European journal of pain : EJP
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Multiple mechanisms contribute to the stimulus-evoked pain hypersensitivity that may be experienced after peripheral inflammation. Persistent pathological stimuli in many pain conditions affect the expression of certain genes through epigenetic alternations. The main purpose of our study was to investigate the role of epigenetic modification on potassium-chloride co-transporter 2 (KCC2) gene expression in the persistence of inflammatory pain. ⋯ Persistent pain suppresses KCC2 expression through HDAC-mediated histone hypoacetylation and consequently impairs the inhibitory function of inhibitory interneurons. Drugs such as HDAC inhibitors that suppress the influences of persistent pain on the expression of KCC2 may serve as a novel analgesic.
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Diabetic neuropathic pain (DNP) is severe and intractable in clinic. The specific cellular and molecular mechanisms underlying DNP remain elusive and its treatment are limited. We investigated roles of EphB1 receptor in the development of DNP. ⋯ Activation of EphB1 receptor in the spinal cord is critical to maintaining the established diabetic neuropathic pain, but not to diabetic pain induction. Spinal blocking EphB1 receptor activation suppresses ongoing diabetic neuropathic pain.