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Biophys J, March 2002, p. 1509-1523, Vol. 82, No. 3
Laboratoire de Physiologie des Eléments Excitables, Université Claude Bernard Lyon 1, F69622 Villeurbanne, France
The effect of micromolar intracellular levels of
ryanodine was tested on the myoplasmic free calcium concentration
([Ca2+]i) measured from a portion of isolated
mouse skeletal muscle fibers voltage-clamped at 
80 mV. When
ryanodine-injected fibers were transiently depolarized to 0 mV, the
early decay phase of [Ca2+]i upon membrane
repolarization was followed by a steady elevated [Ca2+]i level. This effect could be
qualitatively well simulated, assuming that ryanodine binds to release
channels that open during depolarization and that ryanodine-bound
channels do not close upon repolarization. The amplitude of the
postpulse [Ca2+]i elevation depended on the
duration of the depolarization, being hardly detectable for pulses
shorter than 100 ms, and very prominent for duration pulses of seconds.
Within a series of consecutive pulses of the same duration, the effect
of ryanodine produced a staircase increase in resting
[Ca2+]i, the slope of which was approximately
twice larger for depolarizations to 0 or +10 mV than to 30 or 20
mV. Overall results are consistent with the "open-locked" state
because of ryanodine binding to calcium release channels that open
during depolarization. Within the voltage-sensitive range of calcium
release, increasing either the amplitude or the duration of the
depolarization seems to enhance the fraction of release channels
accessible to ryanodine.
Biophys J, March 2002, p. 1509-1523, Vol. 82, No. 3
© 2002 by the Biophysical Society 0006-3495/02/03/1509/15 $2.00
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