Effect of Electrical Field Stimulation on Dorsal Root Ganglion Neuronal Function
Effect of Electrical Field Stimulation on Dorsal Root Ganglion Neuronal Function
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DOI：
10.1111/ner.12028
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发表时间：
2013-07-01
期刊：
影响因子：
2.8
通讯作者：
Hogan, Quinn H.
中科院分区：
文献类型：
--
作者：
Koopmeiners, Andrew S.;Mueller, Samantha;Hogan, Quinn H.
目的神经刺激可为多种疼痛提供镇痛。初级感觉神经元的激活是通过脊髓刺激缓解疼痛的基础，也可以通过在背根神经节（DRG）水平的刺激来实现。DRG也是疼痛发病机制的部位，特别是在神经性疼痛中。因此，我们研究的假设，场刺激的DRG直接抑制感觉神经元的兴奋性。材料与方法采用Fura-2微荧光法测定离体大鼠DRG细胞内Ca ~（2+）浓度和膜电位。通过神经元去极化期间产生的动作电位（AP）数量、轴突刺激期间的传导速度和AP传播失败来评估神经元兴奋性。这些是在60 Hz的GFS 90秒之前和之后测量的。资料分析采用卡方检验、配对t检定及变异数分析。结果400 s脉冲和30 V电压的GFS可产生Ca 2+内流，提示DRG神经元激活。与没有GFS的对照神经元（N = 24，p < 0.05）相比，在GFS之后能够激发一个或多个AP的神经元（N = 23）更少，并且与时间对照相比，在GFS之后能够产生多个AP的神经元更少（p < 0.05）。与GFS之前的基线相比，GFS显著降低了传导速度（N = 16，p < 0.05），而对照组中没有变化（N = 18）。通过GFS，16个神经元中的9个神经元的AP可以传播的峰值速率降低，但是18个对照神经元中仅4个神经元的传播效率降低（p < 0.05），并且通过GFS（N = 16，p < 0.05）减少了在不同频率的刺激的集合中产生的AP的总数，但是在时间对照中没有减少（N = 18）。结论电场直接刺激背根神经节可降低神经元兴奋性，可能为镇痛提供一种新的途径。
Objectives Neural stimulation may provide analgesia for a variety of painful conditions. Activation of primary sensory neurons, which underlies pain relief by spinal cord stimulation, also may be achieved by stimulation at the level of the dorsal root ganglion (DRG). The DRG also is a site of pain pathogenesis, particularly in neuropathic pain. We therefore examined the hypothesis that field stimulation of the DRG directly suppresses excitability of sensory neurons. Materials and Methods Intercellular Ca2+ level (Fura-2 microfluorimetry) and membrane potential were recorded in excised rat DRGs with ganglionic field stimulation (GFS) delivered by wire electrodes in the bath solution adjacent to the DRG. Neuronal excitability was evaluated by number of action potentials (APs) generated during neuronal depolarization, conduction velocity during axonal stimulation, and AP propagation failure. These were measured before and after 90sec of GFS at 60Hz. Data analysis employed chi-square, paired t-test, and analysis of variance. Results GFS using 400-sec pulses and 30V generated Ca2+ influx, indicative of DRG neuronal activation. Fewer neurons were able to fire one or more APs after GFS (N = 23) than in control neurons without GFS (N = 24, p < 0.05), and fewer neurons were able to generate multiple APs after GFS compared with time controls (p < 0.05). GFS significantly reduced conduction velocity compared with baseline before GFS (N = 16, p < 0.05) while there was no change in the controls (N = 18). The peak rate at which APs could be propagated was reduced in 9 of 16 neurons by GFS, but propagation efficiency was reduced in only 4 of 18 control neurons (p < 0.05), and the total number of APs generated in an ensemble of stimuli at different frequencies was reduced by GFS (N = 16, p < 0.05) but not in time controls (N = 18). Conclusions Our findings indicate that direct excitation of the DRG by electrical fields reduces neuronal excitability and may provide a new analgesic approach.