scholarly journals ROLE OF SUPERFICIALLY MEMBRANE-BOUND CALCIUM ON EXCITATION-CONTRACTION COUPLING IN FROG SKELETAL MUSCLE

1976 ◽  
Vol 26 (2) ◽  
pp. 117-126 ◽  
Author(s):  
Isao OOTA ◽  
Isao KOSAKA ◽  
Torao NAGAI
Keyword(s):  
Skeletal Muscle ◽  
Frog Skeletal Muscle ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Membrane Bound

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.

The Effect of Lanthanum on Excitation–Contraction Coupling in Frog Skeletal Muscle

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Reduced Rate ◽  
Caffeine Contractures

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.

Electromechanical Coupling II. The Effect of Perchlorate Upon Excitation-Contraction Coupling in Frog Skeletal Muscle Fibres

1982 ◽  
Vol 37 (7-8) ◽  
pp. 707-708
Author(s):  
Michael Gomolla ◽  
Gernot Gottschalk ◽  
Hans-Christoph Lüttgau
Keyword(s):  
Skeletal Muscle ◽  
Electromechanical Coupling ◽  
Muscle Fibres ◽  
Frog Skeletal Muscle ◽  
Large Shift ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Inactivation Process ◽  
Skeletal Muscle Fibres ◽  
Kinetics Of

Abstract In single skeletal muscle Fibres perchlorate causes a large shift of the potential dependence of contraction activation to more negative potentials without a corresponding alteration in the kinetics of the inactivation process.

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.

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