Journal article
Modulation of L-type Ca2+ current but not activation of Ca2+ release by the gamma1 subunit of the dihydropyridine receptor of skeletal muscle
BMC physiology, Vol.1(1), pp.8-8
07/24/2001
DOI: 10.1186/1472-6793-1-8
PMID: 11495636
Abstract
BACKGROUND: The multisubunit (α1S,α2-δ, β1a and γ1) skeletal muscle dihydropyridine receptor (DHPR) transduces membrane depolarization into release of Ca2+ from the sarcoplasmic reticulum (SR) and also acts as an L-type Ca2+ channel. To more fully investigate the function of the γ1 subunit in these two processes, we produced mice lacking this subunit by gene targeting. RESULTS: Mice lacking the DHPR γ1 subunit (γ1 null) survive to adulthood, are fertile and have no obvious gross phenotypic abnormalities. The γ1 subunit is expressed at approximately half the normal level in heterozygous mice (γ1 het). The density of the L-type Ca2+ current in γ1 null and γ1 het myotubes was higher than in controls. Inactivation of the Ca2+ current produced by a long depolarization was slower and incomplete in γ1 null and γ1 het myotubes, and was shifted to a more positive potential than in controls. However, the half-activation potential of intramembrane charge movements was not shifted, and the maximum density of the total charge was unchanged. Also, no shift was observed in the voltage-dependence of Ca2+ transients. γ1 null and γ1 het myotubes had the same peak Ca2+ amplitude vs. voltage relationship as control myotubes. CONCLUSIONS: The L-type Ca2+ channel function, but not the SR Ca2+ release triggering function of the skeletal muscle dihydropyridine receptor, is modulated by the γ1 subunit.
Details
- Title: Subtitle
- Modulation of L-type Ca2+ current but not activation of Ca2+ release by the gamma1 subunit of the dihydropyridine receptor of skeletal muscle
- Creators
- Chris AhernPatricia PowersGloria BiddlecomeLaura RoethePaola VallejoLindsay MortensonCaroline StrubeKevin CampbellRoberto CoronadoRonald Gregg
- Resource Type
- Journal article
- Publication Details
- BMC physiology, Vol.1(1), pp.8-8
- Publisher
- BioMed Central Ltd
- DOI
- 10.1186/1472-6793-1-8
- PMID
- 11495636
- ISSN
- 1472-6793
- eISSN
- 1472-6793
- Language
- English
- Date published
- 07/24/2001
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Iowa Neuroscience Institute
- Record Identifier
- 9984068269702771
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