Brief electrical stimulation of c-fibers in rats produces thermal hyperalgesia lasting weeks.

Nerve injury produces neuropathic pain in some humans, but the nature of the signal triggering the pain is still unknown. When injured, many afferent fibers emit a prolonged discharge of action potentials. This input triggers pain disorders in rats following some, but not other types of total and partial nerve injury. In the present study we report that similar sensory disorders develop in rats by electrically stimulating an intact sciatic nerve. Robust thermal hyperalgesia and weak mechanical allodynia developed rapidly, lasting 3-5 weeks thereafter, but only when activating C-fibers. Thus, a discharge mimicking injury discharge in C-fibers, in the absence of any intended damage to the stimulated nerve, is sufficient to alter chronically central processing of sensory input.