Sleep and Psychiatric Disorders in Persons With Mild Traumatic Brain Injury.

PubMed

Mollayeva, Tatyana; D'Souza, Andrea; Mollayeva, Shirin

2017-08-01

Mild traumatic brain injury (mTBI) frequently challenges the integrity of sleep function by affecting multiple brain areas implicated in controlling the switch between wakefulness and sleep and those involved in circadian and homeostatic processes; the malfunction of each causes a variety of disorders. In this review, we discuss recent data on the dynamics between disorders of sleep and mental/psychiatric disorders in persons with mTBI. This analysis sets the stage for understanding how a variety of physiological, emotional and environmental influences affect sleep and mental activities after injury to the brain. Consideration of the intricate links between sleep and mental functions in future research can increase understanding on the underlying mechanisms of sleep-related and psychiatric comorbidity in mTBI.

A One-Hour Sleep Restriction Impacts Brain Processing in Young Children Across Tasks: Evidence From Event-related Potentials

PubMed Central

Molfese, Dennis L.; Ivanenko, Anna; Key, Alexandra Fonaryova; Roman, Adrienne; Molfese, Victoria J.; O'Brien, Louise M.; Gozal, David; Kota, Srinivas; Hudac, Caitlin M.

2014-01-01

The effect of mild sleep restriction on cognitive functioning in young children is unclear, yet sleep loss may impact children's abilities to attend to tasks with high processing demands. In a preliminary investigation, six children (6.6 - 8.3 years of age) with normal sleep patterns performed three tasks: attention (“Oddball”), speech perception (conconant-vowel syllables) and executive function (Directional Stroop). Event-related potentials (ERP) responses were recorded before (Control) and following one-week of 1-hour per day of sleep restriction. Brain activity across all tasks following Sleep Restriction differed from activity during Control Sleep, indicating that minor sleep restriction impacts children's neurocognitive functioning. PMID:23862635

Differences in activity of cytochrome C oxidase in brain between sleep and wakefulness.

PubMed

Nikonova, Elena V; Vijayasarathy, Camasamudram; Zhang, Lin; Cater, Jacqueline R; Galante, Raymond J; Ward, Stephen E; Avadhani, Narayan G; Pack, Allan I

2005-01-01

Increased mRNA level of subunit 1 cytochrome c oxidase (COXI) during wakefulness and after short-term sleep deprivation has been described in brain. We hypothesized that this might contribute to increased activity of cytochrome oxidase (COX) enzyme during wakefulness, as part of the mechanisms to provide sufficient amounts of adenosine triphosphate to meet increased neuronal energy demands. COX activity was measured in isolated mitochondria from different brain regions in groups of rats with 3 hours of spontaneous sleep, 3 hours of spontaneous wake, and 3 hours of sleep deprivation. The group with 3 hours of spontaneous wake was added to delineate the circadian component of changes in the enzyme activity. Northern blot analysis was performed to examine the mRNA levels of 2 subunits of the enzyme COXI and COXIV, encoded by mitochondrial and nuclear DNA, respectively. Laboratory of Biochemistry, Department of Animal Biology, and Center for Sleep and Respiratory Neurobiology, University of Pennsylvania. 2-month-old male Fischer rats (N = 21) implanted for polygraphic recording. For COX activity, there was a main effect by analysis of variance of experimental group (P < .0001) with significant increases in COX activity in wake and sleep-deprived groups as compared to the sleep group. A main effect of brain region was also significant (P < .001). There was no difference between brain regions in the degree of increase in enzyme activity in wakefulness. Both COXI and COXIV mRNA were increased with wakefulness as compared to sleep. There is an increase in COX activity after both 3 hours of spontaneous wake and 3 hours of sleep deprivation as compared with 3 hours of spontaneous sleep in diverse brain regions, which could be, in part, explained by the increased levels of bigenomic transcripts of the enzyme. This likely contributes to increased adenosine triphosphate production during wakefulness. ADP, adenosine diphosphate; ATP, adenosine triphosphate; COXI, cytochrome c oxidase subunit 1 mRNA; COX, cytochrome c oxidase (protein); CREB, cyclic AMP response element binding protein; DNA, deoxyribonucleic acid; EDTA, ethylenediaminetetraacetic acid; EEG, electroencephalography; EMG, electromyography; GABP, GA binding protein; HEPES, 4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid; mRNA, messenger ribonucleic acid; NADH, nicotinamid adenine dinucleotide, reduced; NDII, NADH dehydrogenase subunit 2 mRNA; NRF, nuclear respiratory factor.

Novel application of brain-targeting polyphenol compounds in sleep deprivation-induced cognitive dysfunction

PubMed Central

Zhao, Wei; Wang, Jun; Bi, Weina; Ferruzzi, Mario; Yemul, Shrishailam; Freire, Daniel; Mazzola, Paolo; Ho, Lap; Dubner, Lauren; Pasinetti, Giulio Maria

2016-01-01

Sleep deprivation produces deficits in hippocampal synaptic plasticity and hippocampal-dependent memory storage. Recent evidence suggests that sleep deprivation disrupts memory consolidation through multiple mechanisms, including the down-regulation of the cAMP-response element-binding protein (CREB) and of mammalian target of rapamycin (mTOR) signaling. In this study, we tested the effects of a Bioactive Dietary Polyphenol Preparation (BDPP), comprised of grape seed polyphenol extract, Concord grape juice, and resveratrol, on the attenuation of sleep deprivation-induced cognitive impairment. We found that BDPP significantly improves sleep deprivation-induced contextual memory deficits, possibly through the activation of CREB and mTOR signaling pathways. We also identified brain-available polyphenol metabolites from BDPP, among which quercetin-3-O-glucuronide activates CREB signaling and malvidin-3-O-glucoside activates mTOR signaling. In combination, quercetin and malvidin-glucoside significantly attenuated sleep deprivation-induced cognitive impairment in -a mouse model of acute sleep deprivation. Our data suggests the feasibility of using select brain-targeting polyphenol compounds derived from BDPP as potential therapeutic agents in promoting resilience against sleep deprivation-induced cognitive dysfunction. PMID:26235983

Regional Slow Waves and Spindles in Human Sleep

PubMed Central

Nir, Yuval; Staba, Richard J.; Andrillon, Thomas; Vyazovskiy, Vladyslav V.; Cirelli, Chiara; Fried, Itzhak; Tononi, Giulio

2011-01-01

SUMMARY The most prominent EEG events in sleep are slow waves, reflecting a slow (<1 Hz) oscillation between up and down states in cortical neurons. It is unknown whether slow oscillations are synchronous across the majority or the minority of brain regions—are they a global or local phenomenon? To examine this, we recorded simultaneously scalp EEG, intracerebral EEG, and unit firing in multiple brain regions of neurosurgical patients. We find that most sleep slow waves and the underlying active and inactive neuronal states occur locally. Thus, especially in late sleep, some regions can be active while others are silent. We also find that slow waves can propagate, usually from medial prefrontal cortex to the medial temporal lobe and hippocampus. Sleep spindles, the other hallmark of NREM sleep EEG, are likewise predominantly local. Thus, intracerebral communication during sleep is constrained because slow and spindle oscillations often occur out-of-phase in different brain regions. PMID:21482364

Experienced Mindfulness Meditators Exhibit Higher Parietal-Occipital EEG Gamma Activity during NREM Sleep

PubMed Central

Ferrarelli, Fabio; Smith, Richard; Dentico, Daniela; Riedner, Brady A.; Zennig, Corinna; Benca, Ruth M.; Lutz, Antoine; Davidson, Richard J.; Tononi, Giulio

2013-01-01

Over the past several years meditation practice has gained increasing attention as a non-pharmacological intervention to provide health related benefits, from promoting general wellness to alleviating the symptoms of a variety of medical conditions. However, the effects of meditation training on brain activity still need to be fully characterized. Sleep provides a unique approach to explore the meditation-related plastic changes in brain function. In this study we performed sleep high-density electroencephalographic (hdEEG) recordings in long-term meditators (LTM) of Buddhist meditation practices (approximately 8700 mean hours of life practice) and meditation naive individuals. We found that LTM had increased parietal-occipital EEG gamma power during NREM sleep. This increase was specific for the gamma range (25–40 Hz), was not related to the level of spontaneous arousal during NREM and was positively correlated with the length of lifetime daily meditation practice. Altogether, these findings indicate that meditation practice produces measurable changes in spontaneous brain activity, and suggest that EEG gamma activity during sleep represents a sensitive measure of the long-lasting, plastic effects of meditative training on brain function. PMID:24015304

Sleep, Memory & Brain Rhythms.

PubMed

Watson, Brendon O; Buzsáki, György

2015-01-01

Sleep occupies roughly one-third of our lives, yet the scientific community is still not entirely clear on its purpose or function. Existing data point most strongly to its role in memory and homeostasis: that sleep helps maintain basic brain functioning via a homeostatic mechanism that loosens connections between overworked synapses, and that sleep helps consolidate and re-form important memories. In this review, we will summarize these theories, but also focus on substantial new information regarding the relation of electrical brain rhythms to sleep. In particular, while REM sleep may contribute to the homeostatic weakening of overactive synapses, a prominent and transient oscillatory rhythm called "sharp-wave ripple" seems to allow for consolidation of behaviorally relevant memories across many structures of the brain. We propose that a theory of sleep involving the division of labor between two states of sleep-REM and non-REM, the latter of which has an abundance of ripple electrical activity-might allow for a fusion of the two main sleep theories. This theory then postulates that sleep performs a combination of consolidation and homeostasis that promotes optimal knowledge retention as well as optimal waking brain function.

Excessive sleep need following traumatic brain injury: a case-control study of 36 patients.

PubMed

Sommerauer, Michael; Valko, Philipp O; Werth, Esther; Baumann, Christian R

2013-12-01

Increased sleep need following traumatic brain injury, referred to in this study as post-traumatic pleiosomnia, is common, but so far its clinical impact and therapeutic implications have not been characterized. We present a case-control study of 36 patients with post-traumatic pleiosomnia, defined by an increased sleep need of at least 2 h per 24 h after traumatic brain injury, compared to 36 controls. We assessed detailed history, sleep-activity patterns with sleep logs and actigraphy, nocturnal sleep with polysomnography and daytime sleep propensity with multiple sleep latency tests. Actigraphy recordings revealed that traumatic brain injury (TBI) patients had longer estimated sleep durations than controls (10.8 h per 24 h, compared to 7.3 h). When using sleep logs, TBI patients underestimated their sleep need. During nocturnal sleep, patients had higher amounts of slow-wave sleep than controls (20 versus 13.8%). Multiple sleep latency tests revealed excessive daytime sleepiness in 15 patients (42%), and 10 of them had signs of chronic sleep deprivation. We conclude that post-traumatic pleiosomnia may be even more frequent than reported previously, because affected patients often underestimate their actual sleep need. Furthermore, these patients exhibit an increase in slow-wave sleep which may reflect recovery mechanisms, intrinsic consequences of diffuse brain damage or relative sleep deprivation. © 2013 European Sleep Research Society.

[Recent progress of neuroimaging studies on sleeping brain].

PubMed

Sasaki, Yuka

2012-06-01

Although sleep is a familiar phenomenon, its functions are yet to be elucidated. Understanding these functions of sleep is an important focus area in neuroscience. Electroencephalography (EEG) has been the predominantly used method in human sleep research but does not provide detailed spatial information about brain activation during sleep. To supplement the spatial information provided by this method, researchers have started using a combination of EEG and various advanced neuroimaging techniques that have been recently developed, including positron emission tomography (PET) and magnetic resonance imaging (MRI). In this paper, we will review the recent progress in sleep studies, especially studies that have used such advanced neuroimaging techniques. First, we will briefly introduce several neuroimaging techniques available for use in sleep studies. Next, we will review the spatiotemporal brain activation patterns during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, the dynamics of functional connectivity during sleep, and the consolidation of learning and memory during sleep; studies on the neural correlates of dreams, which have not yet been identified, will also be discussed. Lastly, possible directions for future research in this area will be discussed.

Tired and misconnected: A breakdown of brain modularity following sleep deprivation.

PubMed

Ben Simon, Eti; Maron-Katz, Adi; Lahav, Nir; Shamir, Ron; Hendler, Talma

2017-06-01

Sleep deprivation (SD) critically affects a range of cognitive and affective functions, typically assessed during task performance. Whether such impairments stem from changes to the brain's intrinsic functional connectivity remain largely unknown. To examine this hypothesis, we applied graph theoretical analysis on resting-state fMRI data derived from 18 healthy participants, acquired during both sleep-rested and sleep-deprived states. We hypothesized that parameters indicative of graph connectivity, such as modularity, will be impaired by sleep deprivation and that these changes will correlate with behavioral outcomes elicited by sleep loss. As expected, our findings point to a profound reduction in network modularity without sleep, evident in the limbic, default-mode, salience and executive modules. These changes were further associated with behavioral impairments elicited by SD: a decrease in salience module density was associated with worse task performance, an increase in limbic module density was predictive of stronger amygdala activation in a subsequent emotional-distraction task and a shift in frontal hub lateralization (from left to right) was associated with increased negative mood. Altogether, these results portray a loss of functional segregation within the brain and a shift towards a more random-like network without sleep, already detected in the spontaneous activity of the sleep-deprived brain. Hum Brain Mapp 38:3300-3314, 2017. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.

Learning-related brain hemispheric dominance in sleeping songbirds.

PubMed

Moorman, Sanne; Gobes, Sharon M H; van de Kamp, Ferdinand C; Zandbergen, Matthijs A; Bolhuis, Johan J

2015-03-12

There are striking behavioural and neural parallels between the acquisition of speech in humans and song learning in songbirds. In humans, language-related brain activation is mostly lateralised to the left hemisphere. During language acquisition in humans, brain hemispheric lateralisation develops as language proficiency increases. Sleep is important for the formation of long-term memory, in humans as well as in other animals, including songbirds. Here, we measured neuronal activation (as the expression pattern of the immediate early gene ZENK) during sleep in juvenile zebra finch males that were still learning their songs from a tutor. We found that during sleep, there was learning-dependent lateralisation of spontaneous neuronal activation in the caudomedial nidopallium (NCM), a secondary auditory brain region that is involved in tutor song memory, while there was right hemisphere dominance of neuronal activation in HVC (used as a proper name), a premotor nucleus that is involved in song production and sensorimotor learning. Specifically, in the NCM, birds that imitated their tutors well were left dominant, while poor imitators were right dominant, similar to language-proficiency related lateralisation in humans. Given the avian-human parallels, lateralised neural activation during sleep may also be important for speech and language acquisition in human infants.

Learning-related brain hemispheric dominance in sleeping songbirds

PubMed Central

Moorman, Sanne; Gobes, Sharon M. H.; van de Kamp, Ferdinand C.; Zandbergen, Matthijs A.; Bolhuis, Johan J.

2015-01-01

There are striking behavioural and neural parallels between the acquisition of speech in humans and song learning in songbirds. In humans, language-related brain activation is mostly lateralised to the left hemisphere. During language acquisition in humans, brain hemispheric lateralisation develops as language proficiency increases. Sleep is important for the formation of long-term memory, in humans as well as in other animals, including songbirds. Here, we measured neuronal activation (as the expression pattern of the immediate early gene ZENK) during sleep in juvenile zebra finch males that were still learning their songs from a tutor. We found that during sleep, there was learning-dependent lateralisation of spontaneous neuronal activation in the caudomedial nidopallium (NCM), a secondary auditory brain region that is involved in tutor song memory, while there was right hemisphere dominance of neuronal activation in HVC (used as a proper name), a premotor nucleus that is involved in song production and sensorimotor learning. Specifically, in the NCM, birds that imitated their tutors well were left dominant, while poor imitators were right dominant, similar to language-proficiency related lateralisation in humans. Given the avian-human parallels, lateralised neural activation during sleep may also be important for speech and language acquisition in human infants. PMID:25761654

The yin and yang of sleep and attention

PubMed Central

Kirszenblat, Leonie; van Swinderen, Bruno

2015-01-01

Sleep is not a single state, but a complex set of brain processes that supports a number of physiological needs. Sleep deprivation is known to affect attention in many animals, suggesting that a key function of sleep is to regulate attention. Conversely, tasks that require more attention drive sleep need and sleep intensity. Attention involves the ability to filter incoming stimuli based on their relative salience, and this is likely to require coordinated synaptic activity across the brain. This capacity may have only become possible with the evolution of related neural mechanisms that support two key sleep functions: stimulus suppression and synaptic plasticity. We argue here that sleep and attention may have co-evolved as brain states that regulate each other. PMID:26602764

Exercise benefits for the aging brain depend on the accompanying cognitive load: insights from sleep electroencephalogram.

PubMed

Horne, Jim

2013-11-01

Although exercise clearly offsets aging effects on the body, its benefits for the aging brain are likely to depend on the extent that physical activity (especially locomotion) facilitates multisensory encounters, curiosity, and interactions with novel environments; this is especially true for exploratory activity, which occupies much of wakefulness for most mammals in the wild. Cognition is inseparable from physical activity, with both interlinked to promote neuroplasticity and more successful brain aging. In these respects and for humans, exercising in a static, featureless, artificially lit indoor setting contrasts with exploratory outdoor walking within a novel environment during daylight. However, little is known about the comparative benefits for the aging brain of longer-term daily regimens of this latter nature including the role of sleep, to the extent that sleep enhances neuroplasticity as shown in short-term laboratory studies. More discerning analyses of sleep electroencephalogram (EEG) slow-wave activity especially 0.5-2-Hz activity would provide greater insights into use-dependent recovery processes during longer-term tracking of these regimens and complement slower changing waking neuropsychologic and resting functional magnetic resonance imaging (fMRI) measures, including those of the brain's default mode network. Although the limited research only points to ephemeral small sleep EEG effects of pure exercise, more enduring effects seem apparent when physical activity incorporates cognitive challenges. In terms of "use it or lose it," curiosity-driven "getting out and about," encountering, interacting with, and enjoying novel situations may well provide the brain with its real exercise, further reflected in changes to the dynamics of sleep. Copyright © 2013 Elsevier B.V. All rights reserved.

Why does rem sleep occur? A wake-up hypothesis.

PubMed

Klemm, W R

2011-01-01

Brain activity differs in the various sleep stages and in conscious wakefulness. Awakening from sleep requires restoration of the complex nerve impulse patterns in neuronal network assemblies necessary to re-create and sustain conscious wakefulness. Herein I propose that the brain uses rapid eye movement (REM) to help wake itself up after it has had a sufficient amount of sleep. Evidence suggesting this hypothesis includes the facts that, (1) when first going to sleep, the brain plunges into Stage N3 (formerly called Stage IV), a deep abyss of sleep, and, as the night progresses, the sleep is punctuated by episodes of REM that become longer and more frequent toward morning, (2) conscious-like dreams are a reliable component of the REM state in which the dreamer is an active mental observer or agent in the dream, (3) the last awakening during a night's sleep usually occurs in a REM episode during or at the end of a dream, (4) both REM and awake consciousness seem to arise out of a similar brainstem ascending arousal system (5) N3 is a functionally perturbed state that eventually must be corrected so that embodied brain can direct adaptive behavior, and (6) cortico-fugal projections to brainstem arousal areas provide a way to trigger increased cortical activity in REM to progressively raise the sleeping brain to the threshold required for wakefulness. This paper shows how the hypothesis conforms to common experience and has substantial predictive and explanatory power regarding the phenomenology of sleep in terms of ontogeny, aging, phylogeny, abnormal/disease states, cognition, and behavioral physiology. That broad range of consistency is not matched by competing theories, which are summarized herein. Specific ways to test this wake-up hypothesis are suggested. Such research could lead to a better understanding of awake consciousness.

Brain and muscle oxygenation monitoring using near-infrared spectroscopy (NIRS) during all-night sleep

NASA Astrophysics Data System (ADS)

Zhang, Zhongxing; Khatami, Ramin

2013-03-01

The hemodynamic changes during natural human sleep are still not well understood. NIRS is ideally suited for monitoring the hemodynamic changes during sleep due to the properties of local measurement, totally safe application and good tolerance to motion. Several studies have been conducted using NIRS in both normal subjects and patients with various sleep disorders during sleep to characterize the hemodynamic changing patterns during different sleep stages and during different symptoms such as obstructive apneas. Here we assessed brain and muscle oxygenation changes in 7 healthy adults during all-night sleep with combined polysomnography measurement to test the notion if hemodynamic changes in sleep are indeed brain specific. We found that muscle and brain showed similar hemodynamic changes during sleep initiation. A decrease in HbO2 and tissue oxygenation index (TOI) while an increase in HHb was observed immediately after sleep onset, and an opposite trend was found after transition with progression to deeper slow-wave sleep (SWS) stage. Spontaneous low frequency oscillations (LFO) and very low frequency oscillations (VLFO) were smaller (Levene's test, p<0.05) during SWS compared to light sleep (LS) and rapid-eye-movement (REM) sleep in both brain and muscle. Spectral analysis of the NIRS signals measured from brain and muscle also showed reductions in VLFO and LFO powers during SWS with respect to LS and REM sleep. These results indicate a systemic attenuation rather than local cerebral reduction of spontaneous hemodynamic activity in SWS. A systemic physiological mechanism may exist to regulate the hemodynamic changes in brain and muscle during sleep.

Behavioral and genetic effects promoted by sleep deprivation in rats submitted to pilocarpine-induced status epilepticus.

PubMed

Matos, Gabriela; Ribeiro, Daniel A; Alvarenga, Tathiana A; Hirotsu, Camila; Scorza, Fulvio A; Le Sueur-Maluf, Luciana; Noguti, Juliana; Cavalheiro, Esper A; Tufik, Sergio; Andersen, Monica L

2012-05-02

The interaction between sleep deprivation and epilepsy has been well described in electrophysiological studies, but the mechanisms underlying this association remain unclear. The present study evaluated the effects of sleep deprivation on locomotor activity and genetic damage in the brains of rats treated with saline or pilocarpine-induced status epilepticus (SE). After 50 days of pilocarpine or saline treatment, both groups were assigned randomly to total sleep deprivation (TSD) for 6 h, paradoxical sleep deprivation (PSD) for 24 h, or be kept in their home cages. Locomotor activity was assessed with the open field test followed by resection of brain for quantification of genetic damage by the single cell gel electrophoresis (comet) assay. Status epilepticus induced significant hyperactivity in the open field test and caused genetic damage in the brain. Sleep deprivation procedures (TSD and PSD) did not affect locomotor activity in epileptic or healthy rats, but resulted in significant DNA damage in brain cells. Although PSD had this effect in both vehicle and epileptic groups, TSD caused DNA damage only in epileptic rats. In conclusion, our results revealed that, despite a lack of behavioral effects of sleep deprivation, TSD and PSD induced genetic damage in rats submitted to pilocarpine-induced SE. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

Sleep and rhythm changes at the time of Trypanosoma brucei invasion of the brain parenchyma in the rat.

PubMed

Seke Etet, Paul F; Palomba, Maria; Colavito, Valeria; Grassi-Zucconi, Gigliola; Bentivoglio, Marina; Bertini, Giuseppe

2012-05-01

Human African trypanosomiasis (HAT), or sleeping sickness, is a severe disease caused by Trypanosoma brucei (T.b.). The disease hallmark is sleep alterations. Brain involvement in HAT is a crucial pathogenetic step for disease diagnosis and therapy. In this study, a rat model of African trypanosomiasis was used to assess changes of sleep-wake, rest-activity, and body temperature rhythms in the time window previously shown as crucial for brain parenchyma invasion by T.b. to determine potential biomarkers of this event. Chronic radiotelemetric monitoring in Sprague-Dawley rats was used to continuously record electroencephalogram, electromyogram, rest-activity, and body temperature in the same animals before (baseline recording) and after infection. Rats were infected with T.b. brucei. Data were acquired from 1 to 20 d after infection (parasite neuroinvasion initiates at 11-13 d post-infection in this model), and were compared to baseline values. Sleep parameters were manually scored from electroencephalographic-electromyographic tracings. Circadian rhythms of sleep time, slow-wave activity, rest-activity, and body temperature were studied using cosinor rhythmometry. Results revealed alterations of most of the analyzed parameters. In particular, sleep pattern and sleep-wake organization plus rest-activity and body temperature rhythms exhibited early quantitative and qualitative alterations, which became marked around the time interval crucial for parasite neuroinvasion or shortly after. Data derived from actigrams showed close correspondence with those from hypnograms, suggesting that rest-activity could be useful to monitor sleep-wake alterations in African trypanosomiasis.

Sleep and the Price of Plasticity: From Synaptic and Cellular Homeostasis to Memory Consolidation and Integration

PubMed Central

Tononi, Giulio; Cirelli, Chiara

2014-01-01

Summary Sleep is universal, tightly regulated, and its loss impairs cognition. But why does the brain need to disconnect from the environment for hours every day? The synaptic homeostasis hypothesis (SHY) proposes that sleep is the price the brain pays for plasticity. During a waking episode, learning statistical regularities about the current environment requires strengthening connections throughout the brain. This increases cellular needs for energy and supplies, decreases signal-to-noise ratios, and saturates learning. During sleep, spontaneous activity renormalizes net synaptic strength and restores cellular homeostasis. Activity-dependent down-selection of synapses can also explain the benefits of sleep on memory acquisition, consolidation, and integration. This happens through the off-line, comprehensive sampling of statistical regularities incorporated in neuronal circuits over a lifetime. This review considers the rationale and evidence for SHY and points to open issues related to sleep and plasticity. PMID:24411729

Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration.

PubMed

Tononi, Giulio; Cirelli, Chiara

2014-01-08

Sleep is universal, tightly regulated, and its loss impairs cognition. But why does the brain need to disconnect from the environment for hours every day? The synaptic homeostasis hypothesis (SHY) proposes that sleep is the price the brain pays for plasticity. During a waking episode, learning statistical regularities about the current environment requires strengthening connections throughout the brain. This increases cellular needs for energy and supplies, decreases signal-to-noise ratios, and saturates learning. During sleep, spontaneous activity renormalizes net synaptic strength and restores cellular homeostasis. Activity-dependent down-selection of synapses can also explain the benefits of sleep on memory acquisition, consolidation, and integration. This happens through the offline, comprehensive sampling of statistical regularities incorporated in neuronal circuits over a lifetime. This Perspective considers the rationale and evidence for SHY and points to open issues related to sleep and plasticity. Copyright © 2014 Elsevier Inc. All rights reserved.

Loss of consciousness is related to hyper-correlated gamma-band activity in anesthetized macaques and sleeping humans.

PubMed

Bola, Michał; Barrett, Adam B; Pigorini, Andrea; Nobili, Lino; Seth, Anil K; Marchewka, Artur

2018-02-15

Loss of consciousness can result from a wide range of causes, including natural sleep and pharmacologically induced anesthesia. Important insights might thus come from identifying neuronal mechanisms of loss and re-emergence of consciousness independent of a specific manipulation. Therefore, to seek neuronal signatures of loss of consciousness common to sleep and anesthesia we analyzed spontaneous electrophysiological activity recorded in two experiments. First, electrocorticography (ECoG) acquired from 4 macaque monkeys anesthetized with different anesthetic agents (ketamine, medetomidine, propofol) and, second, stereo-electroencephalography (sEEG) from 10 epilepsy patients in different wake-sleep stages (wakefulness, NREM, REM). Specifically, we investigated co-activation patterns among brain areas, defined as correlations between local amplitudes of gamma-band activity. We found that resting wakefulness was associated with intermediate levels of gamma-band coupling, indicating neither complete dependence, nor full independence among brain regions. In contrast, loss of consciousness during NREM sleep and propofol anesthesia was associated with excessively correlated brain activity, as indicated by a robust increase of number and strength of positive correlations. However, such excessively correlated brain signals were not observed during REM sleep, and were present only to a limited extent during ketamine anesthesia. This might be related to the fact that, despite suppression of behavioral responsiveness, REM sleep and ketamine anesthesia often involve presence of dream-like conscious experiences. We conclude that hyper-correlated gamma-band activity might be a signature of loss of consciousness common across various manipulations and independent of behavioral responsiveness. Copyright © 2017 Elsevier Inc. All rights reserved.

Brain mechanisms that control sleep and waking

NASA Astrophysics Data System (ADS)

Siegel, Jerome

This review paper presents a brief historical survey of the technological and early research that laid the groundwork for recent advances in sleep-waking research. A major advance in this field occurred shortly after the end of World War II with the discovery of the ascending reticular activating system (ARAS) as the neural source in the brain stem of the waking state. Subsequent research showed that the brain stem activating system produced cortical arousal via two pathways: a dorsal route through the thalamus and a ventral route through the hypothalamus and basal forebrain. The nuclei, pathways, and neurotransmitters that comprise the multiple components of these arousal systems are described. Sleep is now recognized as being composed of two very different states: rapid eye movements (REMs) sleep and non-REM sleep. The major findings on the neural mechanisms that control these two sleep states are presented. This review ends with a discussion of two current views on the function of sleep: to maintain the integrity of the immune system and to enhance memory consolidation.

Analysis of EEG activity during sleep - brain hemisphere symmetry of two classes of sleep spindles

NASA Astrophysics Data System (ADS)

Smolen, Magdalena M.

2009-01-01

This paper presents automatic analysis of some selected human electroencephalographic patterns during deep sleep using the Matching Pursuit (MP) algorithm. The periodicity of deep sleep EEG patterns was observed by calculating autocorrelation functions of their percentage contributions. The study confirmed the increasing trend of amplitude-weighted average frequency of sleep spindles from frontal to posterior derivations. The dominant frequencies from the left and the right brain hemisphere were strongly correlated.

The Neuroprotective Aspects of Sleep.

PubMed

Eugene, Andy R; Masiak, Jolanta

2015-03-01

Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle.

The Neuroprotective Aspects of Sleep

PubMed Central

Eugene, Andy R.; Masiak, Jolanta

2015-01-01

Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle. PMID:26594659

Sleep Homeostasis and Synaptic Plasticity

DTIC Science & Technology

2017-06-01

accrued through learning. But how is wake experience translated into sleep drive? Where in the brain does this occur? Is there a discrete sleep drive...neuronal activity in discrete parts of the brain. At the same time, neuronal biochemistry is very similar – flies and man respond in a similar manner to...null phenotypes by expressing rescue construct in discrete regions Task 1C: Verify rescue brain areas by RNAi knockdown (in wildtype) of gene in areas

Extracellular levels of lactate, but not oxygen, reflect sleep homeostasis in the rat cerebral cortex.

PubMed

Dash, Michael B; Tononi, Giulio; Cirelli, Chiara

2012-07-01

It is well established that brain metabolism is higher during wake and rapid eye movement (REM) sleep than in nonrapid eye movement (NREM) sleep. Most of the brain's energy is used to maintain neuronal firing and glutamatergic transmission. Recent evidence shows that cortical firing rates, extracellular glutamate levels, and markers of excitatory synaptic strength increase with time spent awake and decline throughout NREM sleep. These data imply that the metabolic cost of each behavioral state is not fixed but may reflect sleep-wake history, a possibility that is investigated in the current report. Chronic (4d) electroencephalographic (EEG) recordings in the rat cerebral cortex were coupled with fixed-potential amperometry to monitor the extracellular concentration of oxygen ([oxy]) and lactate ([lac]) on a second-by-second basis across the spontaneous sleep-wake cycle and in response to sleep deprivation. Basic sleep research laboratory. Wistar Kyoto (WKY) adult male rats. N/A. Within 30-60 sec [lac] and [oxy] progressively increased during wake and REM sleep and declined during NREM sleep (n = 10 rats/metabolite), but with several differences. [Oxy], but not [lac], increased more during wake with high motor activity and/or elevated EEG high-frequency power. Meanwhile, only the NREM decline of [lac] reflected sleep pressure as measured by slow-wave activity, mirroring previous results for cortical glutamate. The observed state-dependent changes in cortical [lac] and [oxy] are consistent with higher brain metabolism during waking and REM sleep in comparison with NREM sleep. Moreover, these data suggest that glycolytic activity, most likely through its link with glutamatergic transmission, reflects sleep homeostasis.

Go Signaling in Mushroom Bodies Regulates Sleep in Drosophila

PubMed Central

Guo, Fang; Yi, Wei; Zhou, Mingmin; Guo, Aike

2011-01-01

Study Objectives: Sleep is a fundamental physiological process and its biological mechanisms are poorly understood. In Drosophila melanogaster, heterotrimeric Go protein is abundantly expressed in the brain. However, its post-developmental function has not been extensively explored. Design: Locomotor activity was measured using the Drosophila Activity Monitoring System under a 12:12 LD cycle. Sleep was defined as periods of 5 min with no recorded activity. Results: Pan-neuronal elevation of Go signaling induced quiescence accompanied by an increased arousal threshold in flies. By screening region-specific GAL4 lines, we mapped the sleep-regulatory function of Go signaling to mushroom bodies (MBs), a central brain region which modulates memory, decision making, and sleep in Drosophila. Up-regulation of Go activity in these neurons consolidated sleep while inhibition of endogenous Go via expression of Go RNAi or pertussis toxin reduced and fragmented sleep, indicating that the Drosophila sleep requirement is affected by levels of Go activity in the MBs. Genetic interaction results showed that Go signaling serves as a neuronal transmission inhibitor in a cAMP-independent pathway. Conclusion: Go signaling is a novel signaling pathway in MBs that regulates sleep in Drosophila. Citation: Guo F; Yi W; Zhou M; Guo A. Go signaling in mushroom bodies regulates sleep in drosophila. SLEEP 2011;34(3):273-281. PMID:21358844

Sleep, Plasticity and Memory from Molecules to Whole-Brain Networks

PubMed Central

Abel, Ted; Havekes, Robbert; Saletin, Jared M.; Walker, Matthew P.

2014-01-01

Despite the ubiquity of sleep across phylogeny, its function remains elusive. In this review, we consider one compelling candidate: brain plasticity associated with memory processing. Focusing largely on hippocampus-dependent memory in rodents and humans, we describe molecular, cellular, network, whole-brain and behavioral evidence establishing a role for sleep both in preparation for initial memory encoding, and in the subsequent offline consolidation ofmemory. Sleep and sleep deprivation bidirectionally alter molecular signaling pathways that regulate synaptic strength and control plasticity-related gene transcription and protein translation. At the cellular level, sleep deprivation impairs cellular excitability necessary for inducing synaptic potentiation and accelerates the decay of long-lasting forms of synaptic plasticity. In contrast, NREM and REM sleep enhance previously induced synaptic potentiation, although synaptic de-potentiation during sleep has also been observed. Beyond single cell dynamics, large-scale cell ensembles express coordinated replay of prior learning-related firing patterns during subsequent sleep. This occurs in the hippocampus, in the cortex, and between the hippocampus and cortex, commonly in association with specific NREM sleep oscillations. At the whole-brain level, somewhat analogous learning-associated hippocampal (re)activation during NREM sleep has been reported in humans. Moreover, the same cortical NREM oscillations associated with replay in rodents also promote human hippocampal memory consolidation, and this process can be manipulated using exogenous reactivation cues during sleep. Mirroring molecular findings in rodents, specific NREM sleep oscillations before encoding refresh human hippocampal learning capacity, while deprivation of sleep conversely impairs subsequent hippocampal activity and associated encoding. Together, these cross-descriptive level findings demonstrate that the unique neurobiology of sleep exert powerful effects on molecular, cellular and network mechanism of plasticity that govern both initial learning and subsequent long-term memory consolidation. PMID:24028961

Low Activity Microstates During Sleep.

PubMed

Miyawaki, Hiroyuki; Billeh, Yazan N; Diba, Kamran

2017-06-01

To better understand the distinct activity patterns of the brain during sleep, we observed and investigated periods of diminished oscillatory and population spiking activity lasting for seconds during non-rapid eye movement (non-REM) sleep, which we call "LOW" activity sleep. We analyzed spiking and local field potential (LFP) activity of hippocampal CA1 region alongside neocortical electroencephalogram (EEG) and electromyogram (EMG) in 19 sessions from four male Long-Evans rats (260-360 g) during natural wake/sleep across the 24-hr cycle as well as data from other brain regions obtained from http://crcns.org.1,2. LOW states lasted longer than OFF/DOWN states and were distinguished by a subset of "LOW-active" cells. LOW activity sleep was preceded and followed by increased sharp-wave ripple activity. We also observed decreased slow-wave activity and sleep spindles in the hippocampal LFP and neocortical EEG upon LOW onset, with a partial rebound immediately after LOW. LOW states demonstrated activity patterns consistent with sleep but frequently transitioned into microarousals and showed EMG and LFP differences from small-amplitude irregular activity during quiet waking. Their likelihood decreased within individual non-REM epochs yet increased over the course of sleep. By analyzing data from the entorhinal cortex of rats,1 as well as the hippocampus, the medial prefrontal cortex, the postsubiculum, and the anterior thalamus of mice,2 obtained from http://crcns.org, we confirmed that LOW states corresponded to markedly diminished activity simultaneously in all of these regions. We propose that LOW states are an important microstate within non-REM sleep that provide respite from high-activity sleep and may serve a restorative function. © Sleep Research Society 2017. Published by Oxford University Press [on behalf of the Sleep Research Society].

Early and Later Life Stress Alter Brain Activity and Sleep in Rats

PubMed Central

Mrdalj, Jelena; Pallesen, Ståle; Milde, Anne Marita; Jellestad, Finn Konow; Murison, Robert; Ursin, Reidun; Bjorvatn, Bjørn; Grønli, Janne

2013-01-01

Exposure to early life stress may profoundly influence the developing brain in lasting ways. Neuropsychiatric disorders associated with early life adversity may involve neural changes reflected in EEG power as a measure of brain activity and disturbed sleep. The main aim of the present study was for the first time to characterize possible changes in adult EEG power after postnatal maternal separation in rats. Furthermore, in the same animals, we investigated how EEG power and sleep architecture were affected after exposure to a chronic mild stress protocol. During postnatal day 2–14 male rats were exposed to either long maternal separation (180 min) or brief maternal separation (10 min). Long maternally separated offspring showed a sleep-wake nonspecific reduction in adult EEG power at the frontal EEG derivation compared to the brief maternally separated group. The quality of slow wave sleep differed as the long maternally separated group showed lower delta power in the frontal-frontal EEG and a slower reduction of the sleep pressure. Exposure to chronic mild stress led to a lower EEG power in both groups. Chronic exposure to mild stressors affected sleep differently in the two groups of maternal separation. Long maternally separated offspring showed more total sleep time, more episodes of rapid eye movement sleep and higher percentage of non-rapid eye movement episodes ending in rapid eye movement sleep compared to brief maternal separation. Chronic stress affected similarly other sleep parameters and flattened the sleep homeostasis curves in all offspring. The results confirm that early environmental conditions modulate the brain functioning in a long-lasting way. PMID:23922857

The Effects of Fatigue on Position Determination and Cognitive Workload Using a Visual and 3-Dimensional Auditory Display

DTIC Science & Technology

2004-06-01

in first third of the night. REM sleep is associated with an extremely active brain that is frequently dreaming with bursts of rapid eye movement...these areas. 3. Human Sleep and Fatigue Sleep is nature’s process of resting the body although brain activity continues throughout the rest...midday roughly between 1500 and 1700 (LeClair, 2001). Disruption of one’s circadian rhythm to accommodate adjustments in unconventional working hours

An in depth view of avian sleep.

PubMed

Beckers, Gabriël J L; Rattenborg, Niels C

2015-03-01

Brain rhythms occurring during sleep are implicated in processing information acquired during wakefulness, but this phenomenon has almost exclusively been studied in mammals. In this review we discuss the potential value of utilizing birds to elucidate the functions and underlying mechanisms of such brain rhythms. Birds are of particular interest from a comparative perspective because even though neurons in the avian brain homologous to mammalian neocortical neurons are arranged in a nuclear, rather than a laminar manner, the avian brain generates mammalian-like sleep-states and associated brain rhythms. Nonetheless, until recently, this nuclear organization also posed technical challenges, as the standard surface EEG recording methods used to study the neocortex provide only a superficial view of the sleeping avian brain. The recent development of high-density multielectrode recording methods now provides access to sleep-related brain activity occurring deep in the avian brain. Finally, we discuss how intracerebral electrical imaging based on this technique can be used to elucidate the systems-level processing of hippocampal-dependent and imprinting memories in birds. Copyright © 2014 Elsevier Ltd. All rights reserved.

[Sleep, emotions and the visceral control].

PubMed

Pigarev, I N; Pigareva, M L

2013-01-01

It is known that sleep is connected with sensory isolation of the brain, inactivation of the consciousness and reorganization of the electrical activity in all cerebral cortical areas. On the other hand, sleep deprivation leads to pathology in visceral organs and finally to the death of animals, while there are no obvious changes in the brain itself. It stays the opened question how the changes in the brain activity during sleep could be con- nected with the visceral health? We proposed that the same brain areas and the same neurons, which in wakefulness process the information coming from the distant and proprioreceptors, switch during sleep to the processing of the interoceptive information. Thus, central nervous system is involved into the regulation of the life support functions of the body during sleep. Results of our experiments supported this hypothesis, explained many observations obtained in somnology and offered the mechanisms of several pathological states connected with sleep. However, at the present level of the visceral sleep theory there were no understanding of the well known link between the emotional states of the organisms and transition from wakefulness to sleep, and sleep quality. In this study the attempt is undertaken to combine the visceral theory of sleep with the need- informational theory ofemotions, proposed by P. Simonov. The visceral theory of sleep proposes that in living organisms there is a constant monitoring of the correspondence of the visceral parameters to the genetically determined values. Mismatch signals evoke the feeling of tiredness and the need of sleep. This sleep need en- ters the competition with the other actual needs of the organism. In according with the theory of P. Simonov emotions connected with a particular need play important role in their ranking for satisfaction. We propose that emotional estimation of the sleep need, based on the visceral signals, is realized in the same brain structures which undertake this estimation for other behavioral needs in wakefulness. During sleep, the same brain structures, involved in estimation of emotions, continue to rank the visceral needs and to define their order for processing in the cortical areas and in the highest level of the visceral integration. In the context of the proposed hypothesis, we discuss the results of the studies devoted to investigation of the link between sleep and emotions.

Sleep Deprivation and Neurobehavioral Dynamics

PubMed Central

Basner, Mathias; Rao, Hengyi; Goel, Namni; Dinges, David F.

2013-01-01

Lifestyles involving sleep deprivation are common, despite mounting evidence that both acute total sleep deprivation and chronically restricted sleep degrade neurobehavioral functions associated with arousal, attention, memory and state stability. Current research suggests dynamic differences in the way the central nervous system responds to acute versus chronic sleep restriction, which is reflected in new models of sleep-wake regulation. Chronic sleep restriction likely induces long-term neuromodulatory changes in brain physiology that could explain why recovery from it may require more time than from acute sleep loss. High intraclass correlations in neurobehavioral responses to sleep loss suggest that these trait-like differences are phenotypic and may include genetic components. Sleep deprivation induces changes in brain metabolism and neural activation that involve distributed networks and connectivity. PMID:23523374

Unrecognized Sleep Loss Accumulated in Daily Life Can Promote Brain Hyperreactivity to Food Cue.

PubMed

Katsunuma, Ruri; Oba, Kentaro; Kitamura, Shingo; Motomura, Yuki; Terasawa, Yuri; Nakazaki, Kyoko; Hida, Akiko; Moriguchi, Yoshiya; Mishima, Kazuo

2017-10-01

Epidemiological studies have shown that sleep debt increases the risk of obesity. Experimental total sleep deprivation (TSD) has been reported to activate the reward system in response to food stimuli, but food-related responses in everyday sleep habits, which could lead to obesity, have not been addressed. Here, we report that habitual sleep time at home among volunteers without any sleep concerns was shorter than their optimal sleep time estimated by the 9-day extended sleep intervention, which indicates that participants had already been in sleep debt in their usual sleep habits. The amygdala and anterior insula, which are responsible for both affective responses and reward prediction, were found to exhibit significantly lowered activity in the optimal sleep condition. Additionally, a subsequent one-night period of TSD reactivated the right anterior insula in response to food images; however, the activity level of amygdala remained lowered. These findings indicate that (1) our brain is at risk of hyperactivation to food triggers in everyday life, which could be a risk factor for obesity and lifestyle diseases, and (2) optimal sleep appears to reduce this hypersensitivity to food stimuli. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Eyes Open on Sleep and Wake: In Vivo to In Silico Neural Networks

PubMed Central

Vanvinckenroye, Amaury; Vandewalle, Gilles; Chellappa, Sarah L.

2016-01-01

Functional and effective connectivity of cortical areas are essential for normal brain function under different behavioral states. Appropriate cortical activity during sleep and wakefulness is ensured by the balanced activity of excitatory and inhibitory circuits. Ultimately, fast, millisecond cortical rhythmic oscillations shape cortical function in time and space. On a much longer time scale, brain function also depends on prior sleep-wake history and circadian processes. However, much remains to be established on how the brain operates at the neuronal level in humans during sleep and wakefulness. A key limitation of human neuroscience is the difficulty in isolating neuronal excitation/inhibition drive in vivo. Therefore, computational models are noninvasive approaches of choice to indirectly access hidden neuronal states. In this review, we present a physiologically driven in silico approach, Dynamic Causal Modelling (DCM), as a means to comprehend brain function under different experimental paradigms. Importantly, DCM has allowed for the understanding of how brain dynamics underscore brain plasticity, cognition, and different states of consciousness. In a broader perspective, noninvasive computational approaches, such as DCM, may help to puzzle out the spatial and temporal dynamics of human brain function at different behavioural states. PMID:26885400

What the cerveau isolé preparation tells us nowadays about sleep-wake mechanisms?

PubMed

Gottesmann, C

1988-01-01

The intercollicular transected preparation opened a rich field for investigations of sleep-wake mechanisms. Initial results showed that brain stem ascending influences are essential for maintaining an activated cortex. It was subsequently shown that the forebrain also develops activating influences, since EEG desynchronization of the cortex reappears in the chronic cerveau isolé preparation, and continuous or almost continuous theta rhythm is able to occur in the acute cerveau isolé preparation. A brief "intermediate stage" of sleep occurs during natural sleep just prior to and after paradoxical sleep. It is characterized by cortical spindle bursts, hippocampal low frequency theta activity (two patterns of the acute cerveau isolé preparation) and is accompanied by a very low thalamic transmission level, suggesting a cerveau isolé-like state. The chronic cerveau isolé preparation also demonstrates that the executive processes of paradoxical sleep are located in the lower brain stem, while the occurrence of this sleep stage seems to be modulated by forebrain structures.

Cortical dendritic activity correlates with spindle-rich oscillations during sleep in rodents.

PubMed

Seibt, Julie; Richard, Clément J; Sigl-Glöckner, Johanna; Takahashi, Naoya; Kaplan, David I; Doron, Guy; de Limoges, Denis; Bocklisch, Christina; Larkum, Matthew E

2017-09-25

How sleep influences brain plasticity is not known. In particular, why certain electroencephalographic (EEG) rhythms are linked to memory consolidation is poorly understood. Calcium activity in dendrites is known to be necessary for structural plasticity changes, but this has never been carefully examined during sleep. Here, we report that calcium activity in populations of neocortical dendrites is increased and synchronised during oscillations in the spindle range in naturally sleeping rodents. Remarkably, the same relationship is not found in cell bodies of the same neurons and throughout the cortical column. Spindles during sleep have been suggested to be important for brain development and plasticity. Our results provide evidence for a physiological link of spindles in the cortex specific to dendrites, the main site of synaptic plasticity.Different stages of sleep, marked by particular electroencephalographic (EEG) signatures, have been linked to memory consolidation, but underlying mechanisms are poorly understood. Here, the authors show that dendritic calcium synchronisation correlates with spindle-rich sleep phases.

Sleeping of a Complex Brain Networks with Hierarchical Organization

NASA Astrophysics Data System (ADS)

Zhang, Ying-Yue; Yang, Qiu-Ying; Chen, Tian-Lun

2009-01-01

The dynamical behavior in the cortical brain network of macaque is studied by modeling each cortical area with a subnetwork of interacting excitable neurons. We characterize the system by studying how to perform the transition, which is now topology-dependent, from the active state to that with no activity. This could be a naive model for the wakening and sleeping of a brain-like system, i.e., a multi-component system with two different dynamical behavior.

The role of serotonin and norepinephrine in sleep-waking activity.

PubMed

Morgane, P J; Stern, W C

1975-11-01

A critical review of the evidences relating the biogenic amines serotonin and norepinephrine to the states of slow-wave and rapid eye movement (REM) sleep is presented. Various alternative explanations for specific chemical regulation of the individual sleep states, including the phasic events of REM sleep, are evaluated within the overall framework of the monoamine theory of sleep. Several critical neuropsychopharmacological studies relating to metabolsim of the amines in relation to sleep-waking behavior are presented. Models of the chemical neuronal circuitry involved in sleep-waking activity are derived and interactions between several brainstem nuclei, particularly the raphé complex and locus coeruleus, are discussed. Activity in these aminergic systems in relation to oscillations in the sleep-waking cycles is evaluated. In particular, the assessment of single cell activity in specific chemical systems in relations to chemical models of sleep is reviewed. Overall, it appears that the biogenic amines, especially serotonin and norepinephrine, play key roles in the generation and maintenance of the sleep states. These neurotransmitters participate in some manner in the "triggering" processes necessary for actuating each sleep phase and in regulating the transitions from sleep to waking activity. The biogenic amines are, however, probably not "sleep factors" or direct inducers of the sleep states. Rather, they appear to be components of a multiplicity of interacting chemical circuitry in the brain whose activity maintains various chemical balances in different brain regions. Shifts in these balances appear to be involved in the triggering and maintenance of the various states comprising the vigilance continuum.

Recalling and forgetting dreams: theta and alpha oscillations during sleep predict subsequent dream recall.

PubMed

Marzano, Cristina; Ferrara, Michele; Mauro, Federica; Moroni, Fabio; Gorgoni, Maurizio; Tempesta, Daniela; Cipolli, Carlo; De Gennaro, Luigi

2011-05-04

Under the assumption that dream recall is a peculiar form of declarative memory, we have hypothesized that (1) the encoding of dream contents during sleep should share some electrophysiological mechanisms with the encoding of episodic memories of the awake brain and (2) recalling a dream(s) after awakening from non-rapid eye movement (NREM) and rapid eye movement (REM) sleep should be associated with different brain oscillations. Here, we report that cortical brain oscillations of human sleep are predictive of successful dream recall. In particular, after morning awakening from REM sleep, a higher frontal 5-7 Hz (theta) activity was associated with successful dream recall. This finding mirrors the increase in frontal theta activity during successful encoding of episodic memories in wakefulness. Moreover, in keeping with the different EEG background, a different predictive relationship was found after awakening from stage 2 NREM sleep. Specifically, a lower 8-12 Hz (alpha) oscillatory activity of the right temporal area was associated with a successful dream recall. These findings provide the first evidence of univocal cortical electroencephalographic correlates of dream recall, suggesting that the neurophysiological mechanisms underlying the encoding and recall of episodic memories may remain the same across different states of consciousness.

Increased Sleep Depth in Developing Neural Networks: New Insights from Sleep Restriction in Children

PubMed Central

Kurth, Salome; Dean, Douglas C.; Achermann, Peter; O’Muircheartaigh, Jonathan; Huber, Reto; Deoni, Sean C. L.; LeBourgeois, Monique K.

2016-01-01

Brain networks respond to sleep deprivation or restriction with increased sleep depth, which is quantified as slow-wave activity (SWA) in the sleep electroencephalogram (EEG). When adults are sleep deprived, this homeostatic response is most pronounced over prefrontal brain regions. However, it is unknown how children’s developing brain networks respond to acute sleep restriction, and whether this response is linked to myelination, an ongoing process in childhood that is critical for brain development and cortical integration. We implemented a bedtime delay protocol in 5- to 12-year-old children to obtain partial sleep restriction (1-night; 50% of their habitual sleep). High-density sleep EEG was assessed during habitual and restricted sleep and brain myelin content was obtained using mcDESPOT magnetic resonance imaging. The effect of sleep restriction was analyzed using statistical non-parametric mapping with supra-threshold cluster analysis. We observed a localized homeostatic SWA response following sleep restriction in a specific parieto-occipital region. The restricted/habitual SWA ratio was negatively associated with myelin water fraction in the optic radiation, a developing fiber bundle. This relationship occurred bilaterally over parieto-temporal areas and was adjacent to, but did not overlap with the parieto-occipital region showing the most pronounced homeostatic SWA response. These results provide evidence for increased sleep need in posterior neural networks in children. Sleep need in parieto-temporal areas is related to myelin content, yet it remains speculative whether age-related myelin growth drives the fading of the posterior homeostatic SWA response during the transition to adulthood. Whether chronic insufficient sleep in the sensitive period of early life alters the anatomical generators of deep sleep slow-waves is an important unanswered question. PMID:27708567

Multimodal neuroimaging investigations of alterations to consciousness: the relationship between absence epilepsy and sleep.

PubMed

Bagshaw, Andrew P; Rollings, David T; Khalsa, Sakh; Cavanna, Andrea E

2014-01-01

The link between epilepsy and sleep is well established on many levels. The focus of the current review is on recent neuroimaging investigations into the alterations of consciousness that are observed during absence seizures and the descent into sleep. Functional neuroimaging provides simultaneous cortical and subcortical recording of activity throughout the brain, allowing a detailed definition and characterization of large-scale brain networks and the interactions between them. This has led to the identification of a set of regions which collectively form the consciousness system, which includes contributions from the default mode network (DMN), ascending arousal systems, and the thalamus. Electrophysiological and neuroimaging investigations have also clearly demonstrated the importance of thalamocortical and corticothalamic networks in the evolution of sleep and absence epilepsy, two phenomena in which the subject experiences an alteration to the conscious state and a disconnection from external input. However, the precise relationship between the consciousness system, thalamocortical networks, and consciousness itself remains to be clarified. One of the fundamental challenges is to understand how distributed brain networks coordinate their activity in order to maintain and implement complex behaviors such as consciousness and how modifications to this network activity lead to alterations in consciousness. By taking into account not only the level of activation of individual brain regions but also their connectivity within specific networks and the activity and connectivity of other relevant networks, a more specific quantification of brain states can be achieved. This, in turn, may provide a more fundamental understanding of the alterations to consciousness experienced in sleep and epilepsy. © 2013.

Glycogen metabolism and the homeostatic regulation of sleep.

PubMed

Petit, Jean-Marie; Burlet-Godinot, Sophie; Magistretti, Pierre J; Allaman, Igor

2015-02-01

In 1995 Benington and Heller formulated an energy hypothesis of sleep centered on a key role of glycogen. It was postulated that a major function of sleep is to replenish glycogen stores in the brain that have been depleted during wakefulness which is associated to an increased energy demand. Astrocytic glycogen depletion participates to an increase of extracellular adenosine release which influences sleep homeostasis. Here, we will review some evidence obtained by studies addressing the question of a key role played by glycogen metabolism in sleep regulation as proposed by this hypothesis or by an alternative hypothesis named "glycogenetic" hypothesis as well as the importance of the confounding effect of glucocorticoïds. Even though actual collected data argue in favor of a role of sleep in brain energy balance-homeostasis, they do not support a critical and direct involvement of glycogen metabolism on sleep regulation. For instance, glycogen levels during the sleep-wake cycle are driven by different physiological signals and therefore appear more as a marker-integrator of brain energy status than a direct regulator of sleep homeostasis. In support of this we provide evidence that blockade of glycogen mobilization does not induce more sleep episodes during the active period while locomotor activity is reduced. These observations do not invalidate the energy hypothesis of sleep but indicate that underlying cellular mechanisms are more complex than postulated by Benington and Heller.

Reward-related brain function and sleep in pre/early pubertal and mid/late pubertal adolescents.

PubMed

Holm, Stephanie M; Forbes, Erika E; Ryan, Neal D; Phillips, Mary L; Tarr, Jill A; Dahl, Ronald E

2009-10-01

The onset of adolescence is a time of dramatic changes, including changes in sleep, and a time of new health concerns related to increases in risk-taking, sensation seeking, depression, substance use, and accidents. As part of a larger study examining puberty-specific changes in adolescents' reward-related brain function, the current article focuses on the relationship between functional neuroimaging measures of reward and measures of sleep. A total of 58 healthy participants 11-13 years of age completed a functional magnetic resonance imaging scan using a guessing task with monetary rewards and 4 days of at-home actigraphy and self-reported sleep ratings. Sleep variables included actigraph measures of mean weekend minutes asleep, sleep onset time, and sleep offset time, as well as self-reported sleep quality. During reward anticipation, less activation in the caudate (part of the ventral striatum) was associated with fewer minutes asleep, later sleep onset time, and lower sleep quality. During reward outcome, less caudate activation was associated with later sleep onset time, earlier sleep offset time, and lower sleep quality. It has been hypothesized that adolescents' low reactivity in reward-related brain areas could lead to compensatory increases in reward-driven behavior. This study's findings suggest that sleep could contribute to such behavior. Because decreased sleep has been associated with risky behavior and negative mood, these findings raise concerns about a negative spiral whereby the effects of puberty and sleep deprivation may have synergistic effects on reward processing, contributing to adolescent behavioral and emotional health problems.

Sleep and Plasticity in Schizophrenia

PubMed Central

Sprecher, Kate E.; Ferrarelli, Fabio

2016-01-01

Schizophrenia is a devastating mental illness with a worldwide prevalence of approximately 1 %. Although the clinical features of the disorder were described over one hundred years ago, its neurobiology is still largely elusive despite several decades of research. Schizophrenia is associated with marked sleep disturbances and memory impairment. Above and beyond altered sleep architecture, sleep rhythms including slow waves and spindles are disrupted in schizophrenia. In the healthy brain, these rhythms reflect and participate in plastic processes during sleep. This chapter discusses evidence that schizophrenia patients exhibit dysfunction of sleep-mediated plasticity on a behavioral, cellular, and molecular level and offers suggestions on how the study of sleeping brain activity can shed light on the pathophysiological mechanisms of the disorder. PMID:25608723

Reduced Sleep Spindle Activity in Early-Onset and Elevated Risk for Depression

ERIC Educational Resources Information Center

Lopez, Jorge; Hoffmann, Robert; Armitage, Roseanne

2010-01-01

Objective: Sleep disturbances are common in major depressive disorder (MDD), although polysomnographic (PSG) abnormalities are more prevalent in adults than in children and adolescents with MDD. Sleep spindle activity (SPA) is associated with neuroplasticity mechanisms during brain maturation and is more abundant in childhood and adolescence than…

Initiation of sleep-dependent cortical-hippocampal correlations at wakefulness-sleep transition.

PubMed

Haggerty, Daniel C; Ji, Daoyun

2014-10-01

Sleep is involved in memory consolidation. Current theories propose that sleep-dependent memory consolidation requires active communication between the hippocampus and neocortex. Indeed, it is known that neuronal activities in the hippocampus and various neocortical areas are correlated during slow-wave sleep. However, transitioning from wakefulness to slow-wave sleep is a gradual process. How the hippocampal-cortical correlation is established during the wakefulness-sleep transition is unknown. By examining local field potentials and multiunit activities in the rat hippocampus and visual cortex, we show that the wakefulness-sleep transition is characterized by sharp-wave ripple events in the hippocampus and high-voltage spike-wave events in the cortex, both of which are accompanied by highly synchronized multiunit activities in the corresponding area. Hippocampal ripple events occur earlier than the cortical high-voltage spike-wave events, and hippocampal ripple incidence is attenuated by the onset of cortical high-voltage spike waves. This attenuation leads to a temporary weak correlation in the hippocampal-cortical multiunit activities, which eventually evolves to a strong correlation as the brain enters slow-wave sleep. The results suggest that the hippocampal-cortical correlation is established through a concerted, two-step state change that first synchronizes the neuronal firing within each brain area and then couples the synchronized activities between the two regions. Copyright © 2014 the American Physiological Society.

Zinc-containing yeast extract promotes nonrapid eye movement sleep in mice.

PubMed

Cherasse, Yoan; Saito, Hitomi; Nagata, Nanae; Aritake, Kosuke; Lazarus, Michael; Urade, Yoshihiro

2015-10-01

Zinc is an essential trace element for humans and animals, being located, among other places, in the synaptic vesicles of cortical glutamatergic neurons and hippocampal mossy fibers in the brain. Extracellular zinc has the potential to interact with and modulate many different synaptic targets, including glutamate and GABA receptors. Because of the central role of these neurotransmitters in brain activity, we examined in this study the sleep-promoting activity of zinc by monitoring locomotor activity and electroencephalogram after its administration to mice. Zinc-containing yeast extract (40 and 80 mg/kg) dose dependently increased the total amount of nonrapid eye movement sleep and decreased the locomotor activity. However, this preparation did not change the amount of rapid eye movement sleep or show any adverse effects such as rebound of insomnia during a period of 24 h following the induction of sleep; whereas the extracts containing other divalent cations (manganese, iron, and copper) did not decrease the locomotor activity. This is the first evidence that zinc can induce sleep. Our data open the way to new types of food supplements designed to improve sleep. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Pannexins Are Potential New Players in the Regulation of Cerebral Homeostasis during Sleep-Wake Cycle

PubMed Central

Shestopalov, Valery I.; Panchin, Yuri; Tarasova, Olga S.; Gaynullina, Dina; Kovalzon, Vladimir M.

2017-01-01

During brain homeostasis, both neurons and astroglia release ATP that is rapidly converted to adenosine in the extracellular space. Pannexin-1 (Panx1) hemichannels represent a major conduit of non-vesicular ATP release from brain cells. Previous studies have shown that Panx1−/− mice possess severe disruption of the sleep-wake cycle. Here, we review experimental data supporting the involvement of pannexins (Panx) in the coordination of fundamental sleep-associated brain processes, such as neuronal activity and regulation of cerebrovascular tone. Panx1 hemichannels are likely implicated in the regulation of the sleep-wake cycle via an indirect effect of released ATP on adenosine receptors and through interaction with other somnogens, such as IL-1β, TNFα and prostaglandin D2. In addition to the recently established role of Panx1 in the regulation of endothelium-dependent arterial dilation, similar signaling pathways are the major cellular component of neurovascular coupling. The new discovered role of Panx in sleep regulation may have broad implications in coordinating neuronal activity and homeostatic housekeeping processes during the sleep-wake cycle. PMID:28769767

Pannexins Are Potential New Players in the Regulation of Cerebral Homeostasis during Sleep-Wake Cycle.

PubMed

Shestopalov, Valery I; Panchin, Yuri; Tarasova, Olga S; Gaynullina, Dina; Kovalzon, Vladimir M

2017-01-01

During brain homeostasis, both neurons and astroglia release ATP that is rapidly converted to adenosine in the extracellular space. Pannexin-1 (Panx1) hemichannels represent a major conduit of non-vesicular ATP release from brain cells. Previous studies have shown that Panx1 -/- mice possess severe disruption of the sleep-wake cycle. Here, we review experimental data supporting the involvement of pannexins (Panx) in the coordination of fundamental sleep-associated brain processes, such as neuronal activity and regulation of cerebrovascular tone. Panx1 hemichannels are likely implicated in the regulation of the sleep-wake cycle via an indirect effect of released ATP on adenosine receptors and through interaction with other somnogens, such as IL-1β, TNFα and prostaglandin D2. In addition to the recently established role of Panx1 in the regulation of endothelium-dependent arterial dilation, similar signaling pathways are the major cellular component of neurovascular coupling. The new discovered role of Panx in sleep regulation may have broad implications in coordinating neuronal activity and homeostatic housekeeping processes during the sleep-wake cycle.

Impact of traumatic brain injury on sleep structure, electrocorticographic activity and transcriptome in mice.

PubMed

Sabir, Meriem; Gaudreault, Pierre-Olivier; Freyburger, Marlène; Massart, Renaud; Blanchet-Cohen, Alexis; Jaber, Manar; Gosselin, Nadia; Mongrain, Valérie

2015-07-01

Traumatic brain injury (TBI), including mild TBI (mTBI), is importantly associated with vigilance and sleep complaints. Because sleep is required for learning, plasticity and recovery, we here evaluated the bidirectional relationship between mTBI and sleep with two specific objectives: (1) Test that mTBI rapidly impairs sleep-wake architecture and the dynamics of the electrophysiological marker of sleep homeostasis (i.e., non-rapid eye movement sleep delta (1-4Hz) activity); (2) evaluate the impact of sleep loss following mTBI on the expression of plasticity markers that have been linked to sleep homeostasis and on genome-wide gene expression. A closed-head injury model was used to perform a 48h electrocorticographic (ECoG) recording in mice submitted to mTBI or Sham surgery. mTBI was found to immediately decrease the capacity to sustain long bouts of wakefulness as well as the amplitude of the time course of ECoG delta activity during wakefulness. Significant changes in ECoG spectral activity during wakefulness, non-rapid eye movement and rapid eye movement sleep were observed mainly on the second recorded day. A second experiment was performed to measure gene expression in the cerebral cortex and hippocampus after a mTBI followed either by two consecutive days of 6h sleep deprivation (SD) or of undisturbed behavior (quantitative PCR and next-generation sequencing). mTBI modified the expression of genes involved in immunity, inflammation and glial function (e.g., chemokines, glial markers) and SD changed that of genes linked to circadian rhythms, synaptic activity/neuronal plasticity, neuroprotection and cell death and survival. SD appeared to affect gene expression in the cerebral cortex more importantly after mTBI than Sham surgery including that of the astrocytic marker Gfap, which was proposed as a marker of clinical outcome after TBI. Interestingly, SD impacted the hippocampal expression of the plasticity elements Arc and EfnA3 only after mTBI. Overall, our findings reveal alterations in spectral signature across all vigilance states in the first days after mTBI, and show that sleep loss post-mTBI reprograms the transcriptome in a brain area-specific manner and in a way that could be deleterious to brain recovery. Copyright © 2015 Elsevier Inc. All rights reserved.

Self-organized dynamical complexity in human wakefulness and sleep: different critical brain-activity feedback for conscious and unconscious states.

PubMed

Allegrini, Paolo; Paradisi, Paolo; Menicucci, Danilo; Laurino, Marco; Piarulli, Andrea; Gemignani, Angelo

2015-09-01

Criticality reportedly describes brain dynamics. The main critical feature is the presence of scale-free neural avalanches, whose auto-organization is determined by a critical branching ratio of neural-excitation spreading. Other features, directly associated to second-order phase transitions, are: (i) scale-free-network topology of functional connectivity, stemming from suprathreshold pairwise correlations, superimposable, in waking brain activity, with that of ferromagnets at Curie temperature; (ii) temporal long-range memory associated to renewal intermittency driven by abrupt fluctuations in the order parameters, detectable in human brain via spatially distributed phase or amplitude changes in EEG activity. Herein we study intermittent events, extracted from 29 night EEG recordings, including presleep wakefulness and all phases of sleep, where different levels of mentation and consciousness are present. We show that while critical avalanching is unchanged, at least qualitatively, intermittency and functional connectivity, present during conscious phases (wakefulness and REM sleep), break down during both shallow and deep non-REM sleep. We provide a theory for fragmentation-induced intermittency breakdown and suggest that the main difference between conscious and unconscious states resides in the backwards causation, namely on the constraints that the emerging properties at large scale induce to the lower scales. In particular, while in conscious states this backwards causation induces a critical slowing down, preserving spatiotemporal correlations, in dreamless sleep we see a self-organized maintenance of moduli working in parallel. Critical avalanches are still present, and establish transient auto-organization, whose enhanced fluctuations are able to trigger sleep-protecting mechanisms that reinstate parallel activity. The plausible role of critical avalanches in dreamless sleep is to provide a rapid recovery of consciousness, if stimuli are highly arousing.

Self-organized dynamical complexity in human wakefulness and sleep: Different critical brain-activity feedback for conscious and unconscious states

NASA Astrophysics Data System (ADS)

Allegrini, Paolo; Paradisi, Paolo; Menicucci, Danilo; Laurino, Marco; Piarulli, Andrea; Gemignani, Angelo

2015-09-01

Criticality reportedly describes brain dynamics. The main critical feature is the presence of scale-free neural avalanches, whose auto-organization is determined by a critical branching ratio of neural-excitation spreading. Other features, directly associated to second-order phase transitions, are: (i) scale-free-network topology of functional connectivity, stemming from suprathreshold pairwise correlations, superimposable, in waking brain activity, with that of ferromagnets at Curie temperature; (ii) temporal long-range memory associated to renewal intermittency driven by abrupt fluctuations in the order parameters, detectable in human brain via spatially distributed phase or amplitude changes in EEG activity. Herein we study intermittent events, extracted from 29 night EEG recordings, including presleep wakefulness and all phases of sleep, where different levels of mentation and consciousness are present. We show that while critical avalanching is unchanged, at least qualitatively, intermittency and functional connectivity, present during conscious phases (wakefulness and REM sleep), break down during both shallow and deep non-REM sleep. We provide a theory for fragmentation-induced intermittency breakdown and suggest that the main difference between conscious and unconscious states resides in the backwards causation, namely on the constraints that the emerging properties at large scale induce to the lower scales. In particular, while in conscious states this backwards causation induces a critical slowing down, preserving spatiotemporal correlations, in dreamless sleep we see a self-organized maintenance of moduli working in parallel. Critical avalanches are still present, and establish transient auto-organization, whose enhanced fluctuations are able to trigger sleep-protecting mechanisms that reinstate parallel activity. The plausible role of critical avalanches in dreamless sleep is to provide a rapid recovery of consciousness, if stimuli are highly arousing.

Unihemispheric sleep and asymmetrical sleep: behavioral, neurophysiological, and functional perspectives.

PubMed

Mascetti, Gian Gastone

2016-01-01

Sleep is a behavior characterized by a typical body posture, both eyes' closure, raised sensory threshold, distinctive electrographic signs, and a marked decrease of motor activity. In addition, sleep is a periodically necessary behavior and therefore, in the majority of animals, it involves the whole brain and body. However, certain marine mammals and species of birds show a different sleep behavior, in which one cerebral hemisphere sleeps while the other is awake. In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance. In birds, antipredation vigilance is the main function of unihemispheric sleep, but in domestic chicks, it is also associated with brain lateralization or dominance in the control of behavior. Compared to bihemispheric sleep, unihemispheric sleep would mean a reduction of the time spent sleeping and of the associated recovery processes. However, the behavior and health of aquatic mammals and birds does not seem at all impaired by the reduction of sleep. The neural mechanisms of unihemispheric sleep are unknown, but assuming that the neural structures involved in sleep in cetaceans, seals, and birds are similar to those of terrestrial mammals, it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem. The neural mechanisms promoting wakefulness dominate one side of the brain, while those promoting sleep predominates the other side. For cetaceans, unihemispheric sleep is the only way to sleep, while in seals and birds, unihemispheric sleep events are intermingled with bihemispheric and rapid eye movement sleep events. Electroencephalogram hemispheric asymmetries are also reported during bihemispheric sleep, at awakening, and at sleep onset, as well as being associated with a use-dependent process (local sleep).

Toll-Like Receptor 4 Is a Regulator of Monocyte and Electroencephalographic Responses to Sleep Loss

PubMed Central

Wisor, Jonathan P.; Clegern, William C.; Schmidt, Michelle A.

2011-01-01

Study Objectives: Sleep loss triggers changes in inflammatory signaling pathways in the brain and periphery. The mechanisms that underlie these changes are ill-defined. The Toll-like receptor 4 (TLR4) activates inflammatory signaling cascades in response to endogenous and pathogen-associated ligands known to be elevated in association with sleep loss. TLR4 is therefore a possible mediator of some of the inflammation-related effects of sleep loss. Here we describe the baseline electroencephalographic sleep phenotype and the biochemical and electroencephalographic responses to sleep loss in TLR4-deficient mice. Design, Measurements and Results: TLR4-deficient mice and wild type controls were subjected to electroencephalographic and electromyographic recordings during spontaneous sleep/wake cycles and during and after sleep restriction sessions of 3, 6, and 24-h duration, during which sleep was disrupted by an automated sleep restriction system. Relative to wild type control mice, TLR4-deficient mice exhibited an increase in the duration of the primary daily waking bout occurring at dark onset in a light/dark cycle. The amount of time spent in non-rapid eye movement sleep by TLR4-deficient mice was reduced in proportion to increased wakefulness in the hours immediately after dark onset. Subsequent to sleep restriction, EEG measures of increased sleep drive were attenuated in TLR4-deficient mice relative to wild-type mice. TLR4 was enriched 10-fold in brain cells positive for the cell surface marker CD11b (cells of the monocyte lineage) relative to CD11b-negative cells in wild type mouse brains. To assess whether this population was affected selectively by TLR4 knockout, flow cytometry was used to count F4/80- and CD45-positive cells in the brains of sleep deprived and time of day control mice. While wild-type mice exhibited a significant reduction in the number of CD11b-positive cells in the brain after 24-h sleep restriction, TLR4-deficient mice did not. Conclusion: These data demonstrate that innate immune signaling pathways active in the monocyte lineage, including presumably microglia, detect and mediate in part the cerebral reaction to sleep loss. Citation: Wisor JP; Clegern WC; Schmidt MA. Toll-like receptor 4 is a regulator of monocyte and electroencephalographic responses to sleep loss. SLEEP 2011;34(10):1335–1345. PMID:21966065

Phase-Locked Loop for Precisely Timed Acoustic Stimulation during Sleep

PubMed Central

Santostasi, Giovanni; Malkani, Roneil; Riedner, Brady; Bellesi, Michele; Tononi, Giulio; Paller, Ken A.; Zee, Phyllis C.

2016-01-01

Background A Brain-Computer Interface could potentially enhance the various benefits of sleep. New Method We describe a strategy for enhancing slow-wave sleep (SWS) by stimulating the sleeping brain with periodic acoustic stimuli that produce resonance in the form of enhanced slow-wave activity in the electroencephalogram (EEG). The system delivers each acoustic stimulus at a particular phase of an electrophysiological rhythm using a Phase-Locked Loop (PLL). Results The PLL is computationally economical and well suited to follow and predict the temporal behavior of the EEG during slow-wave sleep. Comparison with Existing Methods Acoustic stimulation methods may be able to enhance SWS without the risks inherent in electrical stimulation or pharmacological methods. The PLL method differs from other acoustic stimulation methods that are based on detecting a single slow wave rather than modeling slow-wave activity over an extended period of time. Conclusions By providing real-time estimates of the phase of ongoing EEG oscillations, the PLL can rapidly adjust to physiological changes, thus opening up new possibilities to study brain dynamics during sleep. Future application of these methods hold promise for enhancing sleep quality and associated daytime behavior and improving physiologic function. PMID:26617321

[Sleep-wake cycle and memory consolidation].

PubMed

Baratti, Carlos M; Boccia, Mariano M; Blake, Mariano G; Acosta, Gabriela B

2007-01-01

Although several hypothesis and theories have been advanced as explanations for the functions of sleep, a unified theory of sleep function remains elusive. Sleep has been implicated in the plastic cerebral changes that underlie learning and memory, in particular those related to memory consolidation of recently acquired new information. Despite steady accumulations of positive findings over the last ten years, the precise role of sleep in memory and brain plasticity is unproven at all. This situation might be solved by more integrated approaches that combine behavioral and neurophysiological measurements in well described in vivo models of neuronal activity and brain plasticity.

Transcranial Electrical Currents to Probe EEG Brain Rhythms and Memory Consolidation during Sleep in Humans

PubMed Central

Marshall, Lisa; Kirov, Roumen; Brade, Julian; Mölle, Matthias; Born, Jan

2011-01-01

Previously the application of a weak electric anodal current oscillating with a frequency of the sleep slow oscillation (∼0.75 Hz) during non-rapid eye movement sleep (NonREM) sleep boosted endogenous slow oscillation activity and enhanced sleep-associated memory consolidation. The slow oscillations occurring during NonREM sleep and theta oscillations present during REM sleep have been considered of critical relevance for memory formation. Here transcranial direct current stimulation (tDCS) oscillating at 5 Hz, i.e., within the theta frequency range (theta-tDCS) is applied during NonREM and REM sleep. Theta-tDCS during NonREM sleep produced a global decrease in slow oscillatory activity conjoint with a local reduction of frontal slow EEG spindle power (8–12 Hz) and a decrement in consolidation of declarative memory, underlining the relevance of these cortical oscillations for sleep-dependent memory consolidation. In contrast, during REM sleep theta-tDCS appears to increase global gamma (25–45 Hz) activity, indicating a clear brain state-dependency of theta-tDCS. More generally, results demonstrate the suitability of oscillating-tDCS as a tool to analyze functions of endogenous EEG rhythms and underlying endogenous electric fields as well as the interactions between EEG rhythms of different frequencies. PMID:21340034

Creating an Environment for Safe and Healthy Sleep in Child Care Programs

ERIC Educational Resources Information Center

Rose, Bobbie

2012-01-01

Along with nutrition, physical activity, and secure attachments, sleep is a basic requirement for a child's growth and brain development. Sleep is important for health and wellness, especially for growing infants and young children. Unfortunately, the amount of time children spend sleeping seems to be declining. If only sleep-deprived children…

Linking sleep and general anesthesia mechanisms: this is no walkover.

PubMed

Bonhomme, V; Boveroux, P; Vanhaudenhuyse, A; Hans, P; Brichant, J F; Jaquet, O; Boly, M; Laureys, S

2011-01-01

This review aims at defining the link between physiological sleep and general anesthesia. Despite common behavioral and electrophysiological characteristics between both states, current literature suggests that the transition process between waking and sleep or anesthesia-induced alteration of consciousness is not driven by the same sequence of events. On the one hand, sleep originates in sub-cortical structures with subsequent repercussions on thalamo-cortical interactions and cortical activity. On the other hand, anesthesia seems to primarily affect the cortex with subsequent repercussions on the activity of sub-cortical networks. This discrepancy has yet to be confirmed by further functional brain imaging and electrophysiological experiments. The relationship between the observed functional modifications of brain activity during anesthesia and the known biochemical targets of hypnotic anesthetic agents also remains to be determined.

Sleep and wakefulness in somnambulism: a spectral analysis study.

PubMed

Guilleminault, C; Poyares, D; Aftab, F A; Palombini, L; Abat, F

2001-08-01

The sleep structure and the dynamics of EEG slow-wave activity (SWA) were investigated in 12 young adults and age- and gender-matched controls. Polysomnography was performed in subjects with well-documented chronic sleepwalking and in matched controls. Blinded visual scoring was performed using the international criteria from the Rechtschaffen and Kales atlas [A manual of standardized technology, techniques and scoring systems for sleep stages of human subjects. Los Angeles: UCLA Brain Information Service, Brain Research Institute, 1968.] and by determining the presence of microarousals as defined in the American Sleep Disorders Association (ASDA) atlas [Sleep 15 (1992) 173.]. An evaluation of SWA overnight was performed on total nocturnal sleep to determine if a difference existed between groups of subjects, since sleepwalking usually originates with slow-wave sleep. Investigation of the delta power in successive nonoverlapping 4-second windows in the 32 seconds just prior to EMG activity associated with a confusional arousal was also conducted. One central EEG lead was used for all analyses. Somnambulistic individuals experienced more disturbed sleep than controls during the first NREM-REM sleep cycle. They had a higher number of ASDA arousals and presented lower peak of SWA during the first cycle that led to a lower SWA decline overnight. When the investigation focused on the short segment immediately preceding a confusional arousal, they presented an important increase in the relative power of low delta (0.75-2 Hz) just prior to the confusional arousal. Sleepwalkers undergo disturbed nocturnal sleep at the beginning of the night. The increased power of low delta just prior to the confusional arousal experienced may not be related to Stages 3-4 NREM sleep. We hypothesize that it may be translated as a cortical reaction to brain activation.

The Memory Function of Noradrenergic Activity in Non-REM Sleep

ERIC Educational Resources Information Center

Gais, Steffen; Rasch, Bjorn; Dahmen, Johannes C.; Sara, Susan; Born, Jan

2011-01-01

There is a long-standing assumption that low noradrenergic activity during sleep reflects mainly the low arousal during this brain state. Nevertheless, recent research has demonstrated that the locus coeruleus, which is the main source of cortical noradrenaline, displays discrete periods of intense firing during non-REM sleep, without any signs of…

Autobiographical memory and hyperassociativity in the dreaming brain: implications for memory consolidation in sleep

PubMed Central

Horton, Caroline L.; Malinowski, Josie E.

2015-01-01

In this paper we argue that autobiographical memory (AM) activity across sleep and wake can provide insight into the nature of dreaming, and vice versa. Activated memories within the sleeping brain reflect one’s personal life history (autobiography). They can appear in largely fragmentary forms and differ from conventional manifestations of episodic memory. Autobiographical memories in dreams can be sampled from non-REM as well as REM periods, which contain fewer episodic references and become more bizarre across the night. Salient fragmented memory features are activated in sleep and re-bound with fragments not necessarily emerging from the same memory, thus de-contextualizing those memories and manifesting as experiences that differ from waking conceptions. The constructive nature of autobiographical recall further encourages synthesis of these hyper-associated images into an episode via recalling and reporting dreams. We use a model of AM to account for the activation of memories in dreams as a reflection of sleep-dependent memory consolidation processes. We focus in particular on the hyperassociative nature of AM during sleep. PMID:26191010

Autobiographical memory and hyperassociativity in the dreaming brain: implications for memory consolidation in sleep.

PubMed

Horton, Caroline L; Malinowski, Josie E

2015-01-01

In this paper we argue that autobiographical memory (AM) activity across sleep and wake can provide insight into the nature of dreaming, and vice versa. Activated memories within the sleeping brain reflect one's personal life history (autobiography). They can appear in largely fragmentary forms and differ from conventional manifestations of episodic memory. Autobiographical memories in dreams can be sampled from non-REM as well as REM periods, which contain fewer episodic references and become more bizarre across the night. Salient fragmented memory features are activated in sleep and re-bound with fragments not necessarily emerging from the same memory, thus de-contextualizing those memories and manifesting as experiences that differ from waking conceptions. The constructive nature of autobiographical recall further encourages synthesis of these hyper-associated images into an episode via recalling and reporting dreams. We use a model of AM to account for the activation of memories in dreams as a reflection of sleep-dependent memory consolidation processes. We focus in particular on the hyperassociative nature of AM during sleep.

