Evidence map›Paper›PMID 27463510›Full record

ArticleMuscle & nerve2017

Chronic peripheral nerve compression disrupts paranodal axoglial junctions.

Yoshinori Otani, Leonid M Yermakov, Jeffrey L Dupree, Keiichiro Susuki

Open access · greenAbstract read
In one paragraph

Article in Muscle & nerve, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Application of SygenBioengineering (Basel, Switzerland) · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Glial βII Spectrin Contributes to Paranode Formation and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  8. Article
  9. 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 2 institutions in 1 country.

Yoshinori OtaniDepartment of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.
Leonid M YermakovDepartment of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.
Jeffrey L DupreeDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
Keiichiro SusukiDepartment of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.
Wright State University · USVirginia Commonwealth University · US

Funding

VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
Identification and Repair of Novel Axonal Pathology in Demyelinating DiseaseI01BX002565 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI DUPREE, JEFFREY L. · 2015 to 2024
–
BLRD VA I01 BX002565NINDS NIH HHS P30 NS047463
6 · The paper itself

Abstract

introductionPeripheral nerves are often exposed to mechanical stress leading to compression neuropathies. The pathophysiology underlying nerve dysfunction by chronic compression is largely unknown.

methodsWe analyzed molecular organization and fine structures at and near nodes of Ranvier in a compression neuropathy model in which a silastic tube was placed around the mouse sciatic nerve.

resultsImmunofluorescence study showed that clusters of cell adhesion complex forming paranodal axoglial junctions were dispersed and overlapped frequently with juxtaparanodal components. These paranodal changes occurred without internodal myelin damage. The distribution and pattern of paranodal disruption suggests that these changes are the direct result of mechanical stress. Electron microscopy confirmed loss of paranodal axoglial junctions.

conclusionsOur data show that chronic nerve compression disrupts paranodal junctions and axonal domains required for proper peripheral nerve function. These results provide important clues toward better understanding of the pathophysiology underlying nerve dysfunction in compression neuropathies. Muscle Nerve 55: 544-554, 2017.

Indexed as

AnimalsAnkyrinsArthrogryposisCell Adhesion MoleculesCell Adhesion Molecules, NeuronalDisease Models, AnimalEvoked Potentials, MotorFemaleFunctional LateralityGene Expression RegulationHereditary Sensory and Motor NeuropathyMiceMice, Inbred C57BLMicroscopy, Electron, TransmissionNerve Growth FactorsNeural ConductionAnk3 protein, mouseAnkyrinsCell Adhesion MoleculesCell Adhesion Molecules, NeuronalCntnap1 protein, mousegliomedin protein, mouseNerve Growth FactorsNfasc protein, mouseShab Potassium Channelsaxon-glia interactionscompression neuropathymouse modelnode of Ranvierparanodal junction

Identifiers

PMID27463510
PMCPMC5272873
OpenAlexW2503237811

What OpenQuestion holds

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LicenceTDM
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.