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 t
ypes of total and partial nerve injury. In the present study we report
that similar sensory disorders develop in rats by electrically stimul
ating an intact sciatic nerve. Robust thermal hyperalgesia and weak me
chanical allodynia developed rapidly, lasting 3-5 weeks thereafter, bu
t only when activating C-fibers. Thus, a discharge mimicking injury di
scharge in C-fibers, in the absence of any intended damage to the stim
ulated nerve, is sufficient to alter chronically central processing of
sensory input. (C) 1998 Elsevier Science Ireland Ltd.