Neuronal noise as an origin of sleep arousals and its role in sudden infant death syndrome

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Science Advances  25 Apr 2018:
Vol. 4, no. 4, eaar6277
DOI: 10.1126/sciadv.aar6277

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  • RE: Response to Bodizs eLetter
    • Hila Dvir
    • Other Contributors:
      • Shlomo Havlin
      • Plamen Ivanov
      • Ronny Bartsch

    Hila Dvir, Shlomo Havlin, Plamen Ivanov, Ronny Bartsch. 

    Response to eLetter for aar6277, Neuronal noise as an origin of sleep arousals and its role in sudden infant death syndrome


    We thank the author of the comment for the interest in our work. 

    We are aware that several mechanisms are involved in sleep and thermoregulation at different levels and time scales -- from neuro-chemical signaling at molecular level, to neuronal networks, to global behavior across brain areas at the system level. We never claimed in our paper that temperature-dependent subthreshold neuronal voltage fluctuations ("neuronal noise") represent the only mechanism to mediate temperature influences on sleep and wake. However, our empirical and modeling studies show that thermal neuronal noise plays an important role in generating arousals during sleep and are responsible for their dynamics and temporal organization.

    Since wake-promoting neuronal (WPN) activation and arousal ascending pathways are responsible for generating cortical arousals (Saper et al., 2001;Saper et al., 2005; Saper et al., 2010), our study naturally focuses on thermal fluctuations of wake-promoting neurons (WPNs). Note that in addition to the global increase or decrease of total sleep and wake as a function of temperature (which appears to be a main focus of the comment), there is a complex scale-invariant temporal organization of brief arousals, which is...

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    Competing Interests: None declared.
  • RE: Neuronal noise as an origin of sleep arousals and its role in sudden infant death syndrome
    • Róbert Bódizs, Senior Research Fellow, Institute of Behavioural Sciences, Semmelweis University, Budapest

    I think the findings and the model presented in this study are interesting. It should be noted however, that the links between thermoregulation and sleep are much more complex than the ones predicted by the neuronal noise-based model presented in this paper. Thus, the predictions of the alternative models should be tested before we conclude that the data supports the neuronal noise model.

    Authors are apparently unaware of the fact that local heating of the preoptic anterior hypothalamic thermodetector area of mammals may induce EEG synchronization and sleep (McGinty and Szymusiak, 2001). The same effect can be elicited by capsaicine-based chemical stimulation of the same neurons (Benedek et al., 1982) suggesting that the thermoregulation and the sleep regulation systems are closely linked. That is the findings of the present study could be explained by an alternative model, which is well known in the literature: instead of the heat-induced decrease in WPN fluctuations, the heat-induced activation of SPN could be involved in the effect.

    In addition, the so called somnogenic cytokines might be involved in the effect. It was reported that the increased ambient temperature induces drowsiness and sleep in mammals (and not only in zebrafish larvae, which in itself is in line with the aims and horizons of the present paper). The neurochemical routes of the ambient temperature induced sleep was shown to be related to the molecule called Tumor Necrosis Factor (TNF; Kr...

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    Competing Interests: None declared.

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