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目的:研究N-甲基-D-天冬氨酸(NMDA)受体2B型受体(NR2B)参与脊髓损伤后慢性神经病理性痛的机制。方法:制作脊髓半横断大鼠模型,von Frey纤维丝测量机械性刺激缩足阈值变化,Western Blot观察脊髓背角NR2B表达时程变化;同时采用行为药理学方法,鞘内给予NR2B特异性拮抗剂ifenprodil,观察对机械性刺激缩足阈值及NR2B表达的影响。结果:脊髓半横断术后大鼠双侧后足出现触诱发痛状态,NR2B在腰段脊髓双侧背角表达上调。鞘内给予ifenprodil逆转了大鼠的痛敏状态,伴随着NR2B在脊髓背角表达下调。结论:NR2B可能参与脊髓损伤后慢性神经病理性痛的发生发展,特异性拮抗NR2B可能是临床治疗脊髓损伤致慢性神经病理性痛的潜在策略。
Objective: To investigate the mechanism of N-methyl-D-aspartate (NMDA) receptor type 2B receptor (NR2B) involved in chronic neuropathic pain after spinal cord injury. Methods: The rat model of spinal cord transection was made. Von Frey filament was used to measure the threshold of mechanical stimulus. Western Blot was used to observe the time course of NR2B expression in spinal dorsal horn. Meanwhile, behavioral pharmacology was used to intrathecally administrate NR2B-specific antagonist Ifenprodil, observe the impact of mechanical stimulus threshold reduction and NR2B expression. Results: The bilateral hindpaw of the rats with spinal cord hemisection showed tactile and painful conditions. The expression of NR2B in the bilateral dorsal horn of the lumbar spinal cord was up-regulated. Intrathecal administration of ifenprodil reversed the hyperalgesia in rats, accompanied by a downregulation of NR2B expression in the dorsal horn of the spinal cord. CONCLUSIONS: NR2B may be involved in the development of chronic neuropathic pain after spinal cord injury. Specific antagonism of NR2B may be a potential strategy for clinical treatment of chronic neuropathic pain induced by spinal cord injury.