Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Identifieur interne : 001F58 ( Istex/Checkpoint ); précédent : 001F57; suivant : 001F59Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Auteurs : I. Parker [États-Unis] ; Y. Yao [États-Unis]Source :
- 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
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
ISTEX:0D331AF8321E2728FB775DC21643C4B3164E485CLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>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></author><author><name sortKey="Yao, Y" sort="Yao, Y" uniqKey="Yao Y" first="Y." last="Yao">Y. Yao</name></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><idno type="wicri:Area/Istex/Curation">000D57</idno><idno type="wicri:Area/Istex/Checkpoint">001F58</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 wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Yao, Y" sort="Yao, Y" uniqKey="Yao Y" first="Y." last="Yao">Y. Yao</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></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><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Parker, I" sort="Parker, I" uniqKey="Parker I" first="I." last="Parker">I. Parker</name></region><name sortKey="Yao, Y" sort="Yao, Y" uniqKey="Yao Y" first="Y." last="Yao">Y. Yao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Ticri/CIDE/explor/OcrV1/Data/Istex/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001F58 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Checkpoint/biblio.hfd -nk 001F58 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Ticri/CIDE
|area= OcrV1
|flux= Istex
|étape= Checkpoint
|type= RBID
|clé= ISTEX:0D331AF8321E2728FB775DC21643C4B3164E485C
|texte= Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
}}
| This area was generated with Dilib version V0.6.32. |  |