Linked Life Data

18046020

Source:http://linkedlifedata.com/resource/pubmed/id/18046020

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-1-31
pubmed:abstractText
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 Ca(2+)/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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
294
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R487-93
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18046020-Action Potentials, pubmed-meshheading:18046020-Anesthesia, pubmed-meshheading:18046020-Animals, pubmed-meshheading:18046020-Calcium, pubmed-meshheading:18046020-Calcium-Calmodulin-Dependent Protein Kinase Type 2, pubmed-meshheading:18046020-Cyclic GMP-Dependent Protein Kinases, pubmed-meshheading:18046020-Electromyography, pubmed-meshheading:18046020-Enzyme Inhibitors, pubmed-meshheading:18046020-Hyperalgesia, pubmed-meshheading:18046020-NG-Nitroarginine Methyl Ester, pubmed-meshheading:18046020-Neuronal Plasticity, pubmed-meshheading:18046020-Nitric Oxide, pubmed-meshheading:18046020-Nitric Oxide Synthase, pubmed-meshheading:18046020-Oxadiazoles, pubmed-meshheading:18046020-Quinoxalines, pubmed-meshheading:18046020-Rats, pubmed-meshheading:18046020-Rats, Wistar, pubmed-meshheading:18046020-Reflex, pubmed-meshheading:18046020-Signal Transduction, pubmed-meshheading:18046020-Spinal Cord
pubmed:year
2008
pubmed:articleTitle
Calcium/calmodulin-dependent kinase II mediates NO-elicited PKG activation to participate in spinal reflex potentiation in anesthetized rats.
pubmed:affiliation
Department of Physiology, College of Medicine, Chung-Shan Medical University, No. 110 Chang-Kuo North Road Section 1, Taichung, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't