Dynamic Structure of NREM Sleep

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A,C—E show diagrams of the combined extent of lesions in the pontine tegmentum of cats producing either EEG activation diagonal dashed lines encircled by heavy dashed lines or EEG synchronization horizontal lines encircled by heavy solid lines. B Graph showing the percent of increase in activation dashed line and decrease in activation solid line relative to the pre-lesion control-based zero for each animal.

Note that lesions that produced EEG synchronization are located at the level of the oral pontine reticular nucleus and those that produced EEG activation are located caudal, dorsal, and lateral to this nucleus. The major role of the cerebellum in motor functions has undervalued its possible involvement in sleep regulation.

Cerebellar participation in sleep can be related to motor activities during sleep but also to intrinsic sleep mechanisms. Together with these actions, the cerebellum has important influences on intrinsic sleep mechanisms as was first indicated by the changes observed in cortical and thalamic electrical activity that follow electrical stimulation and lesion of different cerebellar structures.

Moruzzi reported that diffuse EEG effects could be obtained through the efferent of the nucleus dentatus, this effect was also obtained with low-frequency electrical stimulation of the nucleus fatigius, while high frequency stimulation of this nucleus produced diffuse EEG activation Fadiga et al. Specific superficial thalamocortical responses surface negative-deep positive potentials in the frontal and parietal cortices were also produced by stimulation of the cerebellar nuclei Sasaki et al.

The bioelectrical features of these synchronized bursts are similar to the relaxation rhythms described in cats during periods of relaxed wakefulness or drowsiness Ursin and Sterman, Also, changes in sleep—wakefulness proportions occur after fastigial nuclei, cortical, or middle cerebellar peduncle lesions.

All these studies point to an important participation by the cerebellum in SWC mechanisms through a functional antagonism in the regulation of the proportions of sleep and wakefulness between cerebellar cortex and deep cerebellar nuclei; that is, like the changes occurring after the brachium conjunctivum tract lesions, increased wakefulness, and decreased NREM and REM sleep were reported after bilateral lesions of the fastigial nuclei Giannazzo et al. However, these effects were just the opposite after lesions in the middle cerebellar peduncle Raffaele et al.

However and surprisingly, in spite of the severe neurological deficits produced by cerebellectomy, the quantitative alterations in the proportions of SWC states in cerebellectomized animals are smaller than those produced by localized subcortical or cortical cerebellar lesions. Modifications in the total duration of wakefulness, drowsiness, NREM slow sleep , and REM paradoxical sleep, as well as their episode mean duration and number per recording after different cerebellar lesions. In contrast, the cats with lesions in the cerebellar cortex and white matter of the anterior vermis showed a significant decrease of drowsiness and a significant increase in REM sleep.

A recent study Dang-Vu et al. On the basis of parallel changes that occur in forebrain and cerebellum during NREM sleep, Andre and Arrighi have proposed that forebrain and cerebellum may cooperate strongly in information processing during sleep. The growing data on hippocampal activation during NREM sleep after memory task training Peigneux et al. In addition, we would note that, in humans and other mammals, sleep is not only regulated by the circadian clock, but also by sleep homeostasis.

Humans are awake in the morning because sleep pressure is low after a night of rest Mignot and Huguenard, Throughout the day increased wakefulness-promoting signals, partly driven by the circadian clock, counter the growing sleep debt or sleep pressure, keeping the subject awake. An opposite interaction occurs at night. Sleep would be necessary to normalize the synapses to a basal condition that is sustainable and ensures cellular homeostasis Cirelli and Tononi, NREM sleep homeostasis depends not only on the duration of prior wakefulness but also on intensity, and sleep intensity increases when wakefulness is associated with learning Cirelli, The metabolic factors that initiate sleep are molecules produced by neuronal activity during wakefulness and they increase proportionally with the duration and intensity of arousal.

The accumulation of metabolites up to a critical level would be involved in the initiation of sleep specifically promoting NREM sleep. During the course of sleep metabolite levels would be reduced from the critical concentration to basal levels Datta and MacLean, Many molecules have been implicated in the processes of sleep regulation, but only a few meet the criteria for being considered NREM sleep-regulatory substances. Among these substances are: adenosine, nitric oxide, prostaglandin d2, interleukin-1, tumor necrosis factor, and growth hormone-releasing hormone Krueger et al.

These molecules are involved in regulating the intensity and duration of NREM sleep and they act in biochemical cascades. Neuronal activity during wakefulness increases the synthesis of NREM sleep regulating molecules; this increase, as occurs with the effects of adenosine on the A1-receptor, leads to the inhibition of neuronal activity, thereby increasing sleep pressure, and finally NREM begins Vassalli and Dijk, Currently, NREM and REM sleep are considered behavioral states involving the whole organism and governed by central control mechanisms.

