SOMATOSENSORY SYSTEMS, PAINInvolvement of TRPA1 in ET-1-induced pain-like behavior in miceLiang, Jiexiana; Bi, Huac; Ji, WenjinbAuthor Information aDivision of Anesthesiology, Department of Cardiovascular Surgery, Guangdong General Hospital bDepartment of Anesthesiology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, PR China cCollege of Optometry, Nova Southeastern University, Fort Lauderdale, Florida, USA Correspondence to Wenjin Ji, MD, Department of Anesthesiology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, 96 DongChun Road, Guangzhou 510080, PR China Tel: +86 18929515581; fax: +86 2037638604; e-mail: email@example.com Received 15 August 2009 accepted 23 November 2009 NeuroReport: February 17th, 2010 - Volume 21 - Issue 3 - p 201-205 doi: 10.1097/WNR.0b013e328335b3c5 Buy SDC Metrics Abstract Transient receptor potential ankyrin subfamily member 1 (TRPA1) is a nonselective cation channel known as a noxious cold-activated ion channel. Recent findings implicated its involvement in acute and chronic cold nociception processes. Here, we investigated whether TRPA1 is involved in endothelin-1 (ET-1)-induced spontaneous pain-like behavior in C57BL/6J mice. We found that TRPA1 antagonists, HC-030031 and AP18, significantly reduced the pain-like behavior caused by ET-1. AP18 also significantly reduced the pain caused by cinnamaldehyde, an agonist of TRPA-1. However, AP18 did not alleviate the pain caused by capsaicin. The pain-like behavior caused by ET-1 was inhibited by phospholipase C inhibitor, but not by protein kinase C inhibitor. Low dose of ET-1 could potentiate cinnamaldehyde-induced nociception. Our results suggested that TRPA1 is involved in ET-1-induced spontaneous pain-like behavior in mice. © 2010 Lippincott Williams & Wilkins, Inc.