Evidence map›Paper›PMID 18716216›Full record

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

cGMP produced by NO-sensitive guanylyl cyclase essentially contributes to inflammatory and neuropathic pain by using targets different from cGMP-dependent protein kinase I.

Achim Schmidtko, Wei Gao, Peter König, Sandra Heine, Roberto Motterlini, Peter Ruth, Jens Schlossmann, Doris Koesling, Ellen Niederberger, Irmgard Tegeder and 2 more

Open access · bronzeAbstract read
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 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
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  17. How Nitric Oxide Increases in Diabetic Morphine Tolerated Male Rats.Iranian journal of pharmaceutical research : IJPR · 2017
    Article
  18. Article
  19. [Physiology of pain].Schmerz (Berlin, Germany) · 2015
    Review
  20. Review
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 6 institutions in 2 countries.

Achim SchmidtkoPharmazentrum Frankfurt/ZAFES, Institut für Klinische Pharmakologie, Klinikum der Johann Wolfgang Goethe-Universität, 60590 Frankfurt am Main, Germany. Schmidtko@em.uni-frankfurt.de
Wei Gao
Peter König
Sandra Heine
Roberto Motterlini
Peter Ruth
Jens Schlossmann
Doris Koesling
Ellen Niederberger
Irmgard Tegeder
Andreas Friebe
Gerd Geisslinger
Goethe University Frankfurt · DERuhr University Bochum · DELeibniz-Forschungsinstitut für Molekulare Pharmakologie · DENorthwick Park Institute for Medical Research · GBUniversity of Lübeck · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large body of evidence indicates that the release of nitric oxide (NO) is crucial for the central sensitization of pain pathways during both inflammatory and neuropathic pain. Here, we investigated the distribution of NO-sensitive guanylyl cyclase (NO-GC) in the spinal cord and in dorsal root ganglia, and we characterized the nociceptive behavior of mice deficient in NO-GC (GC-KO mice). We show that NO-GC is distinctly expressed in neurons of the mouse dorsal horn, whereas its distribution in dorsal root ganglia is restricted to non-neuronal cells. GC-KO mice exhibited a considerably reduced nociceptive behavior in models of inflammatory or neuropathic pain, but their responses to acute pain were not impaired. Moreover, GC-KO mice failed to develop pain sensitization induced by intrathecal administration of drugs releasing NO or carbon monoxide. Surprisingly, during spinal nociceptive processing, cGMP produced by NO-GC may activate signaling pathways different from cGMP-dependent protein kinase I (cGKI), whereas cGKI can be activated by natriuretic peptide receptor-B dependent cGMP production. Together, our results provide evidence that NO-GC is crucially involved in the central sensitization of pain pathways during inflammatory and neuropathic pain.

Indexed as

AnimalsBehavior, AnimalCarbon MonoxideCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic GMP-Dependent Protein Kinase Type IFemaleGanglia, SpinalGuanylate CyclaseInflammationMaleMiceMice, KnockoutNeuralgiaNociceptorsPainCarbon MonoxideCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic GMP-Dependent Protein Kinase Type IGuanylate CyclasePrkg1 protein, mouseReceptors, Cytoplasmic and NuclearSoluble Guanylyl Cyclase

Identifiers

PMID18716216
PMCPMC6671070
OpenAlexW2042653860

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.