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• W2898074363 abstract "Chronic pain is a phenomenon that neurosurgeons are well acquainted with and that is notoriously difficult to treat. The pathophysiology of the transition from acute to chronic pain is complex, featuring a combination of social, psychological, and physiological changes that remain frustratingly hard to pick apart. Moreover, few options exist for pharmacological treatment. A recent study by Garriga et al1 in the Journal of Neuroscience helps elucidate some of the epigenetic modifications that occur in neuronal cell bodies as patients transition from acute to chronic pain states. The authors created chronic neuropathic pain in rats and measured the degree of DNA methylation in the dorsal root ganglion. Subjects underwent surgical left-sided L5/L6 spinal nerve ligation and sham surgery on the contralateral side (without nerve ligation). A second group of subjects underwent intrathecal paclitaxel treatment for induction of neuropathic pain sensitivity. The presence of allodynia was confirmed using microfilaments and pressure stimuli applied to the hind paws and checking for signs of paw withdrawal and/or vocalization. The investigators discovered DNA methylation changes both in the acute (3 d post-injury) and chronic (3 wk post-injury) pain stages, with 1% of possible CpG sites showing methylation changes in the acute phase (4.6% of all CpG sites showing increased methylation and 3% showing loss of methylation; Figure). In contrast, the chronic pain stage was associated with a predominantly hypomethylated state, with up to 14% of possible CpG sites showing methylation changes (11.2% showing hypomethylation vs. 2.9% showing hypermethylation). These sites were consistent across multiple subjects, appeared to be distributed across all chromosomes, and were associated with increased gene expression variability. Notably, this work found epigenetic changes in the brain and spinal cord; however, these were less pronounced and trended toward hypermethylation. Lastly, paclitaxel treatment did not induce the same methylation changes. Further supporting that DNA hypomethylation is sufficient to induce pain sensitivity, the investigators injected intrathecal DNA methyltransferase inhibitor (RG108) into naïve subjects, resulting in increased pain-sensitivity. Similarly, feeding the rats with a folate and B12-poor diet—decreasing available methyl donors—reduced pain thresholds in experimental nerve-ligation animals.FIGURE.: DNA methylation changes at A, 3 d and B, 3 wk in spinal nerve root ligated dorsal root ganglion compared to contralateral controls. Dark points show hypomethylated sites while as orange dots show hypermethylated sites. These methylation changes show correlation from the acute to chronic states across 17 869 CpG sites (C, r = 0.62). In a separate DNA methylation analysis by RRBS assay, chronic pain states also D, demonstrate gross hypomethylation changes, and E, changes in a variety of different genomic sites. Republished with permission of Society for Neuroscience, from Nerve injury-induced chronic pain is associated with persistent DNA methylation reprogramming in dorsal root ganglion, Garriga J, Laumet G, Chen SR, et al, copyright July 2018,1 permission conveyed through Copyright Clearance Center, Inc.These findings explore a new and potentially important pathophysiological mechanism of chronic pain. As patients and physicians struggle to deal with the refractory nature of most chronic pain, these findings suggest a potential future avenue for pharmacological treatment." @default.
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• W2898074363 date "2018-10-15" @default.
• W2898074363 modified "2023-10-17" @default.
• W2898074363 title "Chronic Neuropathic Pain Induces DNA Methylation Changes in the Dorsal Root Ganglion" @default.
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• W2898074363 doi "https://doi.org/10.1093/neuros/nyy403" @default.
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