Evidence map›Paper›PMID 23209395›Full record

ArticlePLoS computational biology2012

Weakly circadian cells improve resynchrony.

Alexis B Webb, Stephanie R Taylor, Kurt A Thoroughman, Francis J Doyle, Erik D Herzog

Abstract read
In one paragraph

Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Article
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  7. Review
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  10. Article
  11. Noise-driven cellular heterogeneity in circadian periodicity.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Keeping time in the lamina terminalis: Novel oscillator properties of forebrain sensory circumventricular organs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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

5 authors.

Alexis B WebbDepartment of Biology, Washington University, St. Louis, Missouri, United States of America.
Stephanie R Taylor
Kurt A Thoroughman
Francis J Doyle
Erik D Herzog

Funding

CRCNS: Computational Integration of Human Adaptation and Primate NeurophysiologyR01NS057813 · NINDS · WASHINGTON UNIVERSITY · PI THOROUGHMAN, KURT A · 2006 to 2009
$1.3M
Trial-by-Trial Human Generalization of Sense into ActionR01HD055851 · NICHD · WASHINGTON UNIVERSITY · PI THOROUGHMAN, KURT A · 2007 to 2011
$1.2M
MECHANISMS AND MODELING OF NETWORKED CIRCADIAN PACEMAKER SYNCHRONIZATIONR01GM096873 · NIGMS · WASHINGTON UNIVERSITY · PI DOYLE, FRANCIS J, HENSON, MICHAEL · 2011 to 2014
$1.1M
NICHD NIH HHS R01 HD055851NIGMS NIH HHS R01 GM096873NIGMS NIH HHS R01GM096873NINDS NIH HHS R01 NS057813
6 · The paper itself

Abstract

The mammalian suprachiasmatic nuclei (SCN) contain thousands of neurons capable of generating near 24-h rhythms. When isolated from their network, SCN neurons exhibit a range of oscillatory phenotypes: sustained or damping oscillations, or arrhythmic patterns. The implications of this variability are unknown. Experimentally, we found that cells within SCN explants recover from pharmacologically-induced desynchrony by re-establishing rhythmicity and synchrony in waves, independent of their intrinsic circadian period We therefore hypothesized that a cell's location within the network may also critically determine its resynchronization. To test this, we employed a deterministic, mechanistic model of circadian oscillators where we could independently control cell-intrinsic and network-connectivity parameters. We found that small changes in key parameters produced the full range of oscillatory phenotypes seen in biological cells, including similar distributions of period, amplitude and ability to cycle. The model also predicted that weaker oscillators could adjust their phase more readily than stronger oscillators. Using these model cells we explored potential biological consequences of their number and placement within the network. We found that the population synchronized to a higher degree when weak oscillators were at highly connected nodes within the network. A mathematically independent phase-amplitude model reproduced these findings. Thus, small differences in cell-intrinsic parameters contribute to large changes in the oscillatory ability of a cell, but the location of weak oscillators within the network also critically shapes the degree of synchronization for the population.

Indexed as

Models, NeurologicalAnimalsCells, CulturedCircadian ClocksComputational BiologyMiceNeuronsSuprachiasmatic Nucleus

Identifiers

PMID23209395
PMCPMC3510091

What OpenQuestion holds

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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.