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The "late" Ca channel in squid axons.

L J Mullins, J Requena

    The Journal of General Physiology
    |December 1, 1981
    PubMed
    Summary

    Calcium entry into squid axons is reduced by sodium depletion and enhanced by sodium loading. This suggests sodium

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    The localization of radiophosphate in cells.

    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)·2010

    Area of Science:

    • Neuroscience
    • Cell Physiology
    • Biochemistry

    Background:

    • The squid giant axon is a model system for studying neuronal ion transport.
    • Calcium ions (Ca2+) play crucial roles in neuronal function, including neurotransmitter release and action potential propagation.
    • Aequorin is a photoprotein used to measure intracellular calcium concentrations.

    Purpose of the Study:

    • To investigate the relationship between intracellular sodium concentration ([Na+]i) and calcium entry in squid giant axons.
    • To determine the effects of sodium depletion and loading on calcium influx during neuronal activity.
    • To elucidate the mechanisms underlying calcium inactivation during prolonged depolarization.

    Main Methods:

    • Squid giant axons were injected with aequorin to monitor intracellular calcium levels.
    • Axons were exposed to varying concentrations of potassium (K+) and calcium (Ca2+) in artificial seawater.
    • Sodium depletion was achieved using lithium (Li+) seawater, and sodium loading was induced by stimulation in sodium (Na+) seawater.

    Main Results:

    • High K+ depolarization initially caused a phasic Ca2+ entry and enhanced aequorin glow.
    • Stimulation in Ca2+-free Li+ seawater significantly reduced subsequent Ca2+ entry upon K+ reapplication.
    • Stimulation in Na+ seawater enhanced the axon's response to high K+ depolarization, indicating a recovery or potentiation of Ca2+ influx.
    • Prolonged depolarization in the absence of external Ca2+ did not abolish Ca2+ entry upon subsequent Ca2+ reapplication, suggesting inactivation is related to Ca2+ entry itself.
    • Responses to high-frequency stimulation were significantly lower than those to steady depolarization, especially at low external Ca2+ concentrations.

    Conclusions:

    • Intracellular sodium levels modulate calcium entry in squid giant axons.
    • Sodium depletion inhibits, while sodium loading enhances, calcium influx during neuronal depolarization.
    • Calcium entry itself, rather than mere membrane depolarization, appears to contribute to inactivation mechanisms.
    • These findings have implications for understanding calcium homeostasis and neuronal excitability under varying ionic conditions.

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