Abstract
The time course of the rise in sodium conductance during positive voltage‐clamp pulses was measured in squid giant axons perfused with CsF and immersed in low‐sodium solutions. The initial transients were eliminated by subtraction of records made after blocking the sodium channels with tetrodotoxin. The value of tau m as defined by Hodgkin & Huxley (1952) passed through a well defined maximum at a membrane potential of about ‐35 mV. On fitting the initial inflexion in the rise of INa to the expression mXh instead of m3h, the value of X was found to vary from axon to axon between 2.9 and 4.4, with an average of 3.5. For any given axon, X did not vary significantly with pulse potential. Measurements of tau m were made on approaching each value of the membrane potential both from the negative and from the positive side. The cube law kinetics of the Hodgkin‐Huxley equations were closely obeyed. Application of a negative prepulse to ‐180 mV delayed the rise of conductance by 20 musec at 7 degrees C without obviously changing tau m. Comparisons of the voltage dependence of tau m with that of the time constant tau 1 of the fast relaxation of the asymmetry current measured in the same axon, showed that tau 1 was smaller than tau m except at positive potentials, was less steeply voltage‐dependent, and reached its maximum at a more positive potential.