The calcium homeostasis and the membrane potential of cultured muscle cells from patients with myotonic dystrophy
| Autor: | E. M. G. Joosten, Peter van Mier, A.A.G.M. Benders, Alga E.M. Jacobs, Arie Oosterhof, Ron A. Wevers, Jacques H. Veerkamp |
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| Rok vydání: | 1990 |
| Předmět: |
Adult
Male Cytoplasm medicine.medical_specialty Nifedipine Biology Microtubules Muscular Dystrophies Membrane Potentials Internal medicine medicine Homeostasis Humans Myocyte Molecular Biology Cells Cultured Calcium metabolism Membrane potential Myogenesis Muscles Depolarization Middle Aged Acetylcholine Cell biology Endocrinology Molecular Medicine Calcium Female Calcium Channels medicine.drug |
| Zdroj: | Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1096:14-19 |
| ISSN: | 0925-4439 |
| DOI: | 10.1016/0925-4439(90)90006-b |
| Popis: | Using the fluorescence indicator, quin2, we compared the cytoplasmic Ca 2+ concentration ([Ca 2+ ] i ) of cultured myotubes obtained from control subjects and myotonic dystrophy (MyD) patients. In Ca 2+ -free buffer the [Ca 2+ ] i of the cultured MyD muscle cells was not significantly different from that of the control cells. In the presence of 1 mM external Ca 2+ the cultured MyD muscle cells showed a significantly higher [Ca 2+ ] i , which was due to the influx of Ca 2+ through voltage-operated nifedipine-sensitive Ca 2+ channels. In the presence of external Ca 2+ , MyD myotubes did not respond to acetylcholine, whereas control myotubes showed a transient increase in [Ca 2+ ] i after addition of acetylcholine. This increase was inhibited by the addition of nifedipine. The difference in Ca 2+ -homeostasis between cultured MyD muscle cells and control cells were not due to differences in the resting membrane potential or the inability of the MyD cells to depolarize as a response to acetylcholine. Therefore, culltured MyD muscle cells exhibit altered nifedipine-sensitive voltage-operated channels which are active under conditions in which they are normally present in the inactivie state, and which are unable to respond to depolarization cause by acetylcholine. |
| Databáze: | OpenAIRE |
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