pubmed-article:11526842 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C0039400 | lld:lifeskim |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C1325529 | lld:lifeskim |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C0040223 | lld:lifeskim |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C0683891 | lld:lifeskim |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C0038078 | lld:lifeskim |
pubmed-article:11526842 | lifeskim:mentions | umls-concept:C0750729 | lld:lifeskim |
pubmed-article:11526842 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:11526842 | pubmed:dateCreated | 2001-8-30 | lld:pubmed |
pubmed-article:11526842 | pubmed:abstractText | Changes in the voltage clamp currents of squid giant axons wrought by low axoplasmic TEA+ (tetraethylammonium chloride) concentrations (0.3 mM and above) are described. They are: (a) For positive steps from the resting potential in sea water, the K+ current increases, decreases, then increases, instead of increasing monotonically. (b) For positive steps from the resting potential in 440 mM external K+, the current has an exponentially decaying component, whose decay rate increases with axoplasmic [TEA+]. The control currents increase monotonically. (c) For negative steps from the resting potential in 440 mM external K+, the current record has a peak followed by a decay that is slow relative to the control. The control record decreases monotonically. Qualitatively these findings can be described by a simple kinetic model, from which, with one assumption, it is possible to calculate the rate at which K+ ions move through the K+ channels. An interesting conclusion from (c) is that the channels cannot be closed by the normal voltage-sensitive mechanism (described by Hodgkin and Huxley) until they are free of TEA+. | lld:pubmed |
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pubmed-article:11526842 | pubmed:language | eng | lld:pubmed |
pubmed-article:11526842 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11526842 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11526842 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11526842 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11526842 | pubmed:month | Nov | lld:pubmed |
pubmed-article:11526842 | pubmed:issn | 0022-1295 | lld:pubmed |
pubmed-article:11526842 | pubmed:author | pubmed-author:ArmstrongC... | lld:pubmed |
pubmed-article:11526842 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11526842 | pubmed:volume | 50 | lld:pubmed |
pubmed-article:11526842 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11526842 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11526842 | pubmed:pagination | 491-503 | lld:pubmed |
pubmed-article:11526842 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:11526842 | pubmed:meshHeading | pubmed-meshheading:11526842... | lld:pubmed |
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pubmed-article:11526842 | pubmed:year | 1966 | lld:pubmed |
pubmed-article:11526842 | pubmed:articleTitle | Time course of TEA(+)-induced anomalous rectification in squid giant axons. | lld:pubmed |
pubmed-article:11526842 | pubmed:affiliation | National Institutes of Health, Bethesda, Maryland, USA. | lld:pubmed |
pubmed-article:11526842 | pubmed:publicationType | Journal Article | lld:pubmed |
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