Evidence map›Paper›PMID 18687715›Full record

ArticleThe Journal of physiology2008

Evolution and modulation of intracellular calcium release during long-lasting, depleting depolarization in mouse muscle.

Leandro Royer, Sandrine Pouvreau, Eduardo Ríos

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Phasic Store-Operated CaFrontiers in physiology · 2020
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Calsequestrin depolymerizes when calcium is depleted in the sarcoplasmic reticulum of working muscle.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Article
  17. Article
  18. Fast kinetics of calcium signaling and sensor design.Current opinion in chemical biology · 2015
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Leandro RoyerDepartment of Molecular Biophysics & Physiology, Section of Cellular Signalling, Rush University School of Medicine, Chicago, IL 60612, USA.
Sandrine Pouvreau
Eduardo Ríos
Centre National de la Recherche Scientifique · FRRush University · US

Funding

Skeletal Muscle. Ca Release Control Inside the Sarcoplasmic Reticulum.R01AR049184 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 2003 to 2013
$3.1M
CALCIUM MOVEMENTS IN EXCITATION-CONTRACTION COUPLING.R37AR032808 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 1996 to 2005
$2.6M
NIAMS NIH HHS R01 AR049184NIAMS NIH HHS R37 AR032808
6 · The paper itself

Abstract

Intracellular calcium signals regulate multiple cellular functions. They depend on release of Ca(2+) from cellular stores into the cytosol, a process that in many types of cells appears to be tightly controlled by changes in [Ca(2+)] within the store. In contrast with cardiac muscle, where depletion of Ca(2+) in the sarcoplasmic reticulum is a crucial determinant of termination of Ca(2+) release, in skeletal muscle there is no agreement regarding the sign, or even the existence of an effect of SR Ca(2+) level on Ca(2+) release. To address this issue we measured Ca(2+) transients in mouse flexor digitorum brevis (FDB) skeletal muscle fibres under voltage clamp, using confocal microscopy and the Ca(2+) monitor rhod-2. The evolution of Ca(2+) release flux was quantified during long-lasting depolarizations that reduced severely the Ca(2+) content of the SR. As in all previous determinations in mammals and non-mammals, release flux consisted of an early peak, relaxing to a lower level from which it continued to decay more slowly. Decay of flux in this second stage, which has been attributed largely to depletion of SR Ca(2+), was studied in detail. A simple depletion mechanism without change in release permeability predicts an exponential decay with time. In contrast, flux decreased non-exponentially, to a finite, measurable level that could be maintained for the longest pulses applied (1.8 s). An algorithm on the flux record allowed us to define a quantitative index, the normalized flux rate of change (NFRC), which was shown to be proportional to the ratio of release permeability P and inversely proportional to Ca(2+) buffering power B of the SR, thus quantifying the 'evacuability' or ability of the SR to empty its content. When P and B were constant, flux then decayed exponentially, and NFRC was equal to the exponential rate constant. Instead, in most cases NFRC increased during the pulse, from a minimum reached immediately after the early peak in flux, to a time between 200 and 250 ms, when the index was no longer defined. NFRC increased by 111% on average (in 27 images from 18 cells), reaching 300% in some cases. The increase may reflect an increase in P, a decrease in B, or both. On experimental and theoretical grounds, both changes are to be expected upon SR depletion. A variable evacuability helps maintain a constant Ca(2+) output under conditions of diminishing store Ca(2+) load.

Indexed as

Calcium SignalingAnimalsCalciumElectrophysiologyIn Vitro TechniquesMembrane PotentialsMiceMicroscopy, ConfocalMuscle, SkeletalPatch-Clamp TechniquesSarcoplasmic ReticulumCalcium

Identifiers

PMID18687715
PMCPMC2614033
OpenAlexW1918081174

What OpenQuestion holds

Textmetadata
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.