Although accepting this point of view, there is increasing evidence that NREM sleep and thus sleep might be a fundamental property of local neuronal networks since it can be initiated at small brain assemblies in response to their use, and only later on be consolidated by general central mechanisms Krueger et al. One of the smallest sleep units could be the individual cortical columns in which sensory stimulation produces fluctuating high and low amplitude evoked responses depending on the behavioral state. In sleeping animals, the sleep-like response in cortical columns is characterized by evoked response potentials with a greater amplitude that the evoked responses during wakefulness Rector et al.

Thus, these findings suggest that NREM sleep may be regulated at local neuronal assembly levels and this regulation appears to be a fundamental property of the neural networks and it depends on prior activity in each network Krueger et al. The NREM sleep of each local cortical column can be initiated by metabolically driven changes derived from the manufacture of molecules of sleep-regulatory substances produced by neuronal activity during wakefulness-like activity. The process may involve increased electrical activity, blood flow, extracellular levels of ATP and extra-and intracellular levels of adenosine, all of which would decrease the intracellular ATP level, and this would drive individual columns to enter a sleep-like activity state.

Once a final sleep state was reached this process would be reversed: reduced electrical activity, blood flow, extracellular levels of ATP and extra-and intracellular levels of adenosine would raise the intracellular ATP level in individual local cortical columns, and thus, the cortical column would be prepared for wakefulness.

The sleep or wakefulness states of individual cortical columns could be synchronized through humoral and electrical connections and therefore the sleep or wakefulness of the whole organism would occur as an emergent property of the interaction of individual networks Krueger et al. Nowadays there is an emerging understanding of the role of astrocytes as potential mediators of the known effect of adenosine in sleep regulation and this mediation would involve both neuroenergetic and synaptic plasticity roles Jones, Delta SWA seems to reflect a form of restorative process for cortical local circuits: SWA delta power is increased in cortical areas that have been most active during the day.

Also, imaging techniques have shown that there is a localized decrease in metabolic activity at night in areas that have been activated during the day Mignot and Huguenard, SWA homeostasis may reflect synaptic changes underlying a cellular need for sleep. Nevertheless, Huber et al. Thus, sleep homeostasis can be induced on a local level and can improve performance. More recently, Vyazovskiy et al. In addition, Vyazovskiy et al. During the first NREM sleep after an uninterrupted waking period, neuronal barrel cortex population ON periods are short and frequent, while neuronal silence periods DOWN states are long and frequent.

DOWN states accompanied by an overall decrease in neuronal activity are a phenomenon that is thought to be associated with energy savings. After a sustained sleep period, which reduces the sleep debt, barrel cortex OFF periods decrease and the duration of the ON periods increases.

Therefore, the systematic increase of firing during wakefulness is balanced by staying asleep. Recent data Jones et al. Based on simple energy demands and since the cerebral cortex—thalamus unit is a large part of the human and mammal brain, being awake for longer and longer periods of time seems to be very expensive, hence energy economy by the brain during NREM sleep is one of the prevalent hypotheses to explain NREM sleep pressure Mignot and Huguenard, However, during NREM sleep neurons must down-fire in synchrony rather than simply stay silent; for some authors this circumstance supports the need to transfer memory to different cortical areas, as has been demonstrated to occur between the hippocampus and visual cortex.

To Vyazovskiy et al. This reduction of synapses during sleep increases the signal to noise ratio for the remaining connections, improving performance Mignot and Huguenard, ; Vyazovskiy et al.

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The close reciprocal connections between the thalamus and the cerebral cortex would force NREM sleep homeostatic processes to take place simultaneously in the two structures. The former connections would act on the thalamus—cerebral cortex unit to facilitate the NREM sleep neurophysiological and homeostatic processes and also through neurophysiological and homeostatic mechanisms, the latter subcortical connections would inhibit the other phases of SWC: REM sleep and wakefulness. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

We acknowledge very valuable suggestions from Dr. We thank Ms. Callejo for technical assistance and Ms. Warren for revision of English language usage. National Center for Biotechnology Information , U. Journal List Front Neurol v. Front Neurol. Published online Nov Prepublished online Aug Author information Article notes Copyright and License information Disclaimer. Reviewed by: Matthew R.

This article was submitted to Frontiers in Sleep and Chronobiology, a specialty of Frontiers in Neurology. Received Jul 27; Accepted Oct This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

This article has been cited by other articles in PMC. Keywords: slow wave sleep, sleep need, thalamus—cerebral cortex unit, rostral hypnogenic system, caudal hypnogenic system, NREM sleep homeostasis. Open in a separate window. Figure 1. Figure 2. The Thalamus and the Cerebral Cortex The thalamus and the cerebral cortex work as an indivisible unit in brain functions. Figure 3. Figure 4. Figure 5. Brainstem and Cerebellar Structures As we have mentioned in the introduction, early work with brainstem transections or lesions below the oral pontine tegmentum indicated that sleep-generating structures were located in the lower brainstem.

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Figure 6. Figure 7. Figure 8.

Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. References Alam M.

Dynamic Structure of NREM Sleep

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How Sleep Activates Epileptic Networks?

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