Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/32973
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dc.contributor.authorChen, G.D.en_US
dc.contributor.author董光中zh_TW
dc.contributor.authorPeng, M.L.en_US
dc.contributor.authorWang, P.Y.en_US
dc.contributor.authorLee, S.D.en_US
dc.contributor.authorChang, H.M.en_US
dc.contributor.authorPan, S.F.en_US
dc.contributor.authorChen, M.J.en_US
dc.contributor.authorTung, K.C.en_US
dc.contributor.authorLai, C.Y.en_US
dc.contributor.authorLin, T.B.en_US
dc.date2008zh_TW
dc.date.accessioned2014-06-06T07:44:32Z-
dc.date.available2014-06-06T07:44:32Z-
dc.identifier.issn0363-6119zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/32973-
dc.description.abstractCalcium/calmodulin protein kinase (CaMK)-dependent nitric oxide (NO) and the downstream intracellular messenger cGMP, which is activated by soluble guanylate cyclase (sGC), are believed to induce long-term changes in efficacy of synapses through the activation of protein kinase G (PKG). The aim of this study was to examine the involvement of the CaMKII-dependent NO/sGC/ PKG pathway in a novel form of repetitive stimulation-induced spinal reflex potentiation (SRP). A single-pulse test stimulation (TS; 1/30 Hz) on the afferent nerve evoked a single action potential, while repetitive stimulation (RS; 1 Hz) induced a long-lasting SRP that was abolished by a selective Ca2+/CaMKII inhibitor, autocamtide 2-related inhibitory peptide (AIP). Such an inhibitory effect was reversed by a relative excess of nitric oxide synthase (NOS) substrate, L-arginine. In addition, the RS-induced SRP was abolished by pretreatment with the NOS inhibitor, N-G-nitro-L-arginine-methyl ester (L-NAME). The sGC activator, protoporphyrin IX (PPIX), reversed the blocking effect caused by L-NAME. On the other hand, a sGC blocker, 1H-[1, 2, 4] oxadiazolo[4, 3-alpha] quinoxalin-1-one (ODQ), abolished the RS-induced SRP. Intrathecal applications of the membrane-permeable cGMP analog, 8-bromoguanosine 3',5'-cyclic monophosphate sodium salt monohydrate (8-Br-cGMP), reversed the blocking effect on the RS-induced SRP elicited by the ODQ. Our findings suggest that a CaMKII-dependent NO/sGC/ PKG pathway is involved in the RS-induced SRP, which has pathological relevance to hyperalgesia and allodynia.en_US
dc.language.isoen_USzh_TW
dc.relationAmerican Journal of Physiology-Regulatory Integrative and Comparative Physiologyen_US
dc.relation.ispartofseriesAmerican Journal of Physiology-Regulatory Integrative and Comparative Physiology, Volume 294, Issue 2, Page(s) R487-R493.en_US
dc.relation.urihttp://dx.doi.org/10.1152/ajpregu.00600.2007en_US
dc.subjectspinal reflex potentiationen_US
dc.subjectsoluble guanylate cyclaseen_US
dc.subjectcyclicen_US
dc.subjectmonophosphate sodium salt monohydrateen_US
dc.subjectspinal corden_US
dc.subjectwindupen_US
dc.subjectlong-term potentiationen_US
dc.subjectfiber-evoked potentialsen_US
dc.subjectnitric-oxideen_US
dc.subjectprotein-kinaseen_US
dc.subjectcentral sensitizationen_US
dc.subjectpain hypersensitivityen_US
dc.subjectguanylylen_US
dc.subjectcyclaseen_US
dc.subjectdorsal-hornen_US
dc.subjectsynaptic potentiationen_US
dc.subjectretrograde messengeren_US
dc.titleCalcium/calmodulin-dependent kinase II mediates NO-elicited PKG activation to participate in spinal reflex potentiation in anesthetized ratsen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1152/ajpregu.00600.2007zh_TW
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