Cumulating evidence indicated that chronic pain-associated cellular and molecular changes play an essential role in contributing to the development of social defect symptoms, and more recent findings implicated the critical role of epigenetic mechanisms in chronic pain-related sensitization. Histone variant exchange, in which canonical histones are replaced with their variant counterparts, is an entire branch of epigenetics that has received limited attention in the brain and has never, to our knowledge, been studied in relation to pain-related social defect. Here we hypothesize that H2A.Z, a variant of histone H2A, is actively involved in the regulation of chronic pain related social defect symptoms, probably through downstream effects on gene expression. We hope the histone variant H2A.Z regulation may contribute to the molecular basis of cognitive function and serve as a potential therapeutic target for associated social defect.
H2A.Z, Epigenetic, Pain, Social Defect
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