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Showing papers on "Slow-wave sleep published in 2014"


Journal ArticleDOI
TL;DR: There is a circuit substrate through which GABAergic PZ neurons can potently trigger SWS and modulate the cortical EEG, regardless of the time of day, and this circuit uniquely and potently initiatedSWS and EEG SWA.
Abstract: Work in animals and humans has suggested the existence of a slow wave sleep (SWS)-promoting/electroencephalogram (EEG)-synchronizing center in the mammalian lower brainstem. Although sleep-active GABAergic neurons in the medullary parafacial zone (PZ) are needed for normal SWS, it remains unclear whether these neurons can initiate and maintain SWS or EEG slow-wave activity (SWA) in behaving mice. We used genetically targeted activation and optogenetically based mapping to examine the downstream circuitry engaged by SWS-promoting PZ neurons, and we found that this circuit uniquely and potently initiated SWS and EEG SWA, regardless of the time of day. PZ neurons monosynaptically innervated and released synaptic GABA onto parabrachial neurons, which in turn projected to and released synaptic glutamate onto cortically projecting neurons of the magnocellular basal forebrain; thus, there is a circuit substrate through which GABAergic PZ neurons can potently trigger SWS and modulate the cortical EEG.

245 citations


Journal ArticleDOI
TL;DR: The results showed that patients with PI present a disruption of sleep continuity and a significant reduction of slow wave sleep (SWS) and rapid eye movement (REM) sleep compared to GSC.

240 citations


Journal ArticleDOI
TL;DR: This work draws on recent studies to suggest a link between light NREM and active potentiation, and between deep N REM and homeostatic regulation, and could serve as a key for interpreting the physiology of sleep stages and reconciling inconsistencies in terminology.

226 citations


Journal ArticleDOI
TL;DR: The converging evidence showing that acoustic stimulation is safe and represents an ideal tool for slow wave sleep (SWS) enhancement is reviewed, highlighting the physiology of the K-complex, a peripheral evoked slow wave, and how intensity and frequency of the acoustic stimuli affect sleep enhancement.
Abstract: Even modest sleep restriction, especially the loss of sleep slow wave activity (SWA), is invariably associated with slower electroencephalogram (EEG) activity during wake, the occurrence of local sleep in an otherwise awake brain, and impaired performance due to cognitive and memory deficits. Recent studies not only confirm the beneficial role of sleep in memory consolidation, but also point to a specific role for sleep slow waves. Thus, the implementation of methods to enhance sleep slow waves without unwanted arousals or lightening of sleep could have significant practical implications. Here we first review the evidence that it is possible to enhance sleep slow waves in humans using transcranial direct-current stimulation (tDCS) and transcranial magnetic stimulation. Since these methods are currently impractical and their safety is questionable, especially for chronic long-term exposure, we then discuss novel data suggesting that it is possible to enhance slow waves using sensory stimuli. We consider the physiology of the K-complex (KC), a peripheral evoked slow wave, and show that, among different sensory modalities, acoustic stimulation is the most effective in increasing the magnitude of slow waves, likely through the activation of non-lemniscal ascending pathways to the thalamo-cortical system. In addition, we discuss how intensity and frequency of the acoustic stimuli, as well as exact timing and pattern of stimulation, affect sleep enhancement. Finally, we discuss automated algorithms that read the EEG and, in real-time, adjust the stimulation parameters in a closed-loop manner to obtain an increase in sleep slow waves and avoid undesirable arousals. In conclusion, while discussing the mechanisms that underlie the generation of sleep slow waves, we review the converging evidence showing that acoustic stimulation is safe and represents an ideal tool for slow wave sleep (SWS) enhancement.

