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"More recent studies demonstrated that the reduced BK channel activity in DRG neurons after nerve injury is mediated by the increased BDNF through epigenetic and transcriptional mechanisms, and this BDNF-associated epigenetic regulation on pain is strongly related to the histone H3 and H4 acetylation at BDNF promoter I in the DRG that initiated at day 1 post-injury and lasted for 7 days [57]."