Transient loss of voltage control of Ca2+ release in the presence of maurocalcine in skeletal muscle
Biophysical Journal. 2006-09-01; 91(6): 2206-2215
DOI: 10.1529/biophysj.105.078089
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Pouvreau S(1), Csernoch L, Allard B, Sabatier JM, De Waard M, Ronjat M,
Jacquemond V.
Author information:
(1)Physiologie Intégrative Cellulaire et Moléculaire, Université Claude Bernard
Lyon 1, UMR CNRS 5123, Bâtiment Raphael Dubois, 43 boulevard du 11 novembre
1918, F 69622 Villeurbanne Cedex, France.
In skeletal muscle, sarcoplasmic reticulum (SR) calcium release is controlled by
the plasma membrane voltage through interactions between the voltage-sensing
dihydropyridine receptor (DHPr) and the ryanodine receptor (RYr) calcium release
channel. Maurocalcine (MCa), a scorpion toxin peptide presenting some homology
with a segment of a cytoplasmic loop of the DHPr, has been previously shown to
strongly affect the activity of the isolated RYr. We injected MCa into mouse
skeletal muscle fibers and measured intracellular calcium under voltage-clamp
conditions. Voltage-activated calcium transients exhibited similar properties in
control and in MCa-injected fibers during the depolarizing pulses, and the
voltage dependence of calcium release was similar under the two conditions.
However, MCa was responsible for a pronounced sustained phase of Ca(2+)
elevation that proceeded for seconds following membrane repolarization, with no
concurrent alteration of the membrane current. The magnitude of the underlying
uncontrolled extra phase of Ca(2+) release correlated well with the peak calcium
release during the pulse. Results suggest that MCa binds to RYr that open on
membrane depolarization and that this interaction specifically alters the
process of repolarization-induced closure of the channels.
DOI: 10.1529/biophysj.105.078089
PMCID: PMC1557560
PMID: 16782801 [Indexed for MEDLINE]