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Review
. 2015 Apr;38(4):237-46.
doi: 10.1016/j.tins.2015.02.001. Epub 2015 Mar 9.

Epigenetic mechanisms of chronic pain

Giannina Descalzi  1 , Daigo Ikegami  2 , Toshikazu Ushijima  3 , Eric J Nestler  1 , Venetia Zachariou  4 , Minoru Narita  5
Affiliations
Review

Epigenetic mechanisms of chronic pain

Giannina Descalzi et al. Trends Neurosci. 2015 Apr.

Erratum in

  • Trends Neurosci. 2015 Sep;38(9):579

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.

Keywords: HDAC; animal models; histone modifications; inflammatory pain; methylation; miRNA; neuropathic pain.

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Figures

Figure 1
Figure 1. Epigenetic abnormality in the spinal cord during neuropathic pain
Long-term increases in chemokine expression may cause epigenetic modifications in the spinal cord, and thus may have a crucial role in chronic pain mechanisms. Nerve injury activates primary afferent nociceptors, which transmit information to the dorsal horn of the spinal cord. Activation of secondary neurons in spinal pathways by long-term chemokine expression can induce epigenetic modifications that may produce central sensitization leading to a neuropathic pain-like state. Reproduced from (30).
See this image and copyright information in PMC

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