{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T09:35:25Z","timestamp":1791279325802,"version":"4.1.0"},"reference-count":33,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,9,30]],"date-time":"2014-09-30T00:00:00Z","timestamp":1412035200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:p>\n                    Hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S), formed by multiple enzymes, including cystathionine\u2010\u03b3\u2010lyase (CSE), targets Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2 T\u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels (T channels) and transient receptor potential ankyrin\u20101 (TRPA1), facilitating somatic pain. Pancreatitis\u2010related pain also appears to involve activation of T channels by H\n                    <jats:sub>2<\/jats:sub>\n                    S formed by the upregulated CSE. Therefore, this study investigates the roles of the Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2 isoform and\/or TRPA1 in pancreatic nociception in the absence and presence of pancreatitis. In anesthetized mice, AP18, a TRPA1 inhibitor, abolished the Fos expression in the spinal dorsal horn caused by injection of a TRPA1 agonist into the pancreatic duct. As did mibefradil, a T\u2010channel inhibitor, in our previous report, AP18 prevented the Fos expression following ductal NaHS, an H\n                    <jats:sub>2<\/jats:sub>\n                    S donor. In the mice with cerulein\u2010induced acute pancreatitis, the referred hyperalgesia was suppressed by NNC 55\u20100396 (NNC), a selective T\u2010channel inhibitor; zinc chloride; or ascorbic acid, known to inhibit Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2 selectively among three T\u2010channel isoforms; and knockdown of Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2. In contrast, AP18 and knockdown of TRPA1 had no significant effect on the cerulein\u2010induced referred hyperalgesia, although they significantly potentiated the antihyperalgesic effect of NNC at a subeffective dose. TRPA1 but not Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2 in the dorsal root ganglia was downregulated at a protein level in mice with cerulein\u2010induced pancreatitis. The data indicate that TRPA1 and Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2 mediate the exogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S\u2010induced pancreatic nociception in na\u00efve mice and suggest that, in the mice with pancreatitis, Ca\n                    <jats:sub>v<\/jats:sub>\n                    3.2 targeted by H\n                    <jats:sub>2<\/jats:sub>\n                    S primarily participates in the pancreatic pain, whereas TRPA1 is downregulated and plays a secondary role in pancreatic nociceptive signaling. \u00a9 2014 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jnr.23490","type":"journal-article","created":{"date-parts":[[2014,9,30]],"date-time":"2014-09-30T00:44:30Z","timestamp":1412037870000},"page":"361-369","source":"Crossref","is-referenced-by-count":37,"title":["Roles of Ca\n                    <sub>v<\/sub>\n                    3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis"],"prefix":"10.1002","volume":"93","author":[{"given":"Yuka","family":"Terada","sequence":"first","affiliation":[{"name":"Division of Pharmacology and Pathophysiology Kinki University School of Pharmacy Higashi\u2010Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mayuko","family":"Fujimura","sequence":"additional","affiliation":[{"name":"Division of Pharmacology and Pathophysiology Kinki University School of Pharmacy Higashi\u2010Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachiyo","family":"Nishimura","sequence":"additional","affiliation":[{"name":"Division of Pharmacology and Pathophysiology Kinki University School of Pharmacy Higashi\u2010Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maho","family":"Tsubota","sequence":"additional","affiliation":[{"name":"Division of Pharmacology and 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