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Related Experiment Videos

Uncoupling of electrotonic synapses by calcium.

G Baux, M Simonneau, L Tauc

    Proceedings of the National Academy of Sciences of the United States of America
    |September 1, 1978
    PubMed
    Summary

    Increased intracellular calcium (Ca2+) causes uncoupling of axo-axonal electrical synapses in Navanax. This effect is reversible when metabolic inhibitors are removed, suggesting calcium

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    Control of IsAHP in mouse hippocampus CA1 pyramidal neurons by RyR3-mediated calcium-induced calcium release.

    Pflugers Archiv : European journal of physiology·2007

    Area of Science:

    • Neuroscience
    • Cellular Biology
    • Synaptic Physiology

    Background:

    • Axo-axonal synaptic coupling is crucial for neural circuit function.
    • The role of intracellular calcium (Ca2+) in modulating electrical synapse efficacy is not fully understood.
    • Navanax buccal ganglion provides a model system for studying neuronal communication.

    Purpose of the Study:

    • To investigate the relationship between intracellular Ca2+ levels and axo-axonal synaptic coupling in Navanax.
    • To determine the mechanism by which Ca2+ affects electrical synapse function.
    • To compare the Ca2+-dependent modulation of these synapses with non-neural gap junctions.

    Main Methods:

    • Intracellular injection of Ca2+, Na+, and Sr2+ into Navanax buccal ganglion neurons.
    • Application of ionophore X537A to alter intracellular Ca2+ concentrations.
    • Use of metabolic inhibitors to control cellular conditions.
    • Recording of electrophysiological parameters to assess synaptic coupling.

    Main Results:

    • Increasing intracellular Ca2+ levels, through various methods, led to the uncoupling of electrical synapses.
    • Uncoupling was observed after a delay of at least 90 minutes when metabolic inhibitors were present.
    • Removal of metabolic inhibitors rapidly restored synaptic coupling within 30 minutes.
    • Injected Sr2+ mimicked the uncoupling effect of Ca2+.

    Conclusions:

    • Elevated free Ca2+ concentration at the synaptic junctions is the primary cause of electrical synapse uncoupling.
    • Endogenous Ca2+ release alone is insufficient for uncoupling unless excess Ca2+ has been previously stored.
    • The electrical synapses in Navanax buccal ganglion exhibit Ca2+-dependent modulation similar to gap junctions in other tissues.

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