Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/32973
標題: Calcium/calmodulin-dependent kinase II mediates NO-elicited PKG activation to participate in spinal reflex potentiation in anesthetized rats
作者: Chen, G.D.
董光中
Peng, M.L.
Wang, P.Y.
Lee, S.D.
Chang, H.M.
Pan, S.F.
Chen, M.J.
Tung, K.C.
Lai, C.Y.
Lin, T.B.
關鍵字: spinal reflex potentiation
soluble guanylate cyclase
cyclic
monophosphate sodium salt monohydrate
spinal cord
windup
long-term potentiation
fiber-evoked potentials
nitric-oxide
protein-kinase
central sensitization
pain hypersensitivity
guanylyl
cyclase
dorsal-horn
synaptic potentiation
retrograde messenger
期刊/報告no:: American Journal of Physiology-Regulatory Integrative and Comparative Physiology, Volume 294, Issue 2, Page(s) R487-R493.
摘要: Calcium/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.
URI: http://hdl.handle.net/11455/32973
ISSN: 0363-6119
文章連結: http://dx.doi.org/10.1152/ajpregu.00600.2007
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