Evidence map›Paper›PMID 18684911›Full record

ArticleJournal of neurophysiology2008

Tumor-evoked sensitization of C nociceptors: a role for endothelin.

Darryl T Hamamoto, Sergey G Khasabov, David M Cain, Donald A Simone

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Targeting MOR-mGluRNeuropharmacology · 2019
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Peripheral TGF-β1 signaling is a critical event in bone cancer-induced hyperalgesia in rodents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. New perspectives on the endothelin axis in pain.Pharmacological research · 2011
    Review
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Darryl T HamamotoDepartment of Diagnostic and Biological Sciences, University of Minnesota, 515 Delaware St. SE, 17-252 Moos Tower, Minneapolis, MN 55455, USA.
Sergey G Khasabov
David M Cain
Donald A Simone
Office of Basic Energy Sciences · USTwin Cities Orthopedics · US

Funding

CANNABINOID MODULATION OF HYPERALGESIAR01DA011471 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI SIMONE, DONALD · 2000 to 2014
$4.2M
Neural Mechanisms of Cancer PainR01CA091007 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI SIMONE, DONALD · 2001 to 2011
$2.3M
NCI NIH HHS CA-91007NIDA NIH HHS DA-011471
6 · The paper itself

Abstract

Primary and metastatic cancers that effect bone are frequently associated with pain. Sensitization of primary afferent C nociceptors innervating tissue near the tumor likely contributes to the chronic pain and hyperalgesia accompanying this condition. This study focused on the role of the endogenous peptide endothelin-1 (ET-1) as a potential peripheral algogen implicated in the process of cancer pain. Electrophysiological response properties, including ongoing activity and responses evoked by heat stimuli, of C nociceptors were recorded in vivo from the tibial nerve in anesthetized control mice and mice exhibiting mechanical hyperalgesia following implantation of fibrosarcoma cells into and around the calcaneus bone. ET-1 (100 microM) injected into the receptive fields of C nociceptors innervating the plantar surface of the hind paw evoked an increase in ongoing activity in both control and tumor-bearing mice. Moreover, the selective ETA receptor antagonist, BQ-123 (3 mM), attenuated tumor-evoked ongoing activity in tumor-bearing mice. Whereas ET-1 produced sensitization of C nociceptors to heat stimuli in control mice, C nociceptors in tumor-bearing mice were sensitized to heat, and their responses were not further increased by ET-1. Importantly, administration of BQ-123 attenuated tumor-evoked sensitization of C nociceptors to heat. We conclude that ET-1 at the tumor site contributes to tumor-evoked excitation and sensitization of C nociceptors through an ETA receptor mediated mechanism.

Indexed as

AnimalsBehavior, AnimalCell Line, TumorElectrophysiologyEndothelin A Receptor AntagonistsEndothelinsFibrosarcomaHot TemperatureHyperalgesiaMaleMiceMice, Inbred C3HNeoplasmsNeoplasm TransplantationNerve Fibers, UnmyelinatedNeural Conductioncyclo(Trp-Asp-Pro-Val-Leu)Endothelin A Receptor AntagonistsEndothelinsPeptides, Cyclic

Identifiers

PMID18684911
PMCPMC2576210
OpenAlexW2073005318

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.