Evidence map›Paper›PMID 17667578›Full record

ArticleAnesthesiology2007

Local inflammation in rat dorsal root ganglion alters excitability and ion currents in small-diameter sensory neurons.

Jun-Gang Wang, Judith A Strong, Wenrui Xie, Jun-Ming Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Anesthesiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Article
  3. A Reference Atlas of the Human Dorsal Root Ganglion.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Updates on Pathophysiology of Discogenic Back Pain.Journal of clinical medicine · 2023
    Review
  6. Article
  7. Article
  8. Transplantation of Human Neural Precursor Cells Reverses Syrinx Growth in a Rat Model of Post-Traumatic Syringomyelia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. The Distributions of Voltage-Gated KThe Journal of membrane biology · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  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

4 authors at 1 institution in 1 country.

Jun-Gang WangPain Research Center, Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Judith A Strong
Wenrui Xie
Jun-Ming Zhang
Marymount University · US

Funding

STUDY OF ACTIVITY-DEPENDENT SYMPATHETIC SPROUTINGR01NS045594 · NINDS · UNIVERSITY OF CINCINNATI · PI ZHANG, JUN-MING · 2004 to 2025
$8.6M
STUDY OF CHEMOGENIC LOW BACK PAINR01NS039568 · NINDS · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI ZHANG, JUN-MING · 2000 to 2003
$876k
NINDS NIH HHS NS39568NINDS NIH HHS NS45594NINDS NIH HHS R01 NS039568NINDS NIH HHS R01 NS045594
6 · The paper itself

Abstract

backgroundChronic pain conditions may result from peripheral nerve injury, chronic peripheral inflammation, or sensory ganglia inflammation. However, inflammatory processes may also contribute to peripheral nerve injury responses. To isolate the contribution of local inflammation of sensory ganglia to chronic pain states, the authors previously developed a rat model in which long-lasting pain is induced by inflaming sensory ganglia without injuring the neurons. This results in prolonged mechanical pain, local increases in proinflammatory cytokines, increased neuronal hyperexcitability, and abnormal spontaneous activity.

methodsThe authors used whole cell patch clamp in acutely isolated small-diameter neurons to determine how localized inflammation (3-5 days) of L4 and L5 ganglia altered voltage-gated K and Na currents.

resultsTetrodotoxin-sensitive Na currents increased twofold to threefold in neurons from inflamed ganglia. Tetrodotoxin-resistant Na currents increased more than twofold, but only in cells that bound isolectin B4. These increases occurred without shifts in voltage dependence of activation and inactivation. Similar results are seen in models of peripheral inflammation, except for the large magnitudes. Unlike most pain models, localized inflammation increased rather than decreased voltage-gated K currents, due to increased amplitudes of the sustained (delayed rectifier) and fast-inactivating transient components. The overall effect in current clamp experiments was an increase in excitability as indicated by decreased rheobase and lower action potential threshold.

conclusionsNeuronal inflammation per se, in the absence of nerve injury, causes large increases in Na channel density and enhanced excitability. The unusual finding of increased K current may reflect regulation of excitability in the face of such large increases in Na current.

Indexed as

Neural ConductionAction PotentialsAnesthetics, LocalAnimalsCells, CulturedDisease Models, AnimalElectric ConductivityElectrophysiologyFemaleGanglia, SpinalInflammationIon Channel GatingMembrane PotentialsNeurons, AfferentPatch-Clamp TechniquesPotassium Channels, Voltage-GatedAnesthetics, LocalPotassium Channels, Voltage-GatedSodium ChannelsTetrodotoxin

Identifiers

PMID17667578
PMCPMC1945168
OpenAlexW2008572521

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.