Journal
JOURNAL OF PHARMACOLOGICAL SCIENCES
Volume 123, Issue 3, Pages 284-287Publisher
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1254/jphs.13128SC
Keywords
transient receptor potential ankyrin-1 (TRPA1); proteinase-activated receptor-2 (PAR2); pancreatic pain
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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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