The Effects of Caffeine on Sleep and Maturational Markers in the Rat

PubMed Central

Olini, Nadja; Kurth, Salomé; Huber, Reto

2013-01-01

Adolescence is a critical period for brain maturation during which a massive reorganization of cortical connectivity takes place. In humans, slow wave activity (<4.5 Hz) during NREM sleep was proposed to reflect cortical maturation which relies on use-dependent processes. A stimulant like caffeine, whose consumption has recently increased especially in adolescents, is known to affect sleep wake regulation. The goal of this study was to establish a rat model allowing to assess the relationship between cortical maturation and sleep and to further investigate how these parameters are affected by caffeine consumption. To do so, we assessed sleep and markers of maturation by electrophysiological recordings, behavioral and structural readouts in the juvenile rat. Our results show that sleep slow wave activity follows a similar inverted U-shape trajectory as already known in humans. Caffeine treatment exerted short-term stimulating effects and altered the trajectory of slow wave activity. Moreover, caffeine affected behavioral and structural markers of maturation. Thus, caffeine consumption during a critical developmental period shows long lasting effects on sleep and brain maturation. PMID:24023748

Flurazepam

MedlinePlus

... by slowing activity in the brain to allow sleep. ... nights after you stop taking the medication.Your sleep problems should improve within 7 to 10 days ... start taking flurazepam. Call your doctor if your sleep problems do not improve during this time, if ...

Estazolam

MedlinePlus

... by slowing activity in the brain to allow sleep. ... full night after you take the medication.Your sleep problems should improve within 7 to 10 days ... start taking estazolam. Call your doctor if your sleep problems do not improve during this time, if ...

Going local: insights from EEG and stereo-EEG studies of the human sleep-wake cycle.

PubMed

Ferrara, Michele; De Gennaro, Luigi

2011-01-01

In the present paper, we reviewed a large body of evidence, mainly from quantitative EEG studies of our laboratory, supporting the notion that sleep is a local and use-dependent process. Quantitative analyses of sleep EEG recorded from multiple cortical derivations clearly indicate that every sleep phenomenon, from sleep onset to the awakening, is strictly local in nature. Sleep onset first occurs in frontal areas, and a frontal predominance of low-frequency power persists in the first part of the night, when the homeostatic processes mainly occur, and then it vanishes. Upon awakening, we showed an asynchronous EEG activation of different cortical areas, the more anterior ones being the first to wake up. During extended periods of wakefulness, the increase of sleepiness-related low-EEG frequencies is again evident over the frontal derivations. Similarly, experimental manipulations of sleep length by total sleep deprivation, partial sleep curtailment or even selective slow-wave sleep deprivation lead to a slow-wave activity rebound localized especially on the anterior derivations. Thus, frontal areas are crucially involved in sleep homeostasis. According to the local use-dependent theory, this would derive from a higher sleep need of the frontal cortex, which in turn is due to its higher levels of activity during wakefulness. The fact that different brain regions can simultaneously exhibit different sleep intensities indicates that sleep is not a spatially global and uniform state, as hypothesized in the theory. We have also reviewed recent evidence of localized effects of learning and plasticity on EEG sleep measures. These studies provide crucial support to a key concept in the theory, the one claiming that local sleep characteristics should be use-dependent. Finally, we have reported data corroborating the notion that sleep is not necessarily present simultaneously in the entire brain. Our stereo-EEG recordings clearly indicate that sleep and wakefulness can co-exist in different areas, suggesting that vigilance states are not necessarily temporally discrete states. We conclude that understanding local variations in sleep propensity and depth, especially as a result of brain plasticity, may provide in the near future insightful hints into the fundamental functions of sleep.

Alter spontaneous activity in amygdala and vmPFC during fear consolidation following 24 h sleep deprivation.

PubMed

Feng, Pan; Becker, Benjamin; Feng, Tingyong; Zheng, Yong

2018-05-15

Sleep deprivation (SD) has been associated with cognitive and emotional disruptions, however its impact on the acquisition of fear and subsequent fear memory consolidation remain unknown. To address this question, we measured human brain activity before and after fear acquisition under conditions of 24 h sleep deprivation versus normal sleep using resting-state functional magnetic resonance imaging (rs-fMRI). Additionally, we explored whether the fear acquisition-induced change of brain activity during the fear memory consolidation window can be predicted by subjective fear ratings and autonomic fear response, assessed by skin conductance responses (SCR) during acquisition. Behaviorally, the SD group demonstrated increased subjective and autonomic fear responses compared to controls at the stage of fear acquisition. During the stage of fear consolidation, the SD group displayed decreased ventromedial prefrontal cortex (vmPFC) activity and concomitantly increased amygdala activity. Moreover, in the SD group fear acquisition-induced brain activity changes in amygdala were positively correlated with both, subjective and autonomic fear indices during acquisition, whereas in controls changes vmPFC activity were positively correlated with fear indices during acquisition. Together, the present findings suggested that SD may weaken the top-down ability of the vmPFC to regulate amygdala activity during fear memory consolidation. Moreover, subjective and objective fear at fear acquisition stage can predict the change of brain activity in amygdala in fear memory consolidation following SD. Copyright © 2018 Elsevier Inc. All rights reserved.

Sleep deprivation compromises resting-state emotional regulatory processes: An EEG study.

PubMed

Zhang, Jinxiao; Lau, Esther Yuet Ying; Hsiao, Janet H

2018-03-01

Resting-state spontaneous neural activities consume far more biological energy than stimulus-induced activities, suggesting their significance. However, existing studies of sleep loss and emotional functioning have focused on how sleep deprivation modulates stimulus-induced emotional neural activities. The current study aimed to investigate the impacts of sleep deprivation on the brain network of emotional functioning using electroencephalogram during a resting state. Two established resting-state electroencephalogram indexes (i.e. frontal alpha asymmetry and frontal theta/beta ratio) were used to reflect the functioning of the emotion regulatory neural network. Participants completed an 8-min resting-state electroencephalogram recording after a well-rested night or 24 hr sleep deprivation. The Sleep Deprivation group had a heightened ratio of the power density in theta band to beta band (theta/beta ratio) in the frontal area than the Sleep Control group, suggesting an effective approach with reduced frontal cortical regulation of subcortical drive after sleep deprivation. There was also marginally more left-lateralized frontal alpha power (left frontal alpha asymmetry) in the Sleep Deprivation group compared with the Sleep Control group. Besides, higher theta/beta ratio and more left alpha lateralization were correlated with higher sleepiness and lower vigilance. The results converged in suggesting compromised emotional regulatory processes during resting state after sleep deprivation. Our work provided the first resting-state neural evidence for compromised emotional functioning after sleep loss, highlighting the significance of examining resting-state neural activities within the affective brain network as a default functional mode in investigating the sleep-emotion relationship. © 2018 European Sleep Research Society.

Diminished Auditory Responses during NREM Sleep Correlate with the Hierarchy of Language Processing

PubMed Central

Furman-Haran, Edna; Arzi, Anat; Levkovitz, Yechiel; Malach, Rafael

2016-01-01

Natural sleep provides a powerful model system for studying the neuronal correlates of awareness and state changes in the human brain. To quantitatively map the nature of sleep-induced modulations in sensory responses we presented participants with auditory stimuli possessing different levels of linguistic complexity. Ten participants were scanned using functional magnetic resonance imaging (fMRI) during the waking state and after falling asleep. Sleep staging was based on heart rate measures validated independently on 20 participants using concurrent EEG and heart rate measurements and the results were confirmed using permutation analysis. Participants were exposed to three types of auditory stimuli: scrambled sounds, meaningless word sentences and comprehensible sentences. During non-rapid eye movement (NREM) sleep, we found diminishing brain activation along the hierarchy of language processing, more pronounced in higher processing regions. Specifically, the auditory thalamus showed similar activation levels during sleep and waking states, primary auditory cortex remained activated but showed a significant reduction in auditory responses during sleep, and the high order language-related representation in inferior frontal gyrus (IFG) cortex showed a complete abolishment of responses during NREM sleep. In addition to an overall activation decrease in language processing regions in superior temporal gyrus and IFG, those areas manifested a loss of semantic selectivity during NREM sleep. Our results suggest that the decreased awareness to linguistic auditory stimuli during NREM sleep is linked to diminished activity in high order processing stations. PMID:27310812

Diminished Auditory Responses during NREM Sleep Correlate with the Hierarchy of Language Processing.

PubMed

Wilf, Meytal; Ramot, Michal; Furman-Haran, Edna; Arzi, Anat; Levkovitz, Yechiel; Malach, Rafael

2016-01-01

Natural sleep provides a powerful model system for studying the neuronal correlates of awareness and state changes in the human brain. To quantitatively map the nature of sleep-induced modulations in sensory responses we presented participants with auditory stimuli possessing different levels of linguistic complexity. Ten participants were scanned using functional magnetic resonance imaging (fMRI) during the waking state and after falling asleep. Sleep staging was based on heart rate measures validated independently on 20 participants using concurrent EEG and heart rate measurements and the results were confirmed using permutation analysis. Participants were exposed to three types of auditory stimuli: scrambled sounds, meaningless word sentences and comprehensible sentences. During non-rapid eye movement (NREM) sleep, we found diminishing brain activation along the hierarchy of language processing, more pronounced in higher processing regions. Specifically, the auditory thalamus showed similar activation levels during sleep and waking states, primary auditory cortex remained activated but showed a significant reduction in auditory responses during sleep, and the high order language-related representation in inferior frontal gyrus (IFG) cortex showed a complete abolishment of responses during NREM sleep. In addition to an overall activation decrease in language processing regions in superior temporal gyrus and IFG, those areas manifested a loss of semantic selectivity during NREM sleep. Our results suggest that the decreased awareness to linguistic auditory stimuli during NREM sleep is linked to diminished activity in high order processing stations.

Neuroimaging Insights into the Pathophysiology of Sleep Disorders

PubMed Central

Desseilles, Martin; Dang-Vu, Thanh; Schabus, Manuel; Sterpenich, Virginie; Maquet, Pierre; Schwartz, Sophie

2008-01-01

Neuroimaging methods can be used to investigate whether sleep disorders are associated with specific changes in brain structure or regional activity. However, it is still unclear how these new data might improve our understanding of the pathophysiology underlying adult sleep disorders. Here we review functional brain imaging findings in major intrinsic sleep disorders (i.e., idiopathic insomnia, narcolepsy, and obstructive sleep apnea) and in abnormal motor behavior during sleep (i.e., periodic limb movement disorder and REM sleep behavior disorder). The studies reviewed include neuroanatomical assessments (voxel-based morphometry, magnetic resonance spectroscopy), metabolic/functional investigations (positron emission tomography, single photon emission computed tomography, functional magnetic resonance imaging), and ligand marker measurements. Based on the current state of the research, we suggest that brain imaging is a useful approach to assess the structural and functional correlates of sleep impairments as well as better understand the cerebral consequences of various therapeutic approaches. Modern neuroimaging techniques therefore provide a valuable tool to gain insight into possible pathophysiological mechanisms of sleep disorders in adult humans. Citation: Desseilles M; Dang-Vu TD; Schabus M; Sterpenich V; Maquet P; Schwartz S. Neuroimaging insights into the pathophysiology of sleep disorders. SLEEP 2008;31(6):777–794. PMID:18548822

Sleep, Sleep Disorders, and Mild Traumatic Brain Injury. What We Know and What We Need to Know: Findings from a National Working Group.

PubMed

Wickwire, Emerson M; Williams, Scott G; Roth, Thomas; Capaldi, Vincent F; Jaffe, Michael; Moline, Margaret; Motamedi, Gholam K; Morgan, Gregory W; Mysliwiec, Vincent; Germain, Anne; Pazdan, Renee M; Ferziger, Reuven; Balkin, Thomas J; MacDonald, Margaret E; Macek, Thomas A; Yochelson, Michael R; Scharf, Steven M; Lettieri, Christopher J

2016-04-01

Disturbed sleep is one of the most common complaints following traumatic brain injury (TBI) and worsens morbidity and long-term sequelae. Further, sleep and TBI share neurophysiologic underpinnings with direct relevance to recovery from TBI. As such, disturbed sleep and clinical sleep disorders represent modifiable treatment targets to improve outcomes in TBI. This paper presents key findings from a national working group on sleep and TBI, with a specific focus on the testing and development of sleep-related therapeutic interventions for mild TBI (mTBI). First, mTBI and sleep physiology are briefly reviewed. Next, essential empirical and clinical questions and knowledge gaps are addressed. Finally, actionable recommendations are offered to guide active and efficient collaboration between academic, industry, and governmental stakeholders.

Co-activated yet disconnected-Neural correlates of eye closures when trying to stay awake.

PubMed

Ong, Ju Lynn; Kong, Danyang; Chia, Tiffany T Y; Tandi, Jesisca; Thomas Yeo, B T; Chee, Michael W L

2015-09-01

Spontaneous eye-closures that herald sleep onset become more frequent when we are sleep deprived. Although these are typically associated with decreased responsiveness to external stimuli, it is less clear what occurs in the brain at these transitions to drowsiness and light sleep. To investigate this, task-free fMRI of sleep-deprived participants was acquired. BOLD activity associated with periods of spontaneously occurring eye closures were marked and analyzed. We observed concurrent and extensive hypnagogic co-activation of the extrastriate visual, auditory, and somatosensory cortices as well as the default mode network, consistent with internal sensory activity without external stimulation. Co-activation of fronto-parietal areas known to mediate attentional control could correspond with participants resisting sleep or additional engagement of mental imagery. This constellation of signal changes differed from those elicited by cued eye closures of similar duration and distribution in the same, rested participants. They also differ from signal changes associated with mind-wandering and consolidated light sleep. Concurrent with the observed event-related changes, eye closures elicited additional reduction in functional connectivity within nodes of the DMN and DAN, superposed on already reduced connectivity associated with sleep deprivation. There was concurrent deactivation of the thalamus during eye-closure during the sleep-deprived state but almost similar changes occurred in the well-rested state that may also be relevant. These findings highlight the dynamic shifts in brain activity and connectivity at border between wakefulness and sleep. Copyright © 2015. Published by Elsevier Inc.

Prediction of general mental ability based on neural oscillation measures of sleep.

PubMed

Bódizs, Róbert; Kis, Tamás; Lázár, Alpár Sándor; Havrán, Linda; Rigó, Péter; Clemens, Zsófia; Halász, Péter

2005-09-01

The usual assessment of general mental ability (or intelligence) is based on performance attained in reasoning and problem-solving tasks. Differences in general mental ability have been associated with event-related neural activity patterns of the wakeful working brain or physical, chemical and electrical brain features measured during wakeful resting conditions. Recent evidences suggest that specific sleep electroencephalogram oscillations are related to wakeful cognitive performances. Our aim is to reveal the relationship between non-rapid eye movement sleep-specific oscillations (the slow oscillation, delta activity, slow and fast sleep spindle density, the grouping of slow and fast sleep spindles) and general mental ability assessed by the Raven Progressive Matrices Test (RPMT). The grouping of fast sleep spindles by the cortical slow oscillation in the left frontopolar derivation (Fp1) as well as the density of fast sleep spindles over the right frontal area (Fp2, F4), correlated positively with general mental ability. Data from those selected electrodes that showed the high correlations with general mental ability explained almost 70% of interindividual variance in RPMT scores. Results suggest that individual differences in general mental ability are reflected in fast sleep spindle-related oscillatory activity measured over the frontal cortex.

The Fate of Incoming Stimuli during NREM Sleep is Determined by Spindles and the Phase of the Slow Oscillation.

PubMed

Schabus, Manuel; Dang-Vu, Thien Thanh; Heib, Dominik Philip Johannes; Boly, Mélanie; Desseilles, Martin; Vandewalle, Gilles; Schmidt, Christina; Albouy, Geneviève; Darsaud, Annabelle; Gais, Steffen; Degueldre, Christian; Balteau, Evelyne; Phillips, Christophe; Luxen, André; Maquet, Pierre

2012-01-01

The present study aimed at identifying the neurophysiological responses associated with auditory stimulation during non-rapid eye movement (NREM) sleep using simultaneous electroencephalography (EEG)/functional magnetic resonance imaging (fMRI) recordings. It was reported earlier that auditory stimuli produce bilateral activation in auditory cortex, thalamus, and caudate during both wakefulness and NREM sleep. However, due to the spontaneous membrane potential fluctuations cortical responses may be highly variable during NREM. Here we now examine the modulation of cerebral responses to tones depending on the presence or absence of sleep spindles and the phase of the slow oscillation. Thirteen healthy young subjects were scanned successfully during stage 2-4 NREM sleep in the first half of the night in a 3 T scanner. Subjects were not sleep-deprived and sounds were post hoc classified according to (i) the presence of sleep spindles or (ii) the phase of the slow oscillation during (±300 ms) tone delivery. These detected sounds were then entered as regressors of interest in fMRI analyses. Interestingly wake-like responses - although somewhat altered in size and location - persisted during NREM sleep, except during present spindles (as previously published in Dang-Vu et al., 2011) and the negative going phase of the slow oscillation during which responses became less consistent or even absent. While the phase of the slow oscillation did not alter brain responses in primary sensory cortex, it did modulate responses at higher cortical levels. In addition EEG analyses show a distinct N550 response to tones during the presence of light sleep spindles and suggest that in deep NREM sleep the brain is more responsive during the positive going slope of the slow oscillation. The presence of short temporal windows during which the brain is open to external stimuli is consistent with the fact that even during deep sleep meaningful events can be detected. Altogether, our results emphasize the notion that spontaneous fluctuations of brain activity profoundly modify brain responses to external information across all behavioral states, including deep NREM sleep.

Nurses' Awareness of Preterm Neonates' Sleep in the NICU.

PubMed

Mahmoodi, Nasrin; Arbabisarjou, Azizollah; Rezaeipoor, Mahmood; Pishkar Mofrad, Zahra

2015-11-17

Fetus and neonate spend most of their time sleeping inside and outside the womb. Sleep is considered a crucial action of neonatal period similar to breathing and nutrition. It plays a key role in brain development. Today, it is shown that sleep plays a predominant role in body temperature regulation, energy saving and neuronal detoxification. Sleep is the most important behavioral state of neonates, particularly in preterm ones. Noise, light, invasive treatment and caring activities are among disturbing factors in the neonatal intensive care unit (NICU) that leave negative impacts on brain development through disturbing the sleep process. This descriptive study assessed all NICU nurses of Ali-ibn-Abitaleb hospital using the census sampling method. Demographic data was collected through a questionnaire with 10 questions about active sleep (AS) cycles, also referred to as REM, methods for inducing AS and AS specifications in neonates. The questionnaire was distributed between the nurses. After completion, data was analyzed using SPSS 16 and descriptive statistics method. According to analyses, 24%, 20%, 48% and 92% of nurses gave correct answers to questions about AS cycle, AS in neonates, the role of sleep in saving energy and ideal noise level, respectively. According to results, nurses had a low level of knowledge towards neonatal sleep. All nurses need to know the importance of sleep in preterm neonates. The main role of inducing sleep is to protect the development of the neonates' brain in the NICU. Those nurses who spend a remarkable portion of their time for caring neonates in the NICU play a significant role in neonatal sleep care.

In Vivo Imaging of the Central and Peripheral Effects of Sleep Deprivation and Suprachiasmatic Nuclei Lesion on PERIOD-2 Protein in Mice.

PubMed

Curie, Thomas; Maret, Stephanie; Emmenegger, Yann; Franken, Paul

2015-09-01

That sleep deprivation increases the brain expression of various clock genes has been well documented. Based on these and other findings we hypothesized that clock genes not only underlie circadian rhythm generation but are also implicated in sleep homeostasis. However, long time lags have been reported between the changes in the clock gene messenger RNA levels and their encoded proteins. It is therefore crucial to establish whether also protein levels increase within the time frame known to activate a homeostatic sleep response. We report on the central and peripheral effects of sleep deprivation on PERIOD-2 (PER2) protein both in intact and suprachiasmatic nuclei-lesioned mice. In vivo and in situ PER2 imaging during baseline, sleep deprivation, and recovery. Mouse sleep-recording facility. Per2::Luciferase knock-in mice. N/A. Six-hour sleep deprivation increased PER2 not only in the brain but also in liver and kidney. Remarkably, the effects in the liver outlasted those observed in the brain. Within the brain the increase in PER2 concerned the cerebral cortex mainly, while leaving suprachiasmatic nuclei (SCN) levels unaffected. Against expectation, sleep deprivation did not increase PER2 in the brain of arrhythmic SCN-lesioned mice because of higher PER2 levels in baseline. In contrast, liver PER2 levels did increase in these mice similar to the sham and partially lesioned controls. Our results stress the importance of considering both sleep-wake dependent and circadian processes when quantifying clock-gene levels. Because sleep deprivation alters PERIOD-2 in the brain as well as in the periphery, it is tempting to speculate that clock genes constitute a common pathway mediating the shared and well-known adverse effects of both chronic sleep loss and disrupted circadian rhythmicity on metabolic health. © 2015 Associated Professional Sleep Societies, LLC.

The sequential hypothesis of sleep function. IV. A correlative analysis of sleep variables in learning and nonlearning rats.

PubMed

Langella, M; Colarieti, L; Ambrosini, M V; Giuditta, A

1992-02-01

Female adult rats were trained for a two-way active avoidance task (4 h), and allowed free sleep (3 h). Control rats (C) were left in their home cages during the acquisition period. Dural electrodes and an intraventricular cannula, implanted one week in advance, were used for EEG recording during the period of sleep and for the injection of [3H]thymidine at the beginning of the training session, respectively. Rats were killed at the end of the sleep period, and the DNA-specific activity was determined in the main brain regions and in liver. Correlations among sleep, behavioral and biochemical variables were assessed using Spearman's nonparametric method. In learning rats (L), the number of avoidances was negatively correlated with SS-W variables, and positively correlated with SS-PS variables (episodes of synchronized sleep followed by wakefulness or paradoxical sleep, respectively) and with PS variables. An inverse pattern of correlations was shown by the number of escapes or freezings. No correlations occurred in rats unable to achieve the learning criterion (NL). In L rats, the specific activity of brain DNA was negatively correlated with SS-W variables and positively correlated with SS-PS variables, while essentially no correlation concerned PS variables. On the other hand, in NL rats, comparable correlations were positive with SS-W variables and negative with SS-PS and PS variables. Few and weak correlations occurred in C rats. The data support a role of SS in brain information processing, as postulated by the sequential hypothesis on the function of sleep. In addition, they suggest that the elimination of nonadaptive memory traces may require several SS-W episodes and a terminal SS-PS episode. During PS episodes, adaptive memory traces cleared of nonadaptive components may be copied in more suitable brain sites.

Brain Energetics During the Sleep-Wake Cycle

PubMed Central

DiNuzzo, Mauro; Nedergaard, Maiken

2017-01-01

Brain activity during wakefulness is associated with high metabolic rates that are believed to support information processing and memory encoding. In spite of loss of consciousness, sleep still carries a substantial energy cost. Experimental evidence supports a cerebral metabolic shift taking place during sleep that suppresses aerobic glycolysis, a hallmark of environment-oriented waking behavior and synaptic plasticity. Recent studies reveal that glial astrocytes respond to the reduction of wake-promoting neuromodulators by regulating volume, composition and glymphatic drainage of interstitial fluid. These events are accompanied by changes in neuronal discharge patterns, astrocyte-neuron interactions, synaptic transactions and underlying metabolic features. Internally-generated neuronal activity and network homeostasis are proposed to account for the high sleep-related energy demand. PMID:29024871

Memory Processing: Ripples in the Resting Brain.

PubMed

Walker, Matthew P; Robertson, Edwin M

2016-03-21

Recent work has shown that, during sleep, a functional circuit is created amidst a general breakdown in connectivity following fast-frequency bursts of brain activity. The findings question the unconscious nature of deep sleep, and provide an explanation for its contribution to memory processing. Copyright © 2016 Elsevier Ltd. All rights reserved.

Spontaneous activity of single neurones in the hypothalamus of rabbits during sleep and waking

PubMed Central

Findlay, Alan L. R.; Hayward, James N.

1969-01-01

1. A method is described for recording from single cells in the hypothalamus of unanaesthetized freely moving rabbits. Behaviour, bodily movement, skin and brain temperatures and e.e.g. were monitored. 2. Patterns of unit firing during slow sleep, paradoxical sleep and waking were studied in several regions of the hypothalamus, thalamus and in the septum. 3. Of the 144 cells analysed from waking to slow sleep, fifty-six (39%) decreased mean firing rates, thirty (21%) increased spike discharges and fifty-eight (40%) showed no marked change. Dorsal hypothalamic and massa intermedia thalamic cells fired in brief high frequency clusters during slow sleep with a characteristic `bimodal' interspike interval histogram. Waking and paradoxical sleep abolished these cluster discharges with a concomitant change to an `asymmetric' histogram. 4. Of the thirty-two cells observed during the three states of waking, slow sleep and paradoxical sleep, a majority (twenty-five or 78%) showed their highest rates of spontaneous discharge during paradoxical sleep. Discharge rates of cells sometimes changed in the course of paradoxical sleep according to the presence or absence of phasic events such as myoclonic motor activity. Two hypothalmic cells were almost totally arrested during paradoxical sleep. 5. Analysis of unit firing rates during spontaneous rises in brain temperature during waking and paradoxical sleep revealed that a majority of the neurones (22/24) changed their discharge rates in relation to behaviour rather than to brain temperature. Two cells did appear to respond specifically to the central thermal stimulus. 6. Hypothalamic cells do not behave as a homogeneous population in relation to changes in the state of arousal of the rabbit. Spontaneous changes in cell discharge related to sleep-waking behaviour must be considered in any interpretation of hypothalamic unit activity as related to neuroendocrine or autonomic mechanisms. PMID:4304342

Medical Imaging for Understanding Sleep Regulation

NASA Astrophysics Data System (ADS)

Wong, Kenneth

2011-10-01

Sleep is essential for the health of the nervous system. Lack of sleep has a profound negative effect on cognitive ability and task performance. During sustained military operations, soldiers often suffer from decreased quality and quantity of sleep, increasing their susceptibility to neurological problems and limiting their ability to perform the challenging mental tasks that their missions require. In the civilian sector, inadequate sleep and overt sleep pathology are becoming more common, with many detrimental impacts. There is a strong need for new, in vivo studies of human brains during sleep, particularly the initial descent from wakefulness. Our research team is investigating sleep using a combination of magnetic resonance imaging (MRI), positron emission tomography (PET), and electroencephalography (EEG). High resolution MRI combined with PET enables localization of biochemical processes (e.g., metabolism) to anatomical structures. MRI methods can also be used to examine functional connectivity among brain regions. Neural networks are dynamically reordered during different sleep stages, reflecting the disconnect with the waking world and the essential yet unconscious brain activity that occurs during sleep.[4pt] In collaboration with Linda Larson-Prior, Washington University; Alpay Ozcan, Virginia Tech; Seong Mun, Virginia Tech; and Zang-Hee Cho, Gachon University.

SLEEP - Williams wearing sleep net

NASA Image and Video Library

1998-05-12

STS090-377-011 (17 APRIL-3 MAY 1998) --- Astronaut Dafydd R. (Dave) Williams, mission specialist representing the Canadian Space Agency (CSA), accomplishes more than one purpose when he sleeps in this bunk aboard the Earth-orbiting Space Shuttle Columbia. Conducting a Neurolab sleep experiment, Williams wears equipment which includes a sleep net (mesh cap that monitors and records brain waves); a Respiratory Inductance Plethysmograph (RIP) suit for monitoring respiration; and an activity monitor -- a device (out of view) worn on the wrist to detect and record body movement. Data on brain waves, eye movements, respiration, heart rate, and oxygen concentration are routed to a portable data recorder. The entire system has capabilities similar to a fully equipped sleep laboratory on Earth. The sleeping bag is conventional Shuttle ware and not part of the experiment.

Linking melanism to brain development: expression of a melanism-related gene in barn owl feather follicles covaries with sleep ontogeny

PubMed Central

2013-01-01

Background Intra-specific variation in melanocyte pigmentation, common in the animal kingdom, has caught the eye of naturalists and biologists for centuries. In vertebrates, dark, eumelanin pigmentation is often genetically determined and associated with various behavioral and physiological traits, suggesting that the genes involved in melanism have far reaching pleiotropic effects. The mechanisms linking these traits remain poorly understood, and the potential involvement of developmental processes occurring in the brain early in life has not been investigated. We examined the ontogeny of rapid eye movement (REM) sleep, a state involved in brain development, in a wild population of barn owls (Tyto alba) exhibiting inter-individual variation in melanism and covarying traits. In addition to sleep, we measured melanistic feather spots and the expression of a gene in the feather follicles implicated in melanism (PCSK2). Results As in mammals, REM sleep declined with age across a period of brain development in owlets. In addition, inter-individual variation in REM sleep around this developmental trajectory was predicted by variation in PCSK2 expression in the feather follicles, with individuals expressing higher levels exhibiting a more precocial pattern characterized by less REM sleep. Finally, PCSK2 expression was positively correlated with feather spotting. Conclusions We demonstrate that the pace of brain development, as reflected in age-related changes in REM sleep, covaries with the peripheral activation of the melanocortin system. Given its role in brain development, variation in nestling REM sleep may lead to variation in adult brain organization, and thereby contribute to the behavioral and physiological differences observed between adults expressing different degrees of melanism. PMID:23886007

Plasticity of brain wave network interactions and evolution across physiologic states

PubMed Central

Liu, Kang K. L.; Bartsch, Ronny P.; Lin, Aijing; Mantegna, Rosario N.; Ivanov, Plamen Ch.

2015-01-01

Neural plasticity transcends a range of spatio-temporal scales and serves as the basis of various brain activities and physiologic functions. At the microscopic level, it enables the emergence of brain waves with complex temporal dynamics. At the macroscopic level, presence and dominance of specific brain waves is associated with important brain functions. The role of neural plasticity at different levels in generating distinct brain rhythms and how brain rhythms communicate with each other across brain areas to generate physiologic states and functions remains not understood. Here we perform an empirical exploration of neural plasticity at the level of brain wave network interactions representing dynamical communications within and between different brain areas in the frequency domain. We introduce the concept of time delay stability (TDS) to quantify coordinated bursts in the activity of brain waves, and we employ a system-wide Network Physiology integrative approach to probe the network of coordinated brain wave activations and its evolution across physiologic states. We find an association between network structure and physiologic states. We uncover a hierarchical reorganization in the brain wave networks in response to changes in physiologic state, indicating new aspects of neural plasticity at the integrated level. Globally, we find that the entire brain network undergoes a pronounced transition from low connectivity in Deep Sleep and REM to high connectivity in Light Sleep and Wake. In contrast, we find that locally, different brain areas exhibit different network dynamics of brain wave interactions to achieve differentiation in function during different sleep stages. Moreover, our analyses indicate that plasticity also emerges in frequency-specific networks, which represent interactions across brain locations mediated through a specific frequency band. Comparing frequency-specific networks within the same physiologic state we find very different degree of network connectivity and link strength, while at the same time each frequency-specific network is characterized by a different signature pattern of sleep-stage stratification, reflecting a remarkable flexibility in response to change in physiologic state. These new aspects of neural plasticity demonstrate that in addition to dominant brain waves, the network of brain wave interactions is a previously unrecognized hallmark of physiologic state and function. PMID:26578891

Shared Genetic Control of Brain Activity During Sleep and Insulin Secretion: A Laboratory-Based Family Study.

PubMed

Morselli, Lisa L; Gamazon, Eric R; Tasali, Esra; Cox, Nancy J; Van Cauter, Eve; Davis, Lea K

2018-01-01

Over the past 20 years, a large body of experimental and epidemiologic evidence has linked sleep duration and quality to glucose homeostasis, although the mechanistic pathways remain unclear. The aim of the current study was to determine whether genetic variation influencing both sleep and glucose regulation could underlie their functional relationship. We hypothesized that the genetic regulation of electroencephalographic (EEG) activity during non-rapid eye movement sleep, a highly heritable trait with fingerprint reproducibility, is correlated with the genetic control of metabolic traits including insulin sensitivity and β-cell function. We tested our hypotheses through univariate and bivariate heritability analyses in a three-generation pedigree with in-depth phenotyping of both sleep EEG and metabolic traits in 48 family members. Our analyses accounted for age, sex, adiposity, and the use of psychoactive medications. In univariate analyses, we found significant heritability for measures of fasting insulin sensitivity and β-cell function, for time spent in slow-wave sleep, and for EEG spectral power in the delta, theta, and sigma ranges. Bivariate heritability analyses provided the first evidence for a shared genetic control of brain activity during deep sleep and fasting insulin secretion rate. © 2017 by the American Diabetes Association.

Comparison of obese adults with poor versus good sleep quality during a functional neuroimaging delay discounting task: A pilot study.

PubMed

Martin, Laura E; Pollack, Lauren; McCune, Ashley; Schulte, Erica; Savage, Cary R; Lundgren, Jennifer D

2015-10-30

This study aimed to determine if obese adults with poor versus good sleep quality demonstrate reduced self-regulatory capacity and different patterns of neural activation when making impulsive monetary choices. Six obese, good quality sleepers (M age=44.7 years, M BMI=38.1 kg/m(2)) were compared to 13 obese, poor quality sleepers (M age=42.6, M BMI=39.2 kg/m(2)) on sleep and eating behavior and brain activation in prefrontal and insular regions while engaging in a delay discounting task during functional magnetic resonance imaging (fMRI). Poor quality sleepers demonstrated significantly lower brain activation in the right inferior frontal gyrus, right middle frontal gyrus, and bilateral insula when making immediate and smaller (impulsive) monetary choices compared to the baseline condition. Behaviorally, poor compared to good quality sleepers reported higher scores in the night eating questionnaire. Obese adults with poor sleep quality demonstrate decreased brain activation in multiple regions that regulate cognitive control and interceptive awareness, possibly reducing self-regulatory capacity when making immediately gratifying decisions. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Stroop Task-Related Brain Activity in Patients With Insomnia: Changes After Cognitive-Behavioral Therapy for Insomnia.

PubMed

Hwang, Jeong Yeon; Kim, Nambeom; Kim, Soohyun; Park, Juhyun; Choi, Jae-Won; Kim, Seog Ju; Kang, Chang-Ki; Lee, Yu Jin

2018-02-16

In the present study, we compared differences in brain activity during the Stroop task between patients with chronic insomnia disorder (CID) and good sleepers (GS). Furthermore, we evaluated changes in Stroop task-related brain activity after cognitive-behavioral therapy for insomnia (CBT-I). The final analysis included 21 patients with CID and 25 GS. All participants underwent functional magnetic resonance imaging (fMRI) while performing the color-word Stroop task. CBT-I, consisting of 5 sessions, was administered to 14 patients with CID in the absence of medication. After CBT-I, fMRI was repeated in the patients with CID while performing the same task. Sleep-related questionnaires and sleep variables from a sleep diary were also obtained before and after CBT-I. No significant differences in behavioral performance in the Stroop task or task-related brain activation were observed between the CID and GS groups. No changes in behavioral performance or brain activity were found after CBT-I. However, clinical improvement in the Insomnia Severity Index (ISI) score was significantly associated with changes in the Stroop task-related regional blood oxygen level-dependent signals in the left supramarginal gyrus. Our findings suggest that cognitive impairment in patients with CID was not detectable by the Stroop task or Stroop task-related brain activation on fMRI. Moreover, there was no altered brain activity during the Stroop task after CBT-I. However, the ISI score reflected changes in the neural correlates of cognitive processes in patients with CID after CBT-I.

Slow waves, sharp waves, ripples, and REM in sleeping dragons.

PubMed

Shein-Idelson, Mark; Ondracek, Janie M; Liaw, Hua-Peng; Reiter, Sam; Laurent, Gilles

2016-04-29

Sleep has been described in animals ranging from worms to humans. Yet the electrophysiological characteristics of brain sleep, such as slow-wave (SW) and rapid eye movement (REM) activities, are thought to be restricted to mammals and birds. Recording from the brain of a lizard, the Australian dragon Pogona vitticeps, we identified SW and REM sleep patterns, thus pushing back the probable evolution of these dynamics at least to the emergence of amniotes. The SW and REM sleep patterns that we observed in lizards oscillated continuously for 6 to 10 hours with a period of ~80 seconds. The networks controlling SW-REM antagonism in amniotes may thus originate from a common, ancient oscillator circuit. Lizard SW dynamics closely resemble those observed in rodent hippocampal CA1, yet they originate from a brain area, the dorsal ventricular ridge, that has no obvious hodological similarity with the mammalian hippocampus. Copyright © 2016, American Association for the Advancement of Science.

In Vivo Imaging of the Central and Peripheral Effects of Sleep Deprivation and Suprachiasmatic Nuclei Lesion on PERIOD-2 Protein in Mice

PubMed Central

Curie, Thomas; Maret, Stephanie; Emmenegger, Yann; Franken, Paul

2015-01-01

Study Objectives: That sleep deprivation increases the brain expression of various clock genes has been well documented. Based on these and other findings we hypothesized that clock genes not only underlie circadian rhythm generation but are also implicated in sleep homeostasis. However, long time lags have been reported between the changes in the clock gene messenger RNA levels and their encoded proteins. It is therefore crucial to establish whether also protein levels increase within the time frame known to activate a homeostatic sleep response. We report on the central and peripheral effects of sleep deprivation on PERIOD-2 (PER2) protein both in intact and suprachiasmatic nuclei-lesioned mice. Design: In vivo and in situ PER2 imaging during baseline, sleep deprivation, and recovery. Settings: Mouse sleep-recording facility. Participants: Per2::Luciferase knock-in mice. Interventions: N/A. Measurements and Results: Six-hour sleep deprivation increased PER2 not only in the brain but also in liver and kidney. Remarkably, the effects in the liver outlasted those observed in the brain. Within the brain the increase in PER2 concerned the cerebral cortex mainly, while leaving suprachiasmatic nuclei (SCN) levels unaffected. Against expectation, sleep deprivation did not increase PER2 in the brain of arrhythmic SCN-lesioned mice because of higher PER2 levels in baseline. In contrast, liver PER2 levels did increase in these mice similar to the sham and partially lesioned controls. Conclusions: Our results stress the importance of considering both sleep-wake dependent and circadian processes when quantifying clock-gene levels. Because sleep deprivation alters PERIOD-2 in the brain as well as in the periphery, it is tempting to speculate that clock genes constitute a common pathway mediating the shared and well-known adverse effects of both chronic sleep loss and disrupted circadian rhythmicity on metabolic health. Citation: Curie T, Maret S, Emmenegger Y, Franken P. In vivo imaging of the central and peripheral effects of sleep deprivation and suprachiasmatic nuclei lesion on PERIOD-2 protein in mice. SLEEP 2015;38(9):1381–1394. PMID:25581923

Drosophila Neuropeptide F Signaling Independently Regulates Feeding and Sleep-Wake Behavior.

PubMed

Chung, Brian Y; Ro, Jennifer; Hutter, Sabine A; Miller, Kylie M; Guduguntla, Lakshmi S; Kondo, Shu; Pletcher, Scott D

2017-06-20

Proper regulation of sleep-wake behavior and feeding is essential for organismal health and survival. While previous studies have isolated discrete neural loci and substrates important for either sleep or feeding, how the brain is organized to coordinate both processes with respect to one another remains poorly understood. Here, we provide evidence that the Drosophila Neuropeptide F (NPF) network forms a critical component of both adult sleep and feeding regulation. Activation of NPF signaling in the brain promotes wakefulness and adult feeding, likely through its cognate receptor NPFR. Flies carrying a loss-of-function NPF allele do not suppress sleep following prolonged starvation conditions, suggesting that NPF acts as a hunger signal to keep the animal awake. NPF-expressing cells, specifically those expressing the circadian photoreceptor cryptochrome, are largely responsible for changes to sleep behavior caused by NPF neuron activation, but not feeding, demonstrating that different NPF neurons separately drive wakefulness and hunger. Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.

Sleep and Predicted Cognitive Performance of New Cadets during Cadet Basic Training at the United States Military Academy

DTIC Science & Technology

2005-09-01

7 B. SLEEP ARCHITECTURE..................................7 1. Circadian Rhythm and Human Sleep Drive...body temperature. Van Dongen & Dinges, 2000 ....10 Figure 2. EEG of Human Brain Activity During Sleep. http://ist-socrates.berkeley.edu/~jmp...the predicted levels of human performance based on circadian rhythms , amount and quality of sleep, and combines cognitive performance 5 predictions

Different Simultaneous Sleep States in the Hippocampus and Neocortex.

PubMed

Emrick, Joshua J; Gross, Brooks A; Riley, Brett T; Poe, Gina R

2016-12-01

Investigators assign sleep-waking states using brain activity collected from a single site, with the assumption that states occur at the same time throughout the brain. We sought to determine if sleep-waking states differ between two separate structures: the hippocampus and neocortex. We measured electrical signals (electroencephalograms and electromyograms) during sleep from the hippocampus and neocortex of five freely behaving adult male rats. We assigned sleep-waking states in 10-sec epochs based on standard scoring criteria across a 4-h recording, then analyzed and compared states and signals from simultaneous epochs between sites. We found that the total amount of each state, assigned independently using the hippocampal and neocortical signals, was similar between the hippocampus and neocortex. However, states at simultaneous epochs were different as often as they were the same (P = 0.82). Furthermore, we found that the progression of states often flowed through asynchronous state-pairs led by the hippocampus. For example, the hippocampus progressed from transition-to-rapid eye movement sleep to rapid eye movement sleep before the neocortex more often than in synchrony with the neocortex (38.7 ± 16.2% versus 15.8 ± 5.6% mean ± standard error of the mean). We demonstrate that hippocampal and neocortical sleep-waking states often differ in the same epoch. Consequently, electrode location affects estimates of sleep architecture, state transition timing, and perhaps even percentage of time in sleep states. Therefore, under normal conditions, models assuming brain state homogeneity should not be applied to the sleeping or waking brain. © 2016 Associated Professional Sleep Societies, LLC.

Cardiovascular and respiratory dynamics during normal and pathological sleep

NASA Astrophysics Data System (ADS)

Penzel, Thomas; Wessel, Niels; Riedl, Maik; Kantelhardt, Jan W.; Rostig, Sven; Glos, Martin; Suhrbier, Alexander; Malberg, Hagen; Fietze, Ingo

2007-03-01

Sleep is an active and regulated process with restorative functions for physical and mental conditions. Based on recordings of brain waves and the analysis of characteristic patterns and waveforms it is possible to distinguish wakefulness and five sleep stages. Sleep and the sleep stages modulate autonomous nervous system functions such as body temperature, respiration, blood pressure, and heart rate. These functions consist of a sympathetic tone usually related to activation and to parasympathetic (or vagal) tone usually related to inhibition. Methods of statistical physics are used to analyze heart rate and respiration to detect changes of the autonomous nervous system during sleep. Detrended fluctuation analysis and synchronization analysis and their applications to heart rate and respiration during sleep in healthy subjects and patients with sleep disorders are presented. The observed changes can be used to distinguish sleep stages in healthy subjects as well as to differentiate normal and disturbed sleep on the basis of heart rate and respiration recordings without direct recording of brain waves. Of special interest are the cardiovascular consequences of disturbed sleep because they present a risk factor for cardiovascular disorders such as arterial hypertension, cardiac ischemia, sudden cardiac death, and stroke. New derived variables can help to find indicators for these health risks.

Sleep: A synchrony of cell activity-driven small network states

PubMed Central

Krueger, James M.; Huang, Yanhua; Rector, David M.; Buysse, Daniel J.

2013-01-01

We posit a bottom-up sleep regulatory paradigm in which state changes are initiated within small networks as a consequence of local cell activity. Bottom-up regulatory mechanisms are prevalent throughout nature, occurring in vastly different systems and levels of organization. Synchronization of state without top-down regulation is a fundamental property of large collections of small semi-autonomous entities. We posit that such synchronization mechanisms are sufficient and necessary for whole organism sleep onset. Within brain we posit that small networks of highly interconnected neurons and glia, e.g. cortical columns, are semi-autonomous units oscillating between sleep-like and wake-like states. We review evidence showing that cells, small networks, and regional areas of brain share sleep-like properties with whole animal sleep. A testable hypothesis focused on how sleep is initiated within local networks is presented. We posit that the release of cell activity-dependent molecules, such as ATP and nitric oxide, into the extracellular space initiates state changes within the local networks where they are produced. We review mechanisms of ATP induction of sleep regulatory substances (SRS) and their actions on receptor trafficking. Finally, we provide an example of how such local metabolic and state changes provide mechanistic explanations for clinical conditions such as insomnia. PMID:23651209

Valeriana wallichii root extract improves sleep quality and modulates brain monoamine level in rats.

PubMed

Sahu, Surajit; Ray, Koushik; Yogendra Kumar, M S; Gupta, Shilpa; Kauser, Hina; Kumar, Sanjeev; Mishra, Kshipra; Panjwani, Usha

2012-07-15

The present study was performed to investigate the effects of Valeriana wallichi (VW) aqueous root extract on sleep-wake profile and level of brain monoamines on Sprague-Dawley rats. Electrodes and transmitters were implanted to record EEG and EMG in freely moving condition and the changes were recorded telemetrically after oral administration of VW in the doses of 100, 200 and 300 mg/kg body weight. Sleep latency was decreased and duration of non-rapid eye movement (NREM) sleep was increased in a dose dependent manner. A significant decrease of sleep latency and duration of wakefulness were observed with VW at doses of 200 and 300 mg/kg. Duration of NREM sleep as well as duration of total sleep was increased significantly after treatment with VW at the doses of 200 and 300 mg/kg. VW also increased EEG slow wave activity during NREM sleep at the doses of 200 and 300 mg/kg. Level of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT) and hydroxy indole acetic acid (HIAA) were measured in frontal cortex and brain stem after VW treatment at the dose of 200mg/kg. NE and 5HT level were decreased significantly in both frontal cortex and brain stem. DA and HIAA level significantly decreased only in cortex. DOPAC level was not changed in any brain region studied. In conclusion it can be said that VW water extract has a sleep quality improving effect which may be dependent upon levels of monoamines in cortex and brainstem. Copyright © 2012 Elsevier GmbH. All rights reserved.

Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation

PubMed Central

Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich

2017-01-01

Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep. PMID:28980941

Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation.

PubMed

Holst, Sebastian C; Sousek, Alexandra; Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich; Tafti, Mehdi; Landolt, Hans-Peter

2017-10-05

Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep.

Urodynamic function during sleep-like brain states in urethane anesthetized rats.

PubMed

Crook, J; Lovick, T

2016-01-28

The aim was to investigate urodynamic parameters and functional excitability of the periaqueductal gray matter (PAG) during changes in sleep-like brain states in urethane anesthetized rats. Simultaneous recordings of detrusor pressure, external urethral sphincter (EUS) electromyogram (EMG), cortical electroencephalogram (EEG), and single-unit activity in the PAG were made during repeated voiding induced by continuous infusion of saline into the bladder. The EEG cycled between synchronized, high-amplitude slow wave activity (SWA) and desynchronized low-amplitude fast activity similar to slow wave and 'activated' sleep-like brain states. During (SWA, 0.5-1.5 Hz synchronized oscillation of the EEG waveform) voiding became more irregular than in the 'activated' brain state (2-5 Hz low-amplitude desynchronized EEG waveform) and detrusor void pressure threshold, void volume threshold and the duration of bursting activity in the external urethral sphincter EMG were raised. The spontaneous firing rate of 23/52 neurons recorded within the caudal PAG and adjacent tegmentum was linked to the EEG state, with the majority of responsive cells (92%) firing more slowly during SWA. Almost a quarter of the cells recorded (12/52) showed phasic changes in firing rate that were linked to the occurrence of voids. Inhibition (n=6), excitation (n=4) or excitation/inhibition (n=2) was seen. The spontaneous firing rate of 83% of the micturition-responsive cells was sensitive to changes in EEG state. In nine of the 12 responsive cells (75%) the responses were reduced during SWA. We propose that during different sleep-like brain states changes in urodynamic properties occur which may be linked to changing excitability of the micturition circuitry in the periaqueductal gray. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.

Sleep, consciousness and the spontaneous and evoked electrical activity of the brain. Is there a cortical integrating mechanism?

PubMed

Evans, B M

2003-02-01

The physiological mechanisms that underlie consciousness and unconsciousness are the sleep/wake mechanisms. Deep sleep is a state of physiological reversible unconsciousness. The change from that state to wakefulness is mediated by the reticular activating mechanism. The reverse change from wakefulness to sleep is also an active process effected by an arousal inhibitory mechanism based on a partial blockade of the thalamus and upper brain stem, associated with thalamic sleep spindles and also with cortical sub-delta activity (<1 Hz). The deactivation of the thalamus has been demonstrated both electrically and by positron emission tomography during deep sleep. Normally, wakefulness is associated with instant awareness (defined as the ability to integrate all sensory information from the external environment and the internal environment of the body). Awareness may be a function of the thalamo-cortical network in the cerebral hemispheres, which forms the final path of the sleep/wake mechanism. Anatomical and physiological studies suggest that there may be a double thalamo-cortical network; one relating to cortical and thalamic areas with specific functions and the other global, involving all cortical areas and so-called 'non-specific' thalamic nuclei. The global system might function as a cortical integrating mechanism permitting the spread of information between the specific cortical areas and thus underlying awareness. The global system may also be responsible for much of the spontaneous and evoked electrical activity of the brain. The cognitive change between sleep and wakefulness is accompanied by changes in the autonomic system, the cerebral blood flow and cerebral metabolism. Awareness is an essential component of total consciousness (defined as continuous awareness of the external and internal environment, both past and present, together with the emotions arising from it). In addition to awareness, full consciousness requires short-term and explicit memory and intact emotional responses.

Sleep Disrupts High-Level Speech Parsing Despite Significant Basic Auditory Processing.

PubMed

Makov, Shiri; Sharon, Omer; Ding, Nai; Ben-Shachar, Michal; Nir, Yuval; Zion Golumbic, Elana

2017-08-09

The extent to which the sleeping brain processes sensory information remains unclear. This is particularly true for continuous and complex stimuli such as speech, in which information is organized into hierarchically embedded structures. Recently, novel metrics for assessing the neural representation of continuous speech have been developed using noninvasive brain recordings that have thus far only been tested during wakefulness. Here we investigated, for the first time, the sleeping brain's capacity to process continuous speech at different hierarchical levels using a newly developed Concurrent Hierarchical Tracking (CHT) approach that allows monitoring the neural representation and processing-depth of continuous speech online. Speech sequences were compiled with syllables, words, phrases, and sentences occurring at fixed time intervals such that different linguistic levels correspond to distinct frequencies. This enabled us to distinguish their neural signatures in brain activity. We compared the neural tracking of intelligible versus unintelligible (scrambled and foreign) speech across states of wakefulness and sleep using high-density EEG in humans. We found that neural tracking of stimulus acoustics was comparable across wakefulness and sleep and similar across all conditions regardless of speech intelligibility. In contrast, neural tracking of higher-order linguistic constructs (words, phrases, and sentences) was only observed for intelligible speech during wakefulness and could not be detected at all during nonrapid eye movement or rapid eye movement sleep. These results suggest that, whereas low-level auditory processing is relatively preserved during sleep, higher-level hierarchical linguistic parsing is severely disrupted, thereby revealing the capacity and limits of language processing during sleep. SIGNIFICANCE STATEMENT Despite the persistence of some sensory processing during sleep, it is unclear whether high-level cognitive processes such as speech parsing are also preserved. We used a novel approach for studying the depth of speech processing across wakefulness and sleep while tracking neuronal activity with EEG. We found that responses to the auditory sound stream remained intact; however, the sleeping brain did not show signs of hierarchical parsing of the continuous stream of syllables into words, phrases, and sentences. The results suggest that sleep imposes a functional barrier between basic sensory processing and high-level cognitive processing. This paradigm also holds promise for studying residual cognitive abilities in a wide array of unresponsive states. Copyright © 2017 the authors 0270-6474/17/377772-10$15.00/0.

State-dependent changes in cortical gain control as measured by auditory evoked responses to varying intensity stimuli.

PubMed

Phillips, Derrick J; Schei, Jennifer L; Meighan, Peter C; Rector, David M

2011-11-01

Auditory evoked potential (AEP) components correspond to sequential activation of brain structures within the auditory pathway and reveal neural activity during sensory processing. To investigate state-dependent modulation of stimulus intensity response profiles within different brain structures, we assessed AEP components across both stimulus intensity and state. We implanted adult female Sprague-Dawley rats (N = 6) with electrodes to measure EEG, EKG, and EMG. Intermittent auditory stimuli (6-12 s) varying from 50 to 75 dBa were delivered over a 24-h period. Data were parsed into 2-s epochs and scored for wake/sleep state. All AEP components increased in amplitude with increased stimulus intensity during wake. During quiet sleep, however, only the early latency response (ELR) showed this relationship, while the middle latency response (MLR) increased at the highest 75 dBa intensity, and the late latency response (LLR) showed no significant change across the stimulus intensities tested. During rapid eye movement sleep (REM), both ELR and LLR increased, similar to wake, but MLR was severely attenuated. Stimulation intensity and the corresponding AEP response profile were dependent on both brain structure and sleep state. Lower brain structures maintained stimulus intensity and neural response relationships during sleep. This relationship was not observed in the cortex, implying state-dependent modification of stimulus intensity coding. Since AEP amplitude is not modulated by stimulus intensity during sleep, differences between paired 75/50 dBa stimuli could be used to determine state better than individual intensities.

Scaling and intermittency of brain events as a manifestation of consciousness

NASA Astrophysics Data System (ADS)

Paradisi, P.; Allegrini, P.; Gemignani, A.; Laurino, M.; Menicucci, D.; Piarulli, A.

2013-01-01

We discuss the critical brain hypothesis and its relationship with intermittent renewal processes displaying power-law decay in the distribution of waiting times between two consecutive renewal events. In particular, studies on complex systems in a "critical" condition show that macroscopic variables, integrating the activities of many individual functional units, undergo fluctuations with an intermittent serial structure characterized by avalanches with inverse-power-law (scale-free) distribution densities of sizes and inter-event times. This condition, which is denoted as "fractal intermittency", was found in the electroencephalograms of subjects observed during a resting state wake condition. It remained unsolved whether fractal intermittency correlates with the stream of consciousness or with a non-task-driven default mode activity, also present in non-conscious states, like deep sleep. After reviewing a method of scaling analysis of intermittent systems based of eventdriven random walks, we show that during deep sleep fractal intermittency breaks down, and reestablishes during REM (Rapid Eye Movement) sleep, with essentially the same anomalous scaling of the pre-sleep wake condition. From the comparison of the pre-sleep wake, deep sleep and REM conditions we argue that the scaling features of intermittent brain events are related to the level of consciousness and, consequently, could be exploited as a possible indicator of consciousness in clinical applications.

Virtual reality and consciousness inference in dreaming.

PubMed

Hobson, J Allan; Hong, Charles C-H; Friston, Karl J

2014-01-01

This article explores the notion that the brain is genetically endowed with an innate virtual reality generator that - through experience-dependent plasticity - becomes a generative or predictive model of the world. This model, which is most clearly revealed in rapid eye movement (REM) sleep dreaming, may provide the theater for conscious experience. Functional neuroimaging evidence for brain activations that are time-locked to rapid eye movements (REMs) endorses the view that waking consciousness emerges from REM sleep - and dreaming lays the foundations for waking perception. In this view, the brain is equipped with a virtual model of the world that generates predictions of its sensations. This model is continually updated and entrained by sensory prediction errors in wakefulness to ensure veridical perception, but not in dreaming. In contrast, dreaming plays an essential role in maintaining and enhancing the capacity to model the world by minimizing model complexity and thereby maximizing both statistical and thermodynamic efficiency. This perspective suggests that consciousness corresponds to the embodied process of inference, realized through the generation of virtual realities (in both sleep and wakefulness). In short, our premise or hypothesis is that the waking brain engages with the world to predict the causes of sensations, while in sleep the brain's generative model is actively refined so that it generates more efficient predictions during waking. We review the evidence in support of this hypothesis - evidence that grounds consciousness in biophysical computations whose neuronal and neurochemical infrastructure has been disclosed by sleep research.

Different Simultaneous Sleep States in the Hippocampus and Neocortex

PubMed Central

Emrick, Joshua J.; Gross, Brooks A.; Riley, Brett T.; Poe, Gina R.

2016-01-01

Study Objectives: Investigators assign sleep-waking states using brain activity collected from a single site, with the assumption that states occur at the same time throughout the brain. We sought to determine if sleep-waking states differ between two separate structures: the hippocampus and neocortex. Methods: We measured electrical signals (electroencephalograms and electromyograms) during sleep from the hippocampus and neocortex of five freely behaving adult male rats. We assigned sleep-waking states in 10-sec epochs based on standard scoring criteria across a 4-h recording, then analyzed and compared states and signals from simultaneous epochs between sites. Results: We found that the total amount of each state, assigned independently using the hippocampal and neocortical signals, was similar between the hippocampus and neocortex. However, states at simultaneous epochs were different as often as they were the same (P = 0.82). Furthermore, we found that the progression of states often flowed through asynchronous state-pairs led by the hippocampus. For example, the hippocampus progressed from transition-to-rapid eye movement sleep to rapid eye movement sleep before the neocortex more often than in synchrony with the neocortex (38.7 ± 16.2% versus 15.8 ± 5.6% mean ± standard error of the mean). Conclusions: We demonstrate that hippocampal and neocortical sleep-waking states often differ in the same epoch. Consequently, electrode location affects estimates of sleep architecture, state transition timing, and perhaps even percentage of time in sleep states. Therefore, under normal conditions, models assuming brain state homogeneity should not be applied to the sleeping or waking brain. Citation: Emrick JJ, Gross BA, Riley BT, Poe GR. Different simultaneous sleep states in the hippocampus and neocortex. SLEEP 2016;39(12):2201–2209. PMID:27748240

Cerebral correlates of delta waves during non-REM sleep revisited.

PubMed

Dang-Vu, Thien Thanh; Desseilles, Martin; Laureys, Steven; Degueldre, Christian; Perrin, Fabien; Phillips, Christophe; Maquet, Pierre; Peigneux, Philippe

2005-10-15

We aimed at characterizing the neural correlates of delta activity during Non Rapid Eye Movement (NREM) sleep in non-sleep-deprived normal young adults, based on the statistical analysis of a positron emission tomography (PET) sleep data set. One hundred fifteen PET scans were obtained using H(2)(15)O under continuous polygraphic monitoring during stages 2-4 of NREM sleep. Correlations between regional cerebral blood flow (rCBF) and delta power (1.5-4 Hz) spectral density were analyzed using statistical parametric mapping (SPM2). Delta power values obtained at central scalp locations negatively correlated during NREM sleep with rCBF in the ventromedial prefrontal cortex, the basal forebrain, the striatum, the anterior insula, and the precuneus. These regions embrace the set of brain areas in which rCBF decreases during slow wave sleep (SWS) as compared to Rapid Eye Movement (REM) sleep and wakefulness (Maquet, P., Degueldre, C., Delfiore, G., Aerts, J., Peters, J.M., Luxen, A., Franck, G., 1997. Functional neuroanatomy of human slow wave sleep. J. Neurosci. 17, 2807-S2812), supporting the notion that delta activity is a valuable prominent feature of NREM sleep. A strong association was observed between rCBF in the ventromedial prefrontal regions and delta power, in agreement with electrophysiological studies. In contrast to the results of a previous PET study investigating the brain correlates of delta activity (Hofle, N., Paus, T., Reutens, D., Fiset, P., Gotman, J., Evans, A.C., Jones, B.E., 1997. Regional cerebral blood flow changes as a function of delta and spindle activity during slow wave sleep in humans. J. Neurosci. 17, 4800-4808), in which waking scans were mixed with NREM sleep scans, no correlation was found with thalamus activity. This latter result stresses the importance of an extra-thalamic delta rhythm among the synchronous NREM sleep oscillations. Consequently, this rCBF distribution might preferentially reflect a particular modulation of the cellular processes involved in the generation of cortical delta waves during NREM sleep.

Do birds sleep in flight?

NASA Astrophysics Data System (ADS)

Rattenborg, Niels C.

2006-09-01

The following review examines the evidence for sleep in flying birds. The daily need to sleep in most animals has led to the common belief that birds, such as the common swift ( Apus apus), which spend the night on the wing, sleep in flight. The electroencephalogram (EEG) recordings required to detect sleep in flight have not been performed, however, rendering the evidence for sleep in flight circumstantial. The neurophysiology of sleep and flight suggests that some types of sleep might be compatible with flight. As in mammals, birds exhibit two types of sleep, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep. Whereas, SWS can occur in one or both brain hemispheres at a time, REM sleep only occurs bihemispherically. During unihemispheric SWS, the eye connected to the awake hemisphere remains open, a state that may allow birds to visually navigate during sleep in flight. Bihemispheric SWS may also be possible during flight when constant visual monitoring of the environment is unnecessary. Nevertheless, the reduction in muscle tone that usually accompanies REM sleep makes it unlikely that birds enter this state in flight. Upon landing, birds may need to recover the components of sleep that are incompatible with flight. Periods of undisturbed postflight recovery sleep may be essential for maintaining adaptive brain function during wakefulness. The recent miniaturization of EEG recording devices now makes it possible to measure brain activity in flight. Determining if and how birds sleep in flight will contribute to our understanding of a largely unexplored aspect of avian behavior and may also provide insight into the function of sleep.

Comparing Neural Correlates of REM Sleep in Posttraumatic Stress Disorder and Depression: A Neuroimaging Study

PubMed Central

Ebdlahad, Sommer; Nofzinger, Eric A.; James, Jeffrey A.; Buysse, Daniel J.; Price, Julie C.; Germain, Anne

2013-01-01

Rapid eye movement (REM) sleep disturbances predict poor clinical outcomes in posttraumatic stress disorder (PTSD) and major depressive disorder (MDD). In MDD, REM sleep is characterized by activation of limbic and paralimbic brain regions compared to wakefulness. The neural correlates of PTSD during REM sleep remain scarcely explored, and comparisons of PTSD and MDD have not been conducted. The present study sought to compare brain activity patterns during wakefulness and REM sleep in 13 adults with PTSD and 12 adults with MDD using [18F]-fluoro-2-deoxy-D-glucose positron emission tomography (PET). PTSD was associated with greater increases in relative regional cerebral metabolic rate of glucose (rCMRglc) in limbic and paralimbic structures in REM sleep compared to wakefulness. Post-hoc comparisons indicated that MDD was associated with greater limbic and paralimbic rCMRglc during wakefulness but not REM sleep compared to PTSD. Our findings suggest that PTSD is associated with increased REM sleep limbic and paralimbic metabolism, whereas MDD is associated with wake and REM hypermetabolism in these areas. These observations suggest that PTSD and MDD disrupt REM sleep through different neurobiological processes. Optimal sleep treatments between the two disorders may differ: REM-specific therapy may be more effective in PTSD. PMID:24367137

The Role of Glia in Sleep Regulation and Function.

PubMed

Frank, Marcos G

2018-01-28

The cellular mechanisms governing the expression, regulation, and function of sleep are not entirely understood. The traditional view is that these mechanisms are neuronal. An alternative view is that glial brain cells may play important roles in these processes. Their ubiquity in the central nervous system makes them well positioned to modulate neuronal circuits that gate sleep and wake. Their ability to respond to chemical neuronal signals suggests that they form feedback loops with neurons that may globally regulate neuronal activity. Their potential role in detoxifying the brain, regulating neuronal metabolism, and promoting synaptic plasticity raises the intriguing possibility that glia mediate important functions ascribed to sleep.

Exercise and sleep in aging: emphasis on serotonin.

PubMed

Melancon, M O; Lorrain, D; Dionne, I J

2014-10-01

Reductions in central serotonin activity with aging might be involved in sleep-related disorders in later life. Although the beneficial effects of aerobic exercise on sleep are not new, sleep represents a complex recurring state of unconsciousness involving many lines of transmitters which remains only partly clear despite intense ongoing research. It is known that serotonin released into diencephalon and cerebrum might play a key inhibitory role to help promote sleep, likely through an active inhibition of supraspinal neural networks. Several lines of evidence support the stimulatory effects of exercise on higher serotonergic pathways. Hence, exercise has proved to elicit acute elevations in forebrain serotonin concentrations, an effect that waned upon cessation of exercise. While adequate exercise training might lead to adaptations in higher serotonergic networks (desensitization of forebrain receptors), excessive training has been linked to serious brain serotonergic maladaptations accompanied by insomnia. Dietary supplementation of tryptophan (the only serotonin precursor) is known to stimulate serotonergic activity and promote sleep, whereas acute tryptophan depletion causes deleterious effects on sleep. Regarding sleep-wake regulation, exercise has proved to accelerate resynchronization of the biological clock to new light-dark cycles following imposition of phase shifts in laboratory animals. Noteworthy, the effect of increased serotonergic transmission on wake state appears to be biphasic, i.e. promote wake and thereafter drowsiness. Therefore, it might be possible that acute aerobic exercise would act on sleep by increasing activity of ascending brain serotonergic projections, though additional work is warranted to better understand the implication of serotonin in the exercise-sleep axis. Copyright © 2014 Elsevier Masson SAS. All rights reserved.

[EFFECTS OF ELECTRICAL STIMULATION OF NUCLEUS RETICULARIS PONTIS ORALIS ON THE SLEEP-WAKING STATES IN KRUSHINSKII-MOLODKINA STRAIN RATS].

PubMed

Vataev, S I; Malgina, N A; Oganesyan, G A

2015-07-01

The effects of electrical stimulation of nucleus reticularis pontis oralis on the behavior and brain electrical activity during all phases of the sleep-waking cycle was studied in Krushinskii-Molodkina strain rats, which have an inherited predisposition to audiogenic seizures. Electrical stimulation with 7 Hz frequency in the deep stage of slow-wave sleep cause appearance the fast-wave sleep. Similar stimulation during fast-wave sleep periods did not effects on the electrographic patterns and EEG spectral characteristics of hippocampus, visual, auditory and somatocnen nrnrenc nf the cnrtey ThPe sfimul1stinns did nnt break a fast-wave sleenhut increased almost twice due the duration of these sleep episodes. After electrical stimulation by same frequency during the wakeftlness and superficial slow-wave sleep states, the patterns and spectral characteristics of brain electrical activity in rats showed no significant changes as compared with controls. The results of this study indicate that the state of the animals sleep-waking cycle at the time of stimulation is a critical variable that influences the responses which are induced by electrical stimulation of the nucleus reticularis pontis oralis.

Upgrading the sleeping brain with targeted memory reactivation.

PubMed

Oudiette, Delphine; Paller, Ken A

2013-03-01

A fundamental feature of human memory is the propensity for beneficial changes in information storage after initial encoding. Recent research findings favor the possibility that memory consolidation during sleep is instrumental for actively maintaining the storehouse of memories that individuals carry through their lives. The information that ultimately remains available for retrieval may tend to be that which is reactivated during sleep. A novel source of support for this idea comes from demonstrations that neurocognitive processing during sleep can benefit memory storage when memories are covertly cued via auditory or olfactory stimulation. Investigations of these subtle manipulations of memory processing during sleep can help elucidate the mechanisms of memory preservation in the human brain. Copyright © 2013 Elsevier Ltd. All rights reserved.

On the functional significance of c-fos induction during the sleep-waking cycle.

PubMed

Cirelli, C; Tononi, G

2000-06-15

A striking finding in recent years has been that the transition from sleep to waking is accompanied in many brain regions by a widespread activation of c-fos and other immediate-early genes (IEGs). IEGs are induced by various electrical or chemical signals to which neural cells are exposed and their protein products act as transcription factors to regulate the expression of other genes. After a few hours of sleep, the expression of these transcription factors in the brain is absent or restricted to very few cells. However, after a few hours of spontaneous waking or sleep deprivation, the expression of c-fos and other IEGs is high in cerebral cortex, hypothalamus, septum, and several thalamic and brainstem nuclei. While cells expressing c-fos during waking are widely distributed, they represent only a subset of all neurons in any given area. These observations raise several questions: Why is c-fos expressed during waking and not during sleep? Is waking always accompanied by c-fos induction? Which subset of cells express c-fos during waking and why only a subset? Once c-fos has been induced, what are the functional consequences of its activation? In this review, we summarize our current understanding of the meaning of c-fos activation in the brain in relation to the sleep-waking cycle and suggest that c-fos induction in the cerebral cortex during waking might be related to the occurrence of plastic phenomena.

Decrease in fMRI brain activation during working memory performed after sleeping under 10 lux light.

PubMed

Kang, Seung-Gul; Yoon, Ho-Kyoung; Cho, Chul-Hyun; Kwon, Soonwook; Kang, June; Park, Young-Min; Lee, Eunil; Kim, Leen; Lee, Heon-Jeong

2016-11-09

The aim of this study was to investigate the effect of exposure to dim light at night (dLAN) when sleeping on functional brain activation during a working-memory tasks. We conducted the brain functional magnetic resonance imaging (fMRI) analysis on 20 healthy male subjects. All participants slept in a polysomnography laboratory without light exposure on the first and second nights and under a dim-light condition of either 5 or 10 lux on the third night. The fMRI scanning was conducted during n-back tasks after second and third nights. Statistical parametric maps revealed less activation in the right inferior frontal gyrus (IFG) after exposure to 10-lux light. The brain activity in the right and left IFG areas decreased more during the 2-back task than during the 1- or 0-back task in the 10-lux group. The exposure to 5-lux light had no significant effect on brain activities. The exposure to dLAN might influence the brain function which is related to the cognition.

β oscillation during slow wave sleep and rapid eye movement sleep in the electroencephalogram of a transgenic mouse model of Huntington's disease.

PubMed

Jeantet, Yannick; Cayzac, Sebastien; Cho, Yoon H

2013-01-01

To search for early abnormalities in electroencephalogram (EEG) during sleep which may precede motor symptoms in a transgenic mouse model of hereditary neurodegenerative Huntington's disease (HD). In the R6/1 transgenic mouse model of HD, rhythmic brain activity in EEG recordings was monitored longitudinally and across vigilance states through the onset and progression of disease. Mice with chronic electrode implants were recorded monthly over wake-sleep cycles (4 hours), beginning at 9-11 weeks (presymptomatic period) through 6-7 months (symptomatic period). Recording data revealed a unique β rhythm (20-35 Hz), present only in R6/1 transgenic mice, which evolves in close parallel with the disease. In addition, there was an unusual relationship between this β oscillation and vigilance states: while nearly absent during the active waking state, the β oscillation appeared with drowsiness and during slow wave sleep (SWS) and, interestingly, strengthened rather than dissipating when the brain returned to an activated state during rapid eye movement (REM) sleep. In addition to providing a new in vivo biomarker and insight into Huntington's disease pathophysiology, this serendipitous observation opens a window onto the rarely explored neurophysiology of the cortico-basal ganglia circuit during SWS and REM sleep.

Glucose Induces Slow-Wave Sleep by Exciting the Sleep-Promoting Neurons in the Ventrolateral Preoptic Nucleus: A New Link between Sleep and Metabolism.

PubMed

Varin, Christophe; Rancillac, Armelle; Geoffroy, Hélène; Arthaud, Sébastien; Fort, Patrice; Gallopin, Thierry

2015-07-08

Sleep-active neurons located in the ventrolateral preoptic nucleus (VLPO) play a crucial role in the induction and maintenance of slow-wave sleep (SWS). However, the cellular and molecular mechanisms responsible for their activation at sleep onset remain poorly understood. Here, we test the hypothesis that a rise in extracellular glucose concentration in the VLPO can promote sleep by increasing the activity of sleep-promoting VLPO neurons. We find that infusion of a glucose concentration into the VLPO of mice promotes SWS and increases the density of c-Fos-labeled neurons selectively in the VLPO. Moreover, we show in patch-clamp recordings from brain slices that VLPO neurons exhibiting properties of sleep-promoting neurons are selectively excited by glucose within physiological range. This glucose-induced excitation implies the catabolism of glucose, leading to a closure of ATP-sensitive potassium (KATP) channels. The extracellular glucose concentration monitors the gating of KATP channels of sleep-promoting neurons, highlighting that these neurons can adapt their excitability according to the extracellular energy status. Together, these results provide evidence that glucose may participate in the mechanisms of SWS promotion and/or consolidation. Although the brain circuitry underlying vigilance states is well described, the molecular mechanisms responsible for sleep onset remain largely unknown. Combining in vitro and in vivo experiments, we demonstrate that glucose likely contributes to sleep onset facilitation by increasing the excitability of sleep-promoting neurons in the ventrolateral preoptic nucleus (VLPO). We find here that these neurons integrate energetic signals such as ambient glucose directly to regulate vigilance states accordingly. Glucose-induced excitation of sleep-promoting VLPO neurons should therefore be involved in the drowsiness that one feels after a high-sugar meal. This novel mechanism regulating the activity of VLPO neurons reinforces the fundamental and intimate link between sleep and metabolism. Copyright © 2015 the authors 0270-6474/15/359900-12$15.00/0.

Unobtrusive sleep state measurements in preterm infants - A review.

PubMed

Werth, Jan; Atallah, Louis; Andriessen, Peter; Long, Xi; Zwartkruis-Pelgrim, Elly; Aarts, Ronald M

2017-04-01

Sleep is important for the development of preterm infants. During sleep, neural connections are formed and the development of brain regions is triggered. In general, various rudimentary sleep states can be identified in the preterm infant, namely active sleep (AS), quiet sleep (QS) and intermediate sleep (IS). As the infant develops, sleep states change in length and organization, with these changes as important indicators of brain development. As a result, several methods have been deployed to distinguish between the different preterm infant sleep states, among which polysomnography (PSG) is the most frequently used. However, this method is limited by the use of adhesive electrodes or patches that are attached to the body by numerous cables that can disturb sleep. Given the importance of sleep, this review explores more unobtrusive methods that can identify sleep states without disturbing the infant. To this end, after a brief introduction to preterm sleep states, an analysis of the physiological characteristics associated with the different sleep states is provided and various methods of measuring these physiological characteristics are explored. Finally, the advantages and disadvantages of each of these methods are evaluated and recommendations for neonatal sleep monitoring proposed. Copyright © 2016 Elsevier Ltd. All rights reserved.

[Sleep regulatory mechanisms].

PubMed

Sei, Hiroyoshi; Shimizu, Noriyuki; Kitaoka, Kazuyoshi; Chikahisa, Sachiko

2012-07-01

The fact that resting wakefulness does not satisfy the need for sleep suggests that sleep has a critical role for the brain, probably for its maintenance or repair. Neuronal oxidative stress, neuroinflammation, or energy insufficiency in the brain is now considered to be a trigger or cause for sleep induction. And the timing for sleep is controlled by circadian clock which also exists in the brain. Sleep is occurred in the brain, which is regulated by the brain itself. "Why do we sleep ?" Although everyone wants to know the answer for this issue, scientists should still question that "How do we sleep"?

GABA-BZD Receptor Modulating Mechanism of Panax quinquefolius against 72-h Sleep Deprivation Induced Anxiety like Behavior: Possible Roles of Oxidative Stress, Mitochondrial Dysfunction and Neuroinflammation

PubMed Central

Chanana, Priyanka; Kumar, Anil

2016-01-01

Rationale: Panax quinquefolius (American Ginseng) is known for its therapeutic potential against various neurological disorders, but its plausible mechanism of action still remains undeciphered. GABA (Gamma Amino Butyric Acid) plays an important role in sleep wake cycle homeostasis. Thus, there exists rationale in exploring the GABA-ergic potential of Panax quinquefolius as neuroprotective strategy in sleep deprivation induced secondary neurological problems. Objective: The present study was designed to explore the possible GABA-ergic mechanism in the neuro-protective effect of Panax quinquefolius against 72-h sleep deprivation induced anxiety like behavior, oxidative stress, mitochondrial dysfunction, HPA-axis activation and neuroinflammation. Materials and Methods: Male laca mice were sleep deprived for 72-h by using Grid suspended over water method. Panax quinquefolius (American Ginseng 50, 100, and 200 mg/kg) was administered alone and in combination with GABA modulators (GABA Cl− channel inhibitor, GABA-benzodiazepine receptor inhibitor and GABAA agonist) for 8 days, starting 5 days prior to 72-h sleep deprivation period. Various behavioral (locomotor activity, mirror chamber test), biochemical (lipid peroxidation, reduced glutathione, catalase, nitrite levels), mitochondrial complexes, neuroinflammation marker (Tumor Necrosis Factor, TNF-alpha), serum corticosterone, and histopathological sections of brains were assessed. Results: Seventy two hours sleep deprivation significantly impaired locomotor activity, caused anxiety-like behavior, conditions of oxidative stress, alterations in mitochondrial enzyme complex activities, raised serum corticosterone levels, brain TNFα levels and led to neuroinflammation like signs in discrete brain areas as compared to naive group. Panax quinquefolius (100 and 200 mg/kg) treatment restored the behavioral, biochemical, mitochondrial, molecular and histopathological alterations. Pre-treatment of GABA Cl− channel inhibitor as well as GABA-benzodiazepine receptor inhibitor, significantly reversed the protective effect of P. quinquefolius (100 mg/kg) in 72-h sleep deprived animals (P < 0.05). However, pretreatment with GABAA agonist, potentiated Panax quinquefolius's protective effect which was significant as compared to their effect per se (p < 0.05). Conclusion: GABA-ergic mechanism could be involved in the neuroprotective effect of P.quinquefolius against sleep deprivation induced anxiety-like behavior, oxidative stress, mitochondrial dysfunction, HPA axis activation and neuroinflammation. PMID:27013946

Peripheral and central blockade of interleukin-6 trans-signaling differentially affects sleep architecture.

PubMed

Oyanedel, Carlos N; Kelemen, Eduard; Scheller, Jürgen; Born, Jan; Rose-John, Stefan

2015-11-01

The immune system is known to essentially contribute to the regulation of sleep. Whereas research in this regard focused on the pro-inflammatory cytokines interleukin-1 and tumor necrosis factor, the role of interleukin-6 (IL-6) in sleep regulation has been less intensely studied, probably due to the so far seemingly ambiguous results. Yet, this picture might simply reflect that the effects of IL-6 are conveyed via two different pathways (with possibly different actions), i.e., in addition to the 'classical' signaling pathway via the membrane bound IL-6 receptor (IL-6R), IL-6 stimulates cells through the alternative 'trans-signaling' pathway via the soluble IL-6R. Here, we concentrated on the contributions of the trans-signaling pathway to sleep regulation. To characterize this contribution, we compared the effect of blocking IL-6 trans-signaling (by the soluble gp130Fc fusion protein) in the brain versus body periphery. Thus, we compared sleep in transgenic mice expressing the soluble gp130Fc protein only in the brain (GFAP mice) or in the body periphery (PEPCK mice), and in wild type mice (WT) during a 24-h period of undisturbed conditions and during 18 h following a 6-h period of sleep deprivation. Compared with WT mice, PEPCK mice displayed less sleep, particularly during the late light phase, and this was accompanied by decreases in slow wave sleep (SWS) and rapid eye movement (REM) sleep. Following sleep deprivation PEPCK mice primarily recovered REM sleep rather than SWS. GFAP mice showed a slight decrease in REM sleep in combination with a profound and persistent increase in EEG theta activity. In conclusion, peripheral and central nervous IL-6 trans-signaling differentially influences brain activity. Peripheral IL-6 trans-signaling appears to more profoundly contribute to sleep regulation, mainly by supporting SWS. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

Gray Matter-Specific Changes in Brain Bioenergetics after Acute Sleep Deprivation: A 31P Magnetic Resonance Spectroscopy Study at 4 Tesla

PubMed Central

Plante, David T.; Trksak, George H.; Jensen, J. Eric; Penetar, David M.; Ravichandran, Caitlin; Riedner, Brady A.; Tartarini, Wendy L.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.; Harper, David G.

2014-01-01

Study Objectives: A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Design: Experimental laboratory study. Setting: Outpatient neuroimaging center at a private psychiatric hospital. Participants: A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Interventions: Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation, and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. Measurements and Results: PCr increased in gray matter after 2 nights of recovery sleep relative to sleep deprivation with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. Conclusions: These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in phosphocreatine after recovery sleep may be related to sleep homeostasis. Citation: Plante DT, Trksak GH, Jensen JE, Penetar DM, Ravichandran C, Riedner BA, Tartarini WL, Dorsey CM, Renshaw PF, Lukas SE, Harper DG. Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla. SLEEP 2014;37(12):1919-1927. PMID:25325507

Sleep Deprivation Decreases [11C]Raclopride’s Binding to Dopamine D2/D3 Receptors in the Human Brain

PubMed Central

Volkow, Nora D.; Wang, Gene-Jack; Telang, Frank; Fowler, Joanna S.; Logan, Jean; Wong, Christopher; Ma, Jim; Pradhan, Kith; Tomasi, Dardo; Thanos, Peter K.; Ferré, Sergi; Jayne, Millard

2009-01-01

Sleep deprivation can markedly impair human performance contributing to accidents and poor productivity. The mechanisms underlying this impairment are not well understood but brain dopamine systems have been implicated. Here we test whether one night of sleep deprivation changes dopamine brain activity. We studied fifteen healthy subjects using positron emission tomography and [11C]raclopride (dopamine D2/3 receptor radioligand) and [11C]cocaine (dopamine transporter radioligand). Subjects were tested twice; after one night of rested sleep and after on night of sleep deprivation. [11C]Raclopride’s specific binding in striatum and thalamus were significantly reduced after sleep deprivation and the magnitude of this reduction correlated with increases in fatigue (tiredness and sleepiness) and with deterioration in cognitive performance (visual attention and working memory). In contrast sleep deprivation did not affect the specific binding of [11C]cocaine in striatum. Since [11C]raclopride competes with endogenous dopamine for binding to D2/D3 receptors, we interpret the decreases in binding to reflect dopamine increases with sleep deprivation. However, we can not rule out the possibility that decreased [11C]raclopride binding reflects decreases in receptor levels or affinity. Sleep deprivation did not affect dopamine transporters (target for most wake-promoting medications) and thus dopamine increases are likely to reflect increases in dopamine cell firing and/or release rather than decreases in dopamine reuptake. Inasmuch as dopamine-enhancing drugs increase wakefulness we postulate that dopamine increases after sleep deprivation is a mechanism by which the brain maintains arousal as the drive to sleep increases but one that is insufficient to counteract behavioral and cognitive impairment. PMID:18716203

Sleep disorders of Whipple's disease of the brain.

