Cortical neuronal activity does not regulate sleep homeostasis

Qiu, Mei‐Hong; Chen, Michael C.; Lü, Jun

doi:10.1016/j.neuroscience.2015.03.070

Cited by 21 publications

(18 citation statements)

References 41 publications

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“…The dissociation between cortical acetylcholine and behavioral arousal is also supported by earlier reports that ablation of cholinergic neurons in basal forebrain either did not affect total wakefulness 62 or had a transient effect on wakefulness, 63 while systemic atropine produced a dissociated state with waking behavior in the presence of a slow wave electroencephalogram. 64 Conversely, cortical acetylcholine is increased after ketamine administration, despite the behavioral phenotype of general anesthesia. 29 Interestingly, the observed stepwise decrease in high gamma frontal-parietal directed connectivity across wakefulness, SWS, and REM sleep parallels progressive reduction in levels of cortical norepinephrine across sleep-wake cycle.…”

Section: Discussionmentioning

confidence: 99%

Neural Correlates of Wakefulness, Sleep, and General Anesthesia

et al. 2016

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Background Significant advances have been made in our understanding of subcortical processes related to anesthetic- and sleep-induced unconsciousness, but the associated changes in cortical connectivity and cortical neurochemistry have yet to be fully clarified. Methods Male Sprague–Dawley rats were instrumented for simultaneous measurement of cortical acetylcholine and electroencephalographic indices of corticocortical connectivity—coherence and symbolic transfer entropy—before, during, and after general anesthesia (propofol, n = 11; sevoflurane, n = 13). In another group of rats (n = 7), these electroencephalographic indices were analyzed during wakefulness, slow wave sleep (SWS), and rapid eye movement (REM) sleep. Results Compared to wakefulness, anesthetic-induced unconsciousness was characterized by a significant decrease in cortical acetylcholine that recovered to preanesthesia levels during recovery wakefulness. Corticocortical coherence and frontal–parietal symbolic transfer entropy in high γ band (85 to 155 Hz) were decreased during anesthetic-induced unconsciousness and returned to preanesthesia levels during recovery wakefulness. Sleep-wake states showed a state-dependent change in coherence and transfer entropy in high γ bandwidth, which correlated with behavioral arousal: high during wakefulness, low during SWS, and lowest during REM sleep. By contrast, frontal–parietal θ connectivity during sleep-wake states was not correlated with behavioral arousal but showed an association with well-established changes in cortical acetylcholine: high during wakefulness and REM sleep and low during SWS. Conclusions Corticocortical coherence and frontal–parietal connectivity in high γ bandwidth correlates with behavioral arousal and is not mediated by cholinergic mechanisms, while θ connectivity correlates with cortical acetylcholine levels.

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Section: Discussionmentioning

confidence: 99%

Neural Correlates of Wakefulness, Sleep, and General Anesthesia

et al. 2016

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“…55 61,62 and following some pharmacological manipulations 63 may reflect an increase in subcortical-neocortical asynchronous states.…”

Section: Broader Implications Of the Findingsmentioning

confidence: 99%

Different Simultaneous Sleep States in the Hippocampus and Neocortex

Emrick

Gross

Riley

et al. 2016

Sleep

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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 transitionto-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.

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“…In one experiment rats were mostly awake for more than 6 hours after receiving systemic repeated injections of atropine, a cholinergic antagonist [44]. The animals were moving and appeared to behave normally, although performance in learning and vigilance tasks was not assessed.…”

Section: Introductionmentioning

confidence: 99%

“…When the effects of atropine abated, the rats showed an increase in NREM sleep duration relative to baseline, associated with an increase in slow wave activity (SWA), a reliable measure of sleep intensity [45]. During the atropine-induced state of wake with slow waves, Fos expression was high in many brainstem and hypothalamic arousal systems, prompting the authors to conclude that activation of these centers, in a seemingly normally behaving animal, was sufficient to trigger a sleep homeostatic response [44]. …”

Section: Introductionmentioning

confidence: 99%

Sleep, synaptic homeostasis and neuronal firing rates

Cirelli

2017

Current Opinion in Neurobiology

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The synaptic homeostasis hypothesis (SHY) states that wake brings about a net overall increase in synaptic strength in many brain circuits that needs to be renormalized by sleep. I will review recent studies that were either specifically designed to test SHY or were interpreted accordingly, including several experiments that focused on changes in neuronal firing rates. I will emphasize that central to SHY is the idea that what is being regulated across the sleep/wake cycle is synaptic strength, not firing rate, and firing rate taken in isolation is not necessarily an adequate proxy for synaptic strength.

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Cortical neuronal activity does not regulate sleep homeostasis

Cited by 21 publications

References 41 publications

Neural Correlates of Wakefulness, Sleep, and General Anesthesia

Neural Correlates of Wakefulness, Sleep, and General Anesthesia

Different Simultaneous Sleep States in the Hippocampus and Neocortex

Sleep, synaptic homeostasis and neuronal firing rates

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