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Mol Pain 2007 Dec 17;3:40. doi: 10.1186/1744-8069-3-40.
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A role of TRPA1 in mechanical hyperalgesia is revealed by pharmacological inhibition.

Petrus M , Peier AM , Bandell M , Hwang SW , Huynh T , Olney N , Jegla T , Patapoutian A .

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.

PubMed ID: 18086313
PMC ID: PMC2222610
Article link: Mol Pain
Grant support: [+]

Species referenced: Xenopus
Genes referenced: bdkrb2 tbx2 trpa1 trpm8 trpv1 trpv2 trpv3 trpv4

Article Images: [+] show captions
References [+] :
Alessandri-Haber, A transient receptor potential vanilloid 4-dependent mechanism of hyperalgesia is engaged by concerted action of inflammatory mediators. 2006, Pubmed