论文部分内容阅读
Neuropathic pain is a refractory disease characterized by maladaptive changes in gene transcription and translation within the sensory pathway.Long noncoding RNAs(lncRNAs)are emerging as new players in gene regulation,but how lncRNAs operate in the development of neuropathic pain is unclear.Here we identify a conserved lncRNA for Kv1.2(named Kv1.2 antisense RNA)in first-order sensory neurons of dorsal root ganglion(DRG).Peripheral nerve injury increases Kv1.2 antisense RNA expression in injured DRG through activation of myeloid zinc finger protein 1,a transcription factor that binds to Kv1.2 antisense RNA gene promoter.Mimicking this increase downregulates Kv1.2,reduces total Kv current,increases excitability in DRG neurons,and produces neuropathic pain symptoms.Blocking this increase reverses nerve injury-induced downregulation of DRG Kv1.2 and attenuates development and maintenance of neuropathic pain symptoms.These findings suggest native Kv1.2 antisense RNA as a new therapeutic target for the treatment of neuropathic pain.