PubMed

Panegyres, P K; Goh, J

2015-02-01

To understand the effects of Whipple's disease (WD) of the brain on sleep function. Clinical and polysomnographic studies of two patients with severe disruption of sleep due to WD: a 48-year-old female with primary WD of the brain and a 41-year-old male with secondary WD of the brain. The patient with primary WD had hypersomnolence with severe obstructive sleep apnoea, reduced sleep efficiency, frequent waking and sleep fragmentation. The patient with secondary WD was also hypersomnolent with oculomastictory myorhythmia. He was shown to have severe sleep initiation insomnia with poor sleep efficiency, severe obstructive sleep apnoea/hypopnoea and oculomasticatory myorhythmia at sleep-wake transitions. WD of the brain may affect sleep biology in its primary and secondary forms leading to hypersomnolence from obstructive sleep apnoea, sleep fragmentation, reduced sleep efficiency, sleep initiation insomnia and intrusive oculomasticatory myorhythmia. © The Author 2014. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

State-dependent and reflex drives to the upper airway: basic physiology with clinical implications

PubMed Central

Hughes, Stuart W.; Malhotra, Atul

2013-01-01

The root cause of the most common and serious of the sleep disorders is impairment of breathing, and a number of factors predispose a particular individual to hypoventilation during sleep. In turn, obstructive hypopneas and apneas are the most common of the sleep-related respiratory problems and are caused by dysfunction of the upper airway as a conduit for airflow. The overarching principle that underpins the full spectrum of clinical sleep-related breathing disorders is that the sleeping brain modifies respiratory muscle activity and control mechanisms and diminishes the ability to respond to respiratory distress. Depression of upper airway muscle activity and reflex responses, and suppression of arousal (i.e., “waking-up”) responses to respiratory disturbance, can also occur with commonly used sedating agents (e.g., hypnotics and anesthetics). Growing evidence indicates that the sometimes critical problems of sleep and sedation-induced depression of breathing and arousal responses may be working through common brain pathways acting on common cellular mechanisms. To identify these state-dependent pathways and reflex mechanisms, as they affect the upper airway, is the focus of this paper. Major emphasis is on the synthesis of established and recent findings. In particular, we specifically focus on 1) the recently defined mechanism of genioglossus muscle inhibition in rapid-eye-movement sleep; 2) convergence of diverse neurotransmitters and signaling pathways onto one root mechanism that may explain pharyngeal motor suppression in sleep and drug-induced brain sedation; 3) the lateral reticular formation as a key hub of respiratory and reflex drives to the upper airway. PMID:23970535

Positive effects of β-amyrin on pentobarbital-induced sleep in mice via GABAergic neurotransmitter system.

PubMed

Jeon, Se Jin; Park, Ho Jae; Gao, Qingtao; Lee, Hyung Eun; Park, Se Jin; Hong, Eunyoung; Jang, Dae Sik; Shin, Chan Young; Cheong, Jae Hoon; Ryu, Jong Hoon

2015-09-15

Sleep loss, insomnia, is considered a sign of imbalance of physiological rhythm, which can be used as pre-clinic diagnosis of various neuropsychiatric disorders. The aim of the present study is to understand the pharmacological actions of α- or β-amyrin, natural triterpene compound, on the sleep in mice. To analyze the sleeping behavior, we used the well-known pentobarbital-induced sleeping model after single administration of either α- or β-amyrin. The sleeping onset time was remarkably decreased and duration was prolonged by β-amyrin (1, 3, or 10mg/kg) but not by α-amyrin (1, 3, or 10mg/kg). These effects were significantly blocked by GABAA receptor antagonist, bicuculline. Moreover, β-amyrin increased brain GABA level compared to the vehicle administration. Overall, the present study suggests that β-amyrin would enhance the total sleeping behavior in pentobarbital-induced sleeping model via the activation of GABAergic neurotransmitter system through GABA content in the brain. Copyright © 2015 Elsevier B.V. All rights reserved.

Enhanced Frontoparietal Synchronized Activation During the Wake-Sleep Transition in Patients with Primary Insomnia

PubMed Central

Corsi-Cabrera, María; Figueredo-Rodríguez, Pedro; del Río-Portilla, Yolanda; Sánchez-Romero, Jorge; Galán, Lídice; Bosch-Bayard, Jorge

2012-01-01

Introduction: Cognitive and brain hyperactivation have been associated with trouble falling asleep and sleep misperception in patients with primary insomnia (PI). Activation and synchronization/temporal coupling in frontal and frontoparietal regions involved in executive control and endogenous attention might be implicated in these symptoms. Methods: Standard polysomnography (PSG) and electroencephalogram (EEG) were recorded in 10 unmedicated young patients (age 19-34 yr) with PI with no other sleep/medical condition, and in 10 matched control subjects. Absolute power, temporal coupling, and topographic source distribution (variable resolution electromagnetic tomography or VARETA) were obtained for all time spent in waking, Stage 1 and Stage 2 of the wake-sleep transition period (WSTP), and the first 3 consecutive min of N3. Subjective sleep quality and continuity were evaluated. Results: In comparison with control subjects, patients with PI exhibited significantly higher frontal beta power and current density, and beta and gamma frontoparietal temporal coupling during waking and Stage 1. Conclusion: These findings suggest that frontal deactivation and disengagement of brain regions involved in executive control, attention, and self-awareness are impaired in patients with PI. The persistence of this activated and coherent network during the wake-sleep transition period (WSTP) may contribute to a better understanding of underlying mechanisms involved in difficulty in falling asleep, in sleep misperception, and in the lighter, poorer, and nonrefreshing sleep experienced by some patients with PI. Citation: Corsi-Cabrera M; Figueredo-Roríguez P; del Río-Portilla Y; Sánchez-Romero J; Galán L; Bosch-Bayard J. Enhanced frontoparietal synchronized activation during the wake-sleep transition in patients with primary insomnia. SLEEP 2012;35(4):501-511. PMID:22467988

Optical imaging of neural and hemodynamic brain activity

NASA Astrophysics Data System (ADS)

Schei, Jennifer Lynn

Optical imaging technologies can be used to record neural and hemodynamic activity. Neural activity elicits physiological changes that alter the optical tissue properties. Specifically, changes in polarized light are concomitant with neural depolarization. We measured polarization changes from an isolated lobster nerve during action potential propagation using both reflected and transmitted light. In transmission mode, polarization changes were largest throughout the center of the nerve, suggesting that most of the optical signal arose from the inner nerve bundle. In reflection mode, polarization changes were largest near the edges, suggesting that most of the optical signal arose from the outer sheath. To overcome irregular cell orientation found in the brain, we measured polarization changes from a nerve tied in a knot. Our results show that neural activation produces polarization changes that can be imaged even without regular cell orientations. Neural activation expends energy resources and elicits metabolic delivery through blood vessel dilation, increasing blood flow and volume. We used spectroscopic imaging techniques combined with electrophysiological measurements to record evoked neural and hemodynamic responses from the auditory cortex of the rat. By using implantable optics, we measured responses across natural wake and sleep states, as well as responses following different amounts of sleep deprivation. During quiet sleep, evoked metabolic responses were larger compared to wake, perhaps because blood vessels were more compliant. When animals were sleep deprived, evoked hemodynamic responses were smaller following longer periods of deprivation. These results suggest that prolonged neural activity through sleep deprivation may diminish vascular compliance as indicated by the blunted vascular response. Subsequent sleep may allow vessels to relax, restoring their ability to deliver blood. These results also suggest that severe sleep deprivation or chronic sleep disturbances could push the vasculature to critical limits, leading to metabolic deficit and the potential for tissue trauma.

Neuronal plasticity and thalamocortical sleep and waking oscillations

PubMed Central

Timofeev, Igor

2011-01-01

Throughout life, thalamocortical (TC) network alternates between activated states (wake or rapid eye movement sleep) and slow oscillatory state dominating slow-wave sleep. The patterns of neuronal firing are different during these distinct states. I propose that due to relatively regular firing, the activated states preset some steady state synaptic plasticity and that the silent periods of slow-wave sleep contribute to a release from this steady state synaptic plasticity. In this respect, I discuss how states of vigilance affect short-, mid-, and long-term synaptic plasticity, intrinsic neuronal plasticity, as well as homeostatic plasticity. Finally, I suggest that slow oscillation is intrinsic property of cortical network and brain homeostatic mechanisms are tuned to use all forms of plasticity to bring cortical network to the state of slow oscillation. However, prolonged and profound shift from this homeostatic balance could lead to development of paroxysmal hyperexcitability and seizures as in the case of brain trauma. PMID:21854960

Mobile phones and sleep - A review

NASA Astrophysics Data System (ADS)

Supe, Sanjay S.

2010-01-01

The increasing use of mobile phones has raised concerns regarding the potential health effects of exposure to the radiofrequency electromagnetic fields. An increasing amount research related to mobile phone use has focussed on the possible effects of mobile phone exposure on human brain activity and function. In particular, the use of sleep research has become a more widely used technique for assessing the possible effects of mobile phones on human health and wellbeing especially in the investigation of potential changes in sleep architecture resulting from mobile phone use. Acute exposure to a mobile phone prior to sleep significantly enhances electroencephalogram spectral power in the sleep spindle frequency range. This mobile phone-induced enhancement in spectral power is largely transitory and does not linger throughout the night. Furthermore, a reduction in rapid eye movement sleep latency following mobile phone exposure was also found, although interestingly, neither this change in rapid eye movement sleep latency or the enhancement in spectral power following mobile phone exposure, led to changes in the overall quality of sleep. In conclusion, a short exposure to the radiofrequency electromagnetic fields emitted by a mobile phone handset immediately prior to sleep is sufficient to induce changes in brain activity in the initial part of sleep. The consequences or functional significance of this effect are currently unknown and it would be premature to draw conclusions about possible health consequences.

Telephone Problem-Solving Treatment Improves Sleep Quality in Service Members With Combat-Related Mild Traumatic Brain Injury: Results From a Randomized Clinical Trial.

PubMed

Vuletic, S; Bell, K R; Jain, S; Bush, N; Temkin, N; Fann, J R; Stanfill, K E; Dikmen, S; Brockway, J A; He, F; Ernstrom, K; Raman, R; Grant, G; Stein, M B; Gahm, G A

2016-01-01

Evaluate sleep quality, its correlates, and the effect of telephone-based problem-solving treatment (PST) in active duty postdeployment service members with mild traumatic brain injury (mTBI) SETTING:: Randomized clinical trial. Active duty service members with combat-related mTBI. Education-only (EO) and PST groups (N = 178 each) received printed study materials and 12 educational brochures. The PST group additionally received up to 12 PST telephone calls addressing participant-selected issues. Outcomes were evaluated postintervention (6 months) and at 12 months. Pittsburgh Sleep Quality Index. Sleep quality was manifestly poor in both groups at baseline (Pittsburgh Sleep Quality Index = 12.5 ± 4). Overall sleep quality was significantly different between the PST and EO groups at 6 months (P = .003) but not at 12 months. Longitudinally, PST significantly improved sleep quality at 6 months (P = .001) but not over the follow-up. Low sleep quality was associated with concussion symptoms, pain, depression, and posttraumatic stress disorder at all time points (P < .0001). Sleep disorders, common in postdeployment service members with mTBI, are strongly associated with the presence of pain, posttraumatic stress disorder, and depression. Telephone-based PST may be an effective therapeutic approach for reducing sleep disorders in this population. Research should focus on maintenance of treatment gains.

Asymmetry and basic pathways in sleep-stage transitions

NASA Astrophysics Data System (ADS)

Lo, Chung-Chuan; Bartsch, Ronny P.; Ivanov, Plamen Ch.

2013-04-01

We study dynamical aspects of sleep micro-architecture. We find that sleep dynamics exhibits a high degree of asymmetry, and that the entire class of sleep-stage transition pathways underlying the complexity of sleep dynamics throughout the night can be characterized by two independent asymmetric transition paths. These basic pathways remain stable under sleep disorders, even though the degree of asymmetry is significantly reduced. Our findings demonstrate an intriguing temporal organization in sleep micro-architecture at short time scales that is typical for physical systems exhibiting self-organized criticality (SOC), and indicates nonequilibrium critical dynamics in brain activity during sleep.

The Relationship between Sleep Quality and Brain Amyloid Burden.

PubMed

Brown, Belinda M; Rainey-Smith, Stephanie R; Villemagne, Victor L; Weinborn, Michael; Bucks, Romola S; Sohrabi, Hamid R; Laws, Simon M; Taddei, Kevin; Macaulay, S Lance; Ames, David; Fowler, Christopher; Maruff, Paul; Masters, Colin L; Rowe, Christopher C; Martins, Ralph N

2016-05-01

To evaluate the association between self-reported sleep quality and levels of brain β-amyloid (Aβ) burden, and to determine the effect of the apolipoprotein E (APOE) ε4 allele on any associations found. This study is a cross-sectional analysis of 184 cognitively healthy men and women aged over 60 y. We measured sleep quality factors: specifically, sleep duration, latency (time taken to fall asleep), disturbances, efficiency, daytime dysfunction, and overall sleep quality, using the Pittsburgh Sleep Quality Index. All participants underwent Aβ positron emission tomography imaging for the quantification of brain Aβ burden and were APOE genotyped. Linear regression analyses were used to evaluate the relationship between sleep quality factors and brain Aβ burden, adjusting for age, body mass index, cardiovascular disease, and symptoms of depression, with APOE ε4 carriage entered as a moderator. Of the sleep factors, longer sleep latency was associated with higher levels of brain Aβ (B = 0.003 [standard error = 0.001], P = 0.02). APOE ε4 allele (carrier/noncarrier) did not moderate the relationship between sleep latency and brain Aβ burden. Our findings suggest a relationship between brain Aβ burden and sleep latency, independent of APOE ε4 genotype. © 2016 Associated Professional Sleep Societies, LLC.

The Developmental Course of Sleep Disturbances Across Childhood Relates to Brain Morphology at Age 7: The Generation R Study.

PubMed

Kocevska, Desana; Muetzel, Ryan L; Luik, Annemarie I; Luijk, Maartje P C M; Jaddoe, Vincent W; Verhulst, Frank C; White, Tonya; Tiemeier, Henning

2017-01-01

Little is known about the impact of sleep disturbances on the structural properties of the developing brain. This study explored associations between childhood sleep disturbances and brain morphology at 7 years. Mothers from the Generation R cohort reported sleep disturbances in 720 children at ages 2 months, 1.5, 2, 3, and 6 years. T1-weighted Magnetic Resonance Imaging (MRI) images were used to assess brain structure at 7 years. Associations of sleep disturbances at each age and of sleep disturbance trajectories with brain volumes (total brain volume, cortical and subcortical grey matter, white matter) were tested with linear regressions. To assess regional differences, sleep disturbance trajectories were tested as determinants for cortical thickness in whole-brain analyses. Sleep disturbances followed a declining trend from toddlerhood onwards. Infant sleep was not associated with brain morphology at age 7. Per SD sleep disturbances (one frequent symptom or two less frequent symptoms) at 2 and 3 years of age, children had -6.3 (-11.7 to -0.8) cm3 and -6.4 (-11.7 to -1.7) cm3 smaller grey matter volumes, respectively. Sleep disturbances at age 6 years were associated with global brain morphology (grey matter: -7.3 (-12.1 to -2.6), p value = .01). Consistently, trajectory analyses showed that more adverse developmental course of childhood sleep disturbances are associated with smaller grey matter volumes and thinner dorsolateral prefrontal cortex. Sleep disturbances from age 2 years onwards are associated with smaller grey matter volumes. Thinner prefrontal cortex in children with adverse sleep disturbance trajectories may reflect effects of sleep disturbances on brain maturation. © Sleep Research Society 2016. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Brain Activation Changes Before and After PAP Treatment in Obstructive Sleep Apnea

PubMed Central

Castronovo, Vincenza; Canessa, Nicola; Strambi, Luigi Ferini; Aloia, Mark S.; Consonni, Monica; Marelli, Sara; Iadanza, Antonella; Bruschi, Alice; Falini, Andrea; Cappa, Stefano F.

2009-01-01

Study Objectives: Obstructive sleep apnea syndrome (OSAS) is associated with cognitive and functional deficits, most of which are corrected after positive airway pressure (PAP) treatment. Previous studies investigating the neural underpinnings of OSAS failed to provide consistent results both on the cerebral substrates underlying cognitive deficits and on the effect of treatment on these anomalies. The aims of the study were a) to investigate whether never-treated OSA patients demonstrated differences in brain activation compared to healthy controls during a cognitive task; and b) to investigate whether any improvements in cognitive functioning found in OSA patients after treatment reflected a change in the underlying cerebral activity. Design: OSA patients and healthy controls underwent functional magnetic resonance imaging (fMRI) scanning. They were compared on performance and brain activation during a 2-back working-memory task. Patients were also re-evaluated after 3 months treatment with PAP. Cognitive functions were evaluated using neurocognitive tests. Sleepiness (ESS), mood (Beck Depression Inventory) and, quality-of-life (SF-36) were also assessed. Setting: The Sleep Disorders Center and CERMAC at the Vita-Salute San Raffaele University. Patients or Participants: 17 OSA patients and 15 age- and education-matched healthy controls. Interventions: PAP treatment for 3 months. Measurements and Results: Compared to controls, never-treated OSA patients showed increased activations in the left frontal cortex, medial precuneus, and hippocampus, and decreased activations in the caudal pons. OSA patients showed decreases in activation with treatment in the left inferior frontal gyrus and anterior cingulate cortex, and bilaterally in the hippocampus. Most neurocognitive domains, impaired at baseline, showed significant improvement after treatment. Conclusions: OSA patients showed an overrecruitment of brain regions compared to controls, in the presence of the same level of performance on a working-memory task. Decreases of activation in prefrontal and hippocampal structures were observed after treatment in comparison to baseline. These findings may reflect a neural compensation mechanism in never-treated patients, which is reduced by effective treatment. Citation: Castronovo V; Canessa N; Ferini Strambi L; Aloia MS; Consonni M; Marelli S; Iadanza A; BruschiA; Falini A; Cappa SF. Brain activation changes before and after PAP treatment in obstructive sleep apnea. SLEEP 2009;32(9):1161-1172. PMID:19750921

A review of current sleep screening applications for smartphones.

PubMed

Behar, Joachim; Roebuck, Aoife; Domingos, João S; Gederi, Elnaz; Clifford, Gari D

2013-07-01

Sleep disorders are a common problem and contribute to a wide range of healthcare issues. The societal and financial costs of sleep disorders are enormous. Sleep-related disorders are often diagnosed with an overnight sleep test called a polysomnogram, or sleep study involving the measurement of brain activity through the electroencephalogram. Other parameters monitored include oxygen saturation, respiratory effort, cardiac activity (through the electrocardiogram), as well as video recording, sound and movement activity. Monitoring can be costly and removes the patients from their normal sleeping environment, preventing repeated unbiased studies. The recent increase in adoption of smartphones, with high quality on-board sensors has led to the proliferation of many sleep screening applications running on the phone. However, with the exception of simple questionnaires, no existing sleep-related application available for smartphones is based on scientific evidence. This paper reviews the existing smartphone applications landscape used in the field of sleep disorders and proposes possible advances to improve screening approaches.

Modulation of the brain's functional network architecture in the transition from wake to sleep

PubMed Central

Larson-Prior, Linda J.; Power, Jonathan D.; Vincent, Justin L.; Nolan, Tracy S.; Coalson, Rebecca S.; Zempel, John; Snyder, Abraham Z.; Schlaggar, Bradley L.; Raichle, Marcus E.; Petersen, Steven E.

2013-01-01

The transition from quiet wakeful rest to sleep represents a period over which attention to the external environment fades. Neuroimaging methodologies have provided much information on the shift in neural activity patterns in sleep, but the dynamic restructuring of human brain networks in the transitional period from wake to sleep remains poorly understood. Analysis of electrophysiological measures and functional network connectivity of these early transitional states shows subtle shifts in network architecture that are consistent with reduced external attentiveness and increased internal and self-referential processing. Further, descent to sleep is accompanied by the loss of connectivity in anterior and posterior portions of the default-mode network and more locally organized global network architecture. These data clarify the complex and dynamic nature of the transitional period between wake and sleep and suggest the need for more studies investigating the dynamics of these processes. PMID:21854969

Shorter sleep duration and better sleep quality are associated with greater tissue density in the brain.

PubMed

Takeuchi, Hikaru; Taki, Yasuyuki; Nouchi, Rui; Yokoyama, Ryoichi; Kotozaki, Yuka; Nakagawa, Seishu; Sekiguchi, Atsushi; Iizuka, Kunio; Yamamoto, Yuki; Hanawa, Sugiko; Araki, Tsuyoshi; Miyauchi, Carlos Makoto; Shinada, Takamitsu; Sakaki, Kohei; Nozawa, Takayuki; Ikeda, Shigeyuki; Yokota, Susumu; Daniele, Magistro; Sassa, Yuko; Kawashima, Ryuta

2018-04-11

Poor sleep quality is associated with unfavorable psychological measurements, whereas sleep duration has complex relationships with such measurements. The aim of this study was to identify the associations between microstructural properties of the brain and sleep duration/sleep quality in a young adult. The associations between mean diffusivity (MD), a measure of diffusion tensor imaging (DTI), and sleep duration/sleep quality were investigated in a study cohort of 1201 normal young adults. Positive correlations between sleep duration and MD of widespread areas of the brain, including the prefrontal cortex (PFC) and the dopaminergic systems, were identified. Negative correlations between sleep quality and MD of the widespread areas of the brain, including the PFC and the right hippocampus, were also detected. Lower MD has been previously associated with more neural tissues in the brain. Further, shorter sleep duration was associated with greater persistence and executive functioning (lower Stroop interference), whereas good sleep quality was associated with states and traits relevant to positive affects. These results suggest that bad sleep quality and longer sleep duration were associated with aberrant neurocognitive measurements in the brain in healthy young adults.

The Impact of Subthalamic Deep Brain Stimulation on Sleep-Wake Behavior: A Prospective Electrophysiological Study in 50 Parkinson Patients.

PubMed

Baumann-Vogel, Heide; Imbach, Lukas L; Sürücü, Oguzkan; Stieglitz, Lennart; Waldvogel, Daniel; Baumann, Christian R; Werth, Esther

2017-05-01

This prospective observational study was designed to systematically examine the effect of subthalamic deep brain stimulation (DBS) on subjective and objective sleep-wake parameters in Parkinson patients. In 50 consecutive Parkinson patients undergoing subthalamic DBS, we assessed motor symptoms, medication, the position of DBS electrodes within the subthalamic nucleus (STN), subjective sleep-wake parameters, 2-week actigraphy, video-polysomnography studies, and sleep electroencepahalogram frequency and dynamics analyses before and 6 months after surgery. Subthalamic DBS improved not only motor symptoms and reduced daily intake of dopaminergic agents but also enhanced subjective sleep quality and reduced sleepiness (Epworth Sleepiness Scale: -2.1 ± 3.8, p < .001). Actigraphy recordings revealed longer bedtimes (+1:06 ± 0:51 hours, p < .001) without shifting of circadian timing. Upon polysomnography, we observed an increase in sleep efficiency (+5.2 ± 17.6%, p = .005) and deep sleep (+11.2 ± 32.2 min, p = .017) and increased accumulation of slow-wave activity over the night (+41.0 ± 80.0%, p = .005). Rapid eye movement sleep features were refractory to subthalamic DBS, and the dynamics of sleep as assessed by state space analyses did not normalize. Increased sleep efficiency was associated with active electrode contact localization more distant from the ventral margin of the left subthalamic nucleus. Subthalamic DBS deepens and consolidates nocturnal sleep and improves daytime wakefulness in Parkinson patients, but several outcomes suggest that it does not normalize sleep. It remains elusive whether modulated activity in the STN directly contributes to changes in sleep-wake behavior, but dorsal positioning of electrodes within the STN is linked to improved sleep-wake outcomes. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla.

PubMed

Plante, David T; Trksak, George H; Jensen, J Eric; Penetar, David M; Ravichandran, Caitlin; Riedner, Brady A; Tartarini, Wendy L; Dorsey, Cynthia M; Renshaw, Perry F; Lukas, Scott E; Harper, David G

2014-12-01

A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Experimental laboratory study. Outpatient neuroimaging center at a private psychiatric hospital. A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation (SD), and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. PCr increased in gray matter after 2 nights of recovery sleep relative to SD with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in PCr after recovery sleep may be related to sleep homeostasis. © 2014 Associated Professional Sleep Societies, LLC.

Thalamocortical Oscillations in the Sleeping and Aroused Brain

NASA Astrophysics Data System (ADS)

Steriade, Mircea; McCormick, David A.; Sejnowski, Terrence J.

1993-10-01

Sleep is characterized by synchronized events in billions of synaptically coupled neurons in thalamocortical systems. The activation of a series of neuromodulatory transmitter systems during awakening blocks low-frequency oscillations, induces fast rhythms, and allows the brain to recover full responsiveness. Analysis of cortical and thalamic networks at many levels, from molecules to single neurons to large neuronal assemblies, with a variety of techniques, ranging from intracellular recordings in vivo and in vitro to computer simulations, is beginning to yield insights into the mechanisms of the generation, modulation, and function of brain oscillations.

SLEEP AND THE FUNCTIONAL CONNECTOME

PubMed Central

Picchioni, Dante; Duyn, Jeff H.; Horovitz, Silvina G.

2013-01-01

Sleep and the functional connectome are research areas with considerable overlap. Neuroimaging studies of sleep based on EEG-PET and EEG-fMRI are revealing the brain networks that support sleep, as well as networks that may support the roles and processes attributed to sleep. For example, phenomena such as arousal and consciousness are substantially modulated during sleep, and one would expect this modulation to be reflected in altered network activity. In addition, recent work suggests that sleep also has a number of adaptive functions that support waking activity. Thus the study of sleep may elucidate the circuits and processes that support waking function and complement information obtained from fMRI during waking conditions. In this review, we will discuss examples of this for memory, arousal, and consciousness after providing a brief background on sleep and on studying it with fMRI. PMID:23707592

Virtual reality and consciousness inference in dreaming

PubMed Central

Hobson, J. Allan; Hong, Charles C.-H.; Friston, Karl J.

2014-01-01

This article explores the notion that the brain is genetically endowed with an innate virtual reality generator that – through experience-dependent plasticity – becomes a generative or predictive model of the world. This model, which is most clearly revealed in rapid eye movement (REM) sleep dreaming, may provide the theater for conscious experience. Functional neuroimaging evidence for brain activations that are time-locked to rapid eye movements (REMs) endorses the view that waking consciousness emerges from REM sleep – and dreaming lays the foundations for waking perception. In this view, the brain is equipped with a virtual model of the world that generates predictions of its sensations. This model is continually updated and entrained by sensory prediction errors in wakefulness to ensure veridical perception, but not in dreaming. In contrast, dreaming plays an essential role in maintaining and enhancing the capacity to model the world by minimizing model complexity and thereby maximizing both statistical and thermodynamic efficiency. This perspective suggests that consciousness corresponds to the embodied process of inference, realized through the generation of virtual realities (in both sleep and wakefulness). In short, our premise or hypothesis is that the waking brain engages with the world to predict the causes of sensations, while in sleep the brain’s generative model is actively refined so that it generates more efficient predictions during waking. We review the evidence in support of this hypothesis – evidence that grounds consciousness in biophysical computations whose neuronal and neurochemical infrastructure has been disclosed by sleep research. PMID:25346710

Advice for the Sleep-Deprived

ERIC Educational Resources Information Center

Wolfe, Pat

2005-01-01

A research has uncovered that adolescent sleep patterns are influenced not so much by the activities of the young adults as by the changes taking place in the biological timing system of their brains. It is evident that teenagers are not getting the amount of sleep they require and suggestions are presented to help diminish if not entirely avoid…

Cytophotometric study of ATPase activity in brain neurons and gliocytes of paradoxical sleep-deprived rats.

PubMed

Klenikova, V A; Taranova, N P

1989-01-01

Conditions were chosen for optimal demonstration of ATPases in brain slices by a modified method of Wachstein and Meisel, and the reaction was shown to obey the Bouguer-Beer laws, confirming that ATPase activity can be determined quantitatively in single cells by cytophotometry. In rats in a state of relative physiological rest specific activity of both Na+, K+-ATPase and Mg++-ATPase in gliocytes of the hippocampus and dorsal raphe was found to be considerably higher than in neurons. Deprivation of the paradoxical phase of sleep of the rats for 24 h led to a significant increase in Na+, K+-ATPase activity in hippocampal neurons and to a decrease in its activity in gliocytes of the hippocampus and dorsal nucleus raphe. It is suggested that these changes in Na+, K+-ATPase activity may be due to some extent to a change in excitability of neurons and depolarization of the glia when sleep is disturbed.

Aberrant brain stem morphometry associated with sleep disturbance in drug-naïve subjects with Alzheimer's disease.

PubMed

Lee, Ji Han; Jung, Won Sang; Choi, Woo Hee; Lim, Hyun Kook

2016-01-01

Among patients with Alzheimer's disease (AD), sleep disturbances are common and serious noncognitive symptoms. Previous studies of AD patients have identified deformations in the brain stem, which may play an important role in the regulation of sleep. The aim of this study was to further investigate the relationship between sleep disturbances and alterations in brain stem morphology in AD. In 44 patients with AD and 40 healthy elderly controls, sleep disturbances were measured using the Neuropsychiatry Inventory sleep subscale. We employed magnetic resonance imaging-based automated segmentation tools to examine the relationship between sleep disturbances and changes in brain stem morphology. Analyses of the data from AD subjects revealed significant correlations between the Neuropsychiatry Inventory sleep-subscale scores and structural alterations in the left posterior lateral region of the brain stem, as well as normalized brain stem volumes. In addition, significant group differences in posterior brain stem morphology were observed between the AD group and the control group. This study is the first to analyze an association between sleep disturbances and brain stem morphology in AD. In line with previous findings, this study lends support to the possibility that brain stem structural abnormalities might be important neurobiological mechanisms underlying sleep disturbances associated with AD. Further longitudinal research is needed to confirm these findings.

Neural Markers of Responsiveness to the Environment in Human Sleep.

PubMed

Andrillon, Thomas; Poulsen, Andreas Trier; Hansen, Lars Kai; Léger, Damien; Kouider, Sid

2016-06-15

Sleep is characterized by a loss of behavioral responsiveness. However, recent research has shown that the sleeping brain is not completely disconnected from its environment. How neural activity constrains the ability to process sensory information while asleep is yet unclear. Here, we instructed human volunteers to classify words with lateralized hand responses while falling asleep. Using an electroencephalographic (EEG) marker of motor preparation, we show how responsiveness is modulated across sleep. These modulations are tracked using classic event-related potential analyses complemented by Lempel-Ziv complexity (LZc), a measure shown to track arousal in sleep and anesthesia. Neural activity related to the semantic content of stimuli was conserved in light non-rapid eye movement (NREM) sleep. However, these processes were suppressed in deep NREM sleep and, importantly, also in REM sleep, despite the recovery of wake-like neural activity in the latter. In NREM sleep, sensory activations were counterbalanced by evoked down states, which, when present, blocked further processing of external information. In addition, responsiveness markers correlated positively with baseline complexity, which could be related to modulation in sleep depth. In REM sleep, however, this relationship was reversed. We therefore propose that, in REM sleep, endogenously generated processes compete with the processing of external input. Sleep can thus be seen as a self-regulated process in which external information can be processed in lighter stages but suppressed in deeper stages. Last, our results suggest drastically different gating mechanisms in NREM and REM sleep. Previous research has tempered the notion that sleepers are isolated from their environment. Here, we pushed this idea forward and examined, across all sleep stages, the brain's ability to flexibly process sensory information, up to the decision level. We extracted an EEG marker of motor preparation to determine the completion of the sensory processing chain and explored how it is constrained by baseline and evoked neural activity. In NREM sleep, slow waves elicited by stimuli appeared to block response preparation. We also used a novel analytic approach (Lempel-Ziv complexity) and showed that the ability to process external information correlates with neural complexity. A reversal of the correlation between complexity and motor indices in REM sleep suggests drastically different gating mechanisms across sleep stages. Copyright © 2016 the authors 0270-6474/16/366583-14$15.00/0.

Effects of CPAP-therapy on brain electrical activity in obstructive sleep apneic patients: a combined EEG study using LORETA and Omega complexity : reversible alterations of brain activity in OSAS.

PubMed

Toth, Marton; Faludi, Bela; Kondakor, Istvan

2012-10-01

Effects of initiation of continuous positive airway pressure (CPAP) therapy on EEG background activity were investigated in patients with obstructive sleep apnea syndrome (OSAS, N = 25) to test possible reversibility of alterations of brain electrical activity caused by chronic hypoxia. Normal control group (N = 14) was also examined. Two EEG examinations were done in each groups: at night and in the next morning. Global and regional (left vs. right, anterior vs. posterior) measures of spatial complexity (Omega complexity) were used to characterize the degree of spatial synchrony of EEG. Low resolution electromagnetic tomography (LORETA) was used to localize generators of EEG activity in separate frequency bands. Before CPAP-treatment, a significantly lower Omega complexity was found globally and over the right hemisphere. Due to CPAP-treatment, these significant differences vanished. Significantly decreased Omega complexity was found in the anterior region after treatment. LORETA showed a decreased activity in all of the beta bands after therapy in the right hippocampus, premotor and temporo-parietal cortex, and bilaterally in the precuneus, paracentral and posterior cingulate cortex. No significant changes were seen in control group. Comparing controls and patients before sleep, an increased alpha2 band activity was seen bilaterally in the precuneus, paracentral and posterior cingulate cortex, while in the morning an increased beta3 band activity in the left precentral and bilateral premotor cortex and a decreased delta band activity in the right temporo-parietal cortex and insula were observed. These findings indicate that effect of sleep on EEG background activity is different in OSAS patients and normal controls. In OSAS patients, significant changes lead to a more normal EEG after a night under CPAP-treatment. Compensatory alterations of brain electrical activity in regions associated with influencing sympathetic outflow, visuospatial abilities, long-term memory and motor performances caused by chronic hypoxia could be reversed by CPAP-therapy.

[Microinjections of heat shock protein 70 kDa into the nucleus reticularis pontis oralis induce inhibition of rapid eye movement sleep in pigeons].

PubMed

Gusel'nikova, E A; Pastukhov, Iu F

2008-03-01

Recently it was indicated that microinjections of heat shock proteins 70 kDa (Hsp70) into the third ventricle of brain in pigeons results in an increase in the duration of slow wave sleep and a decrease in somato-visceral indices. It is suggested that Hsp70 effect may be related to GABA(A) receptors activation in the preoptic area of the hypothalamus. However, what transmitter mechanisms of activation are related to the removal effect (in 2-3 hrs) of rapid eye movement sleep inhibition still remains poorly understood. To solve this problem in the present study, microinjections of Hsp70 into the Nucleus reticularis pontis oralis (NRPO) were done. It is well known that cholinergic neurons of the NRPO are crucial for rapid eye movement sleep generation. The data show that Hsp70 produces more early (for first two hrs) a decrease in number of episodes and total time of rapid eye movement sleep, a diminution of electroencephalogram (EEG) power spectra in the 9-14 Hz band, a decrease in contractile muscle activity and brain temperature. It is suggested that Hsp70 effects are realized due to activation of GABA(A) receptors in the NRPO and induced inhibition of cholinergic mechanisms of rapid eye movement sleep triggering. The microinjections of Hsp70 into the NRPO increase the slow wave sleep total time with long latency (for 8-12 hrs). This effect may be related to influence of Hsp70 on neurons population, which are responsible for slow wave sleep maintenance outside the NRPO.

Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

PubMed Central

Goldstein-Piekarski, Andrea N.; Greer, Stephanie M.; Stark, Shauna; Stark, Craig E.

2016-01-01

Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine). SIGNIFICANCE STATEMENT Sleep deprivation does not impact all people equally. Some individuals show cognitive resilience to the effects of sleep loss, whereas others express striking vulnerability, the reasons for which remain largely unknown. Here, we demonstrate that structural features of the human brain, specifically those within the hippocampus, accurately predict which individuals are susceptible (or conversely, resilient) to memory impairments caused by sleep deprivation. Moreover, this same structural feature determines the success of memory restoration following subsequent recovery sleep. Therefore, structural properties of the human brain represent a novel biomarker predicting individual vulnerability to (and recovery from) the effects of sleep loss, one with occupational relevance in professions where insufficient sleep is pervasive yet memory function is paramount. PMID:26911684

Auditory evoked magnetic fields to speech stimuli in newborns--effect of sleep stages.

PubMed

Pihko, E; Sambeth, A; Leppänen, P H T; Okada, Y; Lauronen, L

2004-11-30

The aim of the study was to examine whether a newborn can detect changes in a speech stimulus consisting of a fricative followed by a vowel /su/. In addition, we studied possible effect of the two sleep stages (active and quiet sleep) on the evoked magnetic responses. In young children (6 years), the same stimulus evokes a prominent deflection, consisting of two peaks. The first one (P1m) is evoked by the beginning of the fricative consonant and has a latency of about 145 ms. The second peak (P2m) with a latency of 340 ms, is evoked by the switch to the vowel. In newborns (n = 10), the waveform resembled that of the older children but latencies of the corresponding peaks were longer, 190 and 435 ms, correspondingly. The results suggest that already the newborn brain detects the change inside the auditory speech stimulus, namely the fricative sound changing into a vowel. However, the immaturity of the brain is reflected in the prolonged latencies. In addition, the responses were higher in amplitude in quiet sleep than in active sleep (F (1.9) = 36.5; p < 0.0002). This is in line with the enhanced somatosensory magnetic fields to tactile stimulation in quiet compared to active sleep in newborns.

β Oscillation during Slow Wave Sleep and Rapid Eye Movement Sleep in the Electroencephalogram of a Transgenic Mouse Model of Huntington’s Disease

PubMed Central

Jeantet, Yannick; Cayzac, Sebastien; Cho, Yoon H.

2013-01-01

Study objectives To search for early abnormalities in electroencephalogram (EEG) during sleep which may precede motor symptoms in a transgenic mouse model of hereditary neurodegenerative Huntington’s disease (HD). Design In the R6/1 transgenic mouse model of HD, rhythmic brain activity in EEG recordings was monitored longitudinally and across vigilance states through the onset and progression of disease. Measurements and results Mice with chronic electrode implants were recorded monthly over wake-sleep cycles (4 hours), beginning at 9–11 weeks (presymptomatic period) through 6–7 months (symptomatic period). Recording data revealed a unique β rhythm (20–35 Hz), present only in R6/1 transgenic mice, which evolves in close parallel with the disease. In addition, there was an unusual relationship between this β oscillation and vigilance states: while nearly absent during the active waking state, the β oscillation appeared with drowsiness and during slow wave sleep (SWS) and, interestingly, strengthened rather than dissipating when the brain returned to an activated state during rapid eye movement (REM) sleep. Conclusions In addition to providing a new in vivo biomarker and insight into Huntington's disease pathophysiology, this serendipitous observation opens a window onto the rarely explored neurophysiology of the cortico-basal ganglia circuit during SWS and REM sleep. PMID:24244517

Update of sleep alterations in depression

PubMed Central

Medina, Andrés Barrera; Lechuga, DeboraYoaly Arana; Escandón, Oscar Sánchez; Moctezuma, Javier Velázquez

2014-01-01

Sleep disturbances in depression are up to 70%. Patients frequently have difficulty in falling asleep, frequent awakenings during the night and non-restorative sleep. Sleep abnormalities in depression are mainly characterized by increased rapid eye movement (REM) sleep and reduced slow wave sleep. Among the mechanisms of sleep disturbances in depression are hyperactivation of the hypothalamic-pituitary-adrenal axis, CLOCK gene polymorphism and primary sleep disorders. The habenula is a structure regulating the activities of monoaminergic neurons in the brain. The hyperactivation of the habenula has also been implicated, together with sleep disturbances, in depression. The presence of depression in primary sleep disorders is common. Sleep disturbances treatment include pharmacotherapy or Cognitive Behavioral Therapy. PMID:26483922

Regional cerebral metabolic correlates of WASO during NREM sleep in insomnia.

PubMed

Nofzinger, Eric A; Nissen, Christoph; Germain, Anne; Moul, Douglas; Hall, Martica; Price, Julie C; Miewald, Jean M; Buysse, Daniel J

2006-07-15

To investigate the non-rapid eye movement (NREM) sleep-related regional cerebral metabolic correlates of wakefulness after sleep onset (WASO) in patients with primary insomnia. Fifteen patients who met DSM-IV criteria for primary insomnia completed 1-week sleep diary (subjective) and polysomnographic (objective) assessments of WASO and regional cerebral glucose metabolic assessments during NREM sleep using [18F] fluoro-2-deoxy-D-glucose positron emission tomography. Whole-brain voxel-by-voxel correlations, as well as region of interest analyses, were performed between subjective and objective WASO and relative regional cerebral metabolism using the statistical software SPM2. Subjective WASO was significantly greater than objective WASO, but the 2 measures were positively correlated. Objective WASO correlated positively with the percentage of stage 2 sleep and negatively with the percentage of stages 3 and 4 sleep. Both subjective and objective WASO positively correlated with NREM sleep-related cerebral glucose metabolism in the pontine tegmentum and in thalamocortical networks in a frontal, anterior temporal, and anterior cingulate distribution. Increased relative metabolism in these brain regions during NREM sleep in patients with insomnia is associated with increased WASO measured either subjectively or objectively. These effects are related to the lighter sleep stages of patients with more WASO and may result from increased activity in arousal systems during sleep and or to activity in higher-order cognitive processes related to goal-directed behavior, conflict monitoring, emotional awareness, anxiety, and fear. Such changes may decrease arousal thresholds and/or increase perceptions of wakefulness in insomnia.

About sleep's role in memory.

PubMed

Rasch, Björn; Born, Jan

2013-04-01

Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

Traveling Slow Oscillations During Sleep: A Marker of Brain Connectivity in Childhood.

PubMed

Kurth, Salome; Riedner, Brady A; Dean, Douglas C; O'Muircheartaigh, Jonathan; Huber, Reto; Jenni, Oskar G; Deoni, Sean C L; LeBourgeois, Monique K

2017-09-01

Slow oscillations, a defining characteristic of the nonrapid eye movement sleep electroencephalogram (EEG), proliferate across the scalp in highly reproducible patterns. In adults, the propagation of slow oscillations is a recognized fingerprint of brain connectivity and excitability. In this study, we (1) describe for the first time maturational features of sleep slow oscillation propagation in children (n = 23; 2-13 years) using high-density (hd) EEG and (2) examine associations between sleep slow oscillatory propagation characteristics (ie, distance, traveling speed, cortical involvement) and white matter myelin microstructure as measured with multicomponent Driven Equilibrium Single Pulse Observation of T1 and T2-magnetic resonance imaging (mcDESPOT-MRI). Results showed that with increasing age, slow oscillations propagated across longer distances (average growth of 0.2 cm per year; R(21) = 0.50, p < .05), while traveling speed and cortical involvement (ie, slow oscillation expanse) remained unchanged across childhood. Cortical involvement (R(20) = 0.44) and slow oscillation speed (R(20) = -0.47; both p < .05, corrected for age) were associated with myelin content in the superior longitudinal fascicle, the largest anterior-posterior, intrahemispheric white matter connectivity tract. Furthermore, slow oscillation distance was moderately associated with whole-brain (R(21) = 0.46, p < .05) and interhemispheric myelin content, the latter represented by callosal myelin water fraction (R(21) = 0.54, p < .01, uncorrected). Thus, we demonstrate age-related changes in slow oscillation propagation distance, as well as regional associations between brain activity during sleep and the anatomical connectivity of white matter microstructure. Our findings make an important contribution to knowledge of the brain connectome using a noninvasive and novel analytic approach. These data also have implications for understanding the emergence of neurodevelopmental disorders and the role of sleep in brain maturation trajectories. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Acidic fibroblast growth factor (FGF) but not basic FGF induces sleep and fever in rabbits.

PubMed

Knefati, M; Somogyi, C; Kapás, L; Bourcier, T; Krueger, J M

1995-07-01

Acidic fibroblast growth factor (FGF) and basic FGF belong to a growth factor family. Interleukin-1, another member of that family, is involved in sleep regulation. FGFs and interleukin-1 share structural and functional features. We therefore determined whether acidic FGF and basic FGF were somnogenic. Male New Zealand White rabbits were provided with electroencephalographic (EEG) electrodes, a brain thermistor, and a lateral intracerebroventricular (icv) cannula. The animals were injected icv with isotonic NaCl (control) and on separate days with one of three doses of acidic or basic FGF (0.01, 0.1, or 1.0 micrograms) or with heat-treated acidic FGF (1.0 micrograms). The EEG, brain temperature, and motor activity were recorded for 23 h. The biological activity of basic FGF was determined in vitro by its ability to induce DNA synthesis in rat aortic smooth muscle cells. Acidic FGF induced prolonged dose-related increases in non-rapid eye movement sleep beginning in the 1st postinjection h and continuing for 12-23 h after the treatment. Acidic FGF also induced fevers of approximately 1 degree C after the 1.0 micrograms dose. Both activities of acidic FGF were lost after heat treatment. In contrast, basic FGF lacked somnogenic and pyrogenic activity, although it did induce DNA synthesis. Current results suggest that acidic FGF is part of the complex cytokine network in brain involved in sleep regulation.

Brain Basics: Understanding Sleep

MedlinePlus

... slow, and muscles relax even further. Your body temperature drops and eye movements stop. Brain wave activity ... functions from daily fluctuations in wakefulness to body temperature, metabolism, and the release of hormones. They control ...

Repetitive Traumatic Brain Injury (or Concussion) Increases Severity of Sleep Disturbance among Deployed Military Personnel

PubMed Central

Bryan, Craig J.

2013-01-01

Study Objectives: Considerable research indicates that sleep disturbances and insomnia are more common and severe among individuals following a traumatic brain injury (TBI). It remains unclear, however, how the experience of multiple TBIs affect sleep disturbances and insomnia. The current study investigated the incidence and severity of insomnia and sleep complaints among active-duty military personnel who have sustained multiple TBIs. Design and Setting: Upon intake at a military TBI clinic located in Iraq, 150 male military patients completed standardized self-report measures and clinical interviews. Measurements and Results: Patients were categorized into three groups according to history of TBI: zero TBIs (n = 18), single TBI (n = 54), multiple TBIs (n = 78). Rates of clinical insomnia significantly increased across TBI groups (P < 0.001):- 5.6% for no TBIs, 20.4% for single TBI, and 50.0% for multiple TBIs. Insomnia severity significantly increased across TBI groups even when controlling for depression, posttraumatic stress disorder, and concussion symptom severity (B = 1.134, standard error = 0.577, P = 0.049). Conclusions: Multiple TBIs are associated with increased risk for and severity of sleep disturbance among male military personnel. Citation: Bryan CJ. Repetitive traumatic brain injury (or concussion) increases severity of sleep disturbance among deployed military personnel. SLEEP 2013;36(6):941-946. PMID:23729938

Novel Intrinsic Ignition Method Measuring Local-Global Integration Characterizes Wakefulness and Deep Sleep

PubMed Central

Tagliazucchi, Enzo; Sanjuán, Ana

2017-01-01

Abstract A precise definition of a brain state has proven elusive. Here, we introduce the novel local-global concept of intrinsic ignition characterizing the dynamical complexity of different brain states. Naturally occurring intrinsic ignition events reflect the capability of a given brain area to propagate neuronal activity to other regions, giving rise to different levels of integration. The ignitory capability of brain regions is computed by the elicited level of integration for each intrinsic ignition event in each brain region, averaged over all events. This intrinsic ignition method is shown to clearly distinguish human neuroimaging data of two fundamental brain states (wakefulness and deep sleep). Importantly, whole-brain computational modelling of this data shows that at the optimal working point is found where there is maximal variability of the intrinsic ignition across brain regions. Thus, combining whole brain models with intrinsic ignition can provide novel insights into underlying mechanisms of brain states. PMID:28966977

Novel Intrinsic Ignition Method Measuring Local-Global Integration Characterizes Wakefulness and Deep Sleep.

PubMed

Deco, Gustavo; Tagliazucchi, Enzo; Laufs, Helmut; Sanjuán, Ana; Kringelbach, Morten L

2017-01-01

A precise definition of a brain state has proven elusive. Here, we introduce the novel local-global concept of intrinsic ignition characterizing the dynamical complexity of different brain states. Naturally occurring intrinsic ignition events reflect the capability of a given brain area to propagate neuronal activity to other regions, giving rise to different levels of integration. The ignitory capability of brain regions is computed by the elicited level of integration for each intrinsic ignition event in each brain region, averaged over all events. This intrinsic ignition method is shown to clearly distinguish human neuroimaging data of two fundamental brain states (wakefulness and deep sleep). Importantly, whole-brain computational modelling of this data shows that at the optimal working point is found where there is maximal variability of the intrinsic ignition across brain regions. Thus, combining whole brain models with intrinsic ignition can provide novel insights into underlying mechanisms of brain states.

Hyperglycemia is associated with simultaneous alterations in electrical brain activity in youths with type 1 diabetes mellitus.

PubMed

Rachmiel, M; Cohen, M; Heymen, E; Lezinger, M; Inbar, D; Gilat, S; Bistritzer, T; Leshem, G; Kan-Dror, E; Lahat, E; Ekstein, D

2016-02-01

To assess the association between hyperglycemia and electrical brain activity in type 1 diabetes mellitus (T1DM). Nine youths with T1DM were monitored simultaneously and continuously by EEG and continuous glucose monitor system, for 40 h. EEG powers of 0.5-80 Hz frequency bands in all the different brain regions were analyzed according to interstitial glucose concentration (IGC) ranges of 4-11 mmol/l, 11-15.5 mmol/l and >15.5 mmol/l. Analysis of variance was used to examine the differences in EEG power of each frequency band between the subgroups of IGC. Analysis was performed separately during wakefulness and sleep, controlling for age, gender and HbA1c. Mean IGC was 11.49 ± 5.26 mmol/l in 1253 combined measurements. IGC>15.5 mmol/l compared to 4-11 mmol/l was associated during wakefulness with increased EEG power of low frequencies and with decreased EEG power of high frequencies. During sleep, it was associated with increased EEG power of low frequencies in all brain areas and of high frequencies in frontal and central areas. Asymptomatic transient hyperglycemia in youth with T1DM is associated with simultaneous alterations in electrical brain activity during wakefulness and sleep. The clinical implications of immediate electrical brain alterations under hyperglycemia need to be studied and may lead to adaptations of management. Copyright © 2015. Published by Elsevier Ireland Ltd.

Brain Damage and Motor Cortex Impairment in Chronic Obstructive Pulmonary Disease: Implication of Nonrapid Eye Movement Sleep Desaturation.

PubMed

Alexandre, Francois; Heraud, Nelly; Sanchez, Anthony M J; Tremey, Emilie; Oliver, Nicolas; Guerin, Philippe; Varray, Alain

2016-02-01

Nonrapid eye movement (NREM) sleep desaturation may cause neuronal damage due to the withdrawal of cerebrovascular reactivity. The current study (1) assessed the prevalence of NREM sleep desaturation in nonhypoxemic patients with chronic obstructive pulmonary disease (COPD) and (2) compared a biological marker of cerebral lesion and neuromuscular function in patients with and without NREM sleep desaturation. One hundred fifteen patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 2 and 3), resting PaO2 of 60-80 mmHg, aged between 40 and 80 y, and without sleep apnea (apnea-hypopnea index < 15) had polysomnographic sleep recordings. In addition, twenty-nine patients (substudy) were assessed i) for brain impairment by serum S100B (biological marker of cerebral lesion), and ii) for neuromuscular function via motor cortex activation and excitability and maximal voluntary quadriceps strength measurement. A total of 51.3% patients (n = 59) had NREM sleep desaturation (NREMDes). Serum S100B was higher in the NREMDes patients of the substudy (n = 14): 45.1 [Q1: 37.7, Q3: 62.8] versus 32.9 [Q1: 25.7, Q3: 39.5] pg.ml(-1) (P = 0.028). Motor cortex activation and excitability were lower in NREMDes patients (both P = 0.03), but muscle strength was comparable between groups (P = 0.58). Over half the nonhypoxemic COPD patients exhibited NREM sleep desaturation associated with higher values of the cerebral lesion biomarker and lower neural drive reaching the quadriceps during maximal voluntary contraction. The lack of muscle strength differences between groups suggests a compensatory mechanism(s). Altogether, the results are consistent with an involvement of NREM sleep desaturation in COPD brain impairment. The study was registered at www.clinicaltrials.gov as NCT01679782. © 2016 Associated Professional Sleep Societies, LLC.

Aberrant Axonal Arborization of PDF Neurons Induced by Aβ42-Mediated JNK Activation Underlies Sleep Disturbance in an Alzheimer's Model.

PubMed

Song, Qian; Feng, Ge; Huang, Zehua; Chen, Xiaoman; Chen, Zhaohuan; Ping, Yong

2017-10-01

Impaired sleep patterns are common symptoms of Alzheimer's disease (AD). Cellular mechanisms underlying sleep disturbance in AD remain largely unknown. Here, using a Drosophila Aβ42 AD model, we show that Aβ42 markedly decreases sleep in a large population, which is accompanied with postdevelopmental axonal arborization of wake-promoting pigment-dispersing factor (PDF) neurons. The arborization is mediated in part via JNK activation and can be reversed by decreasing JNK signaling activity. Axonal arborization and impaired sleep are correlated in Aβ42 and JNK kinase hemipterous mutant flies. Image reconstruction revealed that these aberrant fibers preferentially project to pars intercerebralis (PI), a fly brain region analogous to the mammalian hypothalamus. Moreover, PDF signaling in PI neurons was found to modulate sleep/wake activities, suggesting that excessive release of PDF by these aberrant fibers may lead to the impaired sleep in Aβ42 flies. Finally, inhibition of JNK activation in Aβ42 flies restores nighttime sleep loss, decreases Aβ42 accumulation, and attenuates neurodegeneration. These data provide a new mechanism by which sleep disturbance could be induced by Aβ42 burden, a key initiator of a complex pathogenic cascade in AD.

Vagotomy attenuates brain cytokines and sleep induced by peripherally administered tumor necrosis factor-α and lipopolysaccharide in mice.

PubMed

Zielinski, Mark R; Dunbrasky, Danielle L; Taishi, Ping; Souza, Gianne; Krueger, James M

2013-08-01

Systemic tumor necrosis factor-α (TNF-α) is linked to sleep and sleep altering pathologies in humans. Evidence from animals indicates that systemic and brain TNF-α have a role in regulating sleep. In animals, TNF-α or lipopolysaccharide (LPS) enhance brain pro-inflammatory cytokine expression and sleep after central or peripheral administration. Vagotomy blocks enhanced sleep induced by systemic TNF-α and LPS in rats, suggesting that vagal afferent stimulation by TNF-α enhances pro-inflammatory cytokines in sleep-related brain areas. However, the effects of systemic TNF-α on brain cytokine expression and mouse sleep remain unknown. We investigated the role of vagal afferents on brain cytokines and sleep after systemically applied TNF-α or LPS in mice. Spontaneous sleep was similar in vagotomized and sham-operated controls. Vagotomy attenuated TNF-α- and LPS-enhanced non-rapid eye movement sleep (NREMS); these effects were more evident after lower doses of these substances. Vagotomy did not affect rapid eye movement sleep responses to these substances. NREMS electroencephalogram delta power (0.5-4 Hz range) was suppressed after peripheral TNF-α or LPS injections, although vagotomy did not affect these responses. Compared to sham-operated controls, vagotomy did not affect liver cytokines. However, vagotomy attenuated interleukin-1 beta (IL-1β) and TNF-α mRNA brain levels after TNF-α, but not after LPS, compared to the sham-operated controls. We conclude that vagal afferents mediate peripheral TNF-α-induced brain TNF-α and IL-1β mRNA expressions to affect sleep. We also conclude that vagal afferents alter sleep induced by peripheral pro-inflammatory stimuli in mice similar to those occurring in other species.

Far-red to near infrared emission and scattering spectroscopy for biomedical applications

NASA Astrophysics Data System (ADS)

Zhang, Gang

2001-06-01

The thesis investigates the far-red and near infrared (NIR) spectral region from biomedical tissue samples for monitoring the state of tissues. The NIR emission wing intensity is weak in comparison to the emission in the visible spectral region. The wing emission from biomedical samples has revealed meaningful information about the state of the tissues. A model is presented to explain the shape of the spectral wing based on a continuum of energy levels. The wing can be used to classify different kinds of tissues; especially it can be used to differentiate cancer part from normal human breast tissues. The research work of the far-red emission from thermal damaged tissue samples shows that the emission intensity in this spectral region is proportional to the extent of the thermal damage of the tissue. Near infrared spectral absorption method is used to investigate blood hemodynamics (perfusion and oxygenation) in brain during sleep-wake transition. The result of the research demonstrates that the continuous wave (CW) type near infrared spectroscopy (NIRS) device can be used to investigate brain blood perfusion and oxygenation with a similar precision with frequency domain (FD) type device. The human subject sleep and wake transition, has been monitored by CW type NIRS instrument with traditional electroencephalograph (EEG) method. Parallel change in oxy-Hb and deoxy-Hb is a discrete event that occurs in the transition from both sleep to wakefulness and wakefulness to sleep. These hemodynamic switches are generally about few seconds delayed from the human decided transition point between sleep and wake on the polygraph EEG recording paper. The combination of NIRS and EEG methods monitor the brain activity, gives more information about the brain activity. The sleep apnea investigation was associated with recurrent apneas, insufficient nasal continuous positive airway pressure (CPAP) and the different response of the peripheral and central compartments to breathing events. The different results with finger pulse oximetry and NIRS suggest that optical monitoring of the brain may have advantages that may help clarify the morbidity of obstructive sleep apnea (OSA) Syndrome.

Intrinsic Brain Activity in Altered States of Consciousness

PubMed Central

Boly, M.; Phillips, C.; Tshibanda, L.; Vanhaudenhuyse, A.; Schabus, M.; Dang-Vu, T.T.; Moonen, G.; Hustinx, R.; Maquet, P.; Laureys, S.

2010-01-01

Spontaneous brain activity has recently received increasing interest in the neuroimaging community. However, the value of resting-state studies to a better understanding of brain–behavior relationships has been challenged. That altered states of consciousness are a privileged way to study the relationships between spontaneous brain activity and behavior is proposed, and common resting-state brain activity features observed in various states of altered consciousness are reviewed. Early positron emission tomography studies showed that states of extremely low or high brain activity are often associated with unconsciousness. However, this relationship is not absolute, and the precise link between global brain metabolism and awareness remains yet difficult to assert. In contrast, voxel-based analyses identified a systematic impairment of associative frontoparieto–cingulate areas in altered states of consciousness, such as sleep, anesthesia, coma, vegetative state, epileptic loss of consciousness, and somnambulism. In parallel, recent functional magnetic resonance imaging studies have identified structured patterns of slow neuronal oscillations in the resting human brain. Similar coherent blood oxygen level–dependent (BOLD) systemwide patterns can also be found, in particular in the default-mode network, in several states of unconsciousness, such as coma, anesthesia, and slow-wave sleep. The latter results suggest that slow coherent spontaneous BOLD fluctuations cannot be exclusively a reflection of conscious mental activity, but may reflect default brain connectivity shaping brain areas of most likely interactions in a way that transcends levels of consciousness, and whose functional significance remains largely in the dark. PMID:18591474

Functional brain imaging of a complex navigation task following one night of total sleep deprivation

NASA Technical Reports Server (NTRS)

Strangman, Gary; Thompson, John H.; Strauss, Monica M.; Marshburn, Thomas H.; Sutton, Jeffrey P.

2006-01-01

Study Objectives: To assess the cerebral effects associated with sleep deprivation in a simulation of a complex, real-world, high-risk task. Design and Interventions: A two-week, repeated measures, cross-over experimental protocol, with counterbalanced orders of normal sleep (NS) and total sleep deprivation (TSD). Setting: Each subject underwent functional magnetic resonance imaging (fMRI) while performing a dual-joystick, 3D sensorimotor navigation task (simulated orbital docking). Scanning was performed twice per subject, once following a night of normal sleep (NS), and once following a single night of total sleep deprivation (TSD). Five runs (eight 24s docking trials each) were performed during each scanning session. Participants: Six healthy, young, right-handed volunteers (2 women; mean age 20) participated. Measurements and Results: Behavioral performance on multiple measures was comparable in the two sleep conditions. Neuroimaging results within sleep conditions revealed similar locations of peak activity for NS and TSD, including left sensorimotor cortex, left precuneus (BA 7), and right visual areas (BA 18/19). However, cerebral activation following TSD was substantially larger and exhibited higher amplitude modulations from baseline. When directly comparing NS and TSD, most regions exhibited TSD>NS activity, including multiple prefrontal cortical areas (BA 8/9,44/45,47), lateral parieto-occipital areas (BA 19/39, 40), superior temporal cortex (BA 22), and bilateral thalamus and amygdala. Only left parietal cortex (BA 7) demonstrated NS>TSD activity. Conclusions: The large network of cerebral differences between the two conditions, even with comparable behavioral performance, suggests the possibility of detecting TSD-induced stress via functional brain imaging techniques on complex tasks before stress-induced failures.

About Sleep's Role in Memory

PubMed Central

2013-01-01

Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of “sleep and memory” research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems. PMID:23589831

Testing the involvement of the prefrontal cortex in lucid dreaming: a tDCS study.

PubMed

Stumbrys, Tadas; Erlacher, Daniel; Schredl, Michael

2013-12-01

Recent studies suggest that lucid dreaming (awareness of dreaming while dreaming) might be associated with increased brain activity over frontal regions during rapid eye movement (REM) sleep. By applying transcranial direct current stimulation (tDCS), we aimed to manipulate the activation of the dorsolateral prefrontal cortex (DLPFC) during REM sleep to increase dream lucidity. Nineteen participants spent three consecutive nights in a sleep laboratory. On the second and third nights they randomly received either 1 mA tDCS for 10 min or sham stimulation during each REM period starting with the second one. According to the participants' self-ratings, tDCS over the DLPFC during REM sleep increased lucidity in dreams. The effects, however, were not strong and found only in frequent lucid dreamers. While this indicates some preliminary support for the involvement of the DLPFC in lucid dreaming, further research, controlling for indirect effects of stimulation and including other brain regions, is needed. Copyright © 2013 Elsevier Inc. All rights reserved.

Local Use-Dependent Sleep in Wakefulness Links Performance Errors to Learning

PubMed Central

Quercia, Angelica; Zappasodi, Filippo; Committeri, Giorgia; Ferrara, Michele

2018-01-01

Sleep and wakefulness are no longer to be considered as discrete states. During wakefulness brain regions can enter a sleep-like state (off-periods) in response to a prolonged period of activity (local use-dependent sleep). Similarly, during nonREM sleep the slow-wave activity, the hallmark of sleep plasticity, increases locally in brain regions previously involved in a learning task. Recent studies have demonstrated that behavioral performance may be impaired by off-periods in wake in task-related regions. However, the relation between off-periods in wake, related performance errors and learning is still untested in humans. Here, by employing high density electroencephalographic (hd-EEG) recordings, we investigated local use-dependent sleep in wake, asking participants to repeat continuously two intensive spatial navigation tasks. Critically, one task relied on previous map learning (Wayfinding) while the other did not (Control). Behaviorally awake participants, who were not sleep deprived, showed progressive increments of delta activity only during the learning-based spatial navigation task. As shown by source localization, delta activity was mainly localized in the left parietal and bilateral frontal cortices, all regions known to be engaged in spatial navigation tasks. Moreover, during the Wayfinding task, these increments of delta power were specifically associated with errors, whose probability of occurrence was significantly higher compared to the Control task. Unlike the Wayfinding task, during the Control task neither delta activity nor the number of errors increased progressively. Furthermore, during the Wayfinding task, both the number and the amplitude of individual delta waves, as indexes of neuronal silence in wake (off-periods), were significantly higher during errors than hits. Finally, a path analysis linked the use of the spatial navigation circuits undergone to learning plasticity to off periods in wake. In conclusion, local sleep regulation in wakefulness, associated with performance failures, could be functionally linked to learning-related cortical plasticity. PMID:29666574

Comparison of quantitative EEG characteristics of quiet and active sleep in newborns.

PubMed

Paul, Karel; Krajca, Vladimír; Roth, Zdenek; Melichar, Jan; Petránek, Svojmil

2003-11-01

The aim of the present study was to verify whether the proposed method of computer-supported EEG analysis is able to differentiate the EEG activity in quiet sleep (QS) from that in active sleep (AS) in newborns. A quantitative description of the neonatal EEG may contribute to a more exact evaluation of the functional state of the brain, as well as to a refinement of diagnostics of brain dysfunction manifesting itself frequently as 'dysrhythmia' or 'dysmaturity'. Twenty-one healthy newborns (10 full-term and 11 pre-term) were examined polygraphically (EEG-eight channels, respiration, ECG, EOG and EMG) in the course of sleep. From each EEG record, two 5-min samples (one from QS and one from AS) were subject to an off-line computerized analysis. The obtained data were averaged with respect to the sleep state and to the conceptional age. The number of variables was reduced by means of factor analysis. All factors identified by factor analysis were highly significantly influenced by sleep states in both developmental periods. Likewise, a comparison of the measured variables between QS and AS revealed many statistically significant differences. The variables describing (a) the number and length of quasi-stationary segments, (b) voltage and (c) power in delta and theta bands contributed to the greatest degree to the differentiation of EEGs between both sleep states. The presented method of the computerized EEG analysis which has good discriminative potential is adequately sensitive and describes the neonatal EEG with convenient accuracy.

Sleep Variability in Adolescence is Associated with Altered Brain Development

PubMed Central

Telzer, Eva H.; Goldenberg, Diane; Fuligni, Andrew J.; Lieberman, Matthew D.; Galvan, Adriana

2015-01-01

Despite the known importance of sleep for brain development, and the sharp increase in poor sleep during adolescence, we know relatively little about how sleep impacts the developing brain. We present the first longitudinal study to examine how sleep during adolescence is associated with white matter integrity. We find that greater variability in sleep duration one year prior to a DTI scan is associated with lower white matter integrity above and beyond the effects of sleep duration, and variability in bedtime, whereas sleep variability a few months prior to the scan is not associated with white matter integrity. Thus, variability in sleep duration during adolescence may have long-term impairments on the developing brain. White matter integrity should be increasing during adolescence, and so sleep variability is directly at odds with normative developmental trends. PMID:26093368

Cortical firing and sleep homeostasis.

PubMed

Vyazovskiy, Vladyslav V; Olcese, Umberto; Lazimy, Yaniv M; Faraguna, Ugo; Esser, Steve K; Williams, Justin C; Cirelli, Chiara; Tononi, Giulio

2009-09-24

The need to sleep grows with the duration of wakefulness and dissipates with time spent asleep, a process called sleep homeostasis. What are the consequences of staying awake on brain cells, and why is sleep needed? Surprisingly, we do not know whether the firing of cortical neurons is affected by how long an animal has been awake or asleep. Here, we found that after sustained wakefulness cortical neurons fire at higher frequencies in all behavioral states. During early NREM sleep after sustained wakefulness, periods of population activity (ON) are short, frequent, and associated with synchronous firing, while periods of neuronal silence are long and frequent. After sustained sleep, firing rates and synchrony decrease, while the duration of ON periods increases. Changes in firing patterns in NREM sleep correlate with changes in slow-wave activity, a marker of sleep homeostasis. Thus, the systematic increase of firing during wakefulness is counterbalanced by staying asleep.

Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

PubMed Central

Trksak, George H.; Bracken, Bethany K.; Jensen, J. Eric; Plante, David T.; Penetar, David M.; Tartarini, Wendy L.; Maywalt, Melissa A.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.

2013-01-01

In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent [31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, [31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brain β-NTP (direct measure of adenosine triphosphate), α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse. PMID:24250276

A Subset of Cholinergic Mushroom Body Neurons Requires Go Signaling to Regulate Sleep in Drosophila

PubMed Central

Yi, Wei; Zhang, Yunpeng; Tian, Yinjun; Guo, Jing; Li, Yan; Guo, Aike

2013-01-01

Study Objectives: Identifying the neurochemistry and neural circuitry of sleep regulation is critical for understanding sleep and various sleep disorders. Fruit flies display sleep-like behavior, sharing essential features with sleep of vertebrate. In the fruit fly's central brain, the mushroom body (MB) has been highlighted as a sleep center; however, its neurochemical nature remains unclear, and whether it promotes sleep or wake is still a topic of controversy. Design: We used a video recording system to accurately monitor the locomotor activity and sleep status. Gene expression was temporally and regionally manipulated by heat induction and the Gal4/UAS system. Measurements and Results: We found that expressing pertussis toxin (PTX) in the MB by c309-Gal4 to block Go activity led to unique sleep defects as dramatic sleep increase in daytime and fragmented sleep in nighttime. We narrowed down the c309-Gal4 expressing brain regions to the MB α/β core neurons that are responsible for the Go-mediated sleep effects. Using genetic tools of neurotransmitter-specific Gal80 and RNA interference approach to suppress acetylcholine signal, we demonstrated that these MB α/β core neurons were cholinergic and sleep-promoting neurons, supporting that Go mediates an inhibitory signal. Interestingly, we found that adjacent MB α/β neurons were also cholinergic but wake-promoting neurons, in which Go signal was also required. Conclusion: Our findings in fruit flies characterized a group of sleep-promoting neurons surrounded by a group of wake-promoting neurons. The two groups of neurons are both cholinergic and use Go inhibitory signal to regulate sleep. Citation: Yi W; Zhang Y; Tian Y; Guo J; Li Y; Guo A. A subset of cholinergic mushroom body neurons requires go signaling to regulate sleep in Drosophila. SLEEP 2013;36(12):1809-1821. PMID:24293755

Cellular consequences of sleep deprivation in the brain.

PubMed

Cirelli, Chiara

2006-10-01

Several recent studies have used transcriptomics approaches to characterize the molecular correlates of sleep, waking, and sleep deprivation. This analysis may help in understanding the benefits that sleep brings to the brain at the cellular level. The studies are still limited in number and focus on a few brain regions, but some consistent findings are emerging. Sleep, spontaneous wakefulness, short-term, and long-term sleep deprivation are each associated with the upregulation of hundreds of genes in the cerebral cortex and other brain areas. In fruit flies as well as in mammals, three categories of genes are consistently upregulated during waking and short-term sleep deprivation relative to sleep. They include genes involved in energy metabolism, synaptic potentiation, and the response to cellular stress. In the rat cerebral cortex, transcriptional changes associated with prolonged sleep loss differ significantly from those observed during short-term sleep deprivation. However, it is too early to draw firm conclusions relative to the molecular consequences of sleep deprivation, and more extensive studies using DNA and protein arrays are needed in different species and in different brain regions.

Sleep Deprivation Reveals Altered Brain Perfusion Patterns in Somnambulism.

PubMed

Dang-Vu, Thien Thanh; Zadra, Antonio; Labelle, Marc-Antoine; Petit, Dominique; Soucy, Jean-Paul; Montplaisir, Jacques

2015-01-01

Despite its high prevalence, relatively little is known about the pathophysiology of somnambulism. Increasing evidence indicates that somnambulism is associated with functional abnormalities during wakefulness and that sleep deprivation constitutes an important drive that facilitates sleepwalking in predisposed patients. Here, we studied the neural mechanisms associated with somnambulism using Single Photon Emission Computed Tomography (SPECT) with 99mTc-Ethylene Cysteinate Dimer (ECD), during wakefulness and after sleep deprivation. Ten adult sleepwalkers and twelve controls with normal sleep were scanned using 99mTc-ECD SPECT in morning wakefulness after a full night of sleep. Eight of the sleepwalkers and nine of the controls were also scanned during wakefulness after a night of total sleep deprivation. Between-group comparisons of regional cerebral blood flow (rCBF) were performed to characterize brain activity patterns during wakefulness in sleepwalkers. During wakefulness following a night of total sleep deprivation, rCBF was decreased bilaterally in the inferior temporal gyrus in sleepwalkers compared to controls. Functional neural abnormalities can be observed during wakefulness in somnambulism, particularly after sleep deprivation and in the inferior temporal cortex. Sleep deprivation thus not only facilitates the occurrence of sleepwalking episodes, but also uncovers patterns of neural dysfunction that characterize sleepwalkers during wakefulness.

Up-regulated neuronal COX-2 expression after cortical spreading depression is involved in non-REM sleep induction in rats.

PubMed

Cui, Yilong; Kataoka, Yosky; Inui, Takashi; Mochizuki, Takatoshi; Onoe, Hirotaka; Matsumura, Kiyoshi; Urade, Yoshihiro; Yamada, Hisao; Watanabe, Yasuyoshi

2008-03-01

Cortical spreading depression is an excitatory wave of depolarization spreading throughout cerebral cortex at a rate of 2-5 mm/min and has been implicated in various neurological disorders, such as epilepsy, migraine aura, and trauma. Although sleepiness or sleep is often induced by these neurological disorders, the cellular and molecular mechanism has remained unclear. To investigate whether and how the sleep-wake behavior is altered by such aberrant brain activity, we induced cortical spreading depression in freely moving rats, monitoring REM and non-REM (NREM) sleep and sleep-associated changes in cyclooxygenase (COX)-2 and prostaglandins (PGs). In such a model for aberrant neuronal excitation in the cerebral cortex, the amount of NREM sleep, but not of REM sleep, increased subsequently for several hours, with an up-regulated expression of COX-2 in cortical neurons and considerable production of PGs. A specific inhibitor of COX-2 completely arrested the increase in NREM sleep. These results indicate that up-regulated neuronal COX-2 would be involved in aberrant brain excitation-induced NREM sleep via production of PGs. (c) 2007 Wiley-Liss, Inc.

Differences of brain electrical activity between moderate and severe obstructive sleep apneic patients: a LORETA study.

PubMed

Toth, Marton; Kondakor, Istvan; Faludi, Bela

2016-10-01

The effects of initiation of continuous positive airway pressure (CPAP) therapy on electroencephalographic (EEG) background activity were investigated in patients exhibiting both moderate (n = 13) and severe (n = 12) obstructive sleep apnea syndromes in the testing of the potential differences of alterations of brain electrical activity caused by chronic hypoxia between these two groups. A normal control group (n = 14) was also examined. Two EEG examinations were achieved in each group: before and after first-time CPAP therapy. Low-resolution electromagnetic tomography (LORETA) was implemented towards localizing the generators of EEG activity in separate frequency bands. Prior to CPAP treatment, as a common direction of change, analysis with LORETA demonstrated increased activity in comparison with the patient and control groups. In the moderate group, significant changes were detected in the alpha2 band in the posterior cingulate cortex as well as in the beta1 band in the right posterior parietal cortex and the left supramarginal gyrus. In the severe group, significant changes were found in theta and alpha1 bands in the posterior cingulate cortex. Following CPAP treatment, these significant differences vanished in the severe group. In the moderate group, significantly decreased activity was seen in the beta3 band in the right fusiform gyrus. These findings potentially suggest a normalizing effect of CPAP therapy on EEG background activity in both groups of obstructive sleep apnea syndrome patients. Compensatory alterations of brain electrical activity in regions associated with influencing successful memory retrieval, emotional perception, default mode network, anorexia and fear network caused by chronic intermittent hypoxia could possibly be reversed with the use of CPAP therapy. © 2016 European Sleep Research Society.

Sleep physiology and sleep disorders in childhood

PubMed Central

El Shakankiry, Hanan M

2011-01-01

Sleep has long been considered as a passive phenomenon, but it is now clear that it is a period of intense brain activity involving higher cortical functions. Overall, sleep affects every aspect of a child’s development, particularly higher cognitive functions. Sleep concerns are ranked as the fifth leading concern of parents. Close to one third of all children suffer from sleep disorders, the prevalence of which is increased in certain pediatric populations, such as children with special needs, children with psychiatric or medical diagnoses and children with autism or pervasive developmental disorders. The paper reviews sleep physiology and the impact, classification, and management of sleep disorders in the pediatric age group. PMID:23616721

Sleep facilitates clearance of metabolites from the brain: glymphatic function in aging and neurodegenerative diseases.

PubMed

Mendelsohn, Andrew R; Larrick, James W

2013-12-01

Decline of cognition and increasing risk of neurodegenerative diseases are major problems associated with aging in humans. Of particular importance is how the brain removes potentially toxic biomolecules that accumulate with normal neuronal function. Recently, a biomolecule clearance system using convective flow between the cerebrospinal fluid (CSF) and interstitial fluid (ISF) to remove toxic metabolites in the brain was described. Xie and colleagues now report that in mice the clearance activity of this so-called "glymphatic system" is strongly stimulated by sleep and is associated with an increase in interstitial volume, possibly by shrinkage of astroglial cells. Moreover, anesthesia and attenuation of adrenergic signaling can activate the glymphatic system to clear potentially toxic proteins known to contribute to the pathology of Alzheimer disease (AD) such as beta-amyloid (Abeta). Clearance during sleep is as much as two-fold faster than during waking hours. These results support a new hypothesis to answer the age-old question of why sleep is necessary. Glymphatic dysfunction may pay a hitherto unsuspected role in the pathogenesis of neurodegenerative diseases as well as maintenance of cognition. Furthermore, clinical studies suggest that quality and duration of sleep may be predictive of the onset of AD, and that quality sleep may significantly reduce the risk of AD for apolipoprotein E (ApoE) ɛ4 carriers, who have significantly greater chances of developing AD. Further characterization of the glymphatic system in humans may lead to new therapies and methods of prevention of neurodegenerative diseases. A public health initiative to ensure adequate sleep among middle-aged and older people may prove useful in preventing AD, especially in apolipoprotein E (ApoE) ɛ4 carriers.

Sleep is not just for the brain: transcriptional responses to sleep in peripheral tissues.

PubMed

Anafi, Ron C; Pellegrino, Renata; Shockley, Keith R; Romer, Micah; Tufik, Sergio; Pack, Allan I

2013-05-30

Many have assumed that the primary function of sleep is for the brain. We evaluated the molecular consequences of sleep and sleep deprivation outside the brain, in heart and lung. Using microarrays we compared gene expression in tissue from sleeping and sleep deprived mice euthanized at the same diurnal times. In each tissue, nearly two thousand genes demonstrated statistically significant differential expression as a function of sleep/wake behavioral state. To mitigate the influence of an artificial deprivation protocol, we identified a subset of these transcripts as specifically sleep-enhanced or sleep-repressed by requiring that their expression also change over the course of unperturbed sleep. 3% and 6% of the assayed transcripts showed "sleep specific" changes in the lung and heart respectively. Sleep specific transcripts in these tissues demonstrated highly significant overlap and shared temporal dynamics. Markers of cellular stress and the unfolded protein response were reduced during sleep in both tissues. These results mirror previous findings in brain. Sleep-enhanced pathways reflected the unique metabolic functions of each tissue. Transcripts related to carbohydrate and sulfur metabolic processes were enhanced by sleep in the lung, and collectively favor buffering from oxidative stress. DNA repair and protein metabolism annotations were significantly enriched among the sleep-enhanced transcripts in the heart. Our results also suggest that sleep may provide a Zeitgeber, or synchronizing cue, in the lung as a large cluster of transcripts demonstrated systematic changes in inter-animal variability as a function of both sleep duration and circadian time. Our data support the notion that the molecular consequences of sleep/wake behavioral state extend beyond the brain to include peripheral tissues. Sleep state induces a highly overlapping response in both heart and lung. We conclude that sleep enhances organ specific molecular functions and that it has a ubiquitous role in reducing cellular metabolic stress in both brain and peripheral tissues. Finally, our data suggest a novel role for sleep in synchronizing transcription in peripheral tissues.

Slow oscillating transcranial direct current stimulation during sleep has a sleep-stabilizing effect in chronic insomnia: a pilot study.

PubMed

Saebipour, Mohammad R; Joghataei, Mohammad T; Yoonessi, Ali; Sadeghniiat-Haghighi, Khosro; Khalighinejad, Nima; Khademi, Soroush

2015-10-01

Recent evidence suggests that lack of slow-wave activity may play a fundamental role in the pathogenesis of insomnia. Pharmacological approaches and brain stimulation techniques have recently offered solutions for increasing slow-wave activity during sleep. We used slow (0.75 Hz) oscillatory transcranial direct current stimulation during stage 2 of non-rapid eye movement sleeping insomnia patients for resonating their brain waves to the frequency of sleep slow-wave. Six patients diagnosed with either sleep maintenance or non-restorative sleep insomnia entered the study. After 1 night of adaptation and 1 night of baseline polysomnography, patients randomly received sham or real stimulation on the third and fourth night of the experiment. Our preliminary results show that after termination of stimulations (sham or real), slow oscillatory transcranial direct current stimulation increased the duration of stage 3 of non-rapid eye movement sleep by 33 ± 26 min (P = 0.026), and decreased stage 1 of non-rapid eye movement sleep duration by 22 ± 17.7 min (P = 0.028), compared with sham. Slow oscillatory transcranial direct current stimulation decreased stage 1 of non-rapid eye movement sleep and wake time after sleep-onset durations, together, by 55.4 ± 51 min (P = 0.045). Slow oscillatory transcranial direct current stimulation also increased sleep efficiency by 9 ± 7% (P = 0.026), and probability of transition from stage 2 to stage 3 of non-rapid eye movement sleep by 20 ± 17.8% (P = 0.04). Meanwhile, slow oscillatory transcranial direct current stimulation decreased transitions from stage 2 of non-rapid eye movement sleep to wake by 12 ± 6.7% (P = 0.007). Our preliminary results suggest a sleep-stabilizing role for the intervention, which may mimic the effect of sleep slow-wave-enhancing drugs. © 2015 European Sleep Research Society.

Sleep fragmentation alters brain energy metabolism without modifying hippocampal electrophysiological response to novelty exposure.

PubMed

Baud, Maxime O; Parafita, Julia; Nguyen, Audrey; Magistretti, Pierre J; Petit, Jean-Marie

2016-10-01

Sleep is viewed as a fundamental restorative function of the brain, but its specific role in neural energy budget remains poorly understood. Sleep deprivation dampens brain energy metabolism and impairs cognitive functions. Intriguingly, sleep fragmentation, despite normal total sleep duration, has a similar cognitive impact, and in this paper we ask the question of whether it may also impair brain energy metabolism. To this end, we used a recently developed mouse model of 2 weeks of sleep fragmentation and measured 2-deoxy-glucose uptake and glycogen, glucose and lactate concentration in different brain regions. In order to homogenize mice behaviour during metabolic measurements, we exposed them to a novel environment for 1 h. Using an intra-hippocampal electrode, we first showed that hippocampal electroencephalograph (EEG) response to exploration was unaltered by 1 or 14 days of sleep fragmentation. However, after 14 days, sleep fragmented mice exhibited a lower uptake of 2-deoxy-glucose in cortex and hippocampus and lower cortical lactate levels than control mice. Our results suggest that long-term sleep fragmentation impaired brain metabolism to a similar extent as total sleep deprivation without affecting the neuronal responsiveness of hippocampus to a novel environment. © 2016 European Sleep Research Society.

