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Resting and active K+ channels in the squid axon membrane
Inoue, I. (1995). Resting and active K+ channels in the squid axon membrane, in: Abbott, N.J. et al. (Ed.) Cephalopod neurobiology: neuroscience studies in squid, octopus and cuttlefish. pp. 73-53
In: Abbott, N.J.; Williamson, R.; Maddock, L. (Ed.) (1995). Cephalopod neurobiology: neuroscience studies in squid, octopus and cuttlefish. Oxford University Press: London. ISBN 0-19-854790-0. 542 pp., more

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    VLIZ: Mollusca [8336]

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    Marine

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  • Inoue, I.

Abstract
    Potassium currents (IK) were recorded from giant axons of squid, Sepioteuthis lessoniana under voltage clamp. The K+ accumulation in a space between outer membrane surface and surrounding Schwann cells layer, the so-called Frankenhauser-Hodgkin space (F-H space) due to K+ efflux was completely removed by immersing the nerve fibre in a high osmolarity solution. Under such conditions IK displays the real time course of potassium conductance (gK) of the membrane. Even though the K+ accumulation had been removed completely, IK still decayed after reaching a peak. This decay is due to gK inactivation, and is well fitted by a dual exponential function, with time constants of approximately 10 ms and of the order of 100 ms. Cytochalasin B applied intracellularly was found to block only one component of gK (with the slow inactivation) in a concentration-dependent manner. At 50 µM cytochalasin B, gK lost the slow inactivation component, thus the decaying gK could be fitted by a single exponential function with time constant of approximately 10 ms. The cytochalasin B-sensitive component had quite different characteristics from the delayed rectifier gK: 1) This component was activated along a single exponential time-course with a time constant of 2 ms at 16.5°C following depolarization and then it decayed slowly toward a steady state. 2) Prepulses of -140 to -60 mV did not alter the time course of the cytochalasin B sensitive gK. Because of the slow activation of the drug-sensitive gK, cytochalasin B did not affect the time course of the action potential. On the other hand, cytochalasin B greatly decreased the steady-state K+ conductance. These results suggest that gK of the squid axon membrane consists of at least two components, i.e. a delayed rectifier K+ channel and a steady-state K+ channel. The cytochalasin B resistant gK may represent the real time- and voltage-dependent characteristics of the delayed rectifier.

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