Evidence map›Paper›PMID 29587245›Full record

ArticleRedox biology2018

Mitochondrial ROS cause motor deficits induced by synaptic inactivity: Implications for synapse pruning.

Eva Sidlauskaite, Jack W Gibson, Ian L Megson, Philip D Whitfield, Artak Tovmasyan, Ines Batinic-Haberle, Michael P Murphy, Peter R Moult, James N Cobley

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Proteoforms as the true units of physiological function.European journal of applied physiology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Ten "Cheat Codes" for Measuring Oxidative Stress in Humans.Antioxidants (Basel, Switzerland) · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Impaired dopamine release in Parkinson's disease.Brain : a journal of neurology · 2023
    Review
  16. Review
  17. Common methods in mitochondrial research (Review).International journal of molecular medicine · 2022
    Article
  18. Synapses: The Brain's Energy-Demanding Sites.International journal of molecular sciences · 2022
    Review
  19. Review
  20. Article
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

9 authors at 4 institutions in 2 countries.

Eva SidlauskaiteSchool of Science Engineering and Technology, Abertay University, Dundee DD1 1HG, UK.
Jack W GibsonSchool of Science Engineering and Technology, Abertay University, Dundee DD1 1HG, UK.
Ian L MegsonInstitute of Health Science, University of Highlands and Islands, Inverness IV2 3JH, UK.
Philip D WhitfieldInstitute of Health Science, University of Highlands and Islands, Inverness IV2 3JH, UK.
Artak TovmasyanDepartment of Radiation Oncology, School of Medicine, Duke University, Durham, NC 27710, USA.
Ines Batinic-HaberleDepartment of Radiation Oncology, School of Medicine, Duke University, Durham, NC 27710, USA.
Michael P MurphyMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, CB2 0XY, UK.
Peter R MoultSchool of Science Engineering and Technology, Abertay University, Dundee DD1 1HG, UK.
James N CobleyInstitute of Health Science, University of Highlands and Islands, Inverness IV2 3JH, UK. Electronic address: james.cobley@uhi.ac.uk.
Abertay University · GBUniversity of the Highlands and Islands · GBDuke University · USUniversity of Cambridge · GB

Funding

Medical Research Council MC_UU_00015/3
6 · The paper itself

Abstract

Developmental synapse pruning refines burgeoning connectomes. The basic mechanisms of mitochondrial reactive oxygen species (ROS) production suggest they select inactive synapses for pruning: whether they do so is unknown. To begin to unravel whether mitochondrial ROS regulate pruning, we made the local consequences of neuromuscular junction (NMJ) pruning detectable as motor deficits by using disparate exogenous and endogenous models to induce synaptic inactivity en masse in developing Xenopus laevis tadpoles. We resolved whether: (1) synaptic inactivity increases mitochondrial ROS; and (2) chemically heterogeneous antioxidants rescue synaptic inactivity induced motor deficits. Regardless of whether it was achieved with muscle (α-bungarotoxin), nerve (α-latrotoxin) targeted neurotoxins or an endogenous pruning cue (SPARC), synaptic inactivity increased mitochondrial ROS in vivo. The manganese porphyrins MnTE-2-PyP

Indexed as

AnimalsAntioxidantsBungarotoxinsLarvaMitochondriaMotor ActivityNeuromuscular JunctionParaquatReactive Oxygen SpeciesSpider VenomsSynapsesXenopus laevisalpha-latrotoxinAntioxidantsBungarotoxinsParaquatReactive Oxygen SpeciesSpider VenomsMitochondriaMotor deficitNeuromuscular junctionReactive oxygen speciesSynapseXenopus

Identifiers

PMID29587245
PMCPMC5953219
OpenAlexW2789748760

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.