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Related Experiment Videos

EGTA and motoneuronal after-potentials.

K Krnjević, E Puil, R Werman

    The Journal of Physiology
    |February 1, 1978
    PubMed
    Summary
    This summary is machine-generated.

    Calcium influx into cat spinal motoneurons significantly reduces the delayed afterhyperpolarization (a.h.p.) and associated conductance increases. This suggests calcium ions play a crucial role in generating the a.h.p. following action potentials.

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    Area of Science:

    • Neuroscience
    • Cellular Physiology

    Background:

    • The delayed afterhyperpolarization (a.h.p.) in spinal motoneurons is a critical determinant of firing rate.
    • The ionic mechanisms underlying the a.h.p. are not fully understood, though calcium-dependent potassium conductances are implicated.

    Purpose of the Study:

    • To investigate the role of intracellular calcium (Ca2+) in generating the delayed afterhyperpolarization (a.h.p.) in cat spinal motoneurons.
    • To determine if Ca2+ influx during the action potential is responsible for the increase in potassium conductance underlying the a.h.p.

    Main Methods:

    • Intracellular iontophoretic injections of ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid (EGTA) into cat spinal motoneurons.
    • Measurement of membrane potential, input conductance, and afterhyperpolarizations before and after EGTA injection.

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  • Assessment of effects on action potential shape and other hyperpolarizing potentials.

    • Main Results:

    • EGTA injections significantly reduced the amplitude of the delayed a.h.p. and the associated increase in input conductance.
    • A decrease in resting input conductance and some depolarization were observed, with slow recovery.
    • Other hyperpolarizing potentials (i.p.s.p.s) and action potential characteristics were unaffected by EGTA.

    Conclusions:

    • The findings strongly suggest that the delayed a.h.p. is primarily mediated by a Ca2+-dependent increase in potassium conductance.
    • An influx of Ca2+ during the action potential is likely responsible for activating the potassium channels that generate the a.h.p.
    • This inward Ca2+ current may also contribute to the post-spike depolarizing after-potential.