AIMS It is hypothesized that dorsal root ganglion stimulation (DRGS), sharing some of the mechanisms of traditional spinal cord stimulation (SCS) of the dorsal columns, induces γ-aminobutyric acid (GABA) release from interneurons in the spinal dorsal horn. METHODS We used quantitative immunohistochemical analysis in order to investigate the effect of DRGS on intensity of intracellular GABA-staining levels in the L4-L6 spinal dorsal horn of painful diabetic polyneuropathy (PDPN) animals. To establish the maximal pain relieving effect, we tested for mechanical hypersensitivity to von Frey filaments and animals received 30 minutes of DRGS at day 3 after implantation of the electrode. One day later, 4 Sham-DRGS animals and four responders-to-DRGS received again 30 minutes of DRGS and were perfused at the peak of DRGS-induced pain relief. RESULTS No significant difference in GABA-immunoreactivity was observed between DRGS and Sham-DRGS in lamina 1-3 of the spinal levels L4-6 neither ipsilaterally nor contralaterally. CONCLUSIONS Dorsal root ganglion stimulation does not induce GABA release from the spinal dorsal horn cells, suggesting that the mechanisms underlying DRGS in pain relief are different from those of conventional SCS. The modulation of a GABA-mediated "Gate Control" in the DRG itself, functioning as a prime Gate of nociception, is suggested and discussed.

中文翻译：

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背根神经节刺激缓解疼痛性糖尿病多发性神经病的机制并不依赖于脊髓背角中GABA的释放。

目的假设，背根神经节刺激（DRGS）与背柱的传统脊髓刺激（SCS）共享某些机制，可诱导γ-氨基丁酸（GABA）从脊髓背角中枢神经元释放。方法我们使用定量免疫组化分析来研究DRGS对疼痛性糖尿病多发性神经病（PDPN）动物的L4-L6脊髓背角中细胞内GABA染色水平强度的影响。为了建立最大的止痛效果，我们测试了对von Frey细丝的机械超敏性，并且在植入电极后的第3天，动物接受了30分钟的DRGS。一天后，四只Sham-DRGS动物和四只对DRGS的应答者再次接受了30分钟的DRGS，并在DRGS引起的疼痛缓解高峰期进行了灌注。结果在同侧或对侧脊髓水平L4-6的1-3层中，DRGS和Sham-DRGS之间的GABA免疫反应性均未观察到显着差异。结论背根神经节刺激不能诱导脊髓背角细胞释放GABA，这表明DRGS缓解疼痛的机制与常规SCS不同。建议并讨论了DRG本身中GABA介导的“门控”的调节作用，它是伤害感受的主要门。这表明DRGS缓解疼痛的机制与常规SCS的机制不同。建议并讨论了DRG本身中GABA介导的“门控”的调节作用，它是伤害感受的主要门。这表明DRGS缓解疼痛的机制与常规SCS的机制不同。建议并讨论了DRG本身中GABA介导的“门控”的调节作用，它是伤害感受的主要门。