| pubmed-article:8666062 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C0999699 | lld:lifeskim |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C0205171 | lld:lifeskim |
| pubmed-article:8666062 | lifeskim:mentions | umls-concept:C0065543 | lld:lifeskim |
| pubmed-article:8666062 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8666062 | pubmed:dateCreated | 1996-8-8 | lld:pubmed |
| pubmed-article:8666062 | pubmed:abstractText | The characteristics of maitotoxin-induced single channel currents were studied in guinea-pig single ventricular cells using the cell-attached or inside-out configuration of the patch clamp. When the patch electrode was filled with normal Tyrode solution containing 10 nM maitotoxin, elementary currents flowing through the single channel were observed in the cell-attached patch. The amplitude of the single channel current at the resting potential was 1.6 +/- 0.1 pA. The current-voltage relation of the current was linear and the single channel conductance was 16.0 +/- 0.9 pS. The distribution of open times was fitted by a single exponential function (decay time constant: 27 ms), while that of closed times was fitted by the sum of two exponential functions (decay time constants: 1.6 and 34 ms). When the electrode solution was filled with the Ca(2+)-free Tyrode solution, maitotoxin also induced single channel currents with parameters similar to those in the normal Tyrode solution. Under inside-out patch clamp conditions and in 150 mM Na+ solution on both sides of the patch membrane, maitotoxin also induced single channel currents. Choline+ could not substitute for Na+. These results indicate that maitotoxin induces single ionic channels irrespective of the presence or absence of Ca2+ and that the charge carrier of the single channel current is Na+ rather than Ca2+. The increase in Na+ permeability through maitotoxin-induced channels may be possibly responsible for its biological actions. | lld:pubmed |
| pubmed-article:8666062 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8666062 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8666062 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8666062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8666062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8666062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8666062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8666062 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8666062 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8666062 | pubmed:issn | 0014-2999 | lld:pubmed |
| pubmed-article:8666062 | pubmed:author | pubmed-author:YasumotoTT | lld:pubmed |
| pubmed-article:8666062 | pubmed:author | pubmed-author:MuramatsuII | lld:pubmed |
| pubmed-article:8666062 | pubmed:author | pubmed-author:NishioMM | lld:pubmed |
| pubmed-article:8666062 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8666062 | pubmed:day | 22 | lld:pubmed |
| pubmed-article:8666062 | pubmed:volume | 297 | lld:pubmed |
| pubmed-article:8666062 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8666062 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8666062 | pubmed:pagination | 293-8 | lld:pubmed |
| pubmed-article:8666062 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:meshHeading | pubmed-meshheading:8666062-... | lld:pubmed |
| pubmed-article:8666062 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8666062 | pubmed:articleTitle | Na(+)-permeable channels induced by maitotoxin in guinea-pig single ventricular cells. | lld:pubmed |
| pubmed-article:8666062 | pubmed:affiliation | Department of Pharmacology, Kanazawa Medical University, Ishikawa, Japan. | lld:pubmed |
| pubmed-article:8666062 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8666062 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:8666062 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8666062 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8666062 | lld:pubmed |
