Evidence map›Paper›PMID 23880056›Full record

ArticlePain2013

Effect of antioxidant treatment on spinal GABA neurons in a neuropathic pain model in the mouse.

June Yowtak, Jigong Wang, Hee Young Kim, Ying Lu, Kyungsoon Chung, Jin Mo Chung

Open access · greenAbstract read
In one paragraph

Article in Pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
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  7. Vitamin DCNS neuroscience & therapeutics · 2024
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  10. Review
  11. Article
  12. Review
  13. Article
  14. Oxidative/Nitroxidative Stress and Multiple Sclerosis.Journal of molecular neuroscience : MN · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Reviewing the case for compromised spinal inhibition in neuropathic pain.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  19. Article
  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

6 authors at 1 institution in 1 country.

June YowtakDepartment of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX, USA.
Jigong Wang
Hee Young Kim
Ying Lu
Kyungsoon Chung
Jin Mo Chung
The University of Texas Medical Branch at Galveston · US

Funding

VISCERAL PAINP01NS011255 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CHUNG, JIN M · 1985 to 2012
$13.6M
Mechanisms of Neuropathic PainR01NS031680 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CHUNG, JIN M · 1994 to 2016
$4.1M
NINDS NIH HHS P01 NS011255NINDS NIH HHS R01 NS031680
6 · The paper itself

Abstract

One feature of neuropathic pain is a reduced spinal gamma-aminobutyric acid (GABA)-ergic inhibitory function. However, the mechanisms behind this attenuation remain to be elucidated. This study investigated the involvement of reactive oxygen species in the spinal GABA neuron loss and reduced GABA neuron excitability in spinal nerve ligation (SNL) model of neuropathic pain in mice. The importance of spinal GABAergic inhibition in neuropathic pain was tested by examining the effects of intrathecally administered GABA receptor agonists and antagonists in SNL and naïve mice, respectively. The effects of SNL and antioxidant treatment on GABA neuron loss and functional changes were examined in transgenic GAD67-enhanced green fluorescent protein positive (EGFP+) mice. GABA receptor agonists transiently reversed mechanical hypersensitivity of the hind paw in SNL mice. On the other hand, GABA receptor antagonists made naïve mice mechanically hypersensitive. Stereological analysis showed that the numbers of enhanced green fluorescent protein positive (EGFP+) GABA neurons were significantly decreased in the lateral superficial laminae (I-II) on the ipsilateral L5 spinal cord after SNL. Repeated antioxidant treatments significantly reduced the pain behaviors and prevented the reduction in EGFP+ GABA neurons. The response rate of the tonic firing GABA neurons recorded from SNL mice increased with antioxidant treatment, whereas no change was seen in those recorded from naïve mice, which suggested that oxidative stress impaired some spinal GABA neuron activity in the neuropathic pain condition. Together the data suggest that neuropathic pain, at least partially, is attributed to oxidative stress, which induces both a GABA neuron loss and dysfunction of surviving GABA neurons.

Indexed as

Action PotentialsAnimalsAntioxidantsBehavior, AnimalCell CountCyclic N-OxidesDose-Response Relationship, DrugFree Radical ScavengersGABA AgonistsGABA Antagonistsgamma-Aminobutyric AcidGreen Fluorescent ProteinsHyperalgesiaLigationMiceMice, TransgenicAntioxidantsCyclic N-OxidesFree Radical ScavengersGABA AgonistsGABA Antagonistsgamma-Aminobutyric AcidGreen Fluorescent Proteinsphenyl-N-tert-butylnitroneFree radicalsGABANeuropathic painReactive oxygen speciesSpinal cord dorsal horn neurons

Identifiers

PMID23880056
PMCPMC3816493
OpenAlexW1972794215

What OpenQuestion holds

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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.