We study the hypothesis according to which plasticity in pain signaling and modulating pathways contributes to long-lasting neuropathic pain, which is a common clinical problem. We study plasticity of pain transduction and transmission mechanisms that are of importance for carrying ascending pain signals. Moreover, we study plasticity in descending pain regulation, such as that originating in the amygdala, a major player in emotions. The results potentially help to develop new diagnostic and therapeutic methods for chronic pain. Among experimental methods used are in vivo electrophysiology, neuropharmacological manipulations and behavioral analyses.