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Reduced intramembrane charge movement in the dysgenic skeletal muscle cell
T Shimahara1, R Bournaud, I Inoue
1Laboratoire de Neurobiologie Cellulaire et Moléculaire, CNRS, Gif-sur-Yvette, France.
Abstract:
Intramembrane charge movement in skeletal muscle cells has been proposed to underlie the process leading to Ca release from the sarcoplasmic reticulum. A number of recent studies suggest that the dihydropyridine receptor located in the transverse-tubular membrane is responsible for the generation of intramembrane charge movement. The skeletal muscle cell of the mutant mouse with "Muscular Dysgenesis" is characterized by absence of excitation-contraction coupling. Here we investigated the charge movement in freshly dissociated skeletal muscle cells from dysgenic mice. In 9 out of 34 dysgenic mouse cells the charge movement was completely absent, in the remaining cells the charge movement was never more than 30% of control. The amount of maximum charge movement (Qmax) in mutant muscle cells was less than 30% of Qmax in normal muscle. Nifedipine, a dihydropyridine derivative, reduced the amount of charge movement in normal muscle cells but it was less effective on charge movement in mutant muscle cells. We conclude that there is an alteration of nifedipine-sensitive charge movement in the skeletal muscle cells from the mutant mice.
Insights
Intramembrane charge movement, crucial for muscle contraction, is significantly reduced in dysgenic mice. This suggests a critical role for the dihydropyridine receptor in this process.
Area of Science:
- Muscle physiology
- Cellular electrophysiology
- Molecular biology
Background:
- Intramembrane charge movement in skeletal muscle cells is linked to calcium release from the sarcoplasmic reticulum.
- The dihydropyridine receptor is implicated in generating this charge movement.
Purpose of the Study:
- Investigate charge movement in skeletal muscle cells from "Muscular Dysgenesis" mutant mice.
- Determine the role of the dihydropyridine receptor in excitation-contraction coupling.
Main Methods:
- Electrophysiological recordings of charge movement in freshly dissociated skeletal muscle cells.
- Comparison of charge movement in dysgenic and normal mouse cells.
- Assessment of nifedipine's effect on charge movement.
Main Results:
- Charge movement was absent or significantly reduced (less than 30% of control) in 9 out of 34 dysgenic mouse cells.
- Maximum charge movement (Qmax) in mutant cells was less than 30% of normal.
- Nifedipine was less effective in reducing charge movement in mutant cells compared to normal cells.
Conclusions:
- Skeletal muscle cells from dysgenic mice exhibit altered nifedipine-sensitive charge movement.
- These findings support the involvement of the dihydropyridine receptor in intramembrane charge movement and excitation-contraction coupling.