We examined whether signals from the neuroma or the dorsal root ganglion of
the injured segment are critical for the generation of neuropathic pain. T
o this aim, we used a rat model of peripheral neuropathy made by transectin
g the inferior and superior caudal trunks at the level between the S1 and S
2 spinal nerves under enflurane anesthesia. These animals displayed tail-wi
thdrawal responses to normally innocuous mechanical stimulation applied to
the tail with a von Prey hair (2 g). Also, these animals, compared to pre-s
urgical value, displayed shorter tail-withdrawal latencies following immers
ion of the tail to warm (40 degrees C) or cold (4 degrees C) water. Transec
tion of the S1 spinal nerve between the dorsal root ganglion and neuroma di
d not change the behavioral signs of neuropathic pain. In contrast, S1 dors
al rhizotomy significantly reduced the behavioral signs. The data suggest t
hat signals arising from the dorsal root ganglion cells of the injured segm
ent, but not from the neuroma, are critical for the generation of neuropath
ic pain in this model. (C) 2000 Published by Elsevier Science Ireland Ltd.