Evidence map›Paper›PMID 21949864›Full record

ArticlePloS one2011

Type III Nrg1 back signaling enhances functional TRPV1 along sensory axons contributing to basal and inflammatory thermal pain sensation.

Sarah E Canetta, Edlira Luca, Elyse Pertot, Lorna W Role, David A Talmage

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Structural Similarities between Neuregulin 1-3 Isoforms Determine Their Subcellular Distribution and Signaling Mode in Central Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Type III neuregulin 1 is required for multiple forms of excitatory synaptic plasticity of mouse cortico-amygdala circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  11. Article
  12. 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

5 authors at 2 institutions in 1 country.

Sarah E CanettaDepartment of Neurobiology and Behavior, Columbia University, New York, New York, United States of America.
Edlira Luca
Elyse Pertot
Lorna W Role
David A Talmage
State University of New York · USColumbia University · US

Funding

TRAINING IN CELLULAR, MOLECULAR AND BIOPHYSICAL STUDIEST32GM008224 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI LIEM, RONALD K. · 1987 to 2021
$9.9M
EXPRESSION OF NEURONAL NICOTINIC ACETYLOCHOLINE RECEPTORR01NS029071 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI ROLE, LORNA W · 1991 to 2009
$3.6M
NCRR NIH HHS TL1RR025158NIGMS NIH HHS T32 GM008224NIGMS NIH HHS T32 GM08224NINDS NIH HHS NS29071NINDS NIH HHS R01 NS029071
6 · The paper itself

Abstract

Type III Nrg1, a member of the Nrg1 family of signaling proteins, is expressed in sensory neurons, where it can signal in a bi-directional manner via interactions with the ErbB family of receptor tyrosine kinases (ErbB RTKs). Type III Nrg1 signaling as a receptor (Type III Nrg1 back signaling) can acutely activate phosphatidylinositol-3-kinase (PtdIns3K) signaling, as well as regulate levels of α7* nicotinic acetylcholine receptors, along sensory axons. Transient receptor potential vanilloid 1 (TRPV1) is a cation-permeable ion channel found in primary sensory neurons that is necessary for the detection of thermal pain and for the development of thermal hypersensitivity to pain under inflammatory conditions. Cell surface expression of TRPV1 can be enhanced by activation of PtdIns3K, making it a potential target for regulation by Type III Nrg1. We now show that Type III Nrg1 signaling in sensory neurons affects functional axonal TRPV1 in a PtdIns3K-dependent manner. Furthermore, mice heterozygous for Type III Nrg1 have specific deficits in their ability to respond to noxious thermal stimuli and to develop capsaicin-induced thermal hypersensitivity to pain. Cumulatively, these results implicate Type III Nrg1 as a novel regulator of TRPV1 and a molecular mediator of nociceptive function.

Indexed as

ThermosensingAnimalsAxonsCapsaicinCells, CulturedImmunoblottingInflammationMaleMiceMice, KnockoutNeuregulin-1PainPatch-Clamp TechniquesSensationSensory Receptor CellsSensory System AgentsCapsaicinNeuregulin-1Nrg1 protein, mouseSensory System AgentsTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID21949864
PMCPMC3176819
OpenAlexW2077830428

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.