Local sleep

Krueger, James M.; Nguyen, Joseph; Dykstra-Aiello, Cheryl; Taishi, Ping

doi:10.1016/j.smrv.2018.10.001

Cited by 107 publications

(92 citation statements)

References 99 publications

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“…In summary, our study suggests an important role for the cortex not only in the dynamics of local network oscillations, but also in sleep homeostasis and the global control of sleep-wake states. This finding supports the idea that brain structures fundamentally involved in sleep regulation extend far beyond the traditionally considered subcortical circuitry 4,12,34 .…”

Section: Main Textsupporting

confidence: 85%

“…Electroencephalogram (EEG) slow-wave activity (SWA, EEG spectral power between 0.5-4 Hz) represents a reliable marker of sleep-wake history 6 and has been proposed to underlie many functions of sleep, such as the need for cellular maintenance 8 or synaptic plasticity 9 . Studies suggest that cortical SWA is regulated in a local, use-dependent manner 10,11 supporting the view that sleep emerges within cortical networks as a result of a local accumulation of products of metabolism, such as adenosine 12 . However, the capacity to produce slow waves does not automatically imply a role for the cortex in sleep or sleep homeostasis, either on a local or global level.…”

Section: Main Textmentioning

confidence: 69%

“…Whilst it remains open where and in what form the need to sleep is encoded in mammals 35 , our data leave no doubt that cortical structures play an important role. One possibility is that homeostatic sleep need is generated locally in the cortex itself in an activity-dependent fashion, as it has been earlier proposed 8,12 . Alternatively, cortical structures may be the key site which integrates the information about levels of sleep need, which accumulate during wakefulness elsewhere.…”

Section: Main Textmentioning

confidence: 98%

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A role for the cortex in sleep-wake regulation

Krone

Yamagata

Blanco‐Duque

et al. 2020

Preprint

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The cortex and subcortical circuitry are thought to play distinct roles in the generation of sleep oscillations and global control of vigilance states. Here we show in mice that cell-specific ablation of the key t-SNARE protein SNAP25 in a subset of cortical layer 5 pyramidal and dentate gyrus granule cells results in a marked increase in wakefulness accompanied by a reduced rebound of EEG slow-wave activity after sleep deprivation. The data suggest an important role of the cortex in both global state control and sleep homeostasis.

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Section: Main Textsupporting

confidence: 85%

Section: Main Textmentioning

confidence: 69%

Section: Main Textmentioning

confidence: 98%

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A role for the cortex in sleep-wake regulation

Krone

Yamagata

Blanco‐Duque

et al. 2020

Preprint

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“…Interestingly, in the last few years, science has produced compelling evidence supporting the idea that sleep is under local regulation (48). Local sleep is a complex physiological phenomenon occurring within anatomically discrete brain locations.…”

Section: Discussionmentioning

confidence: 99%

Local sleep-like cortical reactivity in the awake brain after focal injury

Sarasso

D’Ambrosio

Fecchio

et al. 2019

Preprint

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One Sentence Summary: Focal cortical injuries are associated with local intrusion of sleep-like dynamics over the perilesional areas which disrupt local signal complexity and coexist with typical wakefulness cortical reactivity patterns within the same brain. AbstractThe functional consequences of brain injury are known to depend on neuronal alterations extending beyond the area of structural damage. Although a lateralized EEG slowing over the injured hemisphere was known since the early days of clinical neurophysiology, its electrophysiological mechanisms were not systematically investigated. In parallel, basic sleep research has thoroughly characterized the neuronal events underlying EEG slow waves in physiological conditions. These EEG events reflect brief interruptions of neuronal firing (OFF-periods) that can occur locally and have prominent consequences on network and behavioral functions. Notably, the EEG slow waves observed following focal brain injury have been never explicitly connected to local sleep-like neuronal events. In previous works, probing cortical circuits with transcranial magnetic stimulation coupled with EEG (TMS/EEG) proved as an effective way to reveal the tendency of cortical circuits to transiently plunge into silent OFF-periods. Here, using this approach, we show that the intact cortex surrounding focal brain injuries engages locally in pathological sleep-like dynamics. Specifically, we employed TMS/EEG in a cohort of thirty conscious awake patients with chronic focal and multifocal brain injuries of various etiologies. TMS systematically evoked prominent slow waves associated with sleep-like OFF-periods in the area surrounding focal cortico-subcortical lesions. These events were associated with a local disruption of signal complexity and were absent when stimulating the contralateral hemisphere. Perilesional sleep-like OFF-periods may represent a valid read-out of the electrophysiological state of discrete cortical circuits following brain injury as well as a potential target of interventions aimed at fostering functional recovery.

