A review of dorsal root ganglia and primary sensory neuron plasticity mediating inflammatory and chronic neuropathic pain

•Central and peripheral mechanisms mediate both inflammatory and neuropathic pain.•DRGs represent an important peripheral site of plasticity driving neuropathic pain.•Changes in ion channel/receptor function are critical to nociceptor hyperexcitability.•Peripheral BDNF-TrkB signaling contributes to neuropathic pain after SCI.•Understanding peripheral mechanisms may reveal relevant clinical targets for pain.