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Delayed rectification was elicited in frog's skeletal muscles bathed in choline-Ringer's solution, in normal Ringer's solution with tetrodotoxin, in 40 mM Na(2)SO(4) solution with tetrodotoxin, and even in 40 mM K(2)SO(4) solution when the membrane had been previously hyperpolarized. However, after a sustained depolarization current-voltage relations in 40 mM K(2)SO(4) and in 40 mM Na(2)SO(4) solutions revealed a rectifier property in the anomalous direction. This indicates that the increase in potassium conductance which is brought about upon depolarization is a transient phenomenon and is inactivated by a maintained depolarization, and that this potassium inactivation process converts the delayed rectification into the anomalous rectification. In normal Ringer's solution with tetrodotoxin and in the 40 mM Na(2)SO(4) solution with tetrodotoxin the apparent resistance was increased when the membrane was hyperpolarized beyond about -150 mv. This is thought to be due to a decrease of K conductance caused by a strong hyperpolarizing current. In the 40 mM Na(2)SO(4) solution with tetrodotoxin a de- or hyperpolarizing current pulse induced a prolonged depolarizing response. During the early phase of this response the effective resistance was lower, and during the following phase greater than that in the resting fiber. An interpretation in terms of the ionic hypothesis was made of the nature of this response.
Nakajima et al. (Sat,) studied this question.