title: Epigenetic mechanisms of chronic pain.
abstract: Neuropathic and inflammatory pain promote a large number of persisting adaptations at the cellular and molecular level, allowing even transient tissue or nerve damage to elicit changes in cells that contribute to the development of chronic pain and associated symptoms. There is evidence that injury-induced changes in chromatin structure drive stable changes in gene expression and neural function, which may cause several symptoms, including allodynia, hyperalgesia, anxiety, and depression. Recent findings on epigenetic changes in the spinal cord and brain during chronic pain may guide fundamental advances in new treatments. Here, we provide a brief overview of epigenetic regulation in the nervous system and then discuss the still-limited literature that directly implicates epigenetic modifications in chronic pain syndromes.
authors.affiliation: Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
authors.forename: Giannina
authors.initials: G
authors.lastname: Descalzi
authors.affiliation: Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan.
authors.forename: Daigo
authors.initials: D
authors.lastname: Ikegami
authors.affiliation: Division of Epigenomics, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan; Life Science Tokyo Advanced Research Center (L-StaR), 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan.
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Ushijima
authors.affiliation: Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Nestler
authors.affiliation: Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: venetia.zachariou@mssm.edu.
authors.forename: Venetia
authors.initials: V
authors.lastname: Zachariou
authors.affiliation: Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan; Life Science Tokyo Advanced Research Center (L-StaR), 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan. Electronic address: narita@hoshi.ac.jp.
authors.forename: Minoru
authors.initials: M
authors.lastname: Narita
mesh_terms: D000818:Animals; D059350:Chronic Pain / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology / Q000523:psychology; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic / Q000235:genetics*; D006657:Histones / Q000378:metabolism / Q000502:physiology; D006801:Humans
chemical_list: D006657:Histones
keywords: HDAC; animal models; histone modifications; inflammatory pain; methylation; miRNA; neuropathic pain