Sleep function: current questions and new approaches (original) (raw)
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NeuroMolecular Medicine, 2004
Electroencephalographic slow-wave activity (EEG SWA) is an electrophysiological signature of slow (0.5 to 4.0 Hz), synchronized, oscillatory neocortical activity. In healthy individuals, EEG SWA is maximally expressed during nonrapid-eye-movement (non-REM) sleep, and intensifies as a function of prior wake duration. Many of the cellular and network mechanisms generating EEG SWA have been identified, but a number of questions remain unanswered. For example, although EEG SWA is a marker of sleep need, its precise relationship with sleep homeostasis and its roles in the brain are unknown. In this review, the authors discuss their current understanding of the neural mechanisms and possible functions of EEG SWA.
Cortical neuronal activity determines the dynamics of local sleep homeostasis
2019
The homeostatic regulation of sleep manifests as a relative constancy of its total daily amount, and the compensation of sleep loss by an increase in its subsequent duration and intensity. Theoretical descriptions of this phenomenon define 'Process S', a variable with dynamics dependent only on sleep-wake history and whose levels are reflected in EEG slow wave activity. While numerous hypotheses have been advanced regarding the substrate and role of Process S, such as synaptic or energy homeostasis, it remains unclear whether these dynamics are fundamentally driven by a need to homeostatically regulate specific variables, or by an unknown innate process which enforces that a certain daily sleep quota is obtained. Sleep is typically defined based on brain-derived criteria, such as behaviour or EEG power spectra, and variation in brain activity during wakefulness has been linked to variation in Process S accumulation. We therefore hypothesised that Process S dynamics might be ...
eLife, 2020
Sleep homeostasis manifests as a relative constancy of its daily amount and intensity. Theoretical descriptions define ‘Process S’, a variable with dynamics dependent on global sleep-wake history, and reflected in electroencephalogram (EEG) slow wave activity (SWA, 0.5–4 Hz) during sleep. The notion of sleep as a local, activity-dependent process suggests that activity history must be integrated to determine the dynamics of global Process S. Here, we developed novel mathematical models of Process S based on cortical activity recorded in freely behaving mice, describing local Process S as a function of the deviation of neuronal firing rates from a locally defined set-point, independent of global sleep-wake state. Averaging locally derived Processes S and their rate parameters yielded values resembling those obtained from EEG SWA and global vigilance states. We conclude that local Process S dynamics reflects neuronal activity integrated over time, and global Process S reflects local p...
Cortical Neuronal Mechanisms of Sleep Homeostasis
Журнал высшей нервной деятельности им. И. В. Павлова, 2013
The longer we are awake, the deeper is our subsequent sleep. On the other hand, the shorter and more fragmented is our sleep, the more difficult it is for us to maintain wakefulness and stable cognitive per formance the next day. This relationship between wakefulness and subsequent sleep becomes especially apparent after sleep deprivation or during chronic sleep restriction, which is experienced by millions of people in our society, as well as in multiple neurological, respiratory and other chronic diseases. Invari ably, poor sleep leads to fatigue, sleepiness, marked cognitive deficits and impaired mood. The crucial question is what happens to the brain after a period of being awake or asleep, and where in the brain and why do these changes occur. This review summarizes information about neurophysiological substrates of sleep homeostatic processes at the cellular and network levels. It is suggested that sensory, behavioral and cognitive deficits after sleep deprivation resulting from the imbalance between local and global neu ronal interactions can be reversed only by physiological sleep.
2020
Sleep homeostasis manifests as a relative constancy of its daily amount and intensity. Theoretical descriptions define 'Process S', a variable with dynamics dependent on global sleepwake history, and reflected in electroencephalogram (EEG) slow wave activity (SWA, 0.5-4 Hz) during sleep. The notion of sleep as a local, activity-dependent process suggests that activity history must be integrated to determine the dynamics of global Process S. Here, we developed novel mathematical models of Process S based on cortical activity recorded in freely behaving mice, describing local Process S as a function of the deviation of neuronal firing rates from a locally defined set-point, independent of global sleep-wake state. Averaging locally derived Processes S and their rate parameters yielded values resembling those obtained from EEG SWA and global vigilance states. We conclude that local Process S dynamics reflects neuronal activity integrated over time, and global Process S reflects local processes integrated over space.
