The activity of myelinated primary afferents was recorded from the dorsal roots 1–3 days after creation of a painful peripheral neuropathy in rats. The effects on spontaneous discharge of acute transections at various points along the injured sciatic nerve and the dorsal root were determined, as were the effects of K⁺ channel blockers applied topically to two putative sites of impulse origin: the injured region of the nerve and the dorsal root ganglion (DRG). Transections just proximal to the nerve injury and just distal to the DRG failed to halt the discharge, but spontaneous discharge disappeared when the transection was made just proximal to the DRG (i.e. between the DRG and recording electrode). K⁺ channel blockers (4-aminopyridine and gallamine triethiodide) applied to the DRG increased the frequency of spontaneous discharge or initiated activity from silent fibers. Applications of K⁺ channel blockers to the injured region of the nerve were without effect. Thus, the spontaneous discharge and the sensitivity to K⁺ channel blockade seen in Aβ and Aδ primary afferents at the time of the onset of the neuropathic pain syndrome appear to originate in the DRG.