194 citations


Journal ArticleDOI
TL;DR: Several recent studies have related consolidation of procedural memories to SWS (or non-REM sleep)-dependent consolidation processes, and proposed future research questions to advance the understanding of the role of different sleep stages for memory consolidation.
Abstract: Sleep benefits memory consolidation. Previous theoretical accounts have proposed a differential role of slow-wave sleep (SWS), rapid-eye-movement (REM) sleep, and stage N2 sleep for different types of memories. For example the dual process hypothesis proposes that SWS is beneficial for declarative memories, whereas REM sleep is important for consolidation of non-declarative, procedural and emotional memories. In fact, numerous recent studies do provide further support for the crucial role of SWS (or non-REM sleep) in declarative memory consolidation. However, recent evidence for the benefit of REM sleep for non-declarative memories is rather scarce. In contrast, several recent studies have related consolidation of procedural memories (and some also emotional memories) to SWS (or non-REM sleep)-dependent consolidation processes. We will review this recent evidence, and propose future research questions to advance our understanding of the role of different sleep stages for memory consolidation.

180 citations


Journal ArticleDOI
TL;DR: Sleep structure and duration underwent significant alterations throughout the aging process in the general population and there was an important correlation between age, sleep respiratory parameters and PLM index.

148 citations


Journal ArticleDOI
TL;DR: Stimulation enhanced slow oscillation power in children with ADHD and boosted memory performance to the same level as in healthy children indicate that increasing slow oscillating direct current stimulation during sleep by toDCS can alleviate declarative memory deficits.

141 citations


Journal ArticleDOI
TL;DR: The enhancing potential of sleep is discussed, mainly focusing on the domain of learning and memory, by discussing different methodological caveats and ethical issues that should be considered when thinking about using sleep for cognitive enhancement in everyday applications.
Abstract: Sleep is essential for effective cognitive functioning Loosing even a few hours of sleep can have detrimental effects on a wide variety of cognitive processes such as attention, language, reasoning, decision making, learning and memory While sleep is necessary to ensure normal healthy cognitive functioning, it can also enhance performance beyond the boundaries of the normal condition This article discusses the enhancing potential of sleep, mainly focusing on the domain of learning and memory Sleep is known to facilitate the consolidation of memories learned before sleep as well as the acquisition of new memories to be learned after sleep According to a widely held model this beneficial effect of sleep relies on the neuronal reactivation of memories during sleep that is associated with sleep-specific brain oscillations (slow oscillations, spindles, ripples) as well as a characteristic neurotransmitter milieu Recent research indicates that memory processing during sleep can be boosted by (i) cueing memory reactivation during sleep; (ii) stimulating sleep-specific brain oscillations; and (iii) targeting specific neurotransmitter systems pharmacologically Olfactory and auditory cues can be used, for example, to increase reactivation of associated memories during post-learning sleep Intensifying neocortical slow oscillations (the hallmark of slow wave sleep (SWS)) by electrical or auditory stimulation and modulating specific neurotransmitters such as noradrenaline and glutamate likewise facilitates memory processing during sleep With this evidence in mind, this article concludes by discussing different methodological caveats and ethical issues that should be considered when thinking about using sleep for cognitive enhancement in everyday applications

139 citations


Journal ArticleDOI
TL;DR: Research on marijuana and sleep has progressed with findings on the effects of marijuana withdrawal on objective and subjective measures of sleep and mechanisms of sleep disturbance in alcoholics and the effect of medical marijuana on sleep and daytime functioning.
Abstract: Substance use disorders (SUD) are common and individuals who suffer from them are prone to relapse. One of the most common consequences of the use of and withdrawal from substances of abuse is sleep disturbance. Substances of abuse affect sleep physiology, including the neurotransmitter systems that regulate the sleep-wake system. Emerging research now highlights an interactive effect between sleep disorders and substance use. New findings in alcohol and sleep research have utilized sophisticated research designs and expanded the scope of EEG and circadian rhythm analyses. Research on marijuana and sleep has progressed with findings on the effects of marijuana withdrawal on objective and subjective measures of sleep. Treatment studies have focused primarily on sleep in alcohol use disorders. Therapies for insomnia in cannabis disorders are needed. Future research is poised to further address mechanisms of sleep disturbance in alcoholics and the effect of medical marijuana on sleep and daytime functioning.

137 citations


Journal ArticleDOI
Li Lan1, Li Pan1, Zhiwei Lian1, Hongyuan Huang, Yanbing Lin 
TL;DR: In this article, the effects of air temperature on sleep quality and thermal comfort of sleeping people were investigated by experimenting on human subjects, and subjective assessments on thermal comfort were performed both before and after sleep.

