scholarly journals Minor sarcoplasmic reticulum membrane components that modulate excitation-contraction coupling in striated muscles

2009 ◽  
Vol 587 (13) ◽  
pp. 3071-3079 ◽  
Author(s):  
Susan Treves ◽  
Mirko Vukcevic ◽  
Marcin Maj ◽  
Raphael Thurnheer ◽  
Barbara Mosca ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Striated Muscles ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Sarcoplasmic Reticulum Membrane ◽  
Membrane Components

Membranes, calcium, and coupling

1987 ◽  
Vol 65 (4) ◽  
pp. 686-690 ◽  
Author(s):  
R. S. Eisenberg
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Electrical Coupling ◽  
Eukaryotic Cell ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Sarcoplasmic Reticulum Membrane ◽  
Voltage Change ◽  
Membrane Compartments ◽  
T System

Every eukaryotic cell contains systems linking the extracellular space and internal membrane compartments. These systems allow cells to communicate and, ultimately they allow the nervous system to control most of the cytoplasmic activity. In skeletal muscle, this system is called "excitation–contraction coupling." While much is known of the early and late steps in coupling, the critical link between the cell (i.e., here the T system) membrane and sarcoplasmic reticulum membrane is not known. Electrical coupling cannot easily account for experimental results; here we show that the Ca2+ influx is not causally related to the excitation–contraction coupling. The most likely mechanism seems to be a variant of the "remote control model" in which a voltage change and accompanying charge movement in the T membrane activates an enzyme tethered to the cytoplasmic leaflet of the T membrane but spanning part of the T – sarcoplasmic reticulum gap.

Ryanodine receptors of striated muscles: a complex channel capable of multiple interactions

1997 ◽  
Vol 77 (3) ◽  
pp. 699-729 ◽  
Author(s):  
C. Franzini-Armstrong ◽  
F. Protasi
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Striated Muscle ◽  
Surface Membrane ◽  
Ryanodine Receptors ◽  
Striated Muscles ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Dihydropyridine Receptors ◽  
Long Range Interactions ◽  
Cardiac Muscles

The ryanodine receptor (RyR) is a high-conductance Ca2+ channel of the sarcoplasmic reticulum in muscle and of the endoplasmic reticulum in other cells. In striated muscle fibers, RyRs are responsible for the rapid release of Ca2+ that activates contraction. Ryanodine receptors are complex molecules, with unusually large cytoplasmic domains containing numerous binding sites for agents that control the state of activity of the channel-forming domain of the molecule. Structural considerations indicate that long-range interactions between cytoplasmic and intramembrane domains control channel function. Ryanodine receptors are located in specialized regions of the SR, where they are structurally and functionally associated with other intrinsic proteins and, indirectly, also with the luminal Ca2(+)-binding protein calsequestrin. Activation of RyRs during the early part of the excitation-contraction coupling cascade is initiated by the activity of surface-membrane Ca2+ channels, the dihydropyridine receptors (DHPRs). Skeletal and cardiac muscles contain different RyR and DHPR isoforms and both contribute to the diversity in cardiac and skeletal excitation-contraction coupling mechanisms. The architecture of the sarcoplasmic reticulum-surface junctions determines the types of RyR-DHPR interactions in the two muscle types.

Localisation of intracellular calcium stores in the striated muscles of the jellyfishPolyorchis penicillatus: possible involvement in excitation–contraction coupling

2001 ◽  
Vol 204 (21) ◽  
pp. 3727-3736 ◽  
Author(s):  
Y.-C. James Lin ◽  
Andrew N. Spencer
Keyword(s):  
Energy Loss ◽  
Electron Energy Loss Spectroscopy ◽  
Potassium Dichromate ◽  
Calcium Stores ◽  
Striated Muscles ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Membrane Bound ◽  
Electron Energy Loss ◽  
Sarcolemmal Vesicles

SUMMARYWhen jellyfish striated muscles were stimulated directly, the amplitude of contractile tension increased as the stimulation frequency increased. Application of 10 mmol l–1 caffeine reduced the amplitude of contractile tension and abolished this facilitatory relationship, indicating that calcium stores participate in excitation–contraction coupling. Calcium stores were identified ultrastructurally using enzymatic histochemistry to localize CaATPases, and potassium dichromate to precipitate calcium. Electron energy-loss spectroscopy was used to verify the presence of calcium in precipitates. Both CaATPase and calcium were localised in membrane-bound vesicles beneath the sarcolemma. We concluded that sub-sarcolemmal vesicles could act as calcium stores and participate in excitation–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.

scholarly journals THE ULTRASTRUCTURE OF FROG VENTRICULAR CARDIAC MUSCLE AND ITS RELATIONSHIP TO MECHANISMS OF EXCITATION-CONTRACTION COUPLING

1968 ◽  
Vol 38 (1) ◽  
pp. 99-114 ◽  
Author(s):  
Nancy A. Staley ◽  
Ellis S. Benson
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Striated Muscle ◽  
Structural Features ◽  
Mammalian Skeletal Muscle ◽  
Striated Muscles ◽  
Thin Filaments ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Dense Granules

Frog ventricular cardiac muscle has structural features which set it apart from frog and mammalian skeletal muscle and mammalian cardiac muscle. In describing these differences, our attention focused chiefly on the distribution of cellular membranes. Abundant inter cellular clefts, the absence of tranverse tubules, and the paucity of sarcotubules, together with exceedingly small cell diameters (less than 5 µ), support the suggestion that the mechanism of excitation-contraction coupling differs in these muscle cells from that now thought to be characteristic of striated muscle such as skeletal muscle and mammalian cardiac muscle. These structural dissimilarities also imply that the mechanism of relaxation in frog ventricular muscle differs from that considered typical of other striated muscles. Additional ultrastructural features of frog ventricular heart muscle include spherical electron-opaque bodies on thin filaments, inconstantly present, forming a rank across the I band about 150 mµ from the Z line, and membrane-bounded dense granules resembling neurosecretory granules. The functional significance of these features is not yet clear.

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