Homeostatic and Circadian Contribution to EEG and Molecular State Variables of Sleep Regulation

Curie, Thomas; Mongrain, Valérie; Dorsaz, Stéphane; Mang, Géraldine M.; Emmenegger, Yann; Franken, Paul

doi:10.5665/sleep.2440

Cited by 93 publications

(81 citation statements)

References 86 publications

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“…In parallel, further complicatedness in the understanding of sleep mechanism has been pointed-out due to that circadian and homeostatic factors influence sleep processes (Curie et al, 2013Houben et al, 2014;Borbely et al, 2016). In regard to the homeostatic clout in sleep modulation and consistent with previous reports, it is known that a compensatory enhancement in the intensity and duration of sleep known as ''sleep rebound" is present as a result of significative loss of sleep (Borbely and Achermann, 1999;Schwierin et al, 1999;Ocampo-Garces et al, 2000;Vyazovskiy et al, 2007Vyazovskiy et al, , 2011Borbely et al, 2016).…”

Section: Introductionsupporting

confidence: 52%

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Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

et al. 2016

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Abstract-The endocannabinoid system comprises receptors (CB 1 and CB 2 cannabinoid receptors), enzymes (Fatty Acid Amide Hydrolase [FAAH], which synthesizes the endocannabinoid anandamide), as well as the anandamide membrane transporter (AMT). Importantly, previous experiments have demonstrated that the endocannabinoid system modulates multiple neurobiological functions, including sleep. For instance, SR141716A (the CB 1 cannabinoid receptor antagonist) as well as URB597 (the FAAH inhibitor) increase waking in rats whereas VDM-11 (the blocker of the AMT) enhances sleep in rodents. However, no further evidence is available regarding the neurobiological role of the endocannabinoid system in the homeostatic control of sleep. Therefore, the aim of the current experiment was to test if SR141716A, URB597 or VDM-11 would modulate the sleep rebound after sleep deprivation. Thus, these compounds were systemically injected (5, 10, 20 mg/kg; ip; separately each one) into rats after prolonged waking. We found that SR141716A and URB597 blocked in dose-dependent fashion the sleep rebound whereas animals treated with VDM-11 displayed sleep rebound during the recovery period. Complementary, injection after sleep deprivation of either SR141716A or URB597 enhanced dose-dependently the extracellular levels of dopamine (DA), norepinephrine (NE), epinephrine (EP), serotonin (5-HT), as well as adenosine (AD) while VDM-11 caused a decline in contents of these molecules. These findings suggest that SR141716A or URB597 behave as a potent stimulants since they suppressed the sleep recovery period after prolonged waking. It can be concluded that elements of the endocannabinoid system, such as the CB 1 cannabinoid receptor, FAAH and AMT, modulate the sleep homeostasis after prolonged waking. Ó

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Section: Introductionsupporting

confidence: 52%

“…during the next sleep period, which is known as ''sleep rebound" (Deboer, 2009;Yasenkov and Deboer, 2012;Curie et al, 2013;Mang and Franken, 2015).…”

Section: Discussionmentioning

confidence: 99%

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

et al. 2016

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“…After acute periods of sleep deprivation, there is an observed upregulation of immediate early genes/transcription factors such as Arc, c-fos, BDNF, and NGFI-A in the cerebral cortex. As sleep deprivation lengthens, changes are observed in other gene classes such as heat shock proteins, molecular chaperones, growth factors, adhesion molecules, and components of presynaptic and postsynaptic neurotransmission machinery (for more in-depth reviews of gene expression changes in the cortex, see Cirelli and Tononi 2000;Tononi and Cirelli 2001;Cirelli 2002;Cirelli et al 2006;Mackiewicz et al 2009;Wang et al 2010;Curie et al 2013).…”

Section: Gene Expression As a Results Of Sleep Deprivationmentioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

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Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

