The Journal of Neurophysiology Vol. 80 No. 2 August 1998, pp. 903-913
Copyright ©1998 The American Physiological Society

Excitability of the Squid Giant Axon Revisited

John R. Clay

Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892; and the Marine Biological Laboratory, Woods Hole, Massachusetts 02543

Clay, John R. Excitability of the squid giant axon revisited. J. Neurophysiol. 80: 903-913, 1998. The electrical properties of the giant axon from the common squid Loligo pealei have been reexamined. The primary motivation for this work was the observation that the refractoriness of the axon was significantly greater than the predictions of the standard model of nerve excitability. In particular, the axon fired only once in response to a sustained, suprathreshold stimulus. Similarly, only a single action potential was observed in response to the first pulse of a train of 1-ms duration current pulses, when the pulses were separated in time by ~10 ms. The axon was refractory to all subsequent pulses in the train. The underlying mechanisms for these results concern both the sodium and potassium ion currents I_Na and I_K. Specifically, Na⁺ channel activation has long been known to be coupled to inactivation during a depolarizing voltage-clamp step. This feature appears to be required to simulate the pulse train results in a revised model of nerve excitability. Moreover, the activation curve for I_K has a significantly steeper voltage dependence, especially near its threshold (approximately 60 mV), than in the standard model, which contributes to reduced excitability, and the fully activated current-voltage relation for I_K has a nonlinear, rather than a linear, dependence on driving force. An additional aspect of the revised model is accumulation/depeletion of K⁺ in the space between the axon and the glial cells surrounding the axon, which is significant even during a single action potential and which can account for the 15-20 mV difference between the potassium equilibrium potential E_K and the maximum afterhyperpolarization of the action potential. The modifications in I_K can also account for the shape of voltage changes near the foot of the action potential.

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