Transient loss of voltage control of Ca2+ release in the presence of maurocalcine in skeletal muscle

Sandrine Pouvreau, Laszlo Csernoch, Bruno Allard, Jean Marc Sabatier, Michel De Waard, Michel Ronjat, Vincent Jacquemond

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Abstract

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 Ca2+ 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.

Original languageEnglish
Pages (from-to)2206-2215
Number of pages10
JournalBiophysical journal
Volume91
Issue number6
DOIs
Publication statusPublished - Jan 1 2006

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ASJC Scopus subject areas

  • Biophysics

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