Potassium channel kinetics in squid axons with elevated levels of external potassium concentration.
Potassium ion current in squid axons is usually modified by the effects of ion accumulation in the periaxonal space during voltage-clamp depolarization. The time course of potassium channel activation and ion accumulation usually overlap. A widely accepted procedure for circumventing the effects of accumulation in measurements of activation kinetics consists of measuring the difference in the current at the end of a depolarizing pulse and immediately following return of the membrane potential to the holding level. This instantaneous jump procedure is based upon the assumptions that the potassium channel current-voltage relation (IV) is a linear function of the driving force, and that the IV and the potassium channel-gating kinetics are both independent of ion accumulation. The latter assumption appears to be appropriate for activation kinetics. However, both assumptions concerning the IV are incorrect, in general. Consequently, the jump procedure provides a misleading view of gating kinetics for membrane depolarizations that produce net current flow. Jump conductance measurements for depolarizations that produce little or no net current indicate that the Hodgkin-Huxley n4 model of potassium channel kinetics is appropriate for the physiological range of membrane potentials.
D000818:Animals; D001369:Axons / Q000378:metabolism*; D049832:Decapodiformes / Q000378:metabolism; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism*; D007700:Kinetics; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism*
D007473:Ion Channels; D011188:Potassium