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1 Institut fuer Pharmakologie, Medizinische Universitaet Wien, Wien, Austria
2 Institut fuer Zoologie, Universitaet Salzburg, Salzburg, Austria
* To whom correspondence should be addressed. E-mail: karlheinz.hilber{at}meduniwien.ac.at.
Each skeletal muscle of the body contains a unique composition of so-called "fast" and "slow" muscle fibers, each of which specialized for certain challenges. This composition is not static, and the muscle fibers are capable of adapting their molecular composition by altered gene expression (i.e. fiber type conversion). Whereas changes in the expression of contractile proteins and metabolic enzymes in the course of fiber type conversion are well described, very little is known about possible adaptations in the electrophysiological properties of skeletal muscle cells. Such adaptations may involve changes in the expression and/or function of ion channels. In this study, we investigated the effects of fast-to-slow fiber type conversion on currents through voltage-gated Na+ channels in the mouse skeletal muscle cell line C2C12. Prolonged treatment of cells with 25 nM of the Ca2+ ionophore A23187 caused a significant shift in myosin heavy chain isoform expression from the fast isoforms towards the slow isoform indicating fast-to-slow fiber type conversion. Moreover, Na+ current inactivation was significantly altered. Slow inactivation less strongly inhibited the Na+ currents of fast-to-slow fiber type converted cells. Compared to control cells, the Na+ currents of converted cells were more resistant to block by tetrodotoxin, suggesting an enhanced expression of the cardiac Na+ channel isoform Nav1.5 versus the skeletal muscle isoform Nav1.4. These results implicate that fast-to-slow fiber type conversion of skeletal muscle cells involves functional adaptations of their electrophysiological properties.
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