{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T21:57:52Z","timestamp":1791064672059,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2011,12,13]],"date-time":"2011-12-13T00:00:00Z","timestamp":1323734400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2012,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background\u2002<\/jats:bold> Proteinase activated receptor 2 (PAR\u20102) is expressed by many neurons in the colon, including primary afferent neurons that co\u2010express transient receptor potential vanilloid 1 (TRPV1). Activation of PAR\u20102 receptors was previously found to enhance colonic motility, increase secretion and produce hypersensitivity to mechanical stimuli. This study examined the functional role of TRPV1\/PAR\u20102 expressing neurons that innervate the colon by lesioning TRPV1 bearing neurons with the highly selective and potent TRPV1 agonist resiniferatoxin.<\/jats:p><jats:p><jats:bold>Methods\u2002<\/jats:bold> Colonic motility in response to PAR\u20102 activation was evaluated <jats:italic>in vitro<\/jats:italic> using isolated segments of descending colon and <jats:italic>in vivo<\/jats:italic> using manometry. Colonic mechanical nociceptive thresholds were measured using colorectal distension. Transient receptor potential vanilloid 1 expressing neurons were selectively lesioned with resiniferatoxin.<\/jats:p><jats:p><jats:bold>Key Results\u2002<\/jats:bold>  <jats:italic>In vitro<\/jats:italic>, the PAR\u20102 agonists, trypsin and SLIGRL did not alter contractions of colon segments when applied alone, however, the agents enhanced acetylcholine stimulated contraction. <jats:italic>In vivo<\/jats:italic>, PAR\u20102 agonists administered intraluminally induced contractions of the colon and produced hypersensitivity to colorectal distention. The PAR\u20102 agonist enhancement of colonic contraction was eliminated when TRPV1 expressing neurons were lesioned with resiniferatoxin, but the PAR\u20102 agonist induced hypersensitivity remained in the lesioned animals.<\/jats:p><jats:p><jats:bold>Conclusions &amp; Inferences\u2002<\/jats:bold> Our findings indicate that TRPV1\/PAR\u20102 expressing primary afferent neurons mediate an extrinsic motor reflex pathway in the colon. These data, coupled with our previous studies, also indicate that the recently described colospinal afferent neurons are nociceptive, suggesting that these neurons may be useful targets for the pharmacological control of pain in diseases such as irritable bowel syndrome.<\/jats:p>","DOI":"10.1111\/j.1365-2982.2011.01848.x","type":"journal-article","created":{"date-parts":[[2011,12,14]],"date-time":"2011-12-14T03:03:30Z","timestamp":1323831810000},"source":"Crossref","is-referenced-by-count":11,"title":["Lesioning of TRPV1 expressing primary afferent neurons prevents PAR\u20102 induced motility, but not mechanical hypersensitivity in the rat colon"],"prefix":"10.1111","volume":"24","author":[{"given":"S. K.","family":"Suckow","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. M.","family":"Anderson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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