| pubmed-article:8474849 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8474849 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:8474849 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8474849 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
| pubmed-article:8474849 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:8474849 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:8474849 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:8474849 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:8474849 | pubmed:dateCreated | 1993-5-18 | lld:pubmed |
| pubmed-article:8474849 | pubmed:abstractText | The whole-cell configuration of the patch-clamp technique was used to characterize the biophysical and pharmacological properties of an oscillating K(+)-current that can be induced by intracellular application of GTP[gamma S] in mouse pancreatic B cells (Ammälä et al. 1991). These K+ conductance changes are evoked by periodic increases in the cytoplasmic Ca2+ concentration ([Ca2+]i) and transiently repolarize the B cell, thus inhibiting action-potential firing and giving rise to a bursting pattern. GTP[gamma S]-evoked oscillations in K+ conductance were reversibly suppressed by a high (300 microM) concentration of carbamylcholine. By contrast, alpha 2-adrenoreceptor stimulation by 20 microM clonidine did not interfere with the oscillatory behaviour but evoked a small sustained outward current. At 0 mV membrane potential, the oscillating K(+)-current elicited by GTP[gamma S] was highly sensitive to extracellular tetraethylammonium (TEA; 70% block by 1 mM). The TEA-resistant component, which carried approximately 80% of the current at -40 mV, was affected neither by apamin (1 microM) nor by tolbutamide (500 microM). The current evoked by internal GTP[gamma S] was highly selective for K+, as demonstrated by a 51-mV change in the reversal potential for a sevenfold change in [K+]o. Stationary fluctuation analysis indicated a unitary conductance of 0.5 pS when measured with symmetric (approximately 140 mM) KCl solutions. The estimated single-channel conductance with physiological ionic gradients is 0.1 pS. The results indicate the existence of a novel Ca(2+)-gated K+ conductance in pancreatic B cells. Activation of this K+ current may contribute to the generation of the oscillatory electrical activity characterizing the B cell at intermediate glucose concentrations. | lld:pubmed |
| pubmed-article:8474849 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8474849 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8474849 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8474849 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8474849 | pubmed:issn | 0031-6768 | lld:pubmed |
| pubmed-article:8474849 | pubmed:author | pubmed-author:LarssonOO | lld:pubmed |
| pubmed-article:8474849 | pubmed:author | pubmed-author:BerggrenP OPO | lld:pubmed |
| pubmed-article:8474849 | pubmed:author | pubmed-author:RorsmanPP | lld:pubmed |
| pubmed-article:8474849 | pubmed:author | pubmed-author:BokvistKK | lld:pubmed |
| pubmed-article:8474849 | pubmed:author | pubmed-author:AmmäläCC | lld:pubmed |
| pubmed-article:8474849 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8474849 | pubmed:volume | 422 | lld:pubmed |
| pubmed-article:8474849 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8474849 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8474849 | pubmed:pagination | 443-8 | lld:pubmed |
| pubmed-article:8474849 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:8474849 | pubmed:meshHeading | pubmed-meshheading:8474849-... | lld:pubmed |
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| pubmed-article:8474849 | pubmed:meshHeading | pubmed-meshheading:8474849-... | lld:pubmed |
| pubmed-article:8474849 | pubmed:meshHeading | pubmed-meshheading:8474849-... | lld:pubmed |
| pubmed-article:8474849 | pubmed:meshHeading | pubmed-meshheading:8474849-... | lld:pubmed |
| pubmed-article:8474849 | pubmed:meshHeading | pubmed-meshheading:8474849-... | lld:pubmed |
| pubmed-article:8474849 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8474849 | pubmed:articleTitle | Demonstration of a novel apamin-insensitive calcium-activated K+ channel in mouse pancreatic B cells. | lld:pubmed |
| pubmed-article:8474849 | pubmed:affiliation | Department of Medical Biophysics, Göteborgs Universitet, Sweden. | lld:pubmed |
| pubmed-article:8474849 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8474849 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:8474849 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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