title: Involvement of spinal neurotrophin-3 in electroacupuncture analgesia and inhibition of spinal glial activation in rat model of monoarthritis.
abstract: Although electroacupuncture (EA) has been proven to effectively relieve pain associated with arthritis, the underlying mechanism of EA analgesia requires further investigation. Here, the involvement of spinal neurotrophin-3 (NT-3) in EA's analgesic effects on complete Freund's adjuvant (CFA)-induced inflammatory pain was examined. The present study demonstrated that: 1) repeated EA stimulation of ipsilateral GB30 and GB34 acupoints remarkably suppressed CFA-induced hyperalgesia; 2) EA treatment markedly enhanced the upregulation of spinal NT-3 mRNA and protein levels following CFA injection; 3) antisense oligodeoxynucleotides (ODN) specifically against NT-3 intrathecally administered during EA treatment for 7 days significantly attenuated the EA analgesia; and 4) the suppressed expression of spinal GFAP (astrocytic marker), OX-42 (microglial marker) as well as proinflammatory cytokines, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by EA treatment was significantly attenuated following NT-3 antisense ODN delivery. These results suggested that endogenous NT-3 may be involved in the analgesic effect of EA on inflammatory pain in rats, mediated through the inhibition of spinal glial activity as well as proinflammatory cytokine production.
  
  
  CONCLUSIONS
  The present study may initiate a discussion on the possible roles of NT-3/glia/cytokines in the therapeutic effects of acupuncture and provide insight on the mechanism underlie the analgesic effects of acupuncture on pain associated with arthritis.
authors.affiliation: Department of Integrative Medicine and Neurobiology, Institute of Acupuncture Research, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Wen-Li
authors.initials: WL
authors.lastname: Mi
authors.forename: Qi-Liang
authors.initials: QL
authors.lastname: Mao-Ying
authors.forename: Xiao-Wei
authors.initials: XW
authors.lastname: Wang
authors.forename: Xiu
authors.initials: X
authors.lastname: Li
authors.forename: Chang-Jiang
authors.initials: CJ
authors.lastname: Yang
authors.forename: Jian-Wei
authors.initials: JW
authors.lastname: Jiang
authors.forename: Jin
authors.initials: J
authors.lastname: Yu
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Qiong
authors.initials: Q
authors.lastname: Liu
authors.forename: Yan-Qing
authors.initials: YQ
authors.lastname: Wang
authors.forename: Gen-Cheng
authors.initials: GC
authors.lastname: Wu
mesh_terms: D000698:Analgesia / Q000379:methods; D000818:Animals; D001168:Arthritis / Q000378:metabolism* / Q000628:therapy; D004195:Disease Models, Animal; D015671:Electroacupuncture / Q000379:methods; D018836:Inflammation Mediators / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000235:genetics / Q000502:physiology*; D009457:Neuroglia / Q000378:metabolism* / Q000502:physiology; D020933:Neurotrophin 3 / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000378:metabolism*; D015854:Up-Regulation / Q000235:genetics
chemical_list: D018836:Inflammation Mediators; D020933:Neurotrophin 3; D012333:RNA, Messenger