136 citations


Journal ArticleDOI
TL;DR: A high index of suspicion is crucial for effective diagnosis of sleep apnea because symptoms commonly noted in younger patients, such as obesity or loud snoring, may not be present in older patients.

Journal ArticleDOI
TL;DR: Evidence is provided that meeting the VPA standards of the ACSM is associated with improved mental health and more successful coping among young people, even compared to those who are meeting or exceeding the requirements for MPA.

Journal ArticleDOI
01 Feb 2014-Brain
TL;DR: Structural and functional MRI is used to demonstrate that hyperarousal, its clearest characteristic, involves reduced recruitment and connectivity of the left caudate that may predispose to insomnia and perpetuate it.
Abstract: Insomnia is prevalent, severe and partially heritable. Unfortunately, its neuronal correlates remain enigmatic, hampering the development of mechanistic models and rational treatments. Consistently reported impairments concern fragmented sleep, hyper-arousal and executive dysfunction. Because fronto-striatal networks could well play a role in sleep, arousal regulation and executive functioning, the present series of studies used an executive task to evaluate fronto-striatal functioning in disturbed sleep. Patients with insomnia showed reduced recruitment of the head of the left caudate nucleus during executive functioning, which was not secondary to altered performance or baseline perfusion. Individual differences in caudate recruitment were associated with hyper-arousal severity. Seed-based functional connectivity analysis suggested that attenuated input from a projecting orbitofrontal area with reduced grey matter density contributes to altered caudate recruitment in patients with insomnia. Attenuated caudate recruitment persisted after successful treatment of insomnia, warranting evaluation as a potential vulnerability trait. A similar selective reduction in caudate recruitment could be elicited in participants without sleep complaints by slow-wave sleep fragmentation, providing a model to facilitate investigation of the causes and consequences of insomnia.

Journal ArticleDOI
TL;DR: This work proposes that cortical slow oscillations, occurring within specific functionally interconnected neuronal networks during NREM sleep, enable information processing, synaptic plasticity, and prophylactic cellular maintenance during sleep and accounts for the overall architecture of normal sleep.
Abstract: The overall function of sleep is hypothesized to provide "recovery" after preceding waking activities, thereby ensuring optimal functioning during subsequent wakefulness. However, the functional significance of the temporal dynamics of sleep, manifested in the slow homeostatic process and the alternation between non-rapid eye movement (NREM) and REM sleep remains unclear. We propose that NREM and REM sleep have distinct and complementary contributions to the overall function of sleep. Specifically, we suggest that cortical slow oscillations, occurring within specific functionally interconnected neuronal networks during NREM sleep, enable information processing, synaptic plasticity, and prophylactic cellular maintenance ("recovery process"). In turn, periodic excursions into an activated brain state-REM sleep-appear to be ideally placed to perform "selection" of brain networks, which have benefited from the process of "recovery," based on their offline performance. Such two-stage modus operandi of the sleep process would ensure that its functions are fulfilled according to the current need and in the shortest time possible. Our hypothesis accounts for the overall architecture of normal sleep and opens up new perspectives for understanding pathological conditions associated with abnormal sleep patterns.

Journal ArticleDOI
TL;DR: It is proposed that sleep-related interventions might modulate the reorganisation of memories and provide new inroads into treatment, particularly relevant for mental disorders.

