Contribution of TRPA1 as a Downstream Signal of Proteinase-Activated Receptor-2 to Pancreatic Pain

Yuka Terada; Mayuko Fujimura; Sachiyo Nishimura; Maho Tsubota; Fumiko Sekiguchi; Hiroyuki Nishikawa; Atsufumi Kawabata

doi:10.1254/jphs.13128SC

Short Communication

Contribution of TRPA1 as a Downstream Signal of Proteinase-Activated Receptor-2 to Pancreatic Pain

Yuka Terada, Mayuko Fujimura, Sachiyo Nishimura, Maho Tsubota, Fumiko Sekiguchi, Hiroyuki Nishikawa, Atsufumi Kawabata

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Keywords: transient receptor potential ankyrin-1 (TRPA1), proteinase-activated receptor-2 (PAR2), pancreatic pain

JOURNAL FREE ACCESS

2013 Volume 123 Issue 3 Pages 284-287

DOI https://doi.org/10.1254/jphs.13128SC

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Abstract

We examined if TRPA1, like TRPV1, contributes to pancreatic nociceptor excitation following proteinase-activated receptor-2 (PAR2) stimulation and to pancreatitis-related pain in mice. A PAR2-activating peptide, infused into the pancreatic duct, caused spinal Fos expression, which was prevented by AP18, a TRPA1 inhibitor. Repeated administration of cerulein caused referred hyperalgesia accompanying pancreatitis, which was reversed by SB366791, a TRPV1 inhibitor, but not AP18. AP18, administered in combination with a subeffective dose of SB366791, significantly suppressed the referred hyperalgesia. Our findings suggest that TRPA1, like TRPV1, mediates PAR2-triggered pancreatic nociception and that TRPA1 in collaboration with TRPV1 latently contributes to pancreatitis-related pain.

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