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pubmed-article:14502585pubmed:dateCreated2003-9-22lld:pubmed
pubmed-article:14502585pubmed:abstractTextThe effect of PbCl2 on membrane potential and intracellular divalent metal cation concentrations of rat thymocytes was examined by flow cytometry. PbCl2 at concentrations of 0.3 microM or higher (up to 10 microM) produced persistent, dose-dependent hyperpolarization (decrease in the intensity of di-BA-C4 fluorescence). Removal of external Ca2+ did not significantly affect the PbCl2-induced hyperpolarization. Charybdotoxin, a specific antagonist of Ca(2+)-dependent K+ conductance, greatly attenuated the PbCl2-induced hyperpolarization. PbCl2 increased the intensity of fluo-3 fluorescence under both normal Ca2+ and nominally Ca(2+)-free conditions. These results suggest that Pb2+ enters thymocytes, causing an increase in fluo-3 fluorescence, and activates Ca(2+)-dependent K+ channels, resulting in hyperpolarization. The persistent activation of K+ channels by Pb2+, leading to persistent hyperpolarization, may be one mechanism whereby Pb2+ alters immune function, as membrane potential changes influence physiological functions of lymphocytes.lld:pubmed
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pubmed-article:14502585pubmed:authorpubmed-author:HiramaSeigoSlld:pubmed
pubmed-article:14502585pubmed:copyrightInfoCopyright 2003 Wiley Periodicals, Inc.lld:pubmed
pubmed-article:14502585pubmed:issnTypePrintlld:pubmed
pubmed-article:14502585pubmed:volume18lld:pubmed
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pubmed-article:14502585pubmed:pagination321-6lld:pubmed
pubmed-article:14502585pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:14502585pubmed:year2003lld:pubmed
pubmed-article:14502585pubmed:articleTitlePbCl2-induced hyperpolarization of rat thymocytes: involvement of charybdotoxin-sensitive K+ channels.lld:pubmed
pubmed-article:14502585pubmed:affiliationLaboratory of Cellular Signaling, Faculty of Integrated Arts and Sciences, University of Tokushima, Tokushima 770-8502, Japan.lld:pubmed
pubmed-article:14502585pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:14502585pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed