A Markovian model of the cardiac Ca release channel, based on experimental
single-channel gating data, was constructed to understand the transient
nature of Ca release. The rate constants for a minimal gating scheme
with one Ca-free resting state, and with two open and three closed
states with one bound Ca$^2+$, were optimized to simulate the
following experimental findings. In steady state the channel displays
three modes of activity: inactivated 1 mode without openings, low-activity
L mode with single openings, and high-activity H mode with bursts
of openings. At the onset of a Ca$^2+$ step, the channel first
activates in H mode and then slowly relaxes to a mixture of all three
modes, the distribution of which depends on the new Ca$^2+$.
The corresponding ensemble current shows rapid activation, which
is followed by a slow partial inactivation. The transient reactivation
of the channel (increment detection) in response to successive additions
of Ca$^2+$ is then explained by the model as a gradual recruitment
of channels from the extant pool of channels in the resting state.
For channels in a living cell, the model predicts a high level of
peak activation, a high extent of inactivation, and rapid deactivation,
which could underlie the observed characteristics of the elementary
release events (calcium sparks).
%0 Journal Article
%1 Zahr_1996_2996
%A Zahradn�kov�, A.
%A Zahradn�k, I.
%D 1996
%J Biophys. J.
%K 8968571 Animals, Calcium Calcium, Cations, Chains, Channel Channel, Channels, Comparative Computer Divalent, Endoplasmic Factors, Gating, Gov't, Heart, Ion Kinetics, Markov Models, Monovalent, Myocardium, Non-U.S. Probability, Receptor Release Research Reticulum, Ryanodine Simulation, Study, Support, Theoret, Time ical,
%N 6
%P 2996--3012
%T A minimal gating model for the cardiac calcium release channel.
%U http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=8968571
%V 71
%X A Markovian model of the cardiac Ca release channel, based on experimental
single-channel gating data, was constructed to understand the transient
nature of Ca release. The rate constants for a minimal gating scheme
with one Ca-free resting state, and with two open and three closed
states with one bound Ca$^2+$, were optimized to simulate the
following experimental findings. In steady state the channel displays
three modes of activity: inactivated 1 mode without openings, low-activity
L mode with single openings, and high-activity H mode with bursts
of openings. At the onset of a Ca$^2+$ step, the channel first
activates in H mode and then slowly relaxes to a mixture of all three
modes, the distribution of which depends on the new Ca$^2+$.
The corresponding ensemble current shows rapid activation, which
is followed by a slow partial inactivation. The transient reactivation
of the channel (increment detection) in response to successive additions
of Ca$^2+$ is then explained by the model as a gradual recruitment
of channels from the extant pool of channels in the resting state.
For channels in a living cell, the model predicts a high level of
peak activation, a high extent of inactivation, and rapid deactivation,
which could underlie the observed characteristics of the elementary
release events (calcium sparks).
@article{Zahr_1996_2996,
abstract = {A Markovian model of the cardiac Ca release channel, based on experimental
single-channel gating data, was constructed to understand the transient
nature of Ca release. The rate constants for a minimal gating scheme
with one Ca-free resting state, and with two open and three closed
states with one bound {C}a$^{2+}$, were optimized to simulate the
following experimental findings. In steady state the channel displays
three modes of activity: inactivated 1 mode without openings, low-activity
L mode with single openings, and high-activity H mode with bursts
of openings. At the onset of a {C}a$^{2+}$ step, the channel first
activates in H mode and then slowly relaxes to a mixture of all three
modes, the distribution of which depends on the new {C}a$^{2+}$.
The corresponding ensemble current shows rapid activation, which
is followed by a slow partial inactivation. The transient reactivation
of the channel (increment detection) in response to successive additions
of {C}a$^{2+}$ is then explained by the model as a gradual recruitment
of channels from the extant pool of channels in the resting state.
For channels in a living cell, the model predicts a high level of
peak activation, a high extent of inactivation, and rapid deactivation,
which could underlie the observed characteristics of the elementary
release events (calcium sparks).},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Zahradn�kov�, A. and Zahradn�k, I.},
biburl = {https://www.bibsonomy.org/bibtex/2707fbfbccbd9eaebbe0d8fd148388fd0/hake},
description = {The whole bibliography file I use.},
file = {Zahr_1996_2996.pdf:Zahr_1996_2996.pdf:PDF},
interhash = {c5bc293454cac888decc19bb52bc1794},
intrahash = {707fbfbccbd9eaebbe0d8fd148388fd0},
journal = {Biophys. J.},
keywords = {8968571 Animals, Calcium Calcium, Cations, Chains, Channel Channel, Channels, Comparative Computer Divalent, Endoplasmic Factors, Gating, Gov't, Heart, Ion Kinetics, Markov Models, Monovalent, Myocardium, Non-U.S. Probability, Receptor Release Research Reticulum, Ryanodine Simulation, Study, Support, Theoret, Time ical,},
month = Dec,
number = 6,
pages = {2996--3012},
pmid = {8968571},
timestamp = {2009-06-03T11:21:38.000+0200},
title = {A minimal gating model for the cardiac calcium release channel.},
url = {http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=8968571},
volume = 71,
year = 1996
}