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) 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.
- 8580321
- adaptation,
- animals,
- biophysics,
- calcium
- calcium,
- cations,
- chains,
- channel
- channel,
- channels,
- comparative
- computer
- divalent,
- dogs,
- endoplasmic
- factors,
- gating,
- gov't,
- heart,
- ical,
- 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,
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