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镇痛性背根神经节刺激选择性地阻断伤害性感觉传入纤维中传入冲动的传导。

Analgesic dorsal root ganglionic field stimulation blocks conduction of afferent impulse trains selectively in nociceptive sensory afferents.

机构信息

Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, United States.

Department of Colon and Rectal Surgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, China.

出版信息

Pain. 2020 Dec;161(12):2872-2886. doi: 10.1097/j.pain.0000000000001982.

DOI:10.1097/j.pain.0000000000001982
PMID:32658148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7669706/
Abstract

Increased excitability of primary sensory neurons after peripheral nerve injury may cause hyperalgesia and allodynia. Dorsal root ganglion field stimulation (GFS) is effective in relieving clinical pain associated with nerve injury and neuropathic pain in animal models. However, its mechanism has not been determined. We examined effects of GFS on transmission of action potentials (APs) from the peripheral to central processes by in vivo single-unit recording from lumbar dorsal roots in sham injured rats and rats with tibial nerve injury (TNI) in fiber types defined by conduction velocity. Transmission of APs directly generated by GFS (20 Hz) in C-type units progressively abated over 20 seconds, whereas GFS-induced Aβ activity persisted unabated, while Aδ showed an intermediate pattern. Activity generated peripherally by electrical stimulation of the sciatic nerve and punctate mechanical stimulation of the receptive field (glabrous skin) was likewise fully blocked by GFS within 20 seconds in C-type units, whereas Aβ units were minimally affected and a subpopulation of Aδ units was blocked. After TNI, the threshold to induce AP firing by punctate mechanical stimulation (von Frey) was reduced, which was reversed to normal during GFS. These results also suggest that C-type fibers, not Aβ, mainly contribute to mechanical and thermal hypersensitivity (von Frey, brush, acetone) after injury. Ganglion field stimulation produces use-dependent blocking of afferent AP trains, consistent with enhanced filtering of APs at the sensory neuron T-junction, particularly in nociceptive units.

摘要

外周神经损伤后初级感觉神经元兴奋性增加可能导致痛觉过敏和感觉异常。背根神经节场刺激(GFS)在缓解与神经损伤相关的临床疼痛和动物模型中的神经病理性疼痛方面是有效的。然而,其机制尚未确定。我们通过在假损伤大鼠和胫骨神经损伤(TNI)大鼠的腰椎背根中进行体内单细胞记录,检查了 GFS 对动作电位(AP)从外周向中枢过程传递的影响,这些大鼠的纤维类型是根据传导速度定义的。GFS 直接产生的 C 型单位中 AP 的传递在 20 秒内逐渐减弱,而 GFS 诱导的 Aβ 活性持续不变,而 Aδ 则呈现中间模式。通过坐骨神经电刺激和触须皮肤感受野(无毛皮肤)的点状机械刺激在外周产生的活动在 20 秒内也被 GFS 完全阻断,而 Aβ 单位受影响最小,Aδ 单位的一个亚群被阻断。TNI 后,用点状机械刺激(von Frey)诱导 AP 放电的阈值降低,在 GFS 期间恢复正常。这些结果还表明,在损伤后,C 型纤维而不是 Aβ 主要导致机械和热敏感性增加(von Frey、刷子、丙酮)。神经节场刺激产生传入 AP 列车的使用依赖性阻断,这与感觉神经元 T 型连接处 AP 的增强过滤一致,特别是在伤害性单位中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/2a92c78c2c7b/nihms-1607496-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/aae623805f46/nihms-1607496-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/2a92c78c2c7b/nihms-1607496-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/aae623805f46/nihms-1607496-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/db7c68db84b6/nihms-1607496-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/80e6a561a983/nihms-1607496-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/cf04aa255f96/nihms-1607496-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/f73aba779f9c/nihms-1607496-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/d2ac3d225b1d/nihms-1607496-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/62100d6d31a7/nihms-1607496-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/e3d279324f87/nihms-1607496-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28da/7669706/2a92c78c2c7b/nihms-1607496-f0009.jpg

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