Effect of electroacupuncture on motor and sensory functions of lower limbs and GABA receptor in spinal cord of rats with neuropathic pain

Objective To explore the effects of electroacupuncture (EA) at ST36 (Zusanli) and BL60 (Kunlun) on improving hyperalgesia and lower-limb motor function of the rat model with lumbar 5 (L5) spinal nerve ligation (SNL), as well as the effects on the microglial cells, BDNF/TrkB signaling pathway activation, and GABAA receptor in model rats’ spinal cord dorsal horn.Design Animal experimental study.Setting Laboratory Animal Research Center, Zhejiang Chinese Medical University.Interventions A total of 56 Sprague–Dawley rats were randomly assigned to the sham SNL group, the SNL group, the SNL plus EA group, and the SNL plus sham EA group (each group n = 14). The lumbar 5 (L5) spinal nerve in the sham SNL group was only exposed for 2–3 min and not ligated. The SNL plus EA group received EA treatment once daily from postoperative day 7 for 7 consecutive days. Acupuncture needles were inserted superficially at the same acupoints to a depth of 0.5 mm, but no electrical stimulation was applied in the SNL plus sham EA group.Outcome Measures The motor and sensory functions of each group were assessed using the MWT (mechanical withdrawal threshold), TWL (thermal withdrawal latency), lower-limb motor function score and balance beam test. The concentration variation of Iba-1, BDNF, TrkB, and GABAA α2 in the rat spinal cord was identified using Western blot and quantitative real-time PCR.Results After 7 days of intervention, the pain threshold of the SNL plus EA group significantly increased compared with the SNL group, accompanied by lower motor dysfunction scores. Moreover, the SNL plus EA group had significantly reduced Iba-1, BDNF, and TrkB while elevated GABAA α2 protein expression versus the SNL group (P < 0.05). Likewise, the mRNA expression of Iba-1, BDNF, and TrkB was decreased while GABAA α2 mRNA expression was increased in the SNL plus EA group versus the SNL group (P < 0.05).Conclusions EA at ST36 and BL60 can improve the neuropathic pain rat model's hyperalgesia and lower-limb motor function. The analgesic effects were achieved by increasing the GABAA α2 receptor expression in the spinal cord of NP rats and promoting GABA's suppression of pain signal transmission via inhibiting the microglia activation and the BDNF/TrkB signaling pathway.