{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T21:29:28Z","timestamp":1787002168017,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":212,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background and purpose:<\/jats:title>\n                    <jats:p>We investigated the mechanisms underlying the pruritogenic response induced by trypsin in mice, to assess the relevance of neurogenic inflammation components in this response.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental approach:<\/jats:title>\n                    <jats:p>Itching was induced by an intradermal injection of trypsin in the mouse neck. The animals were observed for 40\u2003min and their scratching behaviour was quantified.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key results:<\/jats:title>\n                    <jats:p>\n                      Trypsin\u2010induced itching was blocked by the lima bean trypsin inhibitor, the selective proteinase\u2010activated receptor\u20102 (PAR\u20102) antagonist FSLLRY and PAR\u20102 receptor desensitization. An important involvement of mast cells was observed, as chronic pretreatment with the mast cell degranulator compound 48\/80 or the mast cell stabilizer disodium cromoglycate prevented scratching. Also, trypsin response was inhibited by the selective COX\u20102 inhibitor celecoxib and by the selective kinin B\n                      <jats:sub>2<\/jats:sub>\n                      (FR173657) and B\n                      <jats:sub>1<\/jats:sub>\n                      (SSR240612) receptor antagonists. Moreover, an essential role for the mediators of neurogenic inflammation was established, as the selective NK\n                      <jats:sub>1<\/jats:sub>\n                      (FK888), NK\n                      <jats:sub>3<\/jats:sub>\n                      (SR142801) and calcitonin gene\u2010related peptide (CGRP\n                      <jats:sub>8\u221237<\/jats:sub>\n                      fragment) receptor antagonists inhibited trypsin\u2010induced itching. Similarly, blockade of transient receptor potential vanilloid 1 (TRPV1) receptors by the selective TRPV1 receptor antagonist SB366791, or by genetic deletion of TRPV1 receptor reduced this behaviour in mice. C\u2010fibre desensitization showed a very similar result.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and implications:<\/jats:title>\n                    <jats:p>Trypsin intradermal injection proved to be a reproducible model for the study of itching and the involvement of PAR\u20102 receptors. Also, trypsin\u2010induced itching seems to be widely dependent on neurogenic inflammation, with a role for TRPV1 receptors. In addition, several other mediators located in the sensory nerves and skin also seem to contribute to this process.<\/jats:p>\n                    <jats:p>\n                      <jats:italic>British Journal of Pharmacology<\/jats:italic>\n                      (2008)\n                      <jats:bold>154<\/jats:bold>\n                      , 1094\u20131103; doi:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/bjp.2008.172\">10.1038\/bjp.2008.172<\/jats:ext-link>\n                      ; published online 5 May 2008\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1038\/bjp.2008.172","type":"journal-article","created":{"date-parts":[[2008,5,5]],"date-time":"2008-05-05T05:58:47Z","timestamp":1209967127000},"page":"1094-1103","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":84,"title":["Evidence for the role of neurogenic 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