• H S Na, K H Ko, S K Back, B Sung, D J Yoo, and S K Hong.
• Neuroscience Research Institute and Department of Physiology, Korea University College of Medicine, 126-1, Anam-dong 5 ga, Sungbuk-gu, 136-705, Seoul, South Korea. hsna@kuccnx.korea.ac.kr
• Neurosci. Lett. 2000 Jul 14; 288 (2): 147-50.

AbstractWe examined whether signals from the neuroma or the dorsal root ganglion of the injured segment are critical for the generation of neuropathic pain. To this aim, we used a rat model of peripheral neuropathy made by transecting the inferior and superior caudal trunks at the level between the S1 and S2 spinal nerves under enflurane anesthesia. These animals displayed tail-withdrawal responses to normally innocuous mechanical stimulation applied to the tail with a von Frey hair (2 g). Also, these animals, compared to pre-surgical value, displayed shorter tail-withdrawal latencies following immersion of the tail to warm (40 degrees C) or cold (4 degrees C) water. Transection of the S1 spinal nerve between the dorsal root ganglion and neuroma did not change the behavioral signs of neuropathic pain. In contrast, S1 dorsal rhizotomy significantly reduced the behavioral signs. The data suggest that signals arising from the dorsal root ganglion cells of the injured segment, but not from the neuroma, are critical for the generation of neuropathic pain in this model.

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