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

Matt Petrus, Andrea M. Peier, Michael Bandell, Sun Wook Hwang, Truc Huynh, Nicholas Olney, Tim Jegla, Ardem Patapoutian

Research output: Contribution to journalArticlepeer-review

357 Scopus citations


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.

Original languageEnglish (US)
Article number40
JournalMolecular Pain
StatePublished - Dec 17 2007

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Cellular and Molecular Neuroscience
  • Anesthesiology and Pain Medicine


Dive into the research topics of 'A role of TRPA1 in mechanical hyperalgesia is revealed by pharmacological inhibition'. Together they form a unique fingerprint.

Cite this