Evidence map›Paper›PMID 40926022›Full record

ArticleCommunications biology2025

Mitochondria delay action potential propagation.

Ann M Castelfranco, Pepe Alcami

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

2 authors.

Ann M CastelfrancoBékésy Laboratory of Neurobiology, Pacific Biosciences Research Center, University of Hawai'i at Mānoa, Honolulu, HI, USA.ORCID http://orcid.org/0000-0002-2536-915X
Pepe AlcamiDivision of Neurobiology, Faculty of Biology, Ludwig-Maximilians-Universität München, Planegg - Martinsried, Germany. alcami@bio.lmu.de.ORCID http://orcid.org/0000-0003-1778-6743

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The internal resistance of axons to ionic current flow determines action potential conduction velocity. Although mitochondria support axonal function, axons have been modeled as organelle-free cables, and mitochondrial impact on conduction velocity, specifically by increasing internal resistance, remains understudied. We combine computational modeling and electron microscopy of forebrain premotor axons controlling birdsong production. Modeling shows that when the propagating action potential in an unmyelinated axon encounters a mitochondrion, conduction velocity decreases, delaying the action potential by tenths of microseconds to microseconds, an effect that is stronger in small axons. Axonal mitochondria thereby induce conduction inhomogeneities, accumulating total delays of tenths of milliseconds to ~ a millisecond over 3 millimeters-long axons, in the range of the temporal precision of these neurons. Thus, by partially occupying the axoplasm, mitochondria constrain information processing in vertebrate small-diameter axons. Our model should permit future investigations on the impact of mitochondrial axonal plasticity on action potential temporal coding.

Indexed as

Action PotentialsAxonsMitochondriaNeural ConductionAnimalsFinchesModels, Neurological

Identifiers

PMID40926022
PMCPMC12420829

What OpenQuestion holds

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LicenceCC BY
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.