|
|
||||||||
We used a patch clamp to measure Na currents across 10-15 micron diameter circular patches of frog and rat skeletal muscle membrane. We tested for electrophoretic mobility of Na channels, by applying steady lateral fields (of the order of 10 mV micron-1) across the wall of the patch pipette. Application of steady negative potentials to the inside of the pipette resulted in a fall in the number of functional Na channels in the patch. This fall took several minutes to complete and was reversible. It was assayed by applying suitable depolarizations at approximately 11 sec intervals. When a steady lateral field was applied in the absence of changes in membrane potential of the patch, the loss of Na current was virtually abolished. Thus it was not due to electrophoretic movement of channels, but instead to depolarization of the sarcolemma. Evidently, a very slow inactivation of Na conductance operates in skeletal muscle. In frog muscle, the rate constants for loss and recovery of Na current were about 0.1 min-1 (17 degrees C) at resting potential. Rate constants were higher at more positive and at more negative membrane potentials. Current amplitude was reduced to 0.5 at about -76 mV. Roughly similar results were found in rat omohyoid muscle. A further inactivation mechanism, whose rate was intermediate between conventional fast inactivation and the very slow process described here, was present also in both rat and frog muscle. In frog muscle, lateral fields do not alter the potential dependence of fast inactivation. Either the surface charge due to membrane lipids does not influence inactivation or the lipids immediately surrounding the Na channel are restricted in their mobility.
This article has been cited by other articles:
![]() |
V. Shushakov, C. Stubbe, A. Peuckert, V. Endeward, and N. Maassen Human, Environmental & Exercise: The relationships between plasma potassium, muscle excitability and fatigue during voluntary exercise in humans Exp Physiol, July 1, 2007; 92(4): 705 - 715. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. Ulbricht Sodium Channel Inactivation: Molecular Determinants and Modulation Physiol Rev, October 1, 2005; 85(4): 1271 - 1301. [Abstract] [Full Text] [PDF] |
||||
![]() |
S Talon, M.-A Giroux-Metges, J.-P Pennec, C Guillet, H Gascan, and M Gioux Rapid protein kinase C-dependent reduction of rat skeletal muscle voltage-gated sodium channels by ciliary neurotrophic factor J. Physiol., June 15, 2005; 565(3): 827 - 841. [Abstract] [Full Text] [PDF] |
||||
![]() |
J.-P. Pennec, H. Talarmin, M. Droguet, M.-A. Giroux-Metges, M. Gioux, and G. Dorange Characterization of the voltage-activated currents in cultured atrial myocytes isolated from the heart of the common oyster Crassostrea gigas J. Exp. Biol., October 15, 2004; 207(22): 3935 - 3944. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. R. Clay On the Persistent Sodium Current in Squid Giant Axons J Neurophysiol, January 1, 2003; 89(1): 640 - 644. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. F. Rakowski, D. C. Gadsby, and P. De Weer Single Ion Occupancy and Steady-state Gating of Na Channels in Squid Giant Axon J. Gen. Physiol., February 22, 2002; 119(3): 235 - 250. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. F. Struyk, K. A. Scoggan, D. E. Bulman, and S. C. Cannon The Human Skeletal Muscle Na Channel Mutation R669H Associated with Hypokalemic Periodic Paralysis Enhances Slow Inactivation J. Neurosci., December 1, 2000; 20(23): 8610 - 8617. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. L. Ruff and S. C. Cannon Defective slow inactivation of sodium channels contributes to familial periodic paralysis Neurology, June 13, 2000; 54(11): 2191 - 2192. [Full Text] [PDF] |
||||
![]() |
R. L. Ruff Effects of temperature on slow and fast inactivation of rat skeletal muscle Na+ channels Am J Physiol Cell Physiol, November 1, 1999; 277(5): C937 - C947. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Toib, V. Lyakhov, and S. Marom Interaction between Duration of Activity and Time Course of Recovery from Slow Inactivation in Mammalian Brain Na+ Channels J. Neurosci., March 1, 1998; 18(5): 1893 - 1903. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |