|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 95, 411-437, Copyright © 1990 by The Rockefeller University Press
ARTICLES |
BE Scanley, DA Hanck, T Chay and HA Fozzard
Department of Medicine, University of Chicago, Illinois 60637.
Single sodium channel events were recorded from cell-attached patches on single canine cardiac Purkinje cells at 10-13 degrees C. Data from four patches containing two to four channels and one patch with one channel were selected for quantitative analysis. The channels showed prominent reopening behavior at voltages near threshold, and the number of reopenings declined steeply with depolarization. Mean channel open time was a biphasic function of voltage with the maximum value (1-1.5 ms) occurring between -50 and -40 mV and lower values at more and at less hyperpolarized levels. Inactivation without opening was also prominent near threshold, and this occurrence also declined with depolarization. The waiting time distributions and the probability of being open showed voltage and time dependence as expected from whole- cell current studies. The results were analyzed in terms of a five- state Markovian kinetic model using both histogram analysis and a maximum likelihood method to estimate kinetic parameters. The kinetic parameters of the model fits were similar to those of GH3 pituitary cells (Horn, R., and C. A. Vandenberg. 1984. Journal of General Physiology. 84:505-534) and N1E115 neuroblastoma cells (Aldrich, R. W., and C. F. Stevens. Journal of Neuroscience. 7:418-431). Both histogram and maximum likelihood analysis implied that much of the voltage dependence of cardiac Na current is in its activation behavior, with inactivation showing modest voltage dependence.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  V. A. Maltsev and A. I. Undrovinas A multi-modal composition of the late Na+ current in human ventricular cardiomyocytes Cardiovasc Res, January 1, 2006; 69(1): 116 - 127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Chen, M. Inoue, and M. F. Sheets Reduced voltage dependence of inactivation in the SCN5A sodium channel mutation delF1617 Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2666 - H2676. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. G. KLEBER and Y. RUDY Basic Mechanisms of Cardiac Impulse Propagation and Associated Arrhythmias Physiol Rev, April 1, 2004; 84(2): 431 - 488. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Sen, Y. Sakaguchi, and G. Cui G protein modulates thyroid hormone-induced Na+ channel activation in ventricular myocytes Am J Physiol Heart Circ Physiol, November 1, 2002; 283(5): H2119 - H2129. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. A. Fozzard Cardiac sodium and calcium channels: a history of excitatory currents Cardiovasc Res, July 1, 2002; 55(1): 1 - 8. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-S. Fan, Y. Yuan, and P. Palade FPL-64176 modifies pore properties of L-type Ca2+ channels Am J Physiol Cell Physiol, March 1, 2001; 280(3): C565 - C572. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
E. Carmeliet Cardiac Ionic Currents and Acute Ischemia: From Channels to Arrhythmias Physiol Rev, July 1, 1999; 79(3): 917 - 1017. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. C. McPhee, D. S. Ragsdale, T. Scheuer, and W. A. Catterall A Critical Role for the S4-S5 Intracellular Loop in Domain IV of the Sodium Channel alpha -Subunit in Fast Inactivation J. Biol. Chem., January 9, 1998; 273(2): 1121 - 1129. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kellenberger, T. Scheuer, and W. A. Catterall Movement of the Na+ Channel Inactivation Gate during Inactivation J. Biol. Chem., November 29, 1996; 271(48): 30971 - 30979. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. C. McPhee, D. S. Ragsdale, T. Scheuer, and W. A. Catterall A Critical Role for Transmembrane Segment IVS6 of the Sodium Channel [IMAGE] Subunit in Fast Inactivation J. Biol. Chem., May 19, 1995; 270(20): 12025 - 12034. [Abstract] [Full Text] [PDF]
|
|
|
|
