Evidence map›Paper›PMID 24285879›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Sodium and potassium currents influence Wallerian degeneration of injured Drosophila axons.

Bibhudatta Mishra, Ross Carson, Richard I Hume, Catherine A Collins

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Peripheral Nerve Crush inCold Spring Harbor protocols · 2025
    Article
  3. Multifaceted roles of SARM1 in axon degeneration and signaling.Frontiers in cellular neuroscience · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Degeneration of Injured Axons and Dendrites Requires Restraint of a Protective JNK Signaling Pathway by the Transmembrane Protein Raw.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. The effect of Riluzole on functional recovery of locomotion in the rat sciatic nerve crush model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2017
    Article
  16. Models of axon regeneration in Drosophila.Experimental neurology · 2017
    Review
  17. Article
  18. Article
  19. Review
  20. Live Imaging of Calcium Dynamics during Axon Degeneration Reveals Two Functionally Distinct Phases of Calcium Influx.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    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

4 authors at 1 institution in 1 country.

Bibhudatta MishraDepartment of Molecular Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109-1048.
Ross Carson
Richard I Hume
Catherine A Collins
University of Michigan–Ann Arbor · US

Funding

Regenerative and Degenerative Responses to Axonal InjuryR01NS069844 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CADIGAN, KENNETH M, COLLINS, CATHERINE A · 2010 to 2024
$5.0M
Regenerative and degenerative responses to axonal injuryR56NS069844 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, CATHERINE A · 2020 to 2020
$546k
NINDS NIH HHS NS069844NINDS NIH HHS R01 NS069844NINDS NIH HHS R56 NS069844
6 · The paper itself

Abstract

Axons degenerate after injury and in neuropathies and disease via a self-destruction program whose mechanism is poorly understood. Axons that have lost connection to their cell bodies have altered electrical and synaptic activities, but whether such changes play a role in the axonal degeneration process is not clear. We have used a Drosophila model to study the Wallerian degeneration of motoneuron axons and their neuromuscular junction synapses. We found that degeneration of the distal nerve stump after a nerve crush is greatly delayed when there is increased potassium channel activity (by overexpression of two different potassium channels, Kir2.1 and dORKΔ-C) or decreased voltage-gated sodium channel activity (using mutations in the para sodium channel). Conversely, degeneration is accelerated when potassium channel activity is decreased (by expressing a dominant-negative mutation of Shaker). Despite the effect of altering voltage-gated sodium and potassium channel activity, recordings made after nerve crush demonstrated that the distal stump does not fire action potentials. Rather, a variety of lines of evidence suggest that the sodium and potassium channels manifest their effects upon degeneration through changes in the resting membrane potential, which in turn regulates the level of intracellular free calcium within the isolated distal axon.

Indexed as

Action PotentialsAnimalsAxonsCalciumDrosophilaElectrophysiological PhenomenaImmunohistochemistryMicroscopy, ConfocalNerve CrushNeuromuscular JunctionPotassium ChannelsShaker Superfamily of Potassium ChannelsSodium Channel BlockersSodium ChannelsSynapsesTemperatureCalciumPotassium ChannelsShaker Superfamily of Potassium ChannelsSodium Channel BlockersSodium ChannelsTetrodotoxin

Identifiers

PMID24285879
PMCPMC3841444
OpenAlexW1980072629

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.