Evidence map›Paper›PMID 21854953›Full record

ReviewProgress in brain research2011

Electrophysiological correlates of sleep homeostasis in freely behaving rats.

Vladyslav V Vyazovskiy, Chiara Cirelli, Giulio Tononi

Abstract readReview
In one paragraph

Review in Progress in brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
16.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 111 citations in OpenAlex.

  1. Sleep homeostasis in OSA: a complementary neurophysiological outcome measure.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2026
    Article
  2. A molecular integrator of sleep duration and interruption.bioRxiv : the preprint server for biology · 2026
    Article
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  19. Do Mosquitoes Sleep?Trends in parasitology · 2020
    Review
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Vladyslav V VyazovskiyDepartment of Psychiatry, University of Wisconsin-Madison, Madison, WI, USA. vyazovskiy@wisc.edu
Chiara Cirelli
Giulio Tononi
University of Wisconsin–Madison · US

Funding

Sleep Function and Synaptic Homeostasis: Linking Neurobiology and Mental HealthP20MH077967 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI TONONI, GIULIO · 2007 to 2010
$3.8M
NIH Director's Pioneer Award (RMI)DP1OD000579 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI TONONI, GIULIO · 2005 to 2009
$3.6M
NIH HHS DP1 OD000579NIMH NIH HHS P20 MH077967PHS HHS FA9550-08-1-0244
6 · The paper itself

Abstract

The electrical activity of the brain does not only reflect the current level of arousal, ongoing behavior, or involvement in a specific task but is also influenced by what kind of activity, and how much sleep and waking occurred before. The best marker of sleep-wake history is the electroencephalogram (EEG) spectral power in slow frequencies (slow-wave activity, 0.5-4 Hz, SWA) during sleep, which is high after extended wakefulness and low after consolidated sleep. While sleep homeostasis has been well characterized in various species and experimental paradigms, the specific mechanisms underlying homeostatic changes in brain activity or their functional significance remain poorly understood. However, several recent studies in humans, rats, and computer simulations shed light on the cortical mechanisms underlying sleep regulation. First, it was found that the homeostatic changes in SWA can be fully accounted for by the variations in amplitude and slope of EEG slow waves, which are in turn determined by the efficacy of corticocortical connectivity. Specifically, the slopes of sleep slow waves were steeper in early sleep compared to late sleep. Second, the slope of cortical evoked potentials, which is an established marker of synaptic strength, was steeper after waking, and decreased after sleep. Further, cortical long-term potentiation (LTP) was partially occluded if it was induced after a period of waking, but it could again be fully expressed after sleep. Finally, multiunit activity recordings during sleep revealed that cortical neurons fired more synchronously after waking, and less so after a period of consolidated sleep. The decline of all these electrophysiological measures-the slopes of slow waves and evoked potentials and neuronal synchrony-during sleep correlated with the decline of the traditional marker of sleep homeostasis, EEG SWA. Taken together, these data suggest that homeostatic changes in sleep EEG are the result of altered neuronal firing and synchrony, which in turn arise from changes in functional neuronal connectivity.

Indexed as

AnimalsBehavior, AnimalBrainElectroencephalographyHomeostasisHumansNeuronal PlasticityRatsSleepWakefulness

Identifiers

PMID21854953
PMCPMC3160719
OpenAlexW1494352394

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.