Book ChapterDOI
TL;DR: Evidence for the role of sleep disruption as a risk factor for developing alcohol dependence is discussed in the context of research conducted in adolescents and the utility of sleep-evoked potentials in the assessment of the effects of alcoholism on sleep and the brain and in abstinence-mediated recovery is outlined.
Abstract: Alcohol acts as a sedative that interacts with several neurotransmitter systems important in the regulation of sleep. Acute administration of large amounts of alcohol prior to sleep leads to decreased sleep-onset latency and changes in sleep architecture early in the night, when blood alcohol levels are high, with subsequent disrupted, poor-quality sleep later in the night. Alcohol abuse and dependence are associated with chronic sleep disturbance, lower slow-wave sleep, and more rapid-eye-movement sleep than normal, that last long into periods of abstinence and may play a role in relapse. This chapter outlines the evidence for acute and chronic alcohol effects on sleep architecture and sleep electroencephalogram, evidence for tolerance with repeated administration, and possible underlying neurochemical mechanisms for alcohol's effects on sleep. Also discussed are sex differences as well as effects of alcohol on sleep homeostasis and circadian regulation. Evidence for the role of sleep disruption as a risk factor for developing alcohol dependence is discussed in the context of research conducted in adolescents. The utility of sleep-evoked potentials in the assessment of the effects of alcoholism on sleep and the brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a series of questions that need to be answered to determine the role of sleep and sleep disturbance in the development and maintenance of problem drinking and the potential beneficial effects of the treatment of sleep disorders for maintenance of abstinence in alcoholism.

Journal ArticleDOI
01 Jul 2014-Sleep
TL;DR: The results suggest that sleep can promote cortical synaptic potentiation in vivo, and that this potentiation may be mediated by slow wave sleep spindles.
Abstract: STUDY OBJECTIVES Sleep has been hypothesized to globally reduce synaptic strength. However, recent findings suggest that in the context of learning and memory consolidation, sleep may promote synaptic potentiation. We tested the requirement for sleep in a naturally occurring form of experience-dependent synaptic potentiation in the adult mouse visual cortex (V1), which is initiated by patterned visual experience. DESIGN Visual responses were recorded in individual V1 neurons before and after presentation of an oriented grating stimulus, and after subsequent sleep or sleep deprivation. MEASUREMENTS AND RESULTS We find that V1 response potentiation-associated with a shift in orientation preference in favor of the presented stimulus-occurs only after sleep and only during the entrained circadian sleep phase, and is blocked by sleep deprivation. Induction of plasticity following stimulus presentation is associated with an increase in principal neuron firing in V1, which is present in all behavioral states and occurs regardless of time of day. Sleep dependent potentiation is proportional to phase-locking of neuronal activity with thalamocortical spindle oscillations. CONCLUSIONS Our results suggest that sleep can promote cortical synaptic potentiation in vivo, and that this potentiation may be mediated by slow wave sleep spindles. CITATION Aton SJ, Suresh A, Broussard C, Frank MG. Sleep promotes cortical response potentiation following visual experience.

Journal ArticleDOI
TL;DR: Higher spindle density predicted better performance on verbal learning, visual attention and verbal fluency, whereas spindle frequency and slow wave density or slope predicted fewer cognitive performance variables.
Abstract: Spindles and slow waves are hallmarks of non-rapid eye movement sleep. Both these oscillations are markers of neuronal plasticity, and play a role in memory and cognition. Normal ageing is associated with spindle and slow wave decline and cognitive changes. The present study aimed to assess whether spindle and slow wave characteristics during a baseline night predict cognitive performance in healthy older adults the next morning. Specifically, we examined performance on tasks measuring selective and sustained visual attention, declarative verbal memory, working memory and verbal fluency. Fifty-eight healthy middle-aged and older adults (aged 50-91years) without sleep disorders underwent baseline polysomnographic sleep recording followed by neuropsychological assessment the next morning. Spindles and slow waves were detected automatically on artefact-free non-rapid eye movement sleep electroencephalogram. All-night stage N2 spindle density (no./min) and mean frequency (Hz) and all-night non-rapid eye movement sleep slow wave density (no./min) and mean slope (V/s) were analysed. Pearson's correlations were performed between spindles, slow waves, polysomnography and cognitive performance. Higher spindle density predicted better performance on verbal learning, visual attention and verbal fluency, whereas spindle frequency and slow wave density or slope predicted fewer cognitive performance variables. In addition, rapid eye movement sleep duration was associated with better verbal learning potential. These results suggest that spindle density is a marker of cognitive functioning in older adults and may reflect neuroanatomic integrity. Rapid eye movement sleep may be a marker of age-related changes in acetylcholine transmission, which plays a role in new information encoding.

