Evidence map›Paper›PMID 18417695›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Silencing the Kir4.1 potassium channel subunit in satellite glial cells of the rat trigeminal ganglion results in pain-like behavior in the absence of nerve injury.

Jean-Philippe Vit, Peter T Ohara, Aditi Bhargava, Kanwar Kelley, Luc Jasmin

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
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  5. The Pathophysiological Mechanisms of Glia in Animal Models of Chronic Orofacial Pain: A Systematic Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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48 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

5 authors at 2 institutions in 1 country.

Jean-Philippe VitDepartment of Neurosurgery and Gene Therapeutics Research Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
Peter T Ohara
Aditi Bhargava
Kanwar Kelley
Luc Jasmin
Cedars-Sinai Medical Center · USUniversity of California, San Francisco · US

Funding

Gene Therapy for Nerve InjuryR01NS051336 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JASMIN, LUC · 2006 to 2010
$1.2M
Neuronal/Glial Interactions in Neuropathic PainR21NS058479 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI OHARA, PETER T · 2007 to 2008
$362k
NINDS NIH HHS R01 NS051336NINDS NIH HHS R21 NS058479
6 · The paper itself

Abstract

Growing evidence suggests that changes in the ion buffering capacity of glial cells can give rise to neuropathic pain. In the CNS, potassium ion (K+) buffering is dependent on the glia-specific inward rectifying K+ channel Kir4.1. We recently reported that the satellite glial cells that surround primary sensory neurons located in sensory ganglia of the peripheral nervous system also express Kir4.1, whereas the neurons do not. In the present study, we show that, in the rat trigeminal ganglion, the location of the primary sensory neurons for face sensation, specific silencing of Kir4.1 using RNA interference leads to spontaneous and evoked facial pain-like behavior in freely moving rats. We also show that Kir4.1 in the trigeminal ganglion is reduced after chronic constriction injury of the infraorbital nerve. These findings suggests that neuropathic pain can result from a change in expression of a single K+ channel in peripheral glial cells, raising the possibility of targeting Kir4.1 to treat pain in general and particularly neuropathic pain that occurs in the absence of nerve injury.

Indexed as

AnimalsCell LineGene SilencingHaplorhiniKcnj10 ChannelMaleNeurogliaOptic Nerve InjuriesPainPain MeasurementPotassium Channels, Inwardly RectifyingProtein SubunitsRatsRats, Sprague-DawleySatellite Cells, PerineuronalTrigeminal GanglionKcnj10 ChannelPotassium Channels, Inwardly RectifyingProtein Subunits

Identifiers

PMID18417695
PMCPMC2533133
OpenAlexW1974360350

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.