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“…Sleep is also regulated by the skeletal muscle, possibly through sleep-promoting (somnogenic) cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNFα) that can be secreted by the muscle (23,24). Other findings indicate that a behaviorally overt sleep is an emergent state that coalesces from local sleep foci that might be, initially, single neurons (25)(26)(27). It is possible, therefore, that a cause that led to the advent of sleep during evolution may reside in individual neurons and other individual cells, as distinguished from higher-order settings such as networks of cells.In what follows, we shall make a distinction between molecularlevel hypotheses about the cause/function of sleep and propositions that are neither molecular nor overtly mechanistic.…”

mentioning

confidence: 99%

On the cause of sleep: Protein fragments, the concept of sentinels, and links to epilepsy

Varshavsky

2019

Proc. Natl. Acad. Sci. U.S.A.

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The molecular-level cause of sleep is unknown. In 2012, we suggested that the cause of sleep stems from cumulative effects of numerous intracellular and extracellular protein fragments. According to the fragment generation (FG) hypothesis, protein fragments (which are continually produced through nonprocessive cleavages by intracellular, intramembrane, and extracellular proteases) can be beneficial but toxic as well, and some fragments are eliminated slowly during wakefulness. We consider the FG hypothesis and propose that, during wakefulness, the degradation of accumulating fragments is delayed within natural protein aggregates such as postsynaptic densities (PSDs) in excitatory synapses and in other dense protein meshworks, owing to an impeded diffusion of the ∼3,000-kDa 26S proteasome. We also propose that a major function of sleep involves a partial and reversible expansion of PSDs, allowing an accelerated destruction of PSD-localized fragments by the ubiquitin/proteasome system. Expansion of PSDs would alter electrochemistry of synapses, thereby contributing to a decreased neuronal firing during sleep. If so, the loss of consciousness, a feature of sleep, would be the consequence of molecular processes (expansions of protein meshworks) that are required for degradation of protein fragments. We consider the concept of FG sentinels, which signal to sleep-regulating circuits that the levels of fragments are going up. Also discussed is the possibility that protein fragments, which are known to be overproduced during an epileptic seizure, may contribute to postictal sleep and termination of seizures. These and related suggestions, described in the paper, are compatible with current evidence about sleep and lead to testable predictions. fragment | extracellular | intracellular | proteolysis | sleep S leep is universal among mammals and other vertebrates.Animals with much smaller nervous systems, such as insects, also sleep (1-8). Mechanisms that control sleep include circadian circuits, which underlie daily rhythms of sleep and other biological variables (9). However, circadian aspects of sleep do not define it entirely, because sleep has the homeostatic property of becoming longer after sleep deprivation (10, 11). In mammals, birds, and lizards, two alternating modes of sleep have been identified, the non-rapid eye movement (NREM) sleep and the rapid eye movement (REM) sleep (12,13). The depth of NREM sleep is yet another sleep variable. In adult humans, NREM sleep occupies ∼80% of the total sleep time. For recent reviews of sleep, see refs. 14-20.Despite advances in the understanding of neuronal circuits as well as genes, proteins, short peptides, and other compounds that regulate sleep, it is largely unknown why sleep exists and what it is for. Maladaptive aspects of sleep include elevated dangers of predation during sleep, the neglect of territorial defense and foraging for food, and the loss of parental care and mating opportunities. It is unknown what features of sleep did not allow these fitness costs to ca...

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Local sleep

Cited by 107 publications

References 99 publications

A role for the cortex in sleep-wake regulation

A role for the cortex in sleep-wake regulation

Local sleep-like cortical reactivity in the awake brain after focal injury

On the cause of sleep: Protein fragments, the concept of sentinels, and links to epilepsy

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