Journal ArticleDOI
01 Dec 2014-Sleep
TL;DR: The results show that optogenetic activation of BF cholinergic neurons during NREM sleep is sufficient to elicit cortical activation and facilitate state transitions, particularly transitions to wakefulness and arousal, at a time scale similar to the activation induced by other subcortical systems.
Abstract: Objectives The basal forebrain cholinergic system is involved in cognitive processes that require an attentive state, an increased level of arousal, and/ or cortical activation associated with low amplitude fast EEG activity. The activity of most neurons in the basal forebrain cholinergic space is tightly correlated with the cortical EEG and the activity state. While most cholinergic neurons fire maximally during waking and REM sleep, the activity of other types of basal forebrain neurons vastly differs across different arousal and sleep states. Numerous studies have suggested a role for the basal forebrain cholinergic neurons in eliciting cortical activation and arousal. However, the intricate local connectivity within the region requires the use of cell-specific manipulation methods to demonstrate such a causal relationship. Design and measurements Here we have combined optogenetics with surface EEG recordings in freely moving mice in order to investigate the effects of acute cholinergic activation on the dynamics of sleep-to-wake transitions. We recorded from naturally sleeping animals and analyzed transitions from NREM sleep to REM sleep and/ or wakefulness in response to photo-stimulation of cholinergic neurons in substantia innominata. Results and conclusions Our results show that optogenetic activation of BF cholinergic neurons during NREM sleep is sufficient to elicit cortical activation and facilitate state transitions, particularly transitions to wakefulness and arousal, at a time scale similar to the activation induced by other subcortical systems. Our results provide in vivo cell-specific demonstration for the role of basal forebrain cholinergic system in induction of wakefulness and arousal.

Journal ArticleDOI
TL;DR: The present article reviews the available evidence on sleep in critically ill children admitted to the PICU, with an emphasis on subjective and objective methods of sleep assessment used and special populations studied, including mechanically ventilated children and children with severe burns.

Journal ArticleDOI
TL;DR: A structured network of sleep brain–brain and brain–heart interactions was found to be sustained mostly by the transitions across different sleep stages, as the information transfer was weaker during specific stages than during the whole night, and vanished progressively when moving from light sleep to deep sleep and to REM sleep.
Abstract: This study proposes an integrated approach, framed in the emerging fields of network physiology and information dynamics, for the quantitative analysis of brain–heart interaction networks during sleep. With this approach, the time series of cardiac vagal autonomic activity and brain wave activities measured respectively as the normalized high frequency component of heart rate variability and the EEG power in the δ, θ, α, σ, and β bands, are considered as realizations of the stochastic processes describing the dynamics of the heart system and of different brain sub-systems. Entropy-based measures are exploited to quantify the predictive information carried by each (sub)system, and to dissect this information into a part actively stored in the system and a part transferred to it from the other connected systems. The application of this approach to polysomnographic recordings of ten healthy subjects led us to identify a structured network of sleep brain–brain and brain–heart interactions, with the node described by the β EEG power acting as a hub which conveys the largest amount of information flowing between the heart and brain nodes. This network was found to be sustained mostly by the transitions across different sleep stages, as the information transfer was weaker during specific stages than during the whole night, and vanished progressively when moving from light sleep to deep sleep and to REM sleep.

Journal ArticleDOI
TL;DR: The results support orexin-A to be a REM sleep stabilizing factor and provide functional signs for effects of orex in-A on sleep alterations and attention in narcolepsy with cataplexy.

Journal ArticleDOI
TL;DR: A bidirectional association between MT and sleep seems likely; therefore, among adolescence, improving sleep should increase MT, and improving MT should increase sleep.

