Evidence map›Paper›PMID 21813679›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

CNGA3: a target of spinal nitric oxide/cGMP signaling and modulator of inflammatory pain hypersensitivity.

Sandra Heine, Stylianos Michalakis, Wiebke Kallenborn-Gerhardt, Ruirui Lu, Hee-Young Lim, Jessica Weiland, Domenico Del Turco, Thomas Deller, Irmgard Tegeder, Martin Biel and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 45 citations in OpenAlex.

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  8. Granulocyte-colony-stimulating factor (G-CSF) signaling in spinal microglia drives visceral sensitization following colitis.Proceedings of the National Academy of Sciences of the United States of America · 2017
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  16. The C-type natriuretic peptide induces thermal hyperalgesia through a noncanonical Gβγ-dependent modulation of TRPV1 channel.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. NADPH oxidase-4 maintains neuropathic pain after peripheral nerve injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

12 authors at 2 institutions in 1 country.

Sandra HeinePharmazentrum Frankfurt/ZAFES, Institut für Klinische Pharmakologie, Klinikum der Johann Wolfgang Goethe-Universität, 60590 Frankfurt am Main, Germany.
Stylianos Michalakis
Wiebke Kallenborn-Gerhardt
Ruirui Lu
Hee-Young Lim
Jessica Weiland
Domenico Del Turco
Thomas Deller
Irmgard Tegeder
Martin Biel
Gerd Geisslinger
Achim Schmidtko
Goethe University Frankfurt · DECenter for Integrated Protein Science Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large body of evidence indicates that nitric oxide (NO) and cGMP contribute to central sensitization of pain pathways during inflammatory pain. Here, we investigated the distribution of cyclic nucleotide-gated (CNG) channels in the spinal cord, and identified the CNG channel subunit CNGA3 as a putative cGMP target in nociceptive processing. In situ hybridization revealed that CNGA3 is localized to inhibitory neurons of the dorsal horn of the spinal cord, whereas its distribution in dorsal root ganglia is restricted to non-neuronal cells. CNGA3 expression is upregulated in the superficial dorsal horn of the mouse spinal cord and in dorsal root ganglia following hindpaw inflammation evoked by zymosan. Mice lacking CNGA3 (CNGA3(-/-) mice) exhibited an increased nociceptive behavior in models of inflammatory pain, whereas their behavior in models of acute or neuropathic pain was normal. Moreover, CNGA3(-/-) mice developed an exaggerated pain hypersensitivity induced by intrathecal administration of cGMP analogs or NO donors. Our results provide evidence that CNGA3 contributes in an inhibitory manner to the central sensitization of pain pathways during inflammatory pain as a target of NO/cGMP signaling.

Indexed as

Analysis of VarianceAnimalsCyclic GMPCyclic Nucleotide-Gated Cation ChannelsDisease Models, AnimalEnzyme InhibitorsGanglia, SpinalGene Expression RegulationGlial Fibrillary Acidic ProteinInflammationMaleMiceMice, Inbred C57BLMice, KnockoutMicrodissectionNaphthalenes1-hydroxy-2-oxo-3-(3-aminopropyl)-3-isopropyl-1-triazene8-((4-chlorophenyl)thio)cyclic-3',5'-GMP8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphorothioateCnga3 protein, mouseCyclic GMPCyclic Nucleotide-Gated Cation ChannelsEnzyme InhibitorsGlial Fibrillary Acidic ProteinNaphthalenesNatriuretic PeptidesNitric OxideRNA, MessengerStathminThionucleotidesTriazenesVesicular Inhibitory Amino Acid Transport ProteinsViaat protein, mouse

Identifiers

PMID21813679
PMCPMC6623383
OpenAlexW2133490942

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.