A Homeostatic Sleep-Stabilizing Pathway in Drosophila Composed of the Sex Peptide Receptor and Its Ligand, the Myoinhibitory Peptide

PubMed Central

Zhang, Qi; Chae, Hyo-Seok; Daubnerová, Ivana; Shafer, Orie T.; Choe, Joonho; Kim, Young-Joon

2014-01-01

Sleep, a reversible quiescent state found in both invertebrate and vertebrate animals, disconnects animals from their environment and is highly regulated for coordination with wakeful activities, such as reproduction. The fruit fly, Drosophila melanogaster, has proven to be a valuable model for studying the regulation of sleep by circadian clock and homeostatic mechanisms. Here, we demonstrate that the sex peptide receptor (SPR) of Drosophila, known for its role in female reproduction, is also important in stabilizing sleep in both males and females. Mutants lacking either the SPR or its central ligand, myoinhibitory peptide (MIP), fall asleep normally, but have difficulty in maintaining a sleep-like state. Our analyses have mapped the SPR sleep function to pigment dispersing factor (pdf) neurons, an arousal center in the insect brain. MIP downregulates intracellular cAMP levels in pdf neurons through the SPR. MIP is released centrally before and during night-time sleep, when the sleep drive is elevated. Sleep deprivation during the night facilitates MIP secretion from specific brain neurons innervating pdf neurons. Moreover, flies lacking either SPR or MIP cannot recover sleep after the night-time sleep deprivation. These results delineate a central neuropeptide circuit that stabilizes the sleep state by feeding a slow-acting inhibitory input into the arousal system and plays an important role in sleep homeostasis. PMID:25333796

A homeostatic sleep-stabilizing pathway in Drosophila composed of the sex peptide receptor and its ligand, the myoinhibitory peptide.

PubMed

Oh, Yangkyun; Yoon, Sung-Eun; Zhang, Qi; Chae, Hyo-Seok; Daubnerová, Ivana; Shafer, Orie T; Choe, Joonho; Kim, Young-Joon

2014-10-01

Sleep, a reversible quiescent state found in both invertebrate and vertebrate animals, disconnects animals from their environment and is highly regulated for coordination with wakeful activities, such as reproduction. The fruit fly, Drosophila melanogaster, has proven to be a valuable model for studying the regulation of sleep by circadian clock and homeostatic mechanisms. Here, we demonstrate that the sex peptide receptor (SPR) of Drosophila, known for its role in female reproduction, is also important in stabilizing sleep in both males and females. Mutants lacking either the SPR or its central ligand, myoinhibitory peptide (MIP), fall asleep normally, but have difficulty in maintaining a sleep-like state. Our analyses have mapped the SPR sleep function to pigment dispersing factor (pdf) neurons, an arousal center in the insect brain. MIP downregulates intracellular cAMP levels in pdf neurons through the SPR. MIP is released centrally before and during night-time sleep, when the sleep drive is elevated. Sleep deprivation during the night facilitates MIP secretion from specific brain neurons innervating pdf neurons. Moreover, flies lacking either SPR or MIP cannot recover sleep after the night-time sleep deprivation. These results delineate a central neuropeptide circuit that stabilizes the sleep state by feeding a slow-acting inhibitory input into the arousal system and plays an important role in sleep homeostasis.

Sleep variability in adolescence is associated with altered brain development.

PubMed

Telzer, Eva H; Goldenberg, Diane; Fuligni, Andrew J; Lieberman, Matthew D; Gálvan, Adriana

2015-08-01

Despite the known importance of sleep for brain development, and the sharp increase in poor sleep during adolescence, we know relatively little about how sleep impacts the developing brain. We present the first longitudinal study to examine how sleep during adolescence is associated with white matter integrity. We find that greater variability in sleep duration one year prior to a DTI scan is associated with lower white matter integrity above and beyond the effects of sleep duration, and variability in bedtime, whereas sleep variability a few months prior to the scan is not associated with white matter integrity. Thus, variability in sleep duration during adolescence may have long-term impairments on the developing brain. White matter integrity should be increasing during adolescence, and so sleep variability is directly at odds with normative developmental trends. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.

REM sleep and emotional face memory in typically-developing children and children with autism.

PubMed

Tessier, Sophie; Lambert, Andréane; Scherzer, Peter; Jemel, Boutheina; Godbout, Roger

2015-09-01

Relationship between REM sleep and memory was assessed in 13 neurotypical and 13 children with Autistic Spectrum Disorder (ASD). A neutral/positive/negative face recognition task was administered the evening before (learning and immediate recognition) and the morning after (delayed recognition) sleep. The number of rapid eye movements (REMs), beta and theta EEG activity over the visual areas were measured during REM sleep. Compared to neurotypical children, children with ASD showed more theta activity and longer reaction time (RT) for correct responses in delayed recognition of neutral faces. Both groups showed a positive correlation between sleep and performance but different patterns emerged: in neurotypical children, accuracy for recalling neutral faces and overall RT improvement overnight was correlated with EEG activity and REMs; in children with ASD, overnight RT improvement for positive and negative faces correlated with theta and beta activity, respectively. These results suggest that neurotypical and children with ASD use different sleep-related brain networks to process faces. Copyright © 2015 Elsevier B.V. All rights reserved.

Sleep disruption and the sequelae associated with traumatic brain injury.

PubMed

Lucke-Wold, Brandon P; Smith, Kelly E; Nguyen, Linda; Turner, Ryan C; Logsdon, Aric F; Jackson, Garrett J; Huber, Jason D; Rosen, Charles L; Miller, Diane B

2015-08-01

Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. Published by Elsevier Ltd.

Sleep disruption and the sequelae associated with traumatic brain injury

PubMed Central

Lucke-Wold, Brandon P.; Smith, Kelly E.; Nguyen, Linda; Turner, Ryan C.; Logsdon, Aric F.; Jackson, Garrett J.; Huber, Jason D.; Rosen, Charles L.; Miller, Diane B.

2016-01-01

Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. PMID:25956251

Associations between Sleep, Cortisol Regulation, and Diet: Possible Implications for the Risk of Alzheimer Disease.

PubMed

Pistollato, Francesca; Sumalla Cano, Sandra; Elio, Iñaki; Masias Vergara, Manuel; Giampieri, Francesca; Battino, Maurizio

2016-07-01

Accumulation of proteinaceous amyloid β plaques and tau oligomers may occur several years before the onset of Alzheimer disease (AD). Under normal circumstances, misfolded proteins get cleared by proteasome degradation, autophagy, and the recently discovered brain glymphatic system, an astroglial-mediated interstitial fluid bulk flow. It has been shown that the activity of the glymphatic system is higher during sleep and disengaged or low during wakefulness. As a consequence, poor sleep quality, which is associated with dementia, might negatively affect glymphatic system activity, thus contributing to amyloid accumulation. The diet is another important factor to consider in the regulation of this complex network. Diets characterized by high intakes of refined sugars, salt, animal-derived proteins and fats and by low intakes of fruit and vegetables are associated with a higher risk of AD and can perturb the circadian modulation of cortisol secretion, which is associated with poor sleep quality. For this reason, diets and nutritional interventions aimed at restoring cortisol concentrations may ease sleep disorders and may facilitate brain clearance, consequentially reducing the risk of cognitive impairment and dementia. Here, we describe the associations that exist between sleep, cortisol regulation, and diet and their possible implications for the risk of cognitive impairment and AD. © 2016 American Society for Nutrition.

Associations between Sleep, Cortisol Regulation, and Diet: Possible Implications for the Risk of Alzheimer Disease12

PubMed Central

Sumalla Cano, Sandra; Elio, Iñaki; Masias Vergara, Manuel; Giampieri, Francesca; Battino, Maurizio

2016-01-01

Accumulation of proteinaceous amyloid β plaques and tau oligomers may occur several years before the onset of Alzheimer disease (AD). Under normal circumstances, misfolded proteins get cleared by proteasome degradation, autophagy, and the recently discovered brain glymphatic system, an astroglial-mediated interstitial fluid bulk flow. It has been shown that the activity of the glymphatic system is higher during sleep and disengaged or low during wakefulness. As a consequence, poor sleep quality, which is associated with dementia, might negatively affect glymphatic system activity, thus contributing to amyloid accumulation. The diet is another important factor to consider in the regulation of this complex network. Diets characterized by high intakes of refined sugars, salt, animal-derived proteins and fats and by low intakes of fruit and vegetables are associated with a higher risk of AD and can perturb the circadian modulation of cortisol secretion, which is associated with poor sleep quality. For this reason, diets and nutritional interventions aimed at restoring cortisol concentrations may ease sleep disorders and may facilitate brain clearance, consequentially reducing the risk of cognitive impairment and dementia. Here, we describe the associations that exist between sleep, cortisol regulation, and diet and their possible implications for the risk of cognitive impairment and AD. PMID:27422503

Brain function assessment in different conscious states.

PubMed

Ozgoren, Murat; Bayazit, Onur; Kocaaslan, Sibel; Gokmen, Necati; Oniz, Adile

2010-06-03

The study of brain functioning is a major challenge in neuroscience fields as human brain has a dynamic and ever changing information processing. Case is worsened with conditions where brain undergoes major changes in so-called different conscious states. Even though the exact definition of consciousness is a hard one, there are certain conditions where the descriptions have reached a consensus. The sleep and the anesthesia are different conditions which are separable from each other and also from wakefulness. The aim of our group has been to tackle the issue of brain functioning with setting up similar research conditions for these three conscious states. In order to achieve this goal we have designed an auditory stimulation battery with changing conditions to be recorded during a 40 channel EEG polygraph (Nuamps) session. The stimuli (modified mismatch, auditory evoked etc.) have been administered both in the operation room and the sleep lab via Embedded Interactive Stimulus Unit which was developed in our lab. The overall study has provided some results for three domains of consciousness. In order to be able to monitor the changes we have incorporated Bispectral Index Monitoring to both sleep and anesthesia conditions. The first stage results have provided a basic understanding in these altered states such that auditory stimuli have been successfully processed in both light and deep sleep stages. The anesthesia provides a sudden change in brain responsiveness; therefore a dosage dependent anesthetic administration has proved to be useful. The auditory processing was exemplified targeting N1 wave, with a thorough analysis from spectrogram to sLORETA. The frequency components were observed to be shifting throughout the stages. The propofol administration and the deeper sleep stages both resulted in the decreasing of N1 component. The sLORETA revealed similar activity at BA7 in sleep (BIS 70) and target propofol concentration of 1.2 microg/mL. The current study utilized similar stimulation and recording system and incorporated BIS dependent values to validate a common approach to sleep and anesthesia. Accordingly the brain has a complex behavior pattern, dynamically changing its responsiveness in accordance with stimulations and states.

Neonatal Sleep Restriction Increases Nociceptive Sensitivity in Adolescent Mice.

PubMed

Araujo, Paula; Coelho, Cesar A; Oliveira, Maria G; Tufik, Sergio; Andersen, Monica L

2018-03-01

Sleep loss in infants may have a negative effect on the functional and structural development of the nociceptive system. We tested the hypothesis that neonatal sleep restriction induces a long-term increase of pain-related behaviors in mice and that this hypersensitivity occurs due to changes in the neuronal activity of nociceptive pathways. We aim to investigate the effects of sleep loss in neonatal mice on pain behaviors of adolescent and adult mice in a sex-dependent manner. We also analyzed neuroanatomical and functional changes in pain pathways associated with behavioral changes. An experimental animal study. A basic sleep research laboratory at Universidade Federal de São Paulo in Brazil. Neonatal mice at postnatal day (PND) 12 were randomly assigned to either control (CTRL), maternal separation (MS), or sleep restriction (SR) groups. MS and SR were performed 2 hours a day for 10 days (PND 12 until PND 21). The gentle handling method was used to prevent sleep. At PND 21, PND 35, or PND 90, the mice were tested for pain-related behaviors. Their brains were harvested and immunohistochemically stained for c-Fos protein in the anterior cingulate cortex, primary somatosensory cortex, and periaqueductal gray (PAG). Neonatal SR significantly increased nociceptive sensitivity in the hot plate test in adolescent mice (-23.5% of pain threshold). This alteration in nociceptive response was accompanied by a decrease in c-Fos expression in PAG (-40% of c-Fos positive cells compared to the CTRL group). The hypersensitivity found in adolescent mice was not present in adult animals, and all mice showed a comparable nociceptive response. Even using a mild manipulation method, in which a minimal amount of handling was applied to maintain wakefulness, sleep deprivation was a stressful event evidenced by higher corticosterone levels. Repeated exposures to sleep loss during early life were able to induce changes in the nociceptive response associated with alterations in neural activity in descending control of pain. Brain maturation, hypersensitivity, neuronal activity, nociception, pain, periaqueductal gray, postnatal development, sleep, sleep deprivation.

Regional Patterns of Elevated Alpha and High-Frequency Electroencephalographic Activity during Nonrapid Eye Movement Sleep in Chronic Insomnia: A Pilot Study.

PubMed

Riedner, Brady A; Goldstein, Michael R; Plante, David T; Rumble, Meredith E; Ferrarelli, Fabio; Tononi, Giulio; Benca, Ruth M

2016-04-01

To examine nonrapid eye movement (NREM) sleep in insomnia using high-density electroencephalography (EEG). All-night sleep recordings with 256 channel high-density EEG were analyzed for 8 insomnia subjects (5 females) and 8 sex and age-matched controls without sleep complaints. Spectral analyses were conducted using unpaired t-tests and topographical differences between groups were assessed using statistical non-parametric mapping. Five minute segments of deep NREM sleep were further analyzed using sLORETA cortical source imaging. The initial topographic analysis of all-night NREM sleep EEG revealed that insomnia subjects had more high-frequency EEG activity (> 16 Hz) compared to good sleeping controls and that the difference between groups was widespread across the scalp. In addition, the analysis also showed that there was a more circumscribed difference in theta (4-8 Hz) and alpha (8-12 Hz) power bands between groups. When deep NREM sleep (N3) was examined separately, the high-frequency difference between groups diminished, whereas the higher regional alpha activity in insomnia subjects persisted. Source imaging analysis demonstrated that sensory and sensorimotor cortical areas consistently exhibited elevated levels of alpha activity during deep NREM sleep in insomnia subjects relative to good sleeping controls. These results suggest that even during the deepest stage of sleep, sensory and sensorimotor areas in insomnia subjects may still be relatively active compared to control subjects and to the rest of the sleeping brain. © 2016 Associated Professional Sleep Societies, LLC.

Nonlinear aspects of the EEG during sleep in children

NASA Astrophysics Data System (ADS)

Berryman, Matthew J.; Coussens, Scott W.; Pamula, Yvonne; Kennedy, Declan; Lushington, Kurt; Shalizi, Cosma; Allison, Andrew; Martin, A. James; Saint, David; Abbott, Derek

2005-05-01

Electroencephalograph (EEG) analysis enables the dynamic behavior of the brain to be examined. If the behavior is nonlinear then nonlinear tools can be used to glean information on brain behavior, and aid in the diagnosis of sleep abnormalities such as obstructive sleep apnea syndrome (OSAS). In this paper the sleep EEGs of a set of normal children and children with mild OSAS are evaluated for nonlinear brain behaviour. We found that there were differences in the nonlinearity of the brain behaviour between different sleep stages, and between the two groups of children.

Lessons from sleeping flies: insights from Drosophila melanogaster on the neuronal circuitry and importance of sleep.

PubMed

Potdar, Sheetal; Sheeba, Vasu

2013-06-01

Sleep is a highly conserved behavior whose role is as yet unknown, although it is widely acknowledged as being important. Here we provide an overview of many vital questions regarding this behavior, that have been addressed in recent years using the genetically tractable model organism Drosophila melanogaster in several laboratories around the world. Rest in D. melanogaster has been compared to mammalian sleep and its homeostatic and circadian regulation have been shown to be controlled by intricate neuronal circuitry involving circadian clock neurons, mushroom bodies, and pars intercerebralis, although their exact roles are not entirely clear. We draw attention to the yet unanswered questions and contradictions regarding the nature of the interactions between the brain regions implicated in the control of sleep. Dopamine, octopamine, γ-aminobutyric acid (GABA), and serotonin are the chief neurotransmitters identified as functioning in different limbs of this circuit, either promoting arousal or sleep by modulating membrane excitability of underlying neurons. Some studies have suggested that certain brain areas may contribute towards both sleep and arousal depending on activation of specific subsets of neurons. Signaling pathways implicated in the sleep circuit include cyclic adenosine monophosphate (cAMP) and epidermal growth factor receptor-extracellular signal-regulated kinase (EGFR-ERK) signaling pathways that operate on different neural substrates. Thus, this field of research appears to be on the cusp of many new and exciting findings that may eventually help in understanding how this complex physiological phenomenon is modulated by various neuronal circuits in the brain. Finally, some efforts to approach the "Holy Grail" of why we sleep have been summarized.

Role of biological membranes in slow-wave sleep.

PubMed

Karnovsky, M L

1991-02-01

Two involvements of cellular membranes in slow-wave sleep (SWS) are discussed. In the first the endoplasmic reticulum (ER) is focussed upon, and in the second, the plasmalemma, where specific binding sites (receptors?) for promoters of slow-wave sleep are believed to be located. The study concerning the ER focuses on an enzyme in the brain, glucose-6-phosphatase, which, although present at low levels, manifests greatly increased activity during SWS compared to the waking state. The work on the plasmalemma has to do with the specific binding of muramyl peptides, inducers of slow-wave sleep, to various cells, and membrane preparations of various sorts, including those from brain tissue. Such cells as macrophages from mice, B-lymphocytes from human blood, and cells from a cell line (C-6 glioma) have been examined in this context.

A Biphasic Change of Regional Blood Volume in the Frontal Cortex during Non-Rapid Eye Movement Sleep: A Near-Infrared Spectroscopy Study.

PubMed

Zhang, Zhongxing; Khatami, Ramin

2015-08-01

Current knowledge on hemodynamics in sleep is limited because available techniques do not allow continuous recordings and mainly focus on cerebral blood flow while neglecting other important parameters, such as blood volume (BV) and vasomotor activity. Observational study. Continuous measures of hemodynamics over the left forehead and biceps were performed using near-infrared spectroscopy (NIRS) during nocturnal polysomnography in 16 healthy participants in sleep laboratory. Temporal dynamics and mean values of cerebral and muscular oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (HHb), and BV during different sleep stages were compared. A biphasic change of cerebral BV was observed which contrasted a monotonic increase of muscular BV during non-rapid eye movement sleep. A significant decrement in cerebral HbO2 and BV accompanied by an increase of HHb was recorded at sleep onset (Phase I). Prior to slow wave sleep (SWS) HbO2 and BV turned to increase whereas HHb began to decrease in subsequent Phase II suggested increased brain perfusion during SWS. The cerebral HbO2 slope correlated to BV slope in Phase I and II, but it only correlated to HHb slope in Phase II. The occurrence time of inflection points correlated to SWS latencies. Initial decrease of brain perfusion with decreased blood volume (BV) and oxygenated hemoglobin (HbO2) together with increasing muscular BV fit thermoregulation process at sleep onset. The uncorrelated and correlated slopes of HbO2 and deoxygenated hemoglobin indicate different mechanisms underlying the biphasic hemodynamic process in light sleep and slow wave sleep (SWS). In SWS, changes in vasomotor activity (i.e., increased vasodilatation) may mediate increasing cerebral and muscular BV. © 2015 Associated Professional Sleep Societies, LLC.

MK-801-induced locomotor activity in long-sleep x short-sleep recombinant inbred mouse strains: correlational analysis with low-dose ethanol and provisional quantitative trait loci.

PubMed

Zahniser, N R; Negri, C A; Hanania, T; Gehle, V M

1999-11-01

Low doses of the N-methyl-D-aspartate receptor (NMDAR) antagonist MK-801 (dizocilpine) or ethanol increase locomotor activity to a lesser extent in long-sleep (LS), than in short-sleep (SS), mice. LS mice also have fewer brain [3H]MK-801 binding sites than SS mice. In this study, LSXSS recombinant inbred (RI) mice were used to investigate whether different NMDAR densities contribute to differential MK-801 activation and whether common genes are involved in initial sensitivity to MK-801-and ethanol-induced activation. Locomotor activity was measured for 90 min after saline or MK-801 injection. Quantitative autoradiographic analysis of [3H]MK-801 binding was used to measure densities of NMDARs in seven brain regions. The ethanol (1-2 g/kg) activation scores from Erwin and colleagues (1997) were used for correlational analysis, as was their method for quantitative trait loci (QTL) analysis. Both saline and MK-801 (0.3 mg/kg, given intraperitoneally) induced a continuum of locomotor responses across the LSXSS RI strains. There was a 4-fold range of MK-801 difference scores (MK-801 score-saline baseline), with the RI 9 and RI 4 strains representing low and high responders, respectively. Dose-response experiments with these two strains confirmed that 0.3 mg/kg MK-801 produced significant activation, similar to previous results with LS and SS mice. However, unlike previous LS/SS results, lower densities of NMDARs were not observed in the RI 9 than in the RI 4 mouse brains. No significant genetic correlations were observed between MK-801-induced and ethanol-induced responses in the LSXSS RI mice. Two provisional MK-801 activation QTLs were identified (p < 0.01) on chromosomes 11 and 19, neither in common with those mapped for ethanol activation. Different densities of brain NMDARs are unlikely to account for the differential activation of LSXSS RI mice by MK-801. Additionally, in the RI mice either separate sets of genes regulate low dose MK-801- and ethanol-induced locomotor responses or the overlapping subset of genes controlling these two behaviors is small (< or =10%).

Dreaming and the brain: from phenomenology to neurophysiology

PubMed Central

Nir, Yuval; Tononi, Giulio

2009-01-01

Dreams are a most remarkable experiment in psychology and neuroscience, conducted every night in every sleeping person. They show that our brain, disconnected from the environment, can generate by itself an entire world of conscious experiences. Content analysis and developmental studies have furthered our understanding of dream phenomenology. In parallel, brain lesion studies, functional imaging, and neurophysiology have advanced our knowledge of the neural basis of dreaming. It is now possible to start integrating these two strands of research in order to address some fundamental questions that dreams pose for cognitive neuroscience: how conscious experiences in sleep relate to underlying brain activity; why the dreamer is largely disconnected from the environment; and whether dreaming is more closely related to mental imagery or to perception. PMID:20079677

Dreaming and the brain: from phenomenology to neurophysiology.

PubMed

Nir, Yuval; Tononi, Giulio

2010-02-01

Dreams are a remarkable experiment in psychology and neuroscience, conducted every night in every sleeping person. They show that the human brain, disconnected from the environment, can generate an entire world of conscious experiences by itself. Content analysis and developmental studies have promoted understanding of dream phenomenology. In parallel, brain lesion studies, functional imaging and neurophysiology have advanced current knowledge of the neural basis of dreaming. It is now possible to start integrating these two strands of research to address fundamental questions that dreams pose for cognitive neuroscience: how conscious experiences in sleep relate to underlying brain activity; why the dreamer is largely disconnected from the environment; and whether dreaming is more closely related to mental imagery or to perception. Published by Elsevier Ltd.

Cerebrovascular Reactivity in Young Subjects with Sleep Apnea

PubMed Central

Buterbaugh, John; Wynstra, Charles; Provencio, Natalie; Combs, Daniel; Gilbert, Michael; Parthasarathy, Sairam

2015-01-01

Study Objectives: Regional brain alterations may be involved in the pathogenesis and adverse consequences of obstructive sleep apnea (OSA). The objectives for the current study were to (1) determine cerebrovascular reactivity in the motor areas that control upper airway musculature in patients with OSA, and (2) determine whether young patients with OSA have decreased cerebrovascular reactivity in response to breath holding. Design: Case-control study. Setting: Academic center. Participants: Twelve subjects with OSA (age 24–42 y; apnea-hypopnea index 17; interquartile range [IQR] 9, 69 per hour) and control subjects (n = 10; age 29–44 y; AHI 2; IQR 1, 3 per hour). Measurements and Results: Subjects underwent blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI) while awake, swallowing, and breath holding. In subjects with OSA, during swallowing, there was less activity in the brainstem than in controls (P = 0.03) that remained reduced after adjusting for cortical motor strip activity (P = 0.036). In OSA subjects, brain regions of increased cerebrovascular reactivity (38; IQR 17, 96 cm3) was smaller than that in controls (199; IQR 5, 423 cm3; P = 0.01). In OSA subjects, brain regions of decreased cerebrovascular reactivity during breath hold was greater (P = 0.01), and the ratio of increased-to-decreased brain regions was lower than that of controls (P = 0.006). Adjustment for cerebral volumes, body mass index, and white matter lesions did not change these results substantively. Conclusions: In patients with obstructive sleep apnea (OSA), diminished change in brainstem activity during swallowing and reduced cerebrovascular reactivity may contribute to the etiopathogenesis and adverse cerebrovascular consequences, respectively. We speculate that decreased cerebral auto-regulation may be causative of gray matter loss in OSA. Citation: Buterbaugh J, Wynstra C, Provencio N, Combs D, Gilbert M, Parthasarathy S. Cerebrovascular reactivity in young subjects with sleep apnea. SLEEP 2015;38(2):241–250. PMID:25409111

Metabolic Response of the Cerebral Cortex Following Gentle Sleep Deprivation and Modafinil Administration

PubMed Central

Petit, Jean-Marie; Tobler, Irene; Kopp, Caroline; Morgenthaler, Florence; Borbély, Alexander A.; Magistretti, Pierre J.

2010-01-01

Study Objectives: The main energy reserve of the brain is glycogen, which is almost exclusively localized in astrocytes. We previously reported that cerebral expression of certain genes related to glycogen metabolism changed following instrumental sleep deprivation in mice. Here, we extended our investigations to another set of genes related to glycogen and glucose metabolism. We also compared the effect of instrumentally and pharmacologically induced prolonged wakefulness, followed (or not) by 3 hours of sleep recovery, on the expression of genes related to brain energy metabolism. Design: Sleep deprivation for 6–7 hours. Setting: Animal sleep research laboratory. Participants: Adults OF1 mice. Interventions: Wakefulness was maintained by “gentle sleep deprivation” method (GSD) or by administration of the wakefulness-promoting drug modafinil (MOD) (200 mg/kg i.p.). Measurements and Results: Levels of mRNAs encoding proteins related to energy metabolism were measured by quantitative real-time PCR in the cerebral cortex. The mRNAs encoding protein targeting to glycogen (PTG) and the glial glucose transporter were significantly increased following both procedures used to prolong wakefulness. Glycogenin mRNA levels were increased only after GSD, while neuronal glucose transporter mRNA only after MOD. These effects were reversed after sleep recovery. A significant enhancement of glycogen synthase activity without any changes in glycogen levels was observed in both conditions. Conclusions: These results indicate the existence of a metabolic adaptation of astrocytes aimed at maintaining brain energy homeostasis during the sleep-wake cycle. Citation: Petit, JM; Tobler I; Kopp C; Morgenthaler F; Borbély AA; Magistretti PJ. Metabolic response of the cerebral cortex following gentle sleep deprivation and modafinil administration. SLEEP 2010;33(7):901–908. PMID:20614850

The Role of Sleep in Emotional Brain Function

PubMed Central

Goldstein, Andrea N.; Walker, Matthew P.

2014-01-01

Rapidly emerging evidence continues to describe an intimate and causal relationship between sleep and emotional brain function. These findings are mirrored by longstanding clinical observations demonstrating that nearly all mood and anxiety disorders co-occur with one or more sleep abnormalities. This review aims to (1) provide a synthesis of recent findings describing the emotional brain and behavioral benefits triggered by sleep, and conversely, the detrimental impairments following a lack of sleep, (2) outline a proposed framework in which sleep, and specifically rapid-eye movement (REM) sleep, supports a process of affective brain homeostasis, optimally preparing the organism for next-day social and emotional functioning, and (3) describe how this hypothesized framework can explain the prevalent relationships between sleep and psychiatric disorders, with a particular focus on post-traumatic stress disorder and major depression. PMID:24499013

Intermittent Short Sleep Results in Lasting Sleep Wake Disturbances and Degeneration of Locus Coeruleus and Orexinergic Neurons.

PubMed

Zhu, Yan; Fenik, Polina; Zhan, Guanxia; Somach, Rebecca; Xin, Ryan; Veasey, Sigrid

2016-08-01

Intermittent short sleep (ISS) is pervasive among students and workers in modern societies, yet the lasting consequences of repeated short sleep on behavior and brain health are largely unexplored. Wake-activated neurons may be at increased risk of metabolic injury across sustained wakefulness. To examine the effects of ISS on wake-activated neurons and wake behavior, wild-type mice were randomized to ISS (a repeated pattern of short sleep on 3 consecutive days followed by 4 days of recovery sleep for 4 weeks) or rested control conditions. Subsets of both groups were allowed a recovery period consisting of 4-week unperturbed activity in home cages with littermates. Mice were examined for immediate and delayed (following recovery) effects of ISS on wake neuron cell metabolics, cell counts, and sleep/wake patterns. ISS resulted in sustained disruption of sleep/wake activity, with increased wakefulness during the lights-on period and reduced wake bout duration and wake time during the lights-off period. Noradrenergic locus coeruleus (LC) and orexinergic neurons showed persistent alterations in morphology, and reductions in both neuronal stereological cell counts and fronto-cortical projections. Surviving wake-activated neurons evidenced persistent reductions in sirtuins 1 and 3 and increased lipofuscin. In contrast, ISS resulted in no lasting injury to the sleep-activated melanin concentrating hormone neurons. Collectively these findings demonstrate for the first time that ISS imparts significant lasting disturbances in sleep/wake activity, degeneration of wake-activated LC and orexinergic neurons, and lasting metabolic changes in remaining neurons most consistent with premature senescence. © 2016 Associated Professional Sleep Societies, LLC.

Sleep, Memory & Brain Rhythms

PubMed Central

Watson, Brendon O.; Buzsáki, György

2015-01-01

Sleep occupies roughly one-third of our lives, yet the scientific community is still not entirely clear on its purpose or function. Existing data point most strongly to its role in memory and homeostasis: that sleep helps maintain basic brain functioning via a homeostatic mechanism that loosens connections between overworked synapses, and that sleep helps consolidate and re-form important memories. In this review, we will summarize these theories, but also focus on substantial new information regarding the relation of electrical brain rhythms to sleep. In particular, while REM sleep may contribute to the homeostatic weakening of overactive synapses, a prominent and transient oscillatory rhythm called “sharp-wave ripple” seems to allow for consolidation of behaviorally relevant memories across many structures of the brain. We propose that a theory of sleep involving the division of labor between two states of sleep–REM and non-REM, the latter of which has an abundance of ripple electrical activity–might allow for a fusion of the two main sleep theories. This theory then postulates that sleep performs a combination of consolidation and homeostasis that promotes optimal knowledge retention as well as optimal waking brain function. PMID:26097242

β-Amyloid accumulation in the human brain after one night of sleep deprivation.

PubMed

Shokri-Kojori, Ehsan; Wang, Gene-Jack; Wiers, Corinde E; Demiral, Sukru B; Guo, Min; Kim, Sung Won; Lindgren, Elsa; Ramirez, Veronica; Zehra, Amna; Freeman, Clara; Miller, Gregg; Manza, Peter; Srivastava, Tansha; De Santi, Susan; Tomasi, Dardo; Benveniste, Helene; Volkow, Nora D

2018-04-24

The effects of acute sleep deprivation on β-amyloid (Aβ) clearance in the human brain have not been documented. Here we used PET and 18 F-florbetaben to measure brain Aβ burden (ABB) in 20 healthy controls tested after a night of rested sleep (baseline) and after a night of sleep deprivation. We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in Aβ burden in the right hippocampus and thalamus. These increases were associated with mood worsening following sleep deprivation, but were not related to the genetic risk (APOE genotype) for Alzheimer's disease. Additionally, baseline ABB in a range of subcortical regions and the precuneus was inversely associated with reported night sleep hours. APOE genotyping was also linked to subcortical ABB, suggesting that different Alzheimer's disease risk factors might independently affect ABB in nearby brain regions. In summary, our findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher Aβ accumulation with chronic less sleep. Copyright © 2018 the Author(s). Published by PNAS.

Deep Sleep and Parietal Cortex Gene Expression Changes Are Related to Cognitive Deficits with Age

PubMed Central

Buechel, Heather M.; Popovic, Jelena; Searcy, James L.; Porter, Nada M.; Thibault, Olivier; Blalock, Eric M.

2011-01-01

Background Age-related cognitive deficits negatively affect quality of life and can presage serious neurodegenerative disorders. Despite sleep disruption's well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep's relationship to cognitive aging. Methodology We measured sleep stages in young adult and aged F344 rats during inactive (enhanced sleep) and active (enhanced wake) periods. Animals were behaviorally characterized on the Morris water maze and gene expression profiles of their parietal cortices were taken. Principal Findings Water maze performance was impaired, and inactive period deep sleep was decreased with age. However, increased deep sleep during the active period was most strongly correlated to maze performance. Transcriptional profiles were strongly associated with behavior and age, and were validated against prior studies. Bioinformatic analysis revealed increased translation and decreased myelin/neuronal pathways. Conclusions The F344 rat appears to serve as a reasonable model for some common sleep architecture and cognitive changes seen with age in humans, including the cognitively disrupting influence of active period deep sleep. Microarray analysis suggests that the processes engaged by this sleep are consistent with its function. Thus, active period deep sleep appears temporally misaligned but mechanistically intact, leading to the following: first, aged brain tissue appears capable of generating the slow waves necessary for deep sleep, albeit at a weaker intensity than in young. Second, this activity, presented during the active period, seems disruptive rather than beneficial to cognition. Third, this active period deep sleep may be a cognitively pathologic attempt to recover age-related loss of inactive period deep sleep. Finally, therapeutic strategies aimed at reducing active period deep sleep (e.g., by promoting active period wakefulness and/or inactive period deep sleep) may be highly relevant to cognitive function in the aging community. PMID:21483696

Sleep is not just for the brain: transcriptional responses to sleep in peripheral tissues

PubMed Central

2013-01-01

Background Many have assumed that the primary function of sleep is for the brain. We evaluated the molecular consequences of sleep and sleep deprivation outside the brain, in heart and lung. Using microarrays we compared gene expression in tissue from sleeping and sleep deprived mice euthanized at the same diurnal times. Results In each tissue, nearly two thousand genes demonstrated statistically significant differential expression as a function of sleep/wake behavioral state. To mitigate the influence of an artificial deprivation protocol, we identified a subset of these transcripts as specifically sleep-enhanced or sleep-repressed by requiring that their expression also change over the course of unperturbed sleep. 3% and 6% of the assayed transcripts showed “sleep specific” changes in the lung and heart respectively. Sleep specific transcripts in these tissues demonstrated highly significant overlap and shared temporal dynamics. Markers of cellular stress and the unfolded protein response were reduced during sleep in both tissues. These results mirror previous findings in brain. Sleep-enhanced pathways reflected the unique metabolic functions of each tissue. Transcripts related to carbohydrate and sulfur metabolic processes were enhanced by sleep in the lung, and collectively favor buffering from oxidative stress. DNA repair and protein metabolism annotations were significantly enriched among the sleep-enhanced transcripts in the heart. Our results also suggest that sleep may provide a Zeitgeber, or synchronizing cue, in the lung as a large cluster of transcripts demonstrated systematic changes in inter-animal variability as a function of both sleep duration and circadian time. Conclusion Our data support the notion that the molecular consequences of sleep/wake behavioral state extend beyond the brain to include peripheral tissues. Sleep state induces a highly overlapping response in both heart and lung. We conclude that sleep enhances organ specific molecular functions and that it has a ubiquitous role in reducing cellular metabolic stress in both brain and peripheral tissues. Finally, our data suggest a novel role for sleep in synchronizing transcription in peripheral tissues. PMID:23721503

Increased Sleep Need and Reduction of Tuberomammillary Histamine Neurons after Rodent Traumatic Brain Injury.

PubMed

Noain, Daniela; Büchele, Fabian; Schreglmann, Sebastian R; Valko, Philipp O; Gavrilov, Yuri V; Morawska, Marta M; Imbach, Lukas L; Baumann, Christian R

2018-01-01

Although sleep-wake disturbances are prevalent and well described after traumatic brain injury, their pathophysiology remains unclear, most likely because human traumatic brain injury is a highly heterogeneous entity that makes the systematic study of sleep-wake disturbances in relation to trauma-induced histological changes a challenging task. Despite increasing interest, specific and effective treatment strategies for post-traumatic sleep-wake disturbances are still missing. With the present work, therefore, we aimed at studying acute and chronic sleep-wake disturbances by electrophysiological means, and at assessing their histological correlates after closed diffuse traumatic brain injury in rats with the ultimate goal of generating a model of post-traumatic sleep-wake disturbances and associated histopathological findings that accurately represents the human condition. We assessed sleep-wake behavior by means of standard electrophysiological recordings before and 1, 7, and 28 days after sham or traumatic brain injury procedures. Sleep-wake findings were then correlated to immunohistochemically labeled and stereologically quantified neuronal arousal systems. Compared with control animals, we found that closed diffuse traumatic brain injury caused increased sleep need one month after trauma, and sleep was more consolidated. As histological correlate, we found a reduced number of histamine immunoreactive cells in the tuberomammillary nucleus, potentially related to increased neuroinflammation. Monoaminergic and hypocretinergic neurotransmitter systems in the hypothalamus and rostral brainstem were not affected, however. These results suggest that our rat traumatic brain injury model reflects human post-traumatic sleep-wake disturbances and associated histopathological findings very accurately, thus providing a study platform for novel treatment strategies for affected patients.

Sleep Deprivation Reveals Altered Brain Perfusion Patterns in Somnambulism

PubMed Central

Dang-Vu, Thien Thanh; Zadra, Antonio; Labelle, Marc-Antoine; Petit, Dominique; Soucy, Jean-Paul; Montplaisir, Jacques

2015-01-01

Background Despite its high prevalence, relatively little is known about the pathophysiology of somnambulism. Increasing evidence indicates that somnambulism is associated with functional abnormalities during wakefulness and that sleep deprivation constitutes an important drive that facilitates sleepwalking in predisposed patients. Here, we studied the neural mechanisms associated with somnambulism using Single Photon Emission Computed Tomography (SPECT) with 99mTc-Ethylene Cysteinate Dimer (ECD), during wakefulness and after sleep deprivation. Methods Ten adult sleepwalkers and twelve controls with normal sleep were scanned using 99mTc-ECD SPECT in morning wakefulness after a full night of sleep. Eight of the sleepwalkers and nine of the controls were also scanned during wakefulness after a night of total sleep deprivation. Between-group comparisons of regional cerebral blood flow (rCBF) were performed to characterize brain activity patterns during wakefulness in sleepwalkers. Results During wakefulness following a night of total sleep deprivation, rCBF was decreased bilaterally in the inferior temporal gyrus in sleepwalkers compared to controls. Conclusions Functional neural abnormalities can be observed during wakefulness in somnambulism, particularly after sleep deprivation and in the inferior temporal cortex. Sleep deprivation thus not only facilitates the occurrence of sleepwalking episodes, but also uncovers patterns of neural dysfunction that characterize sleepwalkers during wakefulness. PMID:26241047

Functions and Mechanisms of Sleep in Flies and Mammals

DTIC Science & Technology

2009-10-01

regulates the structure and/or amount of sleep. We expressed dTrpA1, a warmth- activated cation channel under control of over 50 GAL4 lines to screen a...neurons). While still preliminary, the results of this screen indicate that many brain areas can drive alterations in sleep structure , but many...these neurons. We have identified the serotonin receptor likely to mediate the known interaction between the serotonergic Raphe nucleus and the LC

ELECTROMAGNETIC PHENOMENA WHICH RADIATE FROM THE HUMAN BRAIN DURING INTENSE PSYCHOSENSORIAL ACTIVITY FROM DREAMY, HALLUCINATORY AND TELEPSYCHIC STATES,

DTIC Science & Technology

intense psychosensorial activity (oneirism, hallucinations, telepsychism). Oneirism is the peculiar psychic condition that is favorable to dreams ...normal hallucinatory phenomena during the sleep and dream -like stages of the beginning sleep and of the reverie. As hallucinations, are designated as the...whole gamut of subjective metapsychics (cryptesthesia, spontaneous or pragmatic; lucidity: clairvoyance: telepathy ; rhabdomancy; radiesthesia; graphonomy; cartomancy; chiromancy). (Author)

Fusing Multiple Sensor Modalities for Complex Physiological State Monitoring

DTIC Science & Technology

2012-12-01

sleep-alpha variants (drowsiness alpha activity and REM -alpha bursts) over frontal, central, parietal and occipital regions. Note the higher spectral...contribution of the slowest components (7.8–8.6 Hz) during REM alpha bursts as compared with drowsiness-alpha activity (13...occipital regions of the brain during the drowsiness state as compared to REM sleep and other states, as seen in figure 1 (13). Furthermore, using EEG

Associations of Sleep Quality and Awake Physical Activity with Fluctuations in Nocturnal Blood Pressure in Patients with Cardiovascular Risk Factors

PubMed Central

Kadoya, Manabu; Koyama, Hidenori; Kurajoh, Masafumi; Naka, Mariko; Miyoshi, Akio; Kanzaki, Akinori; Kakutani, Miki; Shoji, Takuhito; Moriwaki, Yuji; Yamamoto, Tetsuya; Inaba, Masaaki; Namba, Mitsuyoshi

2016-01-01

Background Sleep quality and awake physical activity are important behavioral factors involved in the occurrence of cardiovascular diseases, potentially through nocturnal blood pressure (BP) changes. However, the impacts of quantitatively measured sleep quality and awake physical activity on BP fluctuation, and their relationships with several candidate causal factors for nocturnal hypertension are not well elucidated. Methods This cross-sectional study included 303 patients registered in the HSCAA study. Measurements included quantitatively determined sleep quality parameters and awake physical activity obtained by actigraph, nocturnal systolic BP (SBP) fall [100 × (1- sleep SBP/awake SBP ratio)], apnea hypopnea index, urinary sodium and cortisol secretion, plasma aldosterone concentration and renin activity, insulin resistance index, parameters of heart rate variability (HRV), and plasma brain-derived neurotrophic factor (BDNF). Results Simple regression analysis showed that time awake after sleep onset (r = -0.150), a parameter of sleep quality, and awake physical activity (r = 0.164) were significantly correlated with nocturnal SBP fall. Among those, time awake after sleep onset (β = -0.179) and awake physical activity (β = 0.190) were significantly and independently associated with nocturnal SBP fall in multiple regression analysis. In a subgroup of patients without taking anti-hypertensive medications, both time awake after sleep onset (β = -0.336) and awake physical activity (β = 0.489) were more strongly and independently associated with nocturnal SBP falls. Conclusion Sleep quality and awake physical activity were found to be significantly associated with nocturnal SBP fall, and that relationship was not necessarily confounded by candidate causal factors for nocturnal hypertension. PMID:27166822

Astrocyte-derived adenosine is central to the hypnogenic effect of glucose

PubMed Central

Scharbarg, Emeric; Daenens, Marion; Lemaître, Frédéric; Geoffroy, Hélène; Guille-Collignon, Manon; Gallopin, Thierry; Rancillac, Armelle

2016-01-01

Sleep has been hypothesised to maintain a close relationship with metabolism. Here we focus on the brain structure that triggers slow-wave sleep, the ventrolateral preoptic nucleus (VLPO), to explore the cellular and molecular signalling pathways recruited by an increase in glucose concentration. We used infrared videomicroscopy on ex vivo brain slices to establish that glucose induces vasodilations specifically in the VLPO via the astrocytic release of adenosine. Real-time detection by in situ purine biosensors further revealed that the adenosine level doubles in response to glucose, and triples during the wakefulness period. Finally, patch-clamp recordings uncovered the depolarizing effect of adenosine and its A2A receptor agonist, CGS-21680, on sleep-promoting VLPO neurons. Altogether, our results provide new insights into the metabolically driven release of adenosine. We hypothesise that adenosine adjusts the local energy supply to local neuronal activity in response to glucose. This pathway could contribute to sleep-wake transition and sleep intensity. PMID:26755200

Sleep confers a benefit for retention of statistical language learning in 6.5month old infants.

PubMed

Simon, Katharine N S; Werchan, Denise; Goldstein, Michael R; Sweeney, Lucia; Bootzin, Richard R; Nadel, Lynn; Gómez, Rebecca L

2017-04-01

Infants show robust ability to track transitional probabilities within language and can use this information to extract words from continuous speech. The degree to which infants remember these words across a delay is unknown. Given well-established benefits of sleep on long-term memory retention in adults, we examine whether sleep similarly facilitates memory in 6.5month olds. Infants listened to an artificial language for 7minutes, followed by a period of sleep or wakefulness. After a time-matched delay for sleep and wakefulness dyads, we measured retention using the head-turn-preference procedure. Infants who slept retained memory for the extracted words that was prone to interference during the test. Infants who remained awake showed no retention. Within the nap group, retention correlated with three electrophysiological measures (1) absolute theta across the brain, (2) absolute alpha across the brain, and (3) greater fronto-central slow wave activity (SWA). Copyright © 2016 Elsevier Inc. All rights reserved.

Sleep-inducing factors.

PubMed

García-García, Fabio; Acosta-Peña, Eva; Venebra-Muñoz, Arturo; Murillo-Rodríguez, Eric

2009-08-01

Kuniomi Ishimori and Henri Piéron were the first researchers to introduce the concept and experimental evidence for a chemical factor that would presumably accumulate in the brain during waking and eventually induce sleep. This substance was named hypnotoxin. Currently, the variety of substances which have been shown to alter sleep includes peptides, cytokines, neurotransmitters and some substances of lipidic nature, many of which are well known for their involvement in other biological activities. In this chapter, we describe the sleep-inducing properties of the vasoactive intestinal peptide, prolactin, adenosine and anandamide.

Chronic sleep restriction induces long-lasting changes in adenosine and noradrenaline receptor density in the rat brain.

PubMed

Kim, Youngsoo; Elmenhorst, David; Weisshaupt, Angela; Wedekind, Franziska; Kroll, Tina; McCarley, Robert W; Strecker, Robert E; Bauer, Andreas

2015-10-01

Although chronic sleep restriction frequently produces long-lasting behavioural and physiological impairments in humans, the underlying neural mechanisms are unknown. Here we used a rat model of chronic sleep restriction to investigate the role of brain adenosine and noradrenaline systems, known to regulate sleep and wakefulness, respectively. The density of adenosine A1 and A2a receptors and β-adrenergic receptors before, during and following 5 days of sleep restriction was assessed with autoradiography. Rats (n = 48) were sleep-deprived for 18 h day(-1) for 5 consecutive days (SR1-SR5), followed by 3 unrestricted recovery sleep days (R1-R3). Brains were collected at the beginning of the light period, which was immediately after the end of sleep deprivation on sleep restriction days. Chronic sleep restriction increased adenosine A1 receptor density significantly in nine of the 13 brain areas analysed with elevations also observed on R3 (+18 to +32%). In contrast, chronic sleep restriction reduced adenosine A2a receptor density significantly in one of the three brain areas analysed (olfactory tubercle which declined 26-31% from SR1 to R1). A decrease in β-adrenergic receptors density was seen in substantia innominata and ventral pallidum which remained reduced on R3, but no changes were found in the anterior cingulate cortex. These data suggest that chronic sleep restriction can induce long-term changes in the brain adenosine and noradrenaline receptors, which may underlie the long-lasting neurocognitive impairments observed in chronic sleep restriction. © 2015 European Sleep Research Society.

Quantification of fetal magnetoencephalographic activity in low-risk fetuses using burst duration and interburst interval.

PubMed

Vairavan, Srinivasan; Govindan, Rathinaswamy B; Haddad, Naim; Preissl, Hubert; Lowery, Curtis L; Siegel, Eric; Eswaran, Hari

2014-07-01

To identify quantitative MEG indices of spontaneous brain activity for fetal neurological maturation in normal pregnancies and examine the effect of fetal state on these indices. Spontaneous MEG brain activity was examined in 22 low-risk fetal recordings with gestational age (GA) ranging from 30 to 37 weeks. As major quantitative characteristics of spontaneous activity, burst duration (BD) and interburst interval (IBI) were studied in correlation with GA and fetal state. IBI showed a decrease with gestational age (-0.21 s/week, P=0.0031). This trend was only maintained in the quiet-sleep state. With respect to BD, no significant trends were detected with GA and state. IBI can be quantified as a fetal brain maturational parameter. The decrease in IBI over gestation was similar to the trend reported in the preterm neonatal EEG studies. Quiet sleep could be the optimal state to study such MEG maturational indices. With further investigation, indices extracted from spontaneous fetal brain activity may serve as an early warning for fetal neurological distress. Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Sleep on your memory traces: How sleep effects can be explained by Act-In, a functional memory model.

PubMed

Cherdieu, Mélaine; Versace, Rémy; Rey, Amandine E; Vallet, Guillaume T; Mazza, Stéphanie

2018-06-01

Numerous studies have explored the effect of sleep on memory. It is well known that a period of sleep, compared to a similar period of wakefulness, protects memories from interference, improves performance, and might also reorganize memory traces in a way that encourages creativity and rule extraction. It is assumed that these benefits come from the reactivation of brain networks, mainly involving the hippocampal structure, as well as from their synchronization with neocortical networks during sleep, thereby underpinning sleep-dependent memory consolidation and reorganization. However, this memory reorganization is difficult to explain within classical memory models. The present paper aims to describe whether the influence of sleep on memory could be explained using a multiple trace memory model that is consistent with the concept of embodied cognition: the Act-In (activation-integration) memory model. We propose an original approach to the results observed in sleep research on the basis of two simple mechanisms, namely activation and integration. Copyright © 2017 Elsevier Ltd. All rights reserved.

The Role of Implied Motion in Engaging Audiences for Health Promotion: Encouraging Naps on a College Campus

ERIC Educational Resources Information Center

Mackert, Michael; Lazard, Allison; Guadagno, Marie; Hughes Wagner, Jessica

2014-01-01

Objective: Lack of sleep among college students negatively impacts health and academic outcomes. Building on research that implied motion imagery increases brain activity, this project tested visual design strategies to increase viewers' engagement with a health communication campaign promoting napping to improve sleep habits. Participants:…

[Regulation of the phases of the sleep-wakefulness cycle with histamine].

PubMed

Diez-Garcia, A; Garzon, M

2017-03-16

Distributed neural networks in the brain sustain generation of wakefulness and two sleep states: non-REM sleep and REM sleep. These three behavioral states are jointly ingrained in a rhythmic sequence that constitutes the sleep-wakefulness cycle. This paper reviews and updates knowledge about the involvement of the histaminergic system in sleep-wakefulness cycle organization. Histaminergic neurons are exclusively located in the hypothalamic tuberomammillary nucleus, but are the source of a widespread projection system to many brain regions. Histamine neurons are active during waking, especially with high attention need, and remain silent in both non-REM and REM sleep. There have been described four metabotropic histamine receptors, of which H1R, H2R and H3R are present in the nervous system. H1R and H2R are mainly postsynaptic heteroreceptors, whereas H3R is thought to be mostly a presynaptic auto- and hetero-receptor. Histaminergic neurons are excited by hypocretinergic neurons and most of the arousing hypocretin effects are thought to depend on histaminergic actions. Interactions among histaminergic axons and cholinergic nuclei within forebrain and brainstem are particularly important for cortical activation. In contrast, histaminergic tuberomammillary neurons, similarly to other aminergic neurons in locus coeruleus or dorsal raphe nucleus, are inhibited by non-REM sleep-promoting neurons of the preoptic region. Further inhibitory actions on histamine neurons come from adenosine release on tuberomammillary region. Finally, histaminergic neurons inhibit REM-on hypothalamic neurons containing melanine-concentrating hormone, thus supporting a permissive role of tuberomammillary nucleus in REM sleep. Actually, knockout mice for histidine decarboxylase, the enzyme synthetizing histamine, show a significant REM sleep increase.

Dual orexin receptor antagonists - promising agents in the treatment of sleep disorders.

PubMed

Pałasz, Artur; Lapray, Damien; Peyron, Christelle; Rojczyk-Gołębiewska, Ewa; Skowronek, Rafał; Markowski, Grzegorz; Czajkowska, Beata; Krzystanek, Marek; Wiaderkiewicz, Ryszard

2014-01-01

Insomnia is a serious medical and social problem, its prevalence in the general population ranges from 9 to 35% depending on the country and assessment method. Often, patients are subject to inappropriate and therefore dangerous pharmacotherapies that include prolonged administration of hypnotic drugs, benzodiazepines and other GABAA receptor modulators. This usually does not lead to a satisfactory improvement in patients' clinical states and may cause lifelong drug dependence. Brain state transitions require the coordinated activity of numerous neuronal pathways and brain structures. It is thought that orexin-expressing neurons play a crucial role in this process. Due to their interaction with the sleep-wake-regulating neuronal population, they can activate vigilance-promoting regions and prevent unwanted sleep intrusions. Understanding the multiple orexin modulatory effects is crucial in the context of pathogenesis of insomnia and should lead to the development of novel treatments. An important step in this process was the synthesis of dual antagonists of orexin receptors. Crucially, these drugs, as opposed to benzodiazepines, do not change the sleep architecture and have limited side-effects. This new pharmacological approach might be the most appropriate to treat insomnia.

Evoked Electrical and Cerebral Vascular Responses Following Sleep Deprivation

PubMed Central

Schei, Jennifer L.; Rector, David M.

2011-01-01

Neuronal activity elicits vascular dilation, delivering additional blood and metabolites to the activated region. With increasing neural activity, vessels stretch and may become less compliant. Most functional imaging studies assume that limits to vascular expansion are not normally reached except under pathological conditions, with the possibility that metabolism could outpace supply. However, we previously demonstrated that evoked hemodynamic responses were larger during quiet sleep when compared to both waking and REM sleep, suggesting that high basal activity during wake may elicit blunted evoked hemodynamic responses due to vascular expansion limits. We hypothesized that extended brain activity through sleep deprivation will further dilate blood vessels, and exacerbate the blunted evoked hemodynamic responses observed during wake, and dampen responses in subsequent sleep. We measured evoked electrical and hemodynamic responses from rats using auditory clicks (0.5 s, 10 Hz, 2–13 s random ISIs) for one hour following 2, 4, or 6 hours of sleep deprivation. Time-of-day matched controls were recorded continuously for 7 hours. Within quiet sleep periods following deprivation, ERP amplitude did not differ; however, the evoked vascular response was smaller with longer sleep deprivation periods. These results suggest that prolonged neural activity periods through sleep deprivation may diminish vascular compliance as indicated by the blunted vascular response. Subsequent sleep may allow vessels to relax, restoring their ability to deliver blood. These results also suggest that severe sleep deprivation or chronic sleep disturbances could push the vasculature to critical limits, leading to metabolic deficit and the potential for tissue trauma. PMID:21854966

Slow sleep spindle and procedural memory consolidation in patients with major depressive disorder.

PubMed

Nishida, Masaki; Nakashima, Yusaku; Nishikawa, Toru

2016-01-01

Evidence has accumulated, which indicates that, in healthy individuals, sleep enhances procedural memory consolidation, and that sleep spindle activity modulates this process. However, whether sleep-dependent procedural memory consolidation occurs in patients medicated for major depressive disorder remains unclear, as are the pharmacological and physiological mechanisms that underlie this process. Healthy control participants (n=17) and patients medicated for major depressive disorder (n=11) were recruited and subjected to a finger-tapping motor sequence test (MST; nondominant hand) paradigm to compare the averaged scores of different learning phases (presleep, postsleep, and overnight improvement). Participants' brain activity was recorded during sleep with 16 electroencephalography channels (between MSTs). Sleep scoring and frequency analyses were performed on the electroencephalography data. Additionally, we evaluated sleep spindle activity, which divided the spindles into fast-frequency spindle activity (12.5-16 Hz) and slow-frequency spindle activity (10.5-12.5 Hz). Sleep-dependent motor memory consolidation in patients with depression was impaired in comparison with that in control participants. In patients with depression, age correlated negatively with overnight improvement. The duration of slow-wave sleep correlated with the magnitude of motor memory consolidation in patients with depression, but not in healthy controls. Slow-frequency spindle activity was associated with reduction in the magnitude of motor memory consolidation in both groups. Because the changes in slow-frequency spindle activity affected the thalamocortical network dysfunction in patients medicated for depression, dysregulated spindle generation may impair sleep-dependent memory consolidation. Our findings may help to elucidate the cognitive deficits that occur in patients with major depression both in the waking state and during sleep.

Regional Patterns of Elevated Alpha and High-Frequency Electroencephalographic Activity during Nonrapid Eye Movement Sleep in Chronic Insomnia: A Pilot Study

PubMed Central

Riedner, Brady A.; Goldstein, Michael R.; Plante, David T.; Rumble, Meredith E.; Ferrarelli, Fabio; Tononi, Giulio; Benca, Ruth M.

2016-01-01

Study Objectives: To examine nonrapid eye movement (NREM) sleep in insomnia using high-density electroencephalography (EEG). Methods: All-night sleep recordings with 256 channel high-density EEG were analyzed for 8 insomnia subjects (5 females) and 8 sex and age-matched controls without sleep complaints. Spectral analyses were conducted using unpaired t-tests and topographical differences between groups were assessed using statistical non-parametric mapping. Five minute segments of deep NREM sleep were further analyzed using sLORETA cortical source imaging. Results: The initial topographic analysis of all-night NREM sleep EEG revealed that insomnia subjects had more high-frequency EEG activity (> 16 Hz) compared to good sleeping controls and that the difference between groups was widespread across the scalp. In addition, the analysis also showed that there was a more circumscribed difference in theta (4–8 Hz) and alpha (8–12 Hz) power bands between groups. When deep NREM sleep (N3) was examined separately, the high-frequency difference between groups diminished, whereas the higher regional alpha activity in insomnia subjects persisted. Source imaging analysis demonstrated that sensory and sensorimotor cortical areas consistently exhibited elevated levels of alpha activity during deep NREM sleep in insomnia subjects relative to good sleeping controls. Conclusions: These results suggest that even during the deepest stage of sleep, sensory and sensorimotor areas in insomnia subjects may still be relatively active compared to control subjects and to the rest of the sleeping brain. Citation: Riedner BA, Goldstein MR, Plante DT, Rumble ME, Ferrarelli F, Tononi G, Benca RM. Regional patterns of elevated alpha and high-frequency electroencephalographic activity during nonrapid eye movement sleep in chronic insomnia: a pilot study. SLEEP 2016;39(4):801–812. PMID:26943465

PR01 - The Effects of Total Sleep Deprivation and Recovery Sleep on Cognitive Performance and Brain Function

DTIC Science & Technology

2006-08-01

characterizing brain areas using fMRI activation during parametric variations of attentional load.Neuron, 2001, 32: 737–745. Doran, S . M., Van Dongen...four nouns. Three images collected at the begin- ning of each run were omitted form the analysis. The entire task lasted 300 s . Data Analysis fMRI data...The views, opinions and/or findings contained in this report are those of the author( s ) and should not be construed as an official Department of the

The anatomical, cellular and synaptic basis of motor atonia during rapid eye movement sleep

PubMed Central

Chen, Michael C.

2016-01-01

Abstract Rapid eye movement (REM) sleep is a recurring part of the sleep–wake cycle characterized by fast, desynchronized rhythms in the electroencephalogram (EEG), hippocampal theta activity, rapid eye movements, autonomic activation and loss of postural muscle tone (atonia). The brain circuitry governing REM sleep is located in the pontine and medullary brainstem and includes ascending and descending projections that regulate the EEG and motor components of REM sleep. The descending signal for postural muscle atonia during REM sleep is thought to originate from glutamatergic neurons of the sublaterodorsal nucleus (SLD), which in turn activate glycinergic pre‐motor neurons in the spinal cord and/or ventromedial medulla to inhibit motor neurons. Despite work over the past two decades on many neurotransmitter systems that regulate the SLD, gaps remain in our knowledge of the synaptic basis by which SLD REM neurons are regulated and in turn produce REM sleep atonia. Elucidating the anatomical, cellular and synaptic basis of REM sleep atonia control is a critical step for treating many sleep‐related disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy. PMID:27060683

Slow spontaneous hemodynamic oscillations during sleep measured with near-infrared spectroscopy

NASA Astrophysics Data System (ADS)

Virtanen, Jaakko; Näsi, Tiina; Noponen, Tommi; Toppila, Jussi; Salmi, Tapani; Ilmoniemi, Risto J.

2011-07-01

Spontaneous cerebral hemodynamic oscillations below 100 mHz reflect the level of cerebral activity, modulate hemodynamic responses to tasks and stimuli, and may aid in detecting various pathologies of the brain. Near-infrared spectroscopy (NIRS) is ideally suited for both measuring spontaneous hemodynamic oscillations and monitoring sleep, but little research has been performed to combine these two applications. We analyzed 30 all-night NIRS-electroencephalography (EEG) sleep recordings to investigate spontaneous hemodynamic activity relative to sleep stages determined by polysomnography. Signal power of hemodynamic oscillations in the low-frequency (LF, 40-150 mHz) and very-low-frequency (VLF, 3-40 mHz) bands decreased in slow-wave sleep (SWS) compared to light sleep (LS) and rapid-eye-movement (REM) sleep. No statistically significant (p < 0.05) differences in oscillation power between LS and REM were observed. However, the period of VLF oscillations around 8 mHz increased in REM sleep in line with earlier studies with other modalities. These results increase our knowledge of the physiology of sleep, complement EEG data, and demonstrate the applicability of NIRS to studying spontaneous hemodynamic fluctuations during sleep.

The important role of sleep in metabolism.

PubMed

Copinschi, Georges; Leproult, Rachel; Spiegel, Karine

2014-01-01

Both reduction in total sleep duration with slow-wave sleep (SWS) largely preserved and alterations of sleep quality (especially marked reduction of SWS) with preservation of total sleep duration are associated with insulin resistance without compensatory increase in insulin secretion, resulting in impaired glucose tolerance and increased risk of type 2 diabetes. When performed under rigorously controlled conditions of energy intake and physical activity, sleep restriction is also associated with a decrease in circulating levels of leptin (an anorexigenic hormone) and an increase in circulating levels of ghrelin (an orexigenic hormone), hunger and appetite. Furthermore, sleep restriction is also associated with a stimulation of brain regions sensitive to food stimuli, indicating that sleep loss may lead to obesity through the selection of high-calorie food. There is also evidence that sleep restriction could provide a permissive environment for the activation of genes that promote obesity. Indeed, the heritability of body mass index is increased in short sleepers. Thus, chronic sleep curtailment, which is on the rise in modern society, including in children, is likely to contribute to the current epidemics of type 2 diabetes and obesity. © 2014 S. Karger AG, Basel.

Fetal Brain Behavior and Cognitive Development.

ERIC Educational Resources Information Center

Joseph, R.

2000-01-01

Presents information on prenatal brain development, detailing the functions controlled by the medulla, pons, and midbrain, and the implications for cognitive development. Concludes that fetal cognitive motor activity, including auditory discrimination, orienting, the wake-sleep cycle, fetal heart rate accelerations, and defensive reactions,…

Characteristic changes in brain electrical activity due to chronic hypoxia in patients with obstructive sleep apnea syndrome (OSAS): a combined EEG study using LORETA and omega complexity.

PubMed

Toth, Marton; Faludi, Bela; Wackermann, Jiri; Czopf, Jozsef; Kondakor, Istvan

2009-11-01

EEG background activity of patients with obstructive sleep apnea syndrome (OSAS, N = 25) was compared to that of normal controls (N = 14) to reflect alterations of brain electrical activity caused by chronic intermittent hypoxia in OSAS. Global and regional (left vs. right, anterior vs. posterior) measures of spatial complexity (Omega) were used to characterize the degree of spatial synchrony of EEG. Low resolution electromagnetic tomography (LORETA) was used to localize generators of EEG activity in separate frequency bands. Comparing patients to controls, lower Omega complexity was found globally and in the right hemisphere. Using LORETA, an increased medium frequency activity was seen bilaterally in the precuneus, paracentral and posterior cingulate cortex. These findings indicate that alterations caused by chronic hypoxia in brain electrical activity in regions associated with influencing emotional regulation, long-term memory and the default mode network. Global synchronization (lower Omega complexity) may indicate a significantly reduced number of relatively independent, parallel neural processes due to chronic global hypoxic state in apneic patients as well as over the right hemisphere.

Sleep, serotonin, and suicide in Japan.

PubMed

Kohyama, Jun

2011-01-01

This article reviews evidence supporting the hypothesis that suicide rates in Japan could be reduced by elevating serotonin levels via increasing the average duration of sleep. Seven major relevant findings were apparent in the literature: 1) Sleep loss is associated with suicide, but the direction of causality is equivocal. 2) Decreased serotonergic activity may be involved in suicidal behavior. 3) Sleep debt may decrease serotonergic activity. 4) The suicide rate in Japan has remained at a heightened level for the past 12 years. 5) The average sleep duration in Japan has decreased over the past 40 years. 6) The average sleep duration in Japan is among the lowest in the world. 7) The average sleep duration in Japan plateaued in 1995 and has been relatively stable since. From the research reviewed, two major problematic issues were apparent: 1) Most people in Japan receive inadequate sleep. 2) Individuals whose sleep is inadequate are unlikely to be sufficiently physically active to stimulate serotonergic systems to a desirable level. I propose that public health initiatives encouraging a longer duration of sleep may provide a relatively simple way of addressing the disturbing current trend in Japan. The combination of actigraph and brain serotonin level measurement could allow large population-based cohort studies to be designed, to elucidate the causal links between sleep duration, serotonin levels, and suicide rates.

Distinct effects of acute and chronic sleep loss on DNA damage in rats.

PubMed

Andersen, M L; Ribeiro, D A; Bergamaschi, C T; Alvarenga, T A; Silva, A; Zager, A; Campos, R R; Tufik, S

2009-04-30

The aim of this investigation was to evaluate genetic damage induced in male rats by experimental sleep loss for short-term (24 and 96 h) and long-term (21 days) intervals, as well as their respective recovery periods in peripheral blood, brain, liver and heart tissue by the single cell gel (comet) assay. Rats were paradoxically deprived of sleep (PSD) by the platform technique for 24 or 96 h, or chronically sleep-restricted (SR) for 21 days. We also sought to verify the time course of their recovery after 24 h of rebound sleep. The results showed DNA damage in blood cells of rats submitted to PSD for 96 h. Brain tissue showed extensive genotoxic damage in PSD rats (both 24 and 96 h), though the effect was more pronounced in the 96 h group. Rats allowed to recover from the PSD-96 h and SR-21 days treatments showed DNA damage as compared to negative controls. Liver and heart did not display any genotoxicity activity. Corticosterone concentrations were increased after PSD (24 and 96 h) relative to control rats, whereas these levels were unaffected in the SR group. Collectively, these findings reveal that sleep loss was able to induce genetic damage in blood and brain cells, especially following acute exposure. Since DNA damage is an important step in events leading to genomic instability, this study represents a relevant contribution to the understanding of the potential health risks associated with sleep deprivation.

Blood-Brain Barrier Disruption Induced by Chronic Sleep Loss: Low-Grade Inflammation May Be the Link

PubMed Central

Velázquez-Moctezuma, J.

2016-01-01

Sleep is a vital phenomenon related to immunomodulation at the central and peripheral level. Sleep deficient in duration and/or quality is a common problem in the modern society and is considered a risk factor to develop neurodegenerative diseases. Sleep loss in rodents induces blood-brain barrier disruption and the underlying mechanism is still unknown. Several reports indicate that sleep loss induces a systemic low-grade inflammation characterized by the release of several molecules, such as cytokines, chemokines, and acute-phase proteins; all of them may promote changes in cellular components of the blood-brain barrier, particularly on brain endothelial cells. In the present review we discuss the role of inflammatory mediators that increase during sleep loss and their association with general disturbances in peripheral endothelium and epithelium and how those inflammatory mediators may alter the blood-brain barrier. Finally, this manuscript proposes a hypothetical mechanism by which sleep loss may induce blood-brain barrier disruption, emphasizing the regulatory effect of inflammatory molecules on tight junction proteins. PMID:27738642

Sleep Deprivation Promotes Habitual Control over Goal-Directed Control: Behavioral and Neuroimaging Evidence.

PubMed

Chen, Jie; Liang, Jie; Lin, Xiao; Zhang, Yang; Zhang, Yan; Lu, Lin; Shi, Jie

2017-12-06

Sleep is one of the most fundamental processes of life, playing an important role in the regulation of brain function. The long-term lack of sleep can cause memory impairments, declines in learning ability, and executive dysfunction. In the present study, we evaluated the effects of sleep deprivation on instrumental learning behavior, particularly goal-directed and habitual actions in humans, and investigated the underlying neural mechanisms. Healthy college students of either gender were enrolled and randomly divided into sleep deprivation group and sleep control group. fMRI data were collected. We found that one night of sleep deprivation led to greater responsiveness to stimuli that were associated with devalued outcomes in the slips-of-action test, indicating a deficit in the formation of goal-directed control and an overreliance on habits. Furthermore, sleep deprivation had no effect on the expression of acquired goal-directed action. The level of goal-directed action after sleep deprivation was positively correlated with baseline working memory capacity. The neuroimaging data indicated that goal-directed learning mainly recruited the ventromedial PFC (vmPFC), the activation of which was less pronounced during goal-directed learning after sleep deprivation. Activation of the vmPFC during goal-directed learning during training was positively correlated with the level of goal-directed action performance. The present study suggests that people rely predominantly on habits at the expense of goal-directed control after sleep deprivation, and this process involves the vmPFC. These results contribute to a better understanding of the effects of sleep loss on decision-making. SIGNIFICANCE STATEMENT Understanding the cognitive consequences of sleep deprivation has become extremely important over the past half century, given the continued decline in sleep duration in industrialized societies. Our results provide novel evidence that goal-directed action may be particularly vulnerable to sleep loss, and the brain mechanism underlying this effect was explored. Elucidation of the effects of sleep deprivation on decision-making will deepen our understanding of the function of sleep, emphasizing the role of sleep in cognitive impairments and mental health. Copyright © 2017 the authors 0270-6474/17/3711979-14$15.00/0.

State-dependencies of learning across brain scales

PubMed Central

Ritter, Petra; Born, Jan; Brecht, Michael; Dinse, Hubert R.; Heinemann, Uwe; Pleger, Burkhard; Schmitz, Dietmar; Schreiber, Susanne; Villringer, Arno; Kempter, Richard

2015-01-01

Learning is a complex brain function operating on different time scales, from milliseconds to years, which induces enduring changes in brain dynamics. The brain also undergoes continuous “spontaneous” shifts in states, which, amongst others, are characterized by rhythmic activity of various frequencies. Besides the most obvious distinct modes of waking and sleep, wake-associated brain states comprise modulations of vigilance and attention. Recent findings show that certain brain states, particularly during sleep, are essential for learning and memory consolidation. Oscillatory activity plays a crucial role on several spatial scales, for example in plasticity at a synaptic level or in communication across brain areas. However, the underlying mechanisms and computational rules linking brain states and rhythms to learning, though relevant for our understanding of brain function and therapeutic approaches in brain disease, have not yet been elucidated. Here we review known mechanisms of how brain states mediate and modulate learning by their characteristic rhythmic signatures. To understand the critical interplay between brain states, brain rhythms, and learning processes, a wide range of experimental and theoretical work in animal models and human subjects from the single synapse to the large-scale cortical level needs to be integrated. By discussing results from experiments and theoretical approaches, we illuminate new avenues for utilizing neuronal learning mechanisms in developing tools and therapies, e.g., for stroke patients and to devise memory enhancement strategies for the elderly. PMID:25767445

Pharmacological treatment of sleep disorders and its relationship with neuroplasticity.

PubMed

Abad, Vivien C; Guilleminault, Christian

2015-01-01

Sleep and wakefulness are regulated by complex brain circuits located in the brain stem, thalamus, subthalamus, hypothalamus, basal forebrain, and cerebral cortex. Wakefulness and NREM and REM sleep are modulated by the interactions between neurotransmitters that promote arousal and neurotransmitters that promote sleep. Various lines of evidence suggest that sleep disorders may negatively affect neuronal plasticity and cognitive function. Pharmacological treatments may alleviate these effects but may also have adverse side effects by themselves. This chapter discusses the relationship between sleep disorders, pharmacological treatments, and brain plasticity, including the treatment of insomnia, hypersomnias such as narcolepsy, restless legs syndrome (RLS), obstructive sleep apnea (OSA), and parasomnias.

The character of sleep disturbances produced by multiple administrations of atropine the antagonist of brain muscarinic cholinergic system.

PubMed

Maglakelidze, N T; Chkhartishvili, E V; Mchedlidze, O M; Dzadzamiia, Sh Sh; Nachkebiia, N G

2012-03-01

Modification of brain muscarinic cholinergic system normal functioning can be considered as an appropriate strategy for the study of its role in sleep-wakefulness cycle basic mechanisms in general and in the course/maintenance of PS in particular. For this aim systemic application of muscarinic cholinoreceptors antagonists is significant because it gives possibility to modify functioning all of known five sub-types of muscarinic cholinoreceptors and to study the character of sleep disturbances in these conditions. Problem is very topical because the question about the intimate aspects of BMChS involvement in PS maintaining mechanisms still remains unsolved. In cats Atropine systemic administration was made once daily at 10:00 a.m. and continuous EEG registration of sleep-wakefulness cycle ultradian structure, lasting for 10 hour daily, was started immediately. In sum each animal received anti-muscarinic drugs for 12 times. Thereafter drug administrations were ceased and EEG registration of sleep-wakefulness cycle ultradian structure was continued during 10 consecutive days. On the basis of results obtained in these conditions we can conclude that brain muscarinic cholinergic system normal functioning is significant for basic mechanisms of sleep-wakefulness cycle. During wakefulness, at the level of neocortex and hippocampus, MChS supports only EEG activation, while it is one of the main factors in PS triggering and maintaining mechanisms.

Spontaneous sleep-wake cycle and sleep deprivation differently induce Bdnf1, Bdnf4 and Bdnf9a DNA methylation and transcripts levels in the basal forebrain and frontal cortex in rats.

PubMed

Ventskovska, Olena; Porkka-Heiskanen, Tarja; Karpova, Nina N

2015-04-01

Brain-derived neurotrophic factor (Bdnf) regulates neuronal plasticity, slow wave activity and sleep homeostasis. Environmental stimuli control Bdnf expression through epigenetic mechanisms, but there are no data on epigenetic regulation of Bdnf by sleep or sleep deprivation. Here we investigated whether 5-methylcytosine (5mC) DNA modification at Bdnf promoters p1, p4 and p9 influences Bdnf1, Bdnf4 and Bdnf9a expression during the normal inactive phase or after sleep deprivation (SD) (3, 6 and 12 h, end-times being ZT3, ZT6 and ZT12) in rats in two brain areas involved in sleep regulation, the basal forebrain and cortex. We found a daytime variation in cortical Bdnf expression: Bdnf1 expression was highest at ZT6 and Bdnf4 lowest at ZT12. Such variation was not observed in the basal forebrain. Also Bdnf p1 and p9 methylation levels differed only in the cortex, while Bdnf p4 methylation did not vary in either area. Factorial analysis revealed that sleep deprivation significantly induced Bdnf1 and Bdnf4 with the similar pattern for Bdnf9a in both basal forebrain and cortex; 12 h of sleep deprivation decreased 5mC levels at the cortical Bdnf p4 and p9. Regression analysis between the 5mC promoter levels and the corresponding Bdnf transcript expression revealed significant negative correlations for the basal forebrain Bdnf1 and cortical Bdnf9a transcripts in only non-deprived rats, while these correlations were lost after sleep deprivation. Our results suggest that Bdnf transcription during the light phase of undisturbed sleep-wake cycle but not after SD is regulated at least partially by brain site-specific DNA methylation. © 2014 European Sleep Research Society.

Sleep and immune function: glial contributions and consequences of aging

PubMed Central

Ingiosi, Ashley M.; Opp, Mark R.; Krueger, James M.

2013-01-01

The reciprocal interactions between sleep and immune function are well-studied. Insufficient sleep induces innate immune responses as evidenced by increased expression of pro-inflammatory mediators in the brain and periphery. Conversely, immune challenges upregulate immunomodulator expression, which alters central nervous system-mediated processes and behaviors, including sleep. Recent studies indicate that glial cells, namely microglia and astrocytes, are active contributors to sleep and immune system interactions. Evidence suggests glial regulation of these interactions is mediated, in part, by adenosine and adenosine 5′-triphosphate actions at purinergic type 1 and type 2 receptors. Furthermore, microglia and astrocytes may modulate declines in sleep-wake behavior and immunity observed in aging. PMID:23452941

Sleep and immune function: glial contributions and consequences of aging.

PubMed

Ingiosi, Ashley M; Opp, Mark R; Krueger, James M

2013-10-01

The reciprocal interactions between sleep and immune function are well-studied. Insufficient sleep induces innate immune responses as evidenced by increased expression of pro-inflammatory mediators in the brain and periphery. Conversely, immune challenges upregulate immunomodulator expression, which alters central nervous system-mediated processes and behaviors, including sleep. Recent studies indicate that glial cells, namely microglia and astrocytes, are active contributors to sleep and immune system interactions. Evidence suggests glial regulation of these interactions is mediated, in part, by adenosine and adenosine 5'-triphosphate actions at purinergic type 1 and type 2 receptors. Furthermore, microglia and astrocytes may modulate declines in sleep-wake behavior and immunity observed in aging. Copyright © 2013. Published by Elsevier Ltd.

Reduction in menopause-related symptoms associated with use of a noninvasive neurotechnology for autocalibration of neural oscillations.

PubMed

Tegeler, Charles H; Tegeler, Catherine L; Cook, Jared F; Lee, Sung W; Pajewski, Nicholas M

2015-06-01

Increased amplitudes in high-frequency brain electrical activity are reported with menopausal hot flashes. We report outcomes associated with the use of High-resolution, relational, resonance-based, electroencephalic mirroring--a noninvasive neurotechnology for autocalibration of neural oscillations--by women with perimenopausal and postmenopausal hot flashes. Twelve women with hot flashes (median age, 56 y; range, 46-69 y) underwent a median of 13 (range, 8-23) intervention sessions for a median of 9.5 days (range, 4-32). This intervention uses algorithmic analysis of brain electrical activity and near real-time translation of brain frequencies into variable tones for acoustic stimulation. Hot flash frequency and severity were recorded by daily diary. Primary outcomes included hot flash severity score, sleep, and depressive symptoms. High-frequency amplitudes (23-36 Hz) from bilateral temporal scalp recordings were measured at baseline and during serial sessions. Self-reported symptom inventories for sleep and depressive symptoms were collected. The median change in hot flash severity score was -0.97 (range, -3.00 to 1.00; P = 0.015). Sleep and depression scores decreased by -8.5 points (range, -20 to -1; P = 0.022) and -5.5 points (range, -32 to 8; P = 0.015), respectively. The median sum of amplitudes for the right and left temporal high-frequency brain electrical activity was 8.44 μV (range, 6.27-16.66) at baseline and decreased by a median of -2.96 μV (range, -11.05 to -0.65; P = 0.0005) by the final session. Hot flash frequency and severity, symptoms of insomnia and depression, and temporal high-frequency brain electrical activity decrease after High-resolution, relational, resonance-based, electroencephalic mirroring. Larger controlled trials with longer follow-up are warranted.

Deep sleep divides the cortex into opposite modes of anatomical-functional coupling.

PubMed

Tagliazucchi, Enzo; Crossley, Nicolas; Bullmore, Edward T; Laufs, Helmut

2016-11-01

The coupling of anatomical and functional connectivity at rest suggests that anatomy is essential for wake-typical activity patterns. Here, we study the development of this coupling from wakefulness to deep sleep. Globally, similarity between whole-brain anatomical and functional connectivity networks increased during deep sleep. Regionally, we found differential coupling: during sleep, functional connectivity of primary cortices resembled more the underlying anatomical connectivity, while we observed the opposite in associative cortices. Increased anatomical-functional similarity in sensory areas is consistent with their stereotypical, cross-modal response to the environment during sleep. In distinction, looser coupling-relative to wakeful rest-in higher order integrative cortices suggests that sleep actively disrupts default patterns of functional connectivity in regions essential for the conscious access of information and that anatomical connectivity acts as an anchor for the restoration of their functionality upon awakening.

REM sleep rescues learning from interference

PubMed Central

McDevitt, Elizabeth A.; Duggan, Katherine A.; Mednick, Sara C.

2015-01-01

Classical human memory studies investigating the acquisition of temporally-linked events have found that the memories for two events will interfere with each other and cause forgetting (i.e., interference; Wixted, 2004). Importantly, sleep helps consolidate memories and protect them from subsequent interference (Ellenbogen, Hulbert, Stickgold, Dinges, & Thompson-Schill, 2006). We asked whether sleep can also repair memories that have already been damaged by interference. Using a perceptual learning paradigm, we induced interference either before or after a consolidation period. We varied brain states during consolidation by comparing active wake, quiet wake, and naps with either non-rapid eye movement sleep (NREM), or both NREM and REM sleep. When interference occurred after consolidation, sleep and wake both produced learning. However, interference prior to consolidation impaired memory, with retroactive interference showing more disruption than proactive interference. Sleep rescued learning damaged by interference. Critically, only naps that contained REM sleep were able to rescue learning that was highly disrupted by retroactive interference. Furthermore, the magnitude of rescued learning was correlated with the amount of REM sleep. We demonstrate the first evidence of a process by which the brain can rescue and consolidate memories damaged by interference, and that this process requires REM sleep. We explain these results within a theoretical model that considers how interference during encoding interacts with consolidation processes to predict which memories are retained or lost. PMID:25498222

High definition-transcranial direct current stimulation changes older adults' subjective sleep and corresponding resting-state functional connectivity.

PubMed

Sheng, Jing; Xie, Chao; Fan, Dong-Qiong; Lei, Xu; Yu, Jing

2018-07-01

With advanced age, older adults show functional deterioration in sleep. Transcranial direct current stimulation (tDCS), a noninvasive brain stimulation, modulates individuals' behavioral performance in various cognitive domains. However, the modulation effect and neural mechanisms of tDCS on sleep, especially for the elderly population are not clear. Here, we aimed to investigate whether high-definition transcranial direct current stimulation (HD-tDCS) could modulate community-dwelling older adults' subjective sleep and whether these potential improvements are associated with the large-scale brain activity alterations recorded by functional magnetic resonance imaging. Thirty-one older adults were randomly allocated to the HD-tDCS group and the control group. HD-tDCS was applied for 25 min at 1.5 mA per day for two weeks. The anode electrode was placed over the left dorsolateral prefrontal cortex, surrounded by 4 cathodes at 7 cm radius. All participants completed sleep neuropsychological assessments and fMRI scans individually before and after intervention. Behaviorally, we observed a HD-tDCS-induced enhancement of older adults' sleep duration. On the aspect of the corresponding neural alterations, we observed that HD-tDCS decreased the functional connectivity between the default mode network (DMN) and subcortical network. More importantly, the decoupling connectivity of the DMN-subcortical network was correlated with the improvements of subjective sleep in the HD-tDCS group. Our findings add novel behavioral and neural evidences about tDCS-induced sleep improvement in community-dwelling older adults. With further development, tDCS may be used as an alternative treatment for sleep disorders and alleviate the dysfunction of brain networks induced by aging. Copyright © 2018 Elsevier B.V. All rights reserved.

