神经病理性痛大鼠海马突触长时程增强的变化

目的 探讨神经病理性痛大鼠海马突触长时程增强(LTP)的变化.方法 成年雄性Wistar大鼠18只,体重190～240 g,随机分为3组(n=6):对照组(C组)、假手术组(S组)和神经病理性痛组(NP组).采用结扎左侧L4,5脊神经的方法 制备大鼠神经病理性痛模型.对照组不制备模型;假手术组仅暴露左侧L4,5脊神经.于模型制备后7、14和21 d时观察大鼠痛行为学及足部形态;于模型制备前(基础状态)、制备后7、14和21 d时测定痛阈;于最后一次痛阈测定结束后3 d时记录海马CA1区兴奋性突触后电位(EPSP),以高频刺激(HFS)诱发LTP,LTP为HFS后EPSP峰值较基础值增大10%以上且维持时间≥60 min,行LTP分级,以评价其程度.结果 NP组模型制备后痛阈低于基础值及C组和S组,LTP程度高于C组和S组(P<0.05).结论 神经损伤可易化大鼠海马CA1区突触LTP,提示神经病理性痛可能与海马突触LTP的易化有关.

Changes in synaptic long-term potentiation in hippocampus in rats with neuropathic pain

Objective To investigate the changes in hippocampal synaptic long-term potentiation (LTP) in rats with neuropathic pain. Methods Eighteen adult male Wistar rats weighing 190-240 g were randomly divided into 3 groups (n = 6 each) : group Ⅰ control (C) ;group Ⅱ sham operation (S) and group Ⅲ neuropathic pain (NP). The animals were anesthetized with intraperitoneal pentobarbital 50 mg/kg. Neuropathic pain was produced by ligation of the left L4.5 spinal nerve. In group S the left L4.5spinal nerve was exposed but not ligated. The behaviour of the rats was evaluated. The pain threshold was measured by electric stimulation. The animals were placed in a special box with a floor made up of 18 steel bars of 0.5 cm in diameter at intervals of 1.2 cm, through which electric stimulation was induced. The intensity of electric stimulation was increased from 0.1 mA to 0.8 mA step by step until the animals screamed and lifted their hind limbs. The stimulation was repeated 6 times. The mean value was taken as pain threshold. Pain threshold was measured before surgery and at 7, 14 and 21 d after surgery. The excitatory postsyuaptie potential (EPSP) in hippocampal CA1 region was measured at 3 days after last measurement of pain threshold. The animals were anesthetized and a hole was drilled in the skull. The recording electrodes were inserted into hippocampal CAI region using stereotaxic technology. The changes in EPSP and input/output (I/O) eurve and LTP were observed. Results The pain threshold was significantly decreased after surgery as compared with the baseline in NP group (group Ⅲ) find was significantly lower than in group C and S. The magnitude of LTP was significantly greater in NS group than in group C and S (P < 0.05). Conclusion Spinal nerve injury can facilitate LTP induction in the hippocampal CAI region, indicating that the facilitation of LTP is involved in the mechanism of neuropathie pain.