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A model for receptor-regulated calcium entry.

J W Putney

    Cell Calcium
    |February 1, 1986
    PubMed
    Summary
    This summary is machine-generated.

    A new model explains sustained cellular calcium (Ca2+) entry. Intracellular Ca2+ pools regulate Ca2+ influx, controlled by inositol (1,4,5) trisphosphate, influencing cellular signaling.

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    Area of Science:

    • Cell Biology
    • Biochemistry
    • Physiology

    Background:

    • Cellular calcium (Ca2+) homeostasis is crucial for numerous biological processes.
    • Surface membrane receptors play a key role in regulating intracellular Ca2+ levels.
    • Previous models did not fully explain sustained Ca2+ entry following receptor activation.

    Purpose of the Study:

    • To propose a novel model for sustained Ca2+ entry into cells.
    • To elucidate the mechanism of receptor-mediated calcium influx.
    • To explain the biphasic nature of agonist-activated Ca2+-mobilization.

    Main Methods:

    • Reassessment of published data on intracellular Ca2+ pool dynamics.
    • Analysis of the role of inositol (1,4,5) trisphosphate in Ca2+ regulation.

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  • Development of a theoretical model for Ca2+ flux.

    • Main Results:

    • Intracellular Ca2+ pools act as regulated gateways for extracellular Ca2+ entry.
    • Pool filling closes the entry pathway, while emptying opens it.
    • Inositol (1,4,5) trisphosphate controls both Ca2+ release and entry.
    • Agonist withdrawal leads to pool-mediated Ca2+ entry until saturation.

    Conclusions:

    • A capacitative model explains sustained Ca2+ entry.
    • A single messenger, inositol (1,4,5) trisphosphate, regulates Ca2+ release and influx.
    • This model reconciles the biphasic Ca2+ mobilization observed in cells.