Pain research is currently undergoing dramatic changes. In the area of basic pain research, new discoveries have been made towards the understanding of pain transmission, modulation and plasticity. However, many of these basic discoveries have not yet led to the development of new drugs for the treatment of chronic pain. One major reason for this disconnection is the lack of translational research and drug discovery based directly on the novel pain mechanism. In this review, I focus on activity-dependent potentiation in pain-related cortical areas and recent translational research on adenylyl cyclase subtype 1 (AC1) as a novel target for treating chronic pain. In particular, I discuss the AC1 inhibitor, NB001, which produces powerful analgesic effects in animal models of chronic pain by inhibiting chronic pain-related cortical potentiation.
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