{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T09:05:47Z","timestamp":1770282347470,"version":"3.49.0"},"reference-count":26,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,1,24]],"date-time":"2013-01-24T00:00:00Z","timestamp":1358985600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Previous studies have identified neuromedin <jats:styled-content style=\"fixed-case\">U<\/jats:styled-content> receptor 2 (<jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content>) as the subtype mediating the effects of neuromedin <jats:styled-content style=\"fixed-case\">U<\/jats:styled-content> on acute chemo\u2010nociception induced by capsaicin or formalin injection. The aims of this study were to determine whether <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content> is required for the development of mechanical hypersensitivity after nerve injury or heat hypersensitivity after inflammation and whether there is a gender difference in the contribution of <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content> to nociception.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Mechanical sensitivity was assessed with von <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>rey filaments in wild type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content>\u2010null mice at baseline and following spared tibial nerve (<jats:styled-content style=\"fixed-case\">STN<\/jats:styled-content>) injury. Heat sensitivity was also assessed at baseline and after induction of inflammation with Freund's complete adjuvant (<jats:styled-content style=\"fixed-case\">FCA<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The response to von <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>rey filaments at baseline was similar for <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content>\u2010null mice and for males and females. The response of male <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content>\u2010null mice was slightly but significantly decreased when exposed to 52\u2009\u00b0<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> but not 58\u2009\u00b0<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> heat stimuli. There was no difference between the stimulus\u2010response curve for <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content>\u2010null mice 7, 13 and 16 days after nerve injury. Similarly, after <jats:styled-content style=\"fixed-case\">FCA<\/jats:styled-content>\u2010induced inflammation, there was no significant difference in heat hyperalgesia between <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content>\u2010null mice or male or female mice in responses to temperatures ranging from 44 to 48\u2009\u00b0<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The present data do not support a significant contribution of <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content> to the development of hypersensitivity after nerve injury or tissue inflammation, suggesting that pharmacological intervention aimed at the <jats:styled-content style=\"fixed-case\">NMUR2<\/jats:styled-content> receptor might not be a valuable approach for the treatment of chronic pain.<\/jats:p><\/jats:sec>","DOI":"10.1002\/j.1532-2149.2013.00288.x","type":"journal-article","created":{"date-parts":[[2013,1,24]],"date-time":"2013-01-24T15:54:07Z","timestamp":1359042847000},"page":"1147-1155","source":"Crossref","is-referenced-by-count":4,"title":["Neuromedin <scp>U R<\/scp>eceptor 2 does not play a role in the development of neuropathic pain following nerve injury in mice"],"prefix":"10.1002","volume":"17","author":[{"given":"A.\u2010K.","family":"Gilbert","sequence":"first","affiliation":[{"name":"AstraZeneca R&amp;D Montreal CNS&amp;Pain Innovative Medicines Unit  Montreal Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Puma","sequence":"additional","affiliation":[{"name":"AstraZeneca R&amp;D Montreal CNS&amp;Pain Innovative Medicines Unit  Montreal Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"X.","family":"Xu","sequence":"additional","affiliation":[{"name":"AstraZeneca R&amp;D M\u00f6lndal  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