAS), especially in the pedunculopontine nucleus, which is in charge of waking and
[...] Read more.
This review highlights the most important discovery in the reticular activating system in the last 10 years, the manifestation of gamma band activity in cells of the reticular activating system (RAS), especially in the pedunculopontine nucleus, which is in charge of waking and rapid eye movement (REM) sleep. The identification of different cell groups manifesting P/Q-type Ca2+ channels that control waking vs. those that manifest N-type channels that control REM sleep provides novel avenues for the differential control of waking vs. REM sleep. Recent discoveries on the development of this system can help explain the developmental decrease in REM sleep and the basic rest-activity cycle. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessReview Sleep, Plasticity and the Pathophysiology of Neurodevelopmental Disorders: The Potential Roles of Protein Synthesis and Other Cellular Processes
Brain Sci. 2014, 4(1), 150-201; doi:10.3390/brainsci4010150
Received: 27 December 2013 / Revised: 26 February 2014 / Accepted: 7 March 2014 / Published: 19 March 2014
Cited by 7 | PDF Full-text (771 KB) | HTML Full-text | XML Full-text
Abstract
Sleep is important for neural plasticity, and plasticity underlies sleep-dependent memory consolidation. It is widely appreciated that protein synthesis plays an essential role in neural plasticity. Studies of sleep-dependent memory and sleep-dependent plasticity have begun to examine alterations in these functions in populations
[...] Read more.
Sleep is important for neural plasticity, and plasticity underlies sleep-dependent memory consolidation. It is widely appreciated that protein synthesis plays an essential role in neural plasticity. Studies of sleep-dependent memory and sleep-dependent plasticity have begun to examine alterations in these functions in populations with neurological and psychiatric disorders. Such an approach acknowledges that disordered sleep may have functional consequences during wakefulness. Although neurodevelopmental disorders are not considered to be sleep disorders per se, recent data has revealed that sleep abnormalities are among the most prevalent and common symptoms and may contribute to the progression of these disorders. The main goal of this review is to highlight the role of disordered sleep in the pathology of neurodevelopmental disorders and to examine some potential mechanisms by which sleep-dependent plasticity may be altered. We will also briefly attempt to extend the same logic to the other end of the developmental spectrum and describe a potential role of disordered sleep in the pathology of neurodegenerative diseases. We conclude by discussing ongoing studies that might provide a more integrative approach to the study of sleep, plasticity, and neurodevelopmental disorders. Full article
(This article belongs to the Special Issue Sleep and Brain Development)
Open AccessReview From Neural Plate to Cortical Arousal—A Neuronal Network Theory of Sleep Derived from in Vitro “Model” Systems for Primordial Patterns of Spontaneous Bioelectric Activity in the Vertebrate Central Nervous System
Brain Sci. 2013, 3(2), 800-820; doi:10.3390/brainsci3020800
Received: 11 March 2013 / Revised: 15 April 2013 / Accepted: 6 May 2013 / Published: 22 May 2013
Cited by 4 | PDF Full-text (2707 KB) | HTML Full-text | XML Full-text
Abstract
In the early 1960s intrinsically generated widespread neuronal discharges were discovered to be the basis for the earliest motor behavior throughout the animal kingdom. The pattern generating system is in fact programmed into the developing nervous system, in a regionally specific manner, already
[...] Read more.
In the early 1960s intrinsically generated widespread neuronal discharges were discovered to be the basis for the earliest motor behavior throughout the animal kingdom. The pattern generating system is in fact programmed into the developing nervous system, in a regionally specific manner, already at the early neural plate stage. Such rhythmically modulated phasic bursts were next discovered to be a general feature of developing neural networks and, largely on the basis of experimental interventions in cultured neural tissues, to contribute significantly to their morpho-physiological maturation. In particular, the level of spontaneous synchronized bursting is homeostatically regulated, and has the effect of constraining the development of excessive network excitability. After birth or hatching, this “slow-wave” activity pattern becomes sporadically suppressed in favor of sensory oriented “waking” behaviors better adapted to dealing with environmental contingencies. It nevertheless reappears periodically as “sleep” at several species-specific points in the diurnal/nocturnal cycle. Although this “default” behavior pattern evolves with development, its essential features are preserved throughout the life cycle, and are based upon a few simple mechanisms which can be both experimentally demonstrated and simulated by computer modeling. In contrast, a late onto- and phylogenetic aspect of sleep, viz., the intermittent “paradoxical” activation of the forebrain so as to mimic waking activity, is much less well understood as regards its contribution to brain development. Some recent findings dealing with this question by means of cholinergically induced “aroused” firing patterns in developing neocortical cell cultures, followed by quantitative electrophysiological assays of immediate and longterm sequelae, will be discussed in connection with their putative implications for sleep ontogeny. Full article
(This article belongs to the Special Issue Sleep and Brain Development)

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