Evidence map›Paper›PMID 29228786›Full record

ArticleASN neuro

Oxidative Stress Induces Disruption of the Axon Initial Segment.

Kareem Clark, Brooke A Sword, Jeffrey L Dupree

Open access · goldAbstract read
In one paragraph

Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Drug-Drug Interactions in Vestibular Diseases, Clinical Problems, and Medico-Legal Implications.International journal of environmental research and public health · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Maturation Dynamics of the Axon Initial Segment (AIS) of Newborn Dentate Granule Cells in Young Adult C57BL/6J Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  11. Type 2 Diabetes Leads to Axon Initial Segment Shortening inFrontiers in cellular neuroscience · 2018
    Article
  12. Article
  13. 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

3 authors at 2 institutions in 1 country.

Kareem Clark1 Department of Anatomy and Neurobiology, 72054 Virginia Commonwealth University , Richmond, VA, USA.
Brooke A Sword3 20125 Hunter Holmes McGuire VA Medical Center , Richmond, VA, USA.
Jeffrey L Dupree1 Department of Anatomy and Neurobiology, 72054 Virginia Commonwealth University , Richmond, VA, USA.
Virginia Commonwealth University · USHunter Holmes McGuire VA Medical Center · US

Funding

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 BX002565
6 · The paper itself

Abstract

The axon initial segment (AIS), the domain responsible for action potential initiation and maintenance of neuronal polarity, is targeted for disruption in a variety of central nervous system pathological insults. Previous work in our laboratory implicates oxidative stress as a potential mediator of structural AIS alterations in two separate mouse models of central nervous system inflammation, as these effects were attenuated following reactive oxygen species scavenging and NADPH oxidase-2 ablation. While these studies suggest a role for oxidative stress in modulation of the AIS, the direct effects of reactive oxygen and nitrogen species (ROS/RNS) on the stability of this domain remain unclear. Here, we demonstrate that oxidative stress, as induced through treatment with 3-morpholinosydnonimine (SIN-1), a spontaneous ROS/RNS generator, drives a reversible loss of AIS protein clustering in primary cortical neurons in vitro. Pharmacological inhibition of both voltage-dependent and intracellular calcium (Ca

Indexed as

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterAnimalsAxon Initial SegmentCalcium Channel AgonistsCalcium Channel BlockersCell SurvivalCerebral CortexDizocilpine MaleateEmbryo, MammalianEnzyme InhibitorsFemaleImmunosuppressive AgentsMiceMice, Inbred C57BLMolsidomineNADPH Oxidase 23-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterCalcium Channel AgonistsCalcium Channel BlockersDizocilpine MaleateEnzyme InhibitorsImmunosuppressive AgentslinsidomineMolsidomineNADPH Oxidase 2Neuroprotective AgentsReactive Oxygen SpeciesTacrolimusaxon initial segmentcalciumcalpainoxidative stressreactive nitrogen speciesreactive oxygen species

Identifiers

PMID29228786
PMCPMC5734465
OpenAlexW2772342323

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.