I will bring special attention to the mechanisms underlying spontaneous ectopia developed at the axons of identified primary afferents, as each fiber type is likely responsible for a distinct positive symptom during neuropathy. I will present experimental evidence showing that, in experimental models of traumatic nerve injury, both damaged and neighbouring intact nociceptors develop ectopic spontaneous discharge that, besides irregular ongoing firing, also follow different patterns such as bursts or clock-like/pacemaker beats. Changes in conductive properties and excitability in peripheral afferents might necessarily have an impact on second-order neurons, thereby contributing to central sensitization. Thanks to pharmacological modulation of ectopic discharges in preclinical studies, we are identifying molecular substrates underlying nociceptor hyperexcitability (such as Kv7 and HCN channels).