{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T15:02:31Z","timestamp":1774450951978,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,8,11]],"date-time":"2017-08-11T00:00:00Z","timestamp":1502409600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Grant-in-Aid for Scientific Research (B)","award":["26293131"],"award-info":[{"award-number":["26293131"]}]},{"name":"Grant-in-Aid for Scientific Research on Priority Areas","award":["21026015"],"award-info":[{"award-number":["21026015"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Scandinavian Med Sci Sports"],"published-print":{"date-parts":[[2018,3]]},"abstract":"We previously demonstrated that nerve growth factor (NGF<\/jats:styled-content>) and glial cell line\u2010derived neurotrophic factor (GDNF<\/jats:styled-content>) were upregulated after lengthening contractions (LC<\/jats:styled-content>) in exercised muscle through B2 bradykinin receptor activation and cyclooxygenase (COX<\/jats:styled-content>)\u20102 upregulation, respectively, and that these trophic factors sensitized nociceptors resulting in mechanical hyperalgesia (delayed\u2010onset muscle soreness,DOMS<\/jats:styled-content>). Here, we examined the prostaglandin receptor subtype involved inDOMS<\/jats:styled-content>. The mechanical withdrawal threshold of the exercised muscle was measured before and afterLC<\/jats:styled-content>in rats administered prostaglandin E2<\/jats:sub>receptor (EP<\/jats:styled-content>) antagonists beforeLC<\/jats:styled-content>, or in wild\u2010type (WT<\/jats:styled-content>),EP<\/jats:styled-content>2 knockout (EP<\/jats:styled-content>2\u2212\/\u2212<\/jats:sup>), andIP<\/jats:styled-content>knockout (IP<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>) mice. The change in expression ofNGF<\/jats:styled-content>,GDNF<\/jats:styled-content>, orCOX<\/jats:styled-content>\u20102mRNA<\/jats:styled-content>was examined using real\u2010timeRT<\/jats:styled-content>\u2010PCR<\/jats:styled-content>in the muscle inEP<\/jats:styled-content>2\u2212\/\u2212<\/jats:sup>andWT<\/jats:styled-content>mice. None of the antagonists toEP<\/jats:styled-content>1,EP<\/jats:styled-content>3, andEP<\/jats:styled-content>4 receptors (ONO<\/jats:styled-content>\u20108713,ONO<\/jats:styled-content>\u2010AE<\/jats:styled-content>5\u2010599, andONO<\/jats:styled-content>\u2010AE<\/jats:styled-content>3\u2010208, respectively) induced a significant difference inDOMS<\/jats:styled-content>compared with controls in rats.WT<\/jats:styled-content>andIP<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>mice developed mechanical hyperalgesia afterLC<\/jats:styled-content>, butEP<\/jats:styled-content>2\u2212\/\u2212<\/jats:sup>mice did not. Upregulation ofNGF<\/jats:styled-content>,GDNF<\/jats:styled-content>, andCOX<\/jats:styled-content>\u20102mRNA<\/jats:styled-content>was observed afterLC<\/jats:styled-content>inWT<\/jats:styled-content>mice but not inEP<\/jats:styled-content>2\u2212\/\u2212<\/jats:sup>mice. Injecting anEP<\/jats:styled-content>2 agonist (ONO<\/jats:styled-content>\u2010AE<\/jats:styled-content>1\u2010259\u201001) into the mouse muscle increased expression ofCOX<\/jats:styled-content>\u20102mRNA<\/jats:styled-content>. These results suggest thatEP<\/jats:styled-content>2 contributes to generating mechanical hyperalgesia through positive feedback upregulation ofCOX<\/jats:styled-content>\u20102 expression in muscle after LC.<\/jats:p>","DOI":"10.1111\/sms.12954","type":"journal-article","created":{"date-parts":[[2017,7,31]],"date-time":"2017-07-31T15:52:41Z","timestamp":1501516361000},"page":"826-833","source":"Crossref","is-referenced-by-count":7,"title":["EP<\/scp>2 receptor plays pivotal roles in generating mechanical hyperalgesia after lengthening contractions"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4746-8845","authenticated-orcid":false,"given":"H.","family":"Ota","sequence":"first","affiliation":[{"name":"Department of Neuroscience II Graduate School of Medicine Nagoya University Nagoya Japan"},{"name":"Department of Judo Therapy Faculty of Medical Technology Teikyo University Utsunomiya Japan"},{"name":"Department of Physical Therapy College of Life 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Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Narumiya","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Graduate School of Medicine Kyoto University Kyoto Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Mizumura","sequence":"additional","affiliation":[{"name":"Department of Neuroscience II Graduate School of Medicine Nagoya University Nagoya Japan"},{"name":"Department of Physical Therapy College of Life and Health Sciences Chubu University Kasugai 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