Objective

To observe the impacts of electroacupuncture (EA) stimulation at “Zusanli and Kunlun Points” on spinal dorsal horn microglia activation in L5 spinal nerve ligation (SNL) rats and BNDF, P2 × 4 and GABAAγ2, and the changes in spinal dorsal horn synaptic plasticity in model rats.

Methods

Adult male SD rats (180–220 g) were selected and randomly divided into 6 groups, including the sham group, the SNL group, the SNL + EA group, the SNL+5-BDBD group, the SNL + EA + 5-BDBD group and the SNL + FEA group. The changes in the Iba-1, BDNF, P2 × 4 and GABAAγ2 in the spinal cord of rats were observed by Western blotting, immunofluorescence, RT-PCR and other techniques; the long-term changes in the potential after the excitatory synapse of the spinal dorsal horn in rats were observed by in vivo electrophysiological technique.

Results

After 7 days of intervention, the fluorescence intensity (FI) of P2 × 4 and Iba-1 in the SNL + EA group was lower than that in the SNL group and higher than that in the sham group(P < 0.01), but the FI of GABA_Aγ2 was higher than that in the SNL group(P < 0.01); the expression of Iba-1, BDNF and P2 × 4 proteins in the SNL + EA group, the SNL+5-BDBD group and the SNL + EA + 5-BDBD group was significantly lower than that in the SNL + FEA group(P < 0.05), but the expression of GABAAγ2 protein was higher (P < 0.05); after treatment with EA, the expression levels of Iba-1 mRNA and P2 × 4 mRNA in the SNL + EA group were lower than those in the SNL group(P < 0.01), but the expression levels of GABAAγ2 mRNA were higher (P < 0.01). Meanwhile, long-term potentiation changes could not be induced in the SNL + EA group.

Conclusion

The EA stimulation at “Zusanli” and “Kunlun” points can improve the pain threshold of rats with neuropathic pain (NP), inhibit the excitatory postsynaptic potential (EPSP), and weaken the excitatory transmission efficiency between synapses during NP.

中文翻译：

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电针对神经病理性疼痛大鼠脊髓中P2×4、GABAA γ 2 表达及长时程增强的影响[J].

客观的

观察电针“足三里、昆仑穴”刺激对L5脊神经结扎（SNL）大鼠和BNDF、P2×4和GABAAγ2脊髓背角小胶质细胞活化的影响，以及脊髓背角突触可塑性的变化在模型大鼠中。

方法

选择成年雄性SD大鼠（180~220 g），随机分为6组，包括假手术组、SNL组、SNL+EA组、SNL+5-BDBD组、SNL+EA+5-BDBD组和 SNL + FEA 组。采用Western blotting、免疫荧光、RT-PCR等技术观察大鼠脊髓中Iba-1、BDNF、P2×4和GABAAγ2的变化；采用体内电生理技术观察大鼠脊髓背角兴奋性突触后电位的长期变化。

结果

干预7天后，SNL+EA组P2×4和Iba-1的荧光强度（FI）低于SNL组，高于假手术组（P < 0.01），但GABA _A γ2的FI高于SNL组（P < 0.01）；SNL+EA组、SNL+5-BDBD组和SNL+EA+5-BDBD组Iba-1、BDNF和P2×4蛋白的表达显着低于SNL+FEA组（P < 0.05），但 GABAAγ2 蛋白表达较高（P < 0.05）；电针治疗后，SNL+电针组Iba-1 mRNA和P2×4 mRNA的表达水平低于SNL组（P < 0.01），而GABAAγ2 mRNA的表达水平高于SNL组（P < 0.01）。 0.01）。同时，

结论

电针刺激“足三里”和“昆仑”点可提高神经病理性疼痛（NP）大鼠的痛阈，抑制兴奋性突触后电位（EPSP），减弱神经病理性疼痛（NP）期间突触间的兴奋传递效率。