Sleep as a biological problem: an overview of frontiers in sleep research
The Journal of Physiological Sciences, 2015
Sleep is a physiological process not only for the rest of the body but also for several brain functions such as mood, memory, and consciousness. Nevertheless, the nature and functions of sleep remain largely unknown due to its extremely complicated nature and lack of optimized technology for the experiments. Here we review the recent progress in the biology of the mammalian sleep, which covers a wide range of research areas: the basic knowledge about sleep, the physiology of cerebral cortex in sleeping animals, the detailed morphological features of thalamocortical networks, the mechanisms underlying fluctuating activity of autonomic nervous systems during rapid eye movement sleep, the cutting-edge technology of tissue clearing for visualization of the whole brain, the ketogenesis-mediated homeostatic regulation of sleep, and the forward genetic approach for identification of novel genes involved in sleep. We hope this multifaceted review will be helpful for researchers who are interested in the biology of sleep.
Current understanding on the neurobiology of sleep and wakefulness
The modern concept of sleep and wakefulness has evolved from the landmark discovery of ascending reticular activating system by Moruzzi and Magoun in 1949. The other major contributions have come from the electrophysiological studies of sleep–wake states following the discovery of electroencephalogram by Hans Berger in 1929. Research studies over the past 60 years have provided us an enormous understanding on the neural basis of sleep–wake states and their regulatory mechanisms. By shuttling through the two behavioral states of sleep and wake, brain coordinates many complex functions essential for cellular homeostasis and adaptation to environment. This review brie fl y summarizes the current awareness on the dynamicity of brain mechanisms of sleep and wakefulness as well as the newer concepts of the biological functions of sleep.
Cognitive neuroscience of sleep
Progress in Brain Research, 2010
Mechanism is at the heart of understanding, and this chapter addresses underlying brain mechanisms and pathways of cognition and the impact of sleep on these processes, especially those serving learning and memory. This chapter reviews the current understanding of the relationship between sleep/waking states and cognition from the perspective afforded by basic neurophysiological investigations. The extensive overlap between sleep mechanisms and the neurophysiology of learning and memory processes provide a foundation for theories of a functional link between the sleep and learning systems. Each of the sleep states, with its attendant alterations in neurophysiology, is associated with facilitation of important functional learning and memory processes. For rapid eye movement (REM) sleep, salient features such as PGO waves, theta synchrony, increased acetylcholine, reduced levels of monoamines and, within the neuron, increased transcription of plasticity-related genes, cumulatively allow for freely occurring bidirectional plasticity (long-term potentiation (LTP) and its reversal, depotentiation). Thus, REM sleep provides a novel neural environment in which the synaptic remodeling essential to learning and cognition can occur, at least within the hippocampal complex. During nonREM sleep Stage 2 spindles, the cessation and subsequent strong bursting of noradrenergic cells and coincident reactivation of hippocampal and cortical targets would also increase synaptic plasticity, allowing targeted bidirectional plasticity in the neocortex as well. In delta nonREM sleep, orderly neuronal reactivation events in phase with slow wave delta activity, together with high protein synthesis levels, would facilitate the events that convert early LTP to long lasting LTP. Conversely, delta sleep does not activate immediate early genes associated with de novo LTP. This nonREM sleep-unique genetic environment combined with low acetylcholine levels may serve to reduce the strength of cortical circuits that activate in the ~50% of delta-coincident reactivation events that do not appear in their waking firing sequence. The chapter reviews the results of manipulation studies, typically total sleep or REM sleep deprivation, that serve to underscore the functional significance of the phenomenological associations. Finally, the implications of sleep neurophysiology for learning and memory will be considered from a larger perspective in which the association of specific sleep states with both potentiation or depotentiation is integrated into mechanistic models of cognition. Long-term potentiation in the dentate gyrus in freely moving rats is reinforced by intraventricular application of norepinephrine, but not oxotremorine. Neurobiol Learn Mem, 83, 72-8. ASTON-JONES, G. & BLOOM, F. E. (1981) Activity of norepinephrine-containing locus coeruleus neurons in behaving rats anticipates fluctuations in the sleep-waking cycle.
Sleep homeostasis in the rat is preserved during chronic sleep restriction
Proceedings of the National Academy of Sciences, 2010
Sleep is homeostatically regulated in all animal species that have been carefully studied so far. The best characterized marker of sleep homeostasis is slow wave activity (SWA), the EEG power between 0.5 and 4 Hz during nonrapid eye movement (NREM) sleep. SWA reflects the accumulation of sleep pressure as a function of duration and/or intensity of prior wake: it increases after spontaneous wake and short-term (3–24 h) sleep deprivation and decreases during sleep. However, recent evidence suggests that during chronic sleep restriction (SR) sleep may be regulated by both allostatic and homeostatic mechanisms. Here, we performed continuous, almost completely artifact-free EEG recordings from frontal, parietal, and occipital cortex in freely moving rats ( n = 11) during and after 5 d of SR. During SR, rats were allowed to sleep during the first 4 h of the light period (4S + ) but not during the following 20 h (20S − ). During the daily 20S − most sleep was prevented, whereas the number ...