Sleep-Wake Differences in Relative Regional Cerebral Metabolic Rate for Glucose among Patients with Insomnia Compared with Good Sleepers.

PubMed

Kay, Daniel B; Karim, Helmet T; Soehner, Adriane M; Hasler, Brant P; Wilckens, Kristine A; James, Jeffrey A; Aizenstein, Howard J; Price, Julie C; Rosario, Bedda L; Kupfer, David J; Germain, Anne; Hall, Martica H; Franzen, Peter L; Nofzinger, Eric A; Buysse, Daniel J

2016-10-01

The neurobiological mechanisms of insomnia may involve altered patterns of activation across sleep-wake states in brain regions associated with cognition, self-referential processes, affect, and sleep-wake promotion. The objective of this study was to compare relative regional cerebral metabolic rate for glucose (rCMR glc ) in these brain regions across wake and nonrapid eye movement (NREM) sleep states in patients with primary insomnia (PI) and good sleeper controls (GS). Participants included 44 PI and 40 GS matched for age (mean = 37 y old, range 21-60), sex, and race. We conducted [ 18 F]fluoro-2-deoxy-D-glucose positron emission tomography scans in PI and GS during both morning wakefulness and NREM sleep at night. Repeated measures analysis of variance was used to test for group (PI vs. GS) by state (wake vs. NREM sleep) interactions in relative rCMR glc . Significant group-by-state interactions in relative rCMR glc were found in the precuneus/posterior cingulate cortex, left middle frontal gyrus, left inferior/superior parietal lobules, left lingual/fusiform/occipital gyri, and right lingual gyrus. All clusters were significant at P corrected < 0.05. Insomnia was characterized by regional alterations in relative glucose metabolism across NREM sleep and wakefulness. Significant group-by-state interactions in relative rCMR glc suggest that insomnia is associated with impaired disengagement of brain regions involved in cognition (left frontoparietal), self-referential processes (precuneus/posterior cingulate), and affect (left middle frontal, fusiform/lingual gyri) during NREM sleep, or alternatively, to impaired engagement of these regions during wakefulness. © 2016 Associated Professional Sleep Societies, LLC.

Recovery of Neurological Function Despite Immediate Sleep Disruption Following Diffuse Brain Injury in the Mouse: Clinical Relevance to Medically Untreated Concussion

PubMed Central

Rowe, Rachel K.; Harrison, Jordan L.; O'Hara, Bruce F.; Lifshitz, Jonathan

2014-01-01

Study Objective: We investigated the relationship between immediate disruption of posttraumatic sleep and functional outcome in the diffuse brain-injured mouse. Design: Adult male C57BL/6 mice were subjected to moderate midline fluid percussion injury (n = 65; 1.4 atm; 6-10 min righting reflex time) or sham injury (n = 44). Cohorts received either intentional sleep disruption (minimally stressful gentle handling) or no sleep disruption for 6 h following injury. Following disruption, serum corticosterone levels (enzyme-linked immunosorbent assay) and posttraumatic sleep (noninvasive piezoelectric sleep cages) were measured. For 1-7 days postinjury, sensorimotor outcome was assessed by Rotarod and a modified Neurological Severity Score (NSS). Cognitive function was measured using Novel Object Recognition (NOR) and Morris water maze (MWM) in the first week postinjury. Setting: Neurotrauma research laboratory. Measurements and Results: Disrupting posttraumatic sleep for 6 h did not affect serum corticosterone levels or functional outcome. In the hour following the first dark onset, sleep-disrupted mice exhibited a significant increase in sleep; however, this increase was not sustained and there was no rebound of lost sleep. Regardless of sleep disruption, mice showed a time-dependent improvement in Rotarod performance, with brain-injured mice having significantly shorter latencies on day 7 compared to sham. Further, brain-injured mice, regardless of sleep disruption, had significantly higher NSS scores postinjury compared with sham. Cognitive behavioral testing showed no group differences among any treatment group measured by MWM and NOR. Conclusion: Short-duration disruption of posttraumatic sleep did not affect functional outcome, measured by motor and cognitive performance. These data raise uncertainty about posttraumatic sleep as a mechanism of recovery from diffuse brain injury. Citation: Rowe RK; Harrison JL; O'Hara BF; Lifshitz J. Recovery of neurological function despite immediate sleep disruption following diffuse brain injury in the mouse: clinical relevance to medically untreated concussion. SLEEP 2014;37(4):743-752. PMID:24899763

Genetic variation in Aquaporin-4 moderates the relationship between sleep and brain Aβ-amyloid burden.

PubMed

Rainey-Smith, Stephanie R; Mazzucchelli, Gavin N; Villemagne, Victor L; Brown, Belinda M; Porter, Tenielle; Weinborn, Michael; Bucks, Romola S; Milicic, Lidija; Sohrabi, Hamid R; Taddei, Kevin; Ames, David; Maruff, Paul; Masters, Colin L; Rowe, Christopher C; Salvado, Olivier; Martins, Ralph N; Laws, Simon M

2018-02-26

The glymphatic system is postulated to be a mechanism of brain Aβ-amyloid clearance and to be most effective during sleep. Ablation of the astrocytic end-feet expressed water-channel protein, Aquaporin-4, in mice, results in impairment of this clearance mechanism and increased brain Aβ-amyloid deposition, suggesting that Aquaporin-4 plays a pivotal role in glymphatic function. Currently there is a paucity of literature regarding the impact of AQP4 genetic variation on sleep, brain Aβ-amyloid burden and their relationship to each other in humans. To address this a cross-sectional observational study was undertaken in cognitively normal older adults from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study. Genetic variants in AQP4 were investigated with respect to self-reported Pittsburgh Sleep Quality Index sleep parameters, positron emission tomography derived brain Aβ-amyloid burden and whether these genetic variants moderated the sleep-Aβ-amyloid burden relationship. One AQP4 variant, rs72878776, was associated with poorer overall sleep quality, while several SNPs moderated the effect of sleep latency (rs491148, rs9951307, rs7135406, rs3875089, rs151246) and duration (rs72878776, rs491148 and rs2339214) on brain Aβ-amyloid burden. This study suggests that AQP4 genetic variation moderates the relationship between sleep and brain Aβ-amyloid burden, which adds weight to the proposed glymphatic system being a potential Aβ-amyloid clearance mechanism and suggests that AQP4 genetic variation may impair this function. Further, AQP4 genetic variation should be considered when interpreting sleep-Aβ relationships.

Interhemispheric differences of the correlation dimension in a human sleep electroencephalogram.

PubMed

Kobayashi, Toshio; Madokoro, Shigeki; Misaki, Kiwamu; Murayama, Jyunichi; Nakagawa, Hiroki; Wada, Yuji

2002-06-01

The interhemispheric differences of the correlation dimension (D2) in the sleep electroencephalogram (EEG) of eight healthy right-handed students was investigated. During slow wave sleep (SWS) the D2 of the central EEG and the temporal left hemisphere (LH) EEG were significantly higher than those in the right hemisphere (RH) EEG; but during rapid eye movement (REM) sleep, the D2 of the central EEG and the occipital RH EEG were significantly higher. The D2 of EEG in the left temporal site during REM sleep were significantly higher than in the right during the first and third sleep cycles, but these were significantly lower during the fourth and fifth sleep cycles. During REM sleep, temporal brain activity may shift from the LH to the RH as morning approaches.

Genomic analysis of sleep deprivation reveals translational regulation in the hippocampus.

PubMed

Vecsey, Christopher G; Peixoto, Lucia; Choi, Jennifer H K; Wimmer, Mathieu; Jaganath, Devan; Hernandez, Pepe J; Blackwell, Jennifer; Meda, Karuna; Park, Alan J; Hannenhalli, Sridhar; Abel, Ted

2012-10-17

Sleep deprivation is a common problem of considerable health and economic impact in today's society. Sleep loss is associated with deleterious effects on cognitive functions such as memory and has a high comorbidity with many neurodegenerative and neuropsychiatric disorders. Therefore, it is crucial to understand the molecular basis of the effect of sleep deprivation in the brain. In this study, we combined genome-wide and traditional molecular biological approaches to determine the cellular and molecular impacts of sleep deprivation in the mouse hippocampus, a brain area crucial for many forms of memory. Microarray analysis examining the effects of 5 h of sleep deprivation on gene expression in the mouse hippocampus found 533 genes with altered expression. Bioinformatic analysis revealed that a prominent effect of sleep deprivation was to downregulate translation, potentially mediated through components of the insulin signaling pathway such as the mammalian target of rapamycin (mTOR), a key regulator of protein synthesis. Consistent with this analysis, sleep deprivation reduced levels of total and phosphorylated mTOR, and levels returned to baseline after 2.5 h of recovery sleep. Our findings represent the first genome-wide analysis of the effects of sleep deprivation on the mouse hippocampus, and they suggest that the detrimental effects of sleep deprivation may be mediated by reductions in protein synthesis via downregulation of mTOR. Because protein synthesis and mTOR activation are required for long-term memory formation, our study improves our understanding of the molecular mechanisms underlying the memory impairments induced by sleep deprivation.

Sleep Duration and Age-Related Changes in Brain Structure and Cognitive Performance

PubMed Central

Lo, June C.; Loh, Kep Kee; Zheng, Hui; Sim, Sam K.Y.; Chee, Michael W.L.

2014-01-01

Study Objectives: To investigate the contribution of sleep duration and quality to age-related changes in brain structure and cognitive performance in relatively healthy older adults. Design: Community-based longitudinal brain and cognitive aging study using a convenience sample. Setting: Participants were studied in a research laboratory. Participants: Relatively healthy adults aged 55 y and older at study commencement. Interventions: N/A. Measurements and Results: Participants underwent magnetic resonance imaging and neuropsychological assessment every 2 y. Subjective assessments of sleep duration and quality and blood samples were obtained. Each hour of reduced sleep duration at baseline augmented the annual expansion rate of the ventricles by 0.59% (P = 0.007) and the annual decline rate in global cognitive performance by 0.67% (P = 0.050) in the subsequent 2 y after controlling for the effects of age, sex, education, and body mass index. In contrast, global sleep quality at baseline did not modulate either brain or cognitive aging. High-sensitivity C-reactive protein, a marker of systemic inflammation, showed no correlation with baseline sleep duration, brain structure, or cognitive performance. Conclusions: In healthy older adults, short sleep duration is associated with greater age-related brain atrophy and cognitive decline. These associations are not associated with elevated inflammatory responses among short sleepers. Citation: Lo JC, Loh KK, Zheng H, Sim SK, Chee MW. Sleep duration and age-related changes in brain structure and cognitive performance. SLEEP 2014;37(7):1171-1178. PMID:25061245

Swing Boat: Inducing and Recording Locomotor Activity in a Drosophila melanogaster Model of Alzheimer’s Disease

PubMed Central

Berlandi, Johannes; Lin, Fang-Ju; Ambrée, Oliver; Rieger, Dirk; Paulus, Werner; Jeibmann, Astrid

2017-01-01

Recent studies indicate that physical activity can slow down progression of neurodegeneration in humans. To date, automated ways to induce activity have been predominantly described in rodent models. To study the impact of activity on behavior and survival in adult Drosophila melanogaster, we aimed to develop a rotating tube device “swing boat” which is capable of monitoring activity and sleep patterns as well as survival rates of flies. For the purpose of a first application, we tested our device on a transgenic fly model of Alzheimer’s disease (AD). Activity of flies was recorded in a climate chamber using the Drosophila Activity Monitoring (DAM) System connected to data acquisition software. Locomotor activity was induced by a rotating tube device “swing boat” by repetitively tilting the tubes for 30 min per day. A non-exercising group of flies was used as control and activity and sleep patterns were obtained. The GAL4-/UAS system was used to drive pan-neuronal expression of human Aβ42 in flies. Immunohistochemical stainings for Aβ42 were performed on paraffin sections of adult fly brains. Daily rotation of the fly tubes evoked a pronounced peak of activity during the 30 min exercise period. Pan-neuronal expression of human Aβ42 in flies caused abnormalities in locomotor activity, reduction of life span and elevated sleep fragmentation in comparison to wild type flies. Furthermore, the formation of amyloid accumulations was observed in the adult fly brain. Gently induced activity over 12 days did not evoke prominent effects in wild type flies but resulted in prolongation of median survival time by 7 days (32.6%) in Aβ42-expressing flies. Additionally, restoration of abnormally decreased night time sleep (10%) and reduced sleep fragmentation (28%) were observed compared to non-exercising Aβ42-expressing flies. On a structural level no prominent effects regarding prevalence of amyloid aggregations and Aβ42 RNA expression were detected following activity induction. The rotating tube device successfully induced activity in flies shown by quantitative activity analysis. Our setup enabled quantitative analysis of activity and sleep patterns as well as of survival rates. Induced activity in a Drosophila model of Alzheimer’s disease improved survival and ameliorated sleep phenotypes. PMID:28912696

Glymphatic clearance controls state-dependent changes in brain lactate concentration.

PubMed

Lundgaard, Iben; Lu, Minh Lon; Yang, Ezra; Peng, Weiguo; Mestre, Humberto; Hitomi, Emi; Deane, Rashid; Nedergaard, Maiken

2017-06-01

Brain lactate concentration is higher during wakefulness than in sleep. However, it is unknown why arousal is linked to an increase in brain lactate and why lactate declines within minutes of sleep. Here, we show that the glymphatic system is responsible for state-dependent changes in brain lactate concentration. Suppression of glymphatic function via acetazolamide treatment, cisterna magna puncture, aquaporin 4 deletion, or changes in body position reduced the decline in brain lactate normally observed when awake mice transition into sleep or anesthesia. Concurrently, the same manipulations diminished accumulation of lactate in cervical, but not in inguinal lymph nodes when mice were anesthetized. Thus, our study suggests that brain lactate is an excellent biomarker of the sleep-wake cycle and increases further during sleep deprivation, because brain lactate is inversely correlated with glymphatic-lymphatic clearance. This analysis provides fundamental new insight into brain energy metabolism by demonstrating that glucose that is not fully oxidized can be exported as lactate via glymphatic-lymphatic fluid transport.

Abnormality of circadian rhythm accompanied by an increase in frontal cortex serotonin in animal model of autism.

PubMed

Tsujino, Naohisa; Nakatani, Yasushi; Seki, Yoshinari; Nakasato, Akane; Nakamura, Michiko; Sugawara, Michiya; Arita, Hideho

2007-02-01

Several clinical reports have indicated that autistic patients often show disturbance of the circadian rhythm, which may be related to dysfunction of the serotonergic system in the brain. Using rats exposed prenatally to valproic acid (VPA) as an animal model of autism, we examined locomotor activity and feeding under a reversed 12-h light/dark cycle, and found disturbance of the circadian rhythm characterized by frequent arousal during the light/sleep phase. In addition, measurement of brain serotonin (5-HT) level using in vivo microdialysis showed that the brain 5-HT level in VPA-exposed rats was significantly higher than that in control rats. These results suggest that a higher brain 5-HT level might be responsible for the irregular sleep/awake rhythm in autism.

Auditory closed-loop stimulation of the sleep slow oscillation enhances memory.

PubMed

Ngo, Hong-Viet V; Martinetz, Thomas; Born, Jan; Mölle, Matthias

2013-05-08

Brain rhythms regulate information processing in different states to enable learning and memory formation. The <1 Hz sleep slow oscillation hallmarks slow-wave sleep and is critical to memory consolidation. Here we show in sleeping humans that auditory stimulation in phase with the ongoing rhythmic occurrence of slow oscillation up states profoundly enhances the slow oscillation rhythm, phase-coupled spindle activity, and, consequently, the consolidation of declarative memory. Stimulation out of phase with the ongoing slow oscillation rhythm remained ineffective. Closed-loop in-phase stimulation provides a straight-forward tool to enhance sleep rhythms and their functional efficacy. Copyright © 2013 Elsevier Inc. All rights reserved.

The median preoptic nucleus reciprocally modulates activity of arousal-related and sleep-related neurons in the perifornical lateral hypothalamus.

PubMed

Suntsova, Natalia; Guzman-Marin, Ruben; Kumar, Sunil; Alam, Md Noor; Szymusiak, Ronald; McGinty, Dennis

2007-02-14

The perifornical-lateral hypothalamic area (PF/LH) contains neuronal groups playing an important role in control of waking and sleep. Among the brain regions that regulate behavioral states, one of the strongest sources of projections to the PF/LH is the median preoptic nucleus (MnPN) containing a sleep-active neuronal population. To evaluate the role of MnPN afferents in the control of PF/LH neuronal activity, we studied the responses of PF/LH cells to electrical stimulation or local chemical manipulation of the MnPN in freely moving rats. Single-pulse electrical stimulation evoked responses in 79% of recorded PF/LH neurons. No cells were activated antidromically. Direct and indirect transsynaptic effects depended on sleep-wake discharge pattern of PF/LH cells. The majority of arousal-related neurons, that is, cells discharging at maximal rates during active waking (AW) or during AW and rapid eye movement (REM) sleep, exhibited exclusively or initially inhibitory responses to stimulation. Sleep-related neurons, the cells with elevated discharge during non-REM and REM sleep or selectively active in REM sleep, exhibited exclusively or initially excitatory responses. Activation of the MnPN via microdialytic application of L-glutamate or bicuculline resulted in reduced discharge of arousal-related and in excitation of sleep-related PF/LH neurons. Deactivation of the MnPN with muscimol caused opposite effects. The results indicate that the MnPN contains subset(s) of neurons, which exert inhibitory control over arousal-related and excitatory control over sleep-related PF/LH neurons. We hypothesize that MnPN sleep-active neuronal group has both inhibitory and excitatory outputs that participate in the inhibitory control of arousal-promoting PF/LH mechanisms.

Night duty and decreased brain activity of medical residents: a wearable optical topography study

PubMed Central

Nishida, Masaki; Kikuchi, Senichiro; Miwakeichi, Fumikazu; Suda, Shiro

2017-01-01

ABSTRACT Background: Overwork, fatigue, and sleep deprivation due to night duty are likely to be detrimental to the performance of medical residents and can consequently affect patient safety. Objective: The aim of this study was to determine the possibility of deterioration of cerebral function of sleep-deprived, fatigued residents using neuroimaging techniques. Design: Six medical residents were instructed to draw blood from artificial vessels installed on the arm of a normal cooperator. Blood was drawn at a similar time of the day, before and after night duty. To assess sleep conditions during night duty, the participants wore actigraphy units throughout the period of night duty. Changes in cerebral hemodynamics, during the course of drawing blood, were measured using a wearable optical topography system. Results: The visual analogue scale scores after night duty correlated negatively with sleep efficiency during the night duty (ρ = −0.812, p = 0.050). The right prefrontal cortex activity was significantly decreased in the second trial after night duty compared with the first (p = 0.028). The extent of [oxy-Hb] decrease, indicating decreased activity, in the right dorsolateral prefrontal cortex correlated negatively with the Epworth sleepiness score after night duty (ρ = −0.841, p = 0.036). Conclusions: Sleep deprivation and fatigue after night duty, caused a decrease in the activity of the right dorsolateral prefrontal cortex of the residents, even with a relatively easy routine. This result implies that the brain activity of medical residents exposed to stress on night duty, although not substantially sleep-deprived, was impaired after the night duty, even though they apparently performed a simple medical technique appropriately. Reconsideration of the shift assignments of medical residents is strongly advised. Abbreviations: DLPFC: Dorsolateral prefrontal cortex; ESS: Epworth sleepiness scale; PSQI: Pittsburgh sleep quality index; ROI: Regions of interest; VAS: Visual analogue scale; WOT: Wearable optical topography PMID:28954586

The resilient brain and the guardians of sleep: New perspectives on old assumptions.

PubMed

Parrino, Liborio; Vaudano, Anna Elisabetta

2018-06-01

Resilience is the capacity of a system, enterprise or a person to maintain its core purpose and integrity in the face of dramatically changed circumstances. In human physiology, resilience is the capacity of adaptively overcoming stress and adversity while maintaining normal psychological and physical functioning. In this review, we investigate the resilient strategies of sleep. First, we discuss the concept of brain resilience, highlighting the modular structure of small-world networking, neuronal plasticity and critical brain behavior. Second, we explore the contribution of sleep to brain resilience listing the putative factors that impair sleep quality and predict susceptibility to sleep disorders. The third part details the manifold mechanisms acting as guardians of sleep, i.e., homeostatic, circadian and ultradian processes, sleep microstructure (K-complexes, delta bursts, arousals, cyclic alternating pattern, spindles), gravity, muscle tone and dreams. Mapping and pooling together the guardians of sleep in a dynamic integrated framework might lead towards an objective measure of sleep resilience and identify effective personalized strategies (biological, pharmacological, behavioral) to restore or protect the core properties of healthy sleep. Copyright © 2017 Elsevier Ltd. All rights reserved.

The 10 Hz Frequency: A Fulcrum For Transitional Brain States.

PubMed

Garcia-Rill, E; D'Onofrio, S; Luster, B; Mahaffey, S; Urbano, F J; Phillips, C

A 10 Hz rhythm is present in the occipital cortex when the eyes are closed (alpha waves), in the precentral cortex at rest ( mu rhythm), in the superior and middle temporal lobe ( tau rhythm), in the inferior olive (projection to cerebellar cortex), and in physiological tremor (underlying all voluntary movement). These are all considered resting rhythms in the waking brain which are "replaced" by higher frequency activity with sensorimotor stimulation. That is, the 10 Hz frequency fulcrum is replaced on the one hand by lower frequencies during sleep, or on the other hand by higher frequencies during volition and cognition. The 10 Hz frequency fulcrum is proposed as the natural frequency of the brain during quiet waking, but is replaced by higher frequencies capable of permitting more complex functions, or by lower frequencies during sleep and inactivity. At the center of the transition shifts to and from the resting rhythm is the reticular activating system, a phylogenetically preserved area of the brain essential for preconscious awareness.

The 10 Hz Frequency: A Fulcrum For Transitional Brain States

PubMed Central

Garcia-Rill, E.; D’Onofrio, S.; Luster, B.; Mahaffey, S.; Urbano, F. J.; Phillips, C.

2016-01-01

A 10 Hz rhythm is present in the occipital cortex when the eyes are closed (alpha waves), in the precentral cortex at rest (mu rhythm), in the superior and middle temporal lobe (tau rhythm), in the inferior olive (projection to cerebellar cortex), and in physiological tremor (underlying all voluntary movement). These are all considered resting rhythms in the waking brain which are “replaced” by higher frequency activity with sensorimotor stimulation. That is, the 10 Hz frequency fulcrum is replaced on the one hand by lower frequencies during sleep, or on the other hand by higher frequencies during volition and cognition. The 10 Hz frequency fulcrum is proposed as the natural frequency of the brain during quiet waking, but is replaced by higher frequencies capable of permitting more complex functions, or by lower frequencies during sleep and inactivity. At the center of the transition shifts to and from the resting rhythm is the reticular activating system, a phylogenetically preserved area of the brain essential for preconscious awareness. PMID:27547831

Sleep duration and age-related changes in brain structure and cognitive performance.

PubMed

Lo, June C; Loh, Kep Kee; Zheng, Hui; Sim, Sam K Y; Chee, Michael W L

2014-07-01

To investigate the contribution of sleep duration and quality to age-related changes in brain structure and cognitive performance in relatively healthy older adults. Community-based longitudinal brain and cognitive aging study using a convenience sample. Participants were studied in a research laboratory. Relatively healthy adults aged 55 y and older at study commencement. N/A. Participants underwent magnetic resonance imaging and neuropsychological assessment every 2 y. Subjective assessments of sleep duration and quality and blood samples were obtained. Each hour of reduced sleep duration at baseline augmented the annual expansion rate of the ventricles by 0.59% (P = 0.007) and the annual decline rate in global cognitive performance by 0.67% (P = 0.050) in the subsequent 2 y after controlling for the effects of age, sex, education, and body mass index. In contrast, global sleep quality at baseline did not modulate either brain or cognitive aging. High-sensitivity C-reactive protein, a marker of systemic inflammation, showed no correlation with baseline sleep duration, brain structure, or cognitive performance. In healthy older adults, short sleep duration is associated with greater age-related brain atrophy and cognitive decline. These associations are not associated with elevated inflammatory responses among short sleepers. Lo JC, Loh KK, Zheng H, Sim SK, Chee MW. Sleep duration and age-related changes in brain structure and cognitive performance.

Rapid eye movement sleep behaviour disorder symptomatic of a brain stem cavernoma.

PubMed

Felix, Sandra; Thobois, Stephane; Peter-Derex, Laure

2016-04-01

A 75-year-old man complained of excessive daytime sleepiness (EDS), difficulty falling asleep and nocturnal agitation during sleep. Restless legs syndrome (RLS) was diagnosed and treated. Because of persistent EDS, snoring and nycturia, a nocturnal polysomnography (PSG) was performed. PSG showed high sleep fragmentation related to a moderate to severe obstructive sleep apnea syndrome. Continuous positive airway pressure treatment (CPAP) was proposed. Because of the persistence of abnormal nocturnal behaviours, characterized by screaming, punching and falling out of bed, a video-PSG with CPAP treatment was performed. The recording showed typical chin electromyography (EMG) activity increase associated with violent movements during rapid eye movement (REM) sleep, suggesting REM sleep behaviour disorders (RBD). Clinical neurological examination found no parkinsonian syndrome, no dysautonomic sign and no neurological focal sign. Dopamine transporter imaging [123I-FP-CIT single photon emission computed tomography (SPECT)] did not find any presynaptic dopaminergic pathways degeneration. Brain magnetic resonance imaging showed a vascular lesion suggestive of cavernoma located in the pons. The present case illustrates the complexity of sleep disturbance diagnosis with a possible entanglement of aetiologies responsible for nocturnal agitation, and confirms that an isolated pons cavernoma should be considered among the rare causes of RBD. © 2016 European Sleep Research Society.

Sleep loss and structural plasticity.

PubMed

Areal, Cassandra C; Warby, Simon C; Mongrain, Valérie

2017-06-01

Wakefulness and sleep are dynamic states during which brain functioning is modified and shaped. Sleep loss is detrimental to many brain functions and results in structural changes localized at synapses in the nervous system. In this review, we present and discuss some of the latest observations of structural changes following sleep loss in some vertebrates and insects. We also emphasize that these changes are region-specific and cell type-specific and that, most importantly, these structural modifications have functional roles in sleep regulation and brain functions. Selected mechanisms driving structural modifications occurring with sleep loss are also discussed. Overall, recent research highlights that extending wakefulness impacts synapse number and shape, which in turn regulate sleep need and sleep-dependent learning/memory. Copyright © 2017 Elsevier Ltd. All rights reserved.

Chronic sleep restriction causes a decrease in hippocampal volume in adolescent rats, which is not explained by changes in glucocorticoid levels or neurogenesis.

PubMed

Novati, A; Hulshof, H J; Koolhaas, J M; Lucassen, P J; Meerlo, P

2011-09-08

Sleep loss strongly affects brain function and may even predispose susceptible individuals to psychiatric disorders. Since a recurrent lack of sleep frequently occurs during adolescence, it has been implicated in the rise in depression incidence during this particular period of life. One mechanism through which sleep loss may contribute to depressive symptomatology is by affecting hippocampal function. In this study, we examined the effects of sleep loss on hippocampal integrity at young age by subjecting adolescent male rats to chronic sleep restriction (SR) for 1 month from postnatal day 30 to 61. They were placed in slowly rotating drums for 20 h per day and were allowed 4 h of rest per day at the beginning of the light phase. Anxiety was measured using an open field and elevated plus maze test, while saccharine preference was used as an indication of anhedonia. All tests were performed after 1 and 4 weeks of SR. We further studied effects of SR on hypothalamic-pituitary-adrenal (HPA) axis activity, and at the end of the experiment, brains were collected to measure hippocampal volume and neurogenesis. Behavior of the SR animals was not affected, except for a transient suppression of saccharine preference after 1 week of SR. Hippocampal volume was significantly reduced in SR rats compared to home cage and forced activity controls. This volume reduction was not paralleled by reduced levels of hippocampal neurogenesis and could neither be explained by elevated levels of glucocorticoids. Thus, our results indicate that insufficient sleep may be a causal factor in the reductions of hippocampal volume that have been reported in human sleep disorders and mood disorders. Since changes in HPA activity or neurogenesis are not causally implicated, sleep disturbance may affect hippocampal volume by other, possibly more direct mechanisms. Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

Promoting Sleep Oscillations and Their Functional Coupling by Transcranial Stimulation Enhances Memory Consolidation in Mild Cognitive Impairment.

PubMed

Ladenbauer, Julia; Ladenbauer, Josef; Külzow, Nadine; de Boor, Rebecca; Avramova, Elena; Grittner, Ulrike; Flöel, Agnes

2017-07-26

Alzheimer's disease (AD) not only involves loss of memory functions, but also prominent deterioration of sleep physiology, which is already evident at the stage of mild cognitive impairment (MCI). Cortical slow oscillations (SO; 0.5-1 Hz) and thalamocortical spindle activity (12-15 Hz) during sleep, and their temporal coordination, are considered critical for memory formation. We investigated the potential of slow oscillatory transcranial direct current stimulation (so-tDCS), applied during a daytime nap in a sleep-state-dependent manner, to modulate these activity patterns and sleep-related memory consolidation in nine male and seven female human patients with MCI. Stimulation significantly increased overall SO and spindle power, amplified spindle power during SO up-phases, and led to stronger synchronization between SO and spindle power fluctuations in EEG recordings. Moreover, visual declarative memory was improved by so-tDCS compared with sham stimulation and was associated with stronger synchronization. These findings indicate a well-tolerated therapeutic approach for disordered sleep physiology and memory deficits in MCI patients and advance our understanding of offline memory consolidation. SIGNIFICANCE STATEMENT In the light of increasing evidence that sleep disruption is crucially involved in the progression of Alzheimer's disease (AD), sleep appears as a promising treatment target in this pathology, particularly to counteract memory decline. This study demonstrates the potential of a noninvasive brain stimulation method during sleep in patients with mild cognitive impairment (MCI), a precursor of AD, and advances our understanding of its mechanism. We provide first time evidence that slow oscillatory transcranial stimulation amplifies the functional cross-frequency coupling between memory-relevant brain oscillations and improves visual memory consolidation in patients with MCI. Copyright © 2017 the authors 0270-6474/17/377111-14$15.00/0.

Sleep deprivation alters functioning within the neural network underlying the covert orienting of attention.

PubMed

Mander, Bryce A; Reid, Kathryn J; Davuluri, Vijay K; Small, Dana M; Parrish, Todd B; Mesulam, M-Marsel; Zee, Phyllis C; Gitelman, Darren R

2008-06-27

One function of spatial attention is to enable goal-directed interactions with the environment through the allocation of neural resources to motivationally relevant parts of space. Studies have shown that responses are enhanced when spatial attention is predictively biased towards locations where significant events are expected to occur. Previous studies suggest that the ability to bias attention predictively is related to posterior cingulate cortex (PCC) activation [Small, D.M., et al., 2003. The posterior cingulate and medial prefrontal cortex mediate the anticipatory allocation of spatial attention. Neuroimage 18, 633-41]. Sleep deprivation (SD) impairs selective attention and reduces PCC activity [Thomas, M., et al., 2000. Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J. Sleep Res. 9, 335-352]. Based on these findings, we hypothesized that SD would affect PCC function and alter the ability to predictively allocate spatial attention. Seven healthy, young adults underwent functional magnetic resonance imaging (fMRI) following normal rest and 34-36 h of SD while performing a task in which attention was shifted in response to peripheral targets preceded by spatially informative (valid), misleading (invalid), or uninformative (neutral) cues. When rested, but not when sleep-deprived, subjects responded more quickly to targets that followed valid cues than those after neutral or invalid cues. Brain activity during validly cued trials with a reaction time benefit was compared to activity in trials with no benefit. PCC activation was greater during trials with a reaction time benefit following normal rest. In contrast, following SD, reaction time benefits were associated with activation in the left intraparietal sulcus, a region associated with receptivity to stimuli at unexpected locations. These changes may render sleep-deprived individuals less able to anticipate the locations of upcoming events, and more susceptible to distraction by stimuli at irrelevant locations.

Plastic changes following imitation-based speech and language therapy for aphasia: a high-density sleep EEG study.

PubMed

Sarasso, Simone; Määttä, Sara; Ferrarelli, Fabio; Poryazova, Rositsa; Tononi, Giulio; Small, Steven L

2014-02-01

BACKGROUND OBJECTIVE: measurement of plastic brain changes induced by a novel rehabilitative approach is a key requirement for validating its biological rationale linking the potential therapeutic gains to the changes in brain physiology. Based on an emerging notion linking cortical plastic changes to EEG sleep slow-wave activity (SWA) regulation, we aimed to assess the acute plastic changes induced by an imitation-based speech therapy in individuals with aphasia by comparing sleep SWA changes before and after therapy. A total of 13 left-hemispheric stroke patients underwent language assessment with the Western Aphasia Battery (WAB) before and after 2 consecutive high-density (hd) EEG sleep recordings interleaved by a daytime session of imitation-based speech therapy (Intensive Mouth Imitation and Talking for Aphasia Therapeutic Effects [IMITATE]). This protocol is thought to stimulate bilateral connections between the inferior parietal lobule and the ventral premotor areas. A single exposure to IMITATE resulted in increases in local EEG SWA during subsequent sleep over the same regions predicted by the therapeutic rationale, particularly over the right hemisphere (unaffected by the lesion). Furthermore, changes in SWA over the left-precentral areas predicted changes in WAB repetition scores in our group, supporting the role of perilesional areas in predicting positive functional responses. Our results suggest that SWA changes occurring in brain areas activated during imitation-based aphasia therapy may reflect the acute plastic changes induced by this intervention. Further testing will be needed to evaluate SWA as a non-invasive assessment of changes induced by the therapy and as a predictor of positive long-term clinical outcome.

P2X7 receptors in body temperature, locomotor activity, and brain mRNA and lncRNA responses to sleep deprivation.

PubMed

Davis, Christopher J; Taishi, Ping; Honn, Kimberly A; Koberstein, John N; Krueger, James M

2016-12-01

The ionotropic purine type 2X7 receptor (P2X7R) is a nonspecific cation channel implicated in sleep regulation and brain cytokine release. Many endogenous rhythms covary with sleep, including locomotor activity and core body temperature. Furthermore, brain-hypothalamic cytokines and purines play a role in the regulation of these physiological parameters as well as sleep. We hypothesized that these parameters are also affected by the absence of the P2X7 receptor. Herein, we determine spontaneous expression of body temperature and locomotor activity in wild-type (WT) and P2X7R knockout (KO) mice and how they are affected by sleep deprivation (SD). We also compare hypothalamic, hippocampal, and cortical cytokine- and purine-related receptor and enzyme mRNA expressions before and after SD in WT and P2X7RKO mice. Next, in a hypothesis-generating survey of hypothalamic long noncoding (lnc) RNAs, we compare lncRNA expression levels between strains and after SD. During baseline conditions, P2X7RKO mice had attenuated temperature rhythms compared with WT mice, although locomotor activity patterns were similar in both strains. After 6 h of SD, body temperature and locomotion were enhanced to a greater extent in P2X7RKO mice than in WT mice during the initial 2-3 h after SD. Baseline mRNA levels of cortical TNF-α and P2X4R were higher in the KO mice than WT mice. In response to SD, the KO mice failed to increase hypothalamic adenosine deaminase and P2X4R mRNAs. Further, hypothalamic lncRNA expressions varied by strain, and with SD. Current data are consistent with a role for the P2X7R in thermoregulation and lncRNA involvement in purinergic signaling. Copyright © 2016 the American Physiological Society.

P2X7 receptors in body temperature, locomotor activity, and brain mRNA and lncRNA responses to sleep deprivation

PubMed Central

Taishi, Ping; Honn, Kimberly A.; Koberstein, John N.; Krueger, James M.

2016-01-01

The ionotropic purine type 2X7 receptor (P2X7R) is a nonspecific cation channel implicated in sleep regulation and brain cytokine release. Many endogenous rhythms covary with sleep, including locomotor activity and core body temperature. Furthermore, brain-hypothalamic cytokines and purines play a role in the regulation of these physiological parameters as well as sleep. We hypothesized that these parameters are also affected by the absence of the P2X7 receptor. Herein, we determine spontaneous expression of body temperature and locomotor activity in wild-type (WT) and P2X7R knockout (KO) mice and how they are affected by sleep deprivation (SD). We also compare hypothalamic, hippocampal, and cortical cytokine- and purine-related receptor and enzyme mRNA expressions before and after SD in WT and P2X7RKO mice. Next, in a hypothesis-generating survey of hypothalamic long noncoding (lnc) RNAs, we compare lncRNA expression levels between strains and after SD. During baseline conditions, P2X7RKO mice had attenuated temperature rhythms compared with WT mice, although locomotor activity patterns were similar in both strains. After 6 h of SD, body temperature and locomotion were enhanced to a greater extent in P2X7RKO mice than in WT mice during the initial 2-3 h after SD. Baseline mRNA levels of cortical TNF-α and P2X4R were higher in the KO mice than WT mice. In response to SD, the KO mice failed to increase hypothalamic adenosine deaminase and P2X4R mRNAs. Further, hypothalamic lncRNA expressions varied by strain, and with SD. Current data are consistent with a role for the P2X7R in thermoregulation and lncRNA involvement in purinergic signaling. PMID:27707719

Notch signaling modulates sleep homeostasis and learning after sleep deprivation in Drosophila.

PubMed

Seugnet, Laurent; Suzuki, Yasuko; Merlin, Gabriel; Gottschalk, Laura; Duntley, Stephen P; Shaw, Paul J

2011-05-24

The role of the transmembrane receptor Notch in the adult brain is poorly understood. Here, we provide evidence that bunched, a negative regulator of Notch, is involved in sleep homeostasis. Genetic evidence indicates that interfering with bunched activity in the mushroom bodies (MBs) abolishes sleep homeostasis. Combining bunched and Delta loss-of-function mutations rescues normal homeostasis, suggesting that Notch signaling may be involved in regulating sensitivity to sleep loss. Preventing the downregulation of Delta by overexpressing a wild-type transgene in MBs reduces sleep homeostasis and, importantly, prevents learning impairments induced by sleep deprivation. Similar resistance to sleep loss is observed with Notch(spl-1) gain-of-function mutants. Immunohistochemistry reveals that the Notch receptor is expressed in glia, whereas Delta is localized in neurons. Importantly, the expression in glia of the intracellular domain of Notch, a dominant activated form of the receptor, is sufficient to prevent learning deficits after sleep deprivation. Together, these results identify a novel neuron-glia signaling pathway dependent on Notch and regulated by bunched. These data highlight the emerging role of neuron-glia interactions in regulating both sleep and learning impairments associated with sleep loss. Copyright © 2011 Elsevier Ltd. All rights reserved.

Altered Sleep Homeostasis in Rev-erbα Knockout Mice.

PubMed

Mang, Géraldine M; La Spada, Francesco; Emmenegger, Yann; Chappuis, Sylvie; Ripperger, Jürgen A; Albrecht, Urs; Franken, Paul

2016-03-01

The nuclear receptor REV-ERBα is a potent, constitutive transcriptional repressor critical for the regulation of key circadian and metabolic genes. Recently, REV-ERBα's involvement in learning, neurogenesis, mood, and dopamine turnover was demonstrated suggesting a specific role in central nervous system functioning. We have previously shown that the brain expression of several core clock genes, including Rev-erbα, is modulated by sleep loss. We here test the consequences of a loss of REV-ERBα on the homeostatic regulation of sleep. EEG/EMG signals were recorded in Rev-erbα knockout (KO) mice and their wild type (WT) littermates during baseline, sleep deprivation, and recovery. Cortical gene expression measurements after sleep deprivation were contrasted to baseline. Although baseline sleep/wake duration was remarkably similar, KO mice showed an advance of the sleep/wake distribution relative to the light-dark cycle. After sleep onset in baseline and after sleep deprivation, both EEG delta power (1-4 Hz) and sleep consolidation were reduced in KO mice indicating a slower increase of homeostatic sleep need during wakefulness. This slower increase might relate to the smaller increase in theta and gamma power observed in the waking EEG prior to sleep onset under both conditions. Indeed, the increased theta activity during wakefulness predicted delta power in subsequent NREM sleep. Lack of Rev-erbα increased Bmal1, Npas2, Clock, and Fabp7 expression, confirming the direct regulation of these genes by REV-ERBα also in the brain. Our results add further proof to the notion that clock genes are involved in sleep homeostasis. Because accumulating evidence directly links REV-ERBα to dopamine signaling the altered homeostatic regulation of sleep reported here are discussed in that context. © 2016 Associated Professional Sleep Societies, LLC.

Phosphorous31 magnetic resonance spectroscopy after total sleep deprivation in healthy adult men.

PubMed

Dorsey, Cynthia M; Lukas, Scott E; Moore, Constance M; Tartarini, Wendy L; Parow, Aimee M; Villafuerte, Rosemond A; Renshaw, Perry F

2003-08-01

To investigate chemical changes in the brains of healthy adults after sleep deprivation and recovery sleep, using phosphorous magnetic resonance spectroscopy. Three consecutive nights (baseline, sleep deprivation, recovery) were spent in the laboratory. Objective sleep measures were assessed on the baseline and recovery nights using polysomnography. Phosphorous magnetic resonance spectroscopy scans took place beginning at 7 am to 8 am on the morning after each of the 3 nights. Sleep laboratory in a private psychiatric teaching hospital. Eleven healthy young men. Following a baseline night of sleep, subjects underwent a night of total sleep deprivation, which involved supervision to ensure the absence of sleep but was not polysomnographically monitored. No significant changes in any measure of brain chemistry were observed the morning after a night of total sleep deprivation. However, after the recovery night, significant increases in total and beta-nucleoside triphosphate and decreases in phospholipid catabolism, measured by an increase in the concentration of glycerylphosphorylcholine, were observed. Chemical changes paralleled some changes in objective sleep measures. Significant chemical changes in the brain were observed following recovery sleep after 1 night of total sleep deprivation. The specific process underlying these changes is unclear due to the large brain region sampled in this exploratory study, but changes may reflect sleep inertia or some aspect of the homeostatic sleep mechanism that underlies the depletion and restoration of sleep. Phosphorous magnetic resonance spectroscopy is a technique that may be of value in further exploration of such sleep-wake functions.

Slow sleep spindle and procedural memory consolidation in patients with major depressive disorder

PubMed Central

Nishida, Masaki; Nakashima, Yusaku; Nishikawa, Toru

2016-01-01

Introduction Evidence has accumulated, which indicates that, in healthy individuals, sleep enhances procedural memory consolidation, and that sleep spindle activity modulates this process. However, whether sleep-dependent procedural memory consolidation occurs in patients medicated for major depressive disorder remains unclear, as are the pharmacological and physiological mechanisms that underlie this process. Methods Healthy control participants (n=17) and patients medicated for major depressive disorder (n=11) were recruited and subjected to a finger-tapping motor sequence test (MST; nondominant hand) paradigm to compare the averaged scores of different learning phases (presleep, postsleep, and overnight improvement). Participants’ brain activity was recorded during sleep with 16 electroencephalography channels (between MSTs). Sleep scoring and frequency analyses were performed on the electroencephalography data. Additionally, we evaluated sleep spindle activity, which divided the spindles into fast-frequency spindle activity (12.5–16 Hz) and slow-frequency spindle activity (10.5–12.5 Hz). Result Sleep-dependent motor memory consolidation in patients with depression was impaired in comparison with that in control participants. In patients with depression, age correlated negatively with overnight improvement. The duration of slow-wave sleep correlated with the magnitude of motor memory consolidation in patients with depression, but not in healthy controls. Slow-frequency spindle activity was associated with reduction in the magnitude of motor memory consolidation in both groups. Conclusion Because the changes in slow-frequency spindle activity affected the thalamocortical network dysfunction in patients medicated for depression, dysregulated spindle generation may impair sleep-dependent memory consolidation. Our findings may help to elucidate the cognitive deficits that occur in patients with major depression both in the waking state and during sleep. PMID:26869818

Cortical connectivity modulation during sleep onset: A study via graph theory on EEG data.

PubMed

Vecchio, Fabrizio; Miraglia, Francesca; Gorgoni, Maurizio; Ferrara, Michele; Iberite, Francesco; Bramanti, Placido; De Gennaro, Luigi; Rossini, Paolo Maria

2017-11-01

Sleep onset is characterized by a specific and orchestrated pattern of frequency and topographical EEG changes. Conventional power analyses of electroencephalographic (EEG) and computational assessments of network dynamics have described an earlier synchronization of the centrofrontal areas rhythms and a spread of synchronizing signals from associative prefrontal to posterior areas. Here, we assess how "small world" characteristics of the brain networks, as reflected in the EEG rhythms, are modified in the wakefulness-sleep transition comparing the pre- and post-sleep onset epochs. The results show that sleep onset is characterized by a less ordered brain network (as reflected by the higher value of small world) in the sigma band for the frontal lobes indicating stronger connectivity, and a more ordered brain network in the low frequency delta and theta bands indicating disconnection on the remaining brain areas. Our results depict the timing and topography of the specific mechanisms for the maintenance of functional connectivity of frontal brain regions at the sleep onset, also providing a possible explanation for the prevalence of the frontal-to-posterior information flow directionality previously observed after sleep onset. Hum Brain Mapp 38:5456-5464, 2017. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.

Malondialdehyde Suppresses Cerebral Function by Breaking Homeostasis between Excitation and Inhibition in Turtle Trachemys scripta

PubMed Central

Li, Fangxu; Yang, Zhilai; Lu, Yang; Wei, Yan; Wang, Jinhui; Yin, Dazhong; He, Rongqiao

2010-01-01

The levels of malondialdehyde (MDA) are high in the brain during carbonyl stress, such as following daily activities and sleep deprivation. To examine our hypothesis that MDA is one of the major substances in the brain leading to fatigue, the influences of MDA on brain functions and neuronal encodings in red-eared turtle (Trachemys scripta) were studied. The intrathecal injections of MDA brought about sleep-like EEG and fatigue-like behaviors in a dose-dependent manner. These changes were found associated with the deterioration of encoding action potentials in cortical neurons. In addition, MDA increased the ratio of γ-aminobutyric acid to glutamate in turtle's brain, as well as the sensitivity of GABAergic neurons to inputs compared to excitatory neurons. Therefore, MDA, as a metabolic product in the brain, may weaken cerebral function during carbonyl stress through breaking the homeostasis between excitatory and inhibitory neurons. PMID:21203547

The Mind/Brain Relationship of the Gifted Child.

ERIC Educational Resources Information Center

Dowdy, Waymon L.,

This paper reviews three studies which examine cognitive processes and brain electrical activity in gifted children. The studies concentrated on mathematically gifted children and/or their sleep patterns. All three studies used the interhemispheric electroencephalogram to examine the gifted child's ability to harness right hemisphere capacities…

Daytime Sleepiness Increases With Age in Early Adolescence: A Sleep Restriction Dose-Response Study.

PubMed

Campbell, Ian G; Burright, Christopher S; Kraus, Amanda M; Grimm, Kevin J; Feinberg, Irwin

2017-05-01

Daytime sleepiness increases across adolescence. This increase is commonly attributed to insufficient sleep durations resulting from increasingly limited time in bed. We tested the effects of 3 sleep schedules on daytime sleepiness and whether these effects changed with age in early adolescence. In 77 children ranging in age from 9.9 to 14 years, objective (multiple sleep latency test [MSLT]) and subjective (Karolinska sleepiness scale [KSS]) sleepiness was measured following 4 consecutive nights of either 7, 8.5, or 10 hours in bed. All participants completed all 3 sleep schedules. The order in which they completed the schedules was not randomized but was accounted for in all statistical analyses. Time in bed restriction decreased sleep duration and increased objective and subjective daytime sleepiness. Although the sleep durations did not change with age, the likelihood of falling asleep during the MSLT increased with age. Nevertheless, sleep restriction produced a greater increase in MSLT-measured sleepiness in younger participants. Subjective sleepiness measured with the KSS increased with shorter sleep duration, but this effect did not change with age. Increasing objective daytime sleepiness in early adolescence cannot simply be attributed to reduced sleep due to restricted sleep schedules. We propose that some of the increased daytime sleepiness of adolescents is a consequence of adolescent brain reorganization driven by synaptic pruning which decreases the intensity of waking brain activity. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Scalp and Source Power Topography in Sleepwalking and Sleep Terrors: A High-Density EEG Study.

PubMed

Castelnovo, Anna; Riedner, Brady A; Smith, Richard F; Tononi, Giulio; Boly, Melanie; Benca, Ruth M

2016-10-01

To examine scalp and source power topography in sleep arousals disorders (SADs) using high-density EEG (hdEEG). Fifteen adult subjects with sleep arousal disorders (SADs) and 15 age- and gender-matched good sleeping healthy controls were recorded in a sleep laboratory setting using a 256 channel EEG system. Scalp EEG analysis of all night NREM sleep revealed a localized decrease in slow wave activity (SWA) power (1-4 Hz) over centro-parietal regions relative to the rest of the brain in SADs compared to good sleeping healthy controls. Source modelling analysis of 5-minute segments taken from N3 during the first half of the night revealed that the local decrease in SWA power was prominent at the level of the cingulate, motor, and sensori-motor associative cortices. Similar patterns were also evident during REM sleep and wake. These differences in local sleep were present in the absence of any detectable clinical or electrophysiological sign of arousal. Overall, results suggest the presence of local sleep differences in the brain of SADs patients during nights without clinical episodes. The persistence of similar topographical changes in local EEG power during REM sleep and wakefulness points to trait-like functional changes that cross the boundaries of NREM sleep. The regions identified by source imaging are consistent with the current neurophysiological understanding of SADs as a disorder caused by local arousals in motor and cingulate cortices. Persistent localized changes in neuronal excitability may predispose affected subjects to clinical episodes. © 2016 Associated Professional Sleep Societies, LLC.

Non-fluent aphasia and neural reorganization after speech therapy: insights from human sleep electrophysiology and functional magnetic resonance imaging.

PubMed

Sarasso, S; Santhanam, P; Määtta, S; Poryazova, R; Ferrarelli, F; Tononi, G; Small, S L

2010-09-01

Stroke is associated with long-term functional deficits. Behavioral interventions are often effective in promoting functional recovery and plastic changes. Recent studies in normal subjects have shown that sleep, and particularly slow wave activity (SWA), is tied to local brain plasticity and may be used as a sensitive marker of local cortical reorganization after stroke. In a pilot study, we assessed the local changes induced by a single exposure to a therapeutic session of IMITATE (Intensive Mouth Imitation and Talking for Aphasia Therapeutic Effects), a behavioral therapy used for recovery in patients with post-stroke aphasia. In addition, we measured brain activity changes with functional magnetic resonance imaging (fMRI) in a language observation task before, during and after the full IMITATE rehabilitative program. Speech production improved both after a single exposure and the full therapy program as measured by the Western Aphasia Battery (WAB) Repetition subscale. We found that IMITATE induced reorganization in functionally-connected, speech-relevant areas in the left hemisphere. These preliminary results suggest that sleep hd-EEGs, and the topographical analysis of SWA parameters, are well suited to investigate brain plastic changes underpinning functional recovery in neurological disorders.

Habitual short sleep impacts frontal switch mechanism in attention to novelty.

PubMed

Gumenyuk, Valentina; Roth, Thomas; Korzyukov, Oleg; Jefferson, Catherine; Bowyer, Susan; Drake, Christopher L

2011-12-01

Reduced time in bed relative to biological sleep need is common. The impact of habitual short sleep on auditory attention has not been studied to date. In the current study, we utilized novelty oddball tasks to evaluate the effect of habitual short sleep on brain function underlying attention control processes measured by the mismatch negativity (MMN, index of pre-attentive stage), P3a (attention-dependent), and P3b (memory-dependent) event related brain potentials (ERPs). An extended time in bed in a separate study was used to evaluate the possible reversal of the impairments of these processes in habitual short sleepers. Ten self-defined short sleepers (total sleep time [TST] ≤ 6 h) and 9 normal-sleeping subjects with TST 7-8 h, participated. ERPs were recorded via a 64-channel EEG system. Two test conditions: "ignore" and "attend" were implemented. The ERPs were analyzed and compared between groups on the 2 task conditions and frontal/central/parietal electrodes by 3-factor ANOVA. Sleep diary data were compared between groups by t-test. Sleep was recorded by the Zeo sleep monitoring system for a week in both habitual and extended sleep conditions at home. The main findings of the present study show that short sleeping individuals had deficiency in activity of the MMN and P3a brain responses over frontal areas compared to normal-sleeping subjects. The P3b amplitude was increased over frontal areas and decreased over parietal with respect to the control group. Extension of time in bed for one week increased TST (from 5.7 h to 7.4 h), and concomitantly MMN amplitude increased from -0.1 μV up to -1.25 μV over frontal areas. Reduced time in bed is associated with deficiency of the neuronal process associated with change detection, which may recover after one week of sleep extension, whereas attention-dependent neural processes do not normalize after this period of time in habitually short sleeping individuals and may require longer recovery periods.

Sleep/wake dependent changes in cortical glucose concentrations.

PubMed

Dash, Michael B; Bellesi, Michele; Tononi, Giulio; Cirelli, Chiara

2013-01-01

Most of the energy in the brain comes from glucose and supports glutamatergic activity. The firing rate of cortical glutamatergic neurons, as well as cortical extracellular glutamate levels, increase with time spent awake and decline throughout non rapid eye movement sleep, raising the question whether glucose levels reflect behavioral state and sleep/wake history. Here chronic (2-3 days) electroencephalographic recordings in the rat cerebral cortex were coupled with fixed-potential amperometry to monitor the extracellular concentration of glucose ([gluc]) on a second-by-second basis across the spontaneous sleep-wake cycle and in response to 3 h of sleep deprivation. [Gluc] progressively increased during non rapid eye movement sleep and declined during rapid eye movement sleep, while during wake an early decline in [gluc] was followed by an increase 8-15 min after awakening. There was a significant time of day effect during the dark phase, when rats are mostly awake, with [gluc] being significantly lower during the last 3-4 h of the night relative to the first 3-4 h. Moreover, the duration of the early phase of [gluc] decline during wake was longer after prolonged wake than after consolidated sleep. Thus, the sleep/wake history may affect the levels of glucose available to the brain upon awakening. © 2012 The Authors Journal of Neurochemistry © 2012 International Society for Neurochemistry.

Sleep-Dependent Memory Consolidation and Incremental Sentence Comprehension: Computational Dependencies during Language Learning as Revealed by Neuronal Oscillations

PubMed Central

Cross, Zachariah R.; Kohler, Mark J.; Schlesewsky, Matthias; Gaskell, M. G.; Bornkessel-Schlesewsky, Ina

2018-01-01

We hypothesize a beneficial influence of sleep on the consolidation of the combinatorial mechanisms underlying incremental sentence comprehension. These predictions are grounded in recent work examining the effect of sleep on the consolidation of linguistic information, which demonstrate that sleep-dependent neurophysiological activity consolidates the meaning of novel words and simple grammatical rules. However, the sleep-dependent consolidation of sentence-level combinatorics has not been studied to date. Here, we propose that dissociable aspects of sleep neurophysiology consolidate two different types of combinatory mechanisms in human language: sequence-based (order-sensitive) and dependency-based (order-insensitive) combinatorics. The distinction between the two types of combinatorics is motivated both by cross-linguistic considerations and the neurobiological underpinnings of human language. Unifying this perspective with principles of sleep-dependent memory consolidation, we posit that a function of sleep is to optimize the consolidation of sequence-based knowledge (the when) and the establishment of semantic schemas of unordered items (the what) that underpin cross-linguistic variations in sentence comprehension. This hypothesis builds on the proposal that sleep is involved in the construction of predictive codes, a unified principle of brain function that supports incremental sentence comprehension. Finally, we discuss neurophysiological measures (EEG/MEG) that could be used to test these claims, such as the quantification of neuronal oscillations, which reflect basic mechanisms of information processing in the brain. PMID:29445333

Circadian factor BMAL1 in histaminergic neurons regulates sleep architecture.

PubMed

Yu, Xiao; Zecharia, Anna; Zhang, Zhe; Yang, Qianzi; Yustos, Raquel; Jager, Polona; Vyssotski, Alexei L; Maywood, Elizabeth S; Chesham, Johanna E; Ma, Ying; Brickley, Stephen G; Hastings, Michael H; Franks, Nicholas P; Wisden, William

2014-12-01

Circadian clocks allow anticipation of daily environmental changes. The suprachiasmatic nucleus (SCN) houses the master clock, but clocks are also widely expressed elsewhere in the body. Although some peripheral clocks have established roles, it is unclear what local brain clocks do. We tested the contribution of one putative local clock in mouse histaminergic neurons in the tuberomamillary nucleus to the regulation of the sleep-wake cycle. Histaminergic neurons are silent during sleep, and start firing after wake onset; the released histamine, made by the enzyme histidine decarboxylase (HDC), enhances wakefulness. We found that hdc gene expression varies with time of day. Selectively deleting the Bmal1 (also known as Arntl or Mop3) clock gene from histaminergic cells removes this variation, producing higher HDC expression and brain histamine levels during the day. The consequences include more fragmented sleep, prolonged wake at night, shallower sleep depth (lower nonrapid eye movement [NREM] δ power), increased NREM-to-REM transitions, hindered recovery sleep after sleep deprivation, and impaired memory. Removing BMAL1 from histaminergic neurons does not, however, affect circadian rhythms. We propose that for mammals with polyphasic/nonwake consolidating sleep, the local BMAL1-dependent clock directs appropriately timed declines and increases in histamine biosynthesis to produce an appropriate balance of wake and sleep within the overall daily cycle of rest and activity specified by the SCN. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

Memory traces of long-range coordinated oscillations in the sleeping human brain.

PubMed

Piantoni, Giovanni; Van Der Werf, Ysbrand D; Jensen, Ole; Van Someren, Eus J W

2015-01-01

Cognition involves coordinated activity across distributed neuronal networks. Neuronal activity during learning triggers cortical plasticity that allows for reorganization of the neuronal network and integration of new information. Animal studies have shown post-learning reactivation of learning-elicited neuronal network activity during subsequent sleep, supporting consolidation of the reorganization. However, no previous studies, to our knowledge, have demonstrated reactivation of specific learning-elicited long-range functional connectivity during sleep in humans. We here show reactivation of learning-induced long-range synchronization of magnetoencephalography power fluctuations in human sleep. Visuomotor learning elicited a specific profile of long-range cortico-cortical synchronization of slow (0.1 Hz) fluctuations in beta band (12-30 Hz) power. The parieto-occipital part of this synchronization profile reappeared in delta band (1-3.5 Hz) power fluctuations during subsequent sleep, but not during the intervening wakefulness period. Individual differences in the reactivated synchronization predicted postsleep performance improvement. The presleep resting-state synchronization profile was not reactivated during sleep. The findings demonstrate reactivation of long-range coordination of neuronal activity in humans, more specifically of reactivation of coupling of infra-slow fluctuations in oscillatory power. The spatiotemporal profile of delta power fluctuations during sleep may subserve memory consolidation by echoing coordinated activation elicited by prior learning. © 2014 Wiley Periodicals, Inc.

Source analysis of MEG activities during sleep (abstract)

NASA Astrophysics Data System (ADS)

Ueno, S.; Iramina, K.

1991-04-01

The present study focuses on magnetic fields of the brain activities during sleep, in particular on K-complexes, vertex waves, and sleep spindles in human subjects. We analyzed these waveforms based on both topographic EEG (electroencephalographic) maps and magnetic fields measurements, called MEGs (magnetoencephalograms). The components of magnetic fields perpendicular to the surface of the head were measured using a dc SQUID magnetometer with a second derivative gradiometer. In our computer simulation, the head is assumed to be a homogeneous spherical volume conductor, with electric sources of brain activity modeled as current dipoles. Comparison of computer simulations with the measured data, particularly the MEG, suggests that the source of K-complexes can be modeled by two current dipoles. A source for the vertex wave is modeled by a single current dipole which orients along the body axis out of the head. By again measuring the simultaneous MEG and EEG signals, it is possible to uniquely determine the orientation of this dipole, particularly when it is tilted slightly off-axis. In sleep stage 2, fast waves of magnetic fields consistently appeared, but EEG spindles appeared intermittently. The results suggest that there exist sources which are undetectable by electrical measurement but are detectable by magnetic-field measurement. Such source can be described by a pair of opposing dipoles of which directions are oppositely oriented.

Hierarchical Neural Representation of Dreamed Objects Revealed by Brain Decoding with Deep Neural Network Features.

PubMed

Horikawa, Tomoyasu; Kamitani, Yukiyasu

2017-01-01

Dreaming is generally thought to be generated by spontaneous brain activity during sleep with patterns common to waking experience. This view is supported by a recent study demonstrating that dreamed objects can be predicted from brain activity during sleep using statistical decoders trained with stimulus-induced brain activity. However, it remains unclear whether and how visual image features associated with dreamed objects are represented in the brain. In this study, we used a deep neural network (DNN) model for object recognition as a proxy for hierarchical visual feature representation, and DNN features for dreamed objects were analyzed with brain decoding of fMRI data collected during dreaming. The decoders were first trained with stimulus-induced brain activity labeled with the feature values of the stimulus image from multiple DNN layers. The decoders were then used to decode DNN features from the dream fMRI data, and the decoded features were compared with the averaged features of each object category calculated from a large-scale image database. We found that the feature values decoded from the dream fMRI data positively correlated with those associated with dreamed object categories at mid- to high-level DNN layers. Using the decoded features, the dreamed object category could be identified at above-chance levels by matching them to the averaged features for candidate categories. The results suggest that dreaming recruits hierarchical visual feature representations associated with objects, which may support phenomenal aspects of dream experience.

The role of sleep in regulating structural plasticity and synaptic strength: Implications for memory and cognitive function.

PubMed

Raven, Frank; Van der Zee, Eddy A; Meerlo, Peter; Havekes, Robbert

2018-06-01

Dendritic spines are the major sites of synaptic transmission in the central nervous system. Alterations in the strength of synaptic connections directly affect the neuronal communication, which is crucial for brain function as well as the processing and storage of information. Sleep and sleep loss bidirectionally alter structural plasticity, by affecting spine numbers and morphology, which ultimately can affect the functional output of the brain in terms of alertness, cognition, and mood. Experimental data from studies in rodents suggest that sleep deprivation may impact structural plasticity in different ways. One of the current views, referred to as the synaptic homeostasis hypothesis, suggests that wake promotes synaptic potentiation whereas sleep facilitates synaptic downscaling. On the other hand, several studies have now shown that sleep deprivation can reduce spine density and attenuate synaptic efficacy in the hippocampus. These data are the basis for the view that sleep promotes hippocampal structural plasticity critical for memory formation. Altogether, the impact of sleep and sleep loss may vary between regions of the brain. A better understanding of the role that sleep plays in regulating structural plasticity may ultimately lead to novel therapeutic approaches for brain disorders that are accompanied by sleep disturbances and sleep loss. Copyright © 2017 Elsevier Ltd. All rights reserved.

Intermittent Short Sleep Results in Lasting Sleep Wake Disturbances and Degeneration of Locus Coeruleus and Orexinergic Neurons

PubMed Central

Zhu, Yan; Fenik, Polina; Zhan, Guanxia; Somach, Rebecca; Xin, Ryan; Veasey, Sigrid

2016-01-01

Study Objectives: Intermittent short sleep (ISS) is pervasive among students and workers in modern societies, yet the lasting consequences of repeated short sleep on behavior and brain health are largely unexplored. Wake-activated neurons may be at increased risk of metabolic injury across sustained wakefulness. Methods: To examine the effects of ISS on wake-activated neurons and wake behavior, wild-type mice were randomized to ISS (a repeated pattern of short sleep on 3 consecutive days followed by 4 days of recovery sleep for 4 weeks) or rested control conditions. Subsets of both groups were allowed a recovery period consisting of 4-week unperturbed activity in home cages with littermates. Mice were examined for immediate and delayed (following recovery) effects of ISS on wake neuron cell metabolics, cell counts, and sleep/wake patterns. Results: ISS resulted in sustained disruption of sleep/wake activity, with increased wakefulness during the lights-on period and reduced wake bout duration and wake time during the lights-off period. Noradrenergic locus coeruleus (LC) and orexinergic neurons showed persistent alterations in morphology, and reductions in both neuronal stereological cell counts and fronto-cortical projections. Surviving wake-activated neurons evidenced persistent reductions in sirtuins 1 and 3 and increased lipofuscin. In contrast, ISS resulted in no lasting injury to the sleep-activated melanin concentrating hormone neurons. Conclusions: Collectively these findings demonstrate for the first time that ISS imparts significant lasting disturbances in sleep/wake activity, degeneration of wake-activated LC and orexinergic neurons, and lasting metabolic changes in remaining neurons most consistent with premature senescence. Citation: Zhu Y, Fenik P, Zhan G, Somach R, Xin R, Veasey S. Intermittent short sleep results in lasting sleep wake disturbances and degeneration of locus coeruleus and orexinergic neurons. SLEEP 2016;39(8):1601–1611. PMID:27306266

Sleep alterations and iron deficiency anemia in infancy

PubMed Central

Peirano, Patricio D.; Algarín, Cecilia R.; Chamorro, Rodrigo A.; Reyes, Sussanne C.; Durán, Samuel A.; Garrido, Marcelo I.; Lozoff, Betsy

2013-01-01

Iron-deficiency anemia (IDA) continues to be the most common single nutrient deficiency in the world. An estimated 20-25% of the world’s infants have IDA, with at least as many having iron deficiency without anemia. Infants are at particular risk due to rapid growth and limited dietary sources of iron. We found that infants with IDA showed different motor activity patterning in all sleep-waking states and several differences in sleep states organization. Sleep alterations were still apparent years after correction of anemia with iron treatment in the absence of subsequent IDA. We suggest that altered sleep patterns may represent an underlying mechanism that interferes with optimal brain functioning during sleep and wakefulness in former IDA children. PMID:20620103

Consciousness, brain, neuroplasticity

PubMed Central

Askenasy, Jean; Lehmann, Joseph

2013-01-01

Subjectivity, intentionality, self-awareness and will are major components of consciousness in human beings. Changes in consciousness and its content following different brain processes and malfunction have long been studied. Cognitive sciences assume that brain activities have an infrastructure, but there is also evidence that consciousness itself may change this infrastructure. The two-way influence between brain and consciousness has been at the center of philosophy and less so, of science. This so-called bottom-up and top-down interrelationship is controversial and is the subject of our article. We would like to ask: how does it happen that consciousness may provoke structural changes in the brain? The living brain means continuous changes at the synaptic level with every new experience, with every new process of learning, memorizing or mastering new and existing skills. Synapses are generated and dissolved, while others are preserved, in an ever-changing process of so-called neuroplasticity. Ongoing processes of synaptic reinforcements and decay occur during wakefulness when consciousness is present, but also during sleep when it is mostly absent. We suggest that consciousness influences brain neuroplasticity both during wakefulness as well as sleep in a top-down way. This means that consciousness really activates synaptic flow and changes brain structures and functional organization. The dynamic impact of consciousness on brain never stops despite the relative stationary structure of the brain. Such a process can be a target for medical intervention, e.g., by cognitive training. PMID:23847580

Recovery of neurological function despite immediate sleep disruption following diffuse brain injury in the mouse: clinical relevance to medically untreated concussion.

PubMed

Rowe, Rachel K; Harrison, Jordan L; O'Hara, Bruce F; Lifshitz, Jonathan

2014-04-01

We investigated the relationship between immediate disruption of posttraumatic sleep and functional outcome in the diffuse brain-injured mouse. Adult male C57BL/6 mice were subjected to moderate midline fluid percussion injury (n = 65; 1.4 atm; 6-10 min righting reflex time) or sham injury (n = 44). Cohorts received either intentional sleep disruption (minimally stressful gentle handling) or no sleep disruption for 6 h following injury. Following disruption, serum corticosterone levels (enzyme-linked immunosorbent assay) and posttraumatic sleep (noninvasive piezoelectric sleep cages) were measured. For 1-7 days postinjury, sensorimotor outcome was assessed by Rotarod and a modified Neurological Severity Score (NSS). Cognitive function was measured using Novel Object Recognition (NOR) and Morris water maze (MWM) in the first week postinjury. Neurotrauma research laboratory. Disrupting posttraumatic sleep for 6 h did not affect serum corticosterone levels or functional outcome. In the hour following the first dark onset, sleep-disrupted mice exhibited a significant increase in sleep; however, this increase was not sustained and there was no rebound of lost sleep. Regardless of sleep disruption, mice showed a time-dependent improvement in Rotarod performance, with brain-injured mice having significantly shorter latencies on day 7 compared to sham. Further, brain-injured mice, regardless of sleep disruption, had significantly higher NSS scores postinjury compared with sham. Cognitive behavioral testing showed no group differences among any treatment group measured by MWM and NOR. Short-duration disruption of posttraumatic sleep did not affect functional outcome, measured by motor and cognitive performance. These data raise uncertainty about posttraumatic sleep as a mechanism of recovery from diffuse brain injury.

Impact of monetary incentives on cognitive performance and error monitoring following sleep deprivation.

PubMed

Hsieh, Shulan; Li, Tzu-Hsien; Tsai, Ling-Ling

2010-04-01

To examine whether monetary incentives attenuate the negative effects of sleep deprivation on cognitive performance in a flanker task that requires higher-level cognitive-control processes, including error monitoring. Twenty-four healthy adults aged 18 to 23 years were randomly divided into 2 subject groups: one received and the other did not receive monetary incentives for performance accuracy. Both subject groups performed a flanker task and underwent electroencephalographic recordings for event-related brain potentials after normal sleep and after 1 night of total sleep deprivation in a within-subject, counterbalanced, repeated-measures study design. Monetary incentives significantly enhanced the response accuracy and reaction time variability under both normal sleep and sleep-deprived conditions, and they reduced the effects of sleep deprivation on the subjective effort level, the amplitude of the error-related negativity (an error-related event-related potential component), and the latency of the P300 (an event-related potential variable related to attention processes). However, monetary incentives could not attenuate the effects of sleep deprivation on any measures of behavior performance, such as the response accuracy, reaction time variability, or posterror accuracy adjustments; nor could they reduce the effects of sleep deprivation on the amplitude of the Pe, another error-related event-related potential component. This study shows that motivation incentives selectively reduce the effects of total sleep deprivation on some brain activities, but they cannot attenuate the effects of sleep deprivation on performance decrements in tasks that require high-level cognitive-control processes. Thus, monetary incentives and sleep deprivation may act through both common and different mechanisms to affect cognitive performance.

What Is the Link Between Hallucinations, Dreams, and Hypnagogic–Hypnopompic Experiences?

PubMed Central

Waters, Flavie; Blom, Jan Dirk; Dang-Vu, Thien Thanh; Cheyne, Allan J.; Alderson-Day, Ben; Woodruff, Peter; Collerton, Daniel

2016-01-01

By definition, hallucinations occur only in the full waking state. Yet similarities to sleep-related experiences such as hypnagogic and hypnopompic hallucinations, dreams and parasomnias, have been noted since antiquity. These observations have prompted researchers to suggest a common aetiology for these phenomena based on the neurobiology of rapid eye movement (REM) sleep. With our recent understanding of hallucinations in different population groups and at the neurobiological, cognitive and interpersonal levels, it is now possible to draw comparisons between the 2 sets of experiences as never before. In the current article, we make detailed comparisons between sleep-related experiences and hallucinations in Parkinson’s disease, schizophrenia and eye disease, at the levels of phenomenology (content, sensory modalities involved, perceptual attributes) and of brain function (brain activations, resting-state networks, neurotransmitter action). Findings show that sleep-related experiences share considerable overlap with hallucinations at the level of subjective descriptions and underlying brain mechanisms. Key differences remain however: (1) Sleep-related perceptions are immersive and largely cut off from reality, whereas hallucinations are discrete and overlaid on veridical perceptions; and (2) Sleep-related perceptions involve only a subset of neural networks implicated in hallucinations, reflecting perceptual signals processed in a functionally and cognitively closed-loop circuit. In summary, both phenomena are non-veridical perceptions that share some phenomenological and neural similarities, but insufficient evidence exists to fully support the notion that the majority of hallucinations depend on REM processes or REM intrusions into waking consciousness. PMID:27358492

Repetitive traumatic brain injury (or concussion) increases severity of sleep disturbance among deployed military personnel.

PubMed

Bryan, Craig J

2013-06-01

Considerable research indicates that sleep disturbances and insomnia are more common and severe among individuals following a traumatic brain injury (TBI). It remains unclear, however, how the experience of multiple TBIs affect sleep disturbances and insomnia. The current study investigated the incidence and severity of insomnia and sleep complaints among active-duty military personnel who have sustained multiple TBIs. Upon intake at a military TBI clinic located in Iraq, 150 male military patients completed standardized self-report measures and clinical interviews. Patients were categorized into three groups according to history of TBI: zero TBIs (n = 18), single TBI (n = 54), multiple TBIs (n = 78). Rates of clinical insomnia significantly increased across TBI groups (P < 0.001):- 5.6% for no TBIs, 20.4% for single TBI, and 50.0% for multiple TBIs. Insomnia severity significantly increased across TBI groups even when controlling for depression, posttraumatic stress disorder, and concussion symptom severity (B = 1.134, standard error = 0.577, P = 0.049). Multiple TBIs are associated with increased risk for and severity of sleep disturbance among male military personnel.

Sleep-Wake Differences in Relative Regional Cerebral Metabolic Rate for Glucose among Patients with Insomnia Compared with Good Sleepers

PubMed Central

Kay, Daniel B.; Karim, Helmet T.; Soehner, Adriane M.; Hasler, Brant P.; Wilckens, Kristine A.; James, Jeffrey A.; Aizenstein, Howard J.; Price, Julie C.; Rosario, Bedda L.; Kupfer, David J.; Germain, Anne; Hall, Martica H.; Franzen, Peter L.; Nofzinger, Eric A.; Buysse, Daniel J.

2016-01-01

Study Objectives: The neurobiological mechanisms of insomnia may involve altered patterns of activation across sleep-wake states in brain regions associated with cognition, self-referential processes, affect, and sleep-wake promotion. The objective of this study was to compare relative regional cerebral metabolic rate for glucose (rCMRglc) in these brain regions across wake and nonrapid eye movement (NREM) sleep states in patients with primary insomnia (PI) and good sleeper controls (GS). Methods: Participants included 44 PI and 40 GS matched for age (mean = 37 y old, range 21–60), sex, and race. We conducted [18F]fluoro-2-deoxy-d-glucose positron emission tomography scans in PI and GS during both morning wakefulness and NREM sleep at night. Repeated measures analysis of variance was used to test for group (PI vs. GS) by state (wake vs. NREM sleep) interactions in relative rCMRglc. Results: Significant group-by-state interactions in relative rCMRglc were found in the precuneus/posterior cingulate cortex, left middle frontal gyrus, left inferior/superior parietal lobules, left lingual/fusiform/occipital gyri, and right lingual gyrus. All clusters were significant at Pcorrected < 0.05. Conclusions: Insomnia was characterized by regional alterations in relative glucose metabolism across NREM sleep and wakefulness. Significant group-by-state interactions in relative rCMRglc suggest that insomnia is associated with impaired disengagement of brain regions involved in cognition (left frontoparietal), self-referential processes (precuneus/posterior cingulate), and affect (left middle frontal, fusiform/lingual gyri) during NREM sleep, or alternatively, to impaired engagement of these regions during wakefulness. Citation: Kay DB, Karim HT, Soehner AM, Hasler BP, Wilckens KA, James JA, Aizenstein HJ, Price JC, Rosario BL, Kupfer DJ, Germain A, Hall MH, Franzen PL, Nofzinger EA, Buysse DJ. Sleep-wake differences in relative regional cerebral metabolic rate for glucose among patients with insomnia compared with good sleepers. SLEEP 2016;39(10):1779–1794. PMID:27568812

Fluorine walk: The impact of fluorine in quinolone amides on their activity against African sleeping sickness.

PubMed

Berninger, Michael; Erk, Christine; Fuß, Antje; Skaf, Joseph; Al-Momani, Ehab; Israel, Ina; Raschig, Martina; Güntzel, Paul; Samnick, Samuel; Holzgrabe, Ulrike

2018-05-25

Human African Trypanosomiasis, also known as African sleeping sickness, is caused by the parasitic protozoa of the genus Trypanosoma. If there is no pharmacological intervention, the parasites can cross the blood-brain barrier (BBB), inevitably leading to death of the patients. Previous investigation identified the quinolone amide GHQ168 as a promising lead compound having a nanomolar activity against T. b. brucei. Here, the role of a fluorine substitution at different positions was investigated in regard to toxicity, pharmacokinetics, and antitrypanosomal activity. This 'fluorine walk' led to new compounds with improved metabolic stability and consistent activity against T. b. brucei. The ability of the new quinolone amides to cross the BBB was confirmed using an 18 F-labelled quinolone amide derivative by means of ex vivo autoradiography of a murine brain. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Visualization of Whole-Night Sleep EEG From 2-Channel Mobile Recording Device Reveals Distinct Deep Sleep Stages with Differential Electrodermal Activity.

PubMed

Onton, Julie A; Kang, Dae Y; Coleman, Todd P

2016-01-01

Brain activity during sleep is a powerful marker of overall health, but sleep lab testing is prohibitively expensive and only indicated for major sleep disorders. This report demonstrates that mobile 2-channel in-home electroencephalogram (EEG) recording devices provided sufficient information to detect and visualize sleep EEG. Displaying whole-night sleep EEG in a spectral display allowed for quick assessment of general sleep stability, cycle lengths, stage lengths, dominant frequencies and other indices of sleep quality. By visualizing spectral data down to 0.1 Hz, a differentiation emerged between slow-wave sleep with dominant frequency between 0.1-1 Hz or 1-3 Hz, but rarely both. Thus, we present here the new designations, Hi and Lo Deep sleep, according to the frequency range with dominant power. Simultaneously recorded electrodermal activity (EDA) was primarily associated with Lo Deep and very rarely with Hi Deep or any other stage. Therefore, Hi and Lo Deep sleep appear to be physiologically distinct states that may serve unique functions during sleep. We developed an algorithm to classify five stages (Awake, Light, Hi Deep, Lo Deep and rapid eye movement (REM)) using a Hidden Markov Model (HMM), model fitting with the expectation-maximization (EM) algorithm, and estimation of the most likely sleep state sequence by the Viterbi algorithm. The resulting automatically generated sleep hypnogram can help clinicians interpret the spectral display and help researchers computationally quantify sleep stages across participants. In conclusion, this study demonstrates the feasibility of in-home sleep EEG collection, a rapid and informative sleep report format, and novel deep sleep designations accounting for spectral and physiological differences.

Consciousness in waking and dreaming: the roles of neuronal oscillation and neuromodulation in determining similarities and differences.

PubMed

Kahn, D; Pace-Schott, E F; Hobson, J A

1997-05-01

State-dependent aspects of consciousness are explored with particular attention to waking and dreaming. First, those phenomenological differences between waking and dreaming that have been established through subjective reports are reviewed. These differences are robustly expressed in most aspects of consciousness including perception, attention, memory, emotion, orientation, and thought. Next, the roles of high frequency neuronal oscillation and neuromodulation are explored in waking and rapid eye movement sleep, the stage of sleep with which the most intense dreaming is associated. The high frequency neuronal oscillations serve similar functions in the wake and rapid eye movement states sleep but neuromodulation is very different in the two states. The collective high frequency oscillatory activity gives coherence to spatially separate neurons but, because of the different neuromodulation, the binding of sensory input in the wake state is very different from the binding of internally perceived input during rapid eye movement sleep. An explanatory model is presented which states that neuromodulation, as well as input source and brain activation level differentiate states of the brain, while the self-organized collective neuronal oscillations unify consciousness via long range correlations.

Scalp and Source Power Topography in Sleepwalking and Sleep Terrors: A High-Density EEG Study

PubMed Central

Castelnovo, Anna; Riedner, Brady A.; Smith, Richard F.; Tononi, Giulio; Boly, Melanie; Benca, Ruth M.

2016-01-01

Study Objectives: To examine scalp and source power topography in sleep arousals disorders (SADs) using high-density EEG (hdEEG). Methods: Fifteen adult subjects with sleep arousal disorders (SADs) and 15 age- and gender-matched good sleeping healthy controls were recorded in a sleep laboratory setting using a 256 channel EEG system. Results: Scalp EEG analysis of all night NREM sleep revealed a localized decrease in slow wave activity (SWA) power (1–4 Hz) over centro-parietal regions relative to the rest of the brain in SADs compared to good sleeping healthy controls. Source modelling analysis of 5-minute segments taken from N3 during the first half of the night revealed that the local decrease in SWA power was prominent at the level of the cingulate, motor, and sensori-motor associative cortices. Similar patterns were also evident during REM sleep and wake. These differences in local sleep were present in the absence of any detectable clinical or electrophysiological sign of arousal. Conclusions: Overall, results suggest the presence of local sleep differences in the brain of SADs patients during nights without clinical episodes. The persistence of similar topographical changes in local EEG power during REM sleep and wakefulness points to trait-like functional changes that cross the boundaries of NREM sleep. The regions identified by source imaging are consistent with the current neurophysiological understanding of SADs as a disorder caused by local arousals in motor and cingulate cortices. Persistent localized changes in neuronal excitability may predispose affected subjects to clinical episodes. Citation: Castelnovo A, Riedner BA, Smith RF, Tononi G, Boly M, Benca RM. Scalp and source power topography in sleepwalking and sleep terrors: a high-density EEG study. SLEEP 2016;39(10):1815–1825. PMID:27568805

Sleep spindles in humans: insights from intracranial EEG and unit recordings

PubMed Central

Andrillon, Thomas; Nir, Yuval; Staba, Richard J.; Ferrarelli, Fabio; Cirelli, Chiara; Tononi, Giulio; Fried, Itzhak

2012-01-01

Sleep spindles are an electroencephalographic (EEG) hallmark of non-rapid eye movement (NREM) sleep and are believed to mediate many sleep-related functions, from memory consolidation to cortical development. Spindles differ in location, frequency, and association with slow waves, but whether this heterogeneity may reflect different physiological processes and potentially serve different functional roles remains unclear. Here we utilized a unique opportunity to record intracranial depth EEG and single-unit activity in multiple brain regions of neurosurgical patients to better characterize spindle activity in human sleep. We find that spindles occur across multiple neocortical regions, and less frequently also in the parahippocampal gyrus and hippocampus. Most spindles are spatially restricted to specific brain regions. In addition, spindle frequency is topographically organized with a sharp transition around the supplementary motor area between fast (13-15Hz) centroparietal spindles often occurring with slow wave up-states, and slow (9-12Hz) frontal spindles occurring 200ms later on average. Spindle variability across regions may reflect the underlying thalamocortical projections. We also find that during individual spindles, frequency decreases within and between regions. In addition, deeper sleep is associated with a reduction in spindle occurrence and spindle frequency. Frequency changes between regions, during individual spindles, and across sleep may reflect the same phenomenon, the underlying level of thalamocortical hyperpolarization. Finally, during spindles neuronal firing rates are not consistently modulated, although some neurons exhibit phase-locked discharges. Overall, anatomical considerations can account well for regional spindle characteristics, while variable hyperpolarization levels can explain differences in spindle frequency. PMID:22159098

Stimulation of the brain with radiofrequency electromagnetic field pulses affects sleep-dependent performance improvement.

