Evidence map›Paper›PMID 22495585›Full record

ArticleThe Journal of physiology2012

Quantitative measurement of mitochondrial membrane potential in cultured cells: calcium-induced de- and hyperpolarization of neuronal mitochondria.

Akos A Gerencser, Christos Chinopoulos, Matthew J Birket, Martin Jastroch, Cathy Vitelli, David G Nicholls, Martin D Brand

Abstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing 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

118 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Phenotypic CRISPR screens identify NLRX1 as an essential activator of the human mitochondrial permeability transition.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Article
  11. TRPM8 Regulates Mitochondrial CaJournal of cellular and molecular medicine · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

58 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

7 authors.

Akos A GerencserBuck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA. agerencser@buckinstitute.org
Christos Chinopoulos
Matthew J Birket
Martin Jastroch
Cathy Vitelli
David G Nicholls
Martin D Brand

Funding

PROTEOMICSP01AG025901 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GIBSON, BRADFORD WAYNE · 2007 to 2011
$8.6M
Mass spectrometry and imaging technologies in GerosciencePL1AG032118 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GIBSON, BRADFORD WAYNE · 2007 to 2011
$4.5M
NIA NIH HHS P01 AG025901NIA NIH HHS PL1 AG032118
6 · The paper itself

Abstract

Mitochondrial membrane potential (ΔΨM) is a central intermediate in oxidative energy metabolism. Although ΔΨM is routinely measured qualitatively or semi-quantitatively using fluorescent probes, its quantitative assay in intact cells has been limited mostly to slow, bulk-scale radioisotope distribution methods. Here we derive and verify a biophysical model of fluorescent potentiometric probe compartmentation and dynamics using a bis-oxonol-type indicator of plasma membrane potential (ΔΨP) and the ΔΨM probe tetramethylrhodamine methyl ester (TMRM) using fluorescence imaging and voltage clamp. Using this model we introduce a purely fluorescence-based quantitative assay to measure absolute values of ΔΨM in millivolts as they vary in time in individual cells in monolayer culture. The ΔΨP-dependent distribution of the probes is modelled by Eyring rate theory. Solutions of the model are used to deconvolute ΔΨP and ΔΨM in time from the probe fluorescence intensities, taking into account their slow, ΔΨP-dependent redistribution and Nernstian behaviour. The calibration accounts for matrix:cell volume ratio, high- and low-affinity binding, activity coefficients, background fluorescence and optical dilution, allowing comparisons of potentials in cells or cell types differing in these properties. In cultured rat cortical neurons, ΔΨM is −139 mV at rest, and is regulated between −108 mV and −158 mV by concerted increases in ATP demand and Ca2+-dependent metabolic activation. Sensitivity analysis showed that the standard error of the mean in the absolute calibrated values of resting ΔΨM including all biological and systematic measurement errors introduced by the calibration parameters is less than 11 mV. Between samples treated in different ways, the typical equivalent error is ∼5 mV.

Indexed as

Membrane Potential, MitochondrialAnimalsCalciumCells, CulturedEnergy MetabolismFluorescent DyesModels, TheoreticalNeuronsPatch-Clamp TechniquesRatsRats, Inbred StrainsRhodaminesVoltage-Sensitive Dye ImagingCalciumFluorescent DyesRhodaminestetramethylrhodamine methyl ester

Identifiers

PMID22495585
PMCPMC3448152

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.