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cAMP potentiates InsP3-induced Ca2+ release from the endoplasmic reticulum in blowfly salivary glands

  • Background Serotonin induces fluid secretion from Calliphora salivary glands by the parallel activation of the InsP3/Ca2+ and cAMP signaling pathways. We investigated whether cAMP affects 5-HT-induced Ca2+ signaling and InsP3-induced Ca2+ release from the endoplasmic reticulum (ER). Results Increasing intracellular cAMP level by bath application of forskolin, IBMX or cAMP in the continuous presence of threshold 5-HT concentrations converted oscillatory [Ca2+]i changes into a sustained increase. Intraluminal Ca2+ measurements in the ER of ß-escin-permeabilized glands with mag-fura-2 revealed that cAMP augmented InsP3-induced Ca2+ release in a concentration-dependent manner. This indicated that cAMP sensitized the InsP3 receptor Ca2+ channel for InsP3. By using cAMP analogs that activated either protein kinase A (PKA) or Epac and the application of PKA-inhibitors, we found that cAMP-induced augmentation of InsP3-induced Ca2+ release was mediated by PKA not by Epac. Recordings of the transepithelial potential of the glandsBackground Serotonin induces fluid secretion from Calliphora salivary glands by the parallel activation of the InsP3/Ca2+ and cAMP signaling pathways. We investigated whether cAMP affects 5-HT-induced Ca2+ signaling and InsP3-induced Ca2+ release from the endoplasmic reticulum (ER). Results Increasing intracellular cAMP level by bath application of forskolin, IBMX or cAMP in the continuous presence of threshold 5-HT concentrations converted oscillatory [Ca2+]i changes into a sustained increase. Intraluminal Ca2+ measurements in the ER of ß-escin-permeabilized glands with mag-fura-2 revealed that cAMP augmented InsP3-induced Ca2+ release in a concentration-dependent manner. This indicated that cAMP sensitized the InsP3 receptor Ca2+ channel for InsP3. By using cAMP analogs that activated either protein kinase A (PKA) or Epac and the application of PKA-inhibitors, we found that cAMP-induced augmentation of InsP3-induced Ca2+ release was mediated by PKA not by Epac. Recordings of the transepithelial potential of the glands suggested that cAMP sensitized the InsP3/Ca2+ signaling pathway for 5-HT, because IBMX potentiated Ca2+-dependent Cl- transport activated by a threshold 5-HT concentration. Conclusion This report shows, for the first time for an insect system, that cAMP can potentiate InsP3-induced Ca2+ release from the ER in a PKA-dependent manner, and that this crosstalk between cAMP and InsP3/Ca2+ signaling pathways enhances transepithelial electrolyte transport.zeige mehrzeige weniger

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Metadaten
Verfasserangaben:Ruth Schmidt, Otto BaumannORCiDGND, Bernd Walz
URN:urn:nbn:de:kobv:517-opus4-429770
DOI:https://doi.org/10.25932/publishup-42977
ISSN:1866-8372
Titel des übergeordneten Werks (Deutsch):Postprints der Universität Potsdam : Mathematisch Naturwissenschaftliche Reihe
Schriftenreihe (Bandnummer):Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe (842)
Publikationstyp:Postprint
Sprache:Englisch
Datum der Erstveröffentlichung:10.03.2020
Erscheinungsjahr:2008
Veröffentlichende Institution:Universität Potsdam
Datum der Freischaltung:10.03.2020
Freies Schlagwort / Tag:cAMP analog; endoplasmic reticulum; fluid secretion; physiological solution; salivary gland
Ausgabe:842
Seitenanzahl:13
Quelle:BMC Physiology 8 (2008) 10 DOI:10.1186/1472-6793-8-10
Organisationseinheiten:Mathematisch-Naturwissenschaftliche Fakultät
DDC-Klassifikation:5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie
6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Peer Review:Referiert
Publikationsweg:Open Access
Lizenz (Englisch):License LogoCreative Commons - Namensnennung 2.0 Generic
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