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Evidence for a synaptically mediated decrease in conductance in a crustacean myocardium

J C Delaleu

    The Journal of Experimental Biology
    |August 1, 1976
    PubMed
    Summary
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    Electrical stimulation of crustacean heart nerves causes inhibitory junctional potentials (IJPs) and a subsequent long-lasting post-stimulus hyperpolarization (PSH). This PSH involves decreased ion conductance, contributing to cardiac inhibitory regulation.

    Area of Science:

    • Cardiovascular Physiology
    • Neurobiology
    • Crustacean Biology

    Background:

    • Neurogenic hearts in crustaceans, like the isopod Porcellio dilatatus, are regulated by cardio-regulatory nerves.
    • Electrical stimulation of these nerves can elicit complex electrophysiological responses in the myocardium.

    Purpose of the Study:

    • To investigate the electrophysiological characteristics of inhibitory junctional potentials (IJPs) and post-stimulus hyperpolarization (PSH) in the isopod heart.
    • To elucidate the ionic mechanisms underlying the PSH and its role in cardiac inhibition.

    Main Methods:

    • Electrical stimulation of cardio-regulatory nerves in the isolated isopod heart.
    • Intracellular recording of myocardial membrane potentials and resistance.
    • Pharmacological manipulation using picrotoxin, K+-free saline, ouabain, lithium saline, and choline solutions.

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  • Ionic manipulation by altering extracellular ion concentrations (Cl-, Na+, K+).

    • Main Results:

    • High-frequency nerve stimulation (>20-25 pulses/s) induced IJPs followed by a prolonged PSH.
    • PSH was associated with increased membrane resistance, sensitive to membrane potential, and reversed around -50 mV.
    • Picrotoxin affected IJPs but not PSH, suggesting distinct inhibitory processes. PSH was dependent on Na+ and K+ but not Cl-.

    Conclusions:

    • The PSH in the isopod heart is proposed to result from a decrease in membrane conductance, likely involving both Na+ and K+.
    • This mechanism plays a significant role in the overall inhibitory regulation of crustacean cardiac function.