Patch-Clamp Recording of Single Channel Activity: Acquisition and Analysis

2013 ◽  
pp. 1825-1832
Author(s):  
Noel Wyn Davies
1995 ◽  
Vol 350 (1334) ◽  
pp. 353-367 ◽  

We introduce and illustrate by examples a new statistical technique, the persistence function, for characterizing ion-channel activity in a single-channel patch-clamp recording. Persistence is a function of both current and time. It is the probability that the current is at a given level (conditional on it having been at that level at an earlier time). Viewed as a function of current it exhibits the prominent conductance levels present in the recording, and viewed as a function of time for a conductance level it portrays the kinetics at that level.


Cell Calcium ◽  
2014 ◽  
Vol 56 (2) ◽  
pp. 96-107 ◽  
Author(s):  
Larry E. Wagner ◽  
Linda A. Groom ◽  
Robert T. Dirksen ◽  
David I. Yule

2000 ◽  
Vol 82 ◽  
pp. 131
Author(s):  
Minoru Wakamori ◽  
Hisanobu Yamada ◽  
Takaharu Okada ◽  
Keiji Imoto ◽  
Yasuo Mori

1997 ◽  
Vol 82 (2) ◽  
pp. 447-452 ◽  
Author(s):  
Terence G. Favero ◽  
, Anthony C. Zable ◽  
, David Colter ◽  
Jonathan J. Abramson

Favero, Terence G., Anthony C. Zable, David Colter, and Jonathan J. Abramson. Lactate inhibits Ca2+-activated Ca2+-channel activity from skeletal muscle sarcoplasmic reticulum. J. Appl. Physiol. 82(2): 447–452, 1997.—Sarcoplasmic reticulum (SR) Ca2+-release channel function is modified by ligands that are generated during about of exercise. We have examined the effects of lactate on Ca2+- and caffeine-stimulated Ca2+ release, [3H]ryanodine binding, and single Ca2+-release channel activity of SR isolated from rabbit white skeletal muscle. Lactate, at concentrations from 10 to 30 mM, inhibited Ca2+- and caffeine-stimulated [3H]ryanodine binding to and inhibited Ca2+- and caffeine-stimulated Ca2+ release from SR vesicles. Lactate also inhibited caffeine activation of single-channel activity in bilayer reconstitution experiments. These findings suggest that intense muscle activity, which generates high concentrations of lactate, will disrupt excitation-contraction coupling. This may lead to decreases in Ca2+ transients promoting a decline in tension development and contribute to muscle fatigue.


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