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Am J Physiol Cell Physiol 281: C690-C699, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 2, C690-C699, August 2001

Stretch-activated cation channels in skeletal muscle myotubes from sarcoglycan-deficient hamsters

Tomoe Y. Nakamura1,3, Yuko Iwata1, Maurilio Sampaolesi1, Hironori Hanada1, Naohiro Saito2, Michael Artman3,4, William A. Coetzee3,4, and Munekazu Shigekawa1

1 Department of Molecular Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565; 2 Research Institute, Kowa Company, Higashimurayama, Tokyo 189-0022, Japan; and 3 Pediatric Cardiology and 4 Physiology and Neurosciences, New York University School of Medicine, New York, New York 10016

Deficiency of delta -sarcoglycan (delta -SG), a component of the dystrophin-glycoprotein complex, causes cardiomyopathy and skeletal muscle dystrophy in Bio14.6 hamsters. Using cultured myotubes prepared from skeletal muscle of normal and Bio14.6 hamsters (J2N-k strain), we investigated the possibility that the delta -SG deficiency may lead to alterations in ionic conductances, which may ultimately lead to myocyte damage. In cell-attached patches (with Ba2+ as the charge carrier), an ~20-pS channel was observed in both control and Bio14.6 myotubes. This channel is also permeable to K+ and Na+ but not to Cl-. Channel activity was increased by pressure-induced stretch and was reduced by GdCl3 (>5 µM). The basal open probability of this channel was fourfold higher in Bio14.6 myotubes, with longer open and shorter closed times. This was mimicked by depolymerization of the actin cytoskeleton. In intact Bio14.6 myotubes, the unidirectional basal Ca2+ influx was enhanced compared with control. This Ca2+ influx was sensitive to GdCl3, signifying that stretch-activated cation channels may have been responsible for Ca2+ influx in Bio14.6 hamster myotubes. These results suggest a possible mechanism by which cell damage might occur in this animal model of muscular dystrophy.

muscular dystrophy; calcium; cell membrane


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