{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:16:33Z","timestamp":1791274593406,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,12,14]],"date-time":"2012-12-14T00:00:00Z","timestamp":1355443200000},"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":[[2013,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Inflammation is a major cause of temporomandibular disorder\u2010related pain. The <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 sodium channel has a critical function in pain perceptions. However, whether and how <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 in the trigeminal ganglion is involved in temporomandibular joint (<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>) inflammatory pain remains to be examined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammation was induced by complete <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>reund's adjuvant in female rats. The expression of trigeminal ganglionic <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 and other sodium channels was examined using real\u2010time polymerase chain reaction or <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>estern blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer <jats:styled-content style=\"fixed-case\">DiI<\/jats:styled-content> was used to confirm <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 in the trigeminal neurons innervating <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>. The functions of trigeminal ganglionic <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 and extracellular signal\u2010regulated kinase 1\/2 (<jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2) phosphorylation were blocked with the microinjection of the <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 antibody or <jats:styled-content style=\"fixed-case\">U<\/jats:styled-content>0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> nociceptive responses.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammation significantly up\u2010regulated <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein; however, the <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> of <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.3 was not affected and those of <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.8 and <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.9 were only slightly up\u2010regulated. <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammation specifically induced <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 in the neurons innervating <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>. In addition, blocking the <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 function significantly attenuated the hyperalgesia of the inflamed <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>. Moreover, <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammation up\u2010regulated <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2 phosphorylation only in the glials; blocking <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2 phosphorylation in the glials blocked <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 up\u2010regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Trigeminal ganglionic <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sub>v<\/jats:sub>1.7 has an important function in the hyperalgesia of the inflamed <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>, which is dependent on the communication with the satellite glials.<\/jats:p><\/jats:sec>","DOI":"10.1002\/j.1532-2149.2012.00262.x","type":"journal-article","created":{"date-parts":[[2012,12,14]],"date-time":"2012-12-14T13:04:31Z","timestamp":1355490271000},"page":"983-994","source":"Crossref","is-referenced-by-count":20,"title":["Involvement of trigeminal ganglionic <scp>N<\/scp>a<sub>v<\/sub>1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on <scp>ERK<\/scp>1\/2 phosphorylation of glial cells in rats"],"prefix":"10.1002","volume":"17","author":[{"given":"R\u2010Y.","family":"Bi","sequence":"first","affiliation":[{"name":"The Third Dental Center Peking University School and Hospital of Stomatology  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"X\u2010X.","family":"Kou","sequence":"additional","affiliation":[{"name":"The Department of Orthodontics Peking University School and Hospital of Stomatology  Beijing 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