Objective: To investigate the role of spinal glial cells activation in neuropathic pain in a recently developed spared nerve injury (SNI) animal model by Decosterd and Woolf. Methods: A lesion was made to two of the t...Objective: To investigate the role of spinal glial cells activation in neuropathic pain in a recently developed spared nerve injury (SNI) animal model by Decosterd and Woolf. Methods: A lesion was made to two of the three terminal branches of the sciatic nerve of rats (tibial and common peroneal nerves) leaving the sural nerve intact. Continuous intrathecai administration of propentofyliine, a glial modulating agent, 1 d before and 5 d after operation, was performed to disrupt spinal cord glia function. The vehicle was intrathecally administrated as control. The paw withdrawal threshold to mechanical stimulation (paw withdrawal mechaical threshold PWMT), body mass and motor function were determined pre- and post-surgery. Results: It produced a prolonged mechanical allodynia in the medial and lateral part of the ipsilateral hind paw in SNL models. The treatment with propentofylline significantly prevented the development of mechanical allodynia located in either medial or lateral plantar surface. Rats in two groups showed normal motor function and body weight increase. Conclusion:SNI model can be applied as a useful method with little variance in searching the mechanism of neuropathic pain. These study suggest that spinal glia activation may contribute to mechanical allodynia induced by SNI.展开更多
目的：研究自发性高血压大鼠降压前后的机械痛阈和热痛阈改变.方法：15只自发性高血压大鼠在实验 d 4～11肌注利血平注射液（1 μg·kg^-1·d^-1）.血压、机械刺激缩足反应阈值和热刺激缩足反应潜伏期作为观察指标.结果：自发...目的：研究自发性高血压大鼠降压前后的机械痛阈和热痛阈改变.方法：15只自发性高血压大鼠在实验 d 4～11肌注利血平注射液（1 μg·kg^-1·d^-1）.血压、机械刺激缩足反应阈值和热刺激缩足反应潜伏期作为观察指标.结果：自发性高血压大鼠经利血平降压治疗后血压明显下降约 50 mmHg 左右,机械痛阈和热痛阈均降低（P＜0.05）.结论：自发性高血压可能对自发性高血压大鼠的伤害性感受系统存在可逆的结构和（或）功能影响.展开更多
文摘Objective: To investigate the role of spinal glial cells activation in neuropathic pain in a recently developed spared nerve injury (SNI) animal model by Decosterd and Woolf. Methods: A lesion was made to two of the three terminal branches of the sciatic nerve of rats (tibial and common peroneal nerves) leaving the sural nerve intact. Continuous intrathecai administration of propentofyliine, a glial modulating agent, 1 d before and 5 d after operation, was performed to disrupt spinal cord glia function. The vehicle was intrathecally administrated as control. The paw withdrawal threshold to mechanical stimulation (paw withdrawal mechaical threshold PWMT), body mass and motor function were determined pre- and post-surgery. Results: It produced a prolonged mechanical allodynia in the medial and lateral part of the ipsilateral hind paw in SNL models. The treatment with propentofylline significantly prevented the development of mechanical allodynia located in either medial or lateral plantar surface. Rats in two groups showed normal motor function and body weight increase. Conclusion:SNI model can be applied as a useful method with little variance in searching the mechanism of neuropathic pain. These study suggest that spinal glia activation may contribute to mechanical allodynia induced by SNI.
