pubmed-article:10022826 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0025462 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0311400 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0282151 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0075586 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0597360 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
pubmed-article:10022826 | lifeskim:mentions | umls-concept:C1523987 | lld:lifeskim |
pubmed-article:10022826 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10022826 | pubmed:dateCreated | 1999-4-26 | lld:pubmed |
pubmed-article:10022826 | pubmed:abstractText | ATP-sensitive potassium (K-ATP) channels couple the metabolic state to cellular excitability in various tissues. Several isoforms of the K-ATP channel subunits, the sulfonylurea receptor (SUR) and inwardly rectifying K channel (Kir6.X), have been cloned, but the molecular composition and functional diversity of native neuronal K-ATP channels remain unresolved. We combined functional analysis of K-ATP channels with expression profiling of K-ATP subunits at the level of single substantia nigra (SN) neurons in mouse brain slices using an RT-multiplex PCR protocol. In contrast to GABAergic neurons, single dopaminergic SN neurons displayed alternative co-expression of either SUR1, SUR2B or both SUR isoforms with Kir6.2. Dopaminergic SN neurons expressed alternative K-ATP channel species distinguished by significant differences in sulfonylurea affinity and metabolic sensitivity. In single dopaminergic SN neurons, co-expression of SUR1 + Kir6.2, but not of SUR2B + Kir6.2, correlated with functional K-ATP channels highly sensitive to metabolic inhibition. In contrast to wild-type, surviving dopaminergic SN neurons of homozygous weaver mouse exclusively expressed SUR1 + Kir6.2 during the active period of dopaminergic neurodegeneration. Therefore, alternative expression of K-ATP channel subunits defines the differential response to metabolic stress and constitutes a novel candidate mechanism for the differential vulnerability of dopaminergic neurons in response to respiratory chain dysfunction in Parkinson's disease. | lld:pubmed |
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pubmed-article:10022826 | pubmed:language | eng | lld:pubmed |
pubmed-article:10022826 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10022826 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10022826 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10022826 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10022826 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10022826 | pubmed:month | Feb | lld:pubmed |
pubmed-article:10022826 | pubmed:issn | 0261-4189 | lld:pubmed |
pubmed-article:10022826 | pubmed:author | pubmed-author:LisiLL | lld:pubmed |
pubmed-article:10022826 | pubmed:author | pubmed-author:BrunsRR | lld:pubmed |
pubmed-article:10022826 | pubmed:author | pubmed-author:RoeperJJ | lld:pubmed |
pubmed-article:10022826 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10022826 | pubmed:day | 15 | lld:pubmed |
pubmed-article:10022826 | pubmed:volume | 18 | lld:pubmed |
pubmed-article:10022826 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10022826 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10022826 | pubmed:pagination | 833-46 | lld:pubmed |
pubmed-article:10022826 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:10022826 | pubmed:meshHeading | pubmed-meshheading:10022826... | lld:pubmed |
pubmed-article:10022826 | pubmed:meshHeading | pubmed-meshheading:10022826... | lld:pubmed |