Fig. 2
The acute to chronic transition of tactile allodynia after nerve injuries. a Schematic illustration of the continuum of neuronal plasticity ranging from “activation” to “modulation” and “modification” for the development of distinct pain states. Detailed forms of neuronal plasticity for PSNs and SC-DH neurons are shown in brief. b Schematic summary of the typical “modification” processes in the SC-DH circuit underlying the development of chronic tactile allodynia after nerve injuries. CCK2, cholecystokinin type 2 receptor; EN, excitatory interneuron; F, function; IL-6, interleukin-6; IN, inhibitory interneuron; MCP-3, monocyte chemotactic protein-3; MOR, μ opioid receptor; PKCγ, protein kinase C gamma; PSN, primary sensory neuron; PTM, post-translational modification; PV, parvalbumin; RVM, rostral ventromedial medulla; S, structure; SC-DH, spinal cord dorsal horn