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Polyamine triggering of exocytosis in Paramecium involves an extracellular Ca2+/(polyvalent cation)-sensing receptor, subplasmalemmal Ca-store mobilization and store-operated Ca2+-influx via unspecific cation channels

Polyamine triggering of exocytosis in Paramecium involves an extracellular Ca2+/(polyvalent cation)-sensing receptor, subplasmalemmal Ca-store mobilization and store-operated Ca2+-influx via unspecific cation channels

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KLAUKE, Norbert, Marie-Pierre BLANCHARD, Helmut PLATTNER, 2000. Polyamine triggering of exocytosis in Paramecium involves an extracellular Ca2+/(polyvalent cation)-sensing receptor, subplasmalemmal Ca-store mobilization and store-operated Ca2+-influx via unspecific cation channels. In: Journal of Membrane Biology. 174(2), pp. 141-156. ISSN 0022-2631. eISSN 1432-1424

@article{Klauke2000Polya-7203, title={Polyamine triggering of exocytosis in Paramecium involves an extracellular Ca2+/(polyvalent cation)-sensing receptor, subplasmalemmal Ca-store mobilization and store-operated Ca2+-influx via unspecific cation channels}, year={2000}, doi={10.1007/s002320001039}, number={2}, volume={174}, issn={0022-2631}, journal={Journal of Membrane Biology}, pages={141--156}, author={Klauke, Norbert and Blanchard, Marie-Pierre and Plattner, Helmut} }

<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/7203"> <dcterms:bibliographicCitation>First publ. in: Journal of Membrane Biology 174 (2000), pp. 141-156</dcterms:bibliographicCitation> <dc:creator>Klauke, Norbert</dc:creator> <dcterms:issued>2000</dcterms:issued> <dcterms:title>Polyamine triggering of exocytosis in Paramecium involves an extracellular Ca2+/(polyvalent cation)-sensing receptor, subplasmalemmal Ca-store mobilization and store-operated Ca2+-influx via unspecific cation channels</dcterms:title> <dc:contributor>Plattner, Helmut</dc:contributor> <dcterms:abstract xml:lang="deu">The polyamine secretagogue, aminoethyldextran (AED), causes a cortical [Ca2+] transient in Paramecium cells, as analyzed by fluorochrome imaging. Our most essential findings are: (i) Cortical Ca2+ signals also occur when AED is applied in presence of the fast Ca2+ chelator, BAPTA. (ii) Extracellular La3+ application causes within seconds a rapid, reversible fluorescence signal whose reversibility can be attributed to a physiological [Ca2+]i transient (while injected La3+ causes a sustained fluorescence signal). (iii) Simply increasing [Ca2+]o causes a similar rapid, short-lived [Ca2+]i transient. All these phenomena, (i¨Ciii), are compatible with activation of an extracellular ¡°Ca2+/(polyvalent cation)-sensing receptor¡± known from some higher eukaryotic systems, where this sensor (responding to Ca2+, La3+ and some multiply charged cations) is linked to cortical calcium stores which, thus, are activated. In Paramecium, such subplasmalemmal stores (¡°alveolar sacs¡±) are physically linked to the cell membrane and they can also be activated by the Ca2+ releasing agent, 4-chloro-m-cresol, just like in Sarcoplasmic Reticulum. Since this drug causes a cortical Ca2+ signal also in absence of Ca2+o we largely exclude a ¡°Ca2+-induced Ca2+ release¡± (CICR) mechanism. Our finding of increased cortical Ca2+ signals after store depletion and re-addition of extracellular Ca2+ can be explained by a ¡°store-operated Ca2+ influx¡± (SOC), i.e., a Ca2+ influx superimposing store activation. AED stimulation in presence of Mn2+o causes fluorescence quenching in Fura-2 loaded cells, indicating involvement of unspecific cation channels. Such channels, known to occur in Paramecium, share some general characteristics of SOCtype Ca2+ influx channels. In conclusion, we assume the following sequence of events during AED stimulated exocytosis: (i) activation of an extracellular Ca2+/polyamine-sensing receptor, (ii) release of Ca2+ from subplasmalemmal stores, (iii) and Ca2+ influx via unspecific cation channels. All three steps are required to produce a steep cortical [Ca2+] signal increase to a level required for full exocytosis activation. In addition, we show formation of [Ca2+] microdomains (¡Ü0.5 mm, ¡Ü33 msec) upon stimulation.</dcterms:abstract> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:32:37Z</dc:date> <dc:creator>Plattner, Helmut</dc:creator> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:32:37Z</dcterms:available> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/7203"/> <dc:contributor>Klauke, Norbert</dc:contributor> <dc:contributor>Blanchard, Marie-Pierre</dc:contributor> <dc:rights>deposit-license</dc:rights> <dc:format>application/pdf</dc:format> <dc:creator>Blanchard, Marie-Pierre</dc:creator> <dc:language>eng</dc:language> <dcterms:rights rdf:resource="https://creativecommons.org/licenses/by-nc-nd/2.0/legalcode"/> </rdf:Description> </rdf:RDF>

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