Development of the Excitation-Contraction Coupling Apparatus in Skeletal Muscle: Association of Sarcoplasmic Reticulum and Transverse Tubules with Myofibrils

1993 ◽  
Vol 160 (1) ◽  
pp. 135-147 ◽  
Author(s):  
Bernhard E. Flucher ◽  
Hiroaki Takekura ◽  
Clara Franzini-Armstrong
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Transverse Tubules ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

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.

Potentiation of the halothane-cooling contractures of mammalian muscles by denervation

1990 ◽  
Vol 68 (9) ◽  
pp. 1207-1213 ◽  
Author(s):  
Margarete M. Trachez ◽  
R. Takashi Sudo ◽  
G. Suarez-Kurtz
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Soleus Muscle ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Denervated Muscles

Denervation potentiated the cooling-induced contractures and the halothane-cooling contractures of isolated extensor digitorum longus and soleus muscles of the mouse. These effects were more striking in extensor digitorum longus than in soleus muscles. Significant increases in the peak amplitudes of the halothane-cooling contractures of both muscles and of the cooling contractures of soleus muscle were observed within 2 and 7 days of denervation. The potentiation of the contractures persisted for 90 days, the period of this study. Denervation (>2 days) endowed extensor digitorum longus with the ability to generate cooling contractures in the absence of halothane. The rate of tension development of cooling-induced contractures in the absence or presence of halothane was significantly greater in denervated (2–90 days) than in innervated muscles. Denervation also reduced the effectiveness of procaine in inhibiting the halothane-cooling contractures. It is proposed that the potentiation of cooling-induced contractures in denervated muscles results primarily from an increase in the rate of efflux and in the quantity of Ca2+ released from the sarcoplasmic reticulum, upon cooling and (or) when challenged with halothane.Key words: denervation, excitation–contraction coupling, halothane, cooling-induced contractures, skeletal muscle.

The Chemical Transmission Mechanism of Excitation-Contraction Coupling in Skeletal Muscle

Physiology ◽  
1987 ◽  
Vol 2 (5) ◽  
pp. 182-186 ◽  
Author(s):  
J Vergara ◽  
K Asotra
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Calcium Release ◽  
Transmission Mechanism ◽  
Temperature Dependent ◽  
Transverse Tubules ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Vertebrate Muscle ◽  
Inositol 1,4,5 Trisphosphate

There is a temperature-dependent lag between depolarization of transverse tubules by the action potential and onset of calcium release from the sacromplasmic reticulum that reveals the occurrence of a chemical step in excitation-contraction coupling. Recent studies suggest that in vertebrate muscle inositol 1,4,5-trisphosphate may act as a chemical link in this process.

Voltage Sensors and Calcium Channels of Excitation-Contraction Coupling

Physiology ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 223-227 ◽  
Author(s):  
E Rios ◽  
G Pizarro
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Channels ◽  
Action Potential ◽  
Structural Data ◽  
Excitation Contraction Coupling ◽  
Voltage Sensors ◽  
Contraction Coupling ◽  
Chemical Mediation ◽  
Mechanical Connection

Three mechanisms are proposed for the transduction from action potential to Ca2+ release from the sarcoplasmic reticulum in skeletal muscle: Chemical mediation, a mechanical connection between transverse tubular membrane and sacroplasmic reticulum, and Ca2+-induced release of Ca2+. New biochemical, biophysical, and structural data favor a mechanical connection and add the possibility that Ca2+-induced Ca2+-release is working in parallel.

scholarly journals SRP-27 is a novel component of the supramolecular signalling complex involved in skeletal muscle excitation–contraction coupling

2008 ◽  
Vol 411 (2) ◽  
pp. 343-349 ◽  
Author(s):  
Christophe Bleunven ◽  
Susan Treves ◽  
Xia Jinyu ◽  
Elisa Leo ◽  
Michel Ronjat ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Western Blot ◽  
Primary Structure ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Macromolecular Complex ◽  
Cdna Clones ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

SRP-27 (sarcoplasmic reticulum protein of 27 kDa) is a newly identified integral membrane protein constituent of the skeletal muscle SR (sarcoplasmic reticulum). We identified its primary structure from cDNA clones isolated from a mouse skeletal muscle cDNA library. ESTs (expressed sequence tags) of SRP-27 were found mainly in cDNA libraries from excitable tissues of mouse. Western blot analysis confirmed the expression of SRP-27 in skeletal muscle and, to a lower extent, in heart and brain. Mild trypsin proteolysis combined with primary-structure prediction analysis suggested that SRP-27 has four transmembrane-spanning alpha helices and its C-terminal domain faces the cytoplasmic side of the endo(sarco)plasmic reticulum. The expression of SRP-27 is higher in fast twitch skeletal muscles compared to slow twitch muscles and peaks during the first month of post-natal development. High-resolution immunohistochemistry and Western blot analysis of subcellular fractions indicated that SRP-27 is distributed in both longitudinal tubules and terminal cisternae of the SR, as well as in the perinuclear membrane systems and the nuclear envelope of myotubes and adult fibres. SRP-27 co-sediments with the RyR (ryanodine receptor) macromolecular complex in high-salt sucrose-gradient centrifugation, and is pulled-down by anti-RyR as well as by maurocalcin, a well characterized RyR modulator. Our results indicate that SRP-27 is part of a SR supramolecular complex, suggesting the involvement of SRP-27 in the structural organization or function of the molecular machinery underlying excitation–contraction coupling.

Avian Extended Junctional SR: 3-D Geometry Rendered in Stereo

1997 ◽  
Vol 3 (S2) ◽  
pp. 247-248
Author(s):  
J.R. Sommer ◽  
T. High ◽  
P. Ingram ◽  
D. Kopf ◽  
R. Nassar ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Muscle Contraction ◽  
Cardiac Myocytes ◽  
Ryanodine Receptor ◽  
Transverse Tubules ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Junctional Sarcoplasmic Reticulum ◽  
Invariant Differentiation

Extended junctional sarcoplasmic reticulum (EJSR) is an invariant differentiation of the sarcoplasmic reticulum (SR) in bird cardiac myocytes (CM) and central to excitation-contraction coupling (ECC). EJSR occurs as both continuous and discontinuous extensions of junctional sarcoplasmic reticulum (JSR), and surrounds and pervades the Z/I band as the “ EJSR Z-rete” whose geometry has mechanistic implications for the function of “couplings” in ECC, in general. “Peripheral coupling(s)” (PC) in birds, and the additional “interior coupling(s)” (IC) at transverse tubules (TT) in mammals, are formed by tight apposition to plasmalemma of JSR, a specialized calcium (Ca) store of the SR. Free SR (FSR; i.e. free of JSR/EJSR specializations) is the rest of the smooth, tubular SR network, which connects intercalated patches of EJSR forming the EJSR Z-retes and, elsewhere, displays both longitudinal and transverse geometries in surrounding the contractile material for the purpose of sequestering Ca after each muscle contraction. Except for EJSR having no plasmalemmal contact, morphologically, EJSR and JSR are homologues:1 both have similar sizes; are studded (approx. 32 nm center-to-center) with junctional processes (JP; ryanodine receptor (RyR)/-Ca-release channels);

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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