摘要
目的 :观察神经病理痛大鼠脊髓背角突触传递可塑性的变化 ,阐明在伤害性刺激及神经损伤时“中枢敏化”(centralsensitization)在神经病理疼痛中的作用。方法 :将Sprague Dawley大鼠的腰 5 /腰 6 (L5 /L6 )脊神经紧结扎造成神经病理痛模型 ,采用电生理学技术记录脊髓背角C 纤维诱发场电位 ,比较模型组与假手术对照组大鼠脊髓背角C 纤维诱发电位LTP诱导的差异。结果 :(1)在神经病理痛大鼠 ,高频、低强度的条件电刺激 (频率 10 0Hz,波宽 0 .5ms,强度 10V ,串长 1s ,串间隔 10s的 4串电刺激 )作用于坐骨神经即可诱导脊髓背角C 纤维诱发电位产生LTP ;然而在假手术对照组大鼠 ,同样的刺激则不能诱导LTP的产生 ,只有高频、高强度的条件电刺激 (强度30～ 4 0V ,其余参数同上 )作用于坐骨神经才可诱导脊髓背角C 纤维诱发电位产生LTP。 (2 )与假手术对照组大鼠相比 ,神经病理痛大鼠脊髓背角C 纤维场电位的诱发阈值显著降低 ,而幅值显著升高。结论 :神经损伤情况下 ,在脊髓背角更容易诱导出C 纤维诱发场电位的LTP ,使脊髓伤害性感觉的突触产生“超敏变化”。
Objective: To observe the change in induction of long term potentiation (LTP) of C fiber evoked potentials in the spinal dorsal horn of neuropathic pain rats, examine the changes in plasticity of synaptic transmission, and explore the effects and mechanisms of central sensitization and neuropathic pain following noxious stimulation or nerve injury. Methods: Neuropathic pain model was produced by tight ligation of the L5/L6 spinal nerve in Sprague Dawley rats and the control group rats were received sham operation. The C fiber evoked field potentials in rat spinal dorsal horn were recorded by extracellular recording techniques. The differences in induction of LTP of C fiber dorsal horn field potentials in sham operated and neuropathic pain rats were compared. Results: (1) In neuropathic pain rats, the LTP in the dorsal horn was induced by high frequency, low intensity conditioning stimulation (100 Hz, 10 V, 0.5 ms, given in 4 trains of 1 s duration at 10 s intervals) of the sciatic nerve, while the same stimulation couldn't induce LTP in sham operated rats. The LTP could only be induced by high frequency, high intensity conditioning stimulation (100 Hz, 30～40 V, 0.5 ms, given in 4 trains of 1 s duration at 10 s intervals) of the sciatic nerve in these control rats. (2) The thresholds for evoking C fiber dorsal horn field potentials were significantly lower and the amplitudes tended to be higher in neuropathic pain rats as compared to controls. Conclusion: These data suggest that the nerve injury itself is likely to induce a state of hyperexcitability at the spinal nociceptive synapses, and further support the notion that the long term synaptic plasticity and the central sensitization may contribute to the development of neuropathic pain.
出处
《北京大学学报（医学版）》
CAS
CSCD
北大核心
2003年第3期226-230,共5页
Journal of Peking University:Health Sciences
基金
国家重点基础研究发展规划项目 (G19990 5 40 0 0 )
国家自然科学基金 ( 3 983 0 160
3 0 170 3 19
3 0 2 40 0 5 9)资助~~
关键词
神经痛
中枢敏化
脊髓背角C纤维
长时程可塑性
神经损伤
Neuralgia/physiopathol
Long term potentiation
Central sensitization
Plasticity
Spinal cord/physiopathol
