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          Institute: MPI für medizinische Forschung     Collection: Abteilung Molekulare Zellforschung     Display Documents

ID: 568805.0, MPI für medizinische Forschung / Abteilung Molekulare Zellforschung
The calcium signal in human neutrophils and its relation to exocytosis investigated by patch−clamp capacitance and Fura−2 measurements
Translation of Title:The calcium signal in human neutrophils and its relation to exocytosis investigated by patch−clamp capacitance and Fura−2 measurements
Authors:Nüße, Oliver; Lindau, Manfred
Date of Publication (YYYY-MM-DD):1993-04-01
Title of Journal:Cell Calcium
Journal Abbrev.:Cell Calcium
Issue / Number:4
Start Page:255
End Page:269
Review Status:Peer-review
Audience:Experts Only
Intended Educational Use:No
Abstract / Description:Intracellular calcium ([Ca2+]i) and exocytosis of human neutrophils were investigated with patch−clamp capacitance and Fura−2 fluorescence measurements. Intracellular application of GTPγS induces a calcium transient and exocytosis. The onset of degranulation occurs at the time where the maximal [Ca2+]i is reached. Despite the close correlation in time, buffering [Ca2+]i at the resting level or at 2 μM leaves the extent and the time course of degranulation unchanged. The decay of the calcium transient is due to diffusional equilibration between the cytosol and the pipette volume. GTPγS activates no cellular mechanisms for Ca2+ reuptake or extrusion. The endogenous calcium buffer capacity can be estimated to be as low as that of 90 μM Fura−2. Stimulation with fMLP also induces degranulation and a calcium transient. The decay of fMLP−induced calcium transients is much faster than that of GTPγS−induced transients and is independent of diffusion indicating that fMLP also induces rapid reuptake or extrusion of Ca2+. Degranulation but not the calcium transient requires the presence of intracellular GTP. Different signalling pathways appear to be involved in GTPγS− and fMLP−stimulated calcium signals. The intracellular calcium release is not an essential signal to initiate exocytosis in neutrophils
Last Change of the Resource (YYYY-MM-DD):--
External Publication Status:published
Document Type:Article
Communicated by:Wulf Kaiser
Affiliations:MPI für medizinische Forschung/Abteilung Molekulare Zellforschung
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