Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Identifieur interne : 000D89 ( Istex/Corpus ); précédent : 000D88; suivant : 000D90Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Auteurs : I. Parker ; Y. YaoSource :
- Cell Calcium [ 0143-4160 ] ; 1993.
Abstract
Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.
Url:
DOI: 10.1016/0143-4160(94)90067-1
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Yao</name><affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0D331AF8321E2728FB775DC21643C4B3164E485C</idno><date when="1994" year="1994">1994</date><idno type="doi">10.1016/0143-4160(94)90067-1</idno><idno type="url">https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000D89</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title><author><name sortKey="Parker, I" sort="Parker, I" uniqKey="Parker I" first="I." last="Parker">I. Parker</name><affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Yao, Y" sort="Yao, Y" uniqKey="Yao Y" first="Y." last="Yao">Y. Yao</name><affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Cell Calcium</title><title level="j" type="abbrev">YCECA</title><idno type="ISSN">0143-4160</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">15</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="276">276</biblScope><biblScope unit="page" to="288">288</biblScope></imprint><idno type="ISSN">0143-4160</idno></series><idno type="istex">0D331AF8321E2728FB775DC21643C4B3164E485C</idno><idno type="DOI">10.1016/0143-4160(94)90067-1</idno><idno type="PII">0143-4160(94)90067-1</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0143-4160</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>I. Parker</name><affiliations><json:string>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</json:string></affiliations></json:item><json:item><name>Y. Yao</name><affiliations><json:string>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. 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Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</p></abstract></profileDesc><revisionDesc><change when="1993-10-07">Registration</change><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YCECA</jid><aid>94900671</aid><ce:pii>0143-4160(94)90067-1</ce:pii><ce:doi>10.1016/0143-4160(94)90067-1</ce:doi><ce:copyright type="unknown" year="1994"></ce:copyright></item-info><head><ce:title>Relation between intracellular Ca<ce:sup>2+</ce:sup> signals and Ca<ce:sup>2+</ce:sup>-activated Cl<ce:sup>−</ce:sup> current in <ce:italic>Xenopus</ce:italic> oocytes</ce:title><ce:author-group><ce:author><ce:given-name>I.</ce:given-name><ce:surname>Parker</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Y.</ce:given-name><ce:surname>Yao</ce:surname></ce:author><ce:affiliation><ce:textfn>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Please send reprint requests to: Dr Ian Parker, Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of California, Irvine, CA 92717, USA.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="27" month="7" year="1993"></ce:date-received><ce:date-accepted day="7" month="10" year="1993"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Activation of inositol 1,4,5-trisphosphate (InsP<ce:inf>3</ce:inf>) signalling in <ce:italic>Xenopus</ce:italic> oocytes causes intracellular Ca<ce:sup>2+</ce:sup> mobilization and thereby activates a Ca<ce:sup>2+</ce:sup>-dependent Cl<ce:sup>−</ce:sup> membrane conductance. Measurements of cytosolic Ca<ce:sup>2+</ce:sup> levels using fluorescent indicators, however, revealed little correspondence with Cl<ce:sup>−</ce:sup> currents. Intracellular photorelease of InsP<ce:inf>3</ce:inf> from a caged precursor evoked transient currents that peaked while the Ca<ce:sup>2+</ce:sup>-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca<ce:sup>2+</ce:sup> signal remained elevated much longer. Also, Cl<ce:sup>−</ce:sup> currents evoked by agonist activation showed transient spikes while a wave of Ca<ce:sup>2+</ce:sup> liberation swept across the cell, but then decreased when the Ca<ce:sup>2+</ce:sup> signal attained a maximal level. Thus, the Cl<ce:sup>−</ce:sup> current corresponded better to the <ce:italic>rate of rise</ce:italic> of intracellular free Ca<ce:sup>2+</ce:sup>, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP<ce:inf>3</ce:inf> and caged Ca<ce:sup>2+</ce:sup> indicated that this relationship did not arise through desensitization or inactivation of the Cl<ce:sup>−</ce:sup> conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca<ce:sup>2+</ce:sup> levels near the plasma membrane was responsible for the decay of Ca<ce:sup>2+</ce:sup>-activated Cl<ce:sup>−</ce:sup> current. Instead, Cl<ce:sup>−</ce:sup> channels may show an adaptive or incremental response to Ca<ce:sup>2+</ce:sup>, which is likely to be important for the encoding and transmission of information by Ca<ce:sup>2+</ce:sup> spikes.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Relation between intracellular Ca</title></titleInfo><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Parker</namePart><affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</affiliation><description>Please send reprint requests to: Dr Ian Parker, Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of California, Irvine, CA 92717, USA.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Yao</namePart><affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued><dateValid encoding="w3cdtf">1993-10-07</dateValid><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. 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