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Unravelling epigenetic mechanisms of chronic pain

Nature Reviews Drug Discovery volume 10, pages 900–901 (2011)Cite this article

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Emerging evidence suggests that the development of chronic pain involves epigenetic modulation of gene expression, but it is unknown how this mechanism operates and which target genes are involved. Now, writing in Nature Medicine, Zhang et al. show that persistent pain suppresses transcription of a gene encoding the enzyme that synthesizes GABA (γ-aminobutyric acid), a neurotransmitter that is involved in pain pathways, through a mechanism that involves modulation of histone acetylation.

Because chronic pain is thought to be partly caused by sustained activation of descending pain-facilitatory pathways projecting from the NRM, the authors next investigated the function of GABA in the NRM. In NRM neurons from rats with persistent pain, there was a decrease in presynaptic neurotransmitter release and a decrease in GABAergic inhibitory postsynaptic currents.

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ORIGINAL RESEARCH PAPER

  1. Zhang, Z. et al. Epigenetic suppression of GAD65 expression mediates persistent pain. Nature Med. 9 Oct 2011 (doi:10.1038/nm.2442)

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  1. Charlotte Harrison
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Harrison, C. Unravelling epigenetic mechanisms of chronic pain. Nat Rev Drug Discov 10, 900–901 (2011). https://doi.org/10.1038/nrd3606

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