Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 568, Issue 3, Pages 867-880Publisher
WILEY
DOI: 10.1113/jphysiol.2005.089318
Keywords
-
Categories
Funding
- NIAMS NIH HHS [AR25201, R56 AR047664, R01 AR047664, AR47664] Funding Source: Medline
- NIGMS NIH HHS [T32 GM008042, GM08042] Funding Source: Medline
Ask authors/readers for more resources
Using a two-microelectrode voltage clamp technique, we investigated possible mechanisms underlying the impaired excitation-contraction coupling in skeletal muscle fibres of the mdx mouse, a model of the human disease Duchenne muscular dystrophy. We evaluated the role of the transverse tubular system (T-system) by using the potentiometric indicator di-8 ANEPPS, and that of the sarcoplasmic reticulum (SR) Ca2+ release by measuring Ca2+ transients with a low affinity indicator in the presence of high EGTA concentrations under voltage clamp conditions. We observed minimal differences in the T-system structure and the T-system electrical propagation was not different between normal and mdx mice. Whereas the maximum Ca2+ release elicited by voltage pulses was reduced by similar to 67% in mdx fibres, in agreement with previous results obtained using AP stimulation, the voltage dependence of SR Ca2+ release was identical to that seen in normal fibres. Taken together, our data suggest that the intrinsic ability of the sarcoplasmic reticulum to release Ca2+ may be altered in the mdx mouse.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available