The role of injury discharge in the induction of neuropathic pain behavior in rats.

When sensory fibers are damaged, a discharge of impulses is emitted, which can last up to a few minutes. In the present study, we examined whether this injury discharge plays a role in triggering 'autotomy'--a behavior involving self-injury in animals that is induced by total denervation of a hind paw. Sensory input from the sciatic and saphenous neuroma is thought to elicit chronic pain sensations which cause the rat to injure the hind paw. In the present experiments: (1) injury discharge was prevented by using a local anesthetic block and (2) injury discharge was artificially prolonged by delivering 150 electrical pulses to the nerve just prior to transection, at a strength sufficient to drive A- and C-fibers. In one group of animals, the nerve was stimulated at 0.5 Hz at which frequency a synchronous, repetitive activity in C-fibers augments the response of some nociceptive dorsal horn neurons by temporal summation ('wind-up'). In 2 other groups, the sciatic nerve was stimulated at 0.1 Hz and 10 Hz. The results show that blocking injury discharge significantly delayed the average time of onset of autotomy and suppressed it in magnitude compared to control rats. In contrast, electrical stimulation, especially at the 'wind-up' frequency, significantly shortened the onset of autotomy and enhanced its severity. Thus, in spite of its short duration, injury discharge affects the subsequent development of neuropathic pain related behavior.