Delta Wave Power: An Independent Sleep Phenotype or Epiphenomenon?

Davis, Christopher J.; Clinton, James M.; Jewett, Kathryn A.; Zielinski, Mark R.; Krueger, James M.

doi:10.5664/jcsm.1346

Cited by 84 publications

(80 citation statements)

References 41 publications

(37 reference statements)

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“…We can also use this as a validation of the use of the “eyes open/eyes closed” dichotomy as a behavioral criterion indicative of the broad state of arousal. The power spectrum in the eyes-closed state in Figure 5 shows strong power below 4Hz which is characteristic of, in fact comprises a major component of the clinical definition for, the transition to slow-wave sleep (Davis et al, 2011). While it is known that transitions between having one’s eyes closed versus open during wakefulness will change electroencephalogram (EEG) power in all frequency bands, both in a lighted room (Barry et al, 2007) and in the dark (the comparable condition for our control study: (Boytsova and Danko, 2010), the changes are concentrated in higher spectral bands, particularly alpha (7–13Hz) and beta (13–30Hz).…”

Section: Resultsmentioning

confidence: 99%

A multi-site array for combined local electrochemistry and electrophysiology in the non-human primate brain

Disney

McKinney

Grissom

et al. 2015

Journal of Neuroscience Methods

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Background Currently, the primary technique employed in circuit-level study of the brain is electrophysiology, recording local field or action potentials (LFPs or APs). However most communication between neurons is chemical and the relationship between electrical activity within neurons and chemical signaling between them is not well understood in vivo, particularly for molecules that signal at least in part by non-synaptic transmission. New Method We describe a multi-contact array and accompanying head stage circuit that together enable concurrent electrophysiological and electrochemical recording. The array is small (<200μm) and can be assembled into a device of arbitrary length. It is therefore well-suited for use in all major in vivo model systems in neuroscience, including non-human primates where the large brain and need for daily insertion and removal of recording devices places particularly strict demands on design. Results We present a protocol for array fabrication. We then show that a device built in the manner described can record LFPs and perform enzyme-based amperometric detection of choline in the awake macaque monkey. Comparison with existing methods Existing methods allow single mode (electrophysiology or electrochemistry) recording. This system is designed for concurrent, dual-mode recording. It is also the only system designed explicitly to meet the challenges of recording in non-human primates. Conclusions Our system offers the possibility for conducting in vivo studies in a range of species that examine the relationship between the electrical activity of neurons and their chemical environment, with exquisite spatial and temporal precision.

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Section: Resultsmentioning

confidence: 99%

A multi-site array for combined local electrochemistry and electrophysiology in the non-human primate brain

Disney

McKinney

Grissom

et al. 2015

Journal of Neuroscience Methods

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“…As described above, in mammals and birds, sleep homeostasis is often approximated by its electrophysiological surrogate, delta power, which reflects SWA during NREM sleep. Some researchers have argued that SWA is actually an epiphenomenon that reflects an unknown physiological process that drives sleep [179]. Certainly SWA can be induced with muscarinic antagonists in an animal that is awake and responsive [180].…”

Section: The Origins Of Sleep Homeostasismentioning

confidence: 99%

Unraveling the Evolutionary Determinants of Sleep

2016

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Summary Despite decades of intense study, the functions of sleep are still shrouded in mystery. The difficulty in understanding these functions can be at least partly attributed to the varied manifestations of sleep in different animals. Daily sleep duration can range from 4–20 hrs among mammals, and sleep can manifest throughout the brain, or it can alternate over time between cerebral hemispheres, depending on the species. Ecological factors are likely to have shaped these and other sleep behaviors during evolution by altering the properties of conserved arousal circuits in the brain. Nonetheless, core functions of sleep are likely to have arisen early and to have persisted to the present day in diverse organisms. This review will discuss the evolutionary forces that may be responsible for phylogenetic differences in sleep and the potential core functions that sleep fulfills.

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“…In particular, somatosensory cortex activity modulates sleep and the electroencephalogram (EEG) (Timofeev et al, 2013). Increased wakefulness, such as that occurring during sleep deprivation (SD), enhances the expression of pro-inflammatory molecules in the somatosensory cortex including interleukin-1 beta (IL-1β) (Zielinski et al, 2011; Imeri and Opp, 2009). IL-1β expression and protein levels in the cortex exhibit diurnal variations that coincide with sleep propensity (Krueger et al, 2010; Taishi et al, 1998; 2012).…”

Section: Introductionmentioning

confidence: 99%

The NLRP3 inflammasome modulates sleep and NREM sleep delta power induced by spontaneous wakefulness, sleep deprivation and lipopolysaccharide

Zielinski

Gerashchenko

Karpova

et al. 2017

Brain, Behavior, and Immunity

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Both sleep loss and pathogens can enhance brain inflammation, sleep, and sleep intensity as indicated by electroencephalogram delta (δ) power. The pro-inflammatory cytokine interleukin-1 beta (IL-1β) is increased in the cortex after sleep deprivation (SD) and in response to the Gram-negative bacterial cell-wall component lipopolysaccharide (LPS), although the exact mechanisms governing these effects are unknown. The nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome protein complex forms in response to changes in the local environment and, in turn, activates caspase-1 to convert IL-1β into its active form. SD enhances the cortical expression of the somnogenic cytokine IL-1β, although the underlying mechanism is, as yet, unidentified. Using NLRP3-gene knockout (KO) mice, we provide evidence that NLRP3 inflammasome activation is a crucial mechanism for the downstream pathway leading to increased IL-1β-enhanced sleep. NLRP3 KO mice exhibited reduced non-rapid eye movement (NREM) sleep during the light period. We also found that sleep amount and intensity (δ activity) were drastically attenuated in NLRP3 KO mice following SD (homeostatic sleep response), as well as after LPS administration, although they were enhanced by central administration of IL-1β. NLRP3, ASC, and IL1β mRNA, IL-1β protein, and caspase-1 activity were greater in the somatosensory cortex at the end of the wake-active period when sleep propensity was high and after SD in wild-type but not NLRP3 KO mice. Thus, our novel and converging findings suggest that the activation of the NLRP3 inflammasome can modulate sleep induced by both increased wakefulness and a bacterial component in the brain.

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Delta Wave Power: An Independent Sleep Phenotype or Epiphenomenon?

Cited by 84 publications

References 41 publications

A multi-site array for combined local electrochemistry and electrophysiology in the non-human primate brain

A multi-site array for combined local electrochemistry and electrophysiology in the non-human primate brain

Unraveling the Evolutionary Determinants of Sleep

The NLRP3 inflammasome modulates sleep and NREM sleep delta power induced by spontaneous wakefulness, sleep deprivation and lipopolysaccharide

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