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In the present study, the modulatory effects of<jats:styled-content style=\"fixed-case\"><jats:italic>N<\/jats:italic><\/jats:styled-content>\u2010methyl\u2010<jats:sc>d<\/jats:sc>\u2010aspartate receptors (<jats:styled-content style=\"fixed-case\">NMDA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>s) and magnesium were investigated in<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>arthritis hypernociception. Male Wistar rats received an intra\u2010articular injection of carrageenan (<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>g) in the<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>, and mechanical hypernociception was measured. The<jats:styled-content style=\"fixed-case\">NMDA\u2010R<\/jats:styled-content>antagonist,<jats:styled-content style=\"fixed-case\">MK<\/jats:styled-content>\u2010801, and magnesium chloride (<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>g<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>l<jats:sub>2<\/jats:sub>) were administered before arthritis induction. Magnesium deficiency was promoted by feeding rats a synthetic magnesium\u2010free diet for 9\u00a0d before injection of<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>g. The<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>g induced mechanical hypernociception that lasted for 120\u00a0h. MK\u2010801 inhibited this hypernociceptive state. MgCl<jats:sub>2<\/jats:sub>pretreatment prevented<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>g\u2010induced hypernociception and altered the nociceptive threshold in the absence of<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>g. Magnesium deficiency increased hypernociception and induced spontaneous hypernociceptive behavior. TMJ arthritis increased the expression of<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>for all<jats:styled-content style=\"fixed-case\"><jats:italic>NMDA\u2010R<\/jats:italic><\/jats:styled-content>subunits and immunostaining of phosphorylated<jats:styled-content style=\"fixed-case\">NR<\/jats:styled-content>1 (phospho\u2010<jats:styled-content style=\"fixed-case\">NR<\/jats:styled-content>1). MgCl<jats:sub>2<\/jats:sub>inhibited expression of<jats:styled-content style=\"fixed-case\">NR<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">B mRNA<\/jats:styled-content>and phospho\u2010NR1 immunostaining and increased expression of NR3<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>. Magnesium deficiency increased expression of both<jats:styled-content style=\"fixed-case\">NR<\/jats:styled-content>1 and<jats:styled-content style=\"fixed-case\">NR<\/jats:styled-content>3<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>s and phospho\u2010<jats:styled-content style=\"fixed-case\">NR<\/jats:styled-content>1 immunostaining in the trigeminal subnucleus caudalis. We found that magnesium modulates nociceptive behavior and induces<jats:styled-content style=\"fixed-case\"><jats:italic>NMDA\u2010R<\/jats:italic><\/jats:styled-content>subunit rearrangement in the subnucleus caudalis. The present results may lead to a better understanding of central processing in the nociceptive trigeminal pathway and the development of new approaches to treat orofacial pain with a<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>origin.<\/jats:p>","DOI":"10.1111\/eos.12093","type":"journal-article","created":{"date-parts":[[2013,11,9]],"date-time":"2013-11-09T08:19:28Z","timestamp":1383985168000},"page":"573-583","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Role of<scp>NMDA<\/scp>receptors in the trigeminal pathway, and the modulatory effect of magnesium in a model of rat temporomandibular joint arthritis"],"prefix":"10.1111","volume":"121","author":[{"given":"Andr\u00e9 L. 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