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“…(Bottom Right) Process S is modeled, assuming S increases only in TDW. For ZT15+SD data points, the simulation uses EEG data collected across ZT12 to 15 in C57BL/6J WT mice sleep-deprived across ZT12 to 18 (77), assuming that TDW expression during SD does not differ between genotypes, as for ZT0 to 6 SD (Fig. 3A).…”

Section: Hcrt Is An Essential Regulator Of the Eeg Determinants Of Spmentioning

confidence: 99%

Hypocretin (orexin) is critical in sustaining theta/gamma-rich waking behaviors that drive sleep need

Vassalli

Franken

2017

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

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121

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Hcrt gene inactivation in mice leads to behavioral state instability, abnormal transitions to paradoxical sleep, and cataplexy, hallmarks of narcolepsy. Sleep homeostasis is, however, considered unimpaired in patients and narcoleptic mice. We find that whereas Hcrt ko/ko mice respond to 6-h sleep deprivation (SD) with a slowwave sleep (SWS) EEG δ (1.0 to 4.0 Hz) power rebound like WT littermates, spontaneous waking fails to induce a δ power reflecting prior waking duration. This correlates with impaired θ (6.0 to 9.5 Hz) and fast-γ (55 to 80 Hz) activity in prior waking. We algorithmically identify a theta-dominated wakefulness (TDW) substate underlying motivated behaviors and typically preceding cataplexy in Hcrt ko/ko mice. Hcrt ko/ko mice fully implement TDW when waking is enforced, but spontaneous TDW episode duration is greatly reduced. A reformulation of the classic sleep homeostasis model, where homeostatic pressure rises exclusively in TDW rather than all waking, predicts δ power dynamics both in Hcrt ko/ko and WT mouse baseline and recovery SWS. The low homeostatic impact of Hcrt ko/ko mouse spontaneous waking correlates with decreased cortical expression of neuronal activityrelated genes (notably Bdnf, Egr1/Zif268, and Per2). Thus, spontaneous TDW stability relies on Hcrt to sustain θ/fast-γ network activity and associated plasticity, whereas other arousal circuits sustain TDW during SD. We propose that TDW identifies a discrete global brain activity mode that is regulated by contextdependent neuromodulators and acts as a major driver of sleep homeostasis. Hcrt loss in Hcrt ko/ko mice causes impaired TDW maintenance in baseline wake and blunted δ power in SWS, reproducing, respectively, narcolepsy excessive daytime sleepiness and poor sleep quality.hypocretin/orexin | narcolepsy | sleep homeostasis | brain theta oscillations | waking substate W akefulness encompasses a wide spectrum of arousal levels, sensorimotor processing modes, and behaviors, reflected in the electroencephalogram (EEG) by a great variety of signal patterns (1). Fourier transform decomposes the signal into multiple frequency ranges, defining δ, θ (5 to 10 Hz), and γ (>30 Hz) oscillatory components. However, although the EEG has been used to define wakefulness and distinguish it from slow-wave and paradoxical sleep (SWS and PS) for decades, a formal cartography of waking substates, associated EEG features, and their significance for the animal is largely lacking. Likewise, definition of the relation between waking quality and subsequent sleep content has evolved little since enunciation of the twoprocess model of sleep regulation (2) in which a sleep/wakedependent homeostatic "process S," reflected in EEG δ power during SWS, regulates sleep propensity as a function of prior waking duration regardless of waking quality. Later studies described behaviors (3, 4) or EEG components (5, 6) that disproportionally affect the sleep homeostat. Different procedural, cognitive, or emotional experience differentially impacts subsequent SWS δ powe...

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Homeostatic and Circadian Contribution to EEG and Molecular State Variables of Sleep Regulation

Abstract: Curie T; Mongrain V; Dorsaz S; Mang GM; Emmenegger Y; Franken P. Homeostatic and circadian contribution to EEG and molecular state variables of sleep regulation. SLEEP 2013;36(3):311-323.

Cited by 93 publications

References 86 publications

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

The impact of sleep loss on hippocampal function

Hypocretin (orexin) is critical in sustaining theta/gamma-rich waking behaviors that drive sleep need

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