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The feature is partly explained by the evidence of epigenetic repression of <jats:styled-content style=\"fixed-case\">Na<jats:sub>v<\/jats:sub><\/jats:styled-content>1.8 sodium channel in the dorsal root ganglion (<jats:styled-content style=\"fixed-case\">DRG<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>We investigated the possibility of trichostatin <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">TSA<\/jats:styled-content>), valproic acid (<jats:styled-content style=\"fixed-case\">VPA<\/jats:styled-content>) and suberoylanilide hydroxamic acid (<jats:styled-content style=\"fixed-case\">SAHA<\/jats:styled-content>) to reverse the unique <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>\u2010fibre sensitivity observed following partial ligation of sciatic nerve in mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Nerve injury\u2010induced down\u2010regulation of <jats:styled-content style=\"fixed-case\">DRG Na<jats:sub>v<\/jats:sub><\/jats:styled-content>1.8 sodium channel and <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>\u2010fibre\u2010related hypoesthesia were reversed by <jats:styled-content style=\"fixed-case\">TSA<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">VPA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">SAHA<\/jats:styled-content> treatments, which inhibit histone deacetylase (<jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>), and increase histone acetylation at the regulatory sequence of <jats:styled-content style=\"fixed-case\">Na<jats:sub>v<\/jats:sub><\/jats:styled-content>1.8.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Implications<\/jats:title><jats:p>Taken together, these studies provide the evidence that hypoesthesia and underlying down\u2010regulation of <jats:styled-content style=\"fixed-case\">Na<jats:sub>v<\/jats:sub><\/jats:styled-content>1.8, negative symptoms observed in nerve injury\u2010induced neuropathic pain models are regulated by an epigenetic chromatin remodelling through <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\u2010related machineries.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.12366","type":"journal-article","created":{"date-parts":[[2013,8,30]],"date-time":"2013-08-30T09:56:09Z","timestamp":1377856569000},"page":"991-998","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":72,"title":["<scp>HDAC<\/scp> inhibitors restore <scp>C<\/scp>\u2010fibre sensitivity in experimental neuropathic pain model"],"prefix":"10.1111","volume":"170","author":[{"given":"Yosuke","family":"Matsushita","sequence":"first","affiliation":[{"name":"Department of Molecular Pharmacology and Neuroscience Nagasaki University Graduate School 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