神经损伤引发实验大鼠痛觉及初级感觉神经元的电生理变化

Nerve Injury Causes Hyperalgesia and Electric-physiologic Variance Hyperexcitability of the Injured Primary Sensory Neurons on Rats

目的：研究神经损伤后，大鼠的痛觉行为改变及初级感觉神经元的电生理变化。方法：用大鼠慢性压迫性神经损伤（Chmnic Constriction Injury，CCI）的痛觉实验模型，正常大鼠为对照，观察大鼠的热痛敏行为；以胞内电生理记录法检测损伤神经元及正常神经元的膜电位特征及其变化。结果：模型组大鼠的损伤侧肢体的缩腿反应潜伏期较对照侧明显缩短；损伤神经元的静息膜电位移向去极化方向且激发动作电位所需阈强度减小。结论：神经损伤可引起大鼠的热痛敏行为，损伤神经元有异位自发放电产生，其兴奋性增加是行为异常的主要成因。

Objective To study the change of pain conduct and variety of electric physiology property of the primary sensory neurons caused by. nerve injury on rats. Methods The rats that received an operation on sciatic nerve to cause nerve chronic constriction injury were used as the pain model of the tested group, and the normal rats as the control group. The hyperalgesia behavior of rats was measured. The electric physiologic property of membrane of the injured and normal primary sensory neurons was studied by intracellular recording technique. Results The withdrawal reflex latency of the injured limb was short comparing with another lateral on CCI rats. The rest membrane potential of injured neurons moved to the depolarizing direction, and its rheobase to kindling a single action potential decreased also, Conclusion The hyperalgesia was resulted by nerve injury. There were ectopic spontaneous discharges on injured primary sensory neurons coming from CCI rats. The ectopic spontaneous discharges hinted hyperexcitability of injured neurons, which is the cause of hyperalgesia.