中山醫學大學機構典藏 CSMUIR:Item 310902500/3788
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    题名: Calcium/calmodulin-dependent kinase II mediates NO-elicited PKG activation to participate in spinal reflex potentiation in anesthetized rats
    作者: Gin-Den Chen;Mei-Lin Peng;Pei-Yi Wang;Shin-Da Lee;Hung-Ming Chang;Shwu-Fen Pan;Mei-Jung Chen;Kwong-Chung Tung;Cheng-Yuan Lai;Tzer-Bin Lin
    贡献者: 中山醫學大學:醫學系
    关键词: spinal reflex potentiation;soluble guanylate cyclase;cyclic monophosphate sodium salt monohydrate;spinal cord;windup
    日期: 2008
    上传时间: 2011-05-20T08:44:59Z (UTC)
    ISSN: 0363-6119
    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, NG-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-α]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: https://ir.csmu.edu.tw:8080/handle/310902500/3788
    http://dx.doi.org/10.1152/ajpregu.00600.2007
    關聯: Am J Physiol Regul Integr Comp Physiol February 1, 2008 294:R487-R493
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