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Calcium entry into cultured mouse astrocytes.

W Walz, D C Wilson

    Neuroscience Letters
    |June 30, 1986
    PubMed
    Summary

    Glial cells do not significantly contribute to calcium (Ca2+) uptake during neuronal activity. Barium

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    Area of Science:

    • Neuroscience
    • Cell Biology
    • Biophysics

    Background:

    • Glial cells play crucial roles in the central nervous system (CNS).
    • Calcium (Ca2+) signaling is vital for neuronal function.
    • Understanding glial Ca2+ uptake is key to comprehending CNS Ca2+ dynamics.

    Purpose of the Study:

    • Investigate the barium-sensitive component of transmembrane Ca2+ influx in mouse astrocytes.
    • Determine the role of glial Ca2+ uptake systems in CNS Ca2+ movements.
    • Clarify the mechanism behind barium-evoked astrocyte depolarizations.

    Main Methods:

    • Utilized cultured mouse astrocytes.
    • Measured 45Ca2+ influx.
    • Assessed the effects of various ions and channel blockers (verapamil, nifedipine, cadmium, cobalt, barium).
    • Examined Ca2+ influx dependence on external Ca2+ and K+ concentrations.

    Main Results:

    • High Ca2+ turnover rate (1.4 min-1) but low flux magnitude (2% of K+ flux).
    • Ca2+ influx insensitive to organic Ca2+ channel blockers but blocked by millimolar concentrations of Cd2+, Co2+, and Ba2+.
    • Influx showed linear dependence on external Ca2+ up to 1.8 mM; unaffected by physiological K+ increases.
    • 50 µM Ba2+ did not affect Ca2+ flux but altered Ca2+:K+ flux ratio.

    Conclusions:

    • Glial Ca2+ entry systems are not involved in the reduction of extracellular Ca2+ during neuronal activity.
    • Barium-evoked astrocyte depolarizations likely result from K+ channel blockade by barium, not direct effects on Ca2+ influx.

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