| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Biophysical Journal 70: 238-245 (1996)
© 1996 the Biophysical Society
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-6602, USA.
ABSTRACT
In this study we have expressed and characterized recombinant cardiac and skeletal muscle sodium channel alpha subunits in tsA-201 cells under identical experimental conditions. Unlike the Xenopus oocyte expression system, in tsA-201 cells (transformed human embryonic kidney) both channels seem to gate rapidly, as in native tissue. In general, hSkM1 gating seemed faster than hH1 both in terms of rate of inactivation and rate of recovery from inactivation as well as time to peak current. The midpoint of the steady-state inactivation curve was approximately 25 mV more negative for hH1 compared with hSkM1. In both isoforms, the steady-state channel availability relationships ("inactivation curves") shifted toward more negative membrane potentials with time. The cardiac isoform showed a minimal shift in the activation curve as a function of time after whole-cell dialysis, whereas hSkM1 showed a continued and marked negative shift in the activation voltage dependence of channel gating. This observation suggests that the mechanism underlying the shift in inactivation voltage dependence may be similar to the one that is causing the shift in the activation voltage dependence in hSkM1 but that this is uncoupled in the cardiac isoform. These results demonstrate the utility and limitations of measuring cardiac and skeletal muscle recombinant Na+ channels in tsA-201 cells. This baseline characterization will be useful for future investigations on channel mutants and pharmacology.
This article has been cited by other articles:
 |
|
 |
|
  K. M. Kahlig, T. H. Rhodes, M. Pusch, T. Freilinger, J. M. Pereira-Monteiro, M. D. Ferrari, A. M. J. M. van den Maagdenberg, M. Dichgans, and A. L. George Jr. Divergent sodium channel defects in familial hemiplegic migraine PNAS, July 15, 2008; 105(28): 9799 - 9804. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Martinez-Marmol, M. David, R. Sanches, M. Roura-Ferrer, N. Villalonga, E. Sorianello, S. M. Webb, A. Zorzano, A. Guma, C. Valenzuela, et al. Voltage-dependent Na+ channel phenotype changes in myoblasts. Consequences for cardiac repair Cardiovasc Res, December 1, 2007; 76(3): 430 - 441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. I. Keller, H. Huang, J. Zhao, R. Frank, V. Suarez, E. Delacretaz, M. Brink, S. Osswald, N. Schwick, and M. Chahine A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation Cardiovasc Res, June 1, 2006; 70(3): 521 - 529. [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]
|
|
|
|
 |
|
 G. N. Filatov and M. M. Rich Hyperpolarized shifts in the voltage dependence of fast inactivation of Nav1.4 and Nav1.5 in a rat model of critical illness myopathy J. Physiol., September 15, 2004; 559(3): 813 - 820. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Shirai, N. Makita, K. Sasaki, H. Yokoi, I. Sakuma, H. Sakurada, J. Akai, A. Kimura, M. Hiraoka, and A. Kitabatake A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease Cardiovasc Res, February 1, 2002; 53(2): 348 - 354. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-F. Desaphy, A. De Luca, P. Tortorella, D. De Vito, A. L. George Jr., and D. Conte Camerino Gating of myotonic Na channel mutants defines the response to mexiletine and a potent derivative Neurology, November 27, 2001; 57(10): 1849 - 1857. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.M. Lupoglazoff, T. Cheav, G. Baroudi, M. Berthet, I. Denjoy, B. Cauchemez, F. Extramiana, M. Chahine, and P. Guicheney Homozygous SCN5A Mutation in Long-QT Syndrome With Functional Two-to-One Atrioventricular Block Circ. Res., July 20, 2001; 89 (2): e16 - e21. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Haeseler, M. Stormer, J. Bufler, R. Dengler, H. Hecker, S. Piepenbrock, and M. Leuwer Propofol Blocks Human Skeletal Muscle Sodium Channels in a Voltage-Dependent Manner Anesth. Analg., May 1, 2001; 92(5): 1192 - 1198. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. N. Wright Irreversible Block of Human Heart (hH1) Sodium Channels by the Plant Alkaloid Lappaconitine Mol. Pharmacol., February 1, 2001; 59(2): 183 - 192. [Abstract] [Full Text]
|
|
|
|
|
|
D. W. Wang, N. Makita, A. Kitabatake, J. R. Balser, and A. L. George Jr Enhanced Na+ Channel Intermediate Inactivation in Brugada Syndrome Circ. Res., October 13, 2000; 87 (8): e37 - e43. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Keller, B. Schu, R. Rüdel, and H. Brinkmeier Cellular Uptake and Efficacy of Antisense Oligonucleotides against RNAs of Two Na+ Channel Isoforms J. Pharmacol. Exp. Ther., October 1, 2000; 295(1): 367 - 372. [Abstract] [Full Text]
|
|
|
|
 |
|
 Y.-F. Xiao, S. N. Wright, G. K. Wang, J. P. Morgan, and A. Leaf Coexpression with beta 1-subunit modifies the kinetics and fatty acid block of hH1alpha Na+ channels Am J Physiol Heart Circ Physiol, July 1, 2000; 279(1): H35 - H46. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Makita, N. Shirai, D. W. Wang, K. Sasaki, A. L. George Jr, M. Kanno, and A. Kitabatake Cardiac Na+ Channel Dysfunction in Brugada Syndrome Is Aggravated by {beta}1-Subunit Circulation, January 4, 2000; 101(1): 54 - 60. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nagatomo, C. T. January, and J. C. Makielski Preferential Block of Late Sodium Current in the LQT3 Delta KPQ Mutant by the Class IC Antiarrhythmic Flecainide Mol. Pharmacol., January 1, 2000; 57(1): 101 - 107. [Abstract] [Full Text]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
J. Wei, D. W. Wang, M. Alings, F. Fish, M. Wathen, D. M. Roden, and A. L. George Jr Congenital Long-QT Syndrome Caused by a Novel Mutation in a Conserved Acidic Domain of the Cardiac Na+ Channel Circulation, June 22, 1999; 99(24): 3165 - 3171. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. Balser Structure and function of the cardiac sodium channels Cardiovasc Res, May 1, 1999; 42(2): 327 - 328. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Deschenes, E. Trottier, and M. Chahine Cysteine scanning analysis of the IFM cluster in the inactivation gate of a human heart sodium channel Cardiovasc Res, May 1, 1999; 42(2): 521 - 529. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nagatomo, Z. Fan, B. Ye, G. S. Tonkovich, C. T. January, J. W. Kyle, and J. C. Makielski Temperature dependence of early and late currents in human cardiac wild-type and long Q-T Delta KPQ Na+ channels Am J Physiol Heart Circ Physiol, December 1, 1998; 275(6): H2016 - H2024. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. A. Maltsev and A. I. Undrovinas Cytoskeleton modulates coupling between availability and activation of cardiac sodium channel Am J Physiol Heart Circ Physiol, October 1, 1997; 273(4): H1832 - H1840. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. W. Wang, K. Yazawa, A. L. George Jr., and P. B. Bennett Characterization of human cardiac Na+ channel mutations in the congenital long QT syndrome PNAS, November 12, 1996; 93(23): 13200 - 13205. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. N. Wright Comparison of aconitine-modified human heart (hH1) and rat skeletal ({micro}1) muscle Na+ channels: an important role for external Na+ ions J. Physiol., February 1, 2002; 538(3): 759 - 771. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
