Evidence map›Paper›PMID 24473263›Full record

ReviewNature neuroscience2014

Regulating excitability of peripheral afferents: emerging ion channel targets.

Stephen G Waxman, Gerald W Zamponi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed
18.5field-weighted citation impact, top 1% 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

224 citing papers in PubMed, 422 citations in OpenAlex.

  1. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
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  4. Functional and molecular diversity of human C-fibers in pain modulation.Current opinion in supportive and palliative care · 2026
    Review
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164 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

2 authors at 2 institutions in 2 countries.

Stephen G Waxman1] Center for Neuroscience & Regeneration Research, Yale University School of Medicine, New Haven, Connecticut, USA. [2] Veterans Affairs Medical Center, West Haven, Connecticut, USA.
Gerald W ZamponiDepartment of Physiology and Pharmacology, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
University of Calgary · CAYale University · US

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

The transmission and processing of pain signals relies critically on the activities of ion channels that are expressed in afferent pain fibers. This includes voltage-gated channels, as well as background (or leak) channels that collectively regulate resting membrane potential and action potential firing properties. Dysregulated ion channel expression in response to nerve injury and inflammation results in enhanced neuronal excitability that underlies chronic neuropathic and inflammatory pain. Pharmacological modulators of ion channels, particularly those that target channels on peripheral neurons, are being pursued as possible analgesics. Over the past few years, a number of different types of ion channels have been implicated in afferent pain signaling. Here we give an overview of recent advances on sodium, calcium, potassium and chloride channels that are emerging as especially attractive targets for the treatment of pain.

Indexed as

Afferent PathwaysAnimalsHumansIon ChannelsPainPeripheral NervesIon Channels

Identifiers

PMID24473263
OpenAlexW2159470318

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.