|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 104, 625-643, Copyright © 1994 by The Rockefeller University Press
ARTICLES |
S Ji, W Sun, AL George Jr, R Horn and RL Barchi
Mahoney Institute of Neurological Sciences, Philadelphia, Pennsylvania 19104.
The TTX-sensitive rat skeletal muscle sodium channel (rSkM1) exhibits two modes of inactivation (fast vs slow) when the alpha subunit is expressed alone in Xenopus oocytes. In this study, two components are found in the voltage dependence of normalized current inactivation, one having a V1/2 in the expected voltage range (approximately -50 mV, I(N)) and the other with a more hyperpolarized V1/2 (approximately -130 mV, IH) at a holding potential of -90 mV. The I(N) component is associated with the gating mode having rapid inactivation and recovery from inactivation of the macroscopic current (N-mode), while IH corresponds to the slow inactivation and recovery mode (H-mode). These two components are interconvertible and their relative contribution to the total current varies with the holding potential: I(N) is favored by hyperpolarization. The interconversion between the two modes is voltage dependent and is well fit to a first-order two-state model with a voltage dependence of e-fold/8.6 mV and a V1/2 of -62 mV. When the rat sodium channel beta 1-subunit is coinjected with rSkM1, IH is essentially eliminated and the inactivation kinetics of macroscopic current becomes rapid. These two current components and their associated gating modes may represent two conformations of the alpha subunit, one of which can be stabilized either by hyperpolarization or by binding of the beta 1 subunit.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  L. Protas, W. Dun, Z. Jia, J. Lu, A. Bucchi, S. Kumari, M. Chen, I. S. Cohen, M. R. Rosen, E. Entcheva, et al. Expression of skeletal but not cardiac Na+ channel isoform preserves normal conduction in a depolarized cardiac syncytium Cardiovasc Res, November 26, 2008; (2008) cvn290v2. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. N. Filatov, M. J. Pinter, and M. M. Rich Resting Potential-dependent Regulation of the Voltage Sensitivity of Sodium Channel Gating in Rat Skeletal Muscle In Vivo J. Gen. Physiol., July 25, 2005; 126(2): 161 - 172. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Qu, J. C. Rogers, S.-F. Chen, K. A. McCormick, T. Scheuer, and W. A. Catterall Functional Roles of the Extracellular Segments of the Sodium Channel alpha Subunit in Voltage-dependent Gating and Modulation by beta 1 Subunits J. Biol. Chem., November 12, 1999; 274(46): 32647 - 32654. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Lehmann-Horn and K. Jurkat-Rott Voltage-Gated Ion Channels and Hereditary Disease Physiol Rev, October 1, 1999; 79(4): 1317 - 1372. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. R. Kay, M. Sugimori, and R. Llinas Kinetic and Stochastic Properties of a Persistent Sodium Current in Mature Guinea Pig Cerebellar Purkinje Cells J Neurophysiol, September 1, 1998; 80(3): 1167 - 1179. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. L. Sah, R. G. Tsushima, and P. H. Backx Effects of local anesthetics on Na+ channels containing the equine hyperkalemic periodic paralysis mutation Am J Physiol Cell Physiol, August 1, 1998; 275(2): C389 - C400. [Abstract] [Full Text] [PDF]
|
|
|
|
