| pubmed-article:19478130 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0027796 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0248868 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C1555029 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:19478130 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:19478130 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19478130 | pubmed:dateCreated | 2009-7-21 | lld:pubmed |
| pubmed-article:19478130 | pubmed:abstractText | The limited data that currently exist for the role of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in neuropathic pain are conflicting. In the present study, we tested the hypothesis that CaMKII is required for the maintenance of neuropathic pain in a rodent model of experimental mononeuropathy. Spinal nerve L(5)/L(6) ligation (SNL) was found to increase the spinal activity of CaMKII (pCaMKII) on the ipsilateral (but not contralateral) side. This effect was blocked by 2-[N-(2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine) (KN93) (intrathecal injection), a CaMKII inhibitor. Acute treatment with KN93 dose-dependently reversed SNL-induced thermal hyperalgesia and mechanical allodynia. The action of KN93 lasted for at least 2 to 4 h. 2-[N-(4-Methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine (KN92) (45 nmol i.t.), an inactive analog of KN93, showed no effect on SNL-induced CaMKII activation, allodynia, or hyperalgesia. We further examined the pharmacologic action of trifluoperazine, a clinically used antipsychotic drug that we found to be a potent CaMKII inhibitor in these assays. Trifluoperazine (administered intraperitoneally or by mouth) dose-dependently reversed SNL-induced mechanical allodynia, thermal hyperalgesia, and CaMKII activation without causing locomotor impairment in mice at the highest doses used. In conclusion, our findings support a critical role of CaMKII in neuropathic pain. Blocking CaMKII or CaMKII-mediated signaling may offer a novel therapeutic target for the treatment of neuropathic pain. | lld:pubmed |
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| pubmed-article:19478130 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19478130 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19478130 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19478130 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19478130 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19478130 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19478130 | pubmed:issn | 1521-0103 | lld:pubmed |
| pubmed-article:19478130 | pubmed:author | pubmed-author:DaleT JTJ | lld:pubmed |
| pubmed-article:19478130 | pubmed:author | pubmed-author:LuoFangF | lld:pubmed |
| pubmed-article:19478130 | pubmed:author | pubmed-author:BRACKW JWJ | lld:pubmed |
| pubmed-article:19478130 | pubmed:author | pubmed-author:WangZaijie... | lld:pubmed |
| pubmed-article:19478130 | pubmed:author | pubmed-author:KirkmireChels... | lld:pubmed |
| pubmed-article:19478130 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19478130 | pubmed:volume | 330 | lld:pubmed |
| pubmed-article:19478130 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19478130 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19478130 | pubmed:pagination | 650-9 | lld:pubmed |
| pubmed-article:19478130 | pubmed:dateRevised | 2010-9-27 | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:meshHeading | pubmed-meshheading:19478130... | lld:pubmed |
| pubmed-article:19478130 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19478130 | pubmed:articleTitle | Acute inhibition of Ca2+/calmodulin-dependent protein kinase II reverses experimental neuropathic pain in mice. | lld:pubmed |
| pubmed-article:19478130 | pubmed:affiliation | Department of Biopharmaceutical Sciences, University of Illinois, Chicago, Illinois 60612, USA. | lld:pubmed |
| pubmed-article:19478130 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19478130 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:19478130 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19478130 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:12322 | entrezgene:pubmed | pubmed-article:19478130 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19478130 | lld:entrezgene |
