scholarly journals The IQ Motif is Crucial for Cav1.1 Function

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Katarina Stroffekova
Keyword(s):  
Skeletal Muscle ◽  
High Voltage ◽  
Functional Coupling ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Whole Cell ◽  
Iq Motif ◽  
Contraction Coupling

Ca2+-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca2+channels. The skeletal muscle Cav1.1 also exhibits Ca2+-/CaM-dependent modulation. Here, whole-cell Ca2+current, Ca2+transient, and maximal, immobilization-resistant charge movement(Qmax)recordings were obtained from cultured mouse myotubes, to test a role of IQ motif in function of Cav1.1. The effect of introducing mutation (IQ to AA) of IQ motif into Cav1.1 was examined. In dysgenic myotubes expressing YFP-Cav1.1AA, neither Ca2+currents nor evoked Ca2+transients were detectable. The loss of Ca2+current and excitation-contraction coupling did not appear to be a consequence of defective trafficking to the sarcolemma. TheQmaxin dysgenic myotubes expressing YFP-Cav1.1AAwas similar to that of normal myotubes. These findings suggest that the IQ motif of the Cav1.1 may be an unrecognized site of structural and functional coupling between DHPR and RyR.

Extracellular divalent cations in excitation–contraction coupling: hypertonic solution effects

1982 ◽  
Vol 60 (4) ◽  
pp. 440-445
Author(s):  
Isao Oota ◽  
Isao Kosaka ◽  
Torao Nagai ◽  
Hideyo Yabu
Keyword(s):  
Skeletal Muscle ◽  
Divalent Cations ◽  
Muscle Fibers ◽  
Hypertonic Solution ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Skeletal Muscle Fibers ◽  
Membrane Bound

It is the purpose of this article to point out that the membrane-bound Ca plays an important role in excitation–contraction (E–C) coupling of skeletal muscle fibers and that other divalent cations are unable to substitute for this role of membrane-bound Ca.

scholarly journals The Role of Ryanodine Receptor Phosphorylation in Skeletal Muscle Excitation-Contraction Coupling

2011 ◽  
Vol 100 (3) ◽  
pp. 592a
Author(s):  
Matthew J. Betzenhauser ◽  
Daniel C. Andersson ◽  
Steven Reiken ◽  
Andrew R. Marks
Keyword(s):  
Skeletal Muscle ◽  
Ryanodine Receptor ◽  
Receptor Phosphorylation ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

scholarly journals The role of action potential changes in depolarization-induced failure of excitation contraction coupling in mouse skeletal muscle

eLife ◽  
2022 ◽  
Vol 11 ◽  
Author(s):  
Xueyong Wang ◽  
Murad Nawaz ◽  
Chris DuPont ◽  
Jessica H Myers ◽  
Steve RA Burke ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Simultaneous Recording ◽  
Periodic Paralysis ◽  
Resting Potential ◽  
Charge Movement ◽  
Vigorous Exercise ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Gating Charge ◽  
Rapid Kinetics

Excitation-contraction coupling (ECC) is the process by which electrical excitation of muscle is converted into force generation. Depolarization of skeletal muscle resting potential contributes to failure of ECC in diseases such as periodic paralysis, intensive care unit acquired weakness and possibly fatigue of muscle during vigorous exercise. When extracellular K+ is raised to depolarize the resting potential, failure of ECC occurs suddenly, over a narrow range of resting potentials. Simultaneous imaging of Ca2+ transients and recording of action potentials (APs) demonstrated failure to generate Ca2+ transients when APs peaked at potentials more negative than –30mV. An AP property that closely correlated with failure of the Ca2+ transient was the integral of AP voltage with respect to time. Simultaneous recording of Ca2+ transients and APs with electrodes separated by 1.6mm revealed AP conduction fails when APs peak below –21mV. We hypothesize propagation of APs and generation of Ca2+ transients are governed by distinct AP properties: AP conduction is governed by AP peak, whereas Ca2+ release from the sarcoplasmic reticulum is governed by AP integral. The reason distinct AP properties may govern distinct steps of ECC is the kinetics of the ion channels involved. Na channels, which govern propagation, have rapid kinetics and are insensitive to AP width (and thus AP integral) whereas Ca2+ release is governed by gating charge movement of Cav1.1 channels, which have slower kinetics such that Ca2+ release is sensitive to AP integral. The quantitative relationships established between resting potential, AP properties, AP conduction and Ca2+ transients provide the foundation for future studies of failure of ECC induced by depolarization of the resting potential.

Role of inositol 1,4,5-trisphosphate in excitation-contraction coupling in skeletal muscle

FEBS Letters ◽  
1986 ◽  
Vol 197 (1-2) ◽  
pp. 1-4 ◽  
Author(s):  
Pompeo Volpe ◽  
Francesco Di Virgilio ◽  
Tullio Pozzan ◽  
Giovanni Salviati
Keyword(s):  
Skeletal Muscle ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Inositol 1,4,5 Trisphosphate
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