Partial peripheral nerve injury sometimes lead to chronic neuropathic pain. This pain is characterized by spontaneous pain accompanied by allodynia and hyperalgesia lasting for varying durations.
To investigate the mechanisms underlying neuropathic pain, we have developed a new rat model for peripheral neuropathy by resecting the superior caudal trunk at the level between S1 and S2 spinal nerves. Although this model is characterized by less injured nerves compared to our old model made by cutting the inferior caudal trunk at the level between S3 and S4 spinal nerves, it still produces strong signs of neuropathic pain, i.e., tail-flick responses to innocuous mechanical stimuli applied to certain spot(s) of the tail with von Frey hairs (mechanical allodynia) and tail flicks or tail flick like responses following immersion of the tail to cold (40°C) or warm (40°C) water (thermal allodynia). Using this new model, we examined the signals from the injured site of the nerve and the dorsal root ganglion cells of the injured nerve which is critical for generation of the neuropathic pain.
To block transmission of the electrical signals arising from the very injured site of the nerve, the neuroma produced in this site was severed with scissors or soaked with bupivacaine. None of these manipulations resulted in alleviation of the signs of neuropathic pain. In contrast, cutting the dorsal root at S1 level (i.e.,
S1 dorsal rhizotomy) significantly reduced or completely removed the neuropathic signs.
These data strongly suggest that signals from the dorsal root ganglion cells, not from the injured site, are crucial for generation of the neuropathic pain.

KeywordsNeuropathic pain, Dorsal root ganglion, Neuroma, Allodynia