Methods Hyperalgesia was induced by injecting complete Freund’s adjuvant (CFA, 0.08 ml, 40 μg Mycobacterium tuberculosis) into one hind paw of each rat. EA treatment, 10 Hz at 3 mA, was given at acupoint GB30 twice for 20 min each, once immediately post-CFA and again 2 hours later. Paw withdrawal latency (PWL) was tested before (-48 h) and 2 and 24 hours after CFA to assess behavioral hyperalgesia. IL-17 antibody (0.2-2 μg/rat) was given intrathecally (i.t.) 24 h before CFA to block the action of basal IL-17 and 2 hours prior to each of two PWL tests to block CFA-induced IL-17. I.t. recombinant IL-17 (10-400 ng/rat) was administered to naive rats to determine its effects on PWL and phosphorylation of NR1 (p-NR1). P-NR1 is known to modulate Nmethyl-D-aspartate receptor (NMDAR) activity and to facilitate pain. Spinal cords were removed for immunostaining of IL-17, double immunostaining of IL-17/cell markers and IL-17 receptor subtype A (IL-17RA)/NR1, and western blot to measure p-NR1 and IL-17RA. Results The data showed that (1) IL-17 is selectively up-regulated in astrocytes, 2) IL-17RA is localized and up-regulated in NR1-immunoreactive neurons, and 3) an IL-17 antibody at 2 μg/rat significantly increased PWL (p<0.05) and decreased p-NR1 and IL-17RA in CFAand IL-17-injected rats compared to control. EA significantly inhibited hyperalgesia, IL-17, IL-17RA, and pNR1.