ArticleThe Journal of physiology2001
Excitation-contraction coupling in skeletal muscle of a mouse lacking the dihydropyridine receptor subunit gamma1.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Age-dependent loss of Crls1 causes myopathy and skeletal muscle regeneration failure.Experimental & molecular medicine · 2024Article
- From α1s splicing to γ1 function: A new twist in subunit modulation of the skeletal muscle L-type Ca2+ channel.The Journal of general physiology · 2022Article
- Calcium current modulation by the γ1 subunit depends on alternative splicing of CaV1.1.The Journal of general physiology · 2022Article
- FABP3-mediated membrane lipid saturation alters fluidity and induces ER stress in skeletal muscle with aging.Nature communications · 2020Article
- A subset of microRNAs in the Dlk1-Dio3 cluster regulates age-associated muscle atrophy by targeting Atrogin-1.Journal of cachexia, sarcopenia and muscle · 2020Article
- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
- Optogenetic approach for targeted activation of global calcium transients in differentiated C2C12 myotubes.Scientific reports · 2017Article
- The CaNature communications · 2017Article
- Stac3 has a direct role in skeletal muscle-type excitation-contraction coupling that is disrupted by a myopathy-causing mutation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- Structure-function of proteins interacting with the α1 pore-forming subunit of high-voltage-activated calcium channels.Frontiers in physiology · 2014Review
- Divergent biophysical properties, gating mechanisms, and possible functions of the two skeletal muscle Ca(V)1.1 calcium channel splice variants.Journal of muscle research and cell motility · 2011Article
- Effects of inserting fluorescent proteins into the alpha1S II-III loop: insights into excitation-contraction coupling.The Journal of general physiology · 2009Article
- Proper restoration of excitation-contraction coupling in the dihydropyridine receptor beta1-null zebrafish relaxed is an exclusive function of the beta1a subunit.The Journal of biological chemistry · 2009Article
- The alpha(1S) III-IV loop influences 1,4-dihydropyridine receptor gating but is not directly involved in excitation-contraction coupling interactions with the type 1 ryanodine receptor.The Journal of biological chemistry · 2008Article
- Differentiation-dependent alterations in the extracellular ATP-evoked calcium fluxes of cultured skeletal muscle cells from mice.Pflugers Archiv : European journal of physiology · 2007Article
- Mini-dystrophin expression down-regulates IP3-mediated calcium release events in resting dystrophin-deficient muscle cells.The Journal of general physiology · 2006Article
- Mini-dystrophin expression down-regulates overactivation of G protein-mediated IP3 signaling pathway in dystrophin-deficient muscle cells.The Journal of general physiology · 2006Article
- Functional roles of the gamma subunit of the skeletal muscle DHP-receptor.Journal of muscle research and cell motility · 2006Review
- Functional interaction of CaV channel isoforms with ryanodine receptors studied in dysgenic myotubes.Biophysical journal · 2005Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. In skeletal muscle, dihydropyridine (DHP) receptors control both Ca(2+) entry (L-type current) and internal Ca(2+) release in a voltage-dependent manner. Here we investigated the question of whether elimination of the skeletal muscle-specific DHP receptor subunit gamma1 affects excitation-contraction (E-C) coupling. We studied intracellular Ca(2+) release and force production in muscle preparations of a mouse deficient in the gamma1 subunit (gamma-/-). 2. The rate of internal Ca(2+) release at large depolarization (+20 mV) was determined in voltage-clamped primary-cultured myotubes derived from satellite cells of adult mice by analysing fura-2 fluorescence signals and estimating the concentration of free and bound Ca(2+). On average, gamma-/- cells showed an increase in release of about one-third of the control value and no alterations in the time course. 3. Voltage of half-maximal activation (V(1/2)) and voltage sensitivity (k) were not significantly different in gamma-/- myotubes, either for internal Ca(2+) release activation or for the simultaneously measured L-type Ca(2+) conductance. The same was true for maximal Ca(2+) inward current and conductance. 4. Contractions evoked by electrical stimuli were recorded in isolated extensor digitorum longus (EDL; fast, glycolytic) and soleus (slow, oxidative) muscles under normal conditions and during fatigue induced by repetitive tetanic stimulation. Neither time course nor amplitudes of twitches and tetani nor force-frequency relations showed significant alterations in the gamma1-deficient muscles. 5. In conclusion, the overall results show that the gamma1 subunit is not essential for voltage-controlled Ca(2+) release and force production.
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