Single channel activity of the cardiac ryanodine-sensitive calcium-release
channel in planar lipid membranes was studied in order to elucidate
the calcium-dependent mechanism of its steady-state behavior. The
single channel kinetics, observed with Cs+ as the charge carrier
at different activating (cis) Ca$^2+$ concentrations in the absence
of ATP and Mg2+, were similar to earlier reports and were extended
by analysis of channel modal behavior. The channel displayed three
episodic levels of open probability defining three gating modes:
H (high activity), L (low activity), and I (no activity). The large
difference in open probabilities between the two active modes resulted
from different bursting patterns and different proportions of two
distinct channel open states. I-mode was without openings and can
be regarded as the inactivated mode of the channel; L-mode was composed
of short and sparse openings; and H-mode openings were longer and
grouped into bursts. Modal gating may explain calcium-release channel
adaptation (as transient prevalence of H-mode after Ca$^2+$ binding)
and the inhibitory effects of drugs (as stabilization of mode I),
and it provides a basis for understanding the regulation of calcium
release.
%0 Journal Article
%1 Zahr_1995_1780
%A Zahradn�kov�, A.
%A Zahradn�k, I.
%D 1995
%J Biophys. J.
%K 8580321 Adaptation, Animals, Biophysics, Calcium Calcium, Cations, Chains, Channel Channel, Channels, Comparative Computer Divalent, Dogs, Endoplasmic Factors, Gating, Gov't, Heart, In Ion Kinetics, Lipids, Markov Membrane Models, Monovalent, Muscle Myocardium, Non-U.S. Physiological, Probability, Proteins, Receptor Release Research Reticulum, Ryanodine Simulation, Study, Support, Theoret, Time Vitro, ical,
%N 5
%P 1780--1788
%T Description of modal gating of the cardiac calcium release channel
in planar lipid membranes.
%U http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=8580321
%V 69
%X Single channel activity of the cardiac ryanodine-sensitive calcium-release
channel in planar lipid membranes was studied in order to elucidate
the calcium-dependent mechanism of its steady-state behavior. The
single channel kinetics, observed with Cs+ as the charge carrier
at different activating (cis) Ca$^2+$ concentrations in the absence
of ATP and Mg2+, were similar to earlier reports and were extended
by analysis of channel modal behavior. The channel displayed three
episodic levels of open probability defining three gating modes:
H (high activity), L (low activity), and I (no activity). The large
difference in open probabilities between the two active modes resulted
from different bursting patterns and different proportions of two
distinct channel open states. I-mode was without openings and can
be regarded as the inactivated mode of the channel; L-mode was composed
of short and sparse openings; and H-mode openings were longer and
grouped into bursts. Modal gating may explain calcium-release channel
adaptation (as transient prevalence of H-mode after Ca$^2+$ binding)
and the inhibitory effects of drugs (as stabilization of mode I),
and it provides a basis for understanding the regulation of calcium
release.
@article{Zahr_1995_1780,
abstract = {Single channel activity of the cardiac ryanodine-sensitive calcium-release
channel in planar lipid membranes was studied in order to elucidate
the calcium-dependent mechanism of its steady-state behavior. The
single channel kinetics, observed with Cs+ as the charge carrier
at different activating (cis) {C}a$^{2+}$ concentrations in the absence
of ATP and Mg2+, were similar to earlier reports and were extended
by analysis of channel modal behavior. The channel displayed three
episodic levels of open probability defining three gating modes:
H (high activity), L (low activity), and I (no activity). The large
difference in open probabilities between the two active modes resulted
from different bursting patterns and different proportions of two
distinct channel open states. I-mode was without openings and can
be regarded as the inactivated mode of the channel; L-mode was composed
of short and sparse openings; and H-mode openings were longer and
grouped into bursts. Modal gating may explain calcium-release channel
adaptation (as transient prevalence of H-mode after {C}a$^{2+}$ binding)
and the inhibitory effects of drugs (as stabilization of mode I),
and it provides a basis for understanding the regulation of calcium
release.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Zahradn�kov�, A. and Zahradn�k, I.},
biburl = {https://www.bibsonomy.org/bibtex/25a2bb00233c8e5016b03d468fe666180/hake},
description = {The whole bibliography file I use.},
file = {Zahr_1995_1780.pdf:Zahr_1995_1780.pdf:PDF},
interhash = {bfb230365a19ceae92236693393f57c1},
intrahash = {5a2bb00233c8e5016b03d468fe666180},
journal = {Biophys. J.},
keywords = {8580321 Adaptation, Animals, Biophysics, Calcium Calcium, Cations, Chains, Channel Channel, Channels, Comparative Computer Divalent, Dogs, Endoplasmic Factors, Gating, Gov't, Heart, In Ion Kinetics, Lipids, Markov Membrane Models, Monovalent, Muscle Myocardium, Non-U.S. Physiological, Probability, Proteins, Receptor Release Research Reticulum, Ryanodine Simulation, Study, Support, Theoret, Time Vitro, ical,},
month = Nov,
number = 5,
pages = {1780--1788},
pmid = {8580321},
timestamp = {2009-06-03T11:21:38.000+0200},
title = {Description of modal gating of the cardiac calcium release channel
in planar lipid membranes.},
url = {http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=8580321},
volume = 69,
year = 1995
}