PubMed

Lustenberger, Caroline; Murbach, Manuel; Dürr, Roland; Schmid, Marc Ralph; Kuster, Niels; Achermann, Peter; Huber, Reto

2013-09-01

Sleep-dependent performance improvements seem to be closely related to sleep spindles (12-15 Hz) and sleep slow-wave activity (SWA, 0.75-4.5 Hz). Pulse-modulated radiofrequency electromagnetic fields (RF EMF, carrier frequency 900 MHz) are capable to modulate these electroencephalographic (EEG) characteristics of sleep. The aim of our study was to explore possible mechanisms how RF EMF affect cortical activity during sleep and to test whether such effects on cortical activity during sleep interact with sleep-dependent performance changes. Sixteen male subjects underwent 2 experimental nights, one of them with all-night 0.25-0.8 Hz pulsed RF EMF exposure. All-night EEG was recorded. To investigate RF EMF induced changes in overnight performance improvement, subjects were trained for both nights on a motor task in the evening and the morning. We obtained good sleep quality in all subjects under both conditions (mean sleep efficiency > 90%). After pulsed RF EMF we found increased SWA during exposure to pulse-modulated RF EMF compared to sham exposure (P < 0.05) toward the end of the sleep period. Spindle activity was not affected. Moreover, subjects showed an increased RF EMF burst-related response in the SWA range, indicated by an increase in event-related EEG spectral power and phase changes in the SWA range. Notably, during exposure, sleep-dependent performance improvement in the motor sequence task was reduced compared to the sham condition (-20.1%, P = 0.03). The changes in the time course of SWA during the exposure night may reflect an interaction of RF EMF with the renormalization of cortical excitability during sleep, with a negative impact on sleep-dependent performance improvement. Copyright © 2013 Elsevier Inc. All rights reserved.

Sleepiness induced by sleep-debt enhanced amygdala activity for subliminal signals of fear.

PubMed

Motomura, Yuki; Kitamura, Shingo; Oba, Kentaro; Terasawa, Yuri; Enomoto, Minori; Katayose, Yasuko; Hida, Akiko; Moriguchi, Yoshiya; Higuchi, Shigekazu; Mishima, Kazuo

2014-08-19

Emotional information is frequently processed below the level of consciousness, where subcortical regions of the brain are thought to play an important role. In the absence of conscious visual experience, patients with visual cortex damage discriminate the valence of emotional expression. Even in healthy individuals, a subliminal mechanism can be utilized to compensate for a functional decline in visual cognition of various causes such as strong sleepiness. In this study, sleep deprivation was simulated in healthy individuals to investigate functional alterations in the subliminal processing of emotional information caused by reduced conscious visual cognition and attention due to an increase in subjective sleepiness. Fourteen healthy adult men participated in a within-subject crossover study consisting of a 5-day session of sleep debt (SD, 4-h sleep) and a 5-day session of sleep control (SC, 8-h sleep). On the last day of each session, participants performed an emotional face-viewing task that included backward masking of nonconscious presentations during magnetic resonance scanning. Finally, data from eleven participants who were unaware of nonconscious face presentations were analyzed. In fear contrasts, subjective sleepiness was significantly positively correlated with activity in the amygdala, ventromedial prefrontal cortex, hippocampus, and insular cortex, and was significantly negatively correlated with the secondary and tertiary visual areas and the fusiform face area. In fear-neutral contrasts, subjective sleepiness was significantly positively correlated with activity of the bilateral amygdala. Further, changes in subjective sleepiness (the difference between the SC and SD sessions) were correlated with both changes in amygdala activity and functional connectivity between the amygdala and superior colliculus in response to subliminal fearful faces. Sleepiness induced functional decline in the brain areas involved in conscious visual cognition of facial expressions, but also enhanced subliminal emotional processing via superior colliculus as represented by activity in the amygdala. These findings suggest that an evolutionally old and auxiliary subliminal hazard perception system is activated as a compensatory mechanism when conscious visual cognition is impaired. In addition, enhancement of subliminal emotional processing might cause involuntary emotional instability during sleep debt through changes in emotional response to or emotional evaluation of external stimuli.

BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories.

PubMed

Gosselin, Nadia; De Beaumont, Louis; Gagnon, Katia; Baril, Andrée-Ann; Mongrain, Valérie; Blais, Hélène; Montplaisir, Jacques; Gagnon, Jean-François; Pelleieux, Sandra; Poirier, Judes; Carrier, Julie

2016-08-10

It is hypothesized that a fundamental function of sleep is to restore an individual's day-to-day ability to learn and to constantly adapt to a changing environment through brain plasticity. Brain-derived neurotrophic factor (BDNF) is among the key regulators that shape brain plasticity. However, advancing age and carrying the BDNF Met allele were both identified as factors that potentially reduce BDNF secretion, brain plasticity, and memory. Here, we investigated the moderating role of BDNF polymorphism on sleep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years of age. All subjects were tested with 1 night of in-laboratory polysomnography followed by a cognitive evaluation the next morning. We found that in subjects carrying the BDNF Val66Val polymorphism, consolidated sleep was associated with significantly better performance on hippocampus-dependent episodic memory tasks the next morning (β-values from 0.290 to 0.434, p ≤ 0.01). In subjects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not associated with better memory performance in most memory tests (β-values from -0.309 to -0.392, p values from 0.06 to 0.15). Strikingly, increased sleep consolidation was associated with poorer performance in learning a short story presented verbally in Met allele carriers (β = -0.585, p = 0.005). This study provides new evidence regarding the interacting roles of consolidated sleep and BDNF polymorphism in the ability to learn and stresses the importance of considering BDNF polymorphism when studying how sleep affects cognition. Individuals with the BDNF Val/Val (valine allele) polymorphism showed better memory performance after a night of consolidated sleep. However, we observed that middle-aged and older individuals who are carriers of the BDNF Met allele displayed no positive association between sleep quality and their ability to learn the next morning. This interaction between sleep and BDNF polymorphism was more salient for hippocampus-dependent tasks than for other cognitive tasks. Our results support the hypothesis that reduced activity-dependent secretion of BDNF impairs the benefits of sleep on synaptic plasticity and next-day memory. Our work advances the field by revealing new evidence of a clear genetic heterogeneity in how sleep consolidation contributes to the ability to learn. Copyright © 2016 the authors 0270-6474/16/368391-09$15.00/0.

Habitual Short Sleep Impacts Frontal Switch Mechanism in Attention to Novelty

PubMed Central

Gumenyuk, Valentina; Roth, Thomas; Korzyukov, Oleg; Jefferson, Catherine; Bowyer, Susan; Drake, Christopher L.

2011-01-01

Study Objectives: Reduced time in bed relative to biological sleep need is common. The impact of habitual short sleep on auditory attention has not been studied to date. In the current study, we utilized novelty oddball tasks to evaluate the effect of habitual short sleep on brain function underlying attention control processes measured by the mismatch negativity (MMN, index of pre-attentive stage), P3a (attention-dependent), and P3b (memory-dependent) event related brain potentials (ERPs). An extended time in bed in a separate study was used to evaluate the possible reversal of the impairments of these processes in habitual short sleepers. Methods: Ten self-defined short sleepers (total sleep time [TST] ≤ 6h) and 9 normal-sleeping subjects with TST 7-8 h, participated. ERPs were recorded via a 64-channel EEG system. Two test conditions: “ignore” and “attend” were implemented. The ERPs were analyzed and compared between groups on the 2 task conditions and frontal/central/parietal electrodes by 3-factor ANOVA. Sleep diary data were compared between groups by t-test. Sleep was recorded by the Zeo sleep monitoring system for a week in both habitual and extended sleep conditions at home. Results: The main findings of the present study show that short sleeping individuals had deficiency in activity of the MMN and P3a brain responses over frontal areas compared to normal-sleeping subjects. The P3b amplitude was increased over frontal areas and decreased over parietal with respect to the control group. Extension of time in bed for one week increased TST (from 5.7 h to 7.4 h), and concomitantly MMN amplitude increased from −0.1μV up to −1.25 μV over frontal areas. Conclusions: Reduced time in bed is associated with deficiency of the neuronal process associated with change detection, which may recover after one week of sleep extension, whereas attention-dependent neural processes do not normalize after this period of time in habitually short sleeping individuals and may require longer recovery periods. Citation: Gumenyuk V; Roth T; Korzyukov O; Jefferson C; Bowyer S; Drake CL. Habitual short sleep impacts frontal switch mechanism in attention to novelty. SLEEP 2011;34(12):1659-1670. PMID:22131603

Sleep Dysfunction and EEG Alterations in Mice Overexpressing Alpha-Synuclein

PubMed Central

McDowell, Kimberly A.; Shin, David; Roos, Kenneth P.; Chesselet, Marie-Françoise

2018-01-01

Background: Sleep disruptions occur early and frequently in Parkinson’s disease (PD). PD patients also show a slowing of resting state activity. Alpha-synuclein is causally linked to PD and accumulates in sleep-related brain regions. While sleep problems occur in over 75% of PD patients and severely impact the quality of life of patients and caregivers, their study is limited by a paucity of adequate animal models. Objective: The objective of this study was to determine whether overexpression of wildtype alpha-synuclein could lead to alterations in sleep patterns reminiscent of those observed in PD by measuring sleep/wake activity with rigorous quantitative methods in a well-characterized genetic mouse model. Methods: At 10 months of age, mice expressing human wildtype alpha-synuclein under the Thy-1 promoter (Thy1-aSyn) and wildtype littermates underwent the subcutaneous implantation of a telemetry device (Data Sciences International) for the recording of electromyograms (EMG) and electroencephalograms (EEG) in freely moving animals. Surgeries and data collection were performed without knowledge of mouse genotype. Results: Thy1-aSyn mice showed increased non-rapid eye movement sleep during their quiescent phase, increased active wake during their active phase, and decreased rapid eye movement sleep over a 24-h period, as well as a shift in the density of their EEG power spectra toward lower frequencies with a significant decrease in gamma power during wakefulness. Conclusions: Alpha-synuclein overexpression in mice produces sleep disruptions and altered oscillatory EEG activity reminiscent of PD, and this model provides a novel platform to assess mechanisms and therapeutic strategies for sleep dysfunction in PD. PMID:24867919

Sleep and stress in man: an approach through exercise and exposure to extreme environments.

PubMed

Buguet, A; Cespuglio, R; Radomski, M W

1998-05-01

In this paper, the effects of exercise on human sleep (in temperate, cold, and hot climates) are compared with those of exposure to extreme environments (tropical, polar climates). Exercise has two effect: (i) when the exercise load is too heavy or if the subject is not trained to the exercise conditions, the hypothalamo-pituitary-adrenocortical axis (HPA) is strongly activated (somatic stress reaction), and a diachronic (delayed) decrease in total sleep time and slow-wave sleep (SWS) occurs with a synchronic (concomitant) sleep disruption (such as a decrease in REM sleep); (ii) a diachronic enhancement of SWS and (or) REM sleep occurs during moderate training and in athletes, with a moderate HPA activation (neurogenic stress reaction). Heat acclimatization (neurogenic stress response) results in a diachronic increase in SWS, contrary to acute heat exposure (somatic stress) which leads to a diachronic decrease in SWS. Nocturnal cold exposure (somatic and (or) neurogenic stress) provokes a synchronic decrease in REM sleep with an activation of stress hormones, which are reduced by previous acclimation (neurogenic pathway); SWS remains undisturbed in the cold, as it occurs at the beginning of the night before body cooling. In conclusion, when the brain can deal with the stressor (neurogenic stress), diachronic increases in SWS and (or) REM sleep occur. When these "central" mechanisms are overloaded, the classical "somatic" stress reaction occurs with diachronic and synchronic disruptions of the sleep structure.

The maturation of cortical sleep rhythms and networks over early development.

PubMed

Chu, C J; Leahy, J; Pathmanathan, J; Kramer, M A; Cash, S S

2014-07-01

Although neuronal activity drives all aspects of cortical development, how human brain rhythms spontaneously mature remains an active area of research. We sought to systematically evaluate the emergence of human brain rhythms and functional cortical networks over early development. We examined cortical rhythms and coupling patterns from birth through adolescence in a large cohort of healthy children (n=384) using scalp electroencephalogram (EEG) in the sleep state. We found that the emergence of brain rhythms follows a stereotyped sequence over early development. In general, higher frequencies increase in prominence with striking regional specificity throughout development. The coordination of these rhythmic activities across brain regions follows a general pattern of maturation in which broadly distributed networks of low-frequency oscillations increase in density while networks of high frequency oscillations become sparser and more highly clustered. Our results indicate that a predictable program directs the development of key rhythmic components and physiological brain networks over early development. This work expands our knowledge of normal cortical development. The stereotyped neurophysiological processes observed at the level of rhythms and networks may provide a scaffolding to support critical periods of cognitive growth. Furthermore, these conserved patterns could provide a sensitive biomarker for cortical health across development. Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

The maturation of cortical sleep rhythms and networks over early development

PubMed Central

Chu, CJ; Leahy, J; Pathmanathan, J; Kramer, MA; Cash, SS

2014-01-01

Objective Although neuronal activity drives all aspects of cortical development, how human brain rhythms spontaneously mature remains an active area of research. We sought to systematically evaluate the emergence of human brain rhythms and functional cortical networks over early development. Methods We examined cortical rhythms and coupling patterns from birth through adolescence in a large cohort of healthy children (n=384) using scalp electroencephalogram (EEG) in the sleep state. Results We found that the emergence of brain rhythms follows a stereotyped sequence over early development. In general, higher frequencies increase in prominence with striking regional specificity throughout development. The coordination of these rhythmic activities across brain regions follows a general pattern of maturation in which broadly distributed networks of low-frequency oscillations increase in density while networks of high frequency oscillations become sparser and more highly clustered. Conclusion Our results indicate that a predictable program directs the development of key rhythmic components and physiological brain networks over early development. Significance This work expands our knowledge of normal cortical development. The stereotyped neurophysiological processes observed at the level of rhythms and networks may provide a scaffolding to support critical periods of cognitive growth. Furthermore, these conserved patterns could provide a sensitive biomarker for cortical health across development. PMID:24418219

Influence of Chronic Moderate Sleep Restriction and Exercise Training on Anxiety, Spatial Memory, and Associated Neurobiological Measures in Mice

PubMed Central

Zielinski, Mark R.; Davis, J. Mark; Fadel, James R.; Youngstedt, Shawn D.

2013-01-01

Sleep deprivation can have deleterious effects on cognitive function and mental health. Moderate exercise training has myriad beneficial effects on cognition and mental health. However, physiological and behavioral effects of chronic moderate sleep restriction and its interaction with common activities, such as moderate exercise training, have received little investigation. The aims of this study were to examine the effects of chronic moderate sleep restriction and moderate exercise training on anxiety-related behavior, spatial memory, and neurobiological correlates in mice. Male mice were randomized to one of four 11-week treatments in a 2 [sleep restriction (~4 h loss/day) vs. ad libitum sleep] × 2 [exercise (1 h/day/6 d/wk) vs. sedentary activity] experimental design. Anxiety-related behavior was assessed with the elevated-plus maze, and spatial learning and memory were assessed with the Morris water maze. Chronic moderate sleep restriction did not alter anxiety-related behavior, but exercise training significantly attenuated anxiety-related behavior. Spatial learning and recall, hippocampal cell activity (i.e., number of c-Fos positive cells), and brain derived neurotrophic factor were significantly lower after chronic moderate sleep restriction, but higher after exercise training. Further, the benefit of exercise training for some memory variables was evident under normal sleep, but not chronic moderate sleep restriction conditions. These data indicate clear detrimental effects of chronic moderate sleep restriction on spatial memory and that the benefits of exercise training were impaired after chronic moderate sleep restriction. PMID:23644185

Is Homeostatic Sleep Regulation Under Low Sleep Pressure Modified by Age?

PubMed Central

Munch, Mirjam; Knoblauch, Vera; Blatter, Katharina; Wirz-Justice, Anna; Cajochen, Christian

2007-01-01

Study Objectives: We have previously shown that healthy older volunteers react with an attenuated frontal predominance of sleep electroencephalogram (EEG) delta activity in response to high sleep pressure. Here, we investigated age-related changes in homeostatic sleep regulation under low sleep pressure conditions, with respect to regional EEG differences and their dynamics. Design: Analysis of the sleep EEG during an 8-hour baseline night, during a 40-hour multiple nap protocol (150 minutes of wakefulness and 75 minutes of sleep) and during the following 8-hour recovery night under constant posture conditions. Setting: Centre for Chronobiology, Psychiatric University Clinics, Basel, Switzerland Participants: Sixteen young (20–31 years) and 15 older (57–74 years) healthy volunteers Interventions: N/A. Measurements and Results: All-night EEG spectra revealed an increase in spindle activity (13–15.25 Hz) for both age groups, but only in the young did we find a significant decrease of delta activity (0.5–1.25 Hz) in response to low sleep pressure conditions, predominantly in occipital brain regions. However, delta activity during the first non-rapid eye movement (NREM) sleep episode was equally reduced in both age groups. This response lasted significantly longer in the young (across the first 2 NREM sleep episodes) than in the older participants (only the first NREM sleep episode). Conclusion: The initial EEG delta response to low sleep pressure was similar in healthy older and young participants. Therefore, age-related sleep deteriorations cannot solely be attributed to alterations in the homeostatic sleep-regulatory system. It is, rather, the interplay of circadian and homeostatic factors of sleep regulation, which is changed with aging. Citation: Munch M; Knoblauch V; Blatter K et al. Is homeostatic sleep regulation under low sleep pressure modified by age? SLEEP 2007;30(6):781-792. PMID:17580600

Unearthing the Phylogenetic Roots of Sleep

PubMed Central

Allada, Ravi; Siegel, Jerome M.

2010-01-01

Why we sleep remains one of the enduring unanswered questions in biology. At its core, sleep can be defined behaviorally as a homeostatically regulated state of reduced movement and sensory responsiveness. The cornerstone of sleep studies in terrestrial mammals, including humans, has been the measurement of coordinated changes in brain activity during sleep measured using the electroencephalogram (EEG). Yet among a diverse set of animals, these EEG sleep traits can vary widely and, in some cases, are absent, raising questions as to whether they define a universal, or even essential, feature of sleep. Over the past decade, behaviorally defined sleep-like states have been identified in a series of genetic model organisms, including fish, flies and worms. Genetic analyses in these systems are revealing a remarkable conservation in the underlying mechanisms controlling sleep behavior. Taken together, these studies suggest an ancient origin for sleep and raise the possibility that model organism genetics may reveal the molecular mechanisms that guide sleep and wake. PMID:18682212

Sleep Duration and White Matter Quality in Middle-Aged Adults

PubMed Central

Yaffe, Kristine; Nasrallah, Ilya; Hoang, Tina D.; Lauderdale, Diane S.; Knutson, Kristen L.; Carnethon, Mercedes R.; Launer, Lenore J.; Lewis, Cora E.; Sidney, Stephen

2016-01-01

Study Objectives: Sleep duration has been associated with risk of dementia and stroke, but few studies have investigated the relationship between sleep duration and brain MRI measures, particularly in middle age. Methods: In a prospective cohort of 613 black and white adults (mean age = 45.4 years) enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study, participants reported typical sleep duration, dichotomized into moderate sleep duration (> 6 to ≤ 8 h) and short sleep duration (≤ 6 h) at baseline (2005–2006). Five years later, we obtained brain MRI markers of white matter including fractional anisotropy, mean diffusivity, and white matter hyperintensities. Results: Compared to moderate sleepers, short sleepers had an elevated ratio of white matter hyperintensities to normal tissue in the parietal region (OR = 2.31, 95% CI: 1.47, 3.61) adjusted for age, race/sex, education, hypertension, stroke/TIA, depression, smoking status, and physical activity. White matter diffusivity was also higher, approximately a 0.2 standard deviation difference, in frontal, parietal, and temporal white matter regions, among those reporting shorter sleep duration in (P < 0.05 for all). Conclusions: Short sleep duration was associated with worse markers of white matter integrity in midlife. These mid-life differences in white matter may underlie the link between poor sleep and risk of dementia and stroke. Citation: Yaffe K, Nasrallah I, Hoang TD, Lauderdale DS, Knutson KL, Carnethon MR, Launer LJ, Lewis CE, Sidney S. Sleep duration and white matter quality in middle-aged adults. SLEEP 2016;39(9):1743–1747. PMID:27397561

Regional cerebral glucose metabolic rate in human sleep assessed by positron emission tomography

DOE Office of Scientific and Technical Information (OSTI.GOV)

Buchsbaum, M.S.; Wu, J.; Hazlett, E.

The cerebral metabolic rate of glucose was measured during nighttime sleep in 36 normal volunteers using positron emission tomography and fluorine-18-labeled 2-deoxyglucose (FDG). In comparison to waking controls, subjects given FDG during non-rapid eye movement (NREM) sleep showed about a 23% reduction in metabolic rate across the entire brain. This decrease was greater for the frontal than temporal or occipital lobes, and greater for basal ganglia and thalamus than cortex. Subjects in rapid eye movement (REM) sleep tended to have higher cortical metabolic rates than walking subjects. The cingulate gyrus was the only cortical structure to show a significant increasemore » in glucose metabolic rate in REM sleep in comparison to waking. The basal ganglia were relatively more active on the right in REM sleep and symmetrical in NREM sleep.« less

Circadian and Brain State Modulation of Network Hyperexcitability in Alzheimer's Disease.

PubMed

Brown, Rosalind; Lam, Alice D; Gonzalez-Sulser, Alfredo; Ying, Andrew; Jones, Mary; Chou, Robert Chang-Chih; Tzioras, Makis; Jordan, Crispin Y; Jedrasiak-Cape, Izabela; Hemonnot, Anne-Laure; Abou Jaoude, Maurice; Cole, Andrew J; Cash, Sydney S; Saito, Takashi; Saido, Takaomi; Ribchester, Richard R; Hashemi, Kevan; Oren, Iris

2018-01-01

Network hyperexcitability is a feature of Alzheimer' disease (AD) as well as numerous transgenic mouse models of AD. While hyperexcitability in AD patients and AD animal models share certain features, the mechanistic overlap remains to be established. We aimed to identify features of network hyperexcitability in AD models that can be related to epileptiform activity signatures in AD patients. We studied network hyperexcitability in mice expressing amyloid precursor protein (APP) with mutations that cause familial AD, and compared a transgenic model that overexpresses human APP (hAPP) (J20), to a knock-in model expressing APP at physiological levels (APP NL/F ). We recorded continuous long-term electrocorticogram (ECoG) activity from mice, and studied modulation by circadian cycle, behavioral, and brain state. We report that while J20s exhibit frequent interictal spikes (IISs), APP NL/F mice do not. In J20 mice, IISs were most prevalent during daylight hours and the circadian modulation was associated with sleep. Further analysis of brain state revealed that IIS in J20s are associated with features of rapid eye movement (REM) sleep. We found no evidence of cholinergic changes that may contribute to IIS-circadian coupling in J20s. In contrast to J20s, intracranial recordings capturing IIS in AD patients demonstrated frequent IIS in non-REM (NREM) sleep. The salient differences in sleep-stage coupling of IIS in APP overexpressing mice and AD patients suggests that different mechanisms may underlie network hyperexcitability in mice and humans. We posit that sleep-stage coupling of IIS should be an important consideration in identifying mouse AD models that most closely recapitulate network hyperexcitability in human AD.

Circadian and Brain State Modulation of Network Hyperexcitability in Alzheimer’s Disease

PubMed Central

Ying, Andrew; Jones, Mary; Chou, Robert Chang-Chih; Jordan, Crispin Y.; Jedrasiak-Cape, Izabela; Abou Jaoude, Maurice; Hashemi, Kevan

2018-01-01

Abstract Network hyperexcitability is a feature of Alzheimer’ disease (AD) as well as numerous transgenic mouse models of AD. While hyperexcitability in AD patients and AD animal models share certain features, the mechanistic overlap remains to be established. We aimed to identify features of network hyperexcitability in AD models that can be related to epileptiform activity signatures in AD patients. We studied network hyperexcitability in mice expressing amyloid precursor protein (APP) with mutations that cause familial AD, and compared a transgenic model that overexpresses human APP (hAPP) (J20), to a knock-in model expressing APP at physiological levels (APPNL/F). We recorded continuous long-term electrocorticogram (ECoG) activity from mice, and studied modulation by circadian cycle, behavioral, and brain state. We report that while J20s exhibit frequent interictal spikes (IISs), APPNL/F mice do not. In J20 mice, IISs were most prevalent during daylight hours and the circadian modulation was associated with sleep. Further analysis of brain state revealed that IIS in J20s are associated with features of rapid eye movement (REM) sleep. We found no evidence of cholinergic changes that may contribute to IIS-circadian coupling in J20s. In contrast to J20s, intracranial recordings capturing IIS in AD patients demonstrated frequent IIS in non-REM (NREM) sleep. The salient differences in sleep-stage coupling of IIS in APP overexpressing mice and AD patients suggests that different mechanisms may underlie network hyperexcitability in mice and humans. We posit that sleep-stage coupling of IIS should be an important consideration in identifying mouse AD models that most closely recapitulate network hyperexcitability in human AD. PMID:29780880

The Impact of Cortical Deafferentation on the Neocortical Slow Oscillation

PubMed Central

Lemieux, Maxime; Chen, Jen-Yung; Lonjers, Peter; Bazhenov, Maxim

2014-01-01

Slow oscillation is the main brain rhythm observed during deep sleep in mammals. Although several studies have demonstrated its neocortical origin, the extent of the thalamic contribution is still a matter of discussion. Using electrophysiological recordings in vivo on cats and computational modeling, we found that the local thalamic inactivation or the complete isolation of the neocortical slabs maintained within the brain dramatically reduced the expression of slow and fast oscillations in affected cortical areas. The slow oscillation began to recover 12 h after thalamic inactivation. The slow oscillation, but not faster activities, nearly recovered after 30 h and persisted for weeks in the isolated slabs. We also observed an increase of the membrane potential fluctuations recorded in vivo several hours after thalamic inactivation. Mimicking this enhancement in a network computational model with an increased postsynaptic activity of long-range intracortical afferents or scaling K+ leak current, but not several other Na+ and K+ intrinsic currents was sufficient for recovering the slow oscillation. We conclude that, in the intact brain, the thalamus contributes to the generation of cortical active states of the slow oscillation and mediates its large-scale synchronization. Our study also suggests that the deafferentation-induced alterations of the sleep slow oscillation can be counteracted by compensatory intracortical mechanisms and that the sleep slow oscillation is a fundamental and intrinsic state of the neocortex. PMID:24741059

How Sleep Activates Epileptic Networks?

PubMed Central

Halász, Peter

2013-01-01

Background. The relationship between sleep and epilepsy has been long ago studied, and several excellent reviews are available. However, recent development in sleep research, the network concept in epilepsy, and the recognition of high frequency oscillations in epilepsy and more new results may put this matter in a new light. Aim. The review address the multifold interrelationships between sleep and epilepsy networks and with networks of cognitive functions. Material and Methods. The work is a conceptual update of the available clinical data and relevant studies. Results and Conclusions. Studies exploring dynamic microstructure of sleep have found important gating mechanisms for epileptic activation. As a general rule interictal epileptic manifestations seem to be linked to the slow oscillations of sleep and especially to the reactive delta bouts characterized by A1 subtype in the CAP system. Important link between epilepsy and sleep is the interference of epileptiform discharges with the plastic functions in NREM sleep. This is the main reason of cognitive impairment in different forms of early epileptic encephalopathies affecting the brain in a special developmental window. The impairment of cognitive functions via sleep is present especially in epileptic networks involving the thalamocortical system and the hippocampocortical memory encoding system. PMID:24159386

Hippocampal Sleep Features: Relations to Human Memory Function

PubMed Central

Ferrara, Michele; Moroni, Fabio; De Gennaro, Luigi; Nobili, Lino

2012-01-01

The recent spread of intracranial electroencephalographic (EEG) recording techniques for presurgical evaluation of drug-resistant epileptic patients is providing new information on the activity of different brain structures during both wakefulness and sleep. The interest has been mainly focused on the medial temporal lobe, and in particular the hippocampal formation, whose peculiar local sleep features have been recently described, providing support to the idea that sleep is not a spatially global phenomenon. The study of the hippocampal sleep electrophysiology is particularly interesting because of its central role in the declarative memory formation. Recent data indicate that sleep contributes to memory formation. Therefore, it is relevant to understand whether specific patterns of activity taking place during sleep are related to memory consolidation processes. Fascinating similarities between different states of consciousness (wakefulness, REM sleep, non-REM sleep) in some electrophysiological mechanisms underlying cognitive processes have been reported. For instance, large-scale synchrony in gamma activity is important for waking memory and perception processes, and its changes during sleep may be the neurophysiological substrate of sleep-related deficits of declarative memory. Hippocampal activity seems to specifically support memory consolidation during sleep, through specific coordinated neurophysiological events (slow waves, spindles, ripples) that would facilitate the integration of new information into the pre-existing cortical networks. A few studies indeed provided direct evidence that rhinal ripples as well as slow hippocampal oscillations are correlated with memory consolidation in humans. More detailed electrophysiological investigations assessing the specific relations between different types of memory consolidation and hippocampal EEG features are in order. These studies will add an important piece of knowledge to the elucidation of the ultimate sleep function. PMID:22529835

EEG oscillations during sleep and dream recall: state- or trait-like individual differences?

PubMed Central

Scarpelli, Serena; D’Atri, Aurora; Gorgoni, Maurizio; Ferrara, Michele; De Gennaro, Luigi

2015-01-01

Dreaming represents a peculiar form of cognitive activity during sleep. On the basis of the well-known relationship between sleep and memory, there has been a growing interest in the predictive role of human brain activity during sleep on dream recall. Neuroimaging studies indicate that rapid eye movement (REM) sleep is characterized by limbic activation and prefrontal cortex deactivation. This pattern could explain the presence of emotional contents in dream reports. Furthermore, the morphoanatomical measures of amygdala and hippocampus predict some features of dream contents (bizarreness, vividness, and emotional load). More relevant for a general view of dreaming mechanisms, empirical data from neuropsychological and electroencephalographic (EEG) studies support the hypothesis that there is a sort of continuity between the neurophysiological mechanisms of encoding and retrieval of episodic memories across sleep and wakefulness. A notable overlap between the electrophysiological mechanisms underlying emotional memory formation and some peculiar EEG features of REM sleep has been suggested. In particular, theta (5–8 Hz) EEG oscillations on frontal regions in the pre-awakening sleep are predictive of dream recall, which parallels the predictive relation during wakefulness between theta activity and successful retrieval of episodic memory. Although some observations support an interpretation more in terms of an intraindividual than interindividual mechanism, the existing empirical evidence still precludes from definitely disentangling if this relation is explained by state- or trait-like differences. PMID:25999908

Longitudinal sleep EEG trajectories indicate complex patterns of adolescent brain maturation.

PubMed

Feinberg, Irwin; Campbell, Ian G

2013-02-15

New longitudinal sleep data spanning ages 6-10 yr are presented and combined with previous data to analyze maturational trajectories of delta and theta EEG across ages 6-18 yr in non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. NREM delta power (DP) increased from age 6 to age 8 yr and then declined. Its highest rate of decline occurred between ages 12 and 16.5 yr. We attribute the delta EEG trajectories to changes in synaptic density. Whatever their neuronal underpinnings, these age curves can guide research into the molecular-genetic mechanisms that underlie adolescent brain development. The DP trajectories in NREM and REM sleep differed strikingly. DP in REM did not initially increase but declined steadily from age 6 to age 16 yr. We hypothesize that the DP decline in REM reflects maturation of the same brain arousal systems that eliminate delta waves in waking EEG. Whereas the DP age curves differed in NREM and REM sleep, theta age curves were similar in both, roughly paralleling the age trajectory of REM DP. The different maturational curves for NREM delta and theta indicate that they serve different brain functions despite having similar within-sleep dynamics and responses to sleep loss. Period-amplitude analysis of NREM and REM delta waveforms revealed that the age trends in DP were driven more by changes in wave amplitude rather than incidence. These data further document the powerful and complex link between sleep and brain maturation. Understanding this relationship would shed light on both brain development and the function of sleep.

Sleep Bruxism in Respiratory Medicine Practice.

PubMed

Mayer, Pierre; Heinzer, Raphael; Lavigne, Gilles

2016-01-01

Sleep bruxism (SB) consists of involuntary episodic and repetitive jaw muscle activity characterized by occasional tooth grinding or jaw clenching during sleep. Prevalence decreases from 20% to 14% in childhood to 8% to 3% in adulthood. Although the causes and mechanisms of idiopathic primary SB are unknown, putative candidates include psychologic risk factors (eg, anxiety, stress due to life events, hypervigilance) and sleep physiologic reactivity (eg, sleep arousals with autonomic activity, breathing events). Although certain neurotransmitters (serotonin, dopamine, noradrenalin, histamine) have been proposed to play an indirect role in SB, their exact contribution to rhythmic masticatory muscle activity (RMMA) (the electromyography marker of SB) genesis remains undetermined. No specific gene is associated with SB; familial environmental influence plays a significant role. To date, no single explanation can account for the SB mechanism. Secondary SB with sleep comorbidities that should be clinically assessed are insomnia, periodic limb movements during sleep, sleep-disordered breathing (eg, apnea-hypopnea), gastroesophageal reflux disease, and neurologic disorders (eg, sleep epilepsy, rapid eye movement behavior disorder). SB is currently quantified by scoring RMMA recordings in parallel with brain, respiratory, and heart activity recordings in a sleep laboratory or home setting. RMMA confirmation with audio-video recordings is recommended for better diagnostic accuracy in the presence of neurologic conditions. Management strategies (diagnostic tests, treatment) should be tailored to the patient's phenotype and comorbidities. In the presence of sleep-disordered breathing, a mandibular advancement appliance or CPAP treatment is preferred over single occlusal splint therapy on the upper jaw. Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Increased Sleep Promotes Survival during a Bacterial Infection in Drosophila

PubMed Central

Kuo, Tzu-Hsing; Williams, Julie A.

2014-01-01

Study Objectives: The relationship between sleep and immune function is not well understood at a functional or molecular level. We therefore used a genetic approach in Drosophila to manipulate sleep and evaluated effects on the ability of flies to fight bacterial infection. Setting: Laboratory. Participants: Drosophila melanogaster. Methods and Results: We used a genetic approach to transiently alter neuronal excitability in the mushroom body, a region in the central brain that is known to regulate sleep. Flies with increased sleep for up to two days prior to a bacterial infection showed increased resistance to the infection and improved survival. These flies also had increased expression levels of a subset of anti-microbial peptide mRNA prior to infection, as well as increased NFκB activity during infection as indicated by in vivo luciferase reporter activity. In contrast, flies that experienced reduced sleep for up to two days prior to infection had no effect on survival or on NFκB activity during infection. However, flies with reduced sleep showed an altered defense mechanism, such that resistance to infection was increased, but at the expense of reduced tolerance. This effect was dependent on environmental condition. Conclusions: Increasing sleep enhanced activity of an NFκB transcription factor, increased resistance to infection, and strongly promoted survival. Together, these findings support the hypothesis that sleep is beneficial to the host by maintaining a robust immune system. Citation: Kuo TH, Williams JA. Increased sleep promotes survival during a bacterial infection in Drosophila. SLEEP 2014;37(6):1077-1086. PMID:24882902

Chronic intermittent hypoxia induces changes on the expression and activity of neprilysin (EC 3.4.24.11) in the brain of rats.

PubMed

de Oliveira, Renato W; Julian, Guilherme S; Perry, Juliana C; Tufik, Sergio; Chagas, Jair R

2018-06-21

Obstructive sleep apnea (OSA) is a frequent sleeping breathing disorder associated with cognitive impairments. Neprilysin (NEP) is responsible for degrading several substrates related to cognition; however, the effect of chronic intermittent hypoxia (CIH) on NEP is still unknown. This study aimed to evaluate the expression and activity of NEP in cognitive-related brain structures of rats submitted to CIH. Western blot, qRT-PCR and enzyme activity assay, demonstrated that a six-week intermittent hypoxia increased NEP expression and activity, selectively in temporal cortex, but not in the hippocampus and frontal cortex. The increase in NEP activity and expression was reverted followed by two weeks recovery in normoxia. These data show that CIH protocol increases the expression and activity of NEP selectively in the temporal cortex. Additional mechanisms must be investigated to elucidate the effects of CIH in cognition. Copyright © 2018 Elsevier B.V. All rights reserved.

Resting brain activity varies with dream recall frequency between subjects.

PubMed

Eichenlaub, Jean-Baptiste; Nicolas, Alain; Daltrozzo, Jérôme; Redouté, Jérôme; Costes, Nicolas; Ruby, Perrine

2014-06-01

Dreaming is still poorly understood. Notably, its cerebral underpinning remains unclear. Neuropsychological studies have shown that lesions in the temporoparietal junction (TPJ) and/or the white matter of the medial prefrontal cortex (MPFC) lead to the global cessation of dream reports, suggesting that these regions of the default mode network have key roles in the dreaming process (forebrain 'dream-on' hypothesis). To test this hypothesis, we measured regional cerebral blood flow (rCBF) using [(15)O]H2O positron emission tomography in healthy subjects with high and low dream recall frequencies (DRFs) during wakefulness (rest) and sleep (rapid eye movement (REM) sleep, N2, and N3). Compared with Low recallers (0.5 ± 0.3 dream recall per week in average), High recallers (5.2 ± 1.4) showed higher rCBF in the TPJ during REM sleep, N3, and wakefulness, and in the MPFC during REM sleep and wakefulness. We demonstrate that the resting states of High recallers and Low recallers differ during sleep and wakefulness. It coheres with previous ERP results and confirms that a high/low DRF is associated with a specific functional organization of the brain. These results support the forebrain 'dream-on' hypothesis and suggest that TPJ and MPFC are not only involved in dream recall during wakefulness but also have a role in dreaming during sleep (production and/or encoding). Increased activity in the TPJ and MPFC might promote the mental imagery and/or memory encoding of dreams. Notably, increased activity in TPJ might facilitate attention orienting toward external stimuli and promote intrasleep wakefulness, facilitating the encoding of the dreams in memory.

Resting Brain Activity Varies with Dream Recall Frequency Between Subjects

PubMed Central

Eichenlaub, Jean-Baptiste; Nicolas, Alain; Daltrozzo, Jérôme; Redouté, Jérôme; Costes, Nicolas; Ruby, Perrine

2014-01-01

Dreaming is still poorly understood. Notably, its cerebral underpinning remains unclear. Neuropsychological studies have shown that lesions in the temporoparietal junction (TPJ) and/or the white matter of the medial prefrontal cortex (MPFC) lead to the global cessation of dream reports, suggesting that these regions of the default mode network have key roles in the dreaming process (forebrain ‘dream-on' hypothesis). To test this hypothesis, we measured regional cerebral blood flow (rCBF) using [15O]H2O positron emission tomography in healthy subjects with high and low dream recall frequencies (DRFs) during wakefulness (rest) and sleep (rapid eye movement (REM) sleep, N2, and N3). Compared with Low recallers (0.5±0.3 dream recall per week in average), High recallers (5.2±1.4) showed higher rCBF in the TPJ during REM sleep, N3, and wakefulness, and in the MPFC during REM sleep and wakefulness. We demonstrate that the resting states of High recallers and Low recallers differ during sleep and wakefulness. It coheres with previous ERP results and confirms that a high/low DRF is associated with a specific functional organization of the brain. These results support the forebrain ‘dream-on' hypothesis and suggest that TPJ and MPFC are not only involved in dream recall during wakefulness but also have a role in dreaming during sleep (production and/or encoding). Increased activity in the TPJ and MPFC might promote the mental imagery and/or memory encoding of dreams. Notably, increased activity in TPJ might facilitate attention orienting toward external stimuli and promote intrasleep wakefulness, facilitating the encoding of the dreams in memory. PMID:24549103

Experimental Evidence for Phase Synchronization Transitions in the Human Cardiorespiratory System

NASA Astrophysics Data System (ADS)

Bartsch, Ronny; Kantelhardt, Jan W.; Penzel, Thomas; Havlin, Shlomo

2007-02-01

Transitions in the dynamics of complex systems can be characterized by changes in the synchronization behavior of their components. Taking the human cardiorespiratory system as an example and using an automated procedure for screening the synchrograms of 112 healthy subjects we study the frequency and the distribution of synchronization episodes under different physiological conditions that occur during sleep. We find that phase synchronization between heartbeat and breathing is significantly enhanced during non-rapid-eye-movement (non-REM) sleep (deep sleep and light sleep) and reduced during REM sleep. Our results suggest that the synchronization is mainly due to a weak influence of the breathing oscillator upon the heartbeat oscillator, which is disturbed in the presence of long-term correlated noise, superimposed by the activity of higher brain regions during REM sleep.

Evaluating Sleep Disturbance: A Review of Methods

NASA Technical Reports Server (NTRS)

Smith, Roy M.; Oyung, R.; Gregory, K.; Miller, D.; Rosekind, M.; Rosekind, Mark R. (Technical Monitor)

1996-01-01

There are three general approaches to evaluating sleep disturbance in regards to noise: subjective, behavioral, and physiological. Subjective methods range from standardized questionnaires and scales to self-report measures designed for specific research questions. There are two behavioral methods that provide useful sleep disturbance data. One behavioral method is actigraphy, a motion detector that provides an empirical estimate of sleep quantity and quality. An actigraph, worn on the non-dominant wrist, provides a 24-hr estimate of the rest/activity cycle. The other method involves a behavioral response, either to a specific probe or stimuli or subject initiated (e.g., indicating wakefulness). The classic, gold standard for evaluating sleep disturbance is continuous physiological monitoring of brain, eye, and muscle activity. This allows detailed distinctions of the states and stages of sleep, awakenings, and sleep continuity. Physiological delta can be obtained in controlled laboratory settings and in natural environments. Current ambulatory physiological recording equipment allows evaluation in home and work settings. These approaches will be described and the relative strengths and limitations of each method will be discussed.

Sleeping brain, learning brain. The role of sleep for memory systems.

PubMed

Peigneux, P; Laureys, S; Delbeuck, X; Maquet, P

2001-12-21

The hypothesis that sleep participates in the consolidation of recent memory traces has been investigated using four main paradigms: (1) effects of post-training sleep deprivation on memory consolidation, (2) effects of learning on post-training sleep, (3) effects of within sleep stimulation on the sleep pattern and on overnight memories, and (4) re-expression of behavior-specific neural patterns during post-training sleep. These studies convincingly support the idea that sleep is deeply involved in memory functions in humans and animals. However, the available data still remain too scarce to confirm or reject unequivocally the recently upheld hypothesis that consolidations of non-declarative and declarative memories are respectively dependent upon REM and NREM sleep processes.

Altered Sleep Homeostasis in Rev-erbα Knockout Mice

PubMed Central

Mang, Géraldine M.; La Spada, Francesco; Emmenegger, Yann; Chappuis, Sylvie; Ripperger, Jürgen A.; Albrecht, Urs; Franken, Paul

2016-01-01

Study Objectives: The nuclear receptor REV-ERBα is a potent, constitutive transcriptional repressor critical for the regulation of key circadian and metabolic genes. Recently, REV-ERBα's involvement in learning, neurogenesis, mood, and dopamine turnover was demonstrated suggesting a specific role in central nervous system functioning. We have previously shown that the brain expression of several core clock genes, including Rev-erbα, is modulated by sleep loss. We here test the consequences of a loss of REV-ERBα on the homeostatic regulation of sleep. Methods: EEG/EMG signals were recorded in Rev-erbα knockout (KO) mice and their wild type (WT) littermates during baseline, sleep deprivation, and recovery. Cortical gene expression measurements after sleep deprivation were contrasted to baseline. Results: Although baseline sleep/wake duration was remarkably similar, KO mice showed an advance of the sleep/wake distribution relative to the light-dark cycle. After sleep onset in baseline and after sleep deprivation, both EEG delta power (1–4 Hz) and sleep consolidation were reduced in KO mice indicating a slower increase of homeostatic sleep need during wakefulness. This slower increase might relate to the smaller increase in theta and gamma power observed in the waking EEG prior to sleep onset under both conditions. Indeed, the increased theta activity during wakefulness predicted delta power in subsequent NREM sleep. Lack of Rev-erbα increased Bmal1, Npas2, Clock, and Fabp7 expression, confirming the direct regulation of these genes by REV-ERBα also in the brain. Conclusions: Our results add further proof to the notion that clock genes are involved in sleep homeostasis. Because accumulating evidence directly links REV-ERBα to dopamine signaling the altered homeostatic regulation of sleep reported here are discussed in that context. Citation: Mang GM, La Spada F, Emmenegger Y, Chappuis S, Ripperger JA, Albrecht U, Franken P. Altered sleep homeostasis in Rev-erbα knockout mice. SLEEP 2016;39(3):589–601. PMID:26564124

Evidence for Neuroinflammatory and Microglial Changes in the Cerebral Response to Sleep Loss

PubMed Central

Wisor, Jonathan P.; Schmidt, Michelle A.; Clegern, William C.

2011-01-01

Study Objectives: Sleep loss has pro-inflammatory effects, but the roles of specific cell populations in mediating these effects have not been delineated. We assessed the modulation of the electroencephalographic and molecular responses to sleep deprivation (S-DEP) by minocycline, a compound that attenuates microglial activation occurring in association with neuroinflammatory events. Design: Laboratory rodents were subjected to assessment of sleep and wake in baseline and sleep deprived conditions. Participants: Adult male CD-1 mice (30-35 g) subjected to telemetric electroencephalography. Interventions: Minocycline was administered daily. Mice were subjected to baseline data collection on the first day of minocycline administration and, on subsequent days, 2 S-DEP sessions, 1 and 3 h in duration, followed by recovery sleep. Following EEG studies, mice were euthanized either at the end of a 3 h S-DEP or as time-of day controls for sampling of brain messenger RNAs. Gene expression was measured by real-time polymerase chain reaction. Measurements and Results: Minocycline-treated mice exhibited a reduction in time spent asleep, relative to saline-treated mice, in the 3-h interval immediately after administration. S-DEP resulted in an increase in EEG slow wave activity relative to baseline in saline-treated mice. This response to S-DEP was abolished in animals subjected to chronic minocycline administration. S-DEP suppressed the expression of the microglial-specific transcript cd11b and the neuroinflammation marker peripheral benzodiazepine receptor, in the brain at the mRNA level. Minocycline attenuated the elevation of c-fos expression by S-DEP. Brain levels of pro-inflammatory cytokine mRNAs interleukin-1β (il-1β), interleukin-6 (il-6), and tumor necrosis factor-α (tnfα) were unaffected by S-DEP, but were elevated in minocycline-treated mice relative to saline-treated mice. Conclusions: The anti-neuroinflammatory agent minocycline prevents either the buildup or expression of sleep need in rodents. The molecular mechanism underlying this effect is not known, but it is not mediated by suppression of il-1β, il-6, and tnfα at the transcript level. Citation: Wisor JP; Schmidt MA; Clegern WC. Evidence for neuroinflammatory and microglial changes in the cerebral response to sleep loss. SLEEP 2011;34(3):261-272. PMID:21358843

Frontal Underactivation During Working Memory Processing in Adults With Acute Partial Sleep Deprivation: A Near-Infrared Spectroscopy Study.

PubMed

Yeung, Michael K; Lee, Tsz L; Cheung, Winnie K; Chan, Agnes S

2018-01-01

Individuals with partial sleep deprivation may have working memory (WM) impairment, but the underlying neural mechanism of this phenomenon is relatively unknown. The present study examined neural processing during WM performance in individuals with and without partial sleep deprivation using near-infrared spectroscopy (NIRS). Forty college students (10 males) were equally split into Sufficient Sleep (SS) and Insufficient Sleep (IS) groups based on self-reports of previous night's sleep duration. Participants in the SS group obtained the recommended amounts of sleep according to various sleep organizations (i.e., >7.0 h), whereas those in the IS group obtained amounts of sleep no greater than the lower limit of the recommendation (i.e., ≤7.0 h). All participants underwent an n -back paradigm with a WM load (i.e., 3-back) and a control condition (i.e., 0-back) while their prefrontal hemodynamics were recorded by NIRS. The IS and SS groups performed the tasks comparably well. However, unlike the SS group, which exhibited bilateral frontal activation indicated by increased oxyhemoglobin concentration and decreased deoxyhemoglobin concentration during WM processing (i.e., 3-back > 0-back), the IS group did not exhibit such activation. In addition, levels of WM-related frontal activation, especially those on the left side, correlated with sleep duration the night before, even when habitual sleep duration was controlled for. The findings suggest the presence of frontal lobe dysfunction in the absence of evident WM difficulties in individuals with acute partial sleep deprivation. They also highlight the importance of a good night's sleep to brain health.

The role of sleep in human declarative memory consolidation.

PubMed

Alger, Sara E; Chambers, Alexis M; Cunningham, Tony; Payne, Jessica D

2015-01-01

Through a variety of methods, researchers have begun unraveling the mystery of why humans spend one-third of their lives asleep. Though sleep likely serves multiple functions, it has become clear that the sleeping brain offers an ideal environment for solidifying newly learned information in the brain. Sleep , which comprises a complex collection of brain states, supports the consolidation of many different types of information. It not only promotes learning and memory stabilization, but also memory reorganization that can lead to various forms of insightful behavior. As this chapter will describe, research provides ample support for these crucial cognitive functions of sleep . Focusing on the declarative memory system in humans, we review the literature regarding the benefits of sleep for both neutral and emotionally salient declarative memory. Finally, we discuss the literature regarding the impact of sleep on emotion regulation.

Glymphatic clearance controls state-dependent changes in brain lactate concentration

PubMed Central

Lu, Minh Lon; Yang, Ezra; Peng, Weiguo; Mestre, Humberto; Hitomi, Emi; Deane, Rashid; Nedergaard, Maiken

2016-01-01

Brain lactate concentration is higher during wakefulness than in sleep. However, it is unknown why arousal is linked to an increase in brain lactate and why lactate declines within minutes of sleep. Here, we show that the glymphatic system is responsible for state-dependent changes in brain lactate concentration. Suppression of glymphatic function via acetazolamide treatment, cisterna magna puncture, aquaporin 4 deletion, or changes in body position reduced the decline in brain lactate normally observed when awake mice transition into sleep or anesthesia. Concurrently, the same manipulations diminished accumulation of lactate in cervical, but not in inguinal lymph nodes when mice were anesthetized. Thus, our study suggests that brain lactate is an excellent biomarker of the sleep–wake cycle and increases further during sleep deprivation, because brain lactate is inversely correlated with glymphatic-lymphatic clearance. This analysis provides fundamental new insight into brain energy metabolism by demonstrating that glucose that is not fully oxidized can be exported as lactate via glymphatic-lymphatic fluid transport. PMID:27481936

Nonimpact brain injury: neuropsychological and behavioral correlates with consideration of physiological findings.

PubMed

Henry, G K; Gross, H S; Herndon, C A; Furst, C J

2000-01-01

This retrospective clinical study investigated the neuropsychological, physiological, and behavioral functioning of 32 adult outpatients up to 65 months following nonimpact brain injury (i.e., whiplash). All participants were administered a flexible battery of cognitive tests, and some underwent neurodiagnostic procedures and sleep studies. Compared with published norms, neuropsychological data revealed significant and persistent age-adjusted cognitive deficits, primarily in the area of executive functioning. Participants frequently complained of problems with behavioral control, sleep, and sexuality. Although structural neuroimaging was not sensitive in detecting brain pathology, quantitative electroencephalography was abnormal in all the participants evaluated, showing frontocentral slowing and increased spike wave activity. We propose that whiplash injury can produce wide-ranging circuitry dysfunction and that test selection is critical in identifying cognitive deficits.

A transition in brain state during propofol-induced unconsciousness.

PubMed

Mukamel, Eran A; Pirondini, Elvira; Babadi, Behtash; Wong, Kin Foon Kevin; Pierce, Eric T; Harrell, P Grace; Walsh, John L; Salazar-Gomez, Andres F; Cash, Sydney S; Eskandar, Emad N; Weiner, Veronica S; Brown, Emery N; Purdon, Patrick L

2014-01-15

Rhythmic oscillations shape cortical dynamics during active behavior, sleep, and general anesthesia. Cross-frequency phase-amplitude coupling is a prominent feature of cortical oscillations, but its role in organizing conscious and unconscious brain states is poorly understood. Using high-density EEG and intracranial electrocorticography during gradual induction of propofol general anesthesia in humans, we discovered a rapid drug-induced transition between distinct states with opposite phase-amplitude coupling and different cortical source distributions. One state occurs during unconsciousness and may be similar to sleep slow oscillations. A second state occurs at the loss or recovery of consciousness and resembles an enhanced slow cortical potential. These results provide objective electrophysiological landmarks of distinct unconscious brain states, and could be used to help improve EEG-based monitoring for general anesthesia.

Age-Dependency of Location of Epileptic Foci in "Continuous Spike-and-Waves during Sleep": A Parallel to the Posterior-Anterior Trajectory of Slow Wave Activity.

PubMed

Bölsterli Heinzle, Bigna Katrin; Bast, Thomas; Critelli, Hanne; Huber, Reto; Schmitt, Bernhard

2017-02-01

Epileptic encephalopathy with continuous spike-and-waves during sleep (CSWS) occurs during childhood and is characterized by an activation of spike wave complexes during slow wave sleep. The location of epileptic foci is variable, as is etiology. A relationship between the epileptic focus and age has been shown in various focal epilepsies following a posterior-anterior trajectory, and a link to brain maturation has been proposed. We hypothesize that in CSWS, maximal spike wave activity, corresponding to the epileptic focus, is related to age and shows a posterior-anterior evolution. In a retrospective cross-sectional study on CSWS (22 EEGs of 22 patients aged 3.1–13.5 years), the location of the epileptic focus is related to age and follows a posterior-anterior course. Younger patients are more likely to have posterior foci than older ones. We propose that the posterior-anterior trajectory of maximal spike waves in CSWS might reflect maturational changes of maximal expression of sleep slow waves, which follow a comparable course. Epileptic spike waves, that is, “hyper-synchronized slow waves” may occur at the place where the highest and therefore most synchronized slow waves meet brain tissue with an increased susceptibility to synchronization. Georg Thieme Verlag KG Stuttgart · New York.

Desynchronization of slow oscillations in the basal ganglia during natural sleep.

PubMed

Mizrahi-Kliger, Aviv D; Kaplan, Alexander; Israel, Zvi; Bergman, Hagai

2018-05-01

Slow oscillations of neuronal activity alternating between firing and silence are a hallmark of slow-wave sleep (SWS). These oscillations reflect the default activity present in all mammalian species, and are ubiquitous to anesthesia, brain slice preparations, and neuronal cultures. In all these cases, neuronal firing is highly synchronous within local circuits, suggesting that oscillation-synchronization coupling may be a governing principle of sleep physiology regardless of anatomical connectivity. To investigate whether this principle applies to overall brain organization, we recorded the activity of individual neurons from basal ganglia (BG) structures and the thalamocortical (TC) network over 70 full nights of natural sleep in two vervet monkeys. During SWS, BG neurons manifested slow oscillations (∼0.5 Hz) in firing rate that were as prominent as in the TC network. However, in sharp contrast to any neural substrate explored thus far, the slow oscillations in all BG structures were completely desynchronized between individual neurons. Furthermore, whereas in the TC network single-cell spiking was locked to slow oscillations in the local field potential (LFP), the BG LFP exhibited only weak slow oscillatory activity and failed to entrain nearby cells. We thus show that synchrony is not inherent to slow oscillations, and propose that the BG desynchronization of slow oscillations could stem from its unique anatomy and functional connectivity. Finally, we posit that BG slow-oscillation desynchronization may further the reemergence of slow-oscillation traveling waves from multiple independent origins in the frontal cortex, thus significantly contributing to normal SWS.

Quantitative differences among EMG activities of muscles innervated by subpopulations of hypoglossal and upper spinal motoneurons during non-REM sleep - REM sleep transitions: a window on neural processes in the sleeping brain.

PubMed

Rukhadze, I; Kamani, H; Kubin, L

2011-12-01

In the rat, a species widely used to study the neural mechanisms of sleep and motor control, lingual electromyographic activity (EMG) is minimal during non-rapid eye movement (non-REM) sleep and then phasic twitches gradually increase after the onset of REM sleep. To better characterize the central neural processes underlying this pattern, we quantified EMG of muscles innervated by distinct subpopulations of hypoglossal motoneurons and nuchal (N) EMG during transitions from non-REM sleep to REM sleep. In 8 chronically instrumented rats, we recorded cortical EEG, EMG at sites near the base of the tongue where genioglossal and intrinsic muscle fibers predominate (GG-I), EMG of the geniohyoid (GH) muscle, and N EMG. Sleep-wake states were identified and EMGs quantified relative to their mean levels in wakefulness in successive 10 s epochs. During non-REM sleep, the average EMG levels differed among the three muscles, with the order being N>GH>GG-I. During REM sleep, due to different magnitudes of phasic twitches, the order was reversed to GG-I>GH>N. GG-I and GH exhibited a gradual increase of twitching that peaked at 70-120 s after the onset of REM sleep and then declined if the REM sleep episode lasted longer. We propose that a common phasic excitatory generator impinges on motoneuron pools that innervate different muscles, but twitching magnitudes are different due to different levels of tonic motoneuronal hyperpolarization. We also propose that REM sleep episodes of average durations are terminated by intense activity of the central generator of phasic events, whereas long REM sleep episodes end as a result of a gradual waning of the tonic disfacilitatory and inhibitory processes.

Sleep Disorders Associated With Mild Traumatic Brain Injury Using Sport Concussion Assessment Tool 3.

PubMed

Tkachenko, Nataliya; Singh, Kanwaljit; Hasanaj, Lisena; Serrano, Liliana; Kothare, Sanjeev V

2016-04-01

Sleep problems affect 30% to 80% of patients with mild traumatic brain injury. We assessed the prevalence of sleep disorders after mild traumatic brain injury and its correlation with other symptoms. Individuals with mild traumatic brain injury were assessed at the New York University Concussion Center during 2013-2014 with the Sports Concussion Assessment Tool, third edition, data following mild traumatic brain injury. The relationship between sleep problems (drowsiness, difficulty falling asleep, fatigue or low energy), psychiatric symptoms (sadness, nervousness or anxiousness), headache, and dizziness were analyzed by Spearman correlation and logistic regression using moderate to severe versus none to mild categorization. Ninety-three patients were retrospectively considered. The most common injury causes were falls (34.4%) and motor vehicle accidents (21.5%). There was a positive correlation between dizziness, headache, psychiatric problems (sadness, anxiety, irritability), and sleep problems (fatigue, drowsiness, and difficulty falling asleep) (P < 0.001). Logistic regression showed a significant association between moderate to severe psychiatric symptoms and moderate to severe sleep symptoms (P < 0.05). Sleep symptoms became more severe with increased time interval from mild traumatic brain injury to Sport Concussion Assessment Tool 3 administration (odds ratio = 1.005, 1.006, and 1.008, P < 0.05). There was significant correlation between motor vehicle accident and drowsiness and difficulty falling asleep (P < 0.05). Medications given in the emergency department had a positive correlation with drowsiness (P < 0.05). Individuals who report moderate to severe headache, dizziness, and psychiatric symptoms have a higher likelihood of reporting moderate to severe sleep disorders following mild traumatic brain injury and should be counseled and initiated with early interventions. Copyright © 2016 Elsevier Inc. All rights reserved.

Comparison of NREM sleep and intravenous sedation through local information processing and whole brain network to explore the mechanism of general anesthesia.

PubMed

Li, Yun; Wang, Shengpei; Pan, Chuxiong; Xue, Fushan; Xian, Junfang; Huang, Yaqi; Wang, Xiaoyi; Li, Tianzuo; He, Huiguang

2018-01-01

The mechanism of general anesthesia (GA) has been explored for hundreds of years, but unclear. Previous studies indicated a possible correlation between NREM sleep and GA. The purpose of this study is to compare them by in vivo human brain function to probe the neuromechanism of consciousness, so as to find out a clue to GA mechanism. 24 healthy participants were equally assigned to sleep or propofol sedation group by sleeping ability. EEG and Ramsay Sedation Scale were applied to determine sleep stage and sedation depth respectively. Resting-state functional magnetic resonance imaging (RS-fMRI) was acquired at each status. Regional homogeneity (ReHo) and seed-based whole brain functional connectivity maps (WB-FC maps) were compared. During sleep, ReHo primarily weakened on frontal lobe (especially preoptic area), but strengthened on brainstem. While during sedation, ReHo changed in various brain areas, including cingulate, precuneus, thalamus and cerebellum. Cingulate, fusiform and insula were concomitance of sleep and sedation. Comparing to sleep, FCs between the cortex and subcortical centers (centralized in cerebellum) were significantly attenuated under sedation. As sedation deepening, cerebellum-based FC maps were diminished, while thalamus- and brainstem-based FC maps were increased. There're huge distinctions in human brain function between sleep and GA. Sleep mainly rely on brainstem and frontal lobe function, while sedation is prone to affect widespread functional network. The most significant differences exist in the precuneus and cingulate, which may play important roles in mechanisms of inducing unconciousness by anesthetics. Institutional Review Board (IRB) ChiCTR-IOC-15007454.

Treatment of Sleep Disorders after Traumatic Brain Injury

PubMed Central

Castriotta, Richard J.; Atanasov, Strahil; Wilde, Mark C.; Masel, Brent E.; Lai, Jenny M.; Kuna, Samuel T.

2009-01-01

Study Objectives: Determine whether treatment of sleep disorders identified in brain injured adults would result in resolution of those sleep disorders and improvement of symptoms and daytime function. Methods: Prospective evaluation of unselected traumatic brain injury patients with nocturnal polysomnography (NPSG), multiple sleep latency test (MSLT), Epworth Sleepiness Scale (ESS), and neuropsychological testing including Psychomotor Vigilance Test (PVT), Profile of Mood States (POMS), and Functional Outcome of Sleep Questionnaire (FOSQ) before and after treatment with continuous positive airway pressure (CPAP) for obstructive sleep apnea (OSA), modafinil (200 mg) for narcolepsy and posttraumatic hypersomnia (PTH), or pramipexole (0.375 mg) for periodic limb movements in sleep (PLMS). Setting: Three academic medical centers. Participants: Fifty-seven (57) adults ≥ 3 months post traumatic brain injury (TBI). Measurements And Results: Abnormal sleep studies were found in 22 subjects (39%), of whom 13 (23%) had OSA, 2 (3%) had PTH, 3 (5%) had narcolepsy, 4 (7%) had PLMS, and 12 had objective excessive daytime sleepiness with MSLT score < 10 minutes. Apneas, hypopneas, and snoring were eliminated by CPAP in OSA subjects, but there was no significant change in MSLT scores. Periodic limb movements were eliminated with pramipexole. One of 3 narcolepsy subjects and 1 of 2 PTH subjects had resolution of hypersomnia with modafinil. There was no significant change in FOSQ, POMS, or PVT results after treatment. Conclusions: Treatment of sleep disorders after TBI may result in polysomnographic resolution without change in sleepiness or neuropsychological function. Citation: Castriotta RJ; Atanasov S; Wilde MC; Masel BE; Lai JM; Kuna ST. Treatment of sleep disorders after traumatic brain injury. J Clin Sleep Med 2009;5(2):137-144. PMID:19968047

Biomedical application of wavelets: analysis of electroencephalograph signals for monitoring depth of anesthesia

NASA Astrophysics Data System (ADS)

Abbate, Agostino; Nayak, A.; Koay, J.; Roy, R. J.; Das, Pankaj K.

1996-03-01

The wavelet transform (WT) has been used to study the nonstationary information in the electroencephalograph (EEG) as an aid in determining the anesthetic depth. A complex analytic mother wavelet is utilized to obtain the time evolution of the various spectral components of the EEG signal. The technique is utilized for the detection and spectral analysis of transient and background processes in the awake and asleep states. It can be observed that the response of both states before the application of the stimulus is similar in amplitude but not in spectral contents, which suggests a background activity of the brain. The brain reacts to the external stimulus in two different modes depending on the state of consciousness of the subject. In the case of awake state, there is an evident increase in response, while for the sleep state a reduction in this activity is observed. This analysis seems to suggest that the brain has an ongoing background process that monitors external stimulus in both the sleep and awake states.

Effects of acute microinjections of the thyroid hormone derivative 3-iodothyronamine to the preoptic region of adult male rats on sleep, thermoregulation and motor activity

PubMed Central

James, Thomas D.; Moffett, Steven X.; Scanlan, Thomas S.; Martin, Joseph V.

2014-01-01

The decarboxylated thyroid hormone derivative 3-iodothyronamine (T1AM) has been reported as having behavioral and physiological consequences distinct from those of thyroid hormones. Here, we investigate the effects of T1AM on EEG-defined sleep after acute administration to the preoptic region of adult male rats. Our laboratory recently demonstrated a decrease in EEG-defined sleep after administration of 3,3′,5-triiodo-L-thyronine (T3) to the same brain region. After injection of T1AM or vehicle solution, EEG, EMG, activity, and core body temperature were recorded for 24 h. Sleep parameters were determined from EEG and EMG data. Earlier investigations found contrasting systemic effects of T3 and T1AM, such as decreased heart rate and body temperature after intraperitoneal T1AM injection. However, nREM sleep was decreased in the present study after injections of 1 or 3 μg T1AM, but not after 0.3 or 10 μg, closely mimicking the previously reported effects of T3 administration to the preoptic region. The biphasic dose–response observed after either T1AM or T3 administration seems to indicate shared mechanisms and/or functions of sleep regulation in the preoptic region. Consistent with systemic administration of T1AM, however, microinjection of T1AM decreased body temperature. The current study is the first to show modulation of sleep by T1AM, and suggests that T1AM and T3 have both shared and independent effects in the adult mammalian brain. PMID:23702093

The brain functional connectome is robustly altered by lack of sleep.

PubMed

Kaufmann, Tobias; Elvsåshagen, Torbjørn; Alnæs, Dag; Zak, Nathalia; Pedersen, Per Ø; Norbom, Linn B; Quraishi, Sophia H; Tagliazucchi, Enzo; Laufs, Helmut; Bjørnerud, Atle; Malt, Ulrik F; Andreassen, Ole A; Roussos, Evangelos; Duff, Eugene P; Smith, Stephen M; Groote, Inge R; Westlye, Lars T

2016-02-15

Sleep is a universal phenomenon necessary for maintaining homeostasis and function across a range of organs. Lack of sleep has severe health-related consequences affecting whole-body functioning, yet no other organ is as severely affected as the brain. The neurophysiological mechanisms underlying these deficits are poorly understood. Here, we characterize the dynamic changes in brain connectivity profiles inflicted by sleep deprivation and how they deviate from regular daily variability. To this end, we obtained functional magnetic resonance imaging data from 60 young, adult male participants, scanned in the morning and evening of the same day and again the following morning. 41 participants underwent total sleep deprivation before the third scan, whereas the remainder had another night of regular sleep. Sleep deprivation strongly altered the connectivity of several resting-state networks, including dorsal attention, default mode, and hippocampal networks. Multivariate classification based on connectivity profiles predicted deprivation state with high accuracy, corroborating the robustness of the findings on an individual level. Finally, correlation analysis suggested that morning-to-evening connectivity changes were reverted by sleep (control group)-a pattern which did not occur after deprivation. We conclude that both, a day of waking and a night of sleep deprivation dynamically alter the brain functional connectome. Copyright © 2015 Elsevier Inc. All rights reserved.

EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation.

PubMed

Freyburger, Marlène; Pierre, Audrey; Paquette, Gabrielle; Bélanger-Nelson, Erika; Bedont, Joseph; Gaudreault, Pierre-Olivier; Drolet, Guy; Laforest, Sylvie; Blackshaw, Seth; Cermakian, Nicolas; Doucet, Guy; Mongrain, Valérie

2016-03-01

Optimal sleep is ensured by the interaction of circadian and homeostatic processes. Although synaptic plasticity seems to contribute to both processes, the specific players involved are not well understood. The EphA4 tyrosine kinase receptor is a cell adhesion protein regulating synaptic plasticity. We investigated the role of EphA4 in sleep regulation using electrocorticography in mice lacking EphA4 and gene expression measurements. EphA4 knockout (KO) mice, Clock(Δ19/Δ19) mutant mice and littermates, C57BL/6J and CD-1 mice, and Sprague-Dawley rats were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SLD), and submitted to a 48 h electrophysiological recording and/or brain sampling at different time of day. EphA4 KO mice showed less rapid eye movement sleep (REMS), enhanced duration of individual bouts of wakefulness and nonrapid eye movement sleep (NREMS) during the light period, and a blunted daily rhythm of NREMS sigma activity. The NREMS delta activity response to SLD was unchanged in EphA4 KO mice. However, SLD increased EphA4 expression in the thalamic/hypothalamic region in C57BL/6J mice. We further show the presence of E-boxes in the promoter region of EphA4, a lower expression of EphA4 in Clock mutant mice, a rhythmic expression of EphA4 ligands in several brain areas, expression of EphA4 in the suprachiasmatic nuclei of the hypothalamus (SCN), and finally an unchanged number of cells expressing Vip, Grp and Avp in the SCN of EphA4 KO mice. Our results suggest that EphA4 is involved in circadian sleep regulation. © 2016 Associated Professional Sleep Societies, LLC.

Acute Sleep Deprivation Induces a Local Brain Transfer Information Increase in the Frontal Cortex in a Widespread Decrease Context.

PubMed

Alonso, Joan F; Romero, Sergio; Mañanas, Miguel A; Alcalá, Marta; Antonijoan, Rosa M; Giménez, Sandra

2016-04-14

Sleep deprivation (SD) has adverse effects on mental and physical health, affecting the cognitive abilities and emotional states. Specifically, cognitive functions and alertness are known to decrease after SD. The aim of this work was to identify the directional information transfer after SD on scalp EEG signals using transfer entropy (TE). Using a robust methodology based on EEG recordings of 18 volunteers deprived from sleep for 36 h, TE and spectral analysis were performed to characterize EEG data acquired every 2 h. Correlation between connectivity measures and subjective somnolence was assessed. In general, TE showed medium- and long-range significant decreases originated at the occipital areas and directed towards different regions, which could be interpreted as the transfer of predictive information from parieto-occipital activity to the rest of the head. Simultaneously, short-range increases were obtained for the frontal areas, following a consistent and robust time course with significant maps after 20 h of sleep deprivation. Changes during sleep deprivation in brain network were measured effectively by TE, which showed increased local connectivity and diminished global integration. TE is an objective measure that could be used as a potential measure of sleep pressure and somnolence with the additional property of directed relationships.

Acute enhancement of non-rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride.

PubMed

Unno, Katsuya; Yamoto, Kurumi; Takeuchi, Kouhei; Kataoka, Aya; Ozaki, Tomoya; Mochizuki, Takatoshi; Honda, Kazuki; Miura, Nobuhiko; Ikeda, Masayuki

2014-02-01

Cadmium (Cd) is a heavy metal widely used or effused by industries. Serious environmental Cd pollution has been reported over the past two centuries, whereas the mechanisms underlying Cd-mediated diseases are not fully understood. Interestingly, an increase in reactive oxygen species (ROS) after Cd exposure has been shown. Our group has demonstrated that sleep is triggered via accumulation of ROS during neuronal activities, and we thus hypothesize the involvement of Cd poisoning in sleep-wake irregularities. In the present study, we analyzed the effects of Cd intake (1-100 ppm CdCl₂ in drinking water) on rats by monitoring sleep encephalograms and locomotor activities. The results demonstrated that 100 ppm CdCl₂ administration for 28 h was sufficient to increase non-rapid-eye-movement (non-REM) sleep and reduce locomotor activities during the night (the rat active phase). In contrast, free-running locomotor rhythms under constant dim red light and their re-entrainment to 12:12-h light/dark cycles were intact under chronic (1 month) 100 ppm CdCl₂ administrations, suggesting a limited influence on circadian clock movements at this dosage. The relative amount of oxidized glutathione increased in the brain after the 28-h 100 ppm CdCl₂ administrations similar to the levels in cultured astrocytes receiving H₂O₂ or CdCl₂ in culture medium. Therefore, we propose Cd-induced sleep as a consequence of oxidative stress. As oxidized glutathione is an endogenous sleep substance, we suggest that Cd rapidly induces sleepiness and influences activity performance by occupying intrinsic sleep-inducing mechanisms. In conclusion, we propose increased non-REM sleep during the active phase as an index of acute Cd exposure. Copyright © 2013 John Wiley & Sons, Ltd.

Functional Anatomy of Non-REM Sleep

PubMed Central

de Andrés, Isabel; Garzón, Miguel; Reinoso-Suárez, Fernando

2011-01-01

The state of non-REM sleep (NREM), or slow wave sleep, is associated with a synchronized EEG pattern in which sleep spindles and/or K complexes and high-voltage slow wave activity (SWA) can be recorded over the entire cortical surface. In humans, NREM is subdivided into stages 2 and 3–4 (presently named N3) depending on the proportions of each of these polygraphic events. NREM is necessary for normal physical and intellectual performance and behavior. An overview of the brain structures involved in NREM generation shows that the thalamus and the cerebral cortex are absolutely necessary for the most significant bioelectric and behavioral events of NREM to be expressed; other structures like the basal forebrain, anterior hypothalamus, cerebellum, caudal brain stem, spinal cord and peripheral nerves contribute to NREM regulation and modulation. In NREM stage 2, sustained hyperpolarized membrane potential levels resulting from interaction between thalamic reticular and projection neurons gives rise to spindle oscillations in the membrane potential; the initiation and termination of individual spindle sequences depends on corticothalamic activities. Cortical and thalamic mechanisms are also involved in the generation of EEG delta SWA that appears in deep stage 3–4 (N3) NREM; the cortex has classically been considered to be the structure that generates this activity, but delta oscillations can also be generated in thalamocortical neurons. NREM is probably necessary to normalize synapses to a sustainable basal condition that can ensure cellular homeostasis. Sleep homeostasis depends not only on the duration of prior wakefulness but also on its intensity, and sleep need increases when wakefulness is associated with learning. NREM seems to ensure cell homeostasis by reducing the number of synaptic connections to a basic level; based on simple energy demands, cerebral energy economizing during NREM sleep is one of the prevalent hypotheses to explain NREM homeostasis. PMID:22110467

Influence of chronic moderate sleep restriction and exercise training on anxiety, spatial memory, and associated neurobiological measures in mice.

PubMed

Zielinski, Mark R; Davis, J Mark; Fadel, James R; Youngstedt, Shawn D

2013-08-01

Sleep deprivation can have deleterious effects on cognitive function and mental health. Moderate exercise training has myriad beneficial effects on cognition and mental health. However, physiological and behavioral effects of chronic moderate sleep restriction and its interaction with common activities, such as moderate exercise training, have received little investigation. The aims of this study were to examine the effects of chronic moderate sleep restriction and moderate exercise training on anxiety-related behavior, spatial memory, and neurobiological correlates in mice. Male mice were randomized to one of four 11-week treatments in a 2 [sleep restriction (∼4h loss/day) vs. ad libitum sleep] × 2 [exercise (1h/day/6 d/wk) vs. sedentary activity] experimental design. Anxiety-related behavior was assessed with the elevated-plus maze, and spatial learning and memory were assessed with the Morris water maze. Chronic moderate sleep restriction did not alter anxiety-related behavior, but exercise training significantly attenuated anxiety-related behavior. Spatial learning and recall, hippocampal cell activity (i.e., number of c-Fos positive cells), and brain derived neurotrophic factor were significantly lower after chronic moderate sleep restriction, but higher after exercise training. Further, the benefit of exercise training for some memory variables was evident under normal sleep, but not chronic moderate sleep restriction conditions. These data indicate clear detrimental effects of chronic moderate sleep restriction on spatial memory and that the benefits of exercise training were impaired after chronic moderate sleep restriction. Published by Elsevier B.V.

Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation.

PubMed

Saletin, Jared M; Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Stark, Shauna; Stark, Craig E; Walker, Matthew P

2016-02-24

Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine). Copyright © 2016 the authors 0270-6474/16/362355-09$15.00/0.

Restricting Time in Bed in Early Adolescence Reduces Both NREM and REM Sleep but Does Not Increase Slow Wave EEG.

PubMed

Campbell, Ian G; Kraus, Amanda M; Burright, Christopher S; Feinberg, Irwin

2016-09-01

School night total sleep time decreases across adolescence (9-18 years) by 10 min/year. This decline is comprised entirely of a selective decrease in NREM sleep; REM sleep actually increases slightly. Decreasing sleep duration across adolescence is often attributed to insufficient time in bed. Here we tested whether sleep restriction in early adolescence produces the same sleep stage changes observed on school nights across adolescence. All-night sleep EEG was recorded in 76 children ranging in age from 9.9 to 14.0 years. Each participant kept 3 different sleep schedules that consisted of 3 nights of 8.5 h in bed followed by 4 nights of either 7, 8.5, or 10 h in bed. Sleep stage durations and NREM delta EEG activity were compared across the 3 time in bed conditions. Shortening time in bed from 10 to 7 hours reduced sleep duration by approximately 2 hours, roughly equal to the decrease in sleep duration we recorded longitudinally across adolescence. However, sleep restriction significantly reduced both NREM (by 83 min) and REM (by 47 min) sleep. Sleep restriction did not affect NREM delta EEG activity. Our findings suggest that the selective NREM reduction and the small increase in REM we observed longitudinally across 9-18 years are not produced by sleep restriction. We hypothesize that the selective NREM decline reflects adolescent brain maturation (synaptic elimination) that reduces the need for the restorative processes of NREM sleep. © 2016 Associated Professional Sleep Societies, LLC.

EEG SPECTRA, BEHAVIORAL STATES AND MOTOR ACTIVITY IN RATS EXPOSED TO ACETYLCHOLINESTERASE INHIBITOR CHLORPYRIFOS.

EPA Science Inventory

Exposure to organophosphate pesticides (OP) has been associated with sleep disorders: insomnia and ?excessive dreaming'. However neuronal mechanisms of these effects have not been analyzed. OP inhibit acetylcholinesterase activity leading to a hyperativity of the brain cholin...

Altered intrinsic regional brain activity in male patients with severe obstructive sleep apnea: a resting-state functional magnetic resonance imaging study

PubMed Central

Peng, De-Chang; Dai, Xi-Jian; Gong, Hong-Han; Li, Hai-Jun; Nie, Xiao; Zhang, Wei

2014-01-01

Background Previous studies have demonstrated that obstructive sleep apnea (OSA) is associated with abnormal brain structural deficits. However, little is known about the changes in local synchronization of spontaneous activity in patients with OSA. The primary aim of the present study was to investigate spontaneous brain activity in patients with OSA compared with good sleepers (GSs) using regional homogeneity (ReHo) analysis based on resting-state functional magnetic resonance imaging (MRI). Methods Twenty-five untreated male patients with severe OSA and 25 male GSs matched for age and years of education were included in this study. The ReHo method was calculated to assess the strength of local signal synchrony and was compared between the two groups. The observed mean ReHo values were entered into Statistical Package for the Social Sciences software to assess their correlation with behavioral performance. Results Compared with GSs, patients with OSA showed significantly lower ReHo in the right medial frontal gyrus (BA11), right superior frontal gyrus (BA10), right cluster of the precuneus and angular gyrus (BA39), and left superior parietal lobule (BA7), and higher ReHo in the right posterior lobe of the cerebellum, right cingulate gyrus (BA23), and bilateral cluster covering the lentiform nucleus, putamen, and insula (BA13). The lower mean ReHo value in the right cluster of the precuneus and angular gyrus had a significant negative correlation with sleep time (r=−0.430, P=0.032), and higher ReHo in the right posterior lobe of the cerebellum showed a significant positive correlation with stage 3 sleep (r=0.458, P=0.021) and in the right cingulate gyrus showed a significant positive correlation with percent rapid eye movement sleep (r=0.405, P=0.045). Conclusion Patients with OSA showed significant regional spontaneous activity deficits in default mode network areas. The ReHo method is a useful noninvasive imaging tool for detection of early changes in cerebral ReHo in patients with OSA. PMID:25278755

Brain reactivity differentiates subjects with high and low dream recall frequencies during both sleep and wakefulness.

PubMed

Eichenlaub, Jean-Baptiste; Bertrand, Olivier; Morlet, Dominique; Ruby, Perrine

2014-05-01

The neurophysiological correlates of dreaming remain unclear. According to the "arousal-retrieval" model, dream encoding depends on intrasleep wakefulness. Consistent with this model, subjects with high and low dream recall frequency (DRF) report differences in intrasleep awakenings. This suggests a possible neurophysiological trait difference between the 2 groups. To test this hypothesis, we compared the brain reactivity (evoked potentials) of subjects with high (HR, N = 18) and low (LR, N = 18) DRF during wakefulness and sleep. During data acquisition, the subjects were presented with sounds to be ignored (first names randomly presented among pure tones) while they were watching a silent movie or sleeping. Brain responses to first names dramatically differed between the 2 groups during both sleep and wakefulness. During wakefulness, the attention-orienting brain response (P3a) and a late parietal response were larger in HR than in LR. During sleep, we also observed between-group differences at the latency of the P3a during N2 and at later latencies during all sleep stages. Our results demonstrate differences in the brain reactivity of HR and LR during both sleep and wakefulness. These results suggest that the ability to recall dreaming is associated with a particular cerebral functional organization, regardless of the state of vigilance.

