The Journal of General Physiology
Cell MicroControls
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text (PDF, 847K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JGP
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kirsch, G. E.
Right arrow Articles by Brown, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kirsch, G. E.
Right arrow Articles by Brown, A. M.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

The Journal of General Physiology, Vol 93, 85-99, Copyright © 1989 by The Rockefeller University Press


ARTICLES

Kinetic properties of single sodium channels in rat heart and rat brain

GE Kirsch and AM Brown
Department of Physiology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas 77030.

Single Na channel currents were compared in ventricular myocytes and cortical neurons of neonatal rats using the gigaseal patch-clamp method to determine whether tissue-specific differences in gating can be detected at the single-channel level. Single-channel currents were recorded in cell-attached and excised membrane patches at test potentials of -70 to -20 mV and at 9-11 degrees C. In both cell- attached and excised patches brain Na channel mean open time progressively increased from less than 1 ms at -70 mV to approximately 2 ms at -20 mV. Near threshold, single openings with dispersed latencies were observed. By contrast, in cell-attached patches, heart Na channel mean open time peaked near -50 mV, was three times brain Na channel mean open time, and declined continuously to approximately 2 ms at -20 mV. Near threshold, openings occurred frequently usually as brief bursts lasting several milliseconds and rarely as prolonged bursts lasting tens of milliseconds. Unlike what occurs in brain tissue where excision did not change gating, in excised heart patches both the frequency of prolonged bursting and the mean open time of single units increased markedly. Brain and cardiac Na channels can therefore be distinguished on the basis of their mean open times and bursting characteristics.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
J. Neurophysiol.Home page
S. Diwakar, J. Magistretti, M. Goldfarb, G. Naldi, and E. D'Angelo
Axonal Na+ Channels Ensure Fast Spike Activation and Back-Propagation in Cerebellar Granule Cells
J Neurophysiol, February 1, 2009; 101(2): 519 - 532.
[Abstract] [Full Text] [PDF]


Home page
J. Med. Genet.Home page
Q Wang, S Chen, Q Chen, X Wan, J Shen, G A Hoeltge, A A Timur, M T Keating, and G E Kirsch
The common SCN5A mutation R1193Q causes LQTS-type electrophysiological alterations of the cardiac sodium channel
J. Med. Genet., May 1, 2004; 41(5): e66 - e66.
[Full Text] [PDF]


Home page
JGPHome page
J. Magistretti and A. Alonso
Fine Gating Properties of Channels Responsible for Persistent Sodium Current Generation in Entorhinal Cortex Neurons
J. Gen. Physiol., November 25, 2002; 120(6): 855 - 873.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
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]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
M. Baruscotti, D. DiFrancesco, and R. B. Robinson
Na+ current contribution to the diastolic depolarization in newborn rabbit SA node cells
Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2303 - H2309.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
J. Magistretti, D. S. Ragsdale, and A. Alonso
High Conductance Sustained Single-Channel Activity Responsible for the Low-Threshold Persistent Na+ Current in Entorhinal Cortex Neurons
J. Neurosci., September 1, 1999; 19(17): 7334 - 7341.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
M. M. Segal and A. F. Douglas
Late Sodium Channel Openings Underlying Epileptiform Activity Are Preferentially Diminished by the Anticonvulsant Phenytoin
J Neurophysiol, June 1, 1997; 77(6): 3021 - 3034.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
R. Dumaine, Q. Wang, M. T. Keating, H. A. Hartmann, P. J. Schwartz, A. M. Brown, and G. E. Kirsch
Multiple Mechanisms of Na+ Channel– Linked Long-QT Syndrome
Circ. Res., May 1, 1996; 78(5): 916 - 924.
[Abstract] [Full Text]


Home page
ScienceHome page
Moorman JR, G. Kirsch, A. Brown, and R. Joho
Changes in sodium channel gating produced by point mutations in a cytoplasmic linker
Science, November 2, 1990; 250(4981): 688 - 691.
[Abstract] [PDF]


Home page
ScienceHome page
T Hoshi, W. Zagotta, and R. Aldrich
Biophysical and molecular mechanisms of Shaker potassium channel inactivation
Science, October 26, 1990; 250(4980): 533 - 538.
[Abstract] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
M. Mantegazza, F. H. Yu, W. A. Catterall, and T. Scheuer
Role of the C-terminal domain in inactivation of brain and cardiac sodium channels
PNAS, December 18, 2001; 98(26): 15348 - 15353.
[Abstract] [Full Text] [PDF]



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents