Objective To observe the effect of electroacupuncture(EA)stimulation of"Weizhong"(BL 40)-"Huantiao"(GB 30)on expression of phosphorylated calcium/calmodulin dependent protein kinaseⅡ(p-CaMKⅡ)and cAMP response element binding protein(p-CREB)in the spinal cord in rats with spared nerve injury(SNI)

so as to explore its mechanism underlying easing neuropathic pain.Methods Sixty SD rats were randomly divided into five groups:control(sham-operation)

model

EA

AP-5(a NMDA receptor antagonist)and L-NAME(a non-selective nitric oxide synthase

NOS inhibitor)(n=12in each group).The neuropathic pain model was established by sectioning the right tibal nerve and common peroneal nerve.EA intervention(2Hz

1mA

increasing 1mA/10min)was applied to"Weizhong"(BL 40)and"Huantiao"(GB 30)on the injured side for30 min

once a day for 7days.Rats of the AP-5and L-NAME groups were treated by intragastric administration of AP-5(0.7mg·kg-1·d-1)and L-NAME(60mg·kg-1·d-1)respectively from the 11 th day after operation

once daily for 7days.The mechanical pain thresholds were measured before the SNI procedure(baseline)and at the 10 th and 16 th day after the procedure.The expression of p-CaMKⅡ protein and p-CREB protein and gene of the spinal cord(L4-L6segments)was determined by Western blot and fluorescence quantitative-polymerase chain reaction(PCR)

separately.Results In comparison to the control group

the mechanical pain threshold was significantly decreased in the model group(P<0.01).After EA intervention

the mechanical pain thresholds of the EA

AP-5and L-NAME groups were obviously increased(P<0.01

P<0.05)on day 16 post SNI procedure.The expression levels of p-CaMKⅡand p-CREB proteins and CREB mRNA in the spinal cord were significantly higher in the model group than in the control group(P<0.05).Compared with the model group

the expression levels of spinal p-CaMKⅡand pCREB proteins and CREB mRNA were obviously down-regulated in the EA group(P<0.05)

but not in the AP-5group and the LNAME group(P>0.05).Conclusion EA intervention of BL 40-GB 30 may alleviate pain in neuropathic pain rats

which may be related to its effects in down-regulating spinal CaMKⅡ-CREB pathway function.