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Vol. 52, Issue 6, 1124-1130, 1997
Departments of
Physiology and Biophysics (C.D., P.P.) and
Pharmacology and Toxicology (P.P.), University of Texas Medical Branch,
Galveston, Texas 77555-0641
The influence of luminal and cytoplasmic Ca2+ on the
ability of ryanodine-sensitive stores to undergo multiple partial
("quantal") releases has been assessed. Increased luminal
Ca2+ levels do indeed modulate sarcoplasmic reticulum
Ca2+ release by lowering the threshold agonist
concentration required to elicit release, but the decrease in luminal
Ca2+ that accompanies a partial release is not sufficient
by itself to terminate release. Similarly, an increase in cytoplasmic
Ca2+ lowers the threshold agonist concentration required to
elicit release; thus, the bulk cytoplasmic Ca2+ levels
attained during a release would only stimulate further release, not
terminate it before it reached completion. Very high cytoplasmic
Ca2+ levels (1-3 mM) also triggered release
but were unable to terminate release before reaching completion. Thus,
even the high local cytoplasmic Ca2+ concentration that
might accompany release would also not terminate release. It is
concluded that Ca2+ feedback can modulate release through
ryanodine receptors but that it does not account for the properties of
quantal release. The low affinity inhibitor tetracaine induces a
decrease in the extent of release that cannot be explained solely by
heterogeneous caffeine sensitivity of the stores. The results are
interpreted in terms of a scheme that includes (i) heterogeneous
sensitivity of stores, conferred in part by differences in luminal
Ca2+ content and (ii) adaptive behavior on the part of
individual ryanodine receptors.
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