• Seung Keun Back, Jaehee Lee, Seung Kil Hong, and Heung Sik Na.
• Medical Science Research Center and Department of Physiology, Korea University College of Medicine, 126-1 Anam-dong 5 Ga, Seongbuk-Ku, Seoul 136-705, Republic of Korea.
• Pain. 2006 Jul 1; 123 (1-2): 117-26.

AbstractThe present study investigated whether the loss of spinal mu-opioid receptors following peripheral nerve injury is related to mechanical allodynia. We compared the quantity of spinal mu-opioid receptor and the effect of its antagonists, such as naloxone and CTOP, on pain behaviors in two groups of rats that showed extremely different severity of mechanical allodynia 2 weeks following partial injury of tail-innervating nerves. One group (allodynic group) exhibited robust signs of mechanical allodynia after the nerve injury, whereas the other group (non-allodynic group) showed little allodynia despite having suffered the same nerve injury. In addition, we investigated the quantity of spinal mu-opioid receptor and the effect of its antagonists on pain behaviors after the rats had recovered from mechanical allodynia 16 weeks following nerve injury. Immunohistochemical and Western blot analyses at 2 weeks after nerve injury indicated that spinal mu-opioid receptor content was more reduced in the allodynic group compared to the non-allodynic group. Intraperitoneal naloxone (2 mg/kg, i.p.) and intrathecal CTOP (10 microg/rat, i.t.) administration dramatically induced mechanical allodynia in the non-allodynic group. However, as in naïve animals, neither the loss of spinal mu-opioid receptors nor antagonist-induced mechanical allodynia was observed in the rats that had recovered from mechanical allodynia. These results suggest that the loss of spinal mu-opioid receptors following peripheral nerve injury is related to mechanical allodynia.

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