中文摘要：

目的：利用在体神经纤维电生理技术记录大鼠背根神经节（DRG）持续受压（CCD）后的异位放电情况，明确瞬时感受器电位离子通道4（TRPV4）是否参与了CCD后受损DRG的异位放电。方法：共采用35只Wistar大鼠。制备大鼠DRG的CCD模型，分别于术前和术后测量损伤侧的机械痛阈和热辐射刺激缩爪反应潜伏期。利用在体神经纤维电生理技术分别记录正常组大鼠DRG及CCD组、CCD＋钌红（RR）组、CCD＋佛波醇（4α—PDD）组受损DRG神经元的异位放电情况。结果：持续压迫明显降低大鼠损伤侧的机械痛阈和热辐射刺激缩爪反应潜伏期（n=30，P〈0．051；CCD组可以记录到受损DRG神经元的异位放电，放电率约为67％，而正常组DRG的异位放电率约为4．5％；以TRP家族阻断剂钌红（RR）100μm孵育受损DRG，较CCD组受损DRG神经元异位放电的频率和波幅均明显下降（n=10，P〈0．05）；以TRPV4特异性激动剂佛波醇（4d—PDD）10μm孵育受损DRG，较CCD组受损DRG异位放电频率和波幅均明显增加（n=10，P〈0．05）。结论：CCD后受损DRG可出现异位放电，TRPV4参与了CCD后受损DRG的异位放电。

英文摘要：

Objective： To investigate the role of transient receptor potential vanilloid 4 （TRPV4） in mediating the ectopic discharges of the injured dorsal root ganglion（DRG） with chronic compression.Method： A total of 35 Wistar rats were used. Chronic compression of dorsal root ganglion（CCD） model was established. Mechanical withdrawal threshold and thermal withdrawal latency were administered before and after operation. The ectopic discharges of normal DRG and injured DRG were recorded by nerve fibers electrophysiological technique in vivo.Result： Mechanical withdrawal threshold and thermal withdrawal latency reduced significantly after CCD （n=30, P〈0.05）; The ectopic discharges were present in 67% of the fibers recorded from DRG neurons injured withchronic compression in contrast to 4.5% from uninjured DRG neurons; Compared with CCD group the frequency and amplitude of ectopic discharges decreased significantly after incubating the injured DRG with TRPs inhibitor1001.Lm RR（n=10, P〈0.05）; Compared with CCD group frequency and amplitude of ectopic discharges increased significantly after incubating the injured DRG with TRPV4 specific activator 101μm 4α-PDD（n=10, P 〈 0.05）.Conclusion： TRPV4 plays a crucial role in mediating ectopic discharges of injured DRG after CCD. Author＇s address Department of Physical Medicine and Rehabilitation, Qilu Hospital of Shandong University,Medical School of Shandong University, Jinan, 250012