Sleep Promotes Consolidation of Emotional Memory in Healthy Children but Not in Children with Attention-Deficit Hyperactivity Disorder

PubMed Central

Prehn-Kristensen, Alexander; Munz, Manuel; Molzow, Ina; Wilhelm, Ines; Wiesner, Christian D.; Baving, Lioba

2013-01-01

Fronto-limbic brain activity during sleep is believed to support the consolidation of emotional memories in healthy adults. Attention deficit-hyperactivity disorder (ADHD) is accompanied by emotional deficits coincidently caused by dysfunctional interplay of fronto-limbic circuits. This study aimed to examine the role of sleep in the consolidation of emotional memory in ADHD in the context of healthy development. 16 children with ADHD, 16 healthy children, and 20 healthy adults participated in this study. Participants completed an emotional picture recognition paradigm in sleep and wake control conditions. Each condition had an immediate (baseline) and delayed (target) retrieval session. The emotional memory bias was baseline–corrected, and groups were compared in terms of sleep-dependent memory consolidation (sleep vs. wake). We observed an increased sleep-dependent emotional memory bias in healthy children compared to children with ADHD and healthy adults. Frontal oscillatory EEG activity (slow oscillations, theta) during sleep correlated negatively with emotional memory performance in children with ADHD. When combining data of healthy children and adults, correlation coefficients were positive and differed from those in children with ADHD. Since children displayed a higher frontal EEG activity than adults these data indicate a decline in sleep-related consolidation of emotional memory in healthy development. In addition, it is suggested that deficits in sleep-related selection between emotional and non-emotional memories in ADHD exacerbate emotional problems during daytime as they are often reported in ADHD. PMID:23734235

Donepezil Improves Episodic Memory in Young Individuals Vulnerable to the Effects of Sleep Deprivation

PubMed Central

Chuah, Lisa Y.M.; Chong, Delise L.; Chen, Annette K.; Rekshan, William R.; Tan, Jiat-Chow; Zheng, Hui; Chee, Michael W.L.

2009-01-01

Study Objectives: We investigated if donepezil, a long-acting orally administered cholinesterase inhibitor, would reduce episodic memory deficits associated with 24 h of sleep deprivation. Design: Double-blind, placebo-controlled, crossover study involving 7 laboratory visits over 2 months. Participants underwent 4 functional MRI scans; 2 sessions (donepezil or placebo) followed a normal night's sleep, and 2 sessions followed a night of sleep deprivation. Setting: The study took place in a research laboratory. Participants: 26 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. Interventions: 5 mg of donepezil was taken once daily for approximately 17 days. Measurements and Results: Subjects were scanned while performing a semantic judgment task and tested for word recognition outside the scanner 45 minutes later. Sleep deprivation increased the frequency of non-responses at encoding and impaired delayed recognition. No benefit of donepezil was evident when participants were well rested. When sleep deprived, individuals who showed greater performance decline improved with donepezil, whereas more resistant individuals did not benefit. Accompanying these behavioral effects, there was corresponding modulation of task-related activation in functionally relevant brain regions. Brain regions identified in relation to donepezil-induced alteration in non-response rates could be distinguished from regions relating to improved recognition memory. This suggests that donepezil can improve delayed recognition in sleep-deprived persons by improving attention as well as enhancing memory encoding. Conclusions: Donepezil reduced decline in recognition performance in individuals vulnerable to the effects of sleep deprivation. Additionally, our findings demonstrate the utility of combined fMRI–behavior evaluation in psychopharmacological studies. Citation: Chuah LYM; Chong DL; Chen AK; Rekshan WR; Tan JC; Zheng H; Chee MWL. Donepezil improves episodic memory in young individuals vulnerable to the effects of sleep deprivation. SLEEP 2009;32(8):999-1010. PMID:19725251

[Electromyography Analysis of Rapid Eye Movement Sleep Behavior Disorder].

PubMed

Nakano, Natsuko; Kinoshita, Fumiya; Takada, Hiroki; Nakayama, Meiho

2018-01-01

Polysomnography (PSG), which records physiological phenomena including brain waves, breathing status, and muscle tonus, is useful for the diagnosis of sleep disorders as a gold standard. However, measurement and analysis are complex for several specific sleep disorders, such as rapid eye movement (REM) sleep behavior disorder (RBD). Usually, brain waves during REM sleep indicate an awakening pattern under relaxed conditions of skeletal and antigravity muscles. However, these muscles are activated during REM sleep when patients suffer from RBD. These activated muscle movements during REM, so-called REM without atonia (RWA) recorded by PSG, may be related to a neurodegenerative disease such as Parkinson's disease. Thus, careful analysis of RWA is significant not only physically, but also clinically. Commonly, manual viewing measurement analysis of RWA is time-consuming. Therefore, quantitative studies on RWA are rarely reported. A software program, developed from Microsoft Office Excel ® , was used to semiautomatically analyze the RWA ratio extracted from PSG to compare with manual viewing measurement analysis. In addition, a quantitative muscle tonus study was carried out to evaluate the effect of medication on RBD patients. Using this new software program, we were able to analyze RWA on the same cases in approximately 15 min as compared with 60 min in the manual viewing measurement analysis. This software program can not only quantify RWA easily but also identify RWA waves for either phasic or tonic bursts. We consider that this software program will support physicians and scientists in their future research on RBD. We are planning to offer this software program for free to physicians and scientists.

Non Benzodiazepines Hypnotics: Another Way to Induce Sleep

DTIC Science & Technology

2000-03-01

caused by disruption environment and we feel intuitively that it must fulfil of circadian rhythm . Another factor that disrupts some restorative function...Many circadian rhythms are circadian rhythms is the conduct of nocturnal operations, linked tightly to our sleep/wake cycle. An adequate a current...The perfect hypnotic should act brain activity and metabolism (38). rapidly, have a short duration of action, not lead to Arousal and wakefulness seem

Across the consciousness continuum—from unresponsive wakefulness to sleep

PubMed Central

Blume, Christine; del Giudice, Renata; Wislowska, Malgorzata; Lechinger, Julia; Schabus, Manuel

2015-01-01

Advances in the development of new paradigms as well as in neuroimaging techniques nowadays enable us to make inferences about the level of consciousness patients with disorders of consciousness (DOC) retain. They, moreover, allow to predict their probable development. Today, we know that certain brain responses (e.g., event-related potentials or oscillatory changes) to stimulation, circadian rhythmicity, the presence or absence of sleep patterns as well as measures of resting state brain activity can serve the diagnostic and prognostic evaluation process. Still, the paradigms we are using nowadays do not allow to disentangle VS/UWS and minimally conscious state (MCS) patients with the desired reliability and validity. Furthermore, even rather well-established methods have, unfortunately, not found their way into clinical routine yet. We here review current literature as well as recent findings from our group and discuss how neuroimaging methods (fMRI, PET) and particularly electroencephalography (EEG) can be used to investigate cognition in DOC or even to assess the degree of residual awareness. We, moreover, propose that circadian rhythmicity and sleep in brain-injured patients are promising fields of research in this context. PMID:25805982

[Non-linear research of alertness levels under sleep deprivation].

PubMed

Xue, Ranting; Zhou, Peng; Gao, Xiang; Dong, Xinming; Wang, Xiaolu; Ming, Dong; Qi, Hongzhi; Wang, Xuemin

2014-06-01

We applied Lempel-Ziv complexity (LZC) combined with brain electrical activity mapping (BEAM) to study the change of alertness under sleep deprivation in our research. Ten subjects were involved in 36 hours sleep deprivation (SD), during which spontaneous electroencephalogram (EEG) experiments and auditory evoked EEG experiments-Oddball were recorded once every 6 hours. Spontaneous and evoked EEG data were calculated and BEAMs were structured. Results showed that during the 36 hours of SD, alertness could be divided into three stages, i. e. the first 12 hours as the high stage, the middle 12 hours as the rapid decline stage and the last 12 hours as the low stage. During the period SD, LZC of Spontaneous EEG decreased over the whole brain to some extent, but remained consistent with the subjective scales. By BEAMs of event related potential, LZC on frontal cortex decreased, but kept consistent with the behavioral responses. Therefore, LZC can be effective to reflect the change of brain alertness. At the same time LZC could be used as a practical index to monitor real-time alertness because of its simple computation and fast calculation.

Reduced sleep spindle activity point to a TRN-MD thalamus-PFC circuit dysfunction in schizophrenia.

PubMed

Ferrarelli, Fabio; Tononi, Giulio

2017-02-01

Sleep disturbances have been reliably reported in patients with schizophrenia, thus suggesting that abnormal sleep may represent a core feature of this disorder. Traditional electroencephalographic studies investigating sleep architecture have found reduced deep non-rapid eye movement (NREM) sleep, or slow wave sleep (SWS), and increased REM density. However, these findings have been inconsistently observed, and have not survived meta-analysis. By contrast, several recent EEG studies exploring brain activity during sleep have established marked deficits in sleep spindles in schizophrenia, including first-episode and early-onset patients, compared to both healthy and psychiatric comparison subjects. Spindles are waxing and waning, 12-16Hz NREM sleep oscillations that are generated within the thalamus by the thalamic reticular nucleus (TRN), and are then synchronized and sustained in the cortex. While the functional role of sleep spindles still needs to be fully established, increasing evidence has shown that sleep spindles are implicated in learning and memory, including sleep dependent memory consolidation, and spindle parameters have been associated to general cognitive ability and IQ. In this article we will review the EEG studies demonstrating sleep spindle deficits in patients with schizophrenia, and show that spindle deficits can predict their reduced cognitive performance. We will then present data indicating that spindle impairments point to a TRN-MD thalamus-prefrontal cortex circuit deficit, and discuss about the possible molecular mechanisms underlying thalamo-cortical sleep spindle abnormalities in schizophrenia. Copyright © 2016 Elsevier B.V. All rights reserved.

Actigraphic investigations on the activity-rest behavior of right- and left-handed students.

PubMed

Lehnkering, Hanna; Strauss, Andreas; Wegner, Brigitte; Siegmund, Renate

2006-01-01

The aim of this study was to explore differences between left-and right-handed subjects in sleep duration. Sleep and activity patterns were continuously registered for 12 days using actometers on 20 left-handed and 20 right-handed medical students in Berlin. Handedness was determined by a modified version of the Edinburgh handedness inventory. Each participant wore one actometer on each wrist. Actiwatch Sleep Analysis Software (CNT, UK) was used to evaluate the data, and statistical calculations were performed with a non-parametric variance analysis. A significant difference in mean sleep duration between left-handers (7.9 h) and right-handers (7.3 h) was determined (p=0.025 for measurement made on the dominant hand and p=0.013 for ones made on the non-dominant hand). In contrast, the maximal phase of daily activity (acrophase) did not show any difference between the two groups. The difference in sleep duration might be caused by either the greater effort required for left-handers to cope in a right-handed world or by structural brain differences.

EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation

PubMed Central

Freyburger, Marlène; Pierre, Audrey; Paquette, Gabrielle; Bélanger-Nelson, Erika; Bedont, Joseph; Gaudreault, Pierre-Olivier; Drolet, Guy; Laforest, Sylvie; Blackshaw, Seth; Cermakian, Nicolas; Doucet, Guy; Mongrain, Valérie

2016-01-01

Study Objectives: Optimal sleep is ensured by the interaction of circadian and homeostatic processes. Although synaptic plasticity seems to contribute to both processes, the specific players involved are not well understood. The EphA4 tyrosine kinase receptor is a cell adhesion protein regulating synaptic plasticity. We investigated the role of EphA4 in sleep regulation using electrocorticography in mice lacking EphA4 and gene expression measurements. Methods: EphA4 knockout (KO) mice, ClockΔ19/Δ19 mutant mice and littermates, C57BL/6J and CD-1 mice, and Sprague-Dawley rats were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SLD), and submitted to a 48 h electrophysiological recording and/or brain sampling at different time of day. Results: EphA4 KO mice showed less rapid eye movement sleep (REMS), enhanced duration of individual bouts of wakefulness and nonrapid eye movement sleep (NREMS) during the light period, and a blunted daily rhythm of NREMS sigma activity. The NREMS delta activity response to SLD was unchanged in EphA4 KO mice. However, SLD increased EphA4 expression in the thalamic/hypothalamic region in C57BL/6J mice. We further show the presence of E-boxes in the promoter region of EphA4, a lower expression of EphA4 in Clock mutant mice, a rhythmic expression of EphA4 ligands in several brain areas, expression of EphA4 in the suprachiasmatic nuclei of the hypothalamus (SCN), and finally an unchanged number of cells expressing Vip, Grp and Avp in the SCN of EphA4 KO mice. Conclusions: Our results suggest that EphA4 is involved in circadian sleep regulation. Citation: Freyburger M, Pierre A, Paquette G, Bélanger-Nelson E, Bedont J, Gaudreault PO, Drolet G, Laforest S, Blackshaw S, Cermakian N, Doucet G, Mongrain V. EphA4 is involved in sleep regulation but not in the electrophysiological response to sleep deprivation. SLEEP 2016;39(3):613–624. PMID:26612390

Association of sleep impairments and gastrointestinal disorders in the context of the visceral theory of sleep.

PubMed

Pigarev, Ivan N; Pigareva, Marina L

2017-01-01

It was noticed long ago that sleep disorders or interruptions to the normal sleep pattern were associated with various gastrointestinal disorders. We review the studies which established the causal link between these disorders and sleep impairment. However, the mechanism of interactions between the quality of sleep and gastrointestinal pathophysiology remained unclear. Recently, the visceral theory of sleep was formulated. This theory proposes that the same brain structures, and particularly the same cortical sensory areas, which in wakefulness are involved in processing of the exteroceptive information, switch during sleep to the processing of information coming from various visceral systems. We review the studies which demonstrated that neurons of the various cortical areas (occipital, parietal, frontal) during sleep began to fire in response to activation coming from the stomach and small intestine. These data demonstrate that, during sleep, the computational power of the central nervous system, including all cortical areas, is engaged in restoration of visceral systems. Thus, the general mechanism of the interaction between quality of sleep and health became clear.

Motivation and affect in REM sleep and the mentation reporting process.

PubMed

Smith, Mark R; Antrobus, John S; Gordon, Evelyn; Tucker, Matthew A; Hirota, Yasutaka; Wamsley, Erin J; Ross, Lars; Doan, Tieu; Chaklader, Annie; Emery, Rebecca N

2004-09-01

Although the emotional and motivational characteristics of dreaming have figured prominently in folk and psychoanalytic conceptions of dream production, emotions have rarely been systematically studied, and motivation, never. Because emotions during sleep lack the somatic components of waking emotions, and they change as the sleeper awakens, their properties are difficult to assess. Recent evidence of limbic system activation during REM sleep suggests a basis in brain architecture for the interaction of motivational and cognitive properties in dreaming. Motivational and emotional content in REM and NREM laboratory mentation reports from 25 participants were compared. Motivational and emotional content was significantly greater in REM than NREM sleep, even after controlling for the greater word count of REM reports.

Induction of slow oscillations by rhythmic acoustic stimulation.

PubMed

Ngo, Hong-Viet V; Claussen, Jens C; Born, Jan; Mölle, Matthias

2013-02-01

Slow oscillations are electrical potential oscillations with a spectral peak frequency of ∼0.8 Hz, and hallmark the electroencephalogram during slow-wave sleep. Recent studies have indicated a causal contribution of slow oscillations to the consolidation of memories during slow-wave sleep, raising the question to what extent such oscillations can be induced by external stimulation. Here, we examined whether slow oscillations can be effectively induced by rhythmic acoustic stimulation. Human subjects were examined in three conditions: (i) with tones presented at a rate of 0.8 Hz ('0.8-Hz stimulation'); (ii) with tones presented at a random sequence ('random stimulation'); and (iii) with no tones presented in a control condition ('sham'). Stimulation started during wakefulness before sleep and continued for the first ∼90 min of sleep. Compared with the other two conditions, 0.8-Hz stimulation significantly delayed sleep onset. However, once sleep was established, 0.8-Hz stimulation significantly increased and entrained endogenous slow oscillation activity. Sleep after the 90-min period of stimulation did not differ between the conditions. Our data show that rhythmic acoustic stimulation can be used to effectively enhance slow oscillation activity. However, the effect depends on the brain state, requiring the presence of stable non-rapid eye movement sleep. © 2012 European Sleep Research Society.

Sleep Restriction Impairs Blood–Brain Barrier Function

PubMed Central

He, Junyun; Hsuchou, Hung; He, Yi; Kastin, Abba J.; Wang, Yuping

2014-01-01

The blood–brain barrier (BBB) is a large regulatory and exchange interface between the brain and peripheral circulation. We propose that changes of the BBB contribute to many pathophysiological processes in the brain of subjects with chronic sleep restriction (CSR). To achieve CSR that mimics a common pattern of human sleep loss, we quantified a new procedure of sleep disruption in mice by a week of consecutive sleep recording. We then tested the hypothesis that CSR compromises microvascular function. CSR not only diminished endothelial and inducible nitric oxide synthase, endothelin1, and glucose transporter expression in cerebral microvessels of the BBB, but it also decreased 2-deoxy-glucose uptake by the brain. The expression of several tight junction proteins also was decreased, whereas the level of cyclooxygenase-2 increased. This coincided with an increase of paracellular permeability of the BBB to the small tracers sodium fluorescein and biotin. CSR for 6 d was sufficient to impair BBB structure and function, although the increase of paracellular permeability returned to baseline after 24 h of recovery sleep. This merits attention not only in neuroscience research but also in public health policy and clinical practice. PMID:25355222

Sleep restriction impairs blood-brain barrier function.

PubMed

He, Junyun; Hsuchou, Hung; He, Yi; Kastin, Abba J; Wang, Yuping; Pan, Weihong

2014-10-29

The blood-brain barrier (BBB) is a large regulatory and exchange interface between the brain and peripheral circulation. We propose that changes of the BBB contribute to many pathophysiological processes in the brain of subjects with chronic sleep restriction (CSR). To achieve CSR that mimics a common pattern of human sleep loss, we quantified a new procedure of sleep disruption in mice by a week of consecutive sleep recording. We then tested the hypothesis that CSR compromises microvascular function. CSR not only diminished endothelial and inducible nitric oxide synthase, endothelin1, and glucose transporter expression in cerebral microvessels of the BBB, but it also decreased 2-deoxy-glucose uptake by the brain. The expression of several tight junction proteins also was decreased, whereas the level of cyclooxygenase-2 increased. This coincided with an increase of paracellular permeability of the BBB to the small tracers sodium fluorescein and biotin. CSR for 6 d was sufficient to impair BBB structure and function, although the increase of paracellular permeability returned to baseline after 24 h of recovery sleep. This merits attention not only in neuroscience research but also in public health policy and clinical practice. Copyright © 2014 the authors 0270-6474/14/3414697-10$15.00/0.

Donepezil improves episodic memory in young individuals vulnerable to the effects of sleep deprivation.

PubMed

Chuah, Lisa Y M; Chong, Delise L; Chen, Annette K; Rekshan, William R; Tan, Jiat-Chow; Zheng, Hui; Chee, Michael W L

2009-08-01

We investigated if donepezil, a long-acting orally administered cholinesterase inhibitor, would reduce episodic memory deficits associated with 24 h of sleep deprivation. Double-blind, placebo-controlled, crossover study involving 7 laboratory visits over 2 months. Participants underwent 4 functional MRI scans; 2 sessions (donepezil or placebo) followed a normal night's sleep, and 2 sessions followed a night of sleep deprivation. The study took place in a research laboratory. 26 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. 5 mg of donepezil was taken once daily for approximately 17 days. Subjects were scanned while performing a semantic judgment task and tested for word recognition outside the scanner 45 minutes later. Sleep deprivation increased the frequency of non-responses at encoding and impaired delayed recognition. No benefit of donepezil was evident when participants were well rested. When sleep deprived, individuals who showed greater performance decline improved with donepezil, whereas more resistant individuals did not benefit. Accompanying these behavioral effects, there was corresponding modulation of task-related activation in functionally relevant brain regions. Brain regions identified in relation to donepezil-induced alteration in non-response rates could be distinguished from regions relating to improved recognition memory. This suggests that donepezil can improve delayed recognition in sleep-deprived persons by improving attention as well as enhancing memory encoding. Donepezil reduced decline in recognition performance in individuals vulnerable to the effects of sleep deprivation. Additionally, our findings demonstrate the utility of combined fMRI-behavior evaluation in psychopharmacological studies.

Disrupted Sleep in Narcolepsy: Exploring the Integrity of Galanin Neurons in the Ventrolateral Preoptic Area.

PubMed

Gavrilov, Yury V; Ellison, Brian A; Yamamoto, Mihoko; Reddy, Hasini; Haybaeck, Johannes; Mignot, Emmanuel; Baumann, Christian R; Scammell, Thomas E; Valko, Philipp O

2016-05-01

To examine the integrity of sleep-promoting neurons of the ventrolateral preoptic nucleus (VLPO) in postmortem brains of narcolepsy type 1 patients. Postmortem examination of five narcolepsy and eight control brains. VLPO galanin neuron count did not differ between narcolepsy patients (11,151 ± 3,656) and controls (13,526 ± 9,544). A normal number of galanin-immunoreactive VLPO neurons in narcolepsy type 1 brains at autopsy suggests that VLPO cell loss is an unlikely explanation for the sleep fragmentation that often accompanies the disease. © 2016 Associated Professional Sleep Societies, LLC.

Comparison of NREM sleep and intravenous sedation through local information processing and whole brain network to explore the mechanism of general anesthesia

PubMed Central

Pan, Chuxiong; Xue, Fushan; Xian, Junfang; Huang, Yaqi; Wang, Xiaoyi; He, Huiguang

2018-01-01

Background The mechanism of general anesthesia (GA) has been explored for hundreds of years, but unclear. Previous studies indicated a possible correlation between NREM sleep and GA. The purpose of this study is to compare them by in vivo human brain function to probe the neuromechanism of consciousness, so as to find out a clue to GA mechanism. Methods 24 healthy participants were equally assigned to sleep or propofol sedation group by sleeping ability. EEG and Ramsay Sedation Scale were applied to determine sleep stage and sedation depth respectively. Resting-state functional magnetic resonance imaging (RS-fMRI) was acquired at each status. Regional homogeneity (ReHo) and seed-based whole brain functional connectivity maps (WB-FC maps) were compared. Results During sleep, ReHo primarily weakened on frontal lobe (especially preoptic area), but strengthened on brainstem. While during sedation, ReHo changed in various brain areas, including cingulate, precuneus, thalamus and cerebellum. Cingulate, fusiform and insula were concomitance of sleep and sedation. Comparing to sleep, FCs between the cortex and subcortical centers (centralized in cerebellum) were significantly attenuated under sedation. As sedation deepening, cerebellum-based FC maps were diminished, while thalamus- and brainstem-based FC maps were increased. Conclusion There’re huge distinctions in human brain function between sleep and GA. Sleep mainly rely on brainstem and frontal lobe function, while sedation is prone to affect widespread functional network. The most significant differences exist in the precuneus and cingulate, which may play important roles in mechanisms of inducing unconciousness by anesthetics. Trial registration Institutional Review Board (IRB) ChiCTR-IOC-15007454. PMID:29486001

Sleep deprivation elevates expectation of gains and attenuates response to losses following risky decisions.

PubMed

Venkatraman, Vinod; Chuah, Y M Lisa; Huettel, Scott A; Chee, Michael W L

2007-05-01

Using a gambling task, we investigated how 24 hours of sleep deprivation modulates the neural response to the making of risky decisions with potentially loss-bearing outcomes. Two experiments involving sleep-deprived subjects were performed. In the first, neural responses to decision making and reward outcome were evaluated. A second control experiment evaluated responses to reward outcome only. Healthy right-handed adults participated in these experiments (26 [mean age 21.3 years] in Experiment 1 and 13 [mean age 21.7 years] in Experiment 2.) Following sleep deprivation, choices involving higher relative risk elicited greater activation in the right nucleus accumbens, signifying an elevated expectation of the higher reward once the riskier choice was made. Concurrently, activation for losses in the insular and orbitofrontal cortices was reduced, denoting a diminished response to losses. This latter finding of reduced insular activation to losses was also true when volunteers were merely shown the results of the computer's decision, that is, without having to make their own choice. These results suggest that sleep deprivation poses a dual threat to competent decision making by modulating activation in nucleus accumbens and insula, brain regions associated with risky decision making and emotional processing.

ERK signaling pathway regulates sleep duration through activity-induced gene expression during wakefulness.

PubMed

Mikhail, Cyril; Vaucher, Angélique; Jimenez, Sonia; Tafti, Mehdi

2017-01-24

Wakefulness is accompanied by experience-dependent synaptic plasticity and an increase in activity-regulated gene transcription. Wake-induced genes are certainly markers of neuronal activity and may also directly regulate the duration of and need for sleep. We stimulated murine cortical cultures with the neuromodulatory signals that are known to control wakefulness in the brain and found that norepinephrine alone or a mixture of these neuromodulators induced activity-regulated gene transcription. Pharmacological inhibition of the various signaling pathways involved in the regulation of gene expression indicated that the extracellular signal-regulated kinase (ERK) pathway is the principal one mediating the effects of waking neuromodulators on gene expression. In mice, ERK phosphorylation in the cortex increased and decreased with wakefulness and sleep. Whole-body or cortical neuron-specific deletion of Erk1 or Erk2 significantly increased the duration of wakefulness in mice, and pharmacological inhibition of ERK phosphorylation decreased sleep duration and increased the duration of wakefulness bouts. Thus, this signaling pathway, which is highly conserved from Drosophila to mammals, is a key pathway that links waking experience-induced neuronal gene expression to sleep duration and quality. Copyright © 2017, American Association for the Advancement of Science.

Overnight Therapy? The Role of Sleep in Emotional Brain Processing

ERIC Educational Resources Information Center

Walker, Matthew P.; van Der Helm, Els

2009-01-01

Cognitive neuroscience continues to build meaningful connections between affective behavior and human brain function. Within the biological sciences, a similar renaissance has taken place, focusing on the role of sleep in various neurocognitive processes and, most recently, on the interaction between sleep and emotional regulation. This review…

Electroencephalographic profiles for differentiation of disorders of consciousness

PubMed Central

2013-01-01

Background Electroencephalography (EEG) is best suited for long-term monitoring of brain functions in patients with disorders of consciousness (DOC). Mathematical tools are needed to facilitate efficient interpretation of long-duration sleep-wake EEG recordings. Methods Starting with matching pursuit (MP) decomposition, we automatically detect and parametrize sleep spindles, slow wave activity, K-complexes and alpha, beta and theta waves present in EEG recordings, and automatically construct profiles of their time evolution, relevant to the assessment of residual brain function in patients with DOC. Results Above proposed EEG profiles were computed for 32 patients diagnosed as minimally conscious state (MCS, 20 patients), vegetative state/unresponsive wakefulness syndrome (VS/UWS, 11 patients) and Locked-in Syndrome (LiS, 1 patient). Their interpretation revealed significant correlations between patients’ behavioral diagnosis and: (a) occurrence of sleep EEG patterns including sleep spindles, slow wave activity and light/deep sleep cycles, (b) appearance and variability across time of alpha, beta, and theta rhythms. Discrimination between MCS and VS/UWS based upon prominent features of these profiles classified correctly 87% of cases. Conclusions Proposed EEG profiles offer user-independent, repeatable, comprehensive and continuous representation of relevant EEG characteristics, intended as an aid in differentiation between VS/UWS and MCS states and diagnostic prognosis. To enable further development of this methodology into clinically usable tests, we share user-friendly software for MP decomposition of EEG (http://braintech.pl/svarog) and scripts used for creation of the presented profiles (attached to this article). PMID:24143892

A prominent role for amygdaloid complexes in the Variability in Heart Rate (VHR) during Rapid Eye Movement (REM) sleep relative to wakefulness.

PubMed

Desseilles, Martin; Vu, Thanh Dang; Laureys, Steven; Peigneux, Philippe; Degueldre, Christian; Phillips, Christophe; Maquet, Pierre

2006-09-01

Rapid eye movement sleep (REMS) is associated with intense neuronal activity, rapid eye movements, muscular atonia and dreaming. Another important feature in REMS is the instability in autonomic, especially in cardiovascular regulation. The neural mechanisms underpinning the variability in heart rate (VHR) during REMS are not known in detail, especially in humans. During wakefulness, the right insula has frequently been reported as involved in cardiovascular regulation but this might not be the case during REMS. We aimed at characterizing the neural correlates of VHR during REMS as compared to wakefulness and to slow wave sleep (SWS), the other main component of human sleep, in normal young adults, based on the statistical analysis of a set of H(2)(15)O positron emission tomography (PET) sleep data acquired during SWS, REMS and wakefulness. The results showed that VHR correlated more tightly during REMS than during wakefulness with the rCBF in the right amygdaloid complex. Moreover, we assessed whether functional relationships between amygdala and any brain area changed depending the state of vigilance. Only the activity within in the insula was found to covary with the amygdala, significantly more tightly during wakefulness than during REMS in relation to the VHR. The functional connectivity between the amygdala and the insular cortex, two brain areas involved in cardiovascular regulation, differs significantly in REMS as compared to wakefulness. This suggests a functional reorganization of central cardiovascular regulation during REMS.

Waking up too early - the consequences of preterm birth on sleep development.

PubMed

Bennet, Laura; Walker, David W; Horne, Rosemary S C

2018-04-24

Good quality sleep of sufficient duration is vital for optimal physiological function and our health. Sleep deprivation is associated with impaired neurocognitive function and emotional control, and increases the risk for cardiometabolic diseases, obesity and cancer. Sleep develops during fetal life with the emergence of a recognisable pattern of sleep states in the preterm fetus associated with the development, maturation, and connectivity within neural networks in the brain. Despite the physiological importance of sleep, surprisingly little is known about how sleep develops in individuals born preterm. Globally, an estimated 15 million babies are born preterm (<37 weeks gestation), and these babies are at significant risk of neural injury and impaired brain development. This review discusses how sleep develops during fetal and neonatal life, how preterm birth impacts on sleep development to adulthood, and the factors which may contribute to impaired brain and sleep development, leading to altered neurocognitive, behavioural and motor capabilities in the infant and child. Going forward, the challenge is to identify specific risk factors for impaired sleep development in preterm babies to allow for the design of interventions that will improve the quality and quantity of sleep throughout life. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.

Restricting Time in Bed in Early Adolescence Reduces Both NREM and REM Sleep but Does Not Increase Slow Wave EEG

PubMed Central

Campbell, Ian G.; Kraus, Amanda M.; Burright, Christopher S.; Feinberg, Irwin

2016-01-01

Study Objectives: School night total sleep time decreases across adolescence (9–18 years) by 10 min/year. This decline is comprised entirely of a selective decrease in NREM sleep; REM sleep actually increases slightly. Decreasing sleep duration across adolescence is often attributed to insufficient time in bed. Here we tested whether sleep restriction in early adolescence produces the same sleep stage changes observed on school nights across adolescence. Methods: All-night sleep EEG was recorded in 76 children ranging in age from 9.9 to 14.0 years. Each participant kept 3 different sleep schedules that consisted of 3 nights of 8.5 h in bed followed by 4 nights of either 7, 8.5, or 10 h in bed. Sleep stage durations and NREM delta EEG activity were compared across the 3 time in bed conditions. Results: Shortening time in bed from 10 to 7 hours reduced sleep duration by approximately 2 hours, roughly equal to the decrease in sleep duration we recorded longitudinally across adolescence. However, sleep restriction significantly reduced both NREM (by 83 min) and REM (by 47 min) sleep. Sleep restriction did not affect NREM delta EEG activity. Conclusions: Our findings suggest that the selective NREM reduction and the small increase in REM we observed longitudinally across 9–18 years are not produced by sleep restriction. We hypothesize that the selective NREM decline reflects adolescent brain maturation (synaptic elimination) that reduces the need for the restorative processes of NREM sleep. Citation: Campbell IG, Kraus AM, Burright CS, Feinberg I. Restricting time in bed in early adolescence reduces both NREM and REM sleep but does not increase slow wave EEG. SLEEP 2016;39(9):1663–1670. PMID:27397569

Cycle-Triggered Cortical Stimulation during Slow Wave Sleep Facilitates Learning a BMI Task: A Case Report in a Non-Human Primate

PubMed Central

Rembado, Irene; Zanos, Stavros; Fetz, Eberhard E.

2017-01-01

Slow wave sleep (SWS) has been identified as the sleep stage involved in consolidating newly acquired information. A growing body of evidence has shown that delta (1–4 Hz) oscillatory activity, the characteristic electroencephalographic signature of SWS, is involved in coordinating interaction between the hippocampus and the neocortex and is thought to take a role in stabilizing memory traces related to a novel task. This case report describes a new protocol that uses neuroprosthetics training of a non-human primate to evaluate the effects of surface cortical electrical stimulation triggered from SWS cycles. The results suggest that stimulation phase-locked to SWS oscillatory activity promoted learning of the neuroprosthetic task. This protocol could be used to elucidate mechanisms of synaptic plasticity underlying off-line learning during sleep and offers new insights into the role of brain oscillations in information processing and memory consolidation. PMID:28450831

The synchronous activity of lateral habenular neurons is essential for regulating hippocampal theta oscillation.

PubMed

Aizawa, Hidenori; Yanagihara, Shin; Kobayashi, Megumi; Niisato, Kazue; Takekawa, Takashi; Harukuni, Rie; McHugh, Thomas J; Fukai, Tomoki; Isomura, Yoshikazu; Okamoto, Hitoshi

2013-05-15

Lateral habenula (LHb) has attracted growing interest as a regulator of serotonergic and dopaminergic neurons in the CNS. However, it remains unclear how the LHb modulates brain states in animals. To identify the neural substrates that are under the influence of LHb regulation, we examined the effects of rat LHb lesions on the hippocampal oscillatory activity associated with the transition of brain states. Our results showed that the LHb lesion shortened the theta activity duration both in anesthetized and sleeping rats. Furthermore, this inhibitory effect of LHb lesion on theta maintenance depended upon an intact serotonergic median raphe, suggesting that LHb activity plays an essential role in maintaining hippocampal theta oscillation via the serotonergic raphe. Multiunit recording of sleeping rats further revealed that firing of LHb neurons showed significant phase-locking activity at each theta oscillation cycle in the hippocampus. LHb neurons showing activity that was coordinated with that of the hippocampal theta were localized in the medial LHb division, which receives afferents from the diagonal band of Broca (DBB), a pacemaker region for the hippocampal theta oscillation. Thus, our findings indicate that the DBB may pace not only the hippocampus, but also the LHb, during rapid eye movement sleep. Since serotonin is known to negatively regulate theta oscillation in the hippocampus, phase-locking activity of the LHb neurons may act, under the influence of the DBB, to maintain the hippocampal theta oscillation by modulating the activity of serotonergic neurons.

Poor sleep quality is associated with increased cortical atrophy in community-dwelling adults.

PubMed

Sexton, Claire E; Storsve, Andreas B; Walhovd, Kristine B; Johansen-Berg, Heidi; Fjell, Anders M

2014-09-09

To examine the relationship between sleep quality and cortical and hippocampal volume and atrophy within a community-based sample, explore the influence of age on results, and assess the possible confounding effects of physical activity levels, body mass index (BMI), and blood pressure. In 147 community-dwelling adults (92 female; age 53.9 ± 15.5 years), sleep quality was measured using the Pittsburgh Sleep Quality Index and correlated with cross-sectional measures of volume and longitudinal measures of atrophy derived from MRI scans separated by an average of 3.5 years. Exploratory post hoc analysis compared correlations between different age groups and included physical activity, BMI, and blood pressure as additional covariates. Poor sleep quality was associated with reduced volume within the right superior frontal cortex in cross-sectional analyses, and an increased rate of atrophy within widespread frontal, temporal, and parietal regions in longitudinal analyses. Results were largely driven by correlations within adults over the age of 60, and could not be explained by variation in physical activity, BMI, or blood pressure. Sleep quality was not associated with hippocampal volume or atrophy. We found that longitudinal measures of cortical atrophy were widely correlated with sleep quality. Poor sleep quality may be a cause or a consequence of brain atrophy, and future studies examining the effect of interventions that improve sleep quality on rates of atrophy may hold key insights into the direction of this relationship. © 2014 American Academy of Neurology.

Interleukin 1 receptor contributes to methamphetamine- and sleep deprivation-induced hypersomnolence

PubMed Central

Schmidt, Michelle A.; Wisor, Jonathan P.

2014-01-01

Methamphetamine-induced wakefulness is dependent on monoamine transporter blockade. Subsequent to methamphetamine-induced wakefulness, the amount of time spent asleep and the depth of sleep are increased relative to baseline sleep. The mechanisms that drive methamphetamine-induced hypersomnolence are not fully understood. We recently observed that methamphetamine exposure elevates the expression of the sleep-promoting cytokine, interleukin-1 β in CD11b-positive monocytes within the brain. Here, we sought to determine whether activation of the interleukin 1 receptor (IL1R) drives the increase in the depth and amount of sleep that occurs subsequent to methamphetamine-induced wakefulness. IL1R-deficient mice and wild type control mice were subjected to systemic methamphetamine (1 and 2mg/kg) and saline treatments. The wake-promoting effect of methamphetamine was modestly potentiated by IL1R-deficiency. Additionally, the increase in time spent in NREMS subsequent to methamphetamine-induced wakefulness in wild type mice was abolished in IL1R-deficient mice. The increase in time spent asleep after 3 h of behaviorally enforced wakefulness was also abolished in IL1R-deficient mice. Increases in EEG slow wave activity triggered by methamphetamine and sleep deprivation were of equal magnitude in IL1R-deficient and wild type mice. These data demonstrate that IL1R activation contributes to hypersomnolence that occurs after sleep loss, whether that sleep loss is triggered pharmacologically by methamphetamine or through behavioral sleep deprivation. PMID:22387068

Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat

PubMed Central

Goldstein-Piekarski, Andrea N.; Greer, Stephanie M.; Saletin, Jared M.

2015-01-01

Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the “embodied” reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive. PMID:26180190

Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat.

PubMed

Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Saletin, Jared M; Walker, Matthew P

2015-07-15

Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the "embodied" reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive. Copyright © 2015 the authors 0270-6474/15/3510135-11$15.00/0.

Sleep in disorders of consciousness

PubMed Central

Cologan, Victor; Schabus, Manvel; Ledoux, Didier; Moonen, Gustave; Maquet, Pierre; Laureys, Steven

2010-01-01

SUMMARY From a behavioral as well as neurobiological point of view, sleep and consciousness are intimately connected. A better understanding of sleep cycles and sleep architecture of patients suffering from disorders of consciousness (DOC) might therefore improve the clinical care for these patients as well as our understanding of the neural correlations of consciousness. Defining sleep in severely brain-injured patients is however problematic as both their electrophysiological and sleep patterns differ in many ways from healthy individuals. This paper discusses the concepts involved in the study of sleep of patients suffering from DOC and critically assesses the applicability of standard sleep criteria in these patients. The available literature on comatose and vegetative states as well as that on locked-in and related states following traumatic or non-traumatic severe brain injury will be reviewed. A wide spectrum of sleep disturbances ranging from almost normal patterns to severe loss and architecture disorganization are reported in cases of DOC and some patterns correlate with diagnosis and prognosis. At the present time the interactions of sleep and consciousness in brain-injured patients are a little studied subject but, the authors suggest, a potentially very interesting field of research. PMID:19524464

Sleep architecture and sleep-related mentation in securely and insecurely attached people

PubMed Central

McNamara, Patrick; Pace-Schott, Edward F.; Johnson, Patricia; Harris, Erica; Auerbach, Sanford

2011-01-01

Based on REM sleep’s brain activation patterns and its participation in consolidation of emotional memories, we tested the hypothesis that measures of REM sleep architecture and REM sleep-related mentation would be associated with attachment orientation. After a habituation night in a sleep lab, a convenience sample of 64 healthy volunteers were awakened 10 minutes into a REM sleep episode and 10 minutes into a control NREM sleep episode in counterbalanced order, then asked to report a dream and to rate themselves and a significant other on a list of trait adjectives. Relative to participants classified as having secure attachment orientations, participants classified as anxious took less time to enter REM sleep and had a higher frequency of REM dreams with aggression and self-denigrating themes. There were no significant differences across attachment groups in other measures of sleep architecture or in post REM-sleep awakening ratings on PANAS subscales reflecting mood and alertness. Selected aspects of REM sleep architecture and mentation appeared to be associated with attachment orientation. We suggest that REM sleep plays a role in processing experiences and emotions related to attachment, and that certain features of sleep and dreaming reflect attachment orientations. PMID:21390907

fMRI during natural sleep as a method to study brain function during early childhood.

PubMed

Redcay, Elizabeth; Kennedy, Daniel P; Courchesne, Eric

2007-12-01

Many techniques to study early functional brain development lack the whole-brain spatial resolution that is available with fMRI. We utilized a relatively novel method in which fMRI data were collected from children during natural sleep. Stimulus-evoked responses to auditory and visual stimuli as well as stimulus-independent functional networks were examined in typically developing 2-4-year-old children. Reliable fMRI data were collected from 13 children during presentation of auditory stimuli (tones, vocal sounds, and nonvocal sounds) in a block design. Twelve children were presented with visual flashing lights at 2.5 Hz. When analyses combined all three types of auditory stimulus conditions as compared to rest, activation included bilateral superior temporal gyri/sulci (STG/S) and right cerebellum. Direct comparisons between conditions revealed significantly greater responses to nonvocal sounds and tones than to vocal sounds in a number of brain regions including superior temporal gyrus/sulcus, medial frontal cortex and right lateral cerebellum. The response to visual stimuli was localized to occipital cortex. Furthermore, stimulus-independent functional connectivity MRI analyses (fcMRI) revealed functional connectivity between STG and other temporal regions (including contralateral STG) and medial and lateral prefrontal regions. Functional connectivity with an occipital seed was localized to occipital and parietal cortex. In sum, 2-4 year olds showed a differential fMRI response both between stimulus modalities and between stimuli in the auditory modality. Furthermore, superior temporal regions showed functional connectivity with numerous higher-order regions during sleep. We conclude that the use of sleep fMRI may be a valuable tool for examining functional brain organization in young children.

Adolescent Changes in Homeostatic Regulation of EEG Activity in the Delta and Theta Frequency Bands during NREM Sleep

PubMed Central

Campbell, Ian G.; Darchia, Nato; Higgins, Lisa M.; Dykan, Igor V.; Davis, Nicole M.; de Bie, Evan; Feinberg, Irwin

2011-01-01

Study Objectives: Slow wave EEG activity in NREM sleep decreases by more than 60% between ages 10 and 20 years. Slow wave EEG activity also declines across NREM periods (NREMPs) within a night, and this decline is thought to represent the dynamics of sleep homeostasis. We used longitudinal data to determine whether these homeostatic dynamics change across adolescence. Design: All-night sleep EEG was recorded semiannually for 6 years. Setting: EEG was recorded with ambulatory recorders in the subjects' homes. Participants: Sixty-seven subjects in 2 cohorts, one starting at age 9 and one starting at age 12 years. Measurements and Results: For NREM delta (1-4 Hz) and theta (4-8 Hz) EEG, we tested whether the proportion of spectral energy contained in the first NREMP changes with age. We also tested for age changes in the parameters of the process S exponential decline. For both delta and theta, the proportion of energy in the first NREMP declined significantly across ages 9 to 18 years. Process S parameters SWA0 and TWA0, respectively, represent slow wave (delta) activity and theta wave activity at the beginning of the night. SWA0 and TWA0 declined significantly (P < 0.0001) across ages 9 to 18. Conclusions: These declines indicate that the intensity of the homeostatic or restorative processes at the beginning of sleep diminished across adolescence. We propose that this change in sleep regulation is caused by the synaptic pruning that occurs during adolescent brain maturation. Citation: Campbell IG; Darchia N; Higgins LM; Dykan IV; Davis NM; de Bie E; Feinberg I. Adolescent changes in homeostatic regulation of EEG activity in the delta and theta frequency bands during NREM sleep. SLEEP 2011;34(1):83-91. PMID:21203377

African trypanosome infections of the nervous system: parasite entry and effects on sleep and synaptic functions.

PubMed

Kristensson, Krister; Nygård, Mikael; Bertini, Giuseppe; Bentivoglio, Marina

2010-06-01

The extracellular parasite Trypanosoma brucei causes human African trypanosomiasis (HAT), also known as sleeping sickness. Trypanosomes are transmitted by tsetse flies and HAT occurs in foci in sub-Saharan Africa. The disease, which is invariably lethal if untreated, evolves in a first hemo-lymphatic stage, progressing to a second meningo-encephalitic stage when the parasites cross the blood-brain barrier. At first, trypanosomes are restricted to circumventricular organs and choroid plexus in the brain outside the blood-brain barrier, and to dorsal root ganglia. Later, parasites cross the blood-brain barrier at post-capillary venules, through a multi-step process similar to that of lymphocytes. Accumulation of parasites in the brain is regulated by cytokines and chemokines. Trypanosomes can alter neuronal function and the most prominent manifestation is represented by sleep alterations. These are characterized, in HAT and experimental rodent infections, by disruption of the sleep-wake 24h cycle and internal sleep structure. Trypanosome infections alter also some, but not all, other endogenous biological rhythms. A number of neural pathways and molecules may be involved in such effects. Trypanosomes secrete prostaglandins including the somnogenic PGD2, and they interact with the host's immune system to cause release of pro-inflammatory cytokines. From the sites of early localization of parasites in the brain and meninges, such molecules could affect adjacent brain areas implicated in sleep-wakefulness regulation, including the suprachiasmatic nucleus and its downstream targets, to cause the changes characteristic of the disease. This raises challenging issues on the effects of cytokines on synaptic functions potentially involved in sleep-wakefulness alterations. (c) 2009 Elsevier Ltd. All rights reserved.

What Is the Link Between Hallucinations, Dreams, and Hypnagogic-Hypnopompic Experiences?

PubMed

Waters, Flavie; Blom, Jan Dirk; Dang-Vu, Thien Thanh; Cheyne, Allan J; Alderson-Day, Ben; Woodruff, Peter; Collerton, Daniel

2016-09-01

By definition, hallucinations occur only in the full waking state. Yet similarities to sleep-related experiences such as hypnagogic and hypnopompic hallucinations, dreams and parasomnias, have been noted since antiquity. These observations have prompted researchers to suggest a common aetiology for these phenomena based on the neurobiology of rapid eye movement (REM) sleep. With our recent understanding of hallucinations in different population groups and at the neurobiological, cognitive and interpersonal levels, it is now possible to draw comparisons between the 2 sets of experiences as never before. In the current article, we make detailed comparisons between sleep-related experiences and hallucinations in Parkinson's disease, schizophrenia and eye disease, at the levels of phenomenology (content, sensory modalities involved, perceptual attributes) and of brain function (brain activations, resting-state networks, neurotransmitter action). Findings show that sleep-related experiences share considerable overlap with hallucinations at the level of subjective descriptions and underlying brain mechanisms. Key differences remain however: (1) Sleep-related perceptions are immersive and largely cut off from reality, whereas hallucinations are discrete and overlaid on veridical perceptions; and (2) Sleep-related perceptions involve only a subset of neural networks implicated in hallucinations, reflecting perceptual signals processed in a functionally and cognitively closed-loop circuit. In summary, both phenomena are non-veridical perceptions that share some phenomenological and neural similarities, but insufficient evidence exists to fully support the notion that the majority of hallucinations depend on REM processes or REM intrusions into waking consciousness. © The Author 2016. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.

The Effects of Experimental Manipulation of Sleep Duration on Neural Response to Food Cues.

PubMed

Demos, Kathryn E; Sweet, Lawrence H; Hart, Chantelle N; McCaffery, Jeanne M; Williams, Samantha E; Mailloux, Kimberly A; Trautvetter, Jennifer; Owens, Max M; Wing, Rena R

2017-11-01

Despite growing literature on neural food cue responsivity in obesity, little is known about how the brain processes food cues following partial sleep deprivation and whether short sleep leads to changes similar to those observed in obesity. We used functional magnetic resonance imaging (fMRI) to test the hypothesis that short sleep leads to increased reward-related and decreased inhibitory control-related processing of food cues.In a within-subject design, 30 participants (22 female, mean age = 36.7 standard deviation = 10.8 years, body mass index range 20.4-40.7) completed four nights of 6 hours/night time-in-bed (TIB; short sleep) and four nights of 9 hours/night TIB (long sleep) in random counterbalanced order in their home environments. Following each sleep condition, participants completed an fMRI scan while viewing food and nonfood images.A priori region of interest analyses revealed increased activity to food in short versus long sleep in regions of reward processing (eg, nucleus accumbens/putamen) and sensory/motor signaling (ie, right paracentral lobule, an effect that was most pronounced in obese individuals). Contrary to the hypothesis, whole brain analyses indicated greater food cue responsivity during short sleep in an inhibitory control region (right inferior frontal gyrus) and ventral medial prefrontal cortex, which has been implicated in reward coding and decision-making (false discovery rate corrected q = 0.05).These findings suggest that sleep restriction leads to both greater reward and control processing in response to food cues. Future research is needed to understand the dynamic functional connectivity between these regions during short sleep and whether the interplay between these neural processes determines if one succumbs to food temptation. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Medical and Psychosocial Correlates of Insomnia Symptoms in Adult Survivors of Pediatric Brain Tumors.

PubMed

Zhou, Eric S; Manley, Peter E; Marcus, Karen J; Recklitis, Christopher J

2016-07-01

Children diagnosed with brain tumors are at risk for insomnia. We evaluated insomnia symptoms, medical and psychosocial correlates, and medical documentation of sleep-related issues in a neuro-oncology clinic. 98 adult survivors of pediatric brain tumors provided data about sleep, psychological distress, and health-related quality of life. Medical records were reviewed for treatment-related information and for documentation of sleep-related issues. 26% of the sample reported insomnia symptoms as evidenced by poor sleep efficiency. Insomnia symptoms were associated with a migraine headache history, but not with other medical or psychosocial outcomes. Approximately one in three medical providers did not document discussing sleep during the survivorship visit. A sizeable number of pediatric brain tumor survivors experience insomnia symptoms. The survivorship visit is an ideal opportunity for providers to conduct a sleep evaluation for this at-risk population and to provide referrals for evidence-based insomnia treatment. © The Author 2015. Published by Oxford University Press on behalf of the Society of Pediatric Psychology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Functions and Mechanisms of Sleep

PubMed Central

Zielinski, Mark R.; McKenna, James T.; McCarley, Robert W.

2017-01-01

Sleep is a complex physiological process that is regulated globally, regionally, and locally by both cellular and molecular mechanisms. It occurs to some extent in all animals, although sleep expression in lower animals may be co-extensive with rest. Sleep regulation plays an intrinsic part in many behavioral and physiological functions. Currently, all researchers agree there is no single physiological role sleep serves. Nevertheless, it is quite evident that sleep is essential for many vital functions including development, energy conservation, brain waste clearance, modulation of immune responses, cognition, performance, vigilance, disease, and psychological state. This review details the physiological processes involved in sleep regulation and the possible functions that sleep may serve. This description of the brain circuitry, cell types, and molecules involved in sleep regulation is intended to further the reader’s understanding of the functions of sleep. PMID:28413828

Sleep Apnea, Sleep Duration and Brain MRI Markers of Cerebral Vascular Disease and Alzheimer's Disease: The Atherosclerosis Risk in Communities Study (ARIC).

PubMed

Lutsey, Pamela L; Norby, Faye L; Gottesman, Rebecca F; Mosley, Thomas; MacLehose, Richard F; Punjabi, Naresh M; Shahar, Eyal; Jack, Clifford R; Alonso, Alvaro

2016-01-01

A growing body of literature has suggested that obstructive sleep apnea (OSA) and habitual short sleep duration are linked to poor cognitive function. Neuroimaging studies may provide insight into this relation. We tested the hypotheses that OSA and habitual short sleep duration, measured at ages 54-73 years, would be associated with adverse brain morphology at ages 67-89 years. Included in this analysis are 312 ARIC study participants who underwent in-home overnight polysomnography in 1996-1998 and brain MRI scans about 15 years later (2012-2013). Sleep apnea was quantified by the apnea-hypopnea index and categorized as moderate/severe (≥15.0 events/hour), mild (5.0-14.9 events/hour), or normal (<5.0 events/hour). Habitual sleep duration was categorized, in hours, as <7, 7 to <8, ≥8. MRI outcomes included number of infarcts (total, subcortical, and cortical) and white matter hyperintensity (WMH) and Alzheimer's disease signature region volumes. Multivariable adjusted logistic and linear regression models were used. All models incorporated inverse probability weighting, to adjust for potential selection bias. At the time of the sleep study participants were 61.7 (SD: 5.0) years old and 54% female; 19% had moderate/severe sleep apnea. MRI imaging took place 14.8 (SD: 1.0) years later, when participants were 76.5 (SD: 5.2) years old. In multivariable models which accounted for body mass index, neither OSA nor abnormal sleep duration were statistically significantly associated with odds of cerebral infarcts, WMH brain volumes or regional brain volumes. In this community-based sample, mid-life OSA and habitually short sleep duration were not associated with later-life cerebral markers of vascular dementia and Alzheimer's disease. However, selection bias may have influenced our results and the modest sample size led to relatively imprecise associations.

Potential role of orexin and sleep modulation in the pathogenesis of Alzheimer's disease.

PubMed

Roh, Jee Hoon; Jiang, Hong; Finn, Mary Beth; Stewart, Floy R; Mahan, Thomas E; Cirrito, John R; Heda, Ashish; Snider, B Joy; Li, Mingjie; Yanagisawa, Masashi; de Lecea, Luis; Holtzman, David M

2014-12-15

Age-related aggregation of amyloid-β (Aβ) is an upstream pathological event in Alzheimer's disease (AD) pathogenesis, and it disrupts the sleep-wake cycle. The amount of sleep declines with aging and to a greater extent in AD. Poor sleep quality and insufficient amounts of sleep have been noted in humans with preclinical evidence of AD. However, how the amount and quality of sleep affects Aβ aggregation is not yet well understood. Orexins (hypocretins) initiate and maintain wakefulness, and loss of orexin-producing neurons causes narcolepsy. We tried to determine whether orexin release or secondary changes in sleep via orexin modulation affect Aβ pathology. Amyloid precursor protein (APP)/Presenilin 1 (PS1) transgenic mice, in which the orexin gene is knocked out, showed a marked decrease in the amount of Aβ pathology in the brain with an increase in sleep time. Focal overexpression of orexin in the hippocampus in APP/PS1 mice did not alter the total amount of sleep/wakefulness and the amount of Aβ pathology. In contrast, sleep deprivation or increasing wakefulness by rescue of orexinergic neurons in APP/PS1 mice lacking orexin increased the amount of Aβ pathology in the brain. Collectively, modulation of orexin and its effects on sleep appear to modulate Aβ pathology in the brain. © 2014 Roh et al.

Neuroimaging of Narcolepsy and Kleine-Levin Syndrome.

PubMed

Hong, Seung Bong

2017-09-01

Narcolepsy is a chronic neurologic disorder with the abnormal regulation of the sleep-wake cycle, resulting in excessive daytime sleepiness, disturbed nocturnal sleep, and manifestations related to rapid eye movement sleep, such as cataplexy, sleep paralysis, and hypnagogic hallucination. Over the past decade, numerous neuroimaging studies have been performed to characterize the pathophysiology and various clinical features of narcolepsy. This article reviews structural and functional brain imaging findings in narcolepsy and Kleine-Levin syndrome. Based on the current state of research, brain imaging is a useful tool to investigate and understand the neuroanatomic correlates and brain abnormalities of narcolepsy and other hypersomnia. Copyright © 2017 Elsevier Inc. All rights reserved.

Sleep extension normalizes ERP of waking auditory sensory gating in healthy habitually short sleeping individuals.

PubMed

Gumenyuk, Valentina; Korzyukov, Oleg; Roth, Thomas; Bowyer, Susan M; Drake, Christopher L

2013-01-01

Chronic sleep loss has been associated with increased daytime sleepiness, as well as impairments in memory and attentional processes. In the present study, we evaluated the neuronal changes of a pre-attentive process of wake auditory sensory gating, measured by brain event-related potential (ERP)--P50 in eight normal sleepers (NS) (habitual total sleep time (TST) 7 h 32 m) vs. eight chronic short sleeping individuals (SS) (habitual TST ≤6 h). To evaluate the effect of sleep extension on sensory gating, the extended sleep condition was performed in chronic short sleeping individuals. Thus, one week of time in bed (6 h 11 m) corresponding to habitual short sleep (hSS), and one week of extended time (∼ 8 h 25 m) in bed corresponding to extended sleep (eSS), were counterbalanced in the SS group. The gating ERP assessment was performed on the last day after each sleep condition week (normal sleep and habitual short and extended sleep), and was separated by one week with habitual total sleep time and monitored by a sleep diary. We found that amplitude of gating was lower in SS group compared to that in NS group (0.3 µV vs. 1.2 µV, at Cz electrode respectively). The results of the group × laterality interaction showed that the reduction of gating amplitude in the SS group was due to lower amplitude over the left hemisphere and central-midline sites relative to that in the NS group. After sleep extension the amplitude of gating increased in chronic short sleeping individuals relative to their habitual short sleep condition. The sleep condition × frontality interaction analysis confirmed that sleep extension significantly increased the amplitude of gating over frontal and central brain areas compared to parietal brain areas.

CAP, epilepsy and motor events during sleep: the unifying role of arousal.

PubMed

Parrino, Liborio; Halasz, Peter; Tassinari, Carlo Alberto; Terzano, Mario Giovanni

2006-08-01

Arousal systems play a topical neurophysiologic role in protecting and tailoring sleep duration and depth. When they appear in NREM sleep, arousal responses are not limited to a single EEG pattern but are part of a continuous spectrum of EEG modifications ranging from high-voltage slow rhythms to low amplitude fast activities. The hierarchic features of arousal responses are reflected in the phase A subtypes of CAP (cyclic alternating pattern) including both slow arousals (dominated by the <1Hz oscillation) and fast arousals (ASDA arousals). CAP is an infraslow oscillation with a periodicity of 20-40s that participates in the dynamic organization of sleep and in the activation of motor events. Physiologic, paraphysiologic and pathologic motor activities during NREM sleep are always associated with a stereotyped arousal pattern characterized by an initial increase in EEG delta power and heart rate, followed by a progressive activation of faster EEG frequencies. These findings suggest that motor patterns are already written in the brain codes (central pattern generators) embraced with an automatic sequence of EEG-vegetative events, but require a certain degree of activation (arousal) to become visibly apparent. Arousal can appear either spontaneously or be elicited by internal (epileptic burst) or external (noise, respiratory disturbance) stimuli. Whether the outcome is a physiologic movement, a muscle jerk or a major epileptic attack will depend on a number of ongoing factors (sleep stage, delta power, neuro-motor network) but all events share the common trait of arousal-activated phenomena.

No effect of odor-induced memory reactivation during REM sleep on declarative memory stability

PubMed Central

Cordi, Maren J.; Diekelmann, Susanne; Born, Jan; Rasch, Björn

2014-01-01

Memory reactivations in hippocampal brain areas are critically involved in memory consolidation processes during sleep. In particular, specific firing patterns of hippocampal place cells observed during learning are replayed during subsequent sleep and rest in rodents. In humans, experimentally inducing hippocampal memory reactivations during slow-wave sleep (but not during wakefulness) benefits consolidation and immediately stabilizes declarative memories against future interference. Importantly, spontaneous hippocampal replay activity can also be observed during rapid eye movement (REM) sleep and some authors have suggested that replay during REM sleep is related to processes of memory consolidation. However, the functional role of reactivations during REM sleep for memory stability is still unclear. Here, we reactivated memories during REM sleep and examined its consequences for the stability of declarative memories. After 3 h of early, slow-wave sleep (SWS) rich sleep, 16 healthy young adults learned a 2-D object location task in the presence of a contextual odor. During subsequent REM sleep, participants were either re-exposed to the odor or to an odorless vehicle, in a counterbalanced within subject design. Reactivation was followed by an interference learning task to probe memory stability after awakening. We show that odor-induced memory reactivation during REM sleep does not stabilize memories against future interference. We propose that the beneficial effect of reactivation during sleep on memory stability might be critically linked to processes characterizing SWS including, e.g., slow oscillatory activity, sleep spindles, or low cholinergic tone, which are required for a successful redistribution of memories from medial temporal lobe regions to neocortical long-term stores. PMID:25225474

A Role for REM Sleep in Recalibrating the Sensitivity of the Human Brain to Specific Emotions

PubMed Central

Gujar, Ninad; McDonald, Steven Andrew; Nishida, Masaki

2011-01-01

Although the impact of sleep on cognitive function is increasingly well established, the role of sleep in modulating affective brain processes remains largely uncharacterized. Using a face recognition task, here we demonstrate an amplified reactivity to anger and fear emotions across the day, without sleep. However, an intervening nap blocked and even reversed this negative emotional reactivity to anger and fear while conversely enhancing ratings of positive (happy) expressions. Most interestingly, only those subjects who obtained rapid eye movement (REM) sleep displayed this remodulation of affective reactivity for the latter 2 emotion categories. Together, these results suggest that the evaluation of specific human emotions is not static across a daytime waking interval, showing a progressive reactivity toward threat-related negative expressions. However, an episode of sleep can reverse this predisposition, with REM sleep depotentiating negative reactivity toward fearful expressions while concomitantly facilitating recognition and ratings of reward-relevant positive expressions. These findings support the view that sleep, and specifically REM neurophysiology, may represent an important factor governing the optimal homeostasis of emotional brain regulation. PMID:20421251

Graph Theoretical Analysis of BOLD Functional Connectivity during Human Sleep without EEG Monitoring.

PubMed

Lv, Jun; Liu, Dongdong; Ma, Jing; Wang, Xiaoying; Zhang, Jue

2015-01-01

Functional brain networks of human have been revealed to have small-world properties by both analyzing electroencephalogram (EEG) and functional magnetic resonance imaging (fMRI) time series. In our study, by using graph theoretical analysis, we attempted to investigate the changes of paralimbic-limbic cortex between wake and sleep states. Ten healthy young people were recruited to our experiment. Data from 2 subjects were excluded for the reason that they had not fallen asleep during the experiment. For each subject, blood oxygen level dependency (BOLD) images were acquired to analyze brain network, and peripheral pulse signals were obtained continuously to identify if the subject was in sleep periods. Results of fMRI showed that brain networks exhibited stronger small-world characteristics during sleep state as compared to wake state, which was in consistent with previous studies using EEG synchronization. Moreover, we observed that compared with wake state, paralimbic-limbic cortex had less connectivity with neocortical system and centrencephalic structure in sleep. In conclusion, this is the first study, to our knowledge, has observed that small-world properties of brain functional networks altered when human sleeps without EEG synchronization. Moreover, we speculate that paralimbic-limbic cortex organization owns an efficient defense mechanism responsible for suppressing the external environment interference when humans sleep, which is consistent with the hypothesis that the paralimbic-limbic cortex may be functionally disconnected from brain regions which directly mediate their interactions with the external environment. Our findings also provide a reasonable explanation why stable sleep exhibits homeostasis which is far less susceptible to outside world.

Oscillations, neural computations and learning during wake and sleep.

PubMed

Penagos, Hector; Varela, Carmen; Wilson, Matthew A

2017-06-01

Learning and memory theories consider sleep and the reactivation of waking hippocampal neural patterns to be crucial for the long-term consolidation of memories. Here we propose that precisely coordinated representations across brain regions allow the inference and evaluation of causal relationships to train an internal generative model of the world. This training starts during wakefulness and strongly benefits from sleep because its recurring nested oscillations may reflect compositional operations that facilitate a hierarchical processing of information, potentially including behavioral policy evaluations. This suggests that an important function of sleep activity is to provide conditions conducive to general inference, prediction and insight, which contribute to a more robust internal model that underlies generalization and adaptive behavior. Copyright © 2017 Elsevier Ltd. All rights reserved.

The neuropharmacology of upper airway motor control in the awake and asleep states: implications for obstructive sleep apnoea

PubMed Central

Horner, Richard L

2001-01-01

Obstructive sleep apnoea is a common and serious breathing problem that is caused by effects of sleep on pharyngeal muscle tone in individuals with narrow upper airways. There has been increasing focus on delineating the brain mechanisms that modulate pharyngeal muscle activity in the awake and asleep states in order to understand the pathogenesis of obstructive apnoeas and to develop novel neurochemical treatments. Although initial clinical studies have met with only limited success, it is proposed that more rational and realistic approaches may be devised for neurochemical modulation of pharyngeal muscle tone as the relevant neurotransmitters and receptors that are involved in sleep-dependent modulation are identified following basic experiments. PMID:11686898

Traumatic Brain Injury, Sleep Quality, and Suicidal Ideation in Iraq/Afghanistan Era Veterans.

PubMed

DeBeer, Bryann B; Kimbrel, Nathan A; Mendoza, Corina; Davidson, Dena; Meyer, Eric C; La Bash, Heidi; Gulliver, Suzy Bird; Morissette, Sandra B

2017-07-01

The objective of this study was to test the hypothesis that sleep quality mediates the association between traumatic brain injury (TBI) history and current suicidal ideation. Measures of TBI history, sleep quality, and suicidal ideation were administered to 130 Iraq/Afghanistan veterans. As expected, sleep quality mediated the effect of TBI history on current suicidal ideation (indirect effect, 0.0082; 95% confidence interval, 0.0019-0.0196), such that history of TBI was associated with worse sleep quality, which was, in turn, associated with increased suicidal ideation. These findings highlight the importance of assessing TBI history and sleep quality during suicide risk assessments for veterans.

Strokes and their relationship with sleep and sleep disorders.

PubMed

Ferre, A; Ribó, M; Rodríguez-Luna, D; Romero, O; Sampol, G; Molina, C A; Álvarez-Sabin, J

2013-03-01

In the current population, strokes are one of the most important causes of morbidity and mortality, to which new risk factors are increasingly being attributed. Of late, there is increased interest in the relationship between sleep disorders and strokes as regards risk and prognosis. This article presents the changes in sleep architecture and brain activity in stroke patients, as well as the interaction between stroke and sleep disorders, including those which may also influence the outcome and recovery from strokes. The different treatments discussed in the literature are also reviewed, as correct treatment of such sleep disorders may not only improve quality of life and reduce after-effects, but can also increase life expectancy. Sleep disorders are becoming increasingly associated with stroke. In addition to being a risk factor, they can also interfere in the outcome and recovery of stroke patients. This article aims to present an exhaustive and current review on strokes and their relationship with sleep alterations and sleep disorders. Copyright © 2010 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.

The putative role of oxidative stress and inflammation in the pathophysiology of sleep dysfunction across neuropsychiatric disorders: Focus on chronic fatigue syndrome, bipolar disorder and multiple sclerosis.

PubMed

Morris, Gerwyn; Stubbs, Brendon; Köhler, Cristiano A; Walder, Ken; Slyepchenko, Anastasiya; Berk, Michael; Carvalho, André F

2018-04-04

Sleep and circadian abnormalities are prevalent and burdensome manifestations of diverse neuro-immune diseases, and may aggravate the course of several neuropsychiatric disorders. The underlying pathophysiology of sleep abnormalities across neuropsychiatric disorders remains unclear, and may involve the inter-play of several clinical variables and mechanistic pathways. In this review, we propose a heuristic framework in which reciprocal interactions of immune, oxidative and nitrosative stress, and mitochondrial pathways may drive sleep abnormalities across potentially neuroprogressive disorders. Specifically, it is proposed that systemic inflammation may activate microglial cells and astrocytes in brain regions involved in sleep and circadian regulation. Activated glial cells may secrete pro-inflammatory cytokines (for example, interleukin-1 beta and tumour necrosis factor alpha), nitric oxide and gliotransmitters, which may influence the expression of key circadian regulators (e.g., the Circadian Locomotor Output Cycles Kaput (CLOCK) gene). Furthermore, sleep disruption may further aggravate oxidative and nitrosative, peripheral immune activation, and (neuro) inflammation across these disorders in a vicious pathophysiological loop. This review will focus on chronic fatigue syndrome, bipolar disorder, and multiple sclerosis as exemplars of neuro-immune disorders. We conclude that novel therapeutic targets exploring immune and oxidative & nitrosative pathways (p.e. melatonin and molecular hydrogen) hold promise in alleviating sleep and circadian dysfunction in these disorders. Copyright © 2018 Elsevier Ltd. All rights reserved.

Lithium ameliorates sleep deprivation-induced mania-like behavior, hypothalamic-pituitary-adrenal (HPA) axis alterations, oxidative stress and elevations of cytokine concentrations in the brain and serum of mice.

PubMed

Valvassori, Samira S; Resende, Wilson R; Dal-Pont, Gustavo; Sangaletti-Pereira, Heron; Gava, Fernanda F; Peterle, Bruna R; Carvalho, André F; Varela, Roger B; Dal-Pizzol, Felipe; Quevedo, João

2017-06-01

The goal of the present study was to investigate the effects of lithium administration on behavior, oxidative stress parameters and cytokine levels in the periphery and brain of mice subjected to an animal model of mania induced by paradoxical sleep deprivation (PSD). Male C57 mice were treated with saline or lithium for 7 days. The sleep deprivation protocol started on the 5th day during for the last 36 hours of the treatment period. Immediately after the sleep deprivation protocol, animals locomotor activity was evaluated and serum and brain samples was extracted to evaluation of corticosterone and adrenocorticotropic hormone circulating levels, oxidative stress parameters and citokynes levels. The results showed that PSD induced hyperactivity in mice, which is considered a mania-like behavior. PSD increased lipid peroxidation and oxidative damage to DNA, as well as causing alterations to antioxidant enzymes in the frontal cortex, hippocampus and serum of mice. In addition, PSD increased the levels of cytokines in the brains of mice. Treatment with lithium prevented the mania-like behavior, oxidative damage and cytokine alterations induced by PSD. Improving our understanding of oxidative damage in biomolecules, antioxidant mechanisms and the inflammatory system - alterations presented in the animal models of mania - is important in helping us to improve our knowledge concerning the pathophysiology of BD, and the mechanisms of action employed by mood stabilizers. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

High Resolution Topography of Age-Related Changes in Non-Rapid Eye Movement Sleep Electroencephalography

PubMed Central

Sprecher, Kate E.; Riedner, Brady A.; Smith, Richard F.; Tononi, Giulio; Davidson, Richard J.; Benca, Ruth M.

2016-01-01

Sleeping brain activity reflects brain anatomy and physiology. The aim of this study was to use high density (256 channel) electroencephalography (EEG) during sleep to characterize topographic changes in sleep EEG power across normal aging, with high spatial resolution. Sleep was evaluated in 92 healthy adults aged 18–65 years old using full polysomnography and high density EEG. After artifact removal, spectral power density was calculated for standard frequency bands for all channels, averaged across the NREM periods of the first 3 sleep cycles. To quantify topographic changes with age, maps were generated of the Pearson’s coefficient of the correlation between power and age at each electrode. Significant correlations were determined by statistical non-parametric mapping. Absolute slow wave power declined significantly with increasing age across the entire scalp, whereas declines in theta and sigma power were significant only in frontal regions. Power in fast spindle frequencies declined significantly with increasing age frontally, whereas absolute power of slow spindle frequencies showed no significant change with age. When EEG power was normalized across the scalp, a left centro-parietal region showed significantly less age-related decline in power than the rest of the scalp. This partial preservation was particularly significant in the slow wave and sigma bands. The effect of age on sleep EEG varies substantially by region and frequency band. This non-uniformity should inform the design of future investigations of aging and sleep. This study provides normative data on the effect of age on sleep EEG topography, and provides a basis from which to explore the mechanisms of normal aging as well as neurodegenerative disorders for which age is a risk factor. PMID:26901503

Quantitative differences among EMG activities of muscles innervated by subpopulations of hypoglossal and upper spinal motoneurons during non-REM sleep - REM sleep transitions: a window on neural processes in the sleeping brain

PubMed Central

RUKHADZE, I.; KAMANI, H.; KUBIN, L.

2017-01-01

In the rat, a species widely used to study the neural mechanisms of sleep and motor control, lingual electromyographic activity (EMG) is minimal during non-rapid eye movement (non-REM) sleep and then phasic twitches gradually increase after the onset of REM sleep. To better characterize the central neural processes underlying this pattern, we quantified EMG of muscles innervated by distinct subpopulations of hypoglossal motoneurons and nuchal (N) EMG during transitions from non-REM sleep to REM sleep. In 8 chronically instrumented rats, we recorded cortical EEG, EMG at sites near the base of the tongue where genioglossal and intrinsic muscle fibers predominate (GG-I), EMG of the geniohyoid (GH) muscle, and N EMG. Sleep-wake states were identified and EMGs quantified relative to their mean levels in wakefulness in successive 10 s epochs. During non-REM sleep, the average EMG levels differed among the three muscles, with the order being N > GH > GG-I. During REM sleep, due to different magnitudes of phasic twitches, the order was reversed to GG-I > GH > N. GG-I and GH exhibited a gradual increase of twitching that peaked at 70–120 s after the onset of REM sleep and then declined if the REM sleep episode lasted longer. We propose that a common phasic excitatory generator impinges on motoneuron pools that innervate different muscles, but twitching magnitudes are different due to different levels of tonic motoneuronal hyperpolarization. We also propose that REM sleep episodes of average durations are terminated by intense activity of the central generator of phasic events, whereas long REM sleep episodes end as a result of a gradual waning of the tonic disfacilitatory and inhibitory processes. PMID:22205596

Analysis and automatic identification of sleep stages using higher order spectra.

PubMed

Acharya, U Rajendra; Chua, Eric Chern-Pin; Chua, Kuang Chua; Min, Lim Choo; Tamura, Toshiyo

2010-12-01

Electroencephalogram (EEG) signals are widely used to study the activity of the brain, such as to determine sleep stages. These EEG signals are nonlinear and non-stationary in nature. It is difficult to perform sleep staging by visual interpretation and linear techniques. Thus, we use a nonlinear technique, higher order spectra (HOS), to extract hidden information in the sleep EEG signal. In this study, unique bispectrum and bicoherence plots for various sleep stages were proposed. These can be used as visual aid for various diagnostics application. A number of HOS based features were extracted from these plots during the various sleep stages (Wakefulness, Rapid Eye Movement (REM), Stage 1-4 Non-REM) and they were found to be statistically significant with p-value lower than 0.001 using ANOVA test. These features were fed to a Gaussian mixture model (GMM) classifier for automatic identification. Our results indicate that the proposed system is able to identify sleep stages with an accuracy of 88.7%.

The Effect of Body Posture on Brain Glymphatic Transport.

PubMed

Lee, Hedok; Xie, Lulu; Yu, Mei; Kang, Hongyi; Feng, Tian; Deane, Rashid; Logan, Jean; Nedergaard, Maiken; Benveniste, Helene

2015-08-05

The glymphatic pathway expedites clearance of waste, including soluble amyloid β (Aβ) from the brain. Transport through this pathway is controlled by the brain's arousal level because, during sleep or anesthesia, the brain's interstitial space volume expands (compared with wakefulness), resulting in faster waste removal. Humans, as well as animals, exhibit different body postures during sleep, which may also affect waste removal. Therefore, not only the level of consciousness, but also body posture, might affect CSF-interstitial fluid (ISF) exchange efficiency. We used dynamic-contrast-enhanced MRI and kinetic modeling to quantify CSF-ISF exchange rates in anesthetized rodents' brains in supine, prone, or lateral positions. To validate the MRI data and to assess specifically the influence of body posture on clearance of Aβ, we used fluorescence microscopy and radioactive tracers, respectively. The analysis showed that glymphatic transport was most efficient in the lateral position compared with the supine or prone positions. In the prone position, in which the rat's head was in the most upright position (mimicking posture during the awake state), transport was characterized by "retention" of the tracer, slower clearance, and more CSF efflux along larger caliber cervical vessels. The optical imaging and radiotracer studies confirmed that glymphatic transport and Aβ clearance were superior in the lateral and supine positions. We propose that the most popular sleep posture (lateral) has evolved to optimize waste removal during sleep and that posture must be considered in diagnostic imaging procedures developed in the future to assess CSF-ISF transport in humans. The rodent brain removes waste better during sleep or anesthesia compared with the awake state. Animals exhibit different body posture during the awake and sleep states, which might affect the brain's waste removal efficiency. We investigated the influence of body posture on brainwide transport of inert tracers of anesthetized rodents. The major finding of our study was that waste, including Aβ, removal was most efficient in the lateral position (compared with the prone position), which mimics the natural resting/sleeping position of rodents. Although our finding awaits testing in humans, we speculate that the lateral position during sleep has advantage with regard to the removal of waste products including Aβ, because clinical studies have shown that sleep drives Aβ clearance from the brain. Copyright © 2015 the authors 0270-6474/15/3511034-11$15.00/0.

The Effect of Body Posture on Brain Glymphatic Transport

PubMed Central

Lee, Hedok; Xie, Lulu; Yu, Mei; Kang, Hongyi; Feng, Tian; Deane, Rashid; Logan, Jean; Nedergaard, Maiken

2015-01-01

The glymphatic pathway expedites clearance of waste, including soluble amyloid β (Aβ) from the brain. Transport through this pathway is controlled by the brain's arousal level because, during sleep or anesthesia, the brain's interstitial space volume expands (compared with wakefulness), resulting in faster waste removal. Humans, as well as animals, exhibit different body postures during sleep, which may also affect waste removal. Therefore, not only the level of consciousness, but also body posture, might affect CSF–interstitial fluid (ISF) exchange efficiency. We used dynamic-contrast-enhanced MRI and kinetic modeling to quantify CSF-ISF exchange rates in anesthetized rodents' brains in supine, prone, or lateral positions. To validate the MRI data and to assess specifically the influence of body posture on clearance of Aβ, we used fluorescence microscopy and radioactive tracers, respectively. The analysis showed that glymphatic transport was most efficient in the lateral position compared with the supine or prone positions. In the prone position, in which the rat's head was in the most upright position (mimicking posture during the awake state), transport was characterized by “retention” of the tracer, slower clearance, and more CSF efflux along larger caliber cervical vessels. The optical imaging and radiotracer studies confirmed that glymphatic transport and Aβ clearance were superior in the lateral and supine positions. We propose that the most popular sleep posture (lateral) has evolved to optimize waste removal during sleep and that posture must be considered in diagnostic imaging procedures developed in the future to assess CSF-ISF transport in humans. SIGNIFICANCE STATEMENT The rodent brain removes waste better during sleep or anesthesia compared with the awake state. Animals exhibit different body posture during the awake and sleep states, which might affect the brain's waste removal efficiency. We investigated the influence of body posture on brainwide transport of inert tracers of anesthetized rodents. The major finding of our study was that waste, including Aβ, removal was most efficient in the lateral position (compared with the prone position), which mimics the natural resting/sleeping position of rodents. Although our finding awaits testing in humans, we speculate that the lateral position during sleep has advantage with regard to the removal of waste products including Aβ, because clinical studies have shown that sleep drives Aβ clearance from the brain. PMID:26245965

Prefrontal atrophy, disrupted NREM slow waves, and impaired hippocampal-dependent memory in aging

PubMed Central

Mander, Bryce A.; Rao, Vikram; Lu, Brandon; Saletin, Jared M.; Lindquist, John R.; Ancoli-Israel, Sonia; Jagust, William; Walker, Matthew P.

2014-01-01

Aging has independently been associated with regional brain atrophy, reduced non-rapid eye movement (NREM) slow-wave activity (SWA), and impaired long-term retention of episodic memories. However, that the interaction of these factors represents a neuropatholgical pathway associated with cognitive decline in later life remains unknown. Here, we show that age-related medial prefrontal cortex (mPFC) grey-matter atrophy is associated with reduced NREM SWA activity in older adults, the extent to which statistically mediates the impairment of overnight sleep-dependent memory retention. Moreover, this memory impairment was further associated with persistent hippocampal activation and reduced task-related hippocampal-prefrontal cortex connectivity, potentially representing impoverished hippocampal-neocortical memory transformation. Together, these data support a model in which age-related mPFC atrophy diminishes SWA, the functional consequence of which is impaired long-term memory. Such findings suggest that sleep disruption in the elderly, mediated by structural brain changes, represent a novel contributing factor to age-related cognitive decline in later life. PMID:23354332

Radio frequency electromagnetic field exposure in humans: Estimation of SAR distribution in the brain, effects on sleep and heart rate.

PubMed

Huber, Reto; Schuderer, Jürgen; Graf, Thomas; Jütz, Kathrin; Borbély, Alexander A; Kuster, Niels; Achermann, Peter

2003-05-01

In two previous studies we demonstrated that radiofrequency electromagnetic fields (RF EMF) similar to those emitted by digital radiotelephone handsets affect brain physiology of healthy young subjects exposed to RF EMF (900 MHz; spatial peak specific absorption rate [SAR] 1 W/kg) either during sleep or during the waking period preceding sleep. In the first experiment, subjects were exposed intermittently during an 8 h nighttime sleep episode and in the second experiment, unilaterally for 30 min prior to a 3 h daytime sleep episode. Here we report an extended analysis of the two studies as well as the detailed dosimetry of the brain areas, including the assessment of the exposure variability and uncertainties. The latter enabled a more in depth analysis and discussion of the findings. Compared to the control condition with sham exposure, spectral power of the non-rapid eye movement sleep electroencephalogram (EEG) was initially increased in the 9-14 Hz range in both experiments. No topographical differences with respect to the effect of RF EMF exposure were observed in the two experiments. Even unilateral exposure during waking induced a similar effect in both hemispheres. Exposure during sleep reduced waking after sleep onset and affected heart rate variability. Exposure prior to sleep reduced heart rate during waking and stage 1 sleep. The lack of asymmetries in the effects on sleep EEG, independent of bi- or unilateral exposure of the cortex, may indicate involvement of subcortical bilateral projections to the cortex in the generation of brain function changes, especially since the exposure of the thalamus was similar in both experiments (approx. 0.1 W/kg). Copyright 2003 Wiley-Liss, Inc.

Three-Dimensional Electroencephalographic Changes on Low-Resolution Brain Electromagnetic Tomography (LORETA) During the Sleep Onset Period.

PubMed

Park, Doo-Heum; Ha, Jee Hyun; Ryu, Seung-Ho; Yu, Jaehak; Shin, Chul-Jin

2015-10-01

Electroencephalographic (EEG) patterns during sleep are markedly different from those measured during the waking state, but the process of falling asleep is not fully understood in terms of biochemical and neurophysiological aspects. We sought to investigate EEG changes that occur during the transitional period from wakefulness to sleep in a 3-dimensional manner to gain a better understanding of the physiological meaning of sleep for the brain. We examined EEG 3-dimensionally using LORETA (low-resolution electromagnetic tomography), to localize the brain region associated with changes that occur during the sleep onset period (SOP). Thirty-channel EEG was recorded in 61 healthy subjects. EEG power spectra and intracortical standardized LORETA were compared between 4 types of 30-second states, including the wakeful stage, transition stage, early sleep stage 1, and late sleep stage 1. Sleep onset began with increased delta and theta power and decreased alpha-1 power in the occipital lobe, and increased theta power in the parietal lobe. Thereafter, global reductions of alpha-1 and alpha-2 powers and greater increases of theta power in the occipito-parietal lobe occurred. As sleep became deeper in sleep stage 1, beta-2 and beta-3, powers decreased mainly in the frontal lobe and some regions of the parieto-temporo-limbic area. These findings suggest that sleep onset includes at least 3 steps in a sequential manner, which include an increase in theta waves in the posterior region of the brain, a global decrease in alpha waves, and a decrease in beta waves in the fronto-central area. © EEG and Clinical Neuroscience Society (ECNS) 2014.

