Evidence map›Paper›PMID 34491202›Full record

ArticleeLife2021

Activity-dependent regulation of mitochondrial motility in developing cortical dendrites.

Catia Ap Silva, Annik Yalnizyan-Carson, M Victoria Fernández Busch, Mike van Zwieten, Matthijs Verhage, Christian Lohmann

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  6. bioRxiv : the preprint server for biology · 2025
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  13. Mitochondria as central hubs in synaptic modulation.Cellular and molecular life sciences : CMLS · 2023
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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

6 authors at 3 institutions in 3 countries.

Catia Ap SilvaDepartment of Synapse and Network Development, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.ORCID 0000-0001-8801-3508
Annik Yalnizyan-CarsonDepartment of Biological Sciences, University of Toronto Scarborough, Toronto, Canada.ORCID 0000-0002-1664-5327
M Victoria Fernández BuschDepartment of Synapse and Network Development, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.ORCID 0000-0001-8636-4988
Mike van ZwietenDepartment of Synapse and Network Development, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.
Matthijs VerhageDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, University Amsterdam, Amsterdam, Netherlands.
Christian LohmannDepartment of Synapse and Network Development, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.ORCID 0000-0002-1780-2419
Netherlands Institute for Neuroscience · NLAmsterdam Neuroscience · NLUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Developing neurons form synapses at a high rate. Synaptic transmission is very energy-demanding and likely requires ATP production by mitochondria nearby. Mitochondria might be targeted to active synapses in young dendrites, but whether such motility regulation mechanisms exist is unclear. We investigated the relationship between mitochondrial motility and neuronal activity in the primary visual cortex of young mice in vivo and in slice cultures. During the first 2 postnatal weeks, mitochondrial motility decreases while the frequency of neuronal activity increases. Global calcium transients do not affect mitochondrial motility. However, individual synaptic transmission events precede local mitochondrial arrest. Pharmacological stimulation of synaptic vesicle release, but not focal glutamate application alone, stops mitochondria, suggesting that an unidentified factor co-released with glutamate is required for mitochondrial arrest. A computational model of synaptic transmission-mediated mitochondrial arrest shows that the developmental increase in synapse number and transmission frequency can contribute substantially to the age-dependent decrease of mitochondrial motility.

Indexed as

AnimalsCalciumDendritesGlutamic AcidMiceMitochondriaNeuronsSynapsesSynaptic TransmissionSynaptic VesiclesCalciumGlutamic Acidcalcium signalingintracellular transportin vivo imagingmouseneurosciencesynaptic transmission

Identifiers

PMID34491202
PMCPMC8423438
OpenAlexW3197254248

What OpenQuestion holds

Textmetadata
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.