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Ca2+ entry through acetylcholine receptor channel in dysgenic myotubes
K Melliti1, R Bournaud, T Shimahara
1Laboratoire de Neurobiologie Cellulaire et Moléculaire CNRS, Gif-sur-Yvette, France.
Archives of Physiology and Biochemistry
|January 1, 1996
Summary
Skeletal muscles lacking dihydropyridine receptors show uncoupled excitation-contraction. Calcium entry via acetylcholine (ACh) receptors is normal in these dysgenic muscles, suggesting other mechanisms drive contraction.
Area of Science:
- Neuroscience
- Muscle Physiology
- Molecular Biology
Background:
- Muscular dysgenesis in mice results in excitation-contraction uncoupling due to absent dihydropyridine receptors.
- Contraction in dysgenic myotubes can be induced by nerve stimulation or acetylcholine (ACh) application.
- These contractions are linked to calcium (Ca2+) influx through ACh receptor channels.
Purpose of the Study:
- To compare calcium entry through ACh receptors in cultured normal and dysgenic myotubes.
- To investigate the mechanisms underlying nerve-stimulated muscle contraction in dysgenic models.
Main Methods:
- Cultured normal and dysgenic mouse myotubes were used.
- Calcium entry through ACh receptors was measured.
- Electrophysiological recordings of ACh-activated ionic channel conductance were performed at elevated external calcium concentrations (110 mM).
Main Results:
- The elementary slope conductance of ACh-activated ionic channels did not differ between normal and dysgenic myotubes.
- This indicates that calcium entry via ACh receptors is not abnormal in dysgenic myotubes.
Conclusions:
- The contraction of dysgenic muscle induced by nerve stimulation is not caused by abnormal calcium entry through ACh receptors.
- Potential mechanisms like sustained high threshold calcium current (Idys) and calcium-induced calcium release may contribute to contractile responses in dysgenic myotubes.