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A role of TRPA1 in mechanical hyperalgesia is revealed by pharmacological inhibition

Academic Article
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Overview

authors

  • Petrus, M.
  • Peier, A. M.
  • Bandell, M.
  • Hwang, S. W.
  • Huynh, T.
  • Olney, N.
  • Jegla, T.
  • Patapoutian, Ardem

publication date

  • December 2007

journal

  • Molecular Pain  Journal

abstract

  • Mechanical hyperalgesia is a clinically-relevant form of pain sensitization that develops through largely unknown mechanisms. TRPA1, a Transient Receptor Potential ion channel, is a sensor of pungent chemicals that may play a role in acute noxious mechanosensation and cold thermosensation. We have developed a specific small molecule TRPA1 inhibitor (AP18) that can reduce cinnameldehyde-induced nociception in vivo. Interestingly, AP18 is capable of reversing CFA-induced mechanical hyperalgesia in mice. Although TRPA1-deficient mice develop normal CFA-induced hyperalgeisa, AP18 is ineffective in the knockout mice, consistent with an on-target mechanism. Therefore, TRPA1 plays a role in sensitization of nociception, and that compensation in TRPA1-deficient mice masks this requirement.

subject areas

  • Animals
  • Behavior, Animal
  • Bradykinin
  • CHO Cells
  • Calcium Signaling
  • Cricetinae
  • Cricetulus
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Humans
  • Hyperalgesia
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Oocytes
  • Pain Measurement
  • Rats
  • Rats, Sprague-Dawley
  • Transfection
  • Transient Receptor Potential Channels
  • Xenopus
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Identity

PubMed Central ID

  • PMC2222610

International Standard Serial Number (ISSN)

  • 1744-8069

Digital Object Identifier (DOI)

  • 10.1186/1744-8069-3-40

PubMed ID

  • 18086313
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Additional Document Info

start page

  • 40

volume

  • 3

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