Evidence map›Paper›PMID 22951907›Full record

ArticleGlia2012

Astrocytic CX43 hemichannels and gap junctions play a crucial role in development of chronic neuropathic pain following spinal cord injury.

Michael J Chen, Benjamin Kress, Xiaoning Han, Katherine Moll, Weiguo Peng, Ru-Rong Ji, Maiken Nedergaard

Open access · greenAbstract read
In one paragraph

Article in Glia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
  4. Article
  5. Article
  6. Review
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  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
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  14. Peripheral and central pathogenesis of postherpetic neuralgia.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
    Review
  15. Review
  16. Inhibition of NFAT5-Dependent Astrocyte Swelling Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  17. Review
  18. Review
  19. Review
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52 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Michael J ChenDepartment of Neurosurgery, Center for Translational Neuromedicine, University of Rochester Medical School, Rochester, New York, USA.
Benjamin Kress
Xiaoning Han
Katherine Moll
Weiguo Peng
Ru-Rong Ji
Maiken Nedergaard
University of Rochester · USBrigham and Women's Hospital · US

Funding

Hemichannels, Astrocytic Release, and Neuropathic PainR01DE022743 · NIDCR · DUKE UNIVERSITY · PI JI, RU-RONG, NEDERGAARD, MAIKEN · 2012 to 2016
$2.0M
Failure of metabolite clearance in a model of multi-lacunar infarctsR01NS078167 · NINDS · UNIVERSITY OF ROCHESTER · PI NEDERGAARD, MAIKEN · 2012 to 2016
$1.8M
The glymphatic system, a new concept in glia biologyR01NS078304 · NINDS · UNIVERSITY OF ROCHESTER · PI NEDERGAARD, MAIKEN · 2012 to 2016
$1.7M
ATP as the instigator of inflammatory responses to spinal cord injuryR01NS075177 · NINDS · UNIVERSITY OF ROCHESTER · PI NEDERGAARD, MAIKEN · 2012 to 2016
$1.6M
NIDCR NIH HHS R01 DE022743NINDS NIH HHS R01 NS075177NINDS NIH HHS R01 NS078167NINDS NIH HHS R01 NS078304
6 · The paper itself

Abstract

Chronic neuropathic pain is a frequent consequence of spinal cord injury (SCI). Yet despite recent advances, upstream releasing mechanisms and effective therapeutic options remain elusive. Previous studies have demonstrated that SCI results in excessive ATP release to the peritraumatic regions and that purinergic signaling, among glial cells, likely plays an essential role in facilitating inflammatory responses and nociceptive sensitization. We sought to assess the role of connexin 43 (Cx43) as a mediator of CNS inflammation and chronic pain. To determine the extent of Cx43 involvement in chronic pain, a weight-drop SCI was performed on transgenic mice with Cx43/Cx30 deletions. SCI induced robust and persistent neuropathic pain including heat hyperalgesia and mechanical allodynia in wild-type control mice, which developed after 4 weeks and was maintained after 8 weeks. Notably, SCI-induced heat hyperalgesia and mechanical allodynia were prevented in transgenic mice with Cx43/Cx30 deletions, but fully developed in transgenic mice with only Cx30 deletion. SCI-induced gliosis, detected as upregulation of glial fibrillary acidic protein in the spinal cord astrocytes at different stages of the injury, was also reduced in the knockout mice with Cx43/Cx30 deletions, when compared with littermate controls. In comparison, a standard regimen of post-SCI treatment of minocycline attenuated neuropathic pain to a significantly lesser degree than Cx43 deletion. These findings suggest Cx43 is critically linked to the development of central neuropathic pain following acute SCI. Since Cx43/Cx30 is expressed by astrocytes, these findings also support an important role of astrocytes in the development of chronic pain.

Indexed as

AnimalsAstrocytesConnexin 43Disease Models, AnimalFemaleGap JunctionsGlial Fibrillary Acidic ProteinHyperalgesiaMiceMice, KnockoutNeuralgiaPain MeasurementPain ThresholdSpinal CordSpinal Cord InjuriesConnexin 43Glial Fibrillary Acidic Protein

Identifiers

PMID22951907
PMCPMC3604747
OpenAlexW1977177662

What OpenQuestion holds

Textmetadata
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.