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Dear Sir: Recently, Armstrong et al. (1973) have reported on the effects of internal perftmion of squid giant axons with the enzyme preparation Pronase. Elegant arguments were developed on the issue of the separate nature of the sodium and potassium conduetances. I wish to comment here on the interpretation of another finding presented by these authors, that of a possible separation between the activation and inactivation processes of the sodium conductance (gNa)Armstrong et al. (1973) found that after internal perfusion with Pronase, the sodium currents were greatly prolonged, showing in fact no indication of a time-dependent inactivation. They suggested that their results could be accounted for if Pronase abolished inactivation, and in adtion reduced ~N,, the maximum possible sodium conductance. Computations made, using Hodgkin-Huxley parameters, showed that this is indeed the ease. By making ~'h (the time constant of inactivation) very long, and reducing ~N, by a factor of about 3, it was possible to produce a good simulation of their Fig. 3 d. The central question of interest, however, is not how to account for the effects of Pronase within the framework of Hodgkin-Huxley kinetics, but rather whether they do in fact bear on the issue of coupled vs. independent activation-inactivation kinetics. This point is illustrated by Fig. I b, which is also an excellent simulation of Fig. 3 d of Armstrong et al. (1973). Part 1 of Fig. 1 a and b has been computed from

Letter: pronase and models for the sodium conductance.