Evidence map›Paper›PMID 24463703›Full record

ArticlePflugers Archiv : European journal of physiology2014

Reduced excitability of gp130-deficient nociceptors is associated with increased voltage-gated potassium currents and Kcna4 channel upregulation.

Michiel Langeslag, Philipp Malsch, Andrea Welling, Michaela Kress

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Pancreatitis pain quality changes at year 1 follow-up, but GP130 remains a biomarker for pain.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024
    Article
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Non-coding RNAs in neuropathic pain.Neuronal signaling · 2020
    Review
  9. Article
  10. Impaired mechanical, heat, and cold nociception in a murine model of genetic TACE/ADAM17 knockdown.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Article
  19. Epigenetic modification of spinal miR-219 expression regulates chronic inflammation pain by targeting CaMKIIγ.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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 3 institutions in 2 countries.

Michiel LangeslagDepartment of Physiology and Biomedical Physics, Division of Physiology, Medical University of Innsbruck, Fritz-Pregl Strasse 3-I, A-6020, Innsbruck, Austria, michiel.langeslag@i-med.ac.at.
Philipp Malsch
Andrea Welling
Michaela Kress
Innsbruck Medical University · ATTechnical University of Munich · DEUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF W 1206
6 · The paper itself

Abstract

Neuropathic pain and pain arising from local inflammation are characterized by increased release of inflammatory mediators like interleukin-6 (IL-6) by immune cells. The levels of IL-6 is increased in various painfull conditions and correlates with the severity of thermal and mechanical hypersensitivity. Deletion of the IL-6 signal transducer glycoprotein 130 (gp130) reduces inflammation associated with hypersensitivity to thermal and mechanical stimuli. In this study, we show that nociceptor-specific deletion of gp130 alters excitability parameters that are linked to changes in the potassium conductance. In SNS-gp130(-/-) sensory neurons, the resting membrane potential was reduced. Moreover the repolarization speed of the action potential and afterhypolarization was augmented, however, voltage-gated Na(+) and Ca(2+) current were not obviously altered. The main difference between gp130-deficient and control neurons was a significant increase in the conductance of both delayed rectifier as well as A-type potassium currents. Taqman RT-PCR analysis revealed significantly higher levels of Kcna4 mRNA, encoding A-type Kv1.4 potassium channel, in neuron cultures from SNS-gp130(-/-) versus control mice, which may account for the electrophysiological data. No difference in other voltage-gated ion channel mRNAs was observed. The present data show for the first time increased A-type K(+) currents and expression of voltage-gated potassium channel Kcna4 (Kv1.4) in SNS-gp130(-/-) nociceptors. This suggests that gp130 acts as a break for the expression of potassium channels and important regulator hub for nociceptor excitability.

Indexed as

AnimalsCalciumGlycoproteinsInterleukin-6Kv1.4 Potassium ChannelMembrane PotentialsMiceNociceptorsPotassiumPotassium Channels, Voltage-GatedRNA, MessengerSensory Receptor CellsSodiumUp-RegulationCalciumGlycoproteinsInterleukin-6Kcna4 protein, mouseKv1.4 Potassium ChannelPotassiumPotassium Channels, Voltage-GatedRNA, MessengerSodium

Identifiers

PMID24463703
OpenAlexW1975551629

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.