Journal ArticleDOI
TL;DR: It is suggested that TMR during sleep can alter memory representations and promote the emergence of explicit knowledge, supporting the notion that reactivation during sleep is a key mechanism in this process.
Abstract: Memories are gradually consolidated after initial encoding, and this can sometimes lead to a transition from implicit to explicit knowledge. The exact physiological processes underlying this reorganization remain unclear. Here, we used a serial reaction time task to determine whether targeted memory reactivation (TMR) of specific memory traces during slow-wave sleep promotes the emergence of explicit knowledge. Human participants learned two 12-item sequences of button presses (A and B). These differed in both cue order and in the auditory tones associated with each of the four fingers (one sequence had four higher-pitched tones). Subsequent overnight sleep was monitored, and the tones associated with one learned sequence were replayed during slow-wave sleep. After waking, participants demonstrated greater explicit knowledge (p = 0.005) and more improved procedural skill (p = 0.04) for the cued sequence relative to the uncued sequence. Furthermore, fast spindles (13.5–15 Hz) at task-related motor regions predicted overnight enhancement in procedural skill (r = 0.71, p = 0.01). Auditory cues had no effect on post-sleep memory performance in a control group who received TMR before sleep. These findings suggest that TMR during sleep can alter memory representations and promote the emergence of explicit knowledge, supporting the notion that reactivation during sleep is a key mechanism in this process.

Journal ArticleDOI
TL;DR: The findings indicate that processes of brain maturation favor experience- dependent plasticity and determine how sensitive a specific brain region is for learning experiences and confirm that SWA is a highly sensitive tool to map maturational differences in experience-dependent plasticity.
Abstract: Experience-dependent plasticity, the ability of the brain to constantly adapt to an ever-changing environment, has been suggested to be highest during childhood and to decline thereafter. However, empirical evidence for this is rather scarce. Slow-wave activity (SWA; EEG activity of 1-4.5 Hz) during deep sleep can be used as a marker of experience-dependent plasticity. For example, performing a visuomotor adaptation task in adults increased SWA during subsequent sleep over a locally restricted region of the right parietal cortex, which is known to be involved in visuomotor adaptation. Here, we investigated whether local experience-dependent changes in SWA vary as a function of brain maturation. Three age groups (children, adolescents, and adults) participated in a high-density EEG study with two conditions (baseline and adaptation) of a visuomotor learning task. Compared with the baseline condition, sleep SWA was increased after visuomotor adaptation in a cluster of eight electrodes over the right parietal cortex. The local boost in SWA was highest in children. Baseline SWA in the parietal cluster and right parietal gray matter volume, which both indicate region-specific maturation, were significantly correlated with the local increase in SWA. Our findings indicate that processes of brain maturation favor experience-dependent plasticity and determine how sensitive a specific brain region is for learning experiences. Moreover, our data confirm that SWA is a highly sensitive tool to map maturational differences in experience-dependent plasticity.

Journal ArticleDOI
TL;DR: Large-scale modeling of the human cortico-cortical anatomical connectivity is employed to evaluate changes in resting-state FC when the model "falls asleep" due to the progressive decrease in arousal-promoting neuromodulation, and it is shown that local slow waves are structured macroscopically in networks that resemble the resting- state networks.
Abstract: The transition from wakefulness to sleep represents the most conspicuous change in behavior and the level of consciousness occurring in the healthy brain. It is accompanied by similarly conspicuous changes in neural dynamics, traditionally exemplified by the change from "desynchronized" electroencephalogram activity in wake to globally synchronized slow wave activity of early sleep. However, unit and local field recordings indicate that the transition is more gradual than it might appear: On one hand, local slow waves already appear during wake; on the other hand, slow sleep waves are only rarely global. Studies with functional magnetic resonance imaging also reveal changes in resting-state functional connectivity (FC) between wake and slow wave sleep. However, it remains unclear how resting-state networks may change during this transition period. Here, we employ large-scale modeling of the human cortico-cortical anatomical connectivity to evaluate changes in resting-state FC when the model "falls asleep" due to the progressive decrease in arousal-promoting neuromodulation. When cholinergic neuromodulation is parametrically decreased, local slow waves appear, while the overall organization of resting-state networks does not change. Furthermore, we show that these local slow waves are structured macroscopically in networks that resemble the resting-state networks. In contrast, when the neuromodulator decrease further to very low levels, slow waves become global and resting-state networks merge into a single undifferentiated, broadly synchronized network.

