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Müller cell function during spreading depression in frog retina.

S Mori, W H Miller, T Tomita

    Proceedings of the National Academy of Sciences of the United States of America
    |April 1, 1976
    PubMed
    Summary
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    Frog retinas undergoing spreading depression (SD) show increased extracellular potassium ([K+]o). Müller cells, acting as potassium electrodes, help clear this excess potassium from the inner plexiform layer during SD.

    Area of Science:

    • Neuroscience
    • Ophthalmology
    • Physiology

    Background:

    • Spreading depression (SD) is a wave of intense neuronal activity.
    • Potassium ion (K+) dynamics are critical in retinal function and dysfunction.
    • Müller cells play a significant role in maintaining retinal homeostasis.

    Purpose of the Study:

    • To investigate potassium potentials during spreading depression in frog retinas.
    • To elucidate the role of Müller cells in regulating extracellular potassium during SD.
    • To identify the source of excess potassium in the inner plexiform layer during SD.

    Main Methods:

    • Utilized K+ microelectrodes for measuring extracellular and intracellular K+ concentrations ([K+]o and [K+]i).
    • Induced spreading depression in frog (Rana pipiens) retinas using Cl--free Ringer's solution.

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  • Performed simultaneous recordings of membrane potential changes in Müller cells.

    • Main Results:

    • Observed a marked increase in extracellular K+ concentration ([K+]o) during SD, peaking in the inner plexiform layer.
    • Demonstrated that Müller cell membrane potential changes mirrored the [K+]o changes, suggesting they function as K+ electrodes.
    • Showed an increase in intracellular K+ ([K+]i) within Müller cells upon SD onset.

    Conclusions:

    • Müller cells act as potassium electrodes in the frog retina during spreading depression.
    • Müller cells actively clear excess extracellular K+ from the inner plexiform layer.
    • Pathologically enhanced synaptic activity in the inner plexiform layer is the likely source of excess K+ during SD.