The epigenetic signature of chronic pain in the mouse brain

Background Peripheral nerve injury can be accompanied by long-term pain-related manifestations, such as affective and cognitive disturbances, suggesting the involvement of supraspinal mechanisms. One particular region of interest is the prefrontal cortex (PFC), an area implicated in depression, anxiety and cognitive impairment, all of which are frequently associated with chronic pain [1-4]. Clinically, pathological pain-related changes in the PFC in individuals with chronic low back pain can be reversed following effective pain management [5]. However, the mechanisms behind pain-induced brain plasticity remain poorly understood. Epigenetics is a term used to describe modifications to genomic DNA that alter gene expression. DNA methylation is an epigenetic mechanism that is involved in gene regulation mainly by silencing promoter activity. We propose that long-term alterations in DNA methylation could provide a molecular substrate for chronic pain-related changes in the CNS, forming a ‘‘memory trace’’ for pain in the brain.