Journal ArticleDOI
TL;DR: The Primary Insomnia-group overestimated Sleep Onset Latency and this overestimation was correlated with elevated EEG activity, and the strong association found between K-alpha (K-complex within one second followed by 8-12 Hz EEG activity) in Stage2 sleep and a lower parasympathetic Autonomic Nervous System dominance (less high frequency HR) in Slow-wave sleep, further assumes a state of hyperarousal continuing through sleep in Primary Ins insomnia.

Journal ArticleDOI
TL;DR: This article puts forward the idea that slow oscillations are the default activity of the cortical network based on both experimental and theoretical evidence and discusses whySlow oscillations emerge from the cortical circuits and what are the dynamic advantages of this activity pattern.
Abstract: The function of sleep remained one of largest enigmas of neuroscience for most of the 20th century. However in recent years different evidence has accumulated in support of a critical role of sleep on functions such as replay and memory consolidation. In particular slow wave sleep, and its underlying corticothalamocortical activity, slow oscillations, could be critical not only for memory but also for the maintenance of the brain's structural and func- tional connectivity. In this article we ask: why slow oscillations? To answer this question we put forward the idea that slow oscillations are the default activity of the cortical network based on both experimental and theoretical evidence. We go on to discuss why slow oscillations emerge from the cortical circuits and what are the dynamic advantages of this activity pattern, such as the resilience to perturbances and the facilitation of transitions between a disconnected (e.g. deep sleep) brain and a connected, awake brain.

Journal ArticleDOI
01 Feb 2014-Sleep
TL;DR: Results of this study provide evidence of a functional deafferentation of the neocortex during nonrapid eye movement (NREM) sleep in humans, which likely accounts for increased sensory awareness thresholds during NREM sleep.
Abstract: Study objectives To determine whether thalamocortical signaling between the thalamus and the neocortex decreases from wakefulness to nonrapid eye movement (NREM) sleep. Design Electroencephalography and functional magnetic resonance imaging data were collected simultaneously at 02:30 after 44 h of sleep deprivation. Setting Clinical research hospital. Participants There were six volunteers (mean age 24.2 y, one male) who yielded sufficient amounts of usable, artifact-free data. All were healthy, right-handed native English speakers who consumed less than 710 mL of caffeinated beverages per day. Psychiatric, neurological, circadian, and sleep disorders were ruled out by reviewing each patient's clinical history. A standard clinical nocturnal polysomnogram was negative for sleep disorders. Interventions N/A. Measurements and results A functional connectivity analysis was performed using the centromedian nucleus as the seed region. We determined the statistical significance of the difference between correlations obtained during wakefulness and during slow wave sleep. Neocortical regions displaying decreased thalamic connectivity were all heteromodal regions (e.g., medial frontal gyrus and posterior cingulate/precuneus), whereas there was a complete absence of neocortical regions displaying increased thalamic connectivity. Although more clusters of significant decreases were observed in stage 2 sleep, these results were similar to the results for slow wave sleep. Conclusions Results of this study provide evidence of a functional deafferentation of the neocortex during nonrapid eye movement (NREM) sleep in humans. This deafferentation likely accounts for increased sensory awareness thresholds during NREM sleep. Decreased thalamocortical connectivity in regions such as the posterior cingulate/precuneus also are observed in coma and general anesthesia, suggesting that changes in thalamocortical connectivity may act as a universal "control switch" for changes in consciousness that are observed in coma, general anesthesia, and natural sleep.

Journal ArticleDOI
07 Jul 2014-PLOS ONE
TL;DR: It is speculated that while simpler forms of learning may occur during sleep, neocortically based memories are not readily established during deep sleep, and neural stimulus processing depends importantly on the slow oscillation phase.
Abstract: The sleeping brain retains some residual information processing capacity. Although direct evidence is scarce, a substantial literature suggests the phase of slow oscillations during deep sleep to be an important determinant for stimulus processing. Here, we introduce an algorithm for predicting slow oscillations in real-time. Using this approach to present stimuli directed at both oscillatory up and down states, we show neural stimulus processing depends importantly on the slow oscillation phase. During ensuing wakefulness, however, we did not observe differential brain or behavioral responses to these stimulus categories, suggesting no enduring memories were formed. We speculate that while simpler forms of learning may occur during sleep, neocortically based memories are not readily established during deep sleep.