Involvement of α7nAChR in electroacupuncture relieving neuropathic pain in the spinal cord of rat with spared nerve injury

Publication date: Available online 4 January 2018
Source:Brain Research Bulletin
Author(s): Ying Wang, Qian Jiang, Yang-yang Xia, Zhi-hua Huang, Cheng Huang
Alpha-7 nicotinic acetylcholine receptor (α7nAChR) was reported to be involved in the modulation of neuropathic pain. Electroacupuncture (EA) has therapeutic effects on neuropathic pain induced by nerve injury, but the underlying mechanisms remain unclear. The present study was designed to investigate whether α7nAChR participates in the relieving effects of 2 Hz EA on neuropathic pain. Paw withdrawal threshold (PWT) was measured to study the EA-mediated analgesic effect in a rat model of spared nerve injury (SNI). The spinal α7nAChR and IL-1β expression levels were determined by RT-PCR, Western blot analysis, and immunofluorescence staining. Additionally, immunofluorescence targeting the expression of CD11b, which is a molecular indicator of microglial activation. The results showed that 2 Hz EA stimulation significantly improved the expression of α7nAChR and reduced the production of IL-1β and CD11b in the spinal cord of rats with SNI-induced neuropathic pain, along with the relief of mechanical hypersensitivity after EA treatment. Moreover, intrathecal injection of alpha-bungarotoxin (α-Bgtx), a selective antagonist for α7nAChR, at the dosage of 1.0 μg/kg, not only suppressed the analgesic effect of EA in SNI rats, but also inhibited the enhancement of α7nAChR expression and the reduction of IL-1β expression induced by EA. In conclusion, our study indicated that 2 Hz EA reduces SNI-induced mechanical hypersensitivity via upregulating α7nAChR and downregulating IL-1β and CD11b in the spinal cord of SNI rats, which might be one of the mechanisms underlying its effectiveness in the neuropathic pain.



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