Fig. 1

The SC-DH circuit for the transformation of touch into pain (i.e., tactile allodynia) after nerve injuries. a Neural circuit framework of neuropathic tactile allodynia based on the gate control theory of pain. b Schematic illustration of the SC-DH circuit for tactile allodynia after nerve injuries. While static tactile allodynia evoked by von Frey hairs is dependent on VT3⁻ excitatory interneurons, morphine-resistant, dynamic tactile allodynia evoked by brushing is dependent on VT3⁺ excitatory interneurons. Moreover, while TAC1⁻NK1R⁺ PTNs are sufficient for reflexive defensive reactions, TAC1⁺NK1R⁺ PTNs are necessary for sustained pain-associated coping behaviors. CCK, cholecystokinin; CR, calretinin; CST, corticospinal tract; DRG, dorsal root ganglion; EN, excitatory interneuron; IN, inhibitory interneuron; LTMR, low-threshold mechanoreceptor; MRGPRD, MAS related GPR family member D; MSC, myelinated Schwann cell; NK1R, neurokinin 1 receptor; PKCγ, protein kinase C gamma; PSDCN, postsynaptic dorsal column neuron; PTN, pain transmission neuron; RORα, retinoid receptor-related orphan receptor; SC-DH, spinal cord dorsal horn; SCTN, spino-cervical tract neuron; SOM, somatostatin; TAC1, preprotachykinin 1; TRPV1, transient receptor potential cation channel, subfamily V, member 1; VT3, vesicular glutamate transporter 3