Evidence map›Paper›PMID 25855183›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Synergistic action of dendritic mitochondria and creatine kinase maintains ATP homeostasis and actin dynamics in growing neuronal dendrites.

Kansai Fukumitsu, Kazuto Fujishima, Azumi Yoshimura, You Kure Wu, John Heuser, Mineko Kengaku

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Review
  3. bioRxiv : the preprint server for biology · 2025
    Article
  4. Neurobiology of mitochondrial dynamics in sleep.The Journal of physiology · 2025
    Review
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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 2 institutions in 2 countries.

Kansai FukumitsuInstitute for Integrated Cell-Material Sciences (WPI-iCeMS) and Graduate School of Biostudies, Kyoto University, Kyoto 606-8501, Japan.
Kazuto FujishimaInstitute for Integrated Cell-Material Sciences (WPI-iCeMS) and.
Azumi YoshimuraInstitute for Integrated Cell-Material Sciences (WPI-iCeMS) and.
You Kure WuInstitute for Integrated Cell-Material Sciences (WPI-iCeMS) and Graduate School of Biostudies, Kyoto University, Kyoto 606-8501, Japan.
John HeuserInstitute for Integrated Cell-Material Sciences (WPI-iCeMS) and.
Mineko KengakuInstitute for Integrated Cell-Material Sciences (WPI-iCeMS) and Graduate School of Biostudies, Kyoto University, Kyoto 606-8501, Japan kengaku@icems.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-1666-3648
Kyoto University · JPMaterial Sciences (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The distribution of mitochondria within mature, differentiated neurons is clearly adapted to their regional physiological needs and can be perturbed under various pathological conditions, but the function of mitochondria in developing neurons has been less well studied. We have studied mitochondrial distribution within developing mouse cerebellar Purkinje cells and have found that active delivery of mitochondria into their dendrites is a prerequisite for proper dendritic outgrowth. Even when mitochondria in the Purkinje cell bodies are functioning normally, interrupting the transport of mitochondria into their dendrites severely disturbs dendritic growth. Additionally, we find that the growth of atrophic dendrites lacking mitochondria can be rescued by activating ATP-phosphocreatine exchange mediated by creatine kinase (CK). Conversely, inhibiting cytosolic CKs decreases dendritic ATP levels and also disrupts dendrite development. Mechanistically, this energy depletion appears to perturb normal actin dynamics and enhance the aggregation of cofilin within growing dendrites, reminiscent of what occurs in neurons overexpressing the dephosphorylated form of cofilin. These results suggest that local ATP synthesis by dendritic mitochondria and ATP-phosphocreatine exchange act synergistically to sustain the cytoskeletal dynamics necessary for dendritic development.

Indexed as

ActinsAdenosine TriphosphateAnimalsCalcium Channel BlockersCarrier ProteinsCells, CulturedCerebellumChelating AgentsCreatine KinaseDendritesDeoxyglucoseDependovirusEgtazic AcidFemaleHippocampusHumans1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl esterActinsAdenosine TriphosphateCalcium Channel BlockersCarrier ProteinsChelating AgentsCreatine KinaseDeoxyglucoseEgtazic AcidLuminescent ProteinsNerve Tissue ProteinsTRAK2 protein, mouseactinATP homeostasiscreatine kinasedendritemitochondriaPurkinje cell

Identifiers

PMID25855183
PMCPMC6605316
OpenAlexW1992041336

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.