RESUMO
BACKGROUND: Neuropathic pain produced by nerve injury has the characteristics of enhanced pain responses - allodynia. To understand the pathophysiology of the neuropathic pain, We evaluated the effect of NMDA antagonists and chemical sympathectomy on the c-fos mRNA expression. METHODS: We have divided rats(Sprague-Dawley, N=24) that their left L5 and L6 nerve were tightly ligated into two groups. In NMDA antagonist group(N=17), We injected 10 g MK801 and 10 g 5-amino-phosphonovalerate in three ways, intrathecally before the ligation, after ligation and subcutaneous continuously. Then behavioral tests for mechanical allodynia and cold allodynia were performed. After the test of allodynia,the expression of c-fos were assessed by Northern blot hybridization. In chemical sympathectomy group(N=7), We injected 70 mg/kg guanethidine into the peritoneum in two ways, before the ligation and after ligation. Then same methods were performed in NMDA antagonist group as well. RESULTS: Intrathecal NMDA antagonists before the ligation supressed the elevation of c-fos mRNA expression. Intrathecal NMDA antagonists on the 7 days after the ligation reduced the c-fos mRNA expression and neuropathic pain. Continuous treatment of subcutaneous NMDA antagonists supressed the development of neuropathic pain and the elevation of c-fos mRNA expression. Chemical sympathectomy before the ligation did not supress the elevation of c-fos mRNA expression. Chemical sympathectomy on the 7 days after the ligation reduced neuropathic pain and the elevation of c-fos mRNA expression. CONCLUSIONS: NMDA receptor is related to the induction and maitenance of neuropatic pain, and sympathetic nervous system has a main role in the already induced neuropathic pain.