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Received September 1, 2003
Revised September 29, 2003
Accepted after revision October 27, 2003
1 Institute of Physiology & Pathophysiology
2 Catholic University of Louvain
3 University of Washington
* To whom correspondence should be addressed. E-mail: rainer.fink{at}urz.uni-heidelberg.de.
L-type calcium currents (iCa) were recorded using the Two-Micro-Electrode Voltage Clamp technique in single short toe muscle fibres of three different mouse strains: (i) C57/SV129 wild-type mice (wt), (ii) mdx mice (an animal model for Duchenne Muscular Dystrophy, DMD) and (iii) transgenically engineered mini-dystrophin (MinD) containing mdx mice. The activation and inactivation properties of iCa were examined in 2 to 18 months old animals. Ca2+-current densities at 0 mV in mdx fibres increased with age, but were always significantly smaller compared to age-matched wild-type fibres. Time-to-peak (TTP) was prolonged in mdx fibres compared to wt fibres. MinD fibres always showed similar TTP and current amplitudes compared to age-matched wt fibres. In all three genotypes, the voltage dependent inactivation and deactivation of iCa were similar. Intracellular resting calcium concentrations [Ca2+]i and the distribution of Dihydropyridine-binding sites were also not different in young animals of all three genotypes, where iCa was markedly reduced in mdx fibres. We conclude, that dystrophin influences L-type Ca2+ channels via a direct or indirect linkage which may be disrupted in mdx mice and may be crucial for proper excitation-contraction coupling initiating Ca2+ release from the sarcoplasmic reticulum. This linkage seems to be fully restored in the presence of mini-dystrophin.
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