Effect of electro-acupuncture on the BDNF-TrkB pathway in the spinal cord of CCI rats.

Microglia, which comprise a sensor for pathological events in the central nervous system, may be triggered by nerve injury and transformed from a quiescent state into an activated state; ionised calcium binding adaptor molecule 1 (Iba1) is a sensitive marker associated with activated microglia. Accumulated evidence suggests that spinal activated microglia and the brain-derived neurotrophic factor (BDNF)-tyrosine kinase receptor B (TrkB) signalling pathway play major roles in the production and development of neuropathic pain. Electro-acupuncture (EA) has a positive effect on relieving chronic neuropathic pain; however, the underlying mechanisms remain unclear. To determine the significance of EA in the treatment of neuropathic pain mediated by activated microglia and the BDNF-TrkB signalling pathway in the spinal cord, the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) values were recorded to assess hyperalgesia and allodynia. In addition, the amount of activated microglia and BDNF were assessed via immunofluorescence. Iba1, BDNF and TrkB mRNA expression levels were examined using qPCR; the protein levels of BDNF, p-TrkB and TrkB in the spinal cord were analysed via western blotting. The present study demonstrated that EA treatment increased the MWT and TWL values. EA significantly inhibited the proportion of activated microglia and BDNF expression in the spinal cord after chronic constrictive injury (CCI). Furthermore, EA decreased the expression of BDNF and TrkB at both the mRNA and protein levels in the spinal cord of CCI rats. These findings suggest that the analgesic effect of EA may be achieved by inhibiting the activation of spinal microglia and subsequently blocking the BDNF-TrkB signalling pathway.

Electro-acupuncture at Governor Vessel improves neurological function in rats with spinal cord injury.

OBJECTIVE: To determine the effects of electro-acupuncture (EA) at Governor Vessel (GV) on the locomotor function in spinal cord injury (SCI) rats and explore the underlying mechanism. METHODS: Thirtytwo male Sprague-Dawley rats were randomly divided into four groups namely: the sham group (with sham operation); the untreated group (without treatment after spinal cord impact); the EA-1 group [EA applied at Baihui (GV 20) and Fengfu (GV 16) after spinal cord impact] and the EA-2 group [with EA applied at Dazhui (GV 14) and Mingmen (GV 4) after spinal cord impact]. Real-time quantitative-polymerase chain reaction (RT-PCR) and Western Blotting were used to assess changes in the mRNA and protein expression levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) at 7 weeks following EA administration. In addition, the Basso-Beattie-Bresnahan (BBB) Locomotor Rating Scale was assessed at 1 day, 1 week, 3 weeks and 7 weeks post-injury. RESULTS: The results showed that EA stimulation induced neuroprotective effects after SCI correlated with the up-regulation of BDNF and NT-3 (P<0.05). Furthermore, EA stimulation at GV 14 and GV 4 could significantly promote the recovery of locomotor function and this may be linked to the up-regulation of BDNF and NT-3 (P<0.05). CONCLUSIONS: EA treatment applied at GV acupoints either within the injury site or adjacent undamaged regions near the brain can improve functional recovery, which may be correlated with the upregulation of BDNF and NT-3. In addition, it would be more effective to administer EA at GV 14 and GV 4 near the injury site of the SCI rats.