How (and why) the immune system makes us sleep

PubMed Central

Imeri, Luca; Opp, Mark R.

2010-01-01

Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value. PMID:19209176

How (and why) the immune system makes us sleep.

PubMed

Imeri, Luca; Opp, Mark R

2009-03-01

Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value.

Inducing task-relevant responses to speech in the sleeping brain.

PubMed

Kouider, Sid; Andrillon, Thomas; Barbosa, Leonardo S; Goupil, Louise; Bekinschtein, Tristan A

2014-09-22

Falling asleep leads to a loss of sensory awareness and to the inability to interact with the environment [1]. While this was traditionally thought as a consequence of the brain shutting down to external inputs, it is now acknowledged that incoming stimuli can still be processed, at least to some extent, during sleep [2]. For instance, sleeping participants can create novel sensory associations between tones and odors [3] or reactivate existing semantic associations, as evidenced by event-related potentials [4-7]. Yet, the extent to which the brain continues to process external stimuli remains largely unknown. In particular, it remains unclear whether sensory information can be processed in a flexible and task-dependent manner by the sleeping brain, all the way up to the preparation of relevant actions. Here, using semantic categorization and lexical decision tasks, we studied task-relevant responses triggered by spoken stimuli in the sleeping brain. Awake participants classified words as either animals or objects (experiment 1) or as either words or pseudowords (experiment 2) by pressing a button with their right or left hand, while transitioning toward sleep. The lateralized readiness potential (LRP), an electrophysiological index of response preparation, revealed that task-specific preparatory responses are preserved during sleep. These findings demonstrate that despite the absence of awareness and behavioral responsiveness, sleepers can still extract task-relevant information from external stimuli and covertly prepare for appropriate motor responses. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

[Sleep psychiatry].

PubMed

Chiba, Shigeru

2013-01-01

Sleep disorders are serious issues in modern society. There has been marked scientific interest in sleep for a century, with the discoveries of the electrical activity of the brain (EEG), sleep-wake system, rapid eye movement (REM) sleep, and circadian rhythm system. Additionally, the advent of video-polysomnography in clinical research has revealed some of the consequences of disrupted sleep and sleep deprivation in psychiatric disorders. Decades of clinical research have demonstrated that sleep disorders are intimately tied to not only physical disease (e. g., lifestyle-related disease) but psychiatric illness. According to The International Classification of Sleep Disorders (2005), sleep disorders are classified into 8 major categories: 1) insomnia, 2) sleep-related breathing disorders, 3) hypersomnias of central origin, 4) circadian rhythm sleep disorders, 5) parasomnias, 6) sleep-related movement disorders, 7) isolated symptoms, and 8) other sleep disorders. Several sleep disorders, including obstructive sleep apnea syndrome, restless legs syndrome, periodic limb movement disorder, sleepwalking, REM sleep behavior disorder, and narcolepsy, may be comorbid or possibly mimic numerous psychiatric disorders, and can even occur due to psychiatric pharmacotherapy. Moreover, sleep disorders may exacerbate underlying psychiatric disorders when left untreated. Therefore, psychiatrists should pay attention to the intimate relationship between sleep disorders and psychiatric symptoms. Sleep psychiatry is an academic field focusing on interrelations between sleep medicine and psychiatry. This mini-review summarizes recent findings in sleep psychiatry. Future research on the bidirectional relation between sleep disturbance and psychiatric symptoms will shed light on the pathophysiological view of psychiatric disorders and sleep disorders.

Sleep Disorders Associated With Alzheimer's Disease: A Perspective

PubMed Central

Brzecka, Anna; Leszek, Jerzy; Ashraf, Ghulam Md; Ejma, Maria; Ávila-Rodriguez, Marco F.; Yarla, Nagendra S.; Tarasov, Vadim V.; Chubarev, Vladimir N.; Samsonova, Anna N.; Barreto, George E.; Aliev, Gjumrakch

2018-01-01

Sleep disturbances, as well as sleep-wake rhythm disturbances, are typical symptoms of Alzheimer's disease (AD) that may precede the other clinical signs of this neurodegenerative disease. Here, we describe clinical features of sleep disorders in AD and the relation between sleep disorders and both cognitive impairment and poor prognosis of the disease. There are difficulties of the diagnosis of sleep disorders based on sleep questionnaires, polysomnography or actigraphy in the AD patients. Typical disturbances of the neurophysiological sleep architecture in the course of the AD include deep sleep and paradoxical sleep deprivation. Among sleep disorders occurring in patients with AD, the most frequent disorders are sleep breathing disorders and restless legs syndrome. Sleep disorders may influence circadian fluctuations of the concentrations of amyloid-β in the interstitial brain fluid and in the cerebrovascular fluid related to the glymphatic brain system and production of the amyloid-β. There is accumulating evidence suggesting that disordered sleep contributes to cognitive decline and the development of AD pathology. In this mini-review, we highlight and discuss the association between sleep disorders and AD. PMID:29904334

Neuroscience-driven discovery and development of sleep therapeutics.

PubMed

Dresler, M; Spoormaker, V I; Beitinger, P; Czisch, M; Kimura, M; Steiger, A; Holsboer, F

2014-03-01

Until recently, neuroscience has given sleep research and discovery of better treatments of sleep disturbances little attention, despite the fact that disturbed sleep has overwhelming impact on human health. Sleep is a complex phenomenon in which specific psychological, electrophysiological, neurochemical, endocrinological, immunological and genetic factors are involved. The brain as both the generator and main object of sleep is obviously of particular interest, which makes a neuroscience-driven view the most promising approach to evaluate clinical implications and applications of sleep research. Polysomnography as the gold standard of sleep research, complemented by brain imaging, neuroendocrine testing, genomics and other laboratory measures can help to create composite biomarkers that allow maximizing the effects of individualized therapies while minimizing adverse effects. Here we review the current state of the neuroscience of sleep, sleep disorders and sleep therapeutics and will give some leads to promote the discovery and development of sleep medicines that are better than those we have today. Copyright © 2013 Elsevier Inc. All rights reserved.

The genetics of insomnia--evidence for epigenetic mechanisms?

PubMed

Palagini, Laura; Biber, Knut; Riemann, Dieter

2014-06-01

Sleep is a complex physiological process and still remains one of the great mysteries of science. Over the past 10 y, genetic research has provided a new avenue to address the regulation and function of sleep. Gene loci that contribute quantitatively to sleep characteristics and variability have already been identified. However, up to now, a genetic basis has been established only for a few sleep disorders. Little is yet known about the genetic background of insomnia, one of the most common sleep disorders. According to the conceptualisation of the 3P model of insomnia, predisposing, precipitating and perpetuating factors contribute to the development and maintenance of insomnia. Growing evidence from studies of predisposing factors suggests a certain degree of heritability for insomnia and for a reactivity of sleep patterns to stressful events, explaining the emergence of insomnia in response to stressful life events. While a genetic susceptibility may modulate the impact of stress on the brain, this finding does not provide us with a complete understanding of the capacity of stress to produce long-lasting perturbations of brain and behaviour. Epigenetic gene-environment interactions have been identified just recently and may provide a more complex understanding of the genetic control of sleep and its disorders. It was recently hypothesised that stress-response-related brain plasticity might be epigenetically controlled and, moreover, several epigenetic mechanisms have been assumed to be involved in the regulation of sleep. Hence, it might be postulated that insomnia may be influenced by an epigenetic control process of both sleep mechanisms and stress-response-related gene-environment interactions having an impact on brain plasticity. This paper reviews the evidence for the genetic basis of insomnia and recent theories about epigenetic mechanisms involved in both sleep regulation and brain-stress response, leading to the hypothesis of an involvement of epigenetic mechanisms in the development and maintenance of insomnia. Copyright © 2013 Elsevier Ltd. All rights reserved.

Reversal of functional changes in the brain associated with obstructive sleep apnoea following 6 months of CPAP.

PubMed

Fatouleh, Rania H; Lundblad, Linda C; Macey, Paul M; McKenzie, David K; Henderson, Luke A; Macefield, Vaughan G

2015-01-01

Obstructive sleep apnoea (OSA) is associated with an increase in the number of bursts of muscle sympathetic nerve activity (MSNA), leading to neurogenic hypertension. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment for preventing collapse of the upper airway in OSA. In addition to improving sleep, CPAP decreases daytime MSNA towards control levels. It remains unknown how this restoration of MSNA occurs, in particular whether CPAP treatment results in a simple readjustment in activity of those brain regions responsible for the initial increase in MSNA or whether other brain regions are recruited to over-ride aberrant brain activity. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI), we aimed to assess brain activity associated with each individual subject's patterns of MSNA prior to and following 6 months of CPAP treatment. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted into the common peroneal nerve in 13 newly diagnosed patients with OSA before and after 6 months of treatment with CPAP and in 15 healthy control subjects while lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min). Fluctuations in BOLD signal intensity in multiple regions covaried with the intensity of the concurrently recorded bursts of MSNA. There was a significant fall in MSNA after 6 months of CPAP (39 ± 2 bursts/min). The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices. These data support our contention that functional changes in these suprabulbar sites are, via projections to the brainstem, driving the augmented sympathetic outflow to the muscle vascular bed in untreated OSA.

Selective Coupling between Theta Phase and Neocortical Fast Gamma Oscillations during REM-Sleep in Mice

PubMed Central

Scheffzük, Claudia; Kukushka, Valeriy I.; Vyssotski, Alexei L.; Draguhn, Andreas

2011-01-01

Background The mammalian brain expresses a wide range of state-dependent network oscillations which vary in frequency and spatial extension. Such rhythms can entrain multiple neurons into coherent patterns of activity, consistent with a role in behaviour, cognition and memory formation. Recent evidence suggests that locally generated fast network oscillations can be systematically aligned to long-range slow oscillations. It is likely that such cross-frequency coupling supports specific tasks including behavioural choice and working memory. Principal Findings We analyzed temporal coupling between high-frequency oscillations and EEG theta activity (4–12 Hz) in recordings from mouse parietal neocortex. Theta was exclusively present during active wakefulness and REM-sleep. Fast oscillations occurred in two separate frequency bands: gamma (40–100 Hz) and fast gamma (120–160 Hz). Theta, gamma and fast gamma were more prominent during active wakefulness as compared to REM-sleep. Coupling between theta and the two types of fast oscillations, however, was more pronounced during REM-sleep. This state-dependent cross-frequency coupling was particularly strong for theta-fast gamma interaction which increased 9-fold during REM as compared to active wakefulness. Theta-gamma coupling increased only by 1.5-fold. Significance State-dependent cross-frequency-coupling provides a new functional characteristic of REM-sleep and establishes a unique property of neocortical fast gamma oscillations. Interactions between defined patterns of slow and fast network oscillations may serve selective functions in sleep-dependent information processing. PMID:22163023

Brain electrical activity and subjective experience during altered states of consciousness: ganzfeld and hypnagogic states.

PubMed

Wackermann, Jiri; Pütz, Peter; Büchi, Simone; Strauch, Inge; Lehmann, Dietrich

2002-11-01

Manifestations of experimentally induced altered states of consciousness in the brain's electrical activity as well as in subjective experience were explored via the hypnagogic state at sleep onset, and the state induced by exposure to an unstructured perceptual field (ganzfeld). Twelve female paid volunteers participated in sessions involving sleep onset, ganzfeld, and eyes-closed relaxed waking, and were repeatedly prompted for recall of their momentary mentation, according to a predefined schedule. Nineteen channel EEG, two channels EOG and EMG were recorded simultaneously. The mentation reports were followed by the subjects' ratings of their experience on a number of ordinal scales. Two-hundred and forty-one mentation reports were collected. EEG epochs immediately preceding the mentation reports were FFT-analysed and the spectra compared between states. The ganzfeld EEG spectrum, showing no signs of decreased vigilance, was very similar to the EEG spectrum of waking states, even showed a minor acceleration of alpha activity. The subjective experience data were reduced to four principal components: Factor I represented the subjective vigilance dimension, as confirmed by correlations with EEG spectral indices. Only Factor IV, the 'absorption' dimension, differentiated between the ganzfeld state (more absorption) and other states. In waking states and in ganzfeld, the subjects estimated elapsed time periods significantly shorter than in states at sleep onset. The results did not support the assumption of a hypnagogic nature of the ganzfeld imagery. Dream-like imagery can occur in various global functional states of the brain; hypnagogic and ganzfeld-induced states should be conceived as special cases of a broader class of 'hypnagoid' phenomena.

Regional reductions in sleep electroencephalography power in obstructive sleep apnea: a high-density EEG study.

PubMed

Jones, Stephanie G; Riedner, Brady A; Smith, Richard F; Ferrarelli, Fabio; Tononi, Giulio; Davidson, Richard J; Benca, Ruth M

2014-02-01

Obstructive sleep apnea (OSA) is associated with significant alterations in neuronal integrity resulting from either hypoxemia and/or sleep loss. A large body of imaging research supports reductions in gray matter volume, alterations in white matter integrity and resting state activity, and functional abnormalities in response to cognitive challenge in various brain regions in patients with OSA. In this study, we used high-density electroencephalography (hdEEG), a functional imaging tool that could potentially be used during routine clinical care, to examine the regional distribution of neural activity in a non-clinical sample of untreated men and women with moderate/severe OSA. Sleep was recorded with 256-channel EEG in relatively healthy subjects with apnea-hypopnea index (AHI) > 10, as well as age-, sex-, and body mass index-matched controls selected from a research population initially recruited for a study on sleep and meditation. Sleep laboratory. Nine subjects with AHI > 10 and nine matched controls. N/A. Topographic analysis of hdEEG data revealed a broadband reduction in EEG power in a circumscribed region overlying the parietal cortex in OSA subjects. This parietal reduction in neural activity was present, to some extent, across all frequency bands in all stages and episodes of nonrapid eye movement sleep. This investigation suggests that regional deficits in electroencephalography (EEG) power generation may be a useful clinical marker for neural disruption in obstructive sleep apnea, and that high-density EEG may have the sensitivity to detect pathological cortical changes early in the disease process.

Incorporation of recent waking-life experiences in dreams correlates with frontal theta activity in REM sleep.

PubMed

Eichenlaub, Jean-Baptiste; van Rijn, Elaine; Gareth Gaskell, M; Lewis, Penelope A; Maby, Emmanuel; Malinowski, Josie; Walker, Matthew P; Boy, Frederic; Blagrove, Mark

2018-06-04

Rapid Eye Movement (REM) sleep and its main oscillatory feature, frontal theta, have been related to the processing of recent emotional memories. As memories constitute much of the source material for our dreams, we explored the link between REM frontal theta and the memory sources of dreaming, so as to elucidate the brain activities behind the formation of dream content. Twenty participants were woken for dream reports in REM and Slow Wave Sleep (SWS) while monitored using electroencephalography. Eighteen participants reported at least one REM dream and 14 at least one SWS dream, and they, and independent judges, subsequently compared their dream reports with log records of their previous daily experiences. The number of references to recent waking-life experiences in REM dreams was positively correlated with frontal theta activity in the REM sleep period. No such correlation was observed for older memories, nor for SWS dreams. The emotional intensity of recent waking-life experiences incorporated into dreams was higher than the emotional intensity of experiences that were not incorporated. These results suggest that the formation of wakefulness-related dream content is associated with REM theta activity, and accords with theories that dreaming reflects emotional memory processing taking place in REM sleep.

[Circadian rhythm disruption and human development].

PubMed

Kohyama, Jun

2013-12-01

Ontogenetic developments of rest-activity, sleep-wakefulness, temperature and several hormone rhythms in humans were reviewed. The reported effects of environment on these alterations were also summarized. Then, disorders or conditions which often encounter during early stage of life and reveal circadian rhythm disruptions were described. These disorders or conditions included severe brain damage, visual disturbance, developmental disorders(autistic spectrum disorder and attention deficit/hyperactivity disorder), Rett syndrome, Angelman syndrome, Smith-Magenis syndrome, epilepsy, Yonaki, and inadequate sleep hygiene. Finally, it was emphasized that we should pay special attention on the development of youngsters who showed sleep disturbance during early stage of life with special reference to the later occurrence of developmental disorders.

Effets des radiofréquences sur le système nerveux central chez lʼhomme : EEG, sommeil, cognition, vascularisation

NASA Astrophysics Data System (ADS)

Ghosn, Rania; Villégier, Anne-Sophie; Selmaoui, Brahim; Thuróczy, Georges; de Sèze, René

2013-05-01

Most of clinical studies on radiofrequency electromagnetic fields (RF) were directed at mobile phone-related exposures, usually at the level of the head, at their effect on some physiological functions including sleep, brain electrical activity (EEG), cognitive processes, brain vascularisation, and more generally on the cardiovascular and endocrine systems. They were frequently carried out on healthy adults. Effects on the amplitude of EEG alpha waves, mainly during sleep, look reproducible. It would however be important to define more precisely whether and how the absence of electromagnetic disturbance between RF exposure and the recording systems is checked. No consensus arises about cognitive effects. Some effects on cerebral vascularisation need complementary work.

Hypothalamic Tuberomammillary Nucleus Neurons: Electrophysiological Diversity and Essential Role in Arousal Stability.

PubMed

Fujita, Akie; Bonnavion, Patricia; Wilson, Miryam H; Mickelsen, Laura E; Bloit, Julien; de Lecea, Luis; Jackson, Alexander C

2017-09-27

Histaminergic (HA) neurons, found in the posterior hypothalamic tuberomammillary nucleus (TMN), extend fibers throughout the brain and exert modulatory influence over numerous physiological systems. Multiple lines of evidence suggest that the activity of HA neurons is important in the regulation of vigilance despite the lack of direct, causal evidence demonstrating its requirement for the maintenance of arousal during wakefulness. Given the strong correlation between HA neuron excitability and behavioral arousal, we investigated both the electrophysiological diversity of HA neurons in brain slices and the effect of their acute silencing in vivo in male mice. For this purpose, we first validated a transgenic mouse line expressing cre recombinase in histidine decarboxylase-expressing neurons ( Hdc -Cre) followed by a systematic census of the membrane properties of both HA and non-HA neurons in the ventral TMN (TMNv) region. Through unsupervised hierarchical cluster analysis, we found electrophysiological diversity both between TMNv HA and non-HA neurons, and among HA neurons. To directly determine the impact of acute cessation of HA neuron activity on sleep-wake states in awake and behaving mice, we examined the effects of optogenetic silencing of TMNv HA neurons in vivo We found that acute silencing of HA neurons during wakefulness promotes slow-wave sleep, but not rapid eye movement sleep, during a period of low sleep pressure. Together, these data suggest that the tonic firing of HA neurons is necessary for the maintenance of wakefulness, and their silencing not only impairs arousal but is sufficient to rapidly and selectively induce slow-wave sleep. SIGNIFICANCE STATEMENT The function of monoaminergic systems and circuits that regulate sleep and wakefulness is often disrupted as part of the pathophysiology of many neuropsychiatric disorders. One such circuit is the posterior hypothalamic histamine (HA) system, implicated in supporting wakefulness and higher brain function, but has been difficult to selectively manipulate owing to cellular heterogeneity in this region. Here we use a transgenic mouse to interrogate both the characteristic firing properties of HA neurons and their specific role in maintaining wakefulness. Our results demonstrate that the acute, cell type-specific silencing of HA neurons during wakefulness is sufficient to not only impair arousal but to rapidly and selectively induce slow-wave sleep. This work furthers our understanding of HA-mediated mechanisms that regulate behavioral arousal. Copyright © 2017 the authors 0270-6474/17/379575-19$15.00/0.

Disrupted Sleep in Narcolepsy: Exploring the Integrity of Galanin Neurons in the Ventrolateral Preoptic Area

PubMed Central

Gavrilov, Yury V.; Ellison, Brian A.; Yamamoto, Mihoko; Reddy, Hasini; Haybaeck, Johannes; Mignot, Emmanuel; Baumann, Christian R.; Scammell, Thomas E.; Valko, Philipp O.

2016-01-01

Study Objectives: To examine the integrity of sleep-promoting neurons of the ventrolateral preoptic nucleus (VLPO) in postmortem brains of narcolepsy type 1 patients. Methods: Postmortem examination of five narcolepsy and eight control brains. Results: VLPO galanin neuron count did not differ between narcolepsy patients (11,151 ± 3,656) and controls (13,526 ± 9,544). Conclusions: A normal number of galanin-immunoreactive VLPO neurons in narcolepsy type 1 brains at autopsy suggests that VLPO cell loss is an unlikely explanation for the sleep fragmentation that often accompanies the disease. Citation: Gavrilov YV, Ellison BA, Yamamoto M, Reddy H, Haybaeck J, Mignot E, Baumann CR, Scammell TE, Valko PO. Disrupted sleep in narcolepsy: exploring the integrity of galanin neurons in the ventrolateral preoptic area. SLEEP 2016;39(5):1059–1062. PMID:26951397

Naturalistic Field Studies of Sleep and Performance

DTIC Science & Technology

2011-05-01

delight: The affective pleasures and pains of  brain   system  for eating and energy regulation  In, L. Dube, A. Bechara, A. Drewnowski, J.  LeBel, P. James...understanding the  brain  organization of sleep in humans and animals and on using  this understanding to link sleep, by way of the underlying...homeostatic (use dependent) drive for sleep. Thompson et al.  (2010) found biological markers at the molecular level of sleep deprivation in the  mouse  brain

Cafeteria feeding induces interleukin-1beta mRNA expression in rat liver and brain.

PubMed

Hansen, M K; Taishi, P; Chen, Z; Krueger, J M

1998-06-01

intake affects gut-immune function and can provide a strong intestinal antigen challenge resulting in activation of host defense mechanisms in the digestive system. Previously, we showed that feeding rats a cafeteria diet increases non-rapid eye movement sleep by a subdiaphragmatic mechanism. Food intake and sleep regulation and the immune system share the regulatory molecule interleukin-1beta (IL-1beta). Thus this study examined the effects of a cafeteria diet on IL-1beta mRNA and IL-1 receptor accessory protein (IL-1RAP) mRNA expression in rat liver and brain. Rats were fed normal rat chow or a palatable diet consisting of bread, chocolate, and shortbread cookies (cafeteria diet). After 3 days, midway between the light period of the light-dark cycle, rats were killed by decapitation. Feeding rats a cafeteria diet resulted in increased IL-1beta mRNA expression in the liver and hypothalamus compared with rats fed only the normal rat chow. In addition, cafeteria feeding decreased IL-1RAP mRNA levels in the liver and brain stem. These results indicate that feeding has direct effects on cytokine production and together with other data suggest that the increased sleep that accompanies increased feeding may be the result of increased brain IL-1beta. These results further suggest that cytokine-to-brain communication may be important in normal physiological conditions, such as feeding, as well as being important during inflammatory responses.

Accelerated echo-planar J-resolved spectroscopic imaging in the human brain using compressed sensing: a pilot validation in obstructive sleep apnea.

PubMed

Sarma, M K; Nagarajan, R; Macey, P M; Kumar, R; Villablanca, J P; Furuyama, J; Thomas, M A

2014-06-01

Echo-planar J-resolved spectroscopic imaging is a fast spectroscopic technique to record the biochemical information in multiple regions of the brain, but for clinical applications, time is still a constraint. Investigations of neural injury in obstructive sleep apnea have revealed structural changes in the brain, but determining the neurochemical changes requires more detailed measurements across multiple brain regions, demonstrating a need for faster echo-planar J-resolved spectroscopic imaging. Hence, we have extended the compressed sensing reconstruction of prospectively undersampled 4D echo-planar J-resolved spectroscopic imaging to investigate metabolic changes in multiple brain locations of patients with obstructive sleep apnea and healthy controls. Nonuniform undersampling was imposed along 1 spatial and 1 spectral dimension of 4D echo-planar J-resolved spectroscopic imaging, and test-retest reliability of the compressed sensing reconstruction of the nonuniform undersampling data was tested by using a brain phantom. In addition, 9 patients with obstructive sleep apnea and 11 healthy controls were investigated by using a 3T MR imaging/MR spectroscopy scanner. Significantly reduced metabolite differences were observed between patients with obstructive sleep apnea and healthy controls in multiple brain regions: NAA/Cr in the left hippocampus; total Cho/Cr and Glx/Cr in the right hippocampus; total NAA/Cr, taurine/Cr, scyllo-Inositol/Cr, phosphocholine/Cr, and total Cho/Cr in the occipital gray matter; total NAA/Cr and NAA/Cr in the medial frontal white matter; and taurine/Cr and total Cho/Cr in the left frontal white matter regions. The 4D echo-planar J-resolved spectroscopic imaging technique using the nonuniform undersampling-based acquisition and compressed sensing reconstruction in patients with obstructive sleep apnea and healthy brain is feasible in a clinically suitable time. In addition to brain metabolite changes previously reported by 1D MR spectroscopy, our results show changes of additional metabolites in patients with obstructive sleep apnea compared with healthy controls. © 2014 by American Journal of Neuroradiology.

Short Meditation Trainings Enhance Non-REM Sleep Low-Frequency Oscillations.

PubMed

Dentico, Daniela; Ferrarelli, Fabio; Riedner, Brady A; Smith, Richard; Zennig, Corinna; Lutz, Antoine; Tononi, Giulio; Davidson, Richard J

2016-01-01

We have recently shown higher parietal-occipital EEG gamma activity during sleep in long-term meditators compared to meditation-naive individuals. This gamma increase was specific for NREM sleep, was present throughout the entire night and correlated with meditation expertise, thus suggesting underlying long-lasting neuroplastic changes induced through prolonged training. The aim of this study was to explore the neuroplastic changes acutely induced by 2 intensive days of different meditation practices in the same group of practitioners. We also repeated baseline recordings in a meditation-naive cohort to account for time effects on sleep EEG activity. High-density EEG recordings of human brain activity were acquired over the course of whole sleep nights following intervention. Sound-attenuated sleep research room. Twenty-four long-term meditators and twenty-four meditation-naïve controls. Two 8-h sessions of either a mindfulness-based meditation or a form of meditation designed to cultivate compassion and loving kindness, hereafter referred to as compassion meditation. We found an increase in EEG low-frequency oscillatory activities (1-12 Hz, centered around 7-8 Hz) over prefrontal and left parietal electrodes across whole night NREM cycles. This power increase peaked early in the night and extended during the third cycle to high-frequencies up to the gamma range (25-40 Hz). There was no difference in sleep EEG activity between meditation styles in long-term meditators nor in the meditation naïve group across different time points. Furthermore, the prefrontal-parietal changes were dependent on meditation life experience. This low-frequency prefrontal-parietal activation likely reflects acute, meditation-related plastic changes occurring during wakefulness, and may underlie a top-down regulation from frontal and anterior parietal areas to the posterior parietal and occipital regions showing chronic, long-lasting plastic changes in long-term meditators.

Looking for a precursor of spontaneous Sleep Slow Oscillations in human sleep: The role of the sigma activity

PubMed Central

Allegrini, Paolo; Bedini, Remo; Bergamasco, Massimo; Laurino, Marco; Sebastiani, Laura; Gemignani, Angelo

2016-01-01

Sleep Slow Oscillations (SSOs), paradigmatic EEG markers of cortical bistability (alternation between cellular downstates and upstates), and sleep spindles, paradigmatic EEG markers of thalamic rhythm, are two hallmarks of sleeping brain. Selective thalamic lesions are reportedly associated to reductions of spindle activity and its spectrum ~14 Hz (sigma), and to alterations of SSO features. This apparent, parallel behavior suggests that thalamo-cortical entrainment favors cortical bistability. Here we investigate temporally-causal associations between thalamic sigma activity and shape, topology, and dynamics of SSOs. We recorded sleep EEG and studied whether spatio-temporal variability of SSO amplitude, negative slope (synchronization in downstate falling) and detection rate are driven by cortical-sigma-activity expression (12–18 Hz), in 3 consecutive 1 s-EEG-epochs preceding each SSO event (Baselines). We analyzed: (i) spatial variability, comparing maps of baseline sigma power and of SSO features, averaged over the first sleep cycle; (ii) event-by-event shape variability, computing for each electrode correlations between baseline sigma power and amplitude/slope of related SSOs; (iii) event-by-event spreading variability, comparing baseline sigma power in electrodes showing an SSO event with the homologous ones, spared by the event. The scalp distribution of baseline sigma power mirrored those of SSO amplitude and slope; event-by-event variability in baseline sigma power was associated with that in SSO amplitude in fronto-central areas; within each SSO event, electrodes involved in cortical bistability presented higher baseline sigma activity than those free of SSO. In conclusion, spatio-temporal variability of thalamocortical entrainment, measured by background sigma activity, is a reliable estimate of the cortical proneness to bistability. PMID:26003553

A Rodent Model of Night-Shift Work Induces Short-Term and Enduring Sleep and Electroencephalographic Disturbances.

PubMed

Grønli, Janne; Meerlo, Peter; Pedersen, Torhild T; Pallesen, Ståle; Skrede, Silje; Marti, Andrea R; Wisor, Jonathan P; Murison, Robert; Henriksen, Tone E G; Rempe, Michael J; Mrdalj, Jelena

2017-02-01

Millions of people worldwide are working at times that overlap with the normal time for sleep. Sleep problems related to the work schedule may mediate the well-established relationship between shift work and increased risk for disease, occupational errors and accidents. Yet, our understanding of causality and the underlying mechanisms that explain this relationship is limited. We aimed to assess the consequences of night-shift work for sleep and to examine whether night-shift work-induced sleep disturbances may yield electrophysiological markers of impaired maintenance of the waking brain state. An experimental model developed in rats simulated a 4-day protocol of night-work in humans. Two groups of rats underwent 8-h sessions of enforced ambulation, either at the circadian time when the animal was physiologically primed for wakefulness (active-workers, mimicking day-shift) or for sleep (rest-workers, mimicking night-shift). The 4-day rest-work schedule induced a pronounced redistribution of sleep to the endogenous active phase. Rest-work also led to higher electroencephalogram (EEG) slow-wave (1-4 Hz) energy in quiet wakefulness during work-sessions, suggesting a degraded waking state. After the daily work-sessions, being in their endogenous active phase, rest-workers slept less and had higher gamma (80-90 Hz) activity during wake than active-workers. Finally, rest-work induced an enduring shift in the main sleep period and attenuated the accumulation of slow-wave energy during NREM sleep. A comparison of recovery data from 12:12 LD and constant dark conditions suggests that reduced time in NREM sleep throughout the recorded 7-day recovery phase induced by rest-work may be modulated by circadian factors. Our data in rats show that enforced night-work-like activity during the normal resting phase has pronounced acute and persistent effects on sleep and waking behavior. The study also underscores the potential importance of animal models for future studies on the health consequences of night-shift work and the mechanisms underlying increased risk for diseases.

Sleep and Learning

NASA Astrophysics Data System (ADS)

Margoliash, Daniel

2010-03-01

The neural basis of cognition represents a grand challenge problem involving multiple disciplines and approaches to the analysis of behavior. Song learning by juvenile songbirds such as zebra finches has proven to have considerable utility for exploring how behavior is represented at multiple levels of brain function. As classically described, young birds are exposed to a ``tutor'' (adult) song and commit that song to memory early in life, then engage in an extended period (weeks) of plastic singing as they slowly learn to match vocal output to the tutor song memory via auditory feedback. In recent years, the role of sleep in learning processes has been actively explored. Young birds isolated from adult songs, then suddenly given access to such songs at circa 40 days of age, show a sudden change in their singing behavior starting on the day following first exposure. Such birds sing songs that have less structure in the mornings than do the songs sung in the afternoons before or after that morning. This fluctuation is directly the result of sleep (not circadian rhythm), and the magnitude of fluctuation is positively correlated with the ultimate similarity to the tutor song. Examining spontaneous neuronal activity in certain brain structures during the night in sleeping adults shows ``replay'' of the patterns of activity the same neurons exhibit during daytime singing, and ``preplay'' of new patterns that will first be incorporated into daytime singing the following day. In experiments on juveniles, nighttime neuronal activity shows dramatic changes associated with song learning, even on the night after the first day of tutor song exposure (preceding changes in singing behavior). Offline processing, especially sleep, has been well documented to participate in memory consolidation in a very broad range of behaviors including in humans. Placing the bird song results in a theoretical framework thereby helps to inform a very broad range of phenomena.

Alpha reactivity to first names differs in subjects with high and low dream recall frequency

PubMed Central

Ruby, Perrine; Blochet, Camille; Eichenlaub, Jean-Baptiste; Bertrand, Olivier; Morlet, Dominique; Bidet-Caulet, Aurélie

2013-01-01

Studies in cognitive psychology showed that personality (openness to experience, thin boundaries, absorption), creativity, nocturnal awakenings, and attitude toward dreams are significantly related to dream recall frequency (DRF). These results suggest the possibility of neurophysiological trait differences between subjects with high and low DRF. To test this hypothesis we compared sleep characteristics and alpha reactivity to sounds in subjects with high and low DRF using polysomnographic recordings and electroencephalography (EEG). We acquired EEG from 21 channels in 36 healthy subjects while they were presented with a passive auditory oddball paradigm (frequent standard tones, rare deviant tones and very rare first names) during wakefulness and sleep (intensity, 50 dB above the subject's hearing level). Subjects were selected as High-recallers (HR, DRF = 4.42 ± 0.25 SEM, dream recalls per week) and Low-recallers (LR, DRF = 0.25 ± 0.02) using a questionnaire and an interview on sleep and dream habits. Despite the disturbing setup, the subjects' quality of sleep was generally preserved. First names induced a more sustained decrease in alpha activity in HR than in LR at Pz (1000–1200 ms) during wakefulness, but no group difference was found in REM sleep. The current dominant hypothesis proposes that alpha rhythms would be involved in the active inhibition of the brain regions not involved in the ongoing brain operation. According to this hypothesis, a more sustained alpha decrease in HR would reflect a longer release of inhibition, suggesting a deeper processing of complex sounds than in LR during wakefulness. A possibility to explain the absence of group difference during sleep is that increase in alpha power in HR may have resulted in awakenings. Our results support this hypothesis since HR experienced more intra sleep wakefulness than LR (30 ± 4 vs. 14 ± 4 min). As a whole our results support the hypothesis of neurophysiological trait differences in high and low-recallers. PMID:23966960

Sleep and gravity.

PubMed

Gonfalone, Alain A

2018-04-01

What is known about sleep results from years of observation at the surface of the Earth. Since a few decade man has been able to reach space, escape from the earth attraction and spend days and nights in a weightless condition. Some major physiological changes have been observed during long stays and in particular the sleep duration in space is shorter than on ground. This paper reviews a novel hypothesis proposing that sleep is partly due to gravity. Gravity is a fundamental part of our environment, but is elusive and difficult to apprehend. At the same time, all creatures on Earth undergo cycles of activity and periods of rest (although not always sleep). Careful analysis of previous research on sleep, on Earth, in space and in water, shows that gravity differs in these three situations, and sleep also varies, at least in its duration. On Earth, Rapid Eye Movement (REM) sleep is conditioned by gravity; in space, astronauts have a shorter sleep duration and this is even more striking when a test subject is immersed in water for a week. In conclusion, sleep is partly due to gravity, which acts on our body and brain during the wake period. Copyright © 2018 The Author. Published by Elsevier Ltd.. All rights reserved.

Sleep Duration Varies as a Function of Glutamate and GABA in Rat Pontine Reticular Formation

PubMed Central

Watson, Christopher J.; Lydic, Ralph; Baghdoyan, Helen A.

2011-01-01

The oral part of the pontine reticular formation (PnO) is a component of the ascending reticular activating system and plays a role in the regulation of sleep and wakefulness. The PnO receives glutamatergic and GABAergic projections from many brain regions that regulate behavioral state. Indirect, pharmacological evidence has suggested that glutamatergic and GABAergic signaling within the PnO alters traits that characterize wakefulness and sleep. No previous studies have simultaneously measured endogenous glutamate and GABA from rat PnO in relation to sleep and wakefulness. The present study utilized in vivo microdialysis coupled on-line to capillary electrophoresis with laser-induced fluorescence to test the hypothesis that concentrations of glutamate and GABA in the PnO vary across the sleep/wake cycle. Concentrations of glutamate and GABA were significantly higher during wakefulness than during NREM sleep and REM sleep. Regression analysis revealed that decreases in glutamate and GABA accounted for a significant portion of the variance in the duration of NREM sleep and REM sleep episodes. These data provide novel support for the hypothesis that endogenous glutamate and GABA in the PnO contribute to the regulation of sleep duration. PMID:21679185

Dopaminergic regulation of sleep and cataplexy in a murine model of narcolepsy.

PubMed

Burgess, Christian R; Tse, Gavin; Gillis, Lauren; Peever, John H

2010-10-01

To determine if the dopaminergic system modulates cataplexy, sleep attacks and sleep-wake behavior in narcoleptic mice. Hypocretin/orexin knockout (i.e., narcoleptic) and wild-type mice were administered amphetamine and specific dopamine receptor modulators to determine their effects on sleep, cataplexy and sleep attacks. Hypocretin knockout (n = 17) and wild-type mice (n = 21). Cataplexy, sleep attacks and sleep-wake behavior were identified using electroencephalogram, electromyogram and videography. These behaviors were monitored for 4 hours after an i.p. injection of saline, amphetamine and specific dopamine receptor modulators (D1- and D2-like receptor modulators). Amphetamine (2 mg/kg), which increases brain dopamine levels, decreased sleep attacks and cataplexy by 61% and 67%, suggesting that dopamine transmission modulates such behaviors. Dopamine receptor modulation also had powerful effects on sleep attacks and cataplexy. Activation (SKF 38393; 20 mg/kg) and blockade (SCH 23390; 1 mg/kg) of D1-like receptors decreased and increased sleep attacks by 77% and 88%, without affecting cataplexy. Pharmacological activation of D2-like receptors (quinpirole; 0.5 mg/kg) increased cataplectic attacks by 172% and blockade of these receptors (eticlopride; 1 mg/kg) potently suppressed them by 97%. Manipulation of D2-like receptors did not affect sleep attacks. We show that the dopaminergic system plays a role in regulating both cataplexy and sleep attacks in narcoleptic mice. We found that cataplexy is modulated by a D2-like receptor mechanism, whereas dopamine modulates sleep attacks by a D1-like receptor mechanism. These results support a role for the dopamine system in regulating sleep attacks and cataplexy in a murine model of narcolepsy.

Protective effect of alprazolam against sleep deprivation-induced behavior alterations and oxidative damage in mice.

PubMed

Singh, Anant; Kumar, Anil

2008-04-01

Sleep deprivation is considered as a risk factor for various diseases. Sleep deprivation leads to behavioral, hormonal, neurochemical and biochemical alterations in the animals. The present study was designed to explore the possible involvement of GABAergic mechanism in protective effect of alprazolam against 72h sleep deprivation-induced behavior alterations and oxidative damage in mice. In the present study, sleep deprivation caused anxiety-like behavior, weight loss, impaired ambulatory movements and oxidative damage as indicated by increase in lipid peroxidation, nitrite level and depletion of reduced glutathione and catalase activity in sleep-deprived mice brain. Treatment with alprazolam (0.25 and 0.5 mg/kg, ip) significantly improved behavioral alterations. Biochemically, alprazolam treatment significantly restored depleted reduced glutathione, catalase activity, reversed raised lipid peroxidation and nitrite level. Combination of flumazenil (0.5 mg/kg) and picrotoxin (0.5 mg/kg) with lower dose of alprazolam (0.25mg/kg) significantly antagonized protective effect of alprazolam. However, combination of muscimol (0.05 mg/kg) with alprazolam (0.25 mg/kg, ip) potentiated protective effect of alprazolam. On the basis of these results, it might be suggested that alprazolam might produce protective effect by involving GABAergic system against sleep deprivation-induced behavior alterations and related oxidative damage.

Sleep-wake disturbances after traumatic brain injury.

PubMed

Ouellet, Marie-Christine; Beaulieu-Bonneau, Simon; Morin, Charles M

2015-07-01

Sleep-wake disturbances are extremely common after a traumatic brain injury (TBI). The most common disturbances are insomnia (difficulties falling or staying asleep), increased sleep need, and excessive daytime sleepiness that can be due to the TBI or other sleep disorders associated with TBI, such as sleep-related breathing disorder or post-traumatic hypersomnia. Sleep-wake disturbances can have a major effect on functional outcomes and on the recovery process after TBI. These negative effects can exacerbate other common sequelae of TBI-such as fatigue, pain, cognitive impairments, and psychological disorders (eg, depression and anxiety). Sleep-wake disturbances associated with TBI warrant treatment. Although evidence specific to patients with TBI is still scarce, cognitive-behavioural therapy and medication could prove helpful to alleviate sleep-wake disturbances in patients with a TBI. Copyright © 2015 Elsevier Ltd. All rights reserved.

Old Brains Come Uncoupled in Sleep: Slow Wave-Spindle Synchrony, Brain Atrophy, and Forgetting.

PubMed

Helfrich, Randolph F; Mander, Bryce A; Jagust, William J; Knight, Robert T; Walker, Matthew P

2018-01-03

The coupled interaction between slow-wave oscillations and sleep spindles during non-rapid-eye-movement (NREM) sleep has been proposed to support memory consolidation. However, little evidence in humans supports this theory. Moreover, whether such dynamic coupling is impaired as a consequence of brain aging in later life, contributing to cognitive and memory decline, is unknown. Combining electroencephalography (EEG), structural MRI, and sleep-dependent memory assessment, we addressed these questions in cognitively normal young and older adults. Directional cross-frequency coupling analyses demonstrated that the slow wave governs a precise temporal coordination of sleep spindles, the quality of which predicts overnight memory retention. Moreover, selective atrophy within the medial frontal cortex in older adults predicted a temporal dispersion of this slow wave-spindle coupling, impairing overnight memory consolidation and leading to forgetting. Prefrontal-dependent deficits in the spatiotemporal coordination of NREM sleep oscillations therefore represent one pathway explaining age-related memory decline. Copyright © 2017 Elsevier Inc. All rights reserved.

Pathological effects of obstructive apneas during the sleep cycle in an animal model of cerebral small vessel disease.

PubMed

Lloyd, Eric E; Durgan, David J; Martini, Sharyl R; Bryan, Robert M

2015-10-01

We tested the hypothesis that apneas during the sleep cycle exacerbate hypertension and accelerate changes that occur with cerebral small vessel disease. Obstructive sleep apnea was modeled by intermittent inflations of a chronically implanted tracheal balloon to occlude the airway during the sleep cycle (termed OSA) in spontaneously hypertensive stroke-prone (SHRSP) rats, a model of cerebral small vessel disease. SHRSP rats and their parent strain, Wistar Kyoto (WKY) rats, were exposed to OSA for 2 weeks (from 9 to 11 or from 18 to 20 weeks). At 9 weeks, hypertension was developing in the SHRSP rats and was firmly established by 18 weeks. OSA exposure increased systolic blood pressure in SHRSP rats by ≈30 mm Hg in both age groups compared with shams that were surgically prepared but not exposed to OSA (P<0.05). OSA exposure also increased systolic blood pressure in WKY rats by 20 and 37 mm Hg at 11 and 20 weeks, respectively (P<0.05). OSA exposure in SHRSP rats compromised blood-brain barrier integrity in white matter at both 11 and 20 weeks of age when compared with SHRSP sham rats (P<0.05). Microglia were activated in SHRSP rats exposed to OSA but not in sham rats at 11 weeks (P<0.05). At 20 weeks, microglia were activated in sham SHRSP rats (P<0.05) compared with WKY sham rats and were not further activated by OSA. Neither was blood-brain barrier integrity altered nor microglia activated in any of the WKY groups. We conclude that OSA accelerates the onset of the cerebral pathologies associated with cerebral small vessel disease in SHRSP, but not WKY, rats. © 2015 American Heart Association, Inc.

Organization of the sleep-related neural systems in the brain of the minke whale (Balaenoptera acutorostrata).

PubMed

Dell, Leigh-Anne; Karlsson, Karl Ae; Patzke, Nina; Spocter, Muhammad A; Siegel, Jerome M; Manger, Paul R

2016-07-01

The current study analyzed the nuclear organization of the neural systems related to the control and regulation of sleep and wake in the basal forebrain, diencephalon, midbrain, and pons of the minke whale, a mysticete cetacean. While odontocete cetaceans sleep in an unusual manner, with unihemispheric slow wave sleep (USWS) and suppressed REM sleep, it is unclear whether the mysticete whales show a similar sleep pattern. Previously, we detailed a range of features in the odontocete brain that appear to be related to odontocete-type sleep, and here present our analysis of these features in the minke whale brain. All neural elements involved in sleep regulation and control found in bihemispheric sleeping mammals and the harbor porpoise were present in the minke whale, with no specific nuclei being absent, and no novel nuclei being present. This qualitative similarity relates to the cholinergic, noradrenergic, serotonergic and orexinergic systems, and the GABAergic elements of these nuclei. Quantitative analysis revealed that the numbers of pontine cholinergic (274,242) and noradrenergic (203,686) neurons, and hypothalamic orexinergic neurons (277,604), are markedly higher than other large-brained bihemispheric sleeping mammals. Small telencephalic commissures (anterior, corpus callosum, and hippocampal), an enlarged posterior commissure, supernumerary pontine cholinergic and noradrenergic cells, and an enlarged peripheral division of the dorsal raphe nuclear complex of the minke whale, all indicate that the suite of neural characteristics thought to be involved in the control of USWS and the suppression of REM in the odontocete cetaceans are present in the minke whale. J. Comp. Neurol. 524:2018-2035, 2016. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.

Brain prolactin is involved in stress-induced REM sleep rebound.

PubMed

Machado, Ricardo Borges; Rocha, Murilo Ramos; Suchecki, Deborah

2017-03-01

REM sleep rebound is a common behavioural response to some stressors and represents an adaptive coping strategy. Animals submitted to multiple, intermittent, footshock stress (FS) sessions during 96h of REM sleep deprivation (REMSD) display increased REM sleep rebound (when compared to the only REMSD ones, without FS), which is correlated to high plasma prolactin levels. To investigate whether brain prolactin plays a role in stress-induced REM sleep rebound two experiments were carried out. In experiment 1, rats were either not sleep-deprived (NSD) or submitted to 96h of REMSD associated or not to FS and brains were evaluated for PRL immunoreactivity (PRL-ir) and determination of PRL concentrations in the lateral hypothalamus and dorsal raphe nucleus. In experiment 2, rats were implanted with cannulas in the dorsal raphe nucleus for prolactin infusion and were sleep-recorded. REMSD associated with FS increased PRL-ir and content in the lateral hypothalamus and all manipulations increased prolactin content in the dorsal raphe nucleus compared to the NSD group. Prolactin infusion in the dorsal raphe nucleus increased the time and length of REM sleep episodes 3h after the infusion until the end of the light phase of the day cycle. Based on these results we concluded that brain prolactin is a major mediator of stress-induced REMS. The effect of PRL infusion in the dorsal raphe nucleus is discussed in light of the existence of a bidirectional relationship between this hormone and serotonin as regulators of stress-induced REM sleep rebound. Copyright © 2016 Elsevier Inc. All rights reserved.

Cyclic Alternating Pattern Is Associated with Cerebral Hemodynamic Variation: A Near-Infrared Spectroscopy Study of Sleep in Healthy Humans

PubMed Central

Toppila, Jussi; Salmi, Tapani; Ilmoniemi, Risto J.

2012-01-01

The cyclic alternating pattern (CAP), that is, cyclic variation of brain activity within non-REM sleep stages, is related to sleep instability and preservation, as well as consolidation of learning. Unlike the well-known electrical activity of CAP, its cerebral hemodynamic counterpart has not been assessed in healthy subjects so far. We recorded scalp and cortical hemodynamics with near-infrared spectroscopy on the forehead and systemic hemodynamics (heart rate and amplitude of the photoplethysmograph) with a finger pulse oximeter during 23 nights in 11 subjects. Electrical CAP activity was recorded with a polysomnogram. CAP was related to changes in scalp, cortical, and systemic hemodynamic signals that resembled the ones seen in arousal. Due to their repetitive nature, CAP sequences manifested as low- and very-low-frequency oscillations in the hemodynamic signals. The subtype A3+B showed the strongest hemodynamic changes. A transient hypoxia occurred during CAP cycles, suggesting that an increased CAP rate, especially with the subtype A3+B, which may result from diseases or fragmented sleep, might have an adverse effect on the cerebral vasculature. PMID:23071658

Cyclic alternating pattern is associated with cerebral hemodynamic variation: a near-infrared spectroscopy study of sleep in healthy humans.

PubMed

Näsi, Tiina; Virtanen, Jaakko; Toppila, Jussi; Salmi, Tapani; Ilmoniemi, Risto J

2012-01-01

The cyclic alternating pattern (CAP), that is, cyclic variation of brain activity within non-REM sleep stages, is related to sleep instability and preservation, as well as consolidation of learning. Unlike the well-known electrical activity of CAP, its cerebral hemodynamic counterpart has not been assessed in healthy subjects so far. We recorded scalp and cortical hemodynamics with near-infrared spectroscopy on the forehead and systemic hemodynamics (heart rate and amplitude of the photoplethysmograph) with a finger pulse oximeter during 23 nights in 11 subjects. Electrical CAP activity was recorded with a polysomnogram. CAP was related to changes in scalp, cortical, and systemic hemodynamic signals that resembled the ones seen in arousal. Due to their repetitive nature, CAP sequences manifested as low- and very-low-frequency oscillations in the hemodynamic signals. The subtype A3+B showed the strongest hemodynamic changes. A transient hypoxia occurred during CAP cycles, suggesting that an increased CAP rate, especially with the subtype A3+B, which may result from diseases or fragmented sleep, might have an adverse effect on the cerebral vasculature.

The future of dream science.

PubMed

Bulkeley, Kelly

2017-10-01

This article describes the future prospects of scientific dream research. Three frontiers of investigation hold special promise: neuroscientific studies of the brain-mind system's activities during sleep (such as during lucid dreaming); systematic analyses of large collections of dream reports from diverse populations of people; and psychotherapeutic explorations of the multiple dimensions of personal and collective meaning woven into the dream experiences of each individual. Several helpful books on the science of sleep and dreaming are mentioned for further study. © 2017 New York Academy of Sciences.

Muramyl Peptide-Enhanced Sleep: Pharmacological Optimization of Performance

DTIC Science & Technology

1991-06-01

assessed. Exieriment C: Effects of PGE2, PGD2, IFNa, VIP, DSIP, 5- HT , hydrocorti- sone, and MDP, on HLADR expression in HTB16 cells . HTB16 cells were...stimulatory effect of IFNy on MHCII expression in astrocytes, or the cell line we used lacks receptors for 5- HT . It is well known that glucocorticoids... Effects of ICV injection of CCK on sleep-wake activity and brain temperature 92 Fig. 7: Growth curves of glioblastoma cell lines HTBl4, HTE16, and H:0i

Determination of halothane-induced sleeping time in the rat: effect of prior administration of centrally active drugs.

PubMed Central

Turnbull, M J; Watkins, J W

1976-01-01

A method is described for the determination of halothane-induced sleeping time in the rat. 2 The sleeping time exhibited a diurnal variation which was due, at least in part, to a change in the sensitivity of the central nervous system (CNS) to the anaesthetic. 3 Tolerance to halothane did not develop in rats repeatedly exposed to the anaesthetic over a period of over 48 hours. 4 Repeated sleeping time determinations have been used to follow changes in the sensitivity of the CNS to the anaesthetic occurring with time. 5 A tolerance to halothane was induced by pretreatment of rats with doses of amylobarbitone, pentobarbitone or meprobamate sufficient to keep animals anaesthetized for approximately 12 hours. This tolerance was followed by a period of halothane-hypersensitivity. 6 Halothane-tolerant animals awakened with higher brain halothane concentrations and were also tolerant to intracerebroventricularly administered pentobarbitone. 7 Halothane-hypertensive rats awakened with lower brain halothane concentrations and were also hypersensitivity to intracerebroventricularly administered pentobarbitone. 8 The possibility that the induction of cross-tolerance to halothane may be indicative of a drug's potential to produce dependence is discussed. PMID:987820

Recalibrating sleep: is recalibration and readjustment of sense organs and brain-body connections the core function of sleep?

PubMed

Smetacek, Victor

2010-10-01

Sleep is an enigma because we all know what it means and does to us, yet a scientific explanation for why animals including humans need to sleep is still lacking. However, the enigma can be resolved if the animal body is regarded as a purposeful machine whose moving parts are coordinated with spatial information provided by a disparate array of sense organs. The performance of all complex machines deteriorates with time due to inevitable instrument drift of the individual sensors combined with wear and tear of the moving parts which result in declining precision and coordination. Peak performance is restored by servicing the machine, which involves calibrating the sensors against baselines and standards, then with one another, and finally readjusting the connections between instruments and moving parts. It follows that the animal body and its sensors will also require regular calibration of sense organs and readjustment of brain-body connections which will need to be carried out while the animal is not in functional but in calibration mode. I suggest that this is the core function of sleep. This recalibration hypothesis of sleep can be tested subjectively. We all know from personal experience that sleep is needed to recover from tiredness that sets in towards the end of a long day. This tiredness, which is quite distinct from mental or muscular exhaustion caused by strenuous exertion, manifests itself in deteriorating general performance: the sense organs lose precision, movements become clumsy and the mind struggles to maintain focus. We can all agree that sleep sharpens the sense organs and restores agility to mind and body. I now propose that the sense of freshness and buoyancy after a good night's sleep is the feeling of recalibrated sensory and motor systems. The hypothesis can be tested rigorously by examining available data on sleep cycles and stages against this background. For instance, REM and deep sleep cycles can be interpreted as successive, separate calibration runs of the vestibulo-ocular reflex and the sensory-motor systems, respectively, amongst other functions running in parallel, such as dreaming. Because the split-second connections between sensory information and emotional responses will also require calibration, some aspects of dreaming could be interpreted in this light. Much of the baffling behaviour and patterns of brain activity of sleeping animals and humans make sense in the framework of this technological paradigm since different animal lineages will have evolved different techniques to achieve calibration. Copyright 2010 Elsevier Ltd. All rights reserved.

The Impact of Sleep Deprivation on the Brain

PubMed

Trošt Bobić, Tatjana; Šečić, Ana; Zavoreo, Iris; Matijević, Valentina; Filipović, Branimir; Kolak, Željka; Bašić Kes, Vanja; Ciliga, Dubravka; Sajković, Dubravka

2016-09-01

Each sleep phase is characterized by specific chemical, cellular and anatomic events of vital importance for normal neural functioning. Different forms of sleep deprivation may lead to a decline of cognitive functions in individuals. Studies in this field make a distinction between total sleep deprivation, chronic sleep restriction, and the situation of sleep disruption. Investigations covering the acute effects of sleep deprivation on the brain show that the discovered behavioral deficits in most cases regenerate after two nights of complete sleep. However, some studies done on mice emphasize the possible chronic effects of long-term sleep deprivation or chronic restriction on the occurrence of neurodegenerative diseases such as Alzheimer’s disease and dementia. In order to better understand the acute and chronic effects of sleep loss, the mechanisms of neural adaptation in the situations of insufficient sleep need to be further investigated. Future integrative research on the impact of sleep deprivation on neural functioning measured through the macro level of cognitive functions and the micro molecular and cell level could contribute to more accurate conclusions about the basic cellular mechanisms responsible for the detected behavioral deficits occurring due to sleep deprivation.

Flexible, foldable, actively multiplexed, high-density electrode array for mapping brain activity in vivo.

PubMed

Viventi, Jonathan; Kim, Dae-Hyeong; Vigeland, Leif; Frechette, Eric S; Blanco, Justin A; Kim, Yun-Soung; Avrin, Andrew E; Tiruvadi, Vineet R; Hwang, Suk-Won; Vanleer, Ann C; Wulsin, Drausin F; Davis, Kathryn; Gelber, Casey E; Palmer, Larry; Van der Spiegel, Jan; Wu, Jian; Xiao, Jianliang; Huang, Yonggang; Contreras, Diego; Rogers, John A; Litt, Brian

2011-11-13

Arrays of electrodes for recording and stimulating the brain are used throughout clinical medicine and basic neuroscience research, yet are unable to sample large areas of the brain while maintaining high spatial resolution because of the need to individually wire each passive sensor at the electrode-tissue interface. To overcome this constraint, we developed new devices that integrate ultrathin and flexible silicon nanomembrane transistors into the electrode array, enabling new dense arrays of thousands of amplified and multiplexed sensors that are connected using fewer wires. We used this system to record spatial properties of cat brain activity in vivo, including sleep spindles, single-trial visual evoked responses and electrographic seizures. We found that seizures may manifest as recurrent spiral waves that propagate in the neocortex. The developments reported here herald a new generation of diagnostic and therapeutic brain-machine interface devices.

Quality of Life, Psychological Burden, and Sleep Quality in Patients With Brain Metastasis Undergoing Whole Brain Radiation Therapy.

PubMed

Teke, Fatma; Bucaktepe, Pakize; Kıbrıslı, Erkan; Demir, Melike; Ibiloglu, Aslıhan; Inal, Ali

2016-10-01

Patients with brain metastasis (BM) usually suffer from poor quality of life (QOL), anxiety, depression, and sleep disorders in their reduced lifespan. The aim of this study was to evaluate QOL, anxiety, depression, and sleep characteristics in patients with BM at the beginning and end of whole brain radiation therapy (WBRT) and three months after treatment. Thirty-three patients undergoing WBRT for BM were featured in this study. The authors used the Karnofsky Performance Status (KPS) scale to measure performance status, the Hospital Anxiety and Depression Scale (HADS) to evaluate anxiety and depression, the SF-36® to evaluate health-related QOL, and the Pittsburgh Sleep Quality Index to evaluate sleep disorders at the start of WBRT, the end of WBRT, and three months after WBRT. Statistically significant improvements were noted in KPS scores from baseline evaluation to the end of WBRT and to three months after WBRT. No significant differences were observed in SF-36 and HADS scores between the start and the end of WBRT. Anxiety scores were negatively correlated with survival at the end of WBRT. Overall survival was better in those who reported better sleep. WBRT improves KPS scores and does not worsen sleep quality or mood, even in patients with poor performance status. When changes in mood and sleep quality are observed, survival and QOL may improve in patients with BM; consequently, nurses should be responsive to these changes.

A Neuron-Based Model of Sleep-Wake Cycles

NASA Astrophysics Data System (ADS)

Postnova, Svetlana; Peters, Achim; Braun, Hans

2008-03-01

In recent years it was discovered that a neuropeptide orexin/hypocretin plays a main role in sleep processes. This peptide is produced by the neurons in the lateral hypothalamus, which project to almost all brain areas. We present a computational model of sleep-wake cycles, which is based on the Hodgkin-Huxley type neurons and considers reciprocal glutaminergic projections between the lateral hypothalamus and the prefrontal cortex. Orexin is released as a neuromodulator and is required to keep the neurons firing, which corresponds to the wake state. When orexin is depleted the neurons are getting silent as observed in the sleep state. They can be reactivated by the circadian signal from the suprachiasmatic nucleus and/or external stimuli (alarm clock). Orexin projections to the thalamocortical neurons also can account for their transition from tonic firing activity during wakefulness to synchronized burst discharges during sleep.

Sleep Extension Normalizes ERP of Waking Auditory Sensory Gating in Healthy Habitually Short Sleeping Individuals

PubMed Central

Gumenyuk, Valentina; Korzyukov, Oleg; Roth, Thomas; Bowyer, Susan M.; Drake, Christopher L.

2013-01-01

Chronic sleep loss has been associated with increased daytime sleepiness, as well as impairments in memory and attentional processes. In the present study, we evaluated the neuronal changes of a pre-attentive process of wake auditory sensory gating, measured by brain event-related potential (ERP) – P50 in eight normal sleepers (NS) (habitual total sleep time (TST) 7 h 32 m) vs. eight chronic short sleeping individuals (SS) (habitual TST ≤6 h). To evaluate the effect of sleep extension on sensory gating, the extended sleep condition was performed in chronic short sleeping individuals. Thus, one week of time in bed (6 h 11 m) corresponding to habitual short sleep (hSS), and one week of extended time (∼ 8 h 25 m) in bed corresponding to extended sleep (eSS), were counterbalanced in the SS group. The gating ERP assessment was performed on the last day after each sleep condition week (normal sleep and habitual short and extended sleep), and was separated by one week with habitual total sleep time and monitored by a sleep diary. We found that amplitude of gating was lower in SS group compared to that in NS group (0.3 µV vs. 1.2 µV, at Cz electrode respectively). The results of the group × laterality interaction showed that the reduction of gating amplitude in the SS group was due to lower amplitude over the left hemisphere and central-midline sites relative to that in the NS group. After sleep extension the amplitude of gating increased in chronic short sleeping individuals relative to their habitual short sleep condition. The sleep condition × frontality interaction analysis confirmed that sleep extension significantly increased the amplitude of gating over frontal and central brain areas compared to parietal brain areas. PMID:23520548

Beyond the neuropsychology of dreaming: Insights into the neural basis of dreaming with new techniques of sleep recording and analysis.

PubMed

Cipolli, Carlo; Ferrara, Michele; De Gennaro, Luigi; Plazzi, Giuseppe

2017-10-01

Recent advances in electrophysiological [e.g., surface high-density electroencephalographic (hd-EEG) and intracranial recordings], video-polysomnography (video-PSG), transcranial stimulation and neuroimaging techniques allow more in-depth and more accurate investigation of the neural correlates of dreaming in healthy individuals and in patients with brain-damage, neurodegenerative diseases, sleep disorders or parasomnias. Convergent evidence provided by studies using these techniques in healthy subjects has led to a reformulation of several unresolved issues of dream generation and recall [such as the inter- and intra-individual differences in dream recall and the predictivity of specific EEG rhythms, such as theta in rapid eye movement (REM) sleep, for dream recall] within more comprehensive models of human consciousness and its variations across sleep/wake states than the traditional models, which were largely based on the neurophysiology of REM sleep in animals. These studies are casting new light on the neural bases (in particular, the activity of dorsal medial prefrontal cortex regions and hippocampus and amygdala areas) of the inter- and intra-individual differences in dream recall, the temporal location of specific contents or properties (e.g., lucidity) of dream experience and the processing of memories accessed during sleep and incorporated into dream content. Hd-EEG techniques, used on their own or in combination with neuroimaging, appear able to provide further important insights into how the brain generates not only dreaming during sleep but also some dreamlike experiences in waking. Copyright © 2016 Elsevier Ltd. All rights reserved.

Effects of growth hormone-releasing hormone on sleep and brain interstitial fluid amyloid-β in an APP transgenic mouse model.

PubMed

Liao, Fan; Zhang, Tony J; Mahan, Thomas E; Jiang, Hong; Holtzman, David M

2015-07-01

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by impairment of cognitive function, extracellular amyloid plaques, intracellular neurofibrillary tangles, and synaptic and neuronal loss. There is substantial evidence that the aggregation of amyloid β (Aβ) in the brain plays a key role in the pathogenesis of AD and that Aβ aggregation is a concentration dependent process. Recently, it was found that Aβ levels in the brain interstitial fluid (ISF) are regulated by the sleep-wake cycle in both humans and mice; ISF Aβ is higher during wakefulness and lower during sleep. Intracerebroventricular infusion of orexin increased wakefulness and ISF Aβ levels, and chronic sleep deprivation significantly increased Aβ plaque formation in amyloid precursor protein transgenic (APP) mice. Growth hormone-releasing hormone (GHRH) is a well-documented sleep regulatory substance which promotes non-rapid eye movement sleep. GHRHR(lit/lit) mice that lack functional GHRH receptor have shorter sleep duration and longer wakefulness during light periods. The current study was undertaken to determine whether manipulating sleep by interfering with GHRH signaling affects brain ISF Aβ levels in APPswe/PS1ΔE9 (PS1APP) transgenic mice that overexpress mutant forms of APP and PSEN1 that cause autosomal dominant AD. We found that intraperitoneal injection of GHRH at dark onset increased sleep and decreased ISF Aβ and that delivery of a GHRH antagonist via reverse-microdialysis suppressed sleep and increased ISF Aβ. The diurnal fluctuation of ISF Aβ in PS1APP/GHRHR(lit/lit) mice was significantly smaller than that in PS1APP/GHRHR(lit/+) mice. However despite decreased sleep in GHRHR deficient mice, this was not associated with an increase in Aβ accumulation later in life. One of several possibilities for the finding is the fact that GHRHR deficient mice have GHRH-dependent but sleep-independent factors which protect against Aβ deposition. Copyright © 2014 Elsevier Inc. All rights reserved.

Brain extracellular glucose assessed by voltammetry throughout the rat sleep-wake cycle.

PubMed

Netchiporouk, L; Shram, N; Salvert, D; Cespuglio, R

2001-04-01

In the present study, cortical extracellular levels of glucose were monitored for the first time throughout the sleep-wake states of the freely moving rat. For this purpose, polygraphic recordings (electroencephalogram of the fronto-occipital cortices and electromyogram of the neck muscles) were achieved in combination with differential normal pulse voltammetry (DNPV) using a specific glucose sensor. Data obtained reveal that the basal extracellular glucose concentration in the conscious rat is 0.59 +/- 0.3 m M while under chloral hydrate anaesthesia (0.4 g/kg, i.p.) it increases up to 180% of its basal concentration. Regarding the sleep-wake cycle, the existence of spontaneous significant variations in the mean glucose level during slow-wave sleep (SWS = +13%) and paradoxical sleep (PS = -11%) compared with the waking state (100%) is also reported. It is to be noticed that during long periods of active waking, glucose level tends towards a decrease that becomes significant after 15 min (active waking = -32%). On the contrary, during long episodes of slow-wave sleep, it tends towards an increase which becomes significant after 12 min (SWS = +28%). It is suggested that voltammetric techniques using enzymatic biosensors are useful tools allowing direct glucose measurements in the freely moving animal. On the whole, paradoxical sleep is pointed out as a state highly dependent on the availability of energy and slow-wave sleep as a period of energy saving.

Recovery sleep after extended wakefulness restores elevated A1 adenosine receptor availability in the human brain

PubMed Central

Elmenhorst, Eva-Maria; Hennecke, Eva; Kroll, Tina; Matusch, Andreas; Aeschbach, Daniel; Bauer, Andreas

2017-01-01

Adenosine and functional A1 adenosine receptor (A1AR) availability are supposed to mediate sleep–wake regulation and cognitive performance. We hypothesized that cerebral A1AR availability after an extended wake period decreases to a well-rested state after recovery sleep. [18F]CPFPX positron emission tomography was used to quantify A1AR availability in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep. Data were additionally compared with A1AR values after 8 h of baseline sleep from an earlier dataset. Polysomnography, cognitive performance, and sleepiness were monitored. Recovery from sleep deprivation was associated with a decrease in A1AR availability in several brain regions, ranging from 11% (insula) to 14% (striatum). A1AR availabilities after recovery did not differ from baseline sleep in the control group. The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to sleep deprivation correlated negatively with the decrease in A1AR availability. Sleep deprivation resulted in a higher A1AR availability in the human brain. The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode. Individuals with a large increase in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase. This pattern implies that differences in endogenous adenosine and A1AR availability might be causal for individual responses to sleep loss. PMID:28373571

Increased Evoked Potentials to Arousing Auditory Stimuli during Sleep: Implication for the Understanding of Dream Recall

PubMed Central

Vallat, Raphael; Lajnef, Tarek; Eichenlaub, Jean-Baptiste; Berthomier, Christian; Jerbi, Karim; Morlet, Dominique; Ruby, Perrine M.

2017-01-01

High dream recallers (HR) show a larger brain reactivity to auditory stimuli during wakefulness and sleep as compared to low dream recallers (LR) and also more intra-sleep wakefulness (ISW), but no other modification of the sleep macrostructure. To further understand the possible causal link between brain responses, ISW and dream recall, we investigated the sleep microstructure of HR and LR, and tested whether the amplitude of auditory evoked potentials (AEPs) was predictive of arousing reactions during sleep. Participants (18 HR, 18 LR) were presented with sounds during a whole night of sleep in the lab and polysomnographic data were recorded. Sleep microstructure (arousals, rapid eye movements (REMs), muscle twitches (MTs), spindles, KCs) was assessed using visual, semi-automatic and automatic validated methods. AEPs to arousing (awakenings or arousals) and non-arousing stimuli were subsequently computed. No between-group difference in the microstructure of sleep was found. In N2 sleep, auditory arousing stimuli elicited a larger parieto-occipital positivity and an increased late frontal negativity as compared to non-arousing stimuli. As compared to LR, HR showed more arousing stimuli and more long awakenings, regardless of the sleep stage but did not show more numerous or longer arousals. These results suggest that the amplitude of the brain response to stimuli during sleep determine subsequent awakening and that awakening duration (and not arousal) is the critical parameter for dream recall. Notably, our results led us to propose that the minimum necessary duration of an awakening during sleep for a successful encoding of dreams into long-term memory is approximately 2 min. PMID:28377708

Coming to grips with a "new" state of consciousness: the study of rapid-eye-movement sleep in the 1960s.

PubMed

Morrison, Adrian R

2013-01-01

The recognition of rapid-eye-movement sleep (REM) and its association with dreaming in 1953 by Aserinsky and Kleitman opened a new world to explore in the brain. Discussions at two major symposia in the early 1960s reveal that a state with characteristics resembling both wakefulness and sleep was overturning accepted views of the regulation of the two states. Participants grappled with the idea that cortical activation could occur during sleep. They struggled with picking a name that would capture the essence of REM without focusing on just one aspect of the state. Questioning whether REM in cats could be homologous with that of humans suggested an anthropocentric focus on human dreaming as the essence of the state. The need for biochemical studies was evident given that deprivation of REM caused a rebound in the amount of subsequent REM, which indicated that simple synaptic activity could not support this phenomenon.

Signals from the brainstem sleep/wake centers regulate behavioral timing via the circadian clock.

PubMed

Abbott, Sabra M; Arnold, Jennifer M; Chang, Qing; Miao, Hai; Ota, Nobutoshi; Cecala, Christine; Gold, Paul E; Sweedler, Jonathan V; Gillette, Martha U

2013-01-01

Sleep-wake cycling is controlled by the complex interplay between two brain systems, one which controls vigilance state, regulating the transition between sleep and wake, and the other circadian, which communicates time-of-day. Together, they align sleep appropriately with energetic need and the day-night cycle. Neural circuits connect brain stem sites that regulate vigilance state with the suprachiasmatic nucleus (SCN), the master circadian clock, but the function of these connections has been unknown. Coupling discrete stimulation of pontine nuclei controlling vigilance state with analytical chemical measurements of intra-SCN microdialysates in mouse, we found significant neurotransmitter release at the SCN and, concomitantly, resetting of behavioral circadian rhythms. Depending upon stimulus conditions and time-of-day, SCN acetylcholine and/or glutamate levels were augmented and generated shifts of behavioral rhythms. These results establish modes of neurochemical communication from brain regions controlling vigilance state to the central circadian clock, with behavioral consequences. They suggest a basis for dynamic integration across brain systems that regulate vigilance states, and a potential vulnerability to altered communication in sleep disorders.

The Emerging Relationship Between Interstitial Fluid-Cerebrospinal Fluid Exchange, Amyloid-β, and Sleep.

PubMed

Boespflug, Erin L; Iliff, Jeffrey J

2018-02-15

Amyloid-β (Aβ) plaques are a key histopathological hallmark of Alzheimer's disease (AD), and soluble Aβ species are believed to play an important role in the clinical development of this disease. Emerging biomarker data demonstrate that Aβ plaque deposition begins decades before the onset of clinical symptoms, suggesting that understanding the biological determinants of the earliest steps in the development of AD pathology may provide key opportunities for AD treatment and prevention. Although a clinical association between sleep disruption and AD has long been appreciated, emerging clinical studies and insights from the basic neurosciences have shed important new light on how sleep and Aβ homeostasis may be connected in the setting of AD. Aβ, like many interstitial solutes, is cleared in part through the exchange of brain interstitial fluid and cerebrospinal fluid along a brain-wide network of perivascular pathways recently termed the glymphatic system. Glymphatic function is primarily a feature of the sleeping brain, rather than the waking brain, and is slowed in the aging and posttraumatic brain. These changes may underlie the diurnal fluctuations in interstitial and cerebrospinal fluid Aβ levels observed in both the rodent and the human. These and other emerging studies suggest that age-related sleep disruption may be one key factor that renders the aging brain vulnerable to Aβ deposition and the development of AD. If this is true, sleep may represent a key modifiable risk factor or therapeutic target in the preclinical phases of AD. Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Sleep affects cortical source modularity in temporal lobe epilepsy: A high-density EEG study.

PubMed

Del Felice, Alessandra; Storti, Silvia Francesca; Manganotti, Paolo

2015-09-01

Interictal epileptiform discharges (IEDs) constitute a perturbation of ongoing cerebral rhythms, usually more frequent during sleep. The aim of the study was to determine whether sleep influences the spread of IEDs over the scalp and whether their distribution depends on vigilance-related modifications in cortical interactions. Wake and sleep 256-channel electroencephalography (EEG) data were recorded in 12 subjects with right temporal lobe epilepsy (TLE) differentiated by whether they had mesial or neocortical TLE. Spikes were selected during wake and sleep. The averaged waking signal was subtracted from the sleep signal and projected on a bidimensional scalp map; sleep and wake spike distributions were compared by using a t-test. The superimposed signal of sleep and wake traces was obtained; the rising phase of the spike, the peak, and the deflections following the spike were identified, and their cortical generator was calculated using low-resolution brain electromagnetic tomography (LORETA) for each group. A mean of 21 IEDs in wake and 39 in sleep per subject were selected. As compared to wake, a larger IED scalp projection was detected during sleep in both mesial and neocortical TLE (p<0.05). A series of EEG deflections followed the spike, the cortical sources of which displayed alternating activations of different cortical areas in wake, substituted by isolated, stationary activations in sleep in mesial TLE and a silencing in neocortical TLE. During sleep, the IED scalp region increases, while cortical interaction decreases. The interaction of cortical modules in sleep and wake in TLE may influence the appearance of IEDs on scalp EEG; in addition, IEDs could be proxies for cerebral oscillation perturbation. Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Expression of interferon-inducible chemokines and sleep/wake changes during early encephalitis in experimental African trypanosomiasis.

PubMed

Laperchia, Claudia; Tesoriero, Chiara; Seke-Etet, Paul F; La Verde, Valentina; Colavito, Valeria; Grassi-Zucconi, Gigliola; Rodgers, Jean; Montague, Paul; Kennedy, Peter G E; Bentivoglio, Marina

2017-08-01

Human African trypanosomiasis or sleeping sickness, caused by the parasite Trypanosoma brucei, leads to neuroinflammation and characteristic sleep/wake alterations. The relationship between the onset of these alterations and the development of neuroinflammation is of high translational relevance, but remains unclear. This study investigates the expression of interferon (IFN)-γ and IFN-inducible chemokine genes in the brain, and the levels of CXCL10 in the serum and cerebrospinal fluid prior to and during the encephalitic stage of trypanosome infection, and correlates these with sleep/wake changes in a rat model of the disease. The expression of genes encoding IFN-γ, CXCL9, CXCL10, and CXCL11 was assessed in the brain of rats infected with Trypanosoma brucei brucei and matched controls using semi-quantitative end-point RT-PCR. Levels of CXCL10 in the serum and cerebrospinal fluid were determined using ELISA. Sleep/wake states were monitored by telemetric recording. Using immunohistochemistry, parasites were found in the brain parenchyma at 14 days post-infection (dpi), but not at 6 dpi. Ifn-γ, Cxcl9, Cxcl10 and Cxcl11 mRNA levels showed moderate upregulation by 14 dpi followed by further increase between 14 and 21 dpi. CXCL10 concentration in the cerebrospinal fluid increased between 14 and 21 dpi, preceded by a rise in the serum CXCL10 level between 6 and 14 dpi. Sleep/wake pattern fragmentation was evident at 14 dpi, especially in the phase of wake predominance, with intrusion of sleep episodes into wakefulness. The results show a modest increase in Cxcl9 and Cxcl11 transcripts in the brain and the emergence of sleep/wake cycle fragmentation in the initial encephalitic stage, followed by increases in Ifn-γ and IFN-dependent chemokine transcripts in the brain and of CXCL10 in the cerebrospinal fluid. The latter parameter and sleep/wake alterations could provide combined humoral and functional biomarkers of the early encephalitic stage in African trypanosomiasis.

Effects of experimental suppression of active (REM) sleep during early development upon adult brain and behavior in the rat.

PubMed

Mirmiran, M; Scholtens, J; van de Poll, N E; Uylings, H B; van der Gugten, J; Boer, G J

1983-04-01

In order to test the hypothesis that active sleep (AS) is important for the normal development of the central nervous system, 3 different deprivation methods were applied to male Wistar rat pups during the first month of life. Daily injection of clomipramine from 8 to 21 days of age reduced the high level of AS to less than the adult value throughout most of the experimental period. Administration of clonidine from 8 to 21 days of life induced an almost total suppression of AS. Instrumental deprivation, using the 'pendulum' method, led to a significant (but less severe) AS reduction during 2-4 weeks of postnatal age. Open-field behavior testing in adulthood revealed a higher than normal level of ambulation in all 3 experimental groups. Masculine sexual responses were deficient, due to a low level of both mounts and ejaculations, in both clomipramine- and clonidine-treated animals. Neither passive avoidance learning nor dark preference tests revealed any differences between the experimental and control rats. Sleep observations showed that there was an abnormally high incidence of large myoclonic jerks during AS in both clomipramine- and clonidine-treated rats. Subsequent measurement of regional brain weights showed a significant reduction in the cerebral cortex and medulla oblongata, as compared with the respective control groups, in both the clomipramine- and the clonidine-treated rats. In addition, DNA and protein determination in the affected brain areas showed a proportional reduction in the cortex and in the medulla. These results demonstrate that interference with normal functioning either of AS per se or of specific monoaminergic transmitter systems during early development can produce long-lasting behavioral as well as brain morphological and biochemical abnormalities in later life.

A neuron-glia interaction involving GABA Transaminase contributes to sleep loss in sleepless mutants

PubMed Central

Chen, Wen-Feng; Maguire, Sarah; Sowcik, Mallory; Luo, Wenyu; Koh, Kyunghee; Sehgal, Amita

2014-01-01

Sleep is an essential process and yet mechanisms underlying it are not well understood. Loss of the Drosophila quiver/sleepless (qvr/sss) gene increases neuronal excitability and diminishes daily sleep, providing an excellent model for exploring the underpinnings of sleep regulation. Here, we used a proteomic approach to identify proteins altered in sss brains. We report that loss of sleepless post-transcriptionally elevates the CG7433 protein, a mitochondrial γ-aminobutyric acid transaminase (GABAT), and reduces GABA in fly brains. Loss of GABAT increases daily sleep and improves sleep consolidation, indicating that GABAT promotes wakefulness. Importantly, disruption of the GABAT gene completely suppresses the sleep phenotype of sss mutants, demonstrating that GABAT is required for loss of sleep in sss mutants. While SSS acts in distinct populations of neurons, GABAT acts in glia to reduce sleep in sss flies. Our results identify a novel mechanism of interaction between neurons and glia that is important for the regulation of sleep. PMID:24637426

EEG slow waves in traumatic brain injury: Convergent findings in mouse and man

PubMed Central

Modarres, Mo; Kuzma, Nicholas N.; Kretzmer, Tracy; Pack, Allan I.; Lim, Miranda M.

2016-01-01

Objective Evidence from previous studies suggests that greater sleep pressure, in the form of EEG-based slow waves, accumulates in specific brain regions that are more active during prior waking experience. We sought to quantify the number and coherence of EEG slow waves in subjects with mild traumatic brain injury (mTBI). Methods We developed a method to automatically detect individual slow waves in each EEG channel, and validated this method using simulated EEG data. We then used this method to quantify EEG-based slow waves during sleep and wake states in both mouse and human subjects with mTBI. A modified coherence index that accounts for information from multiple channels was calculated as a measure of slow wave synchrony. Results Brain-injured mice showed significantly higher theta:alpha amplitude ratios and significantly more slow waves during spontaneous wakefulness and during prolonged sleep deprivation, compared to sham-injured control mice. Human subjects with mTBI showed significantly higher theta:beta amplitude ratios and significantly more EEG slow waves while awake compared to age-matched control subjects. We then quantified the global coherence index of slow waves across several EEG channels in human subjects. Individuals with mTBI showed significantly less EEG global coherence compared to control subjects while awake, but not during sleep. EEG global coherence was significantly correlated with severity of post-concussive symptoms (as assessed by the Neurobehavioral Symptom Inventory scale). Conclusion and implications Taken together, our data from both mouse and human studies suggest that EEG slow wave quantity and the global coherence index of slow waves may represent a sensitive marker for the diagnosis and prognosis of mTBI and post-concussive symptoms. PMID:28018987

EEG slow waves in traumatic brain injury: Convergent findings in mouse and man.

PubMed

Modarres, Mo; Kuzma, Nicholas N; Kretzmer, Tracy; Pack, Allan I; Lim, Miranda M

2016-07-01

Evidence from previous studies suggests that greater sleep pressure, in the form of EEG-based slow waves, accumulates in specific brain regions that are more active during prior waking experience. We sought to quantify the number and coherence of EEG slow waves in subjects with mild traumatic brain injury (mTBI). We developed a method to automatically detect individual slow waves in each EEG channel, and validated this method using simulated EEG data. We then used this method to quantify EEG-based slow waves during sleep and wake states in both mouse and human subjects with mTBI. A modified coherence index that accounts for information from multiple channels was calculated as a measure of slow wave synchrony. Brain-injured mice showed significantly higher theta:alpha amplitude ratios and significantly more slow waves during spontaneous wakefulness and during prolonged sleep deprivation, compared to sham-injured control mice. Human subjects with mTBI showed significantly higher theta:beta amplitude ratios and significantly more EEG slow waves while awake compared to age-matched control subjects. We then quantified the global coherence index of slow waves across several EEG channels in human subjects. Individuals with mTBI showed significantly less EEG global coherence compared to control subjects while awake, but not during sleep. EEG global coherence was significantly correlated with severity of post-concussive symptoms (as assessed by the Neurobehavioral Symptom Inventory scale). Taken together, our data from both mouse and human studies suggest that EEG slow wave quantity and the global coherence index of slow waves may represent a sensitive marker for the diagnosis and prognosis of mTBI and post-concussive symptoms.