Voltage Dependent Charge Movement in Skeletal Muscle: a Possible Step in Excitation–Contraction Coupling

Nature ◽  
1973 ◽  
Vol 242 (5395) ◽  
pp. 244-246 ◽  
Author(s):  
M. F. SCHNEIDER ◽  
W. K. CHANDLER
Keyword(s):  
Skeletal Muscle ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Voltage Dependent

Calmodulin and Excitation-Contraction Coupling

Physiology ◽  
2000 ◽  
Vol 15 (6) ◽  
pp. 281-284 ◽  
Author(s):  
Susan L. Hamilton ◽  
Irina Serysheva ◽  
Gale M. Strasburg
Keyword(s):  
Skeletal Muscle ◽  
Ion Channels ◽  
Sarcoplasmic Reticulum ◽  
Release Channel ◽  
Excitation Contraction Coupling ◽  
Transverse Tubule ◽  
Contraction Coupling ◽  
Voltage Dependent ◽  
Important Regulator ◽  
Precise Role

Excitation-contraction coupling in cardiac and skeletal muscle involves the transverse-tubule voltage-dependent Ca2+ channel and the sarcoplasmic reticulum Ca2+ release channel. Both of these ion channels bind and are modulated by calmodulin in both its Ca2+-bound and Ca2+-free forms. Calmodulin is, therefore, potentially an important regulator of excitation-contraction coupling. Its precise role, however, has not yet been defined.

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.

scholarly journals Separation of intramembrane charging components in low-calcium solutions in frog skeletal muscle.

1991 ◽  
Vol 98 (2) ◽  
pp. 249-263 ◽  
Author(s):  
C L Huang
Keyword(s):  
Voltage Dependence ◽  
Charge Movement ◽  
Pharmacological Effects ◽  
Frog Skeletal Muscle ◽  
Calcium Signals ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Charge Movements

The inactivation of charge movement components by small (-100 to -70 mV) shifts in holding potential was examined in voltage-clamped intact amphibian muscle fibers in low [Ca2+], Mg(2+)-containing solutions. The pulse protocols used both large voltage excursions and smaller potential steps that elicited prolonged (q gamma) transients. Charge species were distinguished through the pharmacological effects of tetracaine. These procedures confirmed earlier observations in cut fibers and identified the following new properties of the q gamma charge. First, q gamma, previously defined as the tetracaine-sensitive charge, is also the component primarily responsible for the voltage-dependent inactivation induced by conditions of low extracellular [Ca2+]. Second, this inactivation separates a transient that includes a "hump" component and which has kinetics and a voltage dependence distinct from the monotonic decay that remains. Third, q gamma, previously associated with delayed charge movements, can also contribute significant charge transfer at early times. These findings suggest that the parallel inhibition of calcium signals and charge movements reported in low [Ca2+] solutions arises from influences on q gamma charge (Brum et al., 1988a, b). They also reconcile reports that implicate tetracaine-sensitive (q gamma) charge in excitation-contraction coupling with evidence that early intramembrane events are also involved in this process (Pizarro et al., 1989). Finally, they are relevant to hypotheses of possible feedback or feed-forward roles of q gamma in excitation-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.

scholarly journals Electrical models of excitation-contraction coupling and charge movement in skeletal muscle.

1980 ◽  
Vol 76 (1) ◽  
pp. 1-31 ◽  
Author(s):  
R T Mathias ◽  
R A Levis ◽  
R S Eisenberg
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Ionic Current ◽  
Charge Movement ◽  
Transient Currents ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Intramembrane Charge Movement ◽  
Terminal Cisternae ◽  
T System

The consequences of ionic current flow from the T system to the sarcoplasmic reticulum (SR) of skeletal muscle are examined. The Appendix analyzes a simple model in which the conductance gx, linking T system and SR, is in series with a parallel resistor and capacitor having fixed values. The conductance gx is supposed to increase rapidly with depolarization and to decrease slowly with repolarization. Nonlinear transient currents computed from this model have some of the properties of gating currents produced by intramembrane charge movement. In particular, the integral of the transient current upon depolarization approximates that upon repolarization. Thus, equality of nonlinear charge movement can occur without intramembrane charge movement. A more complicated model is used in the text to fit the structure of skeletal muscle and other properties of its charge movement. Rectification is introduced into gx and the membrane conductance of the terminal cisternae to give asymmetry in the time-course of the transient currents and saturation in the curve relating charge movement to depolarization, respectively. The more complex model fits experimental data quite well if the longitudinal tubules of the sarcoplasmic reticulum are isolated from the terminal cisternae by a substantial resistance and if calcium release from the terminal cisternae is, for the most part, electrically silent. Specific experimental tests of the model are proposed, and the implications for